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Sexual & Reproductive Health
Nutrition for Women
Part I: Sexual & Reproductive Health
8th edition • Revised December 2009
by Dale Ames Kline, ms, rd, cnsc, ld
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Nutrition for Women
Part I: Sexual & Reproductive Health
8th Edition – Revised December 2009
By Dale Ames Kline, ms, rd, cnsc, ld
Dale Ames Kline, MS, RD, CNSC, LD president of Nutrition Dimension, Inc., has created
continuing education programs since 1984. A former hospital chief clinical dietitian and
nutrition educator in the WIC program, she has written, edited and presented numerous
continuing education seminars and home study courses and has lectured before international, national, state and local groups of medical, fitness and nutrition professionals. Dale
has been active in local, state and regional dietetics associations, was named “Recognized
Young Dietitian of the Year” in 1984 and awarded "Outstanding Nutrition Entrepreneur
of the Year" in 2001 by the Nutrition Entrepreneurs Practice Group. Dale was elected as
a Professional Issues Delegate to the House of Delegaes of ADA in 2003. Dale resides in
Southern Oregon. Education: BA, Tufts University; MS, University of Missouri.
Important - Read Before Proceeding
EXPIRATION DATE: Students must submit this course for continuing education credit no later
than December 31, 2014. Credit will not be awarded for this course after that date.
Course Code: RD106, CHES106, FIT106, AT106
This course approved for
RD, DTR................. 10 CPEU
CDM............10 Clock Hours
CHES......................10 CECH
ACE.......................... 1.0 CEC
NATA (BOC)..............5 CEU
NSCA-CC................0.7 CEU
ACSM........................10 CEU
CFCS..........................10 PDU
Editing/proofreading: Rich Kline, Gwen Hulbert
Design: Knotwork Graphic Design & Typesetting
© 1988-2010 Nutrition Dimension/Gannett Education, Inc.
No part of this course may be reproduced, duplicated or copied in any way without the written permission of the copyright holder. (See note on Page ii)
Sexual & Reproductive Health
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Sexual & Reproductive Health
iii
Contents
Page
Chapter
1
Introduction
3
Chapter One: Premenstrual Syndrome
What is PMS? • Diagnosing PMS • Causes and treatment • Nutritional factors • Carbohy-
drates • Fats and fatty acids • Placebo effect • Dietary recommendations • Vitamin/Mineral Supplements • Herbs
15
Chapter Two: Oral Contraceptives
How oral contraceptives work • Risks and benefits of OCA • Lipid metabolism •
Protein metabolism • Venous thromboembolytic diseass and strokes • Carbohydrate metabo
lism • Vitamin B6 • Other vitamins • Minerals • Bone mineral density • Dietary recommen
dations
31
Chapter Three: Factors Affecting Pregnancy Outcome
Risk factors • Nutrition and fertility • Diseases in later life • Epigenetics
39
Chapter Four: Physiological Changes which Alter Nutrient Needs
Hormones • Blood • Cardiovascular system • Renal function • Liver • Gastrointestinal system Metabolism • Placenta • Fetal growth and gene regulation • Pregnancy and Ω-3 fatty acids
53
Chapter Five: Nutrient Needs in Pregnancy
Calories • Protein • Fat intake • Fiber and Carbohydrates • Sodium • Iron • Zinc and Iron • Folic acid • Zinc • Calcium • Vitamin D • Fluoride • Vitamin B6 • Other vitamins and minerals
79
Chapter Six: Weight Gain in Pregnancy
Optimal weight gain • Evaluating prepregnancy weight • Weight gain recommendations: Normal weight/underweight/overweight • Weight gain in adolescents • Twin pregnancies,
multiple pregnancies and more • Monitoring weight gain • Counseling principles • Exercise Case studies
101
Chapter Seven: Diet Assessment for Pregnancy
Dietary guidelines • MyPyramid for moms • Calories • Food groups: Meat/meat alternatives Dairy group • Fruits/vegetables • Breads/cereals • Feedback form • Assessing the diet
119
Chapter Eight: Special Diet Problems, Supplementation and Exercise
Weight gain • Nausea & vomiting • Heartburn and constipation • Leg cramps • Non-nutritive
sweeteners • Caffeine • Bariatric surgery • Food safety • Herbs • Adolescent pregnancy Supplementation • Pica • Vegetarian diets • Exercise
139
Chapter Nine: Medical Complications
Calcium, magnesium and preeclampsia • Prostaglandins and preeclampsia • Diabetes • Pathophysiology of diabetes • Classification of diabetes • Diabetes onset prior to pregnancy • Gestational diabetes • Nutritional management of pregestational diabetes
HIV and AIDS
155
Chapter Ten: Alcohol, Tobacco & Other Drugs
Fetal alcohol syndrome • Smoking • Drugs • Use of medication in pregnancy • Street drugs
169
References
183
Appendices
201
Examination
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Learning Objectives
Upon successful completion of this course, the student will be able to:
1.
Explain how PMS is diagnosed.
2.
List three dietary changes that may alleviate symptoms associated with PMS.
3.
Describe the metabolic alterations that occur with use of oral contraceptives, and
three nutrients whose requirements change.
4. Explain the relationship of oral contraceptive use and bone mineral density.
5.
Discuss the impact of the nutritional status of pregnant women on pregnancy outcome.
6.
List three factors which influence the nutritional status of a pregnant woman.
7.
Discuss the relationship of fetal development to nutrient requirements, by trimester.
8.
Identify the proper weight gain for the pregnant woman who at conception is normal weight, underweight or overweight.
9.
Plot the weight gain of a pregnant woman on a prenatal weight gain grid.
10.
List the current intake recommendations during pregnancy for the following nutrients: calories, protein, sodium, iron, folic acid, zinc and calcium.
11. Determine a plan of nutrient supplementation for pregnant women who prior to
pregnancy are well nourished, poorly nourished or anemic.
12. Analyze the diet of a pregnant woman, using a food frequency form, to determine if
it meets the dietary recommendations for pregnancy.
13. Recommend three solutions for the common complaints of pregnancy: nausea, vomiting, heartburn and constipation.
14. Design a diet for a gestational diabetic that has the appropriate number and distribution of calories.
15. Explain the current treatment for preeclampsia and its rationale.
16. Explain the effects of maternal cigarette smoking on the fetus and pregnancy outcome.
17. Identify a safe level of consumption of caffeine and alcohol for the pregnant woman.
18. Discuss the importance of Ω-3 fatty acids in fetal development and preeclampsia and
list four sources in the diet.
Sexual & Reproductive Health
1
Introduction
The role of nutrition in sexual and reproductive health, particularly in healthy
pregnancy and childbearing, is the focus of this course.
In the 21 years since the original version of this course was published, research has
continued to document the important role of nutrition in sexual and reproductive
health. Major studies affirming the importance of folic acid in preventing neural tube
defects in babies, for instance, have confirmed recommendations made in the first
edition of this course and led to the fortification of wheat flour with folic acid beginning
in 1998. This has reduced the number of babies born with neural tube defects. It is
gratifying to see early research leading to positive action which improves quality of life
and prevents problems for women and newborns.
While progress has been made in understanding the cause or causes of premenstrual
syndrome, many questions remain. We will review what is known about PMS, including the
role of nutrition in preventing the symptoms of PMS.
The nutritional effects of oral contraceptive use are now well understood. Numerous metabolic changes occur with the use of oral contraceptives, altering nutrient needs.
Dietary recommendations to ensure proper intake of specific nutrients will be discussed
for women in general and for those women who would like to get pregnant following
discontinuation of the pill. The effect of the third-generation hormones and newer
hormone delivery systems will be reviewed.
The course explains how several factors affect the nutritional needs of the pregnant
woman: physiological changes associated with pregnancy, prepregnancy nutritional
status, and pre-existing diseases and conditions.
Evidence has shown that a mother’s prepregnancy weight and her weight gain
during pregnancy are linked to the birth weight of her child. Low birth weight correlates with increased morbidity and mortality for newborns.
In 2009, because more childbearing women are overweight and obese, which can
Sexual & Reproductive Health
2
effect pregnancy outcome, and more retain gained weight after delivery, the Institute of
Medicine (IOM) and the National Research Council of the National Academies published new guidelines for weight gain during pregnancy, the first since 1990. These are
discussed at length.
The incidence of low birth weight babies has declined over the years — however,
the birthweight of babies is increasing to the point of being unhealthy. Education of
proper nutrition and exercise throughout the childbearing years is stressed in the new
IOM weight gain guidelines, which have been incorporated into this course.
Evidence has been accumulating that nutrition in utero may affect the long term
health of the baby, especially its risk for heart disease, diabetes and hypertension. The
role of epigenetics in pregnancy and the health of offspring is introduced.
Dietary practices that can be modified to affect pregnancy outcome will be examined: intake levels of specific nutrients, weight gain, exercise, smoking, use of alcohol
and drugs, pregnancy-induced hypertension, diabetes and bariatric surgery. How to
manage some of the common problems of pregnancy, such as nausea and vomiting,
heartburn, and leg cramps will be covered.
It has been assumed that most women get adequate vitamin D due to exposure to
the sun, but over the past 10 to 15 years researchers have found that many women
living in northern climates do not make enough vitamin D, and in fact may be deficient.
The section looks at the problems with inadequate vitamin D in pregnancy and how to
ensure adequacy.
MyPyramid, which replaces the Food Guide Pyramid, now has a section for pregnancy and breastfeeding. It is a great interactive tool that provides individualized meal
plans, "MyPyramid Plan for Moms," has a menu planner and many educational resources
to help pregnant women make the best food choices. These plans are now in household
measures — cups and ounces — not "servings." To be consistent with MyPyramid, I have
changed the forms and assessment tools to household measurements as well.
Other information in this edition includes periodontal disease and pregnancy, a
vegetarian food guide pyramid, an appendix on weight gain for twin pregnancies, a
discussion of oxidative stress and preeclampsia, and the new FDA guidelines on fish
consumption during pregnancy. Finally, the latest information on the importance of
drug therapy for pregnant women with HIV/AIDS will be discussed.
This is the eighth edition of this course. It is amazing to me how time flies and how
much more is known about nutrition and pregnancy than when I wrote the first edition,
in 1988. I would like to thank the customers of Nutrition Dimension for their overwhelming support of this course and their positive feedback. I would also like to acknowledge the efforts of Brenda Dobson, MS, RD, for research assistance and her dedication to maternal and child health issues.
Sexual & Reproductive Health
3
Chapter One:
Premenstrual Syndrome
Premenstrual Syndrome (PMS) was first described in 1931 by Robert T. Frank,
MD. The symptoms he documented were similar to those used today to diagnose PMS.
The cause of PMS, according to Frank, was an increase in the plasma concentration, and
decrease in the urine concentration, of sex hormones. He reasoned that the cure was to
reduce the hormone levels, and his treatment was radiation of the ovaries, which may
have successfully treated the disorder, but obviously created a host of new problems.
We've come a long way since then, thankfully.
Understanding of the causes and development of effective treatments for PMS has
continued since 1931, but not as fast as many would like. There was very little research
into PMS until the 1970s. Research greatly expanded in the 1980s and continues. Unfortunately, there are still as many questions as answers.
PMS Facts
• Incidence: 75% of menstruating women complain of symptoms
• 3 to 8% diagnosed using strict diagnostic criteria
• 10 to 15% of women have severe, debilitating symptoms
• Onset of symptoms 7 to 14 days prior to menstruation
• Symptoms disappear within 4 days of menstruation
• Diagnosis should be done prospectively
Barnhart, et al., 1995; Bianchi-Demicheli, 2002
Sexual & Reproductive Health
4
WHAT IS PMS?
One reason for the lack of progress is definition and diagnosis. PMS is a set of symptoms, physiological and psychological, that occurs prior to menstruation. These symptoms
cause physical and behavioral changes that interfere with the lives of the women affected,
but are difficult to quantify. Onset of the symptoms occurs seven to 14 days prior to menstruation and disappears within four days of when menstruation begins (Rapkin, 2003).
("Premenstrual Dysphoric Disorder" (PMDD) is used by some practitioners and
researchers interchangeably with PMS. It is generally considered to be similar to PMS,
but as we will see, it is usually more severe. In this course I will consider PMS and
PMDD one disorder but note when there is a clear distinction between the two.)
The incidence of PMS reported in the literature is 5 to 97 percent of menstruating
women — a range that further illustrates the subjective nature of the condition. It is
generally accepted that between 30 and 60 percent of women have had PMS, but that
number declines drastically to 3 to 8 percent when more strict diagnostic criteria are
applied (Barnhart, et al., 1995; Bianchi-Demicheli, et al., 2002).
Of those women with PMS, 10 to 15 percent have severe symptoms that make it
difficult for them to carry on their normal lives and cause them to seek medical help.
Using a figure of 50 million women of reproductive age in this country, that means 37.5
million have some symptoms and 1.5 to 4 million have diagnosable PMS which has
caused them to seek treatment.
The most common reported symptoms are breast swelling and tenderness, headaches, backaches, skin disorders, weight gain, bloating, mood swings, irritability, depression and anxiety. Other symptoms, although not as common, include food carvings
(sweets, chocolate, salt, carbohydrates), nausea, joint pain, dizziness, lethargy, fatigue,
sleep disturbances and aggression.
Further complicating the problem is women’s reluctance to bring this disorder to
the attention of their physicians. Many feel that their symptoms are solely psychological, not physiological. Unfortunately, that had also been the thinking of much of the
medical community until recently, making it difficult for women to talk about this
disorder. Now, although the cause has not been determined, there is acceptance of this
disorder as a disease and not “all in the minds” of the women affected.
Symptoms of PMS
Breast tenderness
Breast swelling
Weight gain
Headache
Depression
Anxiety
Binge eating
Dizziness
Irritability
Lethargy
Fatigue
Aggression
Hyperalgesia
Cramping
Mood swings
Acne
Joint pain
Nausea
Sleep disturbances
Thirst
Bloating
Sexual & Reproductive Health
5
DIAGNOSING PMS
A PMS diagnosis requires not only symptoms, but a characteristic pattern of onset
and disappearance of symptoms, and severity. The onset of symptoms must correspond
to hormonal changes which occur with the phases of a woman’s menstrual cycle, as
shown in the chart below.
Phases of the Menstrual Cycle
Phase
Menstrual
Mid-follicular
Ovulatory
Luteal
Days of Cycle
0- 7
7 - 14
14 - 21
21 - 28
For a woman to be diagnosed as having PMS, her symptoms must correspond with
the luteal phase of the menstrual cycle, disappear at the onset of or during menstruation
and not reappear for at least a week (Barnhart, et al., 1995; Bianchi-Demicheli, et al.,
2002; Dickerson, et al., 2003). There is a consensus in the medical community that it is
the timing of the appearance and disappearance of the symptoms, rather than any
specific symptoms, that leads to a diagnosis of PMS.
To gather the information needed for a diagnosis, questionnaires asking patients to
rate their symptoms are used. These questionnaire should be prospective, based on
events as they occur. Retrospective questionnaires, based on past events and experiences, are not as valuable as respondents tend to overestimate the presence and severity
of symptoms. Mortola (1990) and other researchers have found that a prospective
inventory is easy to complete and is a valid and reliable diagnostic tool.
Most importantly, a comparison between cycles must be done to determine the
changes in the severity of symptoms within a cycle and between cycles. Therefore, the
questionnaire must be kept for several consecutive menstrual cycles.
The symptoms must be severe enough to interfere with normal functions, i.e.
school, work, social activities, relationships. The American College of Obstetricians and
Gynecologists established criteria to diagnose PMS and PMDD, using the Diagnostic
and Statistical Manual of Mental Disorders (DSM-IV) criteria (Rapkin, 2003):
• PMS: one moderate-to-severe mood symptom and one physical symptom
• PMDD: a total of five symptoms with one severe mood symptom
CAUSES AND TREATMENT
Numerous causes of PMS have been theorized but, to date, none have been
proven. PMS is a probably a complex interaction between ovarian steroid production,
endogenous opioid peptides, central nervous system neurotransmitters, prostaglandins,
peripheral and autonomic nervous systems and endocrine systems, but no one is sure of
the exact mechanisms of action.
Sexual & Reproductive Health
6
Mood changes associated with PMS may be caused in part by the ability of
estrogen and progesterone to act within the brain. Receptors in the brain for both
hormones have been identified, as has their ability to stimulate or inhibit brain activities. However, progesterone levels are not abnormal in all women with PMS. Many
have normal progesterone levels throughout the monthly cycle and still have weight
gain and bloating. Treatment with progesterone will correct hormonal imbalances.
However, in an evidence-based review of effective treatments, progesterone has not
been shown to be effective in treating PMS (Douglas, 2002).
In a review of trials of progesterone use to treat PMS, the authors stated they could
not conclude that progesterone treatment was or was not effective (Ford, et al., 2009).
The authors found many flaws in the individual studies, especially differences in criteria between studies, so that comparisons were difficult to draw.
Another theory cites an endogenous opiate peptide imbalance. Opiate peptides are
small protein molecules that have numerous functions as neurotransmitters and
neuromodulators. They affect the levels of norepinephrine and dopamine, regulate
endocrine secretion, influence mood and behavior, alter production and secretion of
hormones, inhibit fluid secretion in the bowel and decrease peristalsis.
Cyclic changes in endogenous opiate peptide activity during the menstrual cycle
may alter the body’s physiology enough to cause some symptoms of PMS, such as
mood changes, water retention and constipation. There is not sufficient evidence to
support this theory at the present time, although research continues.
Other research has focused on alterations in neurotransmitters as the cause of PMS
— specifically, changes in serotonin activity and the serotonin receptor 5-HT. Serotonin
is involved in our moods, especially irritability, anger and depression as well as specific
food cravings (Bianchi-Demicheli, et al., 2002). Estrogen decreases the sensitivity of
serotonin receptors and increases the sensitivity of serotonin antagonists.
During the luteal phase of menstruation, serotonin levels are decreased in the
blood of women with PMS (Ashby, 1988). Women with PMS do have a heightened
sensitivity to the serotonin receptor 5-HT during the luteal phase that increases premenstrually (Freeman, 1992).
Although the exact cause(s) of PMS are unknown, some treatments have been
proven clinically effective. Begging the question "why?", we can review the literature to
see if good scientific evidence exists for the various PMS treatments commonly used.
The consensus is that two treatments are supported by enough quality research to
recommend their use: calcium supplements and selective serotonin reuptake inhibitors
(SSRI) (Douglas, 2002; Rapkin, 2003; Brown, et al, 2009).
Other therapies that have some empirical evidence of benefits include vitamin B6,
evening primrose oil, oral contraceptives, complex carbohydrate drinks, cognitive
behavioral relaxation therapy and aerobic exercise (Douglas, 2002; Rapkin, 2003).
The best approach is to try to alter lifestyle first, such as exercise, diet and stress. If
symptoms still persist after two or three months, then drugs can be used (BianchiDemicheli, et al., 2002).
Sexual & Reproductive Health
7
Serotonin reuptake inhibitors (SSRI) have shown good success in treating PMS and
are the first drug of choice for more severe PMS (Barnhart, et al., 1995; Moline and
Zendell, 2000; Bianchi-Demicheli, et al., 2002; Vleck and Safranek, 2002; Brown, et al.,
2009 ). In a review of 15 randomized controlled trials involving 884 women, the evidence supported the use of SSRI to treat severe PMS (Wyatt, et al., 2006). This conclusion
was supported by a newer meta-analysis of over 2,294 women, in which SSRI drugs
were found to be highly effective in treating severe PMS (Brown, et al., 2009).
SSRI drugs that have been investigated include: fluoxetine (Fluctine®), sertraline
(Zoloft®), paroxetine (Deroxat®), citalopram (Seropram®), venlafaxine (Efexor®) and
fluvoxamine (Luvox®) (Bianchi-Demicheli, et al., 2002; Brown, et al., 2009).
Vitamin E has been used to treat breast tenderness in women with PMS. Women
given 400 IU of vitamin E for two months had substantial relief from breast tenderness
(London, et al., 1987). No more recent studies on vitamin E have been reported.
Debate over the effects of caffeine on breast tenderness continues. Some studies
show that caffeine (from soft drinks, coffee, tea, chocolate or over-the-counter drugs)
increases breast tenderness, while other studies don't. This may be due to the effect of
caffeine on magnesium levels, which will be discussed in the next section.
NUTRITIONAL FACTORS
Deficiencies and imbalances of various vitamins, minerals and nutrients in the
diet have been theorized to cause PMS symptoms. Only one, calcium, has well-documented studies to back up its benefits. Other nutrients, such as magnesium, carbohydrates, vitamin D, vitamin E and vitamin B6 appear to be of benefit, but more studies
are needed. Let's look at what we know.
• Calcium does appear to reduce the symptoms of PMS, especially water retention,
mood changes, food cravings and pain, in doses of 1200 to 1600 mg/day (Thys-Jacobs,
et al., 1998, Ward and Holimon, 1999). Thys-Jacobs and colleagues (1998) conducted a
double-blind, placebo-controlled, multi-center clinical trial comparing calcium supplementation to a placebo on PMS symptoms. The supplemented group showed a significant reduction in symptoms, 48 percent, by the third treatment cycle, compared to a 30
percent reduction in the control group.
Calcium metabolism, including intestinal absorption and parathyroid gene expression, is regulated by estrogen. Alterations of calcium metabolism resulting in hypocalcemia, occur in PMS, leading to symptoms of depression, anxiety and other mood changes
(Thys-Jacobs, 2000). Supplementing with calcium reverses the calcium deficiency,
alleviating those symptoms associated with the low serum calcium levels. Note how
similar the symptoms of hypocalcemia are to those of PMS.
Other studies have found that women with a history of PMS have reduced bone
mass and an increased risk for osteoporosis (Bendich, 2000).
• Vitamin D may also be beneficial to women with PMS. In a study using data from
the prospective Nurses' Health Study II cohort, researches found an inverse relationship
between vitamin D intake and PMS , as well as calcium intake and PMS (Bertone-
Sexual & Reproductive Health
8
Johnson, et al., 2005). As intake of each nutrient increased, the incidence of PMS decreased. The intake of vitamin D in the highest quintile was 706 IU/day, versus 112 IU/
day in the lowest quintile. For calcium, the highest quintile had an intake of 1283 mg/day,
versus 529 mg/day in the lowest quintile. In more recent studies, calcium plus vitamin D,
or calcium alone, were effective in decreasing PMS symptoms (Khajehei et al., 2009;
Ghanbari et al., 2009).
It is recommended that women with PMS supplement approximately 1200 mg/day
of calcium, well within tolerable limits. This amount of calcium will help alleviate PMS
symptoms as well as maximize bone health. Not all the calcium needs to be supplemented; as intake increases, supplementation can decrease. In addition, getting adequate vitamin D is also important, whether from the sun, food or supplementation.
Women living in more northern climates are more likely to be vitamin D-deficient and
should supplement with up to 1000 IU per day (Holick, 2004; Hollis, 2004).
• Vitamin B6 is necessary for the production of the neurotransmitters dopamine,
norepinephrine and serotonin, which control and affect our moods. In women taking
oral contraceptives, vitamin B6 metabolism was altered, causing low serum B6 levels.
When women with low serum B6 levels were supplemented with vitamin B6, metabolism and serum levels were normalized and behavioral changes, such as depression,
mood swings and irritability were helped by the additional vitamin B6.
Some of the mood changes experienced by women using oral contraceptives are
experienced by women with PMS. Supplemental vitamin B6 seems to help some women
not only with mood changes, but other symptoms as well.
Not all women are helped by B6 supplementation. Berman and others (1990), in a
study of the effects of 250 mg of supplemental vitamin B6 on PMS, found that subjects
reported improvement of their symptoms, but noted that there was no significant change
in the biochemical indices of vitamin B6 status. Bendich (2000) found conflicting results
in a review of the literature, while Wyatt and colleagues (1999) believe that supplemental
vitamin B6, up to 100 mg/day, is likely to be of benefit in treating premenstrual symptoms and premenstrual depression. Bendich noted that most of the studies were small,
with flawed methodologies, but that the results of all the studies combined indicate a
potential for vitamin B6 to relieve some PMS symptoms. Newer research is needed to
determine the effectiveness of vitamin B6.
Caution must be used when using vitamin B6. Peripheral nerve damage (reversible
if supplementation stopped soon after symptoms appear) can develop in sensitive
individuals at doses above 100 mg/day, a level below the 200 to 500 mg/day which is
recommended by some PMS practitioners. The tolerable upper limit (UL) for vitamin B6
is 100 mg/day, a level designed to protect the most sensitive individuals (IOM, 1998).
• Magnesium. Serum levels of magnesium and zinc have been shown to be
significantly reduced, and serum copper significantly elevated, in the luteal phase of
menstruation in women with PMS (Posaci, et al., 1994, Chuong and Dawson, 1994). It is
magnesium that appears to play a role in the development of PMS. Excess intake of
alcohol, salt and caffeine can decrease magnesium levels and worsen symptoms in PMS
(Rapkin, 2005).
Sexual & Reproductive Health
9
There are several potential mechanisms by which magnesium may cause or exacerbate PMS. Magnesium is involved in neurotransmitter activity, including serotonin, as
well as neuromuscular function, cell membrane stability and vascular contraction, all of
which are "abnormal" in PMS. Only a few small studies have investigated whether or
not supplemental magnesium can alleviate or reduce symptoms of PMS in doses of 200
to 360 mg/day.
One study found that supplementation of 200 mg magnesium a day significantly
reduced mild fluid retention symptoms of PMS (Walker, 1998). According to Bendich
(2000), these studies are promising but do not conclusively prove clinical benefit. More
studies are needed. However, it will do no harm to supplement magnesium in doses of
250 mg to 400 mg/day.
In a recent study comparing women receiving intravenous magnesium infusion
and controls, there was no difference in the amount of magnesium retained by the two
groups, indicating no magnesium deficiency (Khine et al., 2006). When the subjects
knew they were getting a magnesium infusion, there was an improvement in mood.
When the authors then changed the study to a double-blind, placebo-controlled study,
there was no difference in the effect of the intravenous magnesium on mood.
Changes in blood sugar levels, causing hypoglycemia, have been blamed for PMS.
Evidence does not support this theory, though it is true that some women experience
cravings for sweets and chocolate during PMS, and many increase their caloric intake.
The cravings have not been definitely linked to low blood sugar levels.
In fact, increased appetite may be due to increased progesterone, which has an
appetite-enhancing effect. Many studies, including one by Lissner and coworkers
(1988), have shown that caloric intake varies during the monthly menstrual cycle, most
likely due to hormonal fluctuations. Martini and colleagues (1994) found significant
increases in mean intakes of energy, protein, carbohydrate and fat during the midluteal
phase of the menstrual cycle, compared with the mid-follicular cycle. Cross, et al. (2001)
found that some women with PMS — but not all — increase their nutrient intake during
the premenstrual phase of the menstrual cycle.
CARBOHYDRATES
The types and amounts of carbohydrate in the diet may affect PMS. Wurtman and
colleagues (1989) studied food intake and mood changes during the follicular and luteal
phases of the menstrual cycle.
In one study, 19 patients who claimed to suffer from PMS (and who had mood
scores determined by both a self-test and a psychiatric interview) were monitored for
food intake. They took meals in a common dining room. Women with PMS increased
their caloric intake and ate more carbohydrate-rich foods in the luteal phase of their
menstrual cycles, while the control group did not change its consumption patterns.
Wurtman’s second study investigated the effects of carbohydrate-rich meals on
mood and plasma levels of glucose, insulin and amino acids. Eighteen women with
PMS, and 14 age-matched non-PMS controls, differed significantly in their behavioral
Sexual & Reproductive Health
10
response to a carbohydrate-rich meal during the late luteal phase of their menstrual
cycles, but not during the follicular phase.
Interestingly, the biochemical parameters did not differ in the two groups. Increasing carbohydrate consumption without increasing protein increases the production and
release of serotonin, a brain neurotransmitter involved in mood and behavior.
In a pilot study in 2008, there were no differences in insulin sensitivity between the
follicular and luteal phases of the menstrual cycle, although cravings increased during
the luteal phase while the distribution of calories remained the same (Trout, et al., 2008).
The women in this pilot study ate 55 to 64 percent of their calories from carbohydrate.
Along those same lines, tryptophan is the precursor of serotonin. In women with
documented PMS, a tryptophan-depleting diet significantly aggravates PMS symptoms
(Menkes, et al., 1994). Sayegh and colleagues (1995) had women diagnosed with PMS
drink a specially formulated, carbohydrate-rich beverage that increased serum tryptophan levels. After consumption of the beverage, PMS symptoms — mood, cognitive
function and appetite disturbances — improved.
In a more recent study, a carbohydrate-rich beverage, given twice a day to women
with PMS five days prior to menstruation, decreased mood symptoms in 33 percent of
the women (Freeman, 2002). Only 5 percent of the women given a placebo had improvement in their mood symptoms. More research is needed to determine if carbohydraterich foods or drinks can alleviate PMS symptoms. Again, using this treatment will do no
harm until the scientific evidence proves it is or is not clinically beneficial.
FATS AND FATTY ACIDS
Fatty acids are the precursors to prostaglandins (PG), substances which have
regulatory functions in the body similar to hormones. They can influence dilation of the
veins and arteries, capillary permeability, fluid balance, neurotransmitter activity,
immune function and cerebral blood flow.
Prostaglandin PGE1 stimulates progesterone production and is produced from
omega-6 (Ω-6) fatty acids, primarily linoleic acid. Animal fats, high in arachidonic acid,
decrease progesterone synthesis by producing the prostaglandin PGF2 which discourages progesterone synthesis as shown in the diagram on the next page.
Evening primrose oil, sold as Efamol®, is 5 to 20 percent gamma-linolenic acid
(GLA). In the body GLA is converted to PGE1, with the enzymes and cofactors vitamin
C, B6, niacin, magnesium and zinc. PGE1 prevents fluid retention, is anti-clotting, reduces insulin response to glucose and reduces the neuroendocrine response to low
blood sugar, among other functions.
Evening primrose oil has been investigated as a treatment of PMS, with mixed
results. Some studies reported relief from the use of evening primrose oil, others did
not. In a review of the literature on evening primrose oil and PMS, there was insufficient
evidence to show that evening primrose oil was of much benefit in women with PMS
(Budeiri, et al, 1996; Rapkin, 2005).
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Sexual & Reproductive Health
Dietary Fatty Acids & PMS
Polyunsaturated
Vegetable Oils
Saturated Fats
Animal Fats
Linoleic Acid
Prostaglandin E1
Progesterone increases
Arachidonic Acid
Prostaglandin F2
Progesterone decreases
THE PLACEBO EFFECT
In analyzing all the data available on the relationship of various modes of treatment for PMS, one fact becomes clear: While treatment of any kind seems to help, not
all symptoms are alleviated, and in some women there is no effect. The benefits of
dietary change cannot always be explained by available research. The benefits of many
dietary changes have not been proven, although — anecdotally — they appear to work.
It may be that in combination with other therapies, diet is an effective treatment.
Some of the response to diet and nutritional supplements can be explained by the
placebo effect. Studies quote that from 50 to 90 percent of the benefits from various treatments are due to the placebo effect, as indicated in Hammarback’s 1989 review of PMS.
If a treatment seems to help, is not harmful or expensive, why not try it? If positive
results are due to the placebo effect, so what? When a woman is suffering from PMS and
needs help, changing the diet may be an easy answer. Even if the changes do not relieve
the PMS symptoms, a nutritionally sound diet will be beneficial in the long run.
Until more research is completed, we will not have definitive answers on how diet
and supplements affect PMS. Until then, we can use diet as a form of treatment, since it
is not harmful and may be extremely beneficial.
DIETARY RECOMMENDATIONS
To be effective, dietary changes for PMS need to become a permanent part of a
woman’s life. Nutrition counselors need to ensure that the diets are nutritionally sound,
with safe levels of vitamin and mineral supplements.
• Limit intake of refined sugar to prevent decreased magnesium absorption (Also,
foods that are high in refined sugar tend to be low in most other nutrients.)
• Limit salt intake to 2300 mg/day (Dietary Guidelines for Americans, 2005). Salt
causes water retention and can increase the bloating and weight gain of PMS.
Limit the amount of salt added to food and limit foods high in salt: processed
Sexual & Reproductive Health
12
foods, salty snack foods, canned soups, ham, bacon, luncheon meats, hot dogs,
soy sauce, pickled foods and marinated foods (if salt is used). Read the label to
determine if salt is added to foods bought at the supermarket. Some women find
they only need to limit salt intake for two weeks prior to menstruation.
• Rely as much as possible on plant sources instead of animal sources to meet
protein needs. Plant protein is low in fat, and most of the fat found in these
foods is polyunsaturated. Use low-fat and non-fat dairy products, as they are
excellent sources of calcium and protein, as well as vitamin D.
• Increase intake of complex carbohydrates, including dried peas and beans,
vegetables, grains and fruits. These foods provide magnesium, vitamin C, B6,
folate, zinc and other important nutrients often inadequate in the diet.
Dietary changes without supplementation can help women with PMS. Make
changes slowly. If too many dietary changes are attempted at once, failure is likely.
VITAMIN/MINERAL SUPPLEMENTS
Nutrition supplements have become a part of the treatment for PMS. Studies
investigating the role of specific nutrients and PMS have come up with contradictory
results. Stewart (1987), in a study of 11 women with PMS, found nutritional deficiencies
of vitamin B6 in eight women, and of magnesium and zinc in 10 women.
Other deficiencies found were:
• chromium in five women;
• potassium in four;
• vitamin E in three, and
• vitamin B1 and vitamin B2 in one woman each.
These deficiencies were corrected by vitamin and mineral supplements. Mira, et al.,
(1988) found no nutrient deficiencies in his study of women with PMS, nor did Berman,
et al., (1990). Although Berman found no nutritional deficiencies, the study documented
symptom relief in the women taking 250 mg of supplemental pyridoxine daily.
It is difficult to determine the role of vitamin and mineral supplements in PMS,
with the exception of calcium. Many studies are not conclusive, particularly those on
vitamin B6, E and magnesium. The results are equivocal. There are few studies on other
nutrients, such as vitamin D. With this in mind, the wisest course is to assist women to
supplement vitamins and minerals, if that is their choice and the doses are not harmful.
Supplements that may be of benefit and are not harmful are:
• 1200 to 1600 mg of calcium;
• 250 to 400 mg of magnesium;
• a maximum of 100 mg vitamin B6;
• 15 mg of zinc;
• 400 to 1000 IU vitamin D, and
• 200 IU of vitamin E.
Sexual & Reproductive Health
13
These nutrients can be included in a broad-spectrum multivitamin and mineral
supplement containing most nutrients at or slightly above RDA amounts, or supplemented as individual nutrients. Keep in mind that it may take two to three months to
see benefit from the vitamins and minerals.
The chart below summarizes the dietary changes for women with PMS and the
recommended vitamin and mineral supplements.
Dietary Recommendations for PMS
Reduce:
• refined sugar
• salt
• alcohol, coffee, tea, chocolate,
tobacco
Increase:
• complex carbohydrates
• green leafy vegetables
• legumes and whole grains and
cereals
• fish, poultry, low-fat and non-fat
dairy products
Supplement:
Broad-spectrum multivitamin/
mineral;
• 250 - 400 mg magnesium
• 50 to 100 mg vitamin B6
• 15 mg zinc
• 200 to 400 IU vitamin E
• 1200 to 1600 mg calcium
(reduce if calcium intake is
high)
• 400 - 1000 IU vitamin D
HERBS
The use of herbs in the treatment of PMS has grown rapidly. The herbs most commonly used for PMS include: chasteberry (Vitex agnus-castus), crampbark (Viburnum
opulus), black haw (Viburnum prunifolium) and dong quai (Angelica sinensis). These herbs
can relieve some of the symptoms of PMS.
An in-depth discussion of herbs is beyond the scope of this course, but can be
found in the Nutrition Dimension course, Herbal Supplements, by Leslie Kay. However,
one herb, chasteberry, deserves discussion.
• Chasteberry contains flavonoids and iridoids as well as compounds similar to
sex hormones (Atkinson, 2006). Researchers and herbalists believe that chasteberry
works by decreasing the effects of estrogen and increasing the effects of progesterone. It
is also speculated that chasteberry may bind to opioid receptors, beta-endorphins and
neuroactive flavonoids (Schellenberg, 2001).
In 2001, Schellenberg and colleagues published a double-blind, placebo-controlled
trial of 168 women given either chasteberry or a placebo for three menstrual cycles.
Fifty-two percent of women in the study group and 24 percent of women in the placebo
group reported improvements in symptoms.
In a review of the literature available, Tesch (2002) concludes that chasteberry may
improve symptoms of PMS, but that more research is needed. According to Fugh-
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14
Berman and Kronenberg (2003), there is preliminary data to suggest chasteberry may be
beneficial in women with PMS.
The active ingredients in chasteberry include flavonoids, which are found in many
foods. Christie and colleagues (2004) studied the effect of a flavonoid extract (from plant
foods) on fluid retention in PMS. While the study was small, 30 women, there was
enough improvement in "leg health" scores (amount of fluid retention in the legs) to
conduct a larger study.
In Chinese women, chasteberry decreased symptoms of PMS and was safe and
effective in a dose of 40 mg herbal drug (He et al, 2009).
An in-depth discussion of herbs is beyond the scope of this course, but can be
found in the Nutrition Dimension course, Herbal Supplements, by Leslie Kay.
For health professionals and clients looking for information on PMS, there are many
reliable sites the contain excellent information. Two sites that I have found useful are:
• Association of Reproductive Health Professionals:
<www.arhp.org>
• US Dept. of Health and Human Services, women's health:
<www.womenshealth.gov>
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Chapter Two:
Oral and Hormonal
Contraceptives
Eight to 10 million women in the United States, and up to 100 million women
world-wide, use hormonal contraceptive agents for birth control. (For a complete list
and explanation of various types of birth control methods and side effects go to:
<www.womenshealth.gov>)
Hormonal contraceptives contain synthetic hormones, estrogens and/or progestogens (also called progestins), that inhibit ovulation and alter the metabolism of the
body. Hormonal contraceptives come in different forms. Most common are oral contraceptive agents (OCA), but newer delivery systems are available, including implants,
injectables, patches, vaginal rings, implantable rods and intrauterine devices.
One implant, Implanon®, is a single rod implanted under the skin which releases
hormones for three to five years. It has been used in Europe and became available in
the US in July 2006. Injectable contraceptives are monthly hormone shots. Patches are
put on by the user once a week for three weeks; the fourth week no patch is worn. The
vaginal ring, worn three weeks each month, releases hormones to prevent pregnancy.
Intrauterine devices, inserted by a clinician, can remain in place up to five years.
While less research is available on these newer types of contraceptives, more
studies are becoming available (Depieres, 2002; Davidson, 2003; Inal, et al., 2008;
Cagnacci, et al., 2009).
Since OCA were the predominant form of contraception for over 30 years, there is
much more research available on them. Thus, OCA will be the form of contraception
discussed in detail in this chapter, unless noted otherwise.
Fifty different metabolic reactions caused by the hormones in OCA may impact nutritional needs and requirements. It is important to understand the hormonal and metabolic
changes that result from OCA use in order to adequately counsel women on their nutritional
needs while taking OCA, or when discontinuing their use to prepare for pregnancy.
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Sexual & Reproductive Health
The Association of Reproductive Health Professionals (ARHP) has a web site —
www.arhp.org — that contains many good resources for health professionals and clients
on oral contraceptives.
HOW ORAL CONTRACEPTIVES WORK
At the beginning of the menstrual cycle, follicle stimulating hormone (FSH) increases
and stimulates ovarian follicular growth and maturation, as shown in the graph below. As a
result of the increase in FSH, the levels of estrogen and progesterone increase.
Hormonal Changes During the Menstrual Cycle
FSH
LH
Progesterone
Estrogen
20
Progesterone
Estrogen
10
LH
FSH
0
0
Menstrual
Phase
7
Midfollicular
Phase
14
Ovulatory
Phase
21
28
Luteal
Phase
(premenstrual)
Days of the Menstrual Cycle
When estrogen reaches a critical level, it stimulates the hypothalamic-pituitary axis
to produce more luteinizing hormone (LH) with a smaller surge of FSH. The increased
levels of FSH and LH cause the release of an ovum. Progesterone and estrogen secretion
increase at this time to allow the uterus to prepare for the ovum.
When no egg is present, the estrogen and progesterone levels decrease and the
mucosal lining is sloughed off. The fall in estrogen and progesterone levels stimulates
the hypothalamus and pituitary gland to secrete FSH and the cycle repeats itself.
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Sexual & Reproductive Health
OCA interfere with the production of hormones so that the early rise in FSH and
the mid-cycle LH surge are absent, preventing ovulation. Pregnancy is also prevented
by an alteration in the cervical mucus, which becomes thick and viscous and interferes
with sperm penetration. Changes in the endometrium occur so that the glands do not
produce sufficient glycogen to support the embryo in the endometrium prior to implantation. Finally, the ovary is less responsive to the same amount of gonadotropins (LH,
FSH) so it does not release an egg.
RISKS AND BENEFITS OF OCA
The oral contraceptives in use today are very different from those used 30 years
ago. Instead of the high-dose, single-hormone pill of the 1960s which contained 150
mcg of estrogen, low-dose, mixed-hormone preparations with both estrogen and
progesterone predominate today. The most common dose of estrogen is 30 to 35 mcg.
A third generation of progesterone derivatives will be discussed later in the chapter.
As shown in the chart below, there are benefits and risks to oral contraceptives.
Some health benefits include less anemia from less bleeding, correcting menstrual
disorders, reducing the incidence of some diseases and protecting against other diseases
and certain cancers. The negative side effects of OCA include nausea, vomiting, breakthrough bleeding, bloating, weight gain, edema, central nervous system side effects
(headaches, dizziness, fatigue, nervousness, mood changes), decreased libido, scant
periods, amenorrhea, breast tenderness, hypertension and facial pigmentation. The
lower the dose of OCA, the fewer side effects.
Risks vs. Benefits of OCA
Risks
Thromboembolic disease
Cardiovascular disease
Side effects:
• nausea
• vomiting
• breakthrough bleeding
• weight gain
• bloating
• edema
• fatigue
• psychological changes
• scant periods
• hypertension
• headaches and/or dizziness
Benefits
Effective contraception
Correction of menstrual disorders:
• increased regularity
• decreased flow
• decreased PMS
Decreased incidence of:
• benign breast disease
• ovarian cysts
• pelvic inflammatory disease
• endometriosis
• ectopic pregnancy
Protects against:
• endometrial, ovarian cancer
• osteoporosis (controversial)
Sexual & Reproductive Health
18
Serious health problems such as venous thromboembolic disease (blood clot that
blocks a vein) and cardiovascular disease, specifically stroke and myocardial infarction,
may occur with use of oral contraceptives. As you will see later, the increases in risk for
these more serious diseases is affected by the type and amount of estrogen and the type
of progestogen in a specific pill.
OCA use was thought to prevent bone loss, a risk factor for osteoporosis. The
increased estrogen in OCA decreases the body’s ability to use the calcium stored in the
bones, thereby protecting against bone loss. However, this is not as clear cut as once
thought. Studies are mixed with some showing that OCA prevent loss of bone mineral
density while others show an increased loss of bone mineral density. This will be discussed in more detail later in this chapter.
The estrogen and progestogen in oral contraceptives change the body’s metabolism
both directly (discussed later) and indirectly. Indirectly they cause the adrenal cortex to
produce the stress hormone cortisol. The increase in cortisol has an effect on protein,
carbohydrate and fat metabolism. The chart below summarizes some of the metabolic
alterations caused by oral contraceptives.
Metabolic Alterations with OCA
Lipid
Alterations in
serum lipids:
• total cholesterol
• VLDL
• LDL
• HDL
• triglycerides
Increase in free fatty
acids
Carbohydrate
Alteration in glucose
tolerance
Hyperinsulinemia
Alterations in insulin
sensitivity
Protein
Increased production of
serum proteins:
• transferrin
• albumin
• ceruloplasmin
• C-reactive protein
Changes in blood
coagulation proteins
Mobilization of amino
acids to the liver
LIPID METABOLISM
Increased incidence of cardiovascular disease — ischemic heart disease, myocardial
infarction, hemorrhagic stroke, thrombotic stroke, deep vein thrombosis and thromboembolism — in women using OCA has been reported in epidemiological studies in
the literature.
It is through direct alterations in metabolism that OCA exert their effect. Both the
estrogen and progestogens found in OCA alter serum lipids. The high-dose OCA,
containing 50 to 150 mcg estrogen and 1 to 10 mg of progestogen (or equivalent amount
of other forms of progestogen), have a more profound effect on serum lipids than low-
Sexual & Reproductive Health
19
dose OCA, containing 20 to 35 mcg estrogen and minimal progestogen ( less than 750
mcg norethisterone and up to 100 mcg levonorgestrel).
Third generation progestogens — desogestrel, norgestimate, gestodene and
drospirenone — are derivatives of levonorgestrel and have a different effect on serum
lipids than earlier progestogens used in oral contraceptives. The chart below shows how
the hormones in OCA affect serum lipids.
Note that the newest progestogen, drospirenone (found in Yasmin®) may increase
triglycerides, unlike the other third generation progestogens (Taneepanichskul and
Phupong, 2007).
Serum lipid profiles associated with increased risk for heart disease are increased
total cholesterol and LDL-cholesterol, and decreased HDL-cholesterol. As noted below,
the older progestogens most adversely affect serum lipids by decreasing cardioprotective
HDL and increasing total cholesterol and LDL-cholesterol. The newer progestogens have
the reverse effect, increasing the ratio of the cardioprotective HDL in relation to the LDL
(London, 1992; Kafrissen and Corson, 1992, Porrka, et al., 1995; Machado, et al., 2004).
Effect of Hormones on Serum Lipids
Change in Serum Lipids
Serum Lipid
Estrogen
Levonorgestrel*
Desogestrel**
Unchanged or Unchanged or Unchanged
Triglyceride
£
VLDL
§
§
LDL cholesterol
HDL cholesterol
HDL2 cholesterol
Total cholesterol
*Norethisterone and older progesterones have this same effect on serum lipids.
**Norgestimate and gestodene have the same effect on lipids. Also, they beneficially alter serum LDL:HDL
ratio. London RS, Obstet Gyn Surv, 1992.
§VLDL increase not affected by progestogens, only estrogen component of OCAs.
£ Drospirenone may increase triglycerides.
(In two separate studies conducted in Europe, Jick, et al., (1995) and Lewis, et al.,
(1996) concluded that third generation OCA are associated with reduced risk of myocardial infarction or with no difference, when compared with second generation OCA.
Keep in mind the incidence level is low to begin with.)
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20
Rabe and colleagues (1992) reported that after two years on Norplant®, total serum
cholesterol and triglycerides decreased. All lipoproteins and apolipoproteins, with the
exception of LDL and apolipoprotein AII, decreased as well, including HDL. They
concluded that Norplant may be cardioprotective.
The NuvaRing®, with 15 mcg ethinylestradiol and 120 mcg etonogestrel, was found
to have minimal effect on lipids, compared to OCA (Tuppurainen, et al., 2004).
The implant Implanon® increased cholesterol and triglycerides in one study. More
needs to be done to determine if this is clinically significant (Inal, et al., 2008).
The increase in serum triglycerides and VLDL is related to the estrogen in OCA.
Walsh and Sacks (1993) investigated the mechanism responsible for the increase in these
serum lipids. They found that there was an increase in the production of triglycerides
and VLDL but no decrease in the catabolism of these lipids. The increase in production
does not appear to promote atherosclerosis. Other researchers have also concluded that,
while there may be an increase in triglycerides and VLDL, the levels are within the
normal range (Gaspard, et al., 2004; Guazzelli, et al., 2005).
Triglycerides are converted to large VLDL particles, then small VLDL particles.
People with hypertriglyceridemia have a problem converting the large VLDL to small
VLDL. The large VLDL stay in circulation longer and accumulate cholesterol esters,
which promote arterial plaque. Women taking OCA may produce more VLDL, but they
are converted to small-particle VLDL and catabolized before they accumulate cholesterol, and therefore are not atherogenic.
The good news is that the use of OCA does not seem to affect mortality related to
cardiovascular disease (CVD) (Graff-Iversen, et al., 2006). In this Norwegian study, there
was no difference in the CVD death rate between women who used OCA and those
who did not.
As discussed earlier, low-dose OCA have effects that are much less pronounced
than those of high-dose pills, and are much safer. However, metabolic changes occur
even at very low levels of hormone intake, and must be considered when choosing a
safe method of birth control.
Increased cortisol appears to have an effect on lipid metabolism independent of the
effect of estrogen and progestogen. Cortisol mobilizes fatty acids from adipose tissue
and cells, increasing circulating free fatty acids. Cells in the body then shift away from
utilizing glucose as the predominant energy source to relying on fatty acids for energy.
Ketones, by-products of fat metabolism, increase in the blood as the body increases
the use of fats for energy. Using fatty acids as an energy source has a ketogenic effect,
seen when cortisol is available to mobilize fats from storage. Again, this effect is blunted
in the low-dose OCA.
Any woman with a family history of heart disease or elevated blood lipids is at
increased risk for plaque buildup, a risk factor in coronary heart disease. These women
should be monitored during OCA use and encouraged to make dietary changes to
decrease the amount of fat and cholesterol in the diet.
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21
PROTEIN METABOLISM
The most striking changes seen in protein metabolism are the types and amount of
proteins and enzymes synthesized by the liver. Women using OCA have increases in
ceruloplasmin, retinol binding protein, transferrin, beta1A-globulin, alpha1-antitrypsin,
fibrinogen, renin and alpha2-globulin, as well as decreased albumin.
Some of the proteins that are increased are carrier proteins for minerals — that is, their
role in the body is to transport minerals through the blood. Ceruloplasmin transports
copper, and transferrin transports iron. By increasing carrier proteins, more minerals can be
transported in the blood and the blood levels can increase. This is indeed the case with both
copper and iron. Serum levels of both minerals are increased in women using OCA.
The increase in fibrinogen and other coagulation proteins by the liver makes the
blood more coagulable, increasing the possibility of thromboembolic disease — blood
clots and phlebitis. It is the estrogen component of OCA which is primarily responsible
for these changes. The dose of estrogen in the OCA is positively correlated with the risk
for venous blood clots (Hedon, 1990). As the amount of estrogen in OCA decreases, so
does the risk for thromboembolism.
Brasdevant, et al., (1993) and Massafra, et al., (1993) found that when the dose of
ethinyl estradiol (estrogen) was reduced from 35 mcg to 20 mcg, there was no substantial change in blood clotting factors. Petitti, et al., (1996) found that low-dose OCA did
not appear to increase the risk of stroke and that stroke was a rare event in women of
childbearing age. The incidence of stroke in women aged 15 to 44 was 5.4 per 100,000
women-years for hemorrhagic stroke and 5.6 per 100,000 women-years for ischemic
stroke. Smoking was positively correlated with OCA use and hemorrhagic stroke.
Brasdevant, et al., (1993) also found that the reduced estrogen in OCA decreased
the amount of renin substrate. Alpha2-globulin, a protein, is converted to angiotensin I.
Renin then acts on the angiotensin I to convert it into angiotensin II, a potent vasoconstrictor, which can increase blood pressure in susceptible women. This would aggravate
hypertension. A decrease in renin production, however, would decrease the effect of
OCA on blood pressure.
C-reactive protein (CRP), a marker of inflammation, has recently come under
scrutiny as an indicator for heart disease (Pearson, et al., 2003). In a very small study of
women using OCA, Dreon, et al., (2003) found CRP levels two times higher in women
who used OCA compared to those who did not. All CRP levels were within normal
limits. Gaspard, et al., (2003) found no changes in CRP with OCA use for one year.
The reason for the different findings on the relationship of CRP and OCA use may
be that other factors also influence CRP. Raitakari and colleagues (2005) found that OCA
use does increase CRP, but so does obesity and physical activity — and not all women
using OCA have increased CRP levels. In another study, OCA use increased CRP and
being overweight increased the median CRP level two-fold (Buchbinder, et al, 2008).
Only some of the increase in CRP can be explained by OCA use.
More studies are necessary to determine if there is any clinical significance to the
use of OCA and changes in CRP.
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22
VENOUS THROMBOEMBOLYTIC DISEASES AND STROKES
A surprising discovery is that third generation OCA, with small doses of estrogen,
are responsible for an increase in the incidence of venous thromboembolytic disease
(VTE), including deep vein thrombosis (DVT) and pulmonary embolism. It appears that
third generation progesterones (gestodene and desogestrel), and not estrogen, are the
culprits. These progesterones, unlike first and second generation progesterones norethindrone and levonorgestrel, increase pro-coagulatory and fibrinolytic activity that
leads to a considerable stimulation of fibrin turnover. This may increase the risk of VTE
(Kuhl, et al., 1995; Hedenmalm and Samuelsson, 2005; Jick, et al., 2006).
Jick, et al., (1995) found that the risk for nonfatal DVT expressed as the number per
100,000 women years was: 16.1 for levonorgestrel, 29.3 for desogestrel, and 28.1 for
gestodene. The excessive risk above the older OCA was 16 per 100,000 women years.
Bloemenkamp, et al., (1995) found a 2.5-fold higher risk for DVT in women taking third
generation OCA.
In two studies undertaken by the World Health Organization (WHO) (Lancet,
1995), the same results were found. The risk for VTE was increased, although the rate
was less than previously reported. In one study , users of older OCA had a 3.5 times
higher risk of VTE than non-users, while users of third generation OCA had a 9.1 times
higher risk; the other study came to the same conclusion. It also found that body mass
index (BMI) was correlated with increased risk for VTE. Two newer studies did find that
the duration of use, dose of estrogen and the type of progestogen were associated with
the risk for VTE (Ligegaard, et al., 2009; van Hylckama, et al., 2009).
The longer a woman is on the OCA, the lower the risk for VTE. As the dose of
estrogen decreases (from 50 mcg to 30 to 40 mcg, then to 20 mcg), the risk of VTE correspondingly decreases. There is a different risk ratio for VTE for each type of progestogen. If the estrogen in the OCA is 30 to 40 mcg, the risk for VTE would be 1.91 for
levonorgestrel, 3.37 for norgestimate, 4.38 for gestodene, 5.58 for desogestrel and 7.90
for drospirenone (Ligegaard, et al., 2009). Put another way, the risk for VTE using
gestodene is 4.38 times the risk of a woman not using OCA. The authors of this study
also concluded that progestogen only OCA and intrauterine devices did not increase the
risk of VTE.
Overall, the risk for VTE in OCA users is low. In the general population, the risk of
VTE is 1 in 10,000 and during pregnancy the risk is eight to 10 in 10,000. The use of lowdose OCA increases the risk to three to four in 10,000, while third generation OCA increases that
risk to six in 10,000, less than the risk during pregnancy (Kovacs, 2002).
The risk for strokes is also higher for women who use OCA. Gillum and colleagues
(2000) looked at 16 studies published from January 1960 through November 1999, and
found that non-smoking women using OCA containing 35 mcg estrogen had an additional 4.1 ischemic strokes per 100,000 women. If the dose of estrogen was over 50 mcg,
the risk for stroke was three times higher in OCA users than in non-OCA users. However, no increased risk of ischemic stroke was found in young Australian women using
OCA with less than 50 mcg of estrogen (Siritho, et al., 2003).
Sexual & Reproductive Health
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The pendulum continues to swing: in a review of the literature on the use of OCA
and the risk of stroke, Chan and colleagues (2004) found that cohort studies did not find
a relationship between the use of OCA and an increased risk of stroke. Neither did Yang
(2009) find any significant association between ischemic or hemorrhagic stroke with
OCA use. Case-controlled studies, however, did find a significant association between
thrombotic stroke and the use of OCA. The authors felt that the risk of stroke from OCA
use may be less than previously thought due to the small significance, the methodological problems with many studies and the fact that the dose of estrogen used now is so
much lower than those in the studies.
CARBOHYDRATE METABOLISM
Glucose intolerance and hyperinsulinemia, due to alterations in insulin sensitivity,
are changes in carbohydrate metabolism caused by OCA. Progestogens have more of an
effect on carbohydrate metabolism than estrogens by increasing insulin secretion and
insulin resistance of cells.
Not all progestogens have the same effect on carbohydrate metabolism. Those that
are more androgenic — 19-nortestosterone and norgestrel derivatives — have a more
profound effect than the less androgenic progestogens — desogestrel, norgestimate and
gestodene. Estrogen may impair the initial secretion of insulin by the pancreas but does
not have a sustained effect on carbohydrate metabolism.
During OCA use the cells of the body are somewhat resistant to insulin. The pancreas will increase production, causing hyperinsulinemia. Even with the high levels of
insulin, the serum levels of glucose increase.
Wynn and colleagues (1986) found that serum glucose levels deteriorated over a
three-year period in women taking high-dose OCA; women taking low-dose OCA
showed changed serum glucose at three months, but no further changes. Other researchers have found some slight changes in fasting insulin and glucose levels, but they
never reached significance nor had any clinical relevance (Skouby, et al., 2005; Nessa, et
al., 2005). Insulin sensitivity was found to decrease in women taking OCA with 30 mcg
estrogen and 150 mcg desogestrel (Cagnacci, et al., 2009a). The clinical significance still
needs to be determined.
Studies by London (1992), Kafrissen and Corson (1992), Shoupe (1993), Wilde and
Balfour (1995) and Gaspard, et al., (2003) found that the newer progestogens do not
seem to alter carbohydrate metabolism. These studies looked at fasting serum and
insulin, and rises in serum glucose and insulin after a challenge with glucose, and found
no significant changes in these parameters. They concluded that desogestrel and
norgestimate have a less pronounced effect on carbohydrate metabolism than
nortestosterone and levonorgestrel. The vaginal ring also did not alter insulin sensitivity
in its users (Cagnacci, et al, 2009b).
Average increases in blood glucose are approximately 10 mg/dL. In the normal
individual, this is not enough to cause any problems. The body can adjust. In individuals susceptible to diabetes, the change in glucose tolerance may pose a slight risk of
causing the diabetes to surface.
24
Sexual & Reproductive Health
In OCA users, there is an increase in both free and bound cortisol; this has the
effect of mobilizing glucose for the cells. In addition, an increase is seen in growth
hormone and xanthurenic acid, which bind to insulin. This could be another explanation for altered carbohydrate metabolism. With insulin bound to other compounds, it is
unavailable to move glucose into the cells, so the serum glucose level increases.
Changes with low-dose OCA are minor in comparison to those from high-dose OCA,
but are still a consideration for women using OCA.
VITAMIN B6
Vitamin B6 (pyridoxine) is required for functions in the body that involve amino
acids and proteins. The conversion of tryptophan to niacin and serotonin requires vitamin
B6. When vitamin B6 is deficient, the body is unable to complete this conversion. It then
excretes compounds that are not fully metabolized, indicating that a deficiency exists.
It has been suspected that women using OCA may have inadequate vitamin B6.
Lussana (2003) did find significantly lower vitamin B6 levels in women using oral
contraceptives compared to non-users.
In OCA users, there is an increased excretion of intermediary tryptophan metabolites involved in the conversion of tryptophan to niacin, indicating insufficient vitamin
B6 to complete the metabolic process, as shown below.
Tryptophan Metabolism
Tryptophan
TO
5-hydroxytryptophan
PLP
SEROTONIN
(5-hydroxytryptamine)
PLP = pyridoxal phosphate (vitamin B6)
TO = tryptophan oxygenase
kynurenine
PLP
3-hydroxykynurenine
kynurenic acid
xanthurenic acid
PLP
3-hydroxyanthranilic acid
NIACIN
Researchers found it took 20 to 30 mg of pyridoxal phosphate (vitamin B6), which
is 10 to 15 times the Recommended Daily Allowance (RDA) for vitamin B6, to normalize
tryptophan metabolism.
Sexual & Reproductive Health
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The cause of this vitamin B6 inadequacy could be an increased need for vitamin B6
or interference with its metabolism. Estrogen sulfate esters may interfere with the
activity of a pyridoxine enzyme, PLP, by competing with it for binding sites. Increased
liver production of an enzyme, tryptophan oxygenase, allows more tryptophan to be
converted to niacin, increasing the need for PLP and vitamin B6.
Altered tryptophan metabolism due to a vitamin B6 deficiency may explain behavioral changes in women using OCA. It’s common to hear complaints of anxiety, lethargy, depression, irritability and emotional instability. Vitamin B6 is required to convert
tryptophan to the neurotransmitter serotonin. With inadequate vitamin B6, less serotonin is produced, possibly causing changes in behavior.
An increase in the conversion of tryptophan to niacin increases the need for vitamin B6 in that pathway, so not enough pyridoxine is available for the tryptophan-toserotonin pathway. The increased use of tryptophan would decrease the amount of
unbound tryptophan available to cross the blood-brain barrier, where serotonin is
produced. Furthermore, the intermediary tryptophan metabolites may block the transport of free tryptophan across the blood-brain barrier, decreasing the available tryptophan for conversion to serotonin.
Masse, et al., (1996) investigated the effect of newer OCA on 23 young women. All
had adequate vitamin B6 intake. The plasma and erythrocyte levels were adequate, but a
disturbance in B6 metabolism was detected.
OTHER VITAMINS
• Riboflavin. Riboflavin is necessary to convert pyridoxine (vitamin B6) to pyridoxal phosphate (PLP). With the increased need for pyridoxine in the conversion of
tryptophan, riboflavin may also be needed in increased amounts. In many OCA users,
riboflavin levels are found to be low.
• Folic Acid. Folic acid levels in the serum and red blood cells have been determined to be low in OCA users. Whether it is a problem of absorption, uptake or
utilization by the tissues is not clear. Steegers, et al., (1993) found that use of OCA with
less than 50 mcg of estrogen significantly lowered serum levels of folate and vitamin
B12. Green, et al., (1998), however, found no difference in serum folate and red blood
cell folate levels in adolescent girls.
Folic acid is critical for normal fetal development, especially between the 18th and
27th day of pregnancy, when a woman may not know she is pregnant. During this time
the neural tube develops and then closes. It is within this structure that the central
nervous system develops.
If a woman has been using OCA and has low serum folic acid levels, there could be
a problem during the first trimester from inadequate folic acid. In 1992 the US Public
Health Service (USPHS) recommended that all women of childbearing age who are
capable of becoming pregnant should consume 0.4 mg (400 mcg) of folic acid per day
for the purpose of reducing their risk of having a pregnancy affected with spina bifida
or other neural tube defects (NTD).
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In 1996, the US Food and Drug Administration (FDA) mandated that all enriched
cereal grain products be fortified with folic acid. The Institute of Medicine (1998) recommends that to get adequate amounts of folic acid, women capable of becoming pregnant
should consume 400 mcg a day of folate — from supplements, fortified foods or both —
as well as continue to eat foods high in folate. They go on to say that the evidence
shows that folate from supplements is more protective than from food.
Other dietary sources of folic acid are encouraged, but not relied on to be adequate
for most women. Appendix #12 lists dietary sources of folic acid. Many dietary studies,
including the National Health and Nutrition Examination Survey II (NHANES II) and
NHANES III show that folic acid is not always consumed in RDA amounts.
To see if the fortification of cereal grain products with folic acid was working. The
Centers for Disease Control (CDC) compared serum and red blood cell folate levels for
childbearing-aged women who participated in the 1999 NHANES survey to those who
participated in the third NHANES study (1988 to 1994). From NHANES III to NHANES
1999, mean serum folate concentrations for all women aged 15 to 44 years increased
from 6.3 to 16.2 ng/mL while red blood cell folate increased from 181 to 315 ng/mL
(MMWR, 2000). This met the national health objective of increasing red blood cell folate
levels in non-pregnant women, aged 15 to 44, to 220 ng/mL. In addition, fortification of
foods has resulted in a 26 percent decline in neural tube defects (MMWR, 2004).
There is still room for improvement. The number of women taking folate supplements did not increase from 1998 to 2003. It did go up in 2004, with approximately 40
percent of women of childbearing years taking a folate supplement, and remained at 40
percent in 2007 (MMWR, 2004; MMWR, 2008).
Those least likely to take a folate supplement are non-white, young and less educated, with Hispanics the least likely to take a folate supplement and with the highest
incidence of neural tube defects (MMWR, 2008). There is still a lot more work to do to
increase folate supplementation and intake in childbearing women, which will help to
decrease neural tube defects even further.
• Vitamin A. OCA use increases vitamin A in the serum by as much as 50 percent,
although the levels are not high enough to be toxic. Therefore, the requirement for vitamin
A does not increase and may be lower than the RDA. The most likely problem from
increased serum levels would be in supplementing too much vitamin A, not from getting
too little. Women should be cautioned about the possibility of toxicity from supplementing vitamin A, which is fat-soluble and stored in the body. Instead, supplementation
with beta carotene is preferable, since it is nontoxic even in very high amounts.
• Vitamin C. Vitamin C levels are reduced in the plasma, leukocytes and platelets from
OCA use. Estrogen increases the breakdown of vitamin C by increasing ceruloplasmin
levels. Ceruloplasmin increases the oxidation of ascorbic acid. The increased dietary need is
not great and can be met easily by increasing vitamin C-rich foods in the diet.
• Vitamin B12. Vitamin B12 levels are decreased in the plasma but not in erythrocytes. Green, et al., (1998) found that adolescent girls using OCA had a 33 percent reduction in serum B12 levels. The question remains if the changes seen in vitamin B12 are
Sexual & Reproductive Health
27
caused by an increased need for vitamin B12 or from a redistribution of vitamin B12.
Intake of vitamin B12 is important due to its essential role in fetal development, so any
women who gets pregnant after discontinuing prolonged OCA use should pay attention
to her vitamin B12 status and ensure that intake is adequate.
MINERALS
Mineral levels do change in women using OCA. The chart below summarizes both
vitamin and mineral changes in women using OCA.
Serum copper levels increase, due to the increased production of its carrier protein
ceruloplasmin. Therefore, the requirement for copper does not change.
Plasma and erythrocyte levels of zinc decrease in OCA users. As with folic acid and
vitamin B12, zinc is critical for fetal development, particularly the first trimester. Zinc is
often deficient in the diet; the average intake is less than 70 percent of the RDA. A
woman contemplating pregnancy should take a careful look at her diet to determine its
adequacy for zinc. If it is inadequate, she should consider a supplement.
Iron status in women using OCA improves. An increase in transferrin, the protein
carrier for iron, increases the amount of iron in the blood. Total iron binding capacity
(TIBC) increases significantly as well (Steegers, et al., 1993). Decreased menstrual blood
loss decreases the monthly iron loss. These three factors decrease the likelihood of iron
deficiency anemia in women using OCA.
Nutrient Changes with OCA
MECHANISMS FOR CHANGE
Increased utilization
Decreased serum levels
Changes in storage sites
Increased GI absorption
Decreased bone resorption
SERUM CHANGES
Nutrients Decreasing
Riboflavin
Folic Acid
Vitamin B6
Vitamin B12
Zinc
Magnesium
Nutrients Increasing
Iron
Copper
Vitamin A
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BONE MINERAL DENSITY
The effect of OCA on bone mineral density (BMD) in women appears to be related
to the type of OCA used — depot medroxyprogesterone acetate (Depo-Provera® or
DMPA) injections, levonorgestrel (Norplant) subdermal implants or hormonal pills.
Researchers are looking to see how each type of OCA impacts bone density in the short
term and what, if any, are the long-term clinical consequences, such as increased or
decreased risk of fracture.
Many of the studies done to date are contradictory due to differences in design,
techniques for measuring bone density, age of the participant and type of OCA. With
that in mind, it does appear that hormonal pills and Norplant implants have a positive
effect on bone mineral density, while DMPA or Depo-Provera injections may have a
slightly negative effect on BMD, although the effect is reversible once the injections are
stopped (Cromer, et al., 1996, 1999; Diaz, et al., 1999; Di, et al., 1999; Berenson, et al., 2001;
Nappi, et al., 2005; Kaunitz, 1999; Wanichsetakul, et al., 2002).
Berenson and colleagues (2001) found that BMD decreased by 2.74 in women using
DMPA for 10 to 14 months. The control group had a decrease of 0.37 percent in BMD as
well. Women using OCA with norethendrone had a 2.33 percent increase in BMD, while
those using OCA with desogestrel had an increase in BMD of 0.33 percent. Average
intake of calcium in all groups was 565 mg, well below the recommended level of 1000
to 1300 mg/day. Other researchers have also found an increase in BMD in women using
OCA pills (Elgan, et al., 2003; Lattakova, et al., 2009). Wanichsetakul, et al., (2002) found
the only significant difference in BMD in women using DMPA was in the lumbar spine.
In young women, it appears that the use of DMPA also causes a loss of BMD in the
hip and spine that is greater than in older women and was reversible when the contraceptive was discontinued (Scholes, et al., 2005).
Cromer and colleagues (2008) compared the BMD in DMPA and oral contraceptive
users, to BMD in non contraceptive users. In the 24 months of the study, the bone
mineral density in the spine and femoral neck decreased 1.5 percent and 5.2 percent in
the DMPA users, went up 4.2 percent and 3.0 percent in the oral contraceptive users and
increased 6.3 percent and 3.8 percent in the untreated group. The difference between
DMPA and the other two groups was significant. The biggest BMD loss was in the first
year, with an average loss of 1.4 percent BMD slowing to 0.1 percent the second year.
BMD was within normal limits for all groups.
Contrary to the studies cited above, Prior and colleagues (2001) found OCA users
had significantly lower BMD than non-users in the spine and the trochanter. These
results were not related to length of OCA use or age at first use. This study was a part of
the Canadian Multicentre Osteoporosis Study and contradicts the Berenson study, but
agrees with other studies that found decreased BMD in OCA users (Polatti, et al., 1995;
Drake, et al., 1996; Almstedt, et al., 2005).
In a review of the literature from 1966 through 2005, Martins and colleagues (2006)
determined that the results of the studies investigating combined hormonal contraceptives with BMD and/or fractures are inconclusive. However, there did appear to be a
Sexual & Reproductive Health
29
trend, based on age. Adolescents and young women had generally lower BMD compared to girls who were not using hormonal contraceptives. Premenopausal women
were no different than non-users of OCA. Perimenopausal and postmenopausal OCA
users preserved their BMD compared to non-users, but overall BMD was the same for
OCA users and non-users.
If you consider that a 1 percent increase in BMD is related to a 7 percent decrease in
vertebral fractures, the clinical significance of OCA use is clear (Prior, et al., 2001). If the
use of OCA increases BMD, that has a very positive effect on the number of fractures
and even the incidence of osteoporosis. Should OCA use decrease BMD, the reverse
would be true. Clinicians need a clearer picture of the relationship of OCA use to BMD.
Studies are under way to answer this question.
When deciding the best method of contraception, the age of the woman should be
a consideration. DMPA interferes with accumulation of bone density. Considering that
37 percent of total skeletal mass is accumulated in adolescence, DMPA may not be the
best choice for this group of females. However, for older women it may be a better
choice as they have already accumulated much of their skeletal mass.
Regardless of the choice of OCA, adequate calcium intake is essential. Increasing
calcium intake to recommended levels — 1000 to 1300 mg/day — is able to protect
young women from loss of BMD while using OCA (Teegaarden, et al., 2005). Adequate
vitamin D is necessary as well to absorb the calcium.
DIETARY RECOMMENDATIONS
Caloric intake between OCA users and non-users is similar (Eck, et al., 1997,
Pelkman, et al., 2001). In the study by Eck, OCA users ate 32 to 35 percent of their calories from fat, versus 28.5 to 28.8 percent in the non-users group. Resting energy expenditure varied depending upon the phase of the menstrual cycle. Total REE for the month
was not different between the two groups, but the pattern of energy expenditure during
the various phases was.
Others studies have also found that overall OCA use and use of DMPA is not
associated with altered energy intake, energy expenditure, weight gain or increased
body fat (Lloyd, et al., 2002; Pelkman, et al., 2001).
In a newer study DMPA was found to cause weight gain that was fat and not lean
muscle (Berenson and Rahman, 2009). After 36 months in the study, DMPA users gained
an average of 5.12 kg with 4.94 kg of fat, while OCA users gained 1.47 kg with 1.9 kg fat
and nonhormonal birth control users gained 2.05 kg with 1.17 kg fat. The authors of the
study speculate that the increase in weight and fat with DMPA is not due to an increase
in appetite or decrease in energy expenditure but related to the glucocorticoid-like
activities of the hormone.
Women who choose to use DMPA should be more careful with their diet and be
sure to exercise so they do not gain weight or gain an excessive amount of weight.
Sexual & Reproductive Health
30
The following are dietary recommendations for women using OCA:
• Monitor cholesterol levels and cholesterol intake. This is especially important
for women with a familial history of heart disease, stroke or with elevated blood
lipids. OCA with very low doses of hormones or the newer progestogens may
not present a problem.
• Reduce total fat intake to 30 percent or less of total calories. Decrease saturated
fat intake to less than 10 percent of total fat intake by reducing consumption of
animal proteins and by using non-fat or low-fat dairy products.
• Increase consumption of foods high in vitamins C, B6, B12, folic acid and zinc.
Foods that have a good supply of these nutrients are: green leafy vegetables,
fruits, dried peas and beans, poultry, seafood, grains, vegetables and lean meats.
Folic acid is extremely sensitive to water and heat. By boiling foods, 80 to 90
percent of the folic acid is destroyed. Try to eat dark green vegetables raw to
obtain the most folic acid, or microwave vegetables to reduce loss of folic acid
and other water-soluble vitamins.
• If the diet is inadequate in any of the above nutrients, supplement to 100
percent of the RDA.
• Consume 400 mcg of folic acid to prevent neural tube defects if you are of
childbearing age from supplements, fortified foods or both, as well as eating
foods high in folate. See Appendix #12 for folic acid content of foods.
• For women trying to get pregnant or who get pregnant soon after stopping oral
contraceptives, supplement with vitamins B6, and zinc at 100 percent of the
RDA.
• For women with depression associated with oral contraceptives, supplement
B6 up to 100 mg/day. No side effects have been seen at that dose, but increasing
the dose increases the possibility of side effects. In a study, Ubbink et al. (1987),
found that supplementing with 200 mg of vitamin B6 did not raise serum levels
any higher than 100 mg. The extra vitamin B6 was being excreted, not utilized by
the body. Therefore, the body can only handle so much vitamin B6 at a given
time. Any vitamin B6 above that level will be cleared from the body.
• Consume adequate amounts of calcium. If unable to meet requirements
through food, consider a supplement. The recommended adequate intake is
1300 mg/day for girls up to 18 years of age; 1000 mg for women 18 to 50 years of
age and 1200 mg/day for women over 50 (Institute of Medicine, 1998). Make
sure you are getting adequate vitamin D to absorb the calcium.
Sexual & Reproductive Health
31
Chapter Three:
Factors Affecting
Pregnancy Outcome
The health and eating habits of the mother directly affect the fetus and the outcome of pregnancy. In a country that is well-nourished, with a plentiful food supply, it
is disheartening to realize that malnutrition and poor eating habits lead to maternal,
fetal and neonatal complications. The chart below lists poor outcomes of pregnancy.
Poor Pregnancy Outcomes
• Low birth weight (LBW), <2500 gm birth weight
• Very low birth weight (VLBW), <1500 gm birth weight
• Small for gestational age
• Fetal growth restriction (FGR)
• Prematurity
• Pregnancy complications
• Congenital anomalies
• Neonatal illness
• Maternal or fetal mortality
• Hypertension, cardiovascular disease and other chronic
diseases later in life
All of these poor outcomes can be caused by poor maternal nutrition. That is not to
say that poor diet is the only cause of poor pregnancy outcomes. Many other factors
influence the course and outcome of pregnancy.
Neonatal mortality, defined as deaths during the first 28 days after birth, is related
Sexual & Reproductive Health
32
to the course of pregnancy. Since 1970, when the National Academy of Sciences published Maternal Nutrition and the Course of Pregnancy, there has been a dramatic increase in
the interest of the relationship of nutrition to the course of pregnancy. This interest has
translated into better prenatal care, government programs to teach and feed pregnant
women, and research and training for health professionals. The results are encouraging.
To highlight the relationship of nutrition to pregnancy outcome, births during the
four-year siege of Sarajevo, Bosnia, were studied to see what nutritional effect the war
had on pregnancy outcomes. Infant mortality during the war climbed to 36 per 1,000
live births from a pre-war level of 15.8 per 1,000 live births (Simic, et al., 1995). Morbidity increased from 3.4 percent to 8.2 percent in the same period, while babies born with
congenital malformations increased from 0.4 percent to 3.0 percent during the war.
In the United States, The National Center For Health Statistics (NCHS) in 1990
reported that between the years 1950 and 1987 infant mortality rates declined from 29.2
to 10.1 deaths per 1,000 live births. From 1990 to 1997 the infant mortality rate has fallen
from 9.2 to 7.2 deaths per 1,000 live births. Even better, between 1995 and 2001 the infant
mortality rates dropped another 10 percent to 6.8 per 1,000 live births — the lowest rate
ever recorded (NCHS, 2003).
Between 1950 and 2001, the infant mortality rate declined by 77 percent. For the
first time since 1958, the infant mortality rate increased in 2002 to 6.95 deaths per 1,000
live births (NCHS, 2008) mostly due to an increase in the number of infants born weighing less than 750 gm (1 lb, 10.5 oz). The majority of these infants die within the first year
of life (NCHS, 2008).
Since 2002, the infant mortality rate has declined slightly, with rates of 6.84 in 2003,
6.78 in 2004, 6.86 in 2005 and 6.71 (preliminary) in 2006 (NCHS, 2008). As you can see ,
the infant mortality rate has stayed fairly constant the past few years. This is the first
time there was a plateau and no serious decline in infant mortality rates.
Hispanic women have the highest infant mortality rate — 13.63 — of any ethnic
group, with Cuban women having the lowest — 4.42 (NCHS, 2008).
Preterm infants (born before 37 weeks gestation) account for the highest percentage
of infant deaths, 68.6 percent. Very preterm infants are only 2 percent of births but
account for over half of the infant deaths in 2005. The plateau in infant mortality is due
to the increase in very preterm births but no decline in their mortality (NCHS, 2008).
The incidence of low birth weight (LBW) babies steadily declined between 1960
and 1984, when it was 6.7 percent. In the 1990s the percent of LBW babies increased by 9
percent, to 7.6 percent, due to the increase in multiple births. The rate of LBW babies in
2003 was 7.93 percent, with a continued increase in multiple births (NCHS, 2005). In
2006, the incidence of LBW climbed to 8.3 percent without a rise in multiple births
(NCHS, 2009). The incidence of very low birth weight (VLBW) babies accounted for 1.45
percent of all births in 2003, also influenced by the increase in multiple births. Unfortunately,
the incidence of LBW and VLBW babies is higher in African-American and Hispanic populations. In 2006, the incidence of VLBW babies was 1.49 percent (NCHS, January, 2009).
Sexual & Reproductive Health
33
Other data reported by NCHS is that maternal weight gain has increased. Between
1940 and 1960 the average gain was 22 lb. In 1970 the average gain was 27 lb, increasing
to 33 lb by the 1980s and dropping to 30.5 lb in 1998, where it remained in 2000 (NCHS,
2002). That translates to a 40 percent increase in maternal weight gain from the 1940s to
today. For every 2.2 lb (1 kg) increase in maternal weight gain, there was a 20 to 30 gm
increase in birth weight.
From 1990 to 2006 the percentage of pregnant women gaining more than 40 lb rose
30 percent, from 16.0 to 20.7 percent (NCHS, January, 2009).
Often overlooked is the rate of fetal mortality, defined as spontaneous intrauterine
death any time during pregnancy. Generally, only fetal deaths after 20 weeks are reported. In 2005, the rate was 6.22 per 1,000 live births, down considerably from 7.75 in
1990 (NCHS, April, 2009). The rates for fetal mortality differ by age, ethnic groups,
multiple births and number of previous pregnancies. More research is needed to determine its causes and prevention strategies.
Despite our best efforts, malnutrition and inadequate diets during pregnancy still
exist. Government agencies studying the United States population have found dietary,
biochemical, clinical and anthropometric evidence of poorly nourished Americans.
Lower socioeconomic groups have a larger percentage of malnutrition, but socioeconomic status alone does not ensure an adequate diet.
RISK FACTORS & OUTCOME
When trying to reduce the risk of a poor pregnancy outcome, it is important to
separate factors you can control from those you cannot. The most important controllable
factors in perinatal mortality are prenatal medical care (started in the first trimester) and
adequate nutrition (resulting in proper weight gain) during pregnancy. Late or no
prenatal care is one of the biggest contributors to poor pregnancy outcome.
The purpose of prenatal care is to assess medical and nutritional risks to determine
the best treatment during pregnancy. Many risk factors relate to the nutritional status of
the mother and can be obtained with the obstetrical history, number of previous pregnancies, intervals between pregnancies, birth control methods, birth weight of other
children and weight gain with each pregnancy.
Knowing any pre-existing conditions or illnesses helps determine nutritional
recommendations. Most of all, good prenatal care can prevent complications before they
threaten the health and welfare of either the mother or the fetus.
Appropriate weight gain is critical to a good pregnancy outcome. In 2009, the
Institute of Medicine (IOM) updated the 1990 guidelines for appropriate weight gain
during pregnancy. The new report emphasizes nutrition and weight gain recommendations for overweight and obese women to prevent poor pregnancy outcomes in both the
mother and baby, as this problem has been growing over the years.
Research has linked not just prepregnancy weight to outcome, but specifically
excessive weight gain in overweight or obese women.
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Some of the complications of excessive weight gain include:
• gestational diabetes;
• gestational hypertension;
• preeclampsia;
• Cesarean delivery;
• large-for-gestational-age babies;
• congenital anomalies, and
• short- and long-term health of the baby (Kiel, et al., 2007, ADA, 2009).
Chapter 6 will cover this topic in detail.
Health habits that affect the nutrient status of the mother must also be considered:
smoking, alcohol consumption, drug use, pica, excessive supplementation, fad diet,
weight-loss diet, eating habits and patterns. The chart below summarizes factors affecting pregnancy outcome, with a complete list in Appendix #1.
Factors Affecting Pregnancy Outcome
General Factors
Nutritional status
Prepregnancy weight
Body mass index (BMI)
Parity
Socioeconomic status
Adolescence
Depression
Illnesses
Diabetes
Hypertension
Renal disease
Heart disease
Liver disease
AIDS
Cancer
Infectious disease
Present Pregnancy
Weight gain
Dietary adequacy
Disordered eating
Complications: hypertension,
gestational diabetes
Use of alcohol, drugs, tobacco
Agrichemicals in water
Prenatal care
Hyperemesis gravidarum
Bariatric surgery
Previous Pregnancies
Preeclampsia
LBW, FGR
Stillbirth
Neonatal death
Multiple pregnancies
Pregnancy intervals
The interval between pregnancies appears to influence outcome. As the interval
between pregnancies decreases, the risk of LBW, preterm birth and small size for gestational age (SGA) increases (Zhu, et al., 1999; Khoshnood, et al., 1998). The interval between pregnancies when the risk is lowest is 18 months to 59 months (Conde-Agudelo,
et al., 2006). Women giving births less than 18 months, or more than 59 months, from
Sexual & Reproductive Health
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their previous delivery, had increased risk of delivering babies that were preterm, LBW
and SGA. The risk is greatest when the interval is less than six months. The optimal
interpregnancy interval is 18 to 23 months.
Disordered eating can increase the risk for LBW, preterm and SGA babies (Conti, et
al., 1998). A history of disordered eating did not effect pregnancy outcome, but disordered eating prior to or during pregnancy does increase the risk.
Another risk factor may be agrichemicals in surface water. Women who conceived
during the months when agrichemicals in surface water were highest (April to July) had
the highest incidence of birth defects (Winchester, et al, 2009).
Over the years, researchers have compiled evidence that periodontal disease, such
as periodontitis, adversely effects pregnancy outcome, leading to preterm and very
preterm babies (Sanchez, et al., 2004; Jarjoura, et al., 2005). The rate of preterm delivery
in women with moderate to severe periodontal disease was 28.6 percent, compared to
11.2 percent in healthy women (Offenbacher, et al., 2006). In another study, the rate for
SGA babies was 3.2 percent in healthy women, 6.5 percent in women with mild periodontal disease and 13.8 percent in women with moderate to severe periodontal disease
(Boggess, 2006).
Since periodontal disease is an infectious and inflammatory condition, it may be
that certain cytokines and prostaglandins produced to fight the infection, initiate the
process that leads to preterm delivery and SGA babies (Tucker, 2006). A newer study
(Gomes-Filho, et al., 2009) found no association between periodontal disease and either
prematurity or LBW. At this point the relationship of periodontal disease to birth weight
and prematurity is not clear.
The American Dietetic Association (ADA) has updated a 2002 position paper
entitled Nutrition and Lifestyle for a Healthy Pregnancy Outcome, which reviews the relationship of nutrition and pregnancy outcome (ADA, 2008) and published a new position paper titled Obesity, Reproduction and Pregnancy Outcomes (ADA, 2009).
NUTRITION AND FERTILITY
If nutrition during pregnancy improves pregnancy outcome, what about
periconceptional nutrition? Will diet and/or supplementation increase fertility and rates
of conception, or decrease poor outcomes?
The relationship of nutrition and fertility is being investigated and includes the
following: maternal height, body weight (too low or too high), body composition, eating
disorders, athletic training, vegetarian diets, excessive carotene intake, phytoestrogens
in foods, iron deficiency (serum ferritin below 40 ng/mL), caffeine, coffee intake, alcohol intake (moderate or excessive), cigarette smoking (Brown, 1993) and polycystic
ovarian disease, one of the leading causes of infertility in the country (Scalzo, 2001).
Women trying to conceive may want to avoid alcohol, as alcohol intake may make
it more difficult to conceive (Jensen, et al., 1998). The effect of caffeine on fertility is still
up in the air, with studies showing different effects. Caan, et al., (1998) found no differences in fertility in women consuming high, moderate or low amounts of caffeine.
Sexual & Reproductive Health
36
Jensen et al. (1998), however, found that women consuming over 700 mg/day of caffeine
had a more difficult time conceiving.
Other nutrients consumed prior to pregnancy may effect the course of the pregnancy. Dietary Ω-3 fatty acids now appear to be linked to both maternal reproduction
and the proper development of the brain and retina of the fetus in utero, and the baby
after birth. Inadequate amounts of dietary Ω-3 fatty acids during pregnancy or after birth
may have serious consequences. (This will be discussed in detail in the next chapter.)
Folic acid is required early in pregnancy to prevent neural tube defects.
Periconceptional supplementation with 800 mcg folic acid decreased the incidence of
the occurrence of neural tube defects in pregnant women (Czeizel and Dudas, 1992).
In newer studies, periconceptual supplementation with folate reduced the incidence of neural tube defects and reduced the incidence of early spontaneous preterm
birth by 50 to 70 percent (Wolff, et al., 2009; Bukowski, et al., 2009).
Periconceptional vitamin supplementation with folic acid does not appear to
protect against cleft palate and cleft lip (Czeizel, et al., 1999). Abnormal maternal folate
metabolism, in a preliminary study, increased the risk of offspring with Down Syndrome (James, et al., 1999). Zinc supplementation may prevent some abnormal fetal
development (Keen and Zidenberg-Cher, 1994; King, 2000; Hess and King, 2009).
While much remains to be learned about periconceptional nutrition, it does no
harm to improve dietary intake and take a daily vitamin and mineral supplement, and
may prove beneficial.
We do know about obesity, however. In the US, approximately 25 percent of infertility appears to be caused by overweight and obesity (ADA, 2008). Issues that negatively impact fertility of overweight and obese women include (ADA, 2008):
• increased time to conception
• increased risk for polycystic ovarian syndrome
• higher waist-to-hip ratio
• lower implantation and pregnancy rates with reproductive technology
Overweight or obese women should consider losing weight prior to getting pregnant — especially if they are having difficulty conceiving. Some studies suggest there is
an increase in spontaneous abortions in obese women undergoing fertility treatment
(ACOG, 2005). CDC recommends improving weight status prior to pregnancy.
DISEASES IN LATER LIFE
In a review of the relationship of pregnancy to disease in later life, James (1997)
found that not only are periconceptional nutritional status and nutrition during pregnancy linked to pregnancy outcome, but that they also may be linked to diseases such
as hypertension, heart disease, stroke and diabetes later in life.
It appears that these chronic diseases are related to the size of a baby at birth.
Babies that are either LBW or SGA, but not preterm, have an increased incidence of
these chronic diseases (Godfrey and Baker, 2000).
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It appears that the fetus adapts physiologically, structurally and metabolically
when there is an insult at a critical developmental stage. This is called "programming,"
and the change is permanent. One such insult is not meeting the demand for a specific
nutrient at the time it is required by the fetus. (Langley-Evans, et al., 1998). (Chapter
Five will discuss the timing of fetal nutrient requirements in more detail.)
Epidemiological studies gave the first clue to the relationship of birth weight to
coronary heart disease (CHD). In England, 16,000 babies have been traced from birth to
the present. Infants born with a LBW had significantly higher death rates from CHD. As
birth weight increased, the rate of death from CHD decreased (Osmond, et al., 1993;
Barker, et al., 1993). This relationship has been confirmed in other studies, including the
US Nurses Study, which looked at 70,297 nurses in the United States (Rich-Edwards, et
al., 1997). Now there is widespread acceptance that fetal growth restriction (LBW and
SGA) is associated with CHD in later life.
Painter (2006) studied the effects of the 1944-1945 Dutch famine on the age of onset
of CHD. Compared with individuals not exposed to the famine, the researchers found
an earlier age of onset in the individuals exposed to the famine. However the mortality
rate from all causes in the individuals exposed to the famine does not appear to be
related to famine exposure (Huxley, 2006).
As with CHD, an association has been found between LBW and SGA babies and
high blood pressure and hypertension in over 34 studies; it is unrelated to other lifestyle
factors such as smoking, alcohol intake and obesity in adulthood (Godfrey and Barker, 2000).
The incidence of altered glucose tolerance, insulin resistance and Type 2 diabetes is
higher in people who were LBW babies. In one study, infants weighing less than 5.5 lb
had a 40 percent incidence of Type 2 diabetes and impaired glucose tolerance. That rate
fell to 14 percent among those weighing up to 9.5 lb at birth. The incidence increased if
birth weight was over 9.5 lb at birth (Hales, et al., 1991).
The relationship between LBW and glucose tolerance is independent of lifestyle.
However, poor lifestyle choices can compound the problem. Those individuals who
were born small and are obese in adulthood have the highest incidence of impaired
glucose tolerance and Type 2 diabetes (Hales, et al., 1991).
EPIGENETICS
Epigenetics refers to how genes express themselves, not to the coding sequence of
DNA. Siblings may have the same gene, but in one the gene is “turned on” and in the
other it is “turned off,” which alters the functioning of the gene. There are “marks” or
metabolic changes in DNA, RNA or histones (part of the chromatin in the nucleosome
of the cell) that determine if the gene is “on” or “off,” and these marks can be inherited.
For instance, a common epigenetic change is the methylation of DNA (the addition
of a methyl group to the base cytosine). Hypermethylation causes the gene to turn “off.”
When the cells divide, the change to the DNA is copied and passed on to the next
generation of cells (Ross, 2007). In other cases, a portion of the gene may be
hypomethylated, which expresses the gene (Zeisler, 2009).
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Epigenetics may be the link between our genetic makeup and the environment.
While it is difficult to alter our genes during our lifetime, epigenes can be modified by
diet and environment, then passed down through generations (Stover, 2006). Many of
the diseases associated with aging, such as cancer, heart disease and autoimmune
diseases, may result from epigenetic changes that alter our physiology.
The same may be true during pregnancy. The fetus inherits the genes from its
parents but also inherits the epigenetic codes marks on the genes that control the expression of the gene. In addition, the fetus can also adapt to its environment by altering
its own epigenetic code (Zeisel, 2009).
The methylation of DNA, RNA and histones requires S-adenosylmethionine (SAM),
a methyl donor. The availability of SAM is influenced by the amount of choline, methionine
and folate in the body. Too much or too little can cause epigenetic changes (Zeisel, 2009).
In mice, the agouti gene determines the color of fur. The folic acid intake of pregnant mice determines the offspring's fur color. If the agouti gene promoter region is
turned on, the offspring's coat color is yellow; if it is turned off due to methylation of
DNA, the coat color is darker, as the gene is not able to express itself (Stover, 2006). The
coat color stays with offspring for their entire life. So changing folic acid intake, either
increasing or decreasing it, alters the expression of the agouti gene and fur color in mice.
Pregnant women during the Dutch famine of World War II delivered small babies
due to the lack of food. Their children, even though they had plenty of food while they
were growing up and during pregnancy, also delivered small children, smaller than
would have been predicted (www.epigenome.eu/en/2,48,872, accessed 10/24/07). It is
thought that the lack of food in the first generation altered epigenes related to the size of
offspring and that information was passed on to the next generation.
Epigenetics may explain some inherited susceptibilities to disease, such as asthma,
diabetes, heart disease and obesity (Zeisel, 2009; Waterland, 2009).
The bottom line is that a mother's diet affects not only the short-term health of her
baby, but the long-term health as well. The goal of health care professionals is to determine the nutritional risks that may impact the outcome of the pregnancy, and to intervene before any damage is done to the fetus.
Health professionals, including nutrition professionals, should actively discourage
smoking, alcohol consumption and illicit drug use in order to improve pregnancy
outcomes. If a woman follows sound dietary guidelines and minimizes other lifestyle risks,
she will have done the best she can to create a normal, healthy infant. In fact, if women are
given advice to eat well, gain weight, take prenatal vitamins, don't drink alcohol, don't
do drugs and don't smoke cigarettes, they have a lower incidence of LBW babies than
those women who do not recall getting this prenatal advice (Kogan, et al., 1994).
The following chapters will cover nutrition-related risk factors, explaining what
they are, how to identify and assess them in a pregnant woman, and how to use nutrition to improve the course and outcome of pregnancy.
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Chapter Four:
Physiological Changes Which
Alter Nutrient Needs
During pregnancy, the body undergoes many physiological changes necessary
for a successful pregnancy outcome, as shown below. Every organ in the body will have
additional demands put on it as the pregnancy progresses, increasing the need for
nutrients. Many of these physiological changes have nutritional implications.
Physiological Changes in Pregnancy
Blood
Plasma volume increases
Red blood cells increase
Leukocytes increase
Renal Function
Renal blood flow increases
Glomerular filtration rate increases
Nutrients “spill” into urine
Heart
Cardiac output increases
Heart rate increases
Peripheral vascular resistance increases
Fluid leakage into tissues
Liver
Protein production increases
Cholesterol production increases
Increased workload
GI Tract
Smooth muscles affected
Peristalsis decreases
Placenta
Nutrient & waste transfer
Source of growth factors
Hormones
Pregnancy hormones produced
Increases in estrogen & progesterone
Metabolism
Altered carbohydrate, fat & protein
metabolism
Decreased sensitivity to insulin
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HORMONES
Human chorionic gonadotropin (hCG), produced during pregnancy, prevents the
corpus luteum from returning to its normal size at the end of the female menstrual
cycle. Instead, it stimulates the corpus luteum to secrete more hormones — estrogen
and progesterone — that cause the endometrium to store nutrients. The corpus luteum
grows larger, about two times its original size one month after the pregnancy begins.
The secretion of these sex hormones is vital to early fetal development. By about week
12, the placenta can secrete enough estrogen and progesterone to maintain the pregnancy, so the corpus luteum returns to its normal size and production of hCG decreases.
The increased level of estrogen during pregnancy affects different organ systems of
the body, one of which is stimulation of uterine growth. The heart has an increase in
blood volume, heart rate, stroke volume and cardiac output. The additional blood
volume necessary to carry nutrients and waste products requires the heart to work
harder, and it is able to adapt by increasing output.
An increase in renal retention of sodium is caused by estrogen. Increasing blood
and plasma volume requires additional water; sodium retention increases the amount of
water in the body. An increase in serum proteins produced in the liver is also caused by
increased estrogen production. These proteins carry nutrients, enzymes, albumin, etc.
Each performs a vital function for pregnancy.
Increases in progesterone levels are responsible for an elevation in basal body
temperature, which slightly increases caloric need and stimulation of maternal respiration. Unlike estrogen, progesterone stimulates the kidneys to lose sodium, due in part to
increased aldosterone production, which is involved in water balance. The net result is a
slight loss of sodium from the kidneys, affecting sodium requirements during pregnancy.
The most noticeable effect of increased progesterone is a decrease in activity of
smooth muscles, such as the colon. When peristalsis of the colon decreases, constipation
results. The cardio-esophageal sphincter, located where the esophagus enters the stomach, is a smooth muscle that provides pressure to keep the contents of the stomach from
regurgitating into the esophagus. During pregnancy, this sphincter is relaxed, so heartburn results. Constipation and heartburn are common in pregnancy.
The placental hormone human chorionic somatomammotropin (hCS), also known
as human placental lactogen (hPL) is secreted by the 5th week of pregnancy. It reaches a
peak secretion of 1 to 2 gm/day, paralleling the growth of the placenta. Mammary
tissue growth is stimulated by hCS.
Metabolically, hCS plays a weak role in causing the deposition of protein into
tissues. (Growth hormone is 100 times more effective than hCS in promoting tissue
growth.) Sensitivity of tissues to insulin decreases in the presence of hCS, decreasing
glucose utilization in the mother, thus allowing more glucose to be available for the
fetus. In addition, hCS increases the release of free fatty acids from fat stores, providing
an alternative fuel source for the mother. During pregnancy, there can be a 40 to 60
percent decline in insulin sensitivity due to hCS, as well as an increased production of
adiponectin by maternal and fetal tissue (NAS, 2009).
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BLOOD
Many changes occur in blood volume and the red blood cells, as shown in the
graph below. There is an increase in plasma volume of 40 to 50 percent over non-pregnant levels, while total blood volume expansion is 35 percent. The number of red blood
cells increases by 20 percent. Increase in the plasma volume begins at 6 to 8 weeks
gestation, at which point it steadily rises until it peaks somewhere between the 30th and
34th week.
Plasma volume expands earlier than red blood cells, causing a temporary fall in
hematocrit levels, known as hemodilution of pregnancy. The hematocrit begins to fall
somewhere in mid-pregnancy, around the 20th to 24th week, as the plasma volume (but
not the number of cells) expands rapidly. It is common to see women with normal
hematocrits at the beginning of pregnancy drop below normal as the pregnancy
progresses. By the end of the pregnancy, many return to normal levels.
Expansion of Blood & Components
50
% Expansion
40
30
10
0
Plasma
Blood
Red Blood Cells
Hemoglobin drops during pregnancy by as much as 2 gm/dL, due to the diluting
effect of plasma expansion and the increased need for red blood cell production. The
production of red blood cells does not begin until the second trimester, with the greatest
rise late in the third trimester.
A normal nonpregnant (and prepregnant) hemoglobin value of 13.5 gm/dL decreases to about 11.6 gm/dL in the second trimester of pregnancy, even in iron-supplemented women. In the last trimester of pregnancy, the hemoglobin rises by about 1 gm/
dL to 12.5 gm/dL by the 36th week of gestation. (These values are norms, and vary in
individuals.)
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Expansion of the plasma volume is critical for a successful pregnancy. The increased circulation is needed for the skin to dissipate heat, for kidneys to increase
filtration and for perfusion of the placenta. Red blood cell volume is utilized by the
fetus and by the mother for the additional metabolizing tissue. When the plasma does
not expand sufficiently, problems with the pregnancy can result.
Other changes seen in the blood of pregnant women include an increase in the
number of leukocytes, mostly neutrophils. Some pregnant women, about 20 percent,
may have an increase in the number of immature leukocytes. In addition, there is a twoto four-fold increase in levels of fibrinogen.
Many serum, plasma and blood levels of various nutrients change during pregnancy, therefore it is difficult to use them to assess the nutritional status of pregnant
women. Some nutrients increase, others decrease and still others stay the same. Changes
from trimester to trimester also occur, as is the case with iron, zinc, calcium, vitamin B6
and others. A lower blood level does not necessarily indicate a problem and may only
be a physiologic adaptation to pregnancy.
For example, after the 10th week of pregnancy, triglyceride concentrations may be
up to 20 percent higher in pregnant women than in nonpregnant women. Cholesterol
and fatty acids also increase, but not as much as triglycerides. Serum albumin, on the
other hand, decreases by 8 to 10 percent during the first 10 weeks of pregnancy and
continues to decline another 10 percent for the duration of the pregnancy (King, 2000).
Until each nutrient can be studied and normal pregnancy values determined for
each trimester, it is difficult to interpret nutritional status using laboratory values —
except for the most researched nutrients: iron, calcium and glucose.
CARDIOVASCULAR SYSTEM
The heart must work harder during pregnancy. Total cardiac output is 30 to 40
percent higher in pregnancy. The heart rate increases by approximately 10 to 15 beats
per minute, rising to 85 to 90 beats per minute. The cardiac output per beat also increases, as does the stroke volume (by 30 percent) — the heart can pump more blood
with each beat.
To accomplish this additional work there is a decrease in peripheral vascular
resistance and in arterial blood pressure. Because there is less resistance to the blood
flowing through the arteries and veins, it is easier for the heart to circulate blood and
plasma. Both the systolic and diastolic blood pressure decrease.
One side effect of the decrease in blood pressure and vascular resistance is leakage
of fluid from capillaries into intercellular spaces. This causes edema, noted in one-third
of all pregnant women. Edema is normal in pregnancy and does not need to be treated
the same as in a nonpregnant woman. Using diuretics to treat edema during pregnancy
can cause more harm than good because it decreases the plasma volume expansion.
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RENAL FUNCTION
During pregnancy the kidneys must filter extra waste products, not only for the
mother and her additional tissue, but also for the fetus. To be able to do this, the blood
flow to the kidneys increases by 30 to 40 percent, reaching 600 to 1000 mL/min. The
amount of plasma that is filtered increases by 50 percent.
Due to this increased load, the kidneys are not as efficient in filtering water, electrolytes and solutes — glucose, amino acids, urea and creatinine. As a result, some of these
substances are not cleared as quickly or efficiently and may “spill” into the urine.
In a nonpregnant woman, glucose does not appear in the urine until the blood level
reaches a concentration of 190 mg/dL. In pregnancy, glucose may appear in the urine
with blood concentrations as low as 155 mg/dL. Amino acids, not normally found in the
urine of healthy nonpregnant women, may appear in the urine of healthy pregnant
women and can reach 2 gm/day. Folate excretion can double to 10 to 15 mcg/day, not a
large amount. Some women, however may lose up to 50 mcg/day (Picciano, 1996).
Sodium balance is also affected. With so much blood and plasma being filtered, the
kidneys are not as effective in handling sodium and there tends to be a sodium loss
from the kidneys. Considering the amount of extra work done by the kidneys, they are
amazingly efficient — but not as efficient as in nonpregnant women.
LIVER
The liver has many roles during pregnancy, although its blood flow does not
change. The liver is the site of protein production, which increases. However, due to the
diluting effect of pregnancy, total serum proteins decrease by 20 percent.
Proteins that increase in pregnancy include albumin, which helps maintain the
increased fluid volume, and carrier proteins such as transferrin, ceruloplasmin and
fibrinogen.
Cholesterol and serum lipids increase 25 to 40 percent and 200 to 400 percent
respectively over nonpregnant levels (Hachey, 1994). Some of this change may be due to
alterations in metabolism (discussed later). Another cause may be that cholesterol is a
precursor of steroid hormones, which increase during pregnancy.
The work of the liver increases dramatically during pregnancy. The detoxification of
harmful compounds and substances increases, as does the metabolic workload required for
the mother and fetus. The liver works in concert with the placenta as a multiorgan
system for the exchange of nutrients. This is designed to ensure adequate nutrient
production to meet fetal needs, especially amino acids (Battaglia and Thureen, 1997).
GASTROINTESTINAL SYSTEM
Many of the problems associated with the gastrointestinal tract occur as a result of
decreased smooth muscle activity mentioned earlier, such as increased gastric emptying
time and decreased intestinal tract motility.
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When the stomach gets too full, the contents of the stomach are easily regurgitated
into the esophagus. Hydrochloric acid, used to digest food, irritates the esophagus,
causing heartburn. The solution to this problem is to eat smaller meals low in fat more
frequently. Never letting the stomach get too full decreases the possibility of reflux.
Other tips include: keep the head above the rest of the body (don't lie down, sit up); eat
early so food is digested by bedtime; only eat foods as tolerated; and wear loose clothing.
If the problem persists, a non-aluminum antacid will relieve the symptoms. (An
additional benefit of the antacid is that it has approximately 250 mg calcium/tablet,
which the body will absorb.) Appendix #11 lists some other tips for heartburn during
pregnancy.
Constipation in pregnancy is caused by a decrease in peristalsis, due to smooth
muscle relaxation. The pressure of the fetus in the abdomen can also slow down transit
time of food in the intestinal tract. Increasing fiber and fluids in the diet can relieve
constipation. Natural laxatives can also be used, as long as they are not digested and
just pass through the intestinal tract.
Exercise is another remedy for constipation. Walking, or any activity that does not
stress the body, will help. If everything fails, remember, the constipation will only last as
long as the pregnancy.
Nausea and vomiting are common during the first trimester of pregnancy due to
changes in hormones. Usually, the discomfort lasts for the first 12 to 15 weeks of pregnancy and then disappears. As long as there is adequate weight gain and the woman is
not severely underweight, few problems result.
Appendix #13 lists some tips for managing nausea and vomiting. This topic will
also be covered in more detail in Chapter Eight. However, the most important point to
remember is to listen to your patients and don't close your mind to any possibility. Erick
(1994) found that potato chips and lemonade worked wonders for many of her patients
who had morning sickness. The saltiness of the potato chips calmed the nausea and
caused thirst. The sweet and sour favors of lemonade seemed to keep the nausea at bay.
METABOLISM
Maternal metabolism alters during pregnancy to what is known as “accelerated
starvation,” since it mimics metabolic alterations seen during fasting or starvation.
Decreased concentrations of glucose and amino acids, increased concentrations of free
fatty acids, ketones, triglycerides and cholesterol, and decreased responsiveness to
insulin characterize maternal metabolism, as shown in the chart on the following page.
King (1994, 2000) found that energy metabolism differs greatly among women
during pregnancy depending upon their prepregnancy energy status and their situation
during pregnancy. Actual total requirements may be zero for the undernourished
woman whose body adaptations spare energy for fetal growth. If energy is abundant
and the woman is well-nourished, her needs may be nearly 120,000 kcal during the
course of the pregnancy.
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Maternal Metabolic Changes in Pregnancy
Decreased blood level:
• Glucose
• Amino acids
• Insulin
Increased blood level:
• Free fatty acids, ketones
• Triglycerides
• Cholesterol
• Cytokines - leptin, adiponectin
Overall Changes:
• Shift from glucose to fat as major
energy source
• Decreased responsiveness of
tissues to insulin
• Slight change in blood pH from
ketones
The fetus utilizes mostly glucose for energy. It uses very small amounts of free fatty
acids. The placenta itself is a major metabolic organ, consuming large quantities of
glucose. The only source of these energy substrates is the mother. To get the energy the
mother needs, the body switches from using glucose to using fat as the primary energy
source, saving most glucose for use by the placenta and fetus.
Early in the second trimester, you begin to see a general drop in the mother's serum
glucose levels. Following a meal, however, the maternal metabolism reacts differently,
with transient hyperglycemia, hyperinsulinemia and increased insulin resistance in the
liver, muscle and adipose tissue. The chart below shows hormones whose production
increases during pregnancy and which are responsible for many of the metabolic alterations noted during pregnancy. In addition to hormones, cytokines are involved in
energy expenditure, although the exact mechanisms are only beginning to be elucidated
(NAS, 2009).
Hormones Affecting Metabolism
hCG
• increases estrogen and progesterone
Estrogen
• impairs glucose tolerance
• antagonistic effect to insulin
hPL/hCS
• decreases glucose utilization
Pituitary Prolactin
• decreases insulin sensitivity
• decreases insulin binding within
• causes deposition of protein into tissues
adipose tissue
(weakly)
• stimulates lipolysis
Glucocorticoids (cortisol)
• mobilizes amino acids
Thyroxine
• antagonist to insulin
• increases basal metabolic rate
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PLACENTA
The placenta is an organ located high on the back wall of the uterus. Arteries and
capillaries of the maternal circulation feed into it and veins drain blood from it. The
umbilical cord has two arteries and one vein to supply the fetus. We can say that the
circulations of the mother and fetus meet, but never touch. A membrane separates the
two circulatory systems.
One major function of the placenta is to exchange nutrients, oxygen and waste
products between the mother and the fetus. Nutrients are transferred across the placenta by passive diffusion, facilitated diffusion, active transport, convection and
vesicular transport. The chart below summarizes placental transfer of nutrients.
To be transported by passive diffusion, the concentration of the nutrients must be
higher in the maternal blood than in the fetal blood. If so, the nutrients will cross the
membrane to the fetus. Nutrients that are passively diffused include oxygen, carbon
dioxide, water, electrolytes and many vitamins and minerals.
Placental Nutrient Transport
Passive Diffusion
• Water
• Oxygen
• Carbon dioxide
• Electrolytes
• Many vitamins & minerals
Facilitated Diffusion
• Glucose
Vesicular Transport
• Immunoglobulins
Active Transport
• Amino acids
• Calcium
• Iron
• Potassium
• Phosphorus
• Vitamin B6
Convection
• Volume of fluid flows through
pores in placental membrane and
takes solutes with it
Since the fetus must have glucose for energy, a means to help glucose get to the
fetus has been created. Glucose, transported by facilitated diffusion, attaches to a protein molecule that helps the glucose cross the placenta, even if the maternal glucose
concentration is not much greater than or even lower than the fetal concentration. The
transporter is known as membrane-localized glucose transporter (GLUT).
Other nutrients — amino acids, calcium, iron, potassium, phosphorus and vitamin
B6 — are actively transported from the mother to the fetus. Even if the concentration of
nutrients in the maternal blood is less than the fetal blood, the nutrients will cross the
placenta with the help of an energy-requiring transport system.
The significance of the active transport of these nutrients is that the fetus will get
nutrients at the expense of the mother. If the mother is not consuming enough calcium,
iron or protein, her body stores will be used by the fetus.
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This is the reason iron deficiency anemia can result from pregnancy. If calcium
intake is inadequate, calcium from the bones will be used, causing a thinning of bones.
Protein stores in muscle mass will be broken down if the fetus needs more protein.
Protein levels in fetal circulation can be two times higher than in maternal circulation
(some of the protein and amino acids are used for energy by the fetus).
The reverse is also true. If vitamin B6 is supplemented in large doses and the
maternal blood levels are high, excessive amounts can be actively transported across the
placenta to the fetus. Other nutrients that passively diffuse, if supplemented in large
doses, may cross to the fetus in excessive amounts.
So is the fetus a complete parasite, as is historically believed? The answer is no. If
the mother does not have sufficient vitamins and minerals in her blood, they cannot
cross the placenta, with the exception of the actively transported nutrients noted above.
That means deficiencies in the maternal diet can affect the fetus. The fetus cannot get
nutrients if they are not in sufficient concentration in the maternal blood.
Adequate uterine blood flow is essential for normal nutrient transfer. Any disruption
decreases the nutrients available for placental transfer. A decrease in the expansion of the
plasma fluid volume can disrupt nutrient transfer. When the plasma volume is smaller,
there is less perfusion of the placenta and fewer nutrients are present to cross the placenta.
FETAL GROWTH AND GENE REGULATION
Another role of the placenta, besides nutrient transfer, is the production of growth
factors necessary for the normal development of the placenta and fetus. These growth
factors are peptides and cytokines, which modulate amino acid transport and increase
glucose uptake and utilization, RNA, DNA and protein synthesis, cell replication and
fat accretion (Garnica and Chan, 1997; NAS, 2009). Some growth factors include:
• Insulin-like growth factor (IGF)-I Ty and IGF-II
• Transforming growth factor (TGF)
• Platelet-derived growth factor (PDGF) alpha and beta
• Type I IGF-I receptor (IGF-IR)
• Fibroblast growth factor (FGF)
• Leptin
During pregnancy, the concentration of IGF-1 increases and there is a positive
correlation between fetal and cord plasma concentrations of IGF-I and birthweight
(Garnica and Chan, 1997; Hay, 1999; Jansson and Powell, 2000). IGF-I decreases protein
breakdown and increases protein accretion.
What's interesting is that nutrient supply influences the production of growth
factors. The intracellular glucose concentration regulates IGF-I and IGF-II production
(Hay, 1999; Garnica and Chan, 1997). If inadequate amounts of glucose are available,
less IGF-I and IGF-II are produced, decreasing the weight of the fetus at birth.
Besides the overall weight of the fetus, IGF-I influences the growth of organs,
particularly the brain and the myelinization of the brain (Hay, 1999).
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It may be that lack of sufficient energy affects birth weight not just by denying the
fetus adequate energy, but because the quantity of growth factors is insufficient to
promote optimal growth in utero (Hay, 1999).
Leptin production by the plancenta increases, with a large percent going to the
mother to help her accumulate fat during pregnancy (NAS, 2009).
OMEGA-3 FATTY ACIDS (Ω-3)
Fatty acids are an integral part of every cell membrane, hence they are called
essential fatty acids (EFA). Two, linoleic acid (LA, 18:2 Ω-6) and alpha-linolenic acid
(ALA, 18:3 Ω-3), make up a large portion of the fatty acids found on the cell membranes.
Humans can not synthesize EFA so they must be included in the diet.
EFA are metabolized in the liver to long chain polyunsaturated fatty acids (LCP).
Three of these, arachidonic acid (AA, 20:4 Ω-6), eicosapentaenoic acid (EPA, 20:3 Ω-3)
and docosahexaenoic acid (DHA, 22:6 Ω-3), are incorporated into cell membranes in all
tissues of the body. Linoleic acid is considered the “parent” of the Ω-6 fatty acids and
alpha-linolenic acid is the “parent” of the Ω-3 fatty acids.
The types of fats eaten determine the fatty acid makeup of cells. For instance, if the
diet is high in LA-containing vegetable oils, the cell membrane will have a high concentration of AA. If the diet contains ALA, there will be EPA and DHA incorporated into
the cell membrane. Cell membranes contain both types of LCP but the amounts differ
based on what the mother eats.
Placental and fetal development require that LCP be transported from maternal
circulation, across the placenta, into the fetal venous blood, since the fetus and placenta
can not metabolize EFA to LCP. The LCP are incorporated into the central nervous
system, brain and tissues of the fetus.
The first few weeks after conception — usually before the mother knows she is
pregnant — are the most active period of brain cell division. The last trimester is the
most rapid period of brain growth and requires a substantial amount of DHA, since 50
percent of the LCP in the brain is DHA. It is estimated that the fetus requires a total of
600 gm DHA, or 2.2 gm/day if averaged over the entire pregnancy (Connor, 1996). Another
study estimated that a full-term infant has a total DHA content of 3800 mg (Das, 2003).
Fatty acids are stored in the body and can be delivered to the fetus when needed, so a
mother with a store of DHA can supply it to the fetus.
Pregnancy causes a decline in the EFA and LCP status of the mother, especially
EPA and DHA (Hornstra, 2000). Studies investigating Ω-3 fatty acid intake during
pregnancy have found that maternal DHA concentration drops dramatically during
pregnancy and may develop into a deficiency (Holman, et al., 1991; Innis and Elias,
2003). It is postulated that the mother's ability to supply DHA may be insufficient to
meet the needs of the fetus if she has inadequate stores and/or intake (Connor,
Backgrounder, 1996). Supplementing pregnant women with DHA, 200 mg/day, increased
the amount of DHA in cells. The level of DHA did decline in the supplemented women
during the third trimester, but the decline was less than the placebo group (Montgomery, et al., 2003).
Sexual & Reproductive Health
49
Rebuilding maternal supplies of fatty acids take time, most likely over six months
(Hornstra, 2000). If the interval between pregnancies is short, the supply of EFA and LCP
may not be adequate for the second fetus.
Connor et al. (Lipids, 1996) supplemented the diet of 15 women for nine weeks with 2.6
gm/day of Ω-3 fatty acids, of which 1.01 gm was DHA. The result was an increase in the
DHA content of red blood cells (RBC) from 4.69 to 7.15 percent. Plasma DHA content increased from 2.12 to 3.15 percent at term. Infants had an increase in RBC DHA from 5.86 to
7.92 percent and an increase in plasma DHA from 3.47 to 5.05 percent. The concentration of
DHA in infant RBC and plasma rose 35 and 45 percent respectively.
Other studies have supplemented both Ω-3 and Ω-6 fatty acids and found increases
in fetal and maternal tissue and plasma levels (Hornstra, 2000; Smuts, et al., 2003). If
supplementing EFA or LCP, it is important to supplement both. Too much of one or the
other can create imbalances.
While Ω-6 fatty acids are plentiful in the diet, Ω-3 fatty acids are not. Pregnant women
may not get adequate amounts of dietary Ω-3 fatty acids. If a mother's intake of EFA is low,
body stores can be used. However, much more LA is stored than ALA in body fat, making it
difficult to meet fetal DHA requirements. Since the mother is the fetus' sole source of EPA,
DHA and AA, it is essential to consume adequate Ω-3 fatty acids during pregnancy.
Inadequate LCP may influence the outcome of pregnancy. Researchers have been
investigating whether or not there is a link between insufficient LCP during pregnancy and
duration of pregnancy, fetal growth, infant birth weight, preeclampsia, depression, infant
visual function and infant neurodevelopment.
Foreman-van Drongelen, et al., (1995) found a significant relationship between birth
weight, length and head circumference, and LCP levels in the umbilical artery wall. Higher
umbilical levels of LCP correlated with a more advanced gestational age and anthropometric measurements. DHA, in particular, has been positively associated with birth weight
(Hornstra, 2000). As fetal and cord levels of DHA increase, so does infant birth weight.
In a study that looked at fish intake and preterm delivery, Olsen and colleagues
(2002) found that as intake of seafood (fish) increased, the incidence of preterm deliveries decreased. Women with the highest intake of seafood had a preterm delivery rate of
1.9 percent, while the group with the lowest intake had a 7.1 percent rate of preterm
deliveries. Low birth weight and intrauterine growth retardation also decreased with
increasing seafood intake, while mean birth weight, duration of gestation and birth
weight adjusted for gestational age tended to increase with increasing seafood intake.
These associations were strongest for fish intakes below (or above) 15 gm of fish or 0.15
gm long chain fatty acids a day.
Conner's studies show that increasing dietary Ω-3 fatty acids will increase levels in the
mother and fetus and can affect the outcome of pregnancy and possibly even children's IQ.
Helland et al. (2003) found that supplementation with long chain Ω-3 fatty acids during
pregnancy improved the mental development of children at age 4. While this is a preliminary study, it raises intriguing possibilities. Petridou et al. (1998) studied 109 children with
CP and 278 control children in Greece, and found an inverse relationship between fish
Sexual & Reproductive Health
50
intake and CP — as fish intake went up, the incidence of CP went down. This warrants a
larger, multicenter study.
Not all studies have found a link between LCP and pregnancy outcome. In 2005,
the Agency for Healthcare Research and Quality (AHRQ) reviewed the literature to
determine the health effects of Ω-3 fatty acids on child and maternal health (Lewin, et
al., 2005). They looked at how maternal intake of Ω-3 fatty acids influences:
• duration of gestation;
• SGA babies;
• clinical outcomes in term and preterm babies; and
• growth patterns, neurological, visual or cognitive development outcomes in
term or preterm infants.
The authors of the review concluded that there is a lack of safety data on LCP
supplementation, which needs to be corrected. The relationship of maternal LCP intake
to pregnancy outcomes was either inconclusive or there were no relationships. The
influence of Ω-3 fatty acids on the duration of pregnancy was the one area where there
is some data to support it, but it is by no means conclusive. The full report is available
at:: <www.ahrq.gov/downloads/pub/evidence/pdf/o3maternalchild/o3mch.pdf>
The evidence for Ω-3 fatty acids improving growth patterns, neurological, visual or
cognitive development was also inconclusive. Jensen (2006) published a review of the
studies on the effects of Ω-3 during pregnancy and lactation and found:
Although the results of the studies summarized above are inconsistent, some
evidence suggests that higher Ω-3 fatty acid intakes during pregnancy may
increase gestational duration without obvious adverse effects.
Keep in mind that one reason the studies are inconclusive is the difficulty in designing a study that takes all of the factors of dietary fat intake into account, e.g. ratio of
Ω-3 to Ω-6 fatty acids, dietary intake of Ω-3 and Ω-6 fats, length of time necessary to
change cellular composition of fats, and determining the optimal intake.
At present, we know the importance of adequate LCP during pregnancy, but the
effect of less than optimal amounts is still uncertain, as is how much LCP is optimal.
The recommendations from "expert panels" range from 200 to 300 mg/day DHA
(Simopoulos, et al., 1999; AOCS, 2003), which appear safe. The March of Dimes recommends 200 mg/day of DHA intake (www.marchofdimes.com/pnhec/159_55030.asp).
SOURCES OF Ω-3
The chart on the next page shows the sources of LA, ALA, EPA and DHA. As you
can see, the only sources of LCP are EPA and DHA, found in fish. The body can convert
some of the ALA to EPA and DHA, but it is very inefficient. Only about 5 to 10 percent
of ALA is converted to EPA and a lesser percentage is converted to DHA.
While the necessity of LCP are now recognized for pregnant women, intake of fish
and fish oil supplements to provide LCP can be problematic due to the contamination of
fish with mercury, which the body converts to the toxic methylmercury.
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51
Sources & Metabolism of Fatty Acids
Ω-6 Fatty Acids
Linoleic acid (LA)
Arachidonic acid (AA)
Dietary Sources
Nuts, seeds, vegetable & seed oils
(body converts linoleic acid to arachidonic acid)
Ω-3 Fatty Acids
Alpha-linolenic acid (ALNA)
Dietary Sources
Green plants, algae, rapeseed (canola oil),
soybeans, flax, flaxseed, walnuts
Marine oils, fish
Marine oils, fish
Eicosapentaenoic acid (EPA)
Docosahexaenoic acid (DHA)
Grams of EPA & DHA in 3 oz of:
Sardines 3.3
Mackerel 2.5
Bass
0.8
Oysters 0.6
Trout
Tuna
1.6
0.5
Bluefish 1.5
Crab
0.3
Salmon
Shrimp
1.0
0.3
Notes: The conversion of ALNA to EPA and DHA is inefficient in adults. Preterm and full term infants have
limited ability to convert the ALNA to EPA and DHA, but can convert LA to AA.
EPA is easily converted to DHA in adults and infants.
Presently, the amount of mercury necessary to produce developmental toxicity is
not known and hotly debated (Charnley, 2006). The average mercury intake of pregnant
women is 1.4 mcg/day according to the EPA and 0.8 mcg/day according to the FDA.
To protect pregnant women and their babies, policy-makers have come up with an
amount of mercury considered to have no adverse effects — this "no-adverse-effect
level" (NOAEL) is then divided by a safety factor. The final number is called the "reference dose" (RfD) by the EPA (Charnley, 2006).
To simplify this issue for the public, the EPA and FDA revised their consumer
advisory on fish intake in 2004. The advisory emphasizes the benefits of eating fish, but
for women of childbearing age or planning to get pregnant, there are ways to minimize
mercury intake from fish. They can thus feel confident they are not exposing themselves
and their babies to harmful effects of mercury (FDA, 2004). The three steps to limiting
mercury intake are found in the chart on the next page.
The bottom line is that women who are or may become pregnant can eat some fish,
enough to meet their needs. One 6 oz serving of salmon has 900 to 1400 mg of DHA;
other white fish has 200 to 700 mg DHA/6 oz serving. Tuna (light) has 500 to 1500 mg/6
oz serving. If you consider the requirement of approximately 200 to 300 mg DHA/day,
one serving of white fish and one serving of salmon or tuna will meet that requirement.
Eating plant sources of Ω-3 fatty acids will also contribute to overall DHA intake.
Womenshealth.gov has a fact sheet for use with clients that lists the fish to eat and
not eat during pregnancy and recommended amount. This is available at:
<www.womenshealth.gov/pregnancy/mom-to-be-tools/fish-facts.pdf.>
The March of Dimes has information on their website, that can be used with clients
on omega-3 fatty acids in pregnancy and mercury and fish in pregnancy.
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52
FDA/EPA Consumer Advisory on Methylmercury in Fish
1. Do not eat shark, swordfish, king mackerel or tilefish because they contain
high levels of mercury.
2. Eat up to 12 oz (two average meals) a week of a variety of fish and shellfish
that are lower in mercury.
• Five of the most commonly eaten fish that are low in mercury are shrimp,
canned light tuna, salmon, pollock and catfish.
• Another commonly eaten fish, albacore ("white tuna") has more mercury than
canned light tuna. So when choosing your two meals of fish and shellfish, you
may eat up to 6 oz (one average meal) of albacore tuna per week.
3. Check local advisories about the safety of fish caught by family and friends in your
local lakes, rivers and costal areas. If no advice is available, eat up to 6 oz (one
average meal) per week of fish you catch from local waters, but don't consume any
other fish during that week.
Premature infants can be born with or can develop impaired vision or nervous
system disorders due to insufficient DHA levels in the brain and retina (Salem and Ward,
1993). Even adequate DHA levels at birth can drop rapidly since there are no fat stores to
supply DHA and infants have limited ability to elongate ALA to DHA. For this reason, all
formulas now contain DHA, although the amounts vary in specific formulas.
PLASMA VOLUME EXPANSION AND NUTRIENT TRANSFER
It is essential that plasma volume expands adequately. Otherwise, cardiac output
is impaired and less blood flows to the placenta, decreasing its size and surface area and
ability to transport nutrients to the fetus.
Any disease or treatment that results in decreased plasma expansion, cardiac
output, placental blood flow, placental size or nutrient transfer can cause a poor pregnancy outcome. Decreased placental size and nutrient transfer can increase the risk for
fetal growth retardation, resulting in low birth weight and/or a small-for-gestational
age (SGA) baby. Inadequate glucose can decrease the production of placental growth
factors leading to low birth weight and growth retardation.
Treating edematous pregnant women with diuretics can cause a 50 percent reduction in plasma volume expansion, seriously affecting the fetus and the delivery of
nutrients. Pregnancy is not a time for diuretic use. Improper transfer of nutrients can
alter the outcome of pregnancy, as you will see in the next chapter.
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Chapter Five:
Nutrient Needs in Pregnancy
Nutrition sets the foundation for the life of every child. The quality of the first six
to 12 months of a baby’s life is determined by the mother’s nutritional status and diet
while pregnant. Poor nutrient intake during pregnancy can affect a child for life, if
severe damage results from poor nutritional status and intake.
Pregnancy is a time of growth for both mother and the fetus. The mother’s body
undergoes many changes necessary to carry the fetus to term. The uterus and breasts
increase in size; blood volume and extracellular fluid volume expand. To meet the
nutritional demands of maternal and fetal growth, additional nutrients are necessary.
Meeting the nutritional demands of pregnancy will affect the outcome of the
pregnancy. The fetus relies on the mother for all its nutritional needs. If the nutrients are
unavailable, the fetus will suffer. Nutrition impacts weight gain, birth weight, gestational age, congenital anomalies, nutritional status and birth defects in the fetus as well
as chronic diseases in later life. The importance of proper nutrient intake during pregnancy cannot be overemphasized.
Both the amount of a nutrient and its time of ingestion, in relation to fetal development, are extremely important, as shown in the chart on the next page. The first trimester
of pregnancy is a time of rapid cell division and organ development. Nutrients essential
for this process — zinc, folic acid, vitamins B12 and D and protein — are critical during the
first three months, as are folic acid and essential fatty acids in the months prior to pregnancy.
The second trimester shows continued rapid cell growth and organ development,
and the fetus grows in size. Thus, caloric intake becomes more important during the
second trimester and is particularly important during the third trimester, when the fetus
triples in size and completes development of organ systems.
54
Sexual & Reproductive Health
Timing of Nutrient Intake
2nd Trimester
3rd Trimester
• Hyperplasia
• Hypertrophy
• Organs still developing
• Growth increases
• Plasma volume expands rapidly
• Slow red blood cell increase
• Hypertrophy
• Rapid growth of fetus
• Rapid bone growth and
mineralization
• Red blood cell increase
Nutrients
Nutrients
1st Trimester
• Hyperplasia
• Rapid cell division
• Organs develop
Nutrients
Zinc, folic acid,
protein, Ω-3 & Ω-6
fatty acids, vitamins
B6 and B12 and D
Calories, protein, iron, folic acid,
zinc, vitamins B6 and B12 and D
Calories, protein, iron,
calcium, magnesium, B
vitamins, DHA (Ω-3 fatty
acids) and vitamin D
Understanding when nutrients are required is as important as understanding how
much of a particular nutrient is necessary. A summary of nutrient requirements for
pregnancy is provided in the chart below.
Recommended Dietary Reference Intake for Pregnancy
Vitamins
≤18 Years
A*
750 mcg
D£
5 mcg
15 mg
E**
C§
80 mg
K¶
75 mcg
600 mcg
Folic Acid
Thiamin (B1)
1.4 mg
Riboflavin (B2)
1.4 mg
18 mg
Niacin (B3)
Pyridoxine (B6)
1.9 mg
B12
2.6 mcg
Pantothenic Acid¶
6 mcg
Biotin¶
30 mcg
Choline¶
450 mg
Minerals
≥18 Years
770 mcg
5 mcg
15 mg
85 mg
90 mcg
600 mcg
1.4 mg
1.4 mg
18 mg
1.9 mg
2.6 mcg
6 mcg
30 mcg
450 mg
≤18 Years
Calcium
Chromium¶
Copper
Fluoride¶
Iron
Iodine
Magnesium
Manganese¶
Molybdenum
Phosphorus
Selenium
Zinc
1300 mg
29 mcg
1000 mcg
3 mg
27 mg
220 mcg
400 mg
2 mg
50 mcg
1250 mg
60 mcg
12 mg
≥18 Years
1000 mg
30 mcg
1000 mcg
3 mg
27 mg
220 mcg
350 mg
2 mg
50 mcg
700 mg
60 mcg
11 mg
Note: values are Recommended Dietary Allowances (RDA); those marked ¶ are Adequate Intakes (AI)
* As retinol activity equivalents (RAEs) 1 RAE = 1 μg retinol, 12 μg B-carotene
£ As cholecalciferol. 1 ug cholecalciferol = 40 IU vitamin D.
**alpha tocopherol (Equivalent to approximately 13.5 IU);
§ Smokers require an additional 35 mg/day
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CALORIES
To meet the energy demands of both maternal and fetal tissues, approximately
60,000 kcal are required during the course of pregnancy (IOM, 2002). This requirement
includes the increased metabolic needs of the fetus and maternal tissues, the increased
cardiac output, and the needs of the placenta and uterine muscle. This caloric level may
be overestimated for sedentary women.
Additional caloric needs during the first trimester are minimal. Cellular division is
rapid, but the weight of the fetus during the first trimester is negligible. About 2,100 to
2300 kcal/day is sufficient to meet all additional calorie demands, with most of those
calories needed for maternal tissues.
Caloric needs increase as the pregnancy progresses. During the second and third
trimesters, the caloric needs increase above pre-pregnancy intake. The increase in calories accounts for the more rapid growth of the fetus in the later stages of pregnancy. As
the weight of the mother increases, it takes more energy to do the same amount of work.
Therefore, the exact number of calories to recommend will vary, based on the individual.
The DRI (Dietary Reference Intake) for calories for pregnant women has changed.
When the new Institute of Medicine recommendations came out in 2002, DRI were
based on age, trimester and total calories (IOM, 2002). Prior recommendations were for
a specific number of calories above normal consumption. The new recommendations for
caloric intake are:
• For females aged 14 through 18:
>> 2368 for the first trimester;
>> 2708 for the second trimester; and
>> 2820 for the third trimester.
• For women aged 19 through 50:
>> 2403 for the first trimester;
>> 2743 for the second trimester; and
>> 2855 for the third trimester. (See Appendix #3A.)
In sum, no additional calories for the first trimester, an additional 340 kcal for the
second trimester and an additional 452 kcal for the third trimester in each age group.
Women who remain physically active during pregnancy — especially those who
engage in weight-bearing activities such as walking, bicycling, tennis, jogging — may
have caloric needs higher than sedentary women. Physically active women have been
shown to have babies who weigh less than babies of sedentary women. This is most
likely due to higher caloric needs which were not met during pregnancy. If weight gain
is adequate and sufficient calories are being consumed, the birth weight of the baby is
not affected, regardless of the amount of physical activity. (The Prenatal Weight Gain
Grid, discussed in the next chapter, is the best tool for monitoring weight gain.)
In a recent study to measure the energy costs of pregnancy, based on pre-pregnancy Body Mass Index (BMI), Butte and colleagues (2004) found that women with a
normal pre-pregnancy BMI had a negligible increase in caloric needs the first trimester,
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56
but that their needs increased by 350 kcal/day in the second trimester and 500 kcal/day
in the third trimester. Basal metabolic rates (BMI) increased throughout the pregnancy,
but were not offset by a decrease in activity as once thought. Women with either a low
or normal pre-pregnancy weight had less of an increase in BMR than the high prepregnancy BMI group. One explanation for the higher increase in BMR in the high-BMI
group was increased fat deposition, which was considered unhealthy.
The results of the study by Butte are close to the IOM recommendations in the
second trimester, but are approximately 50 kcal/day higher in the third trimester.
The variability in energy needs and energy expenditure in pregnant women makes
it difficult to advise women what to eat during pregnancy. For normal-weight and
overweight women in developed countries, the need for food may be very small, especially if activity levels decline. These women may not need 2800 kcal in the third trimester. Underweight women may need more. Therefore, “eating to appetite” is probably
the best advice that can be offered (King, et al., 1994; King, 2000).
Many women watch their weight, which can present a problem when they become
pregnant, if they have trouble increasing their intake. Adolescents are extremely weightconscious, trying to keep their intake down to avoid gaining.
PROTEIN
This is the backbone of all new tissues created during pregnancy. Both cells and the
substances necessary for metabolism are made from protein. During pregnancy, the
body conserves protein, especially during the last half of pregnancy when the demand
is greatest. Hormones and growth favors anabolism (tissue growth), so the body retains
nitrogen for amino acid and protein synthesis.
Protein is stored in maternal tissues. The greatest storage occurs in the last 10
weeks of pregnancy. The total amount of protein needed for the fetus, placenta, amniotic fluid, uterus, blood and extracellular fluid is estimated at 925 gm for a normal 270day pregnancy, with 760 gm accumulated in the last 20 weeks (King, 2000; IOM, 2002).
Maternal protein deficiency can have serious fetal consequences. Metabolism is
altered if the quantity and/or quality of protein is inadequate. Even though amino acids
are transported from mother to fetus across a concentration gradient, if the supply is
inadequate in the mother, the fetus will be deficient.
No longer is the requirement for protein during pregnancy based on maternal age.
According to the IOM (2002) report: “For adolescents, the additional need for protein during
the second and third trimesters is assumed to be the same as for adult women.”
The DRI for protein for nonpregnant women is 0.8 gm/kg, or 48 to 52 gm/day.
Adding an additional 25 gm for pregnancy, the daily requirement would be about 70 to
75 gm/day, as shown in the chart on the next page. For multiparous pregnancies, the
recommendation is an additional 50 gm protein/day, with enough calories (1000/day)
to spare the protein, starting the 20th week gestation (IOM, 2002).
The average daily protein intake in the US is 75 to 100 gm, so it appears that protein intake is not usually a problem in pregnant women, at least in this country — with
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57
two exceptions. Vegans need careful planning to meet protein needs. Low-income
women, who lack adequate financial resources to purchase expensive red meat, poultry
and fish, may consume diets low in protein. Work with these women to plan higherprotein meals with low-cost protein sources.
Protein Requirement
1.1 gm/kg/day of protein
or
0.8 gm/kg/day + 25 gm/day additional protein
Example:Weight in pounds ÷ 2.2 = kg
135 pounds ÷ 2.2 = 61.4 kg
(61.4 kg x 1.1) = 70.5 gm
(61.4 kg x 0.8 ) + 25 = 74 gm
Special consideration
+50 gm/day beginning 20th week for multiparous pregnancy*
Note: No longer is the protein requirement for pregnancy based on age.
* Must have adequate calories (1,000/day) to spare protein
Women with seemingly adequate protein intake may indeed have a protein deficiency if their caloric intake is inadequate. To meet the energy demands of pregnancy,
some amino acids will be used for energy. The adequacy of protein in the diet of a
pregnant women must be evaluated in the context of her total diet.
FAT INTAKE
Many pregnant women reduce their dietary fat intake because the general population
is constantly advised to lower total fat consumption. Although the literature documenting
the safety of restricted-fat but energy-adequate diets in pregnancy is incomplete, a diet
limited to 30 percent of calories from fat is acceptable. However, this is true only if total
energy is adequate, if the quality and amount of dietary protein is sufficient, if micronutrients are maintained at recommended levels, and if essential fatty acids supply at least 5
percent of total energy (Hachey, 1994; IOM, 2002).
Very-low-fat diets are not warranted, because they do not supply adequate
amounts of essential fatty acids and fat-soluble vitamins — and as we saw in the previous chapter, inadequate docosahexaenoic acid is linked to LBW babies. In addition, the
bulk of this high-carbohydrate diet may discourage adequate energy intake.
Evidence suggests that Ω-3 fatty acids may improve pregnancy outcome. Observational studies have shown that women who eat higher amounts of fish have longer
pregnancies, higher birth weights, improved placental blood flow and a lower incidence
of preelcampsia (Murtaugh and Weingart, 1995; Makrides, 2008; Carlson, 2009). Supplementation with Ω-3 fatty acid during the third trimester of pregnancy increased the
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58
length of pregnancy (Smuts, et al., 2003). Since the initiation of labor needs prostaglandin F2α and E2, it is plausible that an increase in Ω-3 fatty acids will inhibit the production of these prostaglandins, increasing the duration of pregnancy.
In a multicenter trial in Europe, women who had one preterm birth supplemented
with 2.4 gm/day of Ω-3 fatty acids from fish oil had a lower incidence of a second
preterm birth (Olsen et al., 2000). However, a similar study in the US did not show the
same results (Harper, 2008). One other interesting study showed that women who ate
more than 340 gm of fish per week had children with improved outcomes (scores) for
prosocial behavior, fine motor skills, communication and social development (Hibbeln,
et al., 2007). The authors conclude that the fish intake didn't prevent bad pregnancy
outcomes but instead had beneficial effects on the children.
Recommendations have been set in the US for the amount of fatty acids in the diet of
pregnant women, although the data for determining them was slim (IOM, 2002). Because of
the lack of good data, the Adequate Intake (AI) for individual fatty acids is based on median
intake of pregnant women. The RDI published in 2002 recommend an AI of 13 gm/day of
the Ω-6 linoleic acid and 1.4 gm/day of the Ω-3 alpha-linolenic acid (IOM, 2002). The ratio of
the two fatty acids should be no more than 5 linoleic to 1 alpha-linolenic acid (IOM, 2002).
In Europe, joint recommendations on dietary fat intake in pregnancy and lactation
were released in 2007 and include (Koletzko, et al., 2007):
• average of 200 mg DHA/day DHA;
• intakes of up to 1 gm/day DHA or 2.7 gm/day Ω-3 fatty acids appear safe;
• women of childbearing years should aim to consume one to two servings of oily
fish a week;
• α-linolenic acid, the DHA precursor, is far less effective in DHA deposition in
fetal brain than DHA; and
• dietary inadequacies should be screened for and counseling offered.
Appendix #3A contains the DRI for Ω-3 fatty acids. Keep in mind that these recommendations may not be optimal as the data to make these recommendations was limited. In addition, intake of linoleic acid is usually adequate, but intake of α-linoleic acid
is not. I suspect the recommended AI of these fatty acids will change as more research
becomes available. Appendix #14 contains the Ω-3 fatty acids content of foods.
FIBER AND CARBOHYDRATES
New recommendations for fiber and carbohydrate intake during pregnancy were
revealed in the IOM (2002) report: Dietary Reference Intakes for Energy, Carbohydrate, Fiber,
Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids.
The AI for pregnant women, regardless of age, is 28 gm/day of total fiber. Total
fiber consists of dietary fiber and functional fiber: these two types of fiber are very
different. Dietary fiber consists of non-digestible carbohydrates and lignins that are part
of plants, such as cellulose, pectin, gums, hemicellulose, beta-glucans, oligosaccharides,
fructans and lignans (IOM, 2002). Functional fibers such as pectin, gums, chitin,
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polydextrose, inulin and indigestible dextrins are isolated nondigestible carbohydrates
that have beneficial physiological effects in humans (IOM, 2002). See Appendix #3A for
more information on the sources of various fibers.
Average fiber intake, based on the Continuing Survey of Food Intakes by Individuals
1994-1996 (CSFII), which was adjusted for fiber not in the database, is 17.1 to 18.8 gm/
day for women. The intake is well below the 28 gm/day recommended for pregnancy.
The DRI for carbohydrate during pregnancy is 175 gm/day, which accounts for
both maternal and fetal glucose needs (IOM, 2002). The median intake of carbohydrates
is approximately 180 to 230 gm/day, which is within the recommendations.
Following a low carbohydrate diet is not appropriate during pregnancy. Appendix
#3A contains the DRI for carbohydrates during pregnancy.
SODIUM
Six to 8 liters of water are retained during pregnancy. It takes 19,500 mg of sodium
to retain the additional water. Since there is a slight sodium loss through the kidneys,
some additional dietary sodium is needed during pregnancy.
The additional water is needed to increase the volume of plasma and intracellular
fluid, to maintain blood flow to the kidneys and for perfusion of the placenta. If the
plasma does not expand and the placenta is not perfused, there will be less nutrients
available to the fetus; decreased blood flow to the kidneys increases circulation of toxins.
No salt restriction is necessary during pregnancy. Women who do not salt their
food, cook with salt, or eat salty foods, may on occasion need to increase salt consumption. Some women crave salt when pregnant and may go as far as licking table salt to
alleviate craving. In most cases, those who crave salt are those who do not eat much.
Salt limitation is not the way to relieve edema. Limiting salt may restrict plasma
volume expansion. Treat edema by elevating the feet, sleeping on the left side and
restricting activity. Remember, some edema is normal in pregnant women, and should
be viewed as a sign that plasma volume is expanding. However, it is important to
differentiate normal pregnancy edema from serious edema (2+ to 3+ pitting edema),
which is not normal during pregnancy. Some women may need to limit salt intake to
control blood pressure.
IRON
The total iron needed during pregnancy averages between 1000 and 1100 mg —for
red blood cell production, development of the placenta and fetus, and maintaining
maternal blood volume (anticipating blood losses during delivery), as shown in the
chart on the next page (Hallberg, 1988; Bothwell, 2000; IOM, 2001).
The need for iron is not consistent during pregnancy. During the first trimester, the
iron demands of the fetus are low — maternal iron status is essentially unchanged from
pre-pregnancy. During the second trimester, maternal plasma begins to expand faster
than red blood cells and the demand for iron increases, causing a fall in hemoglobin,
serum iron, and serum ferritin levels, and an increase in transferrin (MMWR, 1998).
Sexual & Reproductive Health
60
Iron Needs During Pregnancy
Tissue
Fetus and placenta
Maternal blood
Iron losses
Total Iron for Pregnancy
Iron retained after delivery
Total Iron Needs
Iron Needs (mg)
320
500
250
1070
150-200
700-800
The greatest demand for iron occurs in the third trimester. Since iron is transported
against a concentration gradient, iron will continually be pulled from maternal stores.
At delivery, it is not uncommon to see levels of hemoglobin and iron higher in umbilical
cord blood than in maternal blood.
The indices of iron status most commonly used are hemoglobin (Hb) and hematocrit (Hct) levels. During pregnancy, these levels begin to drop during the end of the
first trimester, and reach their lowest level at the end of the second trimester (due to the
rapid plasma volume expansion). They may actually begin to rise somewhat during the
third trimester, even though this is the period of highest demand, if the woman is
supplementing with iron or has adequate stores (MMWR, 1998). Otherwise, hemoglobin
and hematocrit levels continue to fall in the third trimester (Bothwell, 2000).
Iron deficiency anemia, with resulting insufficient hemoglobin, can cause complications in pregnancy. Metabolism is altered, there is a smaller increase in plasma and
red cell volume, and less oxygen is transported to the tissues, decreasing energy
production. The immune system can be impaired, decreasing resistance to infection.
Also, placental insufficiency or hypertrophy decreases nutrient transfer to the fetus.
Increased incidence of urinary tract infections, pyelonephritis (inflammation of the
kidney), preeclampsia and pica are seen in anemic women (MMWR, 1998). Complications of anemia affect the outcome of pregnancy — higher incidence of premature
delivery (associated with low birth weight), stillbirth, and perinatal mortality are seen.
There are three stages of iron depletion, with increasing severity.
• Stage one is a depletion of iron stores without interference with Hb production.
Low serum ferritin level, the storage form of iron, with a normal Hb level indicates a depletion of iron stores. Most pregnant women have low or depleted
serum ferritin stores during the third trimester without hemoglobin production
problems, indicating a physiological adaptation to pregnancy. However, low
serum ferritin during the first or second trimester means a woman may progress
to stage two or three.
• Stage two of iron depletion is impaired Hb production, evidenced by a low ratio
of serum iron to total iron-binding capacity (Fe/TIBC), low mean corpuscular
Sexual & Reproductive Health
61
volume (MCV), and normal serum Hb. The serum Hb may be within normal
range, but may have decreased from mid-normal range to low-normal range.
• Stage three, iron deficiency anemia, is characterized by low serum ferritin levels,
low serum iron, decreased Hb and decreased MCV.
The published literature suggests that maternal anemia diagnosed at the beginning
of prenatal care is associated with an increased risk of preterm delivery, while anemia
diagnosed during the third trimester is not. Lack of association during the third trimester may occur, because hemodilution makes it difficult to distinguish between anemia
and expanded plasma volume (Scholl and Hediger, 1994). In fact, Steer (2000) suggests
that Hb levels between 9.5 to 11.5 gm/dL with normal MCV of 84 to 99 fL, minimizes
low birth weight and preterm labor. Hemoglobin levels of 9.5 to 11.5 gm/dL normally
indicate anemia. However, if the MCV is normal, as it is with a value above 84 fL, the
lower Hb is not a concern.
The type of birth control method used by women will affect the iron status at the
beginning of pregnancy. Oral contraceptives decrease blood loss by 50 percent, conserving iron. Intrauterine devices (IUD), although used by few women, double blood loss
during menstruation and thus decrease iron stores.
All pregnant women should have their iron status assessed using Hb and Hct
values. If these are low other tests can be done to determine if a woman has low iron
stores, preventing iron deficiency anemia later in the pregnancy. Smoking and higher
altitudes cause an increase in Hb and Hct levels.
The chart below, adapted from CDC, shows lab values indicating anemia and
adjustments for smoking and living at higher altitudes. Misdiagnosis of anemia occurs
if Hb and Hct are not adjusted.
Lab Indicators of Anemia
Pregnancy:
1st trimester
2nd trimester
3rd trimester
Smoking Adjustment¶
0.5 - <1.0 pack/day
1.0 - <2.0 packs/day
≥ 2.0 packs/day
Hb*
(gm/dl)
Hct**
(%)
<11.0
<10.5
<11.0
<33.0
<32.0
<33.0
+0.3
+0.5
+0.7
+1.0
+1.5
+2.0
*Hb=hemoglobin **Hct = hematrocrit
¶ Add to Hb/Hct value to determine if anemia is present
Source:CDC, USDHHS, MMWR, 47 (RR-3), April 3, 1998.
Altitude (feet)¶
3,000-3,999
4,000-4,999
5,000-5,999
6,000-6,999
7,000-7,999
8,000-8,999
9,000-9,999
10,000-11,000
Hb*
(gm/dl)
Hct**
(%)
+0.2
+0.3
+0.5
+0.7
+1.0
+1.3
+1.6
+2.0
+0.5
+1.0
+1.5
+2.0
+3.0
+4.0
+5.0
+6.0
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Dietary sources of iron, no matter what the choices, are usually not sufficient to meet
the iron demands of pregnancy. The iron requirement of pregnancy is 700 to 800 mg —
most of it needed in the second half of pregnancy. Iron absorption increases during each
trimester, from 0.4 mg/day the first trimester to 1.9 mg/day the second trimester to 5.0
mg/day the third trimester, regardless of the foods eaten (Bothwell, 2000). The DRI for
iron during pregnancy is 27 mg/day from 14 to 50 years of age (IOM, 2001).
If a women consumes of 10 to 15 mg of iron a day during pregnancy, and absorbs
from 0.4 to 5.0 mg/day, based on trimester, the total amount of iron absorbed during
pregnancy is 600 mg, below the 800 mg needed. The difference must be made up by iron
stores or supplements. It is very common to see women iron-deficient at the end of
pregnancy, as measured by levels of serum ferritin.
Iron from animal sources, heme iron, is more easily absorbed than non-heme iron,
from plant sources. Absorption of non-heme iron is decreased by phytates (in whole
grains and legumes), calcium and phosphorus (in milk), tannins (in tea) and polyphenols (in vegetables). Ascorbic acid increases absorption of non-heme and heme iron.
Absorption of non-heme iron ranges from 6 to 13 percent (Charlton and Bothwell, 1983).
Absorption of non-heme iron is inversely related to iron stores. As absorption
increases, stores decrease, and vice versa. Heme iron — found in meat, poultry and fish
— is better absorbed than non-heme iron and few factors interfere with its absorption.
Overall, iron absorption from food is difficult to assess due to the many variables.
It may be possible to increase or decrease the amount of iron absorbed, but not by
much. Reddy, et al., (2000) found that only 16.5 percent of the variance in iron absorption is due to food constituents: meat, phytates and ascorbic acid. No other nutrients
studied — calcium, phosphorus, phenols — influenced iron absorption.
Supplementation can reverse the fall in hemoglobin, serum iron and serum ferritin.
How much to supplement and what method of supplementation to use are widely
debated and researched. Absorption of supplemental iron is affected by the dose, iron
stores and the delivery form — alone or in combination with other vitamins and minerals. Studies have shown that supplementing pregnant women with 30 mg of elemental
iron significantly raises their serum iron levels. High doses of supplemental iron can
cause many GI side effects. The chart on the next page refers.
Most pregnant women are routinely supplemented with 27 mg of ferrous iron,
enough to allow them to absorb 2.5 to 3 mg/day. When considering whether to supplement with iron, certain factors should be considered. Calcium, magnesium or zinc can
decrease iron absorption. Any of these minerals, supplemented at the same time as iron,
can interfere with iron absorption, as can food. Layrisse et al. (1973), found that 50
percent more iron is absorbed when it is given between — not with — meals.
When iron is taken as a part of a multivitamin and mineral preparation, very little
of the iron may be released from the pill. Seligman et al. (1983) found iron release from a
prenatal vitamin and mineral supplement was, at best, 1 percent. This is of particular
concern since the majority of women in the US take a vitamin and mineral supplement
with iron and feel it will meet their iron needs during pregnancy, when in fact it may not.
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Rationale for Iron Supplementation
Dietary iron intake
Dietary iron absorbed (6-25% absorption rate)
10-15 mg/day
0.9-3.75 mg/day
Total dietary iron for pregnancy (270 days):
Absorbable iron from 27mg supplement
Total supplement for pregnancy (270 days):
Total intake from diet and supplements
240-800 mg
2.7 mg
725 mg
965 - 1725 mg
30 mg ferrous iron equals:
150 mg ferrous sulfate
300 mg ferrous gluconate
100 mg ferrous fumarate
Consideration of the effects of iron on other nutrients is important. Breskin, et al.,
(1983) found that women using a vitamin and mineral supplement with 30 to 60 mg of
iron had significantly lower serum zinc levels than when less iron was present. The
Institute of Medicine recommends supplementing with 15 mg of zinc and 2 mg of
copper when iron is supplemented at or above 30 mg/day.
Clinical trials have shown that iron supplementation is effective in raising serum
hemoglobin and ferritin levels (Yip, 1996; Madhavan, et al., 2004). Unfortunately, when
supplementation is done on a widespread basis, it is not as effective due to problems
with compliance. Most women do not like taking iron. It causes many gastrointestinal
disturbances — nausea, constipation, metallic taste in the mouth, loss of appetite, upset
stomach, gas, etc. — so many women just stop taking it. A big part of the non-compliance issue may be that physicians are prescribing too much iron. The higher the dose,
the lower the compliance.
Ridman et al. (1996) compared pregnant women supplemented with a single
weekly dose of 120 mg ferrous sulfate with those receiving a daily dose of 60 mg. The
effects on serum hemoglobin and ferritin were comparable. This raises the possibility
that one weekly dose may be enough for some women. Other studies have also concluded that weekly supplementation with iron is as effective as daily supplementation,
as long as the woman is not anemic at the beginning of the pregnancy (Casanueva, et al.,
2006; Mukhopadhyay, et al., 2004).
To decrease the symptoms associated with iron supplementation, instruct your
client to take iron before bed. Another option is to decrease the total amount taken. If a
woman is not anemic, 30 mg/day or 60 mg/week is adequate and is associated with
minimal side effects. If a woman is anemic, she needs to take a higher dose, which will
be prescribed by her physician. There is no benefit to prescribing iron supplements that
women do not take. It is better to find a smaller dose that is tolerated by the woman.
I have found that liquid iron, such as Floridex,® sold in health food stores, is much
better tolerated than pills. It contain ferrous gluconate, herbals and fruit extracts and
vitamin C to increase absorption.
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The CDC recommends the following to prevent anemia in pregnant women:
• Start oral, low-dose (30 mg/day) iron supplements at first prenatal visit;
• Encourage pregnant woman to eat iron-rich foods;
• Encourage pregnant women to eat foods that enhance absorption; and
• Screen women for anemia at the first prenatal care visit.
ZINC AND IRON
Zinc is essential during the first trimester; iron is not. It is important to ensure
adequate zinc early in pregnancy. Numerous studies have shown that supplementing
with iron increases hemoglobin levels, but reduces serum zinc levels (Breskin, et al.,
1983; O'Brien, et al., 1999).
Since it interferes with zinc, iron supplementation is not recommended during the
first trimester. This is especially true for women with adequate iron stores and serum
hemoglobin levels. They could wait until the second trimester to begin the higher level
of iron supplementation without any problem.
More recently, Harvey and colleagues (2007) found that supplementation with 100
mg iron/day had no detectable adverse effects on zinc metabolism. Note that this study
was small, 13 women, and the study period was the second and third trimesters.
Women who are severely iron-deficient pose a problem. Supplementation with iron
should begin as early as possible, but zinc and copper should be supplemented as well.
O'Brien and colleagues (1999) showed that supplementing with zinc and iron prevented
a fall in zinc levels while increasing serum iron. Taking supplemental iron in the ferrous
form, as a single pill rather than as part of a multi-vitamin and mineral preparation,
between meals, and without tea, coffee or milk (which inhibit absorption), will maximize iron absorption.
Pica, the eating of non-food substances, is often associated with iron deficiency.
Moore and Sears (1994) estimated that pica may occur in as many as half of iron-deficient patients. No one knows if pica causes iron deficiency or if iron deficiency causes a
craving for non-food substances. (Pica will be discussed in Chapter Eight.)
FOLIC ACID
Folic acid is a water-soluble B-complex vitamin, involved in the synthesis of amino
acids as well as purines and pyrimidines (molecules necessary for the production of
RNA, DNA, and red blood cells). Folate is the naturally-occurring form of the vitamin
and folic acid is the synthetic form (which is better absorbed).
A deficiency of folic acid (or folate) leads to impaired cell division and altered
protein synthesis. During the first trimester of pregnancy, when cells are rapidly dividing, adequate folic acid is critical. Poor outcomes of pregnancy have been attributed to
inadequate maternal folate, including spontaneous abortions, fetal malformation,
toxemia, preterm and small-for-gestational-age babies and antepartum hemorrhage
(Pietrzik and Thorand, 1997).
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A folic acid deficiency results in megaloblastic anemia, characterized by large,
nucleated red blood cells. Without sufficient folic acid, red blood cells cannot be synthesized. An MCV greater than 95 fL indicates a folic acid deficiency.
Serum folate levels decrease during pregnancy, beginning at mid-pregnancy, most
likely due to blood volume expansion, increased urinary excretion and hormonal
influences on folate metabolism. Supplementing with folic acid will prevent a deficiency, but may not reverse the physiological changes due to pregnancy. Studies have
also shown increased birth weights and prevention of preterm deliveries in women
with low serum and erythrocyte levels who supplemented with 150 to 200 mcg/day
folic acid (Mukherjee, et al., 1984).
Scholl and colleagues (1996) found that (after controlling for maternal characteristics, energy intake and other correlated nutrients) women with a low mean daily folate
intake (less than 240 mcg/day) had a nearly two-fold greater risk of preterm delivery
and infant LBW. Lower concentrations of serum folate at gestational week 28 were also
associated with a greater risk of preterm delivery and low birth weight. (The study was
observational; so, it is possible that folate may be a marker for other aspects of maternal
lifestyle or nutritional status that are causally related to preterm birth.)
In another study, intakes of folate below 500 mcg/day and serum folate levels below 16.3
ng/mL in the second trimester were associated with an increased risk of preterm delivery
(Siega-Riz, et al., 2004). The average intake of folate in the study was 463 mcg/day.
Deficient levels of folate have been linked to neural tube defects (NTD), such as
spina bifida, myelomeningocele, and anencephaly in infants. The central nervous
system develops inside the neural tube, which forms early in fetal life (between the 18th
and 20th day) and closes between the 24th and 27th day of pregnancy. At this time,
many women do not even know they are pregnant.
Studies done in northern Europe suggest that when women with one child with a
neural tube defect are supplemented with folic acid, the incidence of a second child
with a neural tube defect is decreased significantly (Smithells, et al., 1980, 1983).
A study published by the MRC Vitamin Study Research Group (Lancet, 1991)
resolved the debate over the effectiveness of folic acid supplementation and neural tube
defects. The study, a randomized double-blind prevention trial of 1,817 women, found
that 4 mg of folic acid reduced the incidence of neural tube defects by 72 percent over
the control group. The researchers concluded that :
Folic acid supplementation starting before pregnancy can now be firmly
recommended for all women who have had an affected pregnancy, and
public health measures should be taken to ensure that the diet of all women
who may bear children contains an adequate amount of folic acid.
Further proof of the link between folic acid and NTD came in a retrospective, casecontrol study published in 1993 (Werler, et al., 1993). This study looked at infants with
congenital malformations. It concluded that 0.4 mg of supplemental folic acid,
periconceptionally, can decrease the occurrence of NTD by 60 percent, and a high intake
of dietary folate may do the same thing.
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It has been suggested that abnormal folate metabolism causes some women to
need more folate than others (Pietrzik and Thorand, 1997; Boddie, et al., 2000). In these
women, folate absorption is decreased, necessitating a higher intake to prevent NTD. In
fact, a genetic abnormality in folate metabolism may be a risk factor for Down syndrome. Mothers of Down syndrome children were found to have abnormal folate
metabolism by James, et al., (1999). This, however, was just one study and further
confirmation is needed.
While other factors besides diet can cause NTD — genetics, geographic location,
socioeconomic status, race, nutrition and maternal health — the US Public Health
Service (USPHS) believes there is enough compelling information to make definite
recommendations on folic acid intake:
All women of childbearing age in the United States who are capable of
becoming pregnant should consume 0.4 mg (400 mcg) of folic acid per day
for the purpose of reducing their risk of having a pregnancy affected with
spina bifida or other NTD.
Since 1998, manufacturers can fortify cereal grains and flour (enriched bread, pasta,
flour, breakfast cereal and rice) with 140 mcg folic acid per 100 gm of flour (Hine, 1996).
Keep in mind that some, but not all, enriched bread, pasta and baked goods are made
from folic acid-fortified flour — the label must so indicate. Prepared baked goods may
or may not be made of folic acid-fortified flour.
The folic acid content of foods in the database of a nutrition program may or may
not differentiate between synthetic folic acid and naturally-occurring folate — check
with the company. Determining the folate/folic acid intake of a pregnant women (or
anyone), can thus be difficult.
A serving of a folic acid-fortified grain product provides about 40 mcg of folic acid;
fortified breakfast cereals can provide 25 to 100 percent of the RDI for folic acid. It is
estimated that folic acid fortification of grain will increase folic acid intake by 100 mcg a
day — and, in fact, women probably cannot meet their folic acid requirement without
the fortified grain products (Firth, 1998; Cuskelly, et al., 1999; Kloeblen, 1999). Firth, et al.,
(1998) found that without fortified foods, folic acid intake would only average 288 mcg/day.
In 1998 the IOM made a new recommendation for folate intake during pregnancy,
and another recommendation to prevent NTD. The reason they have two recommendations is that neural tube development occurs during the first four weeks after conception, when the woman is least likely to know she is pregnant. Therefore, all women
capable of getting pregnant should have sufficient levels of folic acid to prevent NTD.
As the IOM report stated:
It is recommended that women capable of becoming pregnant consume
400 mcg of folic acid daily from supplements, fortified foods or both in
addition to consuming food folate from a varied diet.
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The IOM decided that fortification or supplementation of synthetic folic acid, with
its superior absorption, is the only way to ensure women are getting enough folic acid.
Absorption of folate from food is approximately 50 percent, while absorption from
fortified foods is 85 percent and absorption from a supplement is 100 percent (Federal
Register, 1993; Bailey, 1998; Suitor and Baily, 2000). Fortified food eaten with other foods
has an absorption rate 1.7 times more efficient than when eaten alone. (IOM, 1998).
With this knowledge, the IOM Food and Nutrition Board decided to express the
DRI for folate in terms of Dietary Folate Equivalents (DFE), which takes into account the
differing absorption rates of synthetic folic acid and food folate (IOM, 1998).
For pregnant women, the DRI for folate is 600 DFE (600 mcg). To calculate DFE, use
the information in the chart below. Appendix #12 lists folate content of foods. (Keep in
mind that it is difficult to determine the DFE of foods made from flour, as the synthetic
folic acid versus natural folate is not differentiated.)
Dietary Folate Equivalents (DFE)
Source
Food folic acid
Food fortified with folic acid
Folic acid supplements
Absorption
50% absorption
85% absorption
100% absorption
Absorption
compared to food
1.7
2.0
1 DFE in food = 1 mcg folic acid from food
1 DFE in fortified foods = 1.7 mcg folic acid from food
1 DFE from supplement = 2 mcg folic acid from food
Example
400 mcg folic acid supplement = 800 DFE (400 x 2)
1 cup fortified pasta, 85 mcg fortified folic acid = 144 mcg DFE (85 x 1.7)
1/2 cup spinach, 100 mcg folic acid = 100 mcg DFE
Many foods do contain quite a bit of folic acid. Foods high in folic acid are dark
green leafy vegetables, liver, kidneys, legumes, oranges, grains and wheat germ. Cooking vegetables in water and high heat destroys 80 to 90 percent of the folic acid. If the
vegetables are eaten raw, little or no folic acid is lost. Since 50 percent of dietary folic acid
is absorbed in the intestinal tract, it is possible to get adequate folic acid needed for pregnancy from diet alone, but it is better to rely on supplements and folic acid fortified foods.
In December 1993, the FDA approved a health claim that linked folic acid to reduced incidence of NTD. A product must contain 10 percent of the RDI (Reference Daily
Intake), which for folate is 0.4 mg (400 mcg), in order to make a health claim. If the label
claims “high in folate,” it means a serving of food provides 20 percent or more of the
RDI of folate. If the label claims it is a “good source” of folate it means the food provides 10 to 19 percent of the RDI (Kurtzweil, 1996).
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Don't forget, pregnant women need 50 percent more folate than nonpregnant
women, so the RDI is not the best guide for pregnant women, unless you adjust for the
increased pregnancy needs.
Has fortification of grains and flour with folic acid made a difference? The answer is
yes. Quinlivan and Gregory (2003) found that the average intake of folic acid has risen in the
US by 215 to 240 mcg/day, which is two to three times the expected increase of 70 to 130
mcg/day, while Choumenkowitch, et al., (2002) found the increase to be 190 mcg/day.
The CDC compared serum and red blood cell folate levels for childbearing-aged
women. From NHANES III (1988-1994) to NHANES 1999, mean serum folate concentrations for aged 15 to 44 increased from 6.3 to 16.2 ng/mL, while red blood cell folate
increased from 181 to 315 ng/mL (MMWR, 2000). More importantly, the incidence of NDT
has decreased by 26 percent since the onset of folic acid fortification of grains and flour
(MMWR, 2004), a good outcome. However, only 40 percent of childbearing-age women
take a folic acid supplement (MMWR, 2004). Increasing that number can reduce NTD
even further. For more information on folic acid, visit: <www.folicacid.net>
From statistics released in April 2009, it appears that the reduction in incidence of NTD,
in particular spina bifida and anencephalus, has stopped. In 1991 the incidence of spina
bifida per 100,000 live births was 24.88, decreasing to 17.96 in 2005 and 17.99 in 2006
(Matthews, 2009). For anencephalus it was 18.38 in 1991, 10.39 in 2004, 11.11 in 2005 and
11.21 in 2006. Getting more childbearing age-women to supplement folic acid may help to
reduce the incidence of NTD even more.
Folate metabolism is controlled by a number of genes which can have single nucleotide
polymorphisms (SNP) — alterations in the gene that effect enzymes involved in folate
metabolism. One SNP in the MTHFR gene, found in 8 to 15 percent of the population
(Zeisel, 2009), can reduce folate enzymatic activity by 50 percent. Other genes can also have
polymorphisms, altering folate metabolism. Individuals with them may need more folate
than the rest of the population, including pregnant women.
How much folate is required is related to the requirement for choline, which also takes
part in one-carbon transfers and methylation reactions. Choline is found in the diet in eggs
and meat and can be made in the body from phosphatidylcholine. Premenopausal women
make more choline than postmenopausal women, since estrogen induces a gene that increases the production of choline. During pregnancy, estrogen levels are higher, so there is
more choline produced and transferred from the mother to the fetus (Zeisel, 2009). Lack of
sufficient choline may also increase the risk for NTD (Zeisel, 2009).
Like folate, there are SNP in the genes that control choline metabolism and these are
fairly common, increasing the dietary requirements for choline. If you look at the metabolic
pathways for one-carbon transfers, both folate and choline are required. If one of the nutrients is insufficient, you need a higher intake of the other to prevent metabolic abnormalities,
including the development of NTD in pregnancy (Zeisel, 2009).
It could be that the lack of a further decline in the incidence of NTD in the US may not
only be due to women not consuming the recommended amount of folate or folic acid, but
also that some women may have a higher need for folate and/or choline which is not met.
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ZINC
Zinc is involved in over 70 metabolic reactions in the body and is essential for
DNA and RNA production, protein synthesis, cell division and cell replication. Rats can
be made zinc-deficient in as short a period of time as six days, as evidenced by decreased DNA in the brain.
Studies done on rats have shown that a zinc deficiency severely impacts the outcome of pregnancy, causing congenital anomalies and malformations, including abnormal brain development and behavior. It may also cause a reduction in the zinc level in
dental enamel and dentin, increasing susceptibility to dental caries (Beach, et al., 1983).
In humans, the relationship of zinc to pregnancy outcome is much less clear.
Numerous studies have shown a relationship between low serum zinc levels in cord
and/or maternal blood and abnormal deliveries, congenital abnormalities (mostly
involving the central nervous system), low birth weight and preterm delivery. However,
other studies have not (King, 2000).
In an excellent review of zinc and pregnancy, King (2000) discusses over 52 studies
done on humans and concludes that while there is a relationship between zinc status
and outcome, the cause is most likely altered utilization, not deficiency. A diet high in
phytates (cereal-based), supplementing with high amounts of iron, smoking, alcohol
abuse and an acute stress response to infection or trauma, all decrease zinc utilization.
Due to a lack of data on normal values of serum zinc during pregnancy, it is difficult to determine how many pregnant women are zinc-deficient. In addition, serum zinc
levels decline during pregnancy as plasma volume expands (King, 2000).
In a newer review of maternal zinc supplementation, Hess and King (2009) found a
14 percent reduction in premature delivery and positive effect on birthweight in a
subset of zinc-deficient women. Zinc supplementation did not effect iron status.
Approximately 100 mg of additional zinc is needed during the course of pregnancy, much of it during the third trimester. The first and second trimester needs call for
an additional 0.5 and 1.5 mg, respectively, of zinc daily, while 4 mg/day is required in
the third trimester.
Zinc deficiencies in the US have been well documented; it is considered one of the
hardest nutrients to consume in DRI amounts. The average zinc intake is approximately 8
to 14 mg/day, which may or may not meet the 11 to 12 mg/day needed during pregnancy.
Vegetarians may have a lower intake, since the best source of dietary zinc is red
meat and they have a much higher intake of plant and cereal — foods high in phytates.
Most people get 70 percent of their dietary zinc from meat (NRC, 1989). In pregnancy,
the DRI increases to 15 mg. Absorption of zinc is approximately 20 percent.
The timing of zinc intake is as important as the quantity. During the first trimester,
when much blastogenesis occurs, zinc is essential for normal fetal development. Inadequacies cannot be made up later in the pregnancy. Once an organ is malformed, no
amount of zinc can repair the damage. Since zinc is often inadequate in the diet, a
supplement of 10 to 15 mg/day is recommended during the first trimester, especially if
iron is also supplemented (ADA, 2002).
70
Sexual & Reproductive Health
As discussed previously in this chapter, supplementation exceeding 60 mg of
elemental iron can lower plasma zinc concentrations. Thus, iron supplementation
should be delayed until the second trimester to avoid interference with zinc. If the
woman is iron-deficient, smaller doses of iron (taken separately from zinc) will minimize interference with zinc absorption.
Alcohol and cadmium (which is found in cigarettes) interfere with zinc metabolism. Alcohol increases urinary zinc losses and decreases plasma zinc concentration.
Increased placental cadmium levels alter the cadmium-to-zinc ratio and are related to
infant birth weight (Kuhnert, et al., 1988). Therefore, alcohol users and smokers need to
be especially careful to make sure they are receiving adequate zinc in their diet or
through supplements.
Dietary sources of zinc include meat, poultry, oysters, seafood, whole grain cereals,
milk, liver and eggs. With the exception of oysters, foods do not contain a lot of zinc.
For example, one 3 oz serving of meat contains only 1 to 2 mg of zinc, while an 8 oz
glass of milk contains just 0.88 mg of zinc.
CALCIUM
Calcium is necessary for bone and tooth formation in the fetus, as well as muscle
contraction and relaxation, blood clotting and blood pressure regulation. Changes in
calcium metabolism that occur during pregnancy — intestinal absorption, renal reabsorption and bone turnover — are caused by hormonal changes regulating calcium
metabolism, as shown in the diagram below.
Calcium Physiology
Low plasma calcium
Increase in parathyroid hormone (PTH)
Kidney
Increased production
active Vitamin D
Increased calcium
conservation
Absorption of
Calcium increases
plasma calcium
Bone cells
Decreased urinary
calcium excretion
Increased bone
demineralization
Increased
bone loss
plasma calcium
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The need for calcium increases as the pregnancy progresses. Eighty percent of the
calcium required during pregnancy is required during the third trimester, when the
fetal bones are mineralized at a rapid rate. Forbes (1976) determined that approximately
50 mg/day of calcium is transferred from the mother to the fetus, increasing to 330 mg/
day at 35 weeks gestation.
It is estimated that 200 mg/day of calcium is deposited in the fetal skeleton
(Prentice, 1994). To meet this increased need for calcium, absorption increases during
pregnancy, from 33 percent pregnancy to 50 percent during the second trimester and
53.8 percent during the third trimester (Ritchie, et al., 1998).
If the mother's diet is inadequate in calcium, decreased storage of calcium is common, since calcium is transported against a concentration gradient. Serum levels of
calcium are thus not a good indicator of calcium status, since calcium will be pulled out
of the bones to normalize serum levels.
Maternal parathyroid hyperplasia during pregnancy may be due to low calcium
intake. When serum calcium levels fall, the body signals the parathyroid gland to
secrete parathyroid hormone (PTH), which increases intestinal calcium absorption and
decreases loss from the kidneys.
The net result is an increase in serum calcium levels, shutting off the production of
PTH. If the serum levels of calcium are still too low, the level of PTH increases, signaling
the bone cells to release calcium into the serum, thus raising calcium levels high enough
to turn off the parathyroid gland’s production of PTH.
With increased estrogen production during pregnancy, the bone cells are more
resistant to the parathyroid hormone, so it takes higher levels to cause the bones to
begin releasing calcium. The resistance of the bone cells to parathyroid hormone makes
the gland work harder, causing hyperplasia, as shown in the diagram below.
Maternal Parathyroid Hyperplasia
Decreased plasma calcium
Parathyroid gland secretes PTH
Dietary calcium inadequate to increase serum calcium
Estrogen decreases effectiveness of PTH
Parathyroid gland secretes more PTH
Bones demineralized for calcium
Increased plasma calcium
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72
Early in the third trimester, blood pressure begins to elevate, corresponding to the
increased need for calcium. In pregnant women, the great demand for calcium can
lower serum levels.
If calcium is being utilized rapidly, maternal serum calcium levels drop, causing a
rise in blood pressure. O’Brien and Dufour (1994) found that by 34 to 36 weeks gestation, pregnant women with calcium intakes less than 1200 mg/day had higher systolic
and diastolic readings (3 to 6 mm Hg) than pregnant women with higher calcium
intakes. This is above the 5 mm Hg increase in blood pressure commonly seen in all
pregnant women. Supplementing calcium in nonpregnant individuals with high blood
pressure will lower their blood pressure — while calcium supplementation of pregnant
women has not been studied, it may be beneficial and will do no harm.
Calcium may also have a role in reducing the risk of preterm delivery in populations at risk for low calcium intake. Calcium supplementation, in theory, reduces
smooth muscle tone, including uterine muscle. In one study, supplementation with 2
gm/day decreased preterm delivery and low birth weight in an adolescent population
(Murtaugh and Weingart, 1995). If confirmed by further study, calcium supplementation
would be a simple and inexpensive intervention to reduce preterm birth. However, high
doses of calcium may cause constipation and decrease intestinal absorption of iron, zinc
and other minerals.
The DRI for calcium during pregnancy is 1300 mg/day for pregnant women under
age 19 and 1000 mg for those 19 years and older, either from the diet or supplements
(IOM, 1997). Adequate calcium in the third trimester is critical for the fetus, and protects
the mother from depleted calcium stores. The DRI for calcium is the same for pregnant
and non-pregnant women. The IOM, after reviewing the studies, felt that as long as
calcium intake was adequate, there was no effect on maternal bone mineral density
(IOM, 1997).
Food sources of calcium include dairy products, kale, broccoli, greens, tofu (processed with calcium), amaranth, sardines and salmon (with bones), tortillas (made with
lime or calcium carbonate), sesame seeds, almonds and other nuts, soy nuts, okra, white
beans and tempeh.
Foods fortified with calcium are now available, including orange juice, milk,
cheese, yogurt, cereals and bread (Wonder Bread®). Women who are lactose intolerant
can buy a milk called Lactaid®, or a Lactaid pill that breaks down milk sugar, enabling
them to drink milk or eat foods with lactose. Otherwise, they must rely on other foods
high in calcium, calcium-fortified foods or a supplement.
Supplementation of calcium can be from an antacid, as long as it does not contain
aluminum. This is an added benefit if the woman has heartburn, as it “kills two birds
with one stone.” Absorption of calcium is improved if consumed with or at the end of a
light meal (Heaney, et al., 1989). Another good calcium supplement is calcium carbonate
or calcium citrate. Avoid oyster shell calcium, bone meal and dolomite, as they may be
contaminated with heavy metals. Calcium carbonate interferes with iron absorption, so
don’t take them together.
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Adequate calcium is especially important for younger pregnant woman and adolescents. Being pregnant while bones are still forming can decrease bone density, if
calcium intake is low, and increase the likelihood of osteoporosis later in life. While this
holds true for older women as well, it is more detrimental to younger women. Adequate
calcium intake prevents bone loss during pregnancy.
The IOM (1990) states that women under 25 years old with low calcium intakes —
defined as below 600 mg/day — should be supplemented with 600 mg daily. To enhance absorption and limit interaction with iron supplements, the calcium supplements
should be taken at mealtime.
VITAMIN D
In the last few years researchers have begun to document a much higher incidence
of vitamin D deficiency in pregnant women (Hollis and Wagner, 2004a). It was thought
that the majority of the US population met their vitamin D requirement through exposure to sunlight, since diet contains minimal amounts of naturally occurring vitamin D.
However, it is now well documented that individuals living above 35º latitude —
roughly, Washington, DC, Little Rock, AR, and San Jose, CA — have difficulty making
adequate vitamin D in winter, due to the angle of the sun. In addition, individuals with
darker skin need much longer sun exposure, up to 10 times as long, to make the same
amount of vitamin D as people with lighter skin (Hollis and Wagner, 2004b).
The vitamin D requirement for the entire population, including pregnant women,
is really unknown. The DRI was based on unsubstantiated data and determined before
measurement of serum vitamin D — 25(OH)D — was possible. For children, the DRI of
10 mcg (400 IU) was based on the amount of vitamin D in 1 tsp of cod liver oil given to
prevent rickets, while the adult dose of 5 mcg (200 IU) was based on the amount of
vitamin D necessary to prevent osteomalacia in the absence of sunlight (Vieth, 1999).
Vitamin D has functions beyond its role in calcium and bone metabolism. Many
organs and cells of the body contain vitamin D receptors that are necessary for their
normal function. Newly discovered functions of vitamin D include: anti-inflammatory
agent; cell growth regulation, blood pressure, and immunity; stimulates insulin production; decreases autoimmune diseases; and may prevent chronic diseases such as diabetes, cancer, multiple sclerosis, heart disease and schizophrenia (Vieth, 1999).
Vitamin D status of the infant at birth is related to the vitamin D status of the
mother, as the cord blood will contain 50 to 60 percent of the maternal circulating
concentrations of vitamin D (Hollis and Wagner, 2004a).
A vitamin D deficiency in pregnant women can cause problems for the mother and
fetus. Maternal effects of a vitamin D deficiency include decreased serum calcium concentrations and possible decreased weight gain the third trimester (Specker, 1994). Fetal
vitamin D deficiency can delay growth and bone ossification, and cause enamel hypoplasia and problems with calcium regulation (i.e. hypocalcemia and tetany), decrease bone
mineral content and skeletal mineralization as well as cause congenital rickets and
craniotabes (Specker, 1994; van der Meer, et al., 2006). It is also possible that a vitamin D
deficiency may increase the risk for chronic diseases later in life.
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74
Adequate vitamin D appears to increase serum calcium concentrations of the fetus
by the 4th day of life, improves neonatal handling of calcium and prevents osteomalacia
(IOM, 1997; Specker, 2004). It may even influence postnatal mineral homeostasis,
growth and bone mass (Pawley and Bishop, 2004). At issue is whether or not a vitamin
D deficiency decreases maternal weight gain, fetal growth and birth weight.
At this point in time we still do not know how much vitamin D is required during
pregnancy and what constitutes a "normal" serum vitamin D level. The present AI for
vitamin D in pregnancy is 200 IU, but according to Hollis (2007) :
...the current recommended AI of 200 IU/day for vitamin D is useless for
maintaining nutritional status, yet alone improving it. This is especially true
in populations of people of color living in northern latitudes. Clinical studies to date with respect to vitamin D supplementation during pregnancy
and lactation are largely dated and grossly inadequate, and as a result, very
little clinical information can be derived from them.
Some researchers suggest that levels below 25 nmol/L are deficient and above 50
nmol/L are necessary for proper functioning of the body’s cells and organs, with a range
of 78 to 100 nmol/L necessary for bone health and chronic disease prevention (Holick,
2004b). Heaney (2003) suggests that levels below 80 nmol/L are deficient. Higher levels
can be tolerated without any adverse effects. Sunlight can provide between 10,000 and
20,000 IUs per day (Holick, 2004b) and lifeguards and sunbathers can have serum vitamin D levels of up to 250 nmol/L without any signs of toxicity. As vitamin D intake
increases, so does serum vitamin D (Hollis and Wagner, 2004a).
A study published by van der Meer, et al., (2006) uses a definition of vitamin D
deficiency as below 25 nmol/L. In this study of pregnant women in the Netherlands, 8
percent of pregnant Western women and over 50 percent of darker-pigmented pregnant
women were vitamin D deficient. Had the criteria for vitamin D deficiency been set
higher, an even greater number of pregnant women would have been vitamin D deficient.
A 2006 study found a correlation of milk intake to infant birth weight in pregnant women living in Calgary, Canada (51º North), independent of other risk factors. As milk intake increased, so did birth weight (Mannion, et al., 2006). For each 1
mcg (40 IU) increase in vitamin D intake, birth weight increased by 11 gm. No
differences in infant head circumferences and lengths were found between women
with higher and lower milk consumption. No serum vitamin D levels were taken.
In studies of lactating women, 400 IU of vitamin D did not raise serum vitamin D
in the lactating women. In fact, their serum levels declined (Hollis and Wagner, 2004b).
The authors feel that 400 IU recommendation during lactation is way too low, especially
for darker pigmented women and infants and that the recommendation should be as
high as 4000 IU per day for lactating women.
In a newer study to assess the vitamin D status of pregnant women and their
offspring in Pittsburgh, PA (latitude 40º North) by race and season, a surprisingly high
number of women and neonates were vitamin D deficient or vitamin D insufficient,
Sexual & Reproductive Health
75
shown in the chart below (Bodnar, et al., 2007). Many of the women with a vitamin D
deficiency or insufficiency took a prenatal supplement the last trimester of pregnancy
and 45 percent took a supplement prior to pregnancy.
More black women and infants had vitamin D deficiencies and insufficiencies than
white women, due in part to the increased skin pigmentation and the fewer number of
women who took supplements prior to or during pregnancy. White babies born in the
spring had a 75 percent increase in the incidence of vitamin D insufficiency compared to
white babies born in the summer. The variation in vitamin D insufficiency in black
women and babies did not vary as much as the white women and babies.
Vitamin D Deficiency in Mothers & Neonates
37-42 weeks gestation
Serum 25(OH)D, nmol/L
Vitamin D status, %
Deficient: <37.5 nmol/L
Insufficient: 37.5-80 nmol/L
Sufficient: >80 nmol/L
White Women
n=200
Black Women
n=200
80.4
49.4
5.0
41.2
53.8
29.2*
54.1
16.7
Neonates, White
Cord Blood
Serum 25(OH)D
Vitamin D status, %
Deficient: <37.5 nmol/L
Insufficient: 37.5-80 nmol/L
Sufficient: >80 nmol
Neonates, Black
67.4
39.0*
9.7
56.4
33.9
45.6*
46.8
7.6
* Different from white women or white babies.
Adapted from Bodnar et al, 2007.
Without any exposure to sunlight, it is suggested that adults need a minimum of
1000 IU/day vitamin D (Holick, 2004a). Heaney (2004, 2005) found that calcium absorption was not maximized until a serum level of vitamin D reached 75 to 80 nmol/L. To
achieve a serum vitamin D level of 80 nmol/L could require a daily intake of up to 2200
IU (Heaney, 2005). At present, the upper limit recommended for vitamin D is 2000 IU/
day. Toxicity is not seen even at serum vitamin D levels of 250 nmol/L, requiring a
vitamin D intake of 10,000 IU/day (Heaney 2005). Individuals exposed to adequate
sunlight have serum vitamin D concentrations averaging 150 nmol/L (Vieth, 1999).
In 1997, the Dietary Reference Intake for vitamin D was published by the Institute
of Medicine (IOM, 1997). The adequate intake recommended for pregnant women is 5
mcg or 200 IU (IOM, 1997).
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76
At this time, it appears the 1997 recommended levels are too low, but the exact
recommendation still needs to be determined. Drs Hollis and Wagner are conducting a
multiyear, double-blind, placebo-controlled study of the effects of supplementing
pregnant women with up to 4000 IU vitamin D per day. At the present time, if a pregnant woman is not getting adequate sunlight to meet her vitamin D requirement,
supplementation is necessary and levels up to 2000 IU are safe.
FLUORIDE
Primary dentition begins developing by the 10th to 12th week of gestation. In the third
trimester, the first four permanent molars and eight of the permanent incisors begin to
develop. Tooth enamel formed when fluoride is taken is calcium fluorapatite, which is six to
10 times more resistant to acid dissolution than calcium hydroxyapatite, normal enamel.
The effectiveness of a fluoride supplement to improve the quality and strength of the
teeth is being debated. For a long time it was thought that fluoride did not cross the placenta, but evidence shows that fluoride does indeed cross the placenta (Glenn, et al., 1982).
There is no consensus on the use of fluoride supplementation during pregnancy. The
American Dental Association has not endorsed fluoride supplementation during pregnancy and the Institute of Medicine in 1997 concluded there is not enough research to
warrant recommending fluoride supplementation during pregnancy. The DRI for fluoride
for pregnant women is the same as nonpregnant women, 3 mg/day (IOM, 1997).
In 2005 the American Dietetic Association came out with a position paper on Oral
Health and Nutrition (ADA, 2005), which you may want to consult as a reference. In the
position paper, it is recommended that pregnant women not supplement fluoride, but can
use fluoridated toothpaste/rinse and drink fluoridated water.
The 2000 report: Oral Health in America: A Report of the Surgeon General concludes that
fluoride supplementation during pregnancy does not seem to benefit the fetus. Normal
intake of fluoride from food and water is sufficient for pregnant women (US Dept Health
and Human Services, 2000).
VITAMIN B6
Vitamin B6 is required for over 100 enzymatic reactions involving amino acids.
Besides this vitamin's important role in protein metabolism, synthesis of red blood cells
and central nervous system development, it is also involved in carbohydrate and lipid
metabolism, immunity and hormonal functions.
During pregnancy there is a gradual decline in blood levels of vitamin B6 and
vitamin B6 -dependent enzymes, up to 30 percent in non-supplemented women at 30
weeks gestation and 25 percent at delivery. The greatest decline is between the fourth
and eighth month of pregnancy. Lumeng et al. (1976), found that it took 4 to 10 mg of
supplemental pyridoxine to normalize serum vitamin B6 levels to those similar to the
beginning of pregnancy. The question remains if that is even desirable. Studies investigating the relationship of vitamin B6 status to poor pregnancy outcome — preeclampsia
and low birth weight — are inconclusive.
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77
A woman who was taking oral contraceptives 2 to 3 months prior to becoming
pregnant may have marginal serum vitamin B6 levels. In this case, a supplement slightly
higher than the 1.9 mg DRI for pregnancy may be necessary, particularly if the diet was
low in vitamin B6 (IOM, 1997). An additional 2 mg/day will be sufficient. Other women
who would benefit from supplemental vitamin B6 are pregnant adolescents, women
with multiple fetuses and women who are substance abusers.
Supplementing too much vitamin B6 may not be wise, as mentioned earlier. Since
vitamin B6 is actively transported across the placenta, too much vitamin B6 may cross to the
fetus and cause abnormally high fetal levels of vitamin B6 if the maternal concentration is
high. This observation has not been confirmed or denied by research, but seems logical.
OTHER VITAMINS AND MINERALS
Concern has again been raised about the safety of ingesting high doses of vitamin
A (retinol) during pregnancy. Rothman and colleagues (1995) recently published a study
of more than 22,000 women. One of 57 women who consumed more than 10,000 IU of
vitamin A (as retinol, not beta-carotene) daily during pregnancy had a child with birth
defects of the head, heart, brain, or spinal cord.
In 1995, the FDA recommended that women in their childbearing years limit their
intakes of preformed vitamin A to about 100 percent of the Daily Value (5000 IU). In
addition, pregnant women were advised to limit their intake of liver and fortified
cereals. A Tolerable Upper Intake Level (UL) for preformed Vitamin A was established by
the IOM (2001), based on the teratogenicity of preformed Vitamin A as the critical adverse
effect. For all other adults, liver abnormalities were used as the critical adverse effect. The
UL for preformed vitamin A for women of childbearing years is 2800 mcg/day for girls
14 to 18 years of age and 3000 mcg/day for women 19 to 50 years of age (IOM, 2001).
Women should choose fortified foods that contain vitamin A in the form of betacarotene rather than preformed vitamin A, whenever possible. High intakes of fruits
and vegetables rich in beta-carotene and other carotenoids are not a concern. The NAS/
IOM report (2001) recommended that supplementation with preformed vitamin A should be
avoided during the first trimester unless there is specific evidence of a deficiency.
Vitamins and minerals that now have either an DRI or AI include copper, chromium, manganese and molybdenum. The values are shown in Appendix #2 and #3.
Other nutrients, with no DRI or AI established, now have Tolerable Upper Intake Levels
(UL), as noted in Appendix #3. These include: boron, nickel and vanadium.
The DRI for the remaining vitamins and minerals are slightly higher during pregnancy. These nutrients are important for health during pregnancy, but do not affect
pregnancy outcome as much as the nutrients discussed earlier. Appendices #2 and #3
list the DRI for vitamins and minerals.
The 10th edition of the RDA, published in 1989, for the first time included a recommendation for selenium — 65 mcg, which was lowered to 60 mcg with the new recommendations (IOM, 2000). While selenium is important in protecting the body from free
radical damage, no known adverse outcome of pregnancy has been identified in women
Sexual & Reproductive Health
78
with inadequate selenium intake. Much research is needed to determine normal laboratory values, since plasma selenium declines during the course of pregnancy.
The chart below shows the increase in the DRI/AI for pregnant women.
Increased Nutrient Requirements for Pregnant Women
Same
Vitamin E
Vitamin K
Calcium
Phosphorus
Fluoride
31 to 49%
Zinc
Unclear
Vitamin D (amount
needed unclear)
Up to 15%
Energy
Vitamin A
Vitamin B12
Choline
Copper
Magnesium
Selenium
Total fiber
Ω-6 fatty acids
16 to 30 %
Vitamin C
Niacin
Thiamin
Chromium
Manganese
Energy
Carbohydrates
Ω-3 fatty acids
50 to 70%
Vitamin B6
Folate
Iron (≥19 years)
71 to 80%
Iron (≤18 years)
As you can see from this chapter, there is a lot of information available on the
effects of nutrient intake on the outcome of pregnancy. There are still many questions
that remain unanswered, as well. For a pregnant woman the best course of action is to
eat as healthful a diet as possible. The better the diet, the better the chance of a normal,
healthy baby.
Sexual & Reproductive Health
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Chapter Six:
Weight Gain in Pregnancy
Maternal weight gain is correlated with birth weight, and birth weight is correlated with infant morbidity and mortality. As birth weight increases, infant morbidity
and mortality decreases. A baby weighing less than 5.5 lb (2500 gm) is more likely to
have health problems or die soon after birth.
Several factors influence weight gain during pregnancy. One is the duration of the
pregnancy. The shorter the duration of the pregnancy, the less the infant will weigh.
Poor nutritional status and weight gain during pregnancy can cause premature labor
and delivery, as can other medical complications of pregnancy.
Smoking impacts birth weight. The more cigarettes smoked, the greater the decrease in birth weight. Alcohol and substance abuse can also retard growth and the
weight of a newborn. Lack of food, or other decreased caloric intake, can have profound
effects on weight gain. In these instances, the nutritional content is usually inadequate
as well. Encouraging proper weight gain in a pregnant woman is essential. Improper
weight gain is a key factor in a poor outcome of pregnancy.
In May 2009, the Institute of Medicine (IOM), Food and Nutrition Board of the
National Academy of Sciences (NAS) updated the 1990 publication Nutrition During
Pregnancy, Weight Gain and Nutrient Supplements — the first update in 19 years. (The
companion publication, Nutrition During Pregnancy and Lactation: An Implementation Guide
(NAS, 1992) is still a valuable resource, especially for nurses and health educators, as it
includes tips and pointers on evaluating weight gain (and nutrition) during pregnancy.)
The new IOM publication, entitled Weight Gain During Pregnancy: Reexamining the
Guidelines, examines many of the changes in the health of women of childbearing years since
1990 that have necessitated a review of the previous guidelines. Among those changes are
an increase in pre-pregnancy body weight and gestational weight gain (GWG), and new the
racial/ethnic subgroups in the population.
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80
In addition, there has been an increase in overweight and obesity among a subgroup of
women at higher risk for poor pregnancy outcomes, and in women getting pregnant at an
older age, who are more likely to have chronic conditions such as hypertension or diabetes
that increase their risk of pregnancy complications (IOM, 2009). The full report is available
online. You can order a copy, download a pdf or read it on-screen at:
<www.nap.edu/catalog.php?record_id=12584#at>
The committee responsible for the new guidelines was asked to:
• review evidence concerning the relationships between weight gain patterns
before, during and after pregnancy and maternal and child outcomes;
• consider factors within a life-stage framework associated with outcomes such as
lactation performance, postpartum weight retention, cardiovascular and other
chronic diseases;
• recommend revisions to existing guidelines where necessary; and
• help implement the guidelines and recommendations by suggesting methods to
implement them via education of the consumer, practitioner, and with public
health strategies. (Note: this course will cover only the sections of the report that
pertain to the guidelines for weight gain.)
The new guidelines are not very different from those published in 1990, but supporting
research for the 1990 recommendations has increased tremendously. One major change is a
shift in focus from preventing LBW and SGA babies to preventing excessive weight gain
and LGA babies. While there is still concern about inadequate weight gain and LBW and
SGA babies, more women have problems of gaining too much weight, having LGA babies
and retaining the excess weight. This change in focus will need to be incorporated into prepregnancy, pregnancy and post-partum counseling.
Some of the concluding remarks of the committee are very enlightening. They include:
Although the guidelines developed as part of this committee process are not dramatically different from those published previously (IOM, 1990), fully implementing
them would represent a radical change in the care provided to women of childbearing age. Included would be preconceptional services, such as counseling on diet and
physical activity to all overweight and obese women of childbearing age to reach a
healthy weight prior to conception. Also included would be counseling on diet, physical activity to all pregnant and postpartum women will the goal of achieving weight
gain within the guidelines and eliminating postpartum weight retention.
And:
The increase in overweight and obesity among American women of childbearing
age and failure of many pregnant women to gain within the [1990] guidelines alone
justify this radical change in care as women clearly require assistance to achieve the
recommendations in this report in the current environment.
81
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And further:
These new guidelines are based on observational data, which consistently show that
women who gained within the [1990] guidelines experienced better outcomes of pregnancy than those who did not.
OPTIMAL WEIGHT GAIN
How much weight should a pregnant woman gain? Before the 1960s, 15 lb was considered adequate. The amount jumped to 25 lb after 1971. Now optimal weight gain varies
from woman to woman, based on pre-pregnancy BMI. To determine optimal weight gain,
we must know how much weight is gained during the course of pregnancy and where it
is gained. The chart below breaks down the components of weight gain into maternal
tissues and fetal tissues by trimester.
Components of Weight Gain
Cumulative gain (lb) at end of each trimester
Tissue
Fetus
Placenta
Amniotic Fluid
(Fetal Subtotal)
First
Second
Third
Negligible
Negligible
Negligible
--
2.2
0.6
0.9
3.7
8.3
1.6
2.0
11.9
Uterus
Breast
Blood Volume
Extracellular Fluid
(Maternal Subtotal)
0.7
0.2
0.7
0
1.6
1.8
0.7
2.8
0
5.3
2.4
1.1
3.0
6.1
12.6
Total Gain
Fat Stores
1.6
9
24.5
8.5
TOTAL GAIN
33
Source: Brown JE, JNE 24:21-5, 1992.
As you can see, during the first trimester there is little weight gain in fetal tissues.
Most of the gain is in the maternal tissues — about 1.6 lb. In the second trimester the
fetal tissues add approximately 3.7 lb, while the maternal tissues have added 5.3 lb, for
a total gain of 9 lb (for mother and fetus combined) at the end of the second trimester.
By the end of the third trimester the fetal tissues have tripled in size to 11.9 lb. Maternal
tissues have increased to 12.6 lb.
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82
The total gain for the pregnancy is 24.5 lb for both the maternal and fetal tissues.
An additional 8.5 lb of fat is stored for energy use during lactation, for a total weight
gain of 33 lb. Other sources have total gain closer to 28 to 30 lb, when you factor in a
smaller baby, less gain in maternal tissues (King, 2000) and less fat gain (Lederman, et
al., 1997; IOM 2002).
The second determining factor is pre-pregnancy weight. One of the earlier studies that
looked at pregnancy weight, weight gain and infant mortality is the Collaborative Perinatal
Project of the National Institutes of Neurological and Communicative Disorders and Stroke.
This study followed 53,518 pregnancies in 12 US hospitals between 1959 and 1966, recording
events of gestation, labor, delivery, and weight of offspring until 8 years of age (Naeye, 1979,
1990). This study was done before the use of BMI to classify pre-pregnancy weight; instead it
uses percentage of ideal body weight (IBW).
The optimal weight gain, i.e. the lowest perinatal mortality rate, differed for
women who were underweight (up to 90 percent of IBW), normal weight (90 to 135
percent of IBW) or overweight (above 135 percent of IBW) before they got pregnant.
• Normal weight women, 90 to 135 percent of IBW, had the lowest perinatal
mortality rate when they gained over 20 lb. At a 10 lb weight gain, the death rate
was 18 per 1,000 live births; with a 22 to 25 lb gain, it was 10 per 1,000 live births.
As weight gain increases, there is a slight increase in death rate, but not anywhere near as high as with lower weight gains.
• Women weighing less than 90 percent of IBW, who gained only 10 lb during
pregnancy, had the highest perinatal mortality rate, 25 deaths per 1,000 live
births. As the weight gain increased to 30 lb, the perinatal mortality rate decreased to the lowest of all groups, five deaths per 1,000 live births. Women who
are underweight prior to pregnancy have babies that weigh less than women
who are normal or overweight prior to pregnancy (IOM, 1990; Brown, et al.,
1992; Abrams, et al., 2000).
• Obese women — more than 135 percent of IBW — had the lowest perinatal
mortality rate at 15 lb weight gain. As weight gain increased, so did the perinatal
death rate, from a low of 16 per 1,000 live births to a high of 21 per 1,000 live
births.
In the intervening years, research has clearly shown a relationship between pre-pregnancy weight, GWG and pregnancy outcome (IOM, 2009). In fact, a key finding of the 2009
IOM report is that pre-pregnancy BMI is an independent predictor of many adverse outcomes of pregnancy and women should try to enter pregnancy with a normal weight. The
adverse outcomes differ based on pre-pregnancy weight and GWG.
Caulfield, et al., (1998) found that when analyzing weight gain within the IOM recommended ranges, and outcome, based on pre-pregnancy BMI, that the risk for SGA births
declined as weight gain increased, but the risk for large-for-gestational age births increased.
For underweight women, the biggest risk is inadequate weight gain (less than 20
pounds) leading to SGA, increased fetal and infant deaths, and decreased fetal growth
Sexual & Reproductive Health
83
(IOM, 2009). In an evidence based review of the literature for the Agency for Healthcare
Research and Quality (AHRQ), Viswanathan, et al., (2008) found strong evidence that weight
gain below IOM recommendations increased preterm births, SGA and LBW babies. There is
moderate evidence that weight gain below IOM recommendation in all pre-pregnancy
weight groups decreases the likelihood of a woman breastfeeding.
For overweight and obese women, the risk of inadequate GWG is a lesser risk than is
excessive weight gain (more than 20 lb). Too much weight gain during pregnancy may lead
to LGA babies, macrosomia, increased incidence of preeclampsia, diabetes, Caesarean
deliveries and post-partum weight retention (IOM, 2009).
Women entering pregnancy with a BMI in the normal range have the lowest risk for
adverse pregnancy outcomes.
Since 1976, the incidence of obesity in the US in women 12 to 44 years of age has
doubled. According to the National Center for Health Statistics, between 1999 and 2004 twothirds of women of childbearing years are overweight (BMI 25 or higher) and one-third are
obese (BMI 30 or higher) (IOM, 2009). More women of racial and ethnic minorities are obese.
Weight gain during pregnancy has also changed in the last 20 years. Between 1990 and
2005 there has been an increase in the number of women gaining less than 16 lb and more
than 40 lb, and a decrease in the number of women gaining within the recommended rand
of 16 to 40 lb (IOM, 2009). In the same time period a larger proportion of women gaining
more than 40 lb was white women, while the larger proportion gaining less than 15 lb was
among black and Hispanic women (IOM, 2009).
In determining the optimal weight gain for each pre-pregnancy classification, the IOM
committee had to find the right balance between preventing SGA babies on the one hand
and preventing LGA babies on the other. Nohr (2008) studied the effects of pre-pregnancy
BMI and GWG on SGA, LGA and birth weight among 60,000 Danish women. The relative
risk of delivering a SGA baby for women who gained less than normal, 22 lb, versus a
normal gain of 22 to 33 lb, based on pre-pregnancy weight classification was 2.1 for underweight women, 1.7 for normal weight, 1.6 for overweight and 1.3 for obese women.
The risk for LGA babies associated with a very high weight gain, over 44 lb, versus a
medium weight gain of 22 to 33 lb, was 3.7 for underweight women, 2.6 for normal women,
2.0 for overweight women and 1.8 for obese women.
This study by Nohr suggests there is a dampening effect of GWG on birth weight with
increasing pre-pregnancy BMI, and that there is less SGA and more LGA with increasing
GWG (IOM, 2009).
In establishing the new weight gain guidelines, the IOM committee determined the
range of GWG associated with the lowest prevalence of outcomes of greatest concern. The
only pre-pregnancy weight classification that changed was the obese category (BMI 30 or
higher) going from a recommendation of 15 lb to a recommendation of 11 to 20 lb (IOM,
2009). The weight gain recommendations for each pre-pregnancy classification are discussed
below, along with adolescents and twin and multiple fetus.
84
Sexual & Reproductive Health
EVALUATING PRE-PREGNANCY WEIGHT
To determine which pre-pregnancy weight classification a woman falls into, you
must assess her weight for height by calculating BMI. Appendix #4 has a chart that can
be used in lieu of the BMI formulas below.
Formula #2
Formula #1
BMI =
weight (kg)
height (m)
2
x 100
BMI =
weight (lb)
height (in)2
x 703
In an evidence-based review of outcomes of maternal weight gain, Viswanathan, et al.,
(2008) concluded that there is insufficient evidence that any method other than standard
BMI is more predictive of pregnancy outcomes. The 2009 IOM pregnancy weight gain
guidelines use the World Health Organization (WHO) cutoff points for categorizing BMI.
There are four weight categories: underweight, normal weight, overweight and obese. For
each pre-pregnancy weight classification there is a recommended range of total weight gain
during pregnancy and the rate of weight to gain in the second and third trimester of pregnancy. The chart below shows these recommendations.
Recommended Weight Gain by Prepregnancy Weight
Rates of Weight Gain**
2nd and 3rd Trimester
Mean (range) Mean (range)
Range in lbs
kg/week
lbs/week
28 - 40
0.51
1
(0.44-0.58)
(1-1.3)
Total Weight Gain
Prepregnancy BMI*
Low or underweight
(<18.5 kg/m2)
Range in Kg
12.5 - 18
Normal weight
(18.5-24.9 kg/m2)
11.5 - 16
25 - 35
0.42
(0.35-0.50)
1
(0.8-1)
High or overweight
(25.0-29.9 kg/m2)
7 - 11.5
15 - 25
0.28
(0.23-0.33)
0.6
(0.5-0.7)
Obese
(≥30.0 kg/m2)
5-9
11 - 20
0.22
(0.17-0.27)
0.5
(0.4-0.6)
* BMI classification uses WHO standards
**Calculations assume a 0.5-2 kg (1.1-4.4 lbs) weight gain in the first trimester.
Adapted from: Weight gains during pregnancy: Reexamining the guidelines, NAS, 2009.
Sexual & Reproductive Health
85
WEIGHT GAIN RECOMMENDATIONS
NORMAL WEIGHT
Normal weight women — BMI 18.5 to 24.9 — should gain a minimum of 25 lb and
a maximum of 35 lb during pregnancy. Women should be encouraged to gain within the
recommended range and not gain more, as is the trend, as it can lead to poorer outcomes —
large babies, cesarean section and postpartum weight gain (Caulfield, et al., 1998; Suitor,
1997; Baeten, et al., 2001; Jensen, 2003; IOM, 2009).
This range should satisfy even the most compulsive weight-watchers. Doctors who
are sticklers on weight gain may intimidate women into feasting, then starving themselves to “make weight.” This is a bad habit. Restricting calories deprives the fetus of
nutrients essential for development.
The rate of gain is as important as the total gained. A 2 to 4 lb gain is recommended
during the first trimester. (Remember, the total increase in maternal and fetal tissues is only
1.5 to 2 lb.) For the second and third trimesters an average weekly gain of 1 lb, with a range
of 0.8 to 1 lb, is recommended. It is not uncommon for a woman to find out she’s pregnant,
and begin to “eat for two,” doubling her intake. The recommended additional calories
required (340 and 452), only adds about one 8 oz glass of skim milk, one slice of bread, an
apple, and 1 to 2 oz of lean meat or poultry. A woman dramatically increasing her intake can
gain 8 to 12 lb in the first trimester.
Slowing down excessive weight gain, more than 4 to 5 lb a month during the first
trimester, is appropriate. Excess weight gained the first trimester is probably fat, and does
not benefit the fetal or maternal tissues. This woman should still gain 0.5 to 1.5 lb per week
depending upon pre-pregnant weight status.
Early in the second trimester weight gain can also be slowed somewhat, but not in the
third trimester, as that is the time the fetus has a greatest need for calories, when it triples its
weight. A caloric restriction is to be avoided during the third trimester.
WEIGHT GAIN RECOMMENDATIONS
UNDERWEIGHT
Underweight women — a BMI of 12.5 to 18 — should gain 28 to 40 lb. Another
way to look at it is to gain to their IBW, plus an additional 25 lb. According to Lederman
et al., (1997), underweight women who gain the recommended amount of weight have
an increase in total body fat and, at term, have a body fat content similar to normal
weight women at 14 weeks of pregnancy.
Underweight pregnant women should be encouraged to begin gaining weight as soon
as possible. The rate of gain is approximately 5 lb the first trimester and 1.0 lb per week in
the second and third trimesters, with a range of 1 to 1.3 lb per week. Individualize the
weight gain for all underweight women, making it reasonable for them.
Most nutrients are passively diffused across the placenta, and if the concentration
in maternal blood is lower than in fetal blood, the fetus will not get them. The underweight woman has the greatest risk of this happening.
Sexual & Reproductive Health
86
In addition, her stores of nutrients are probably lower than the normal and overweight woman, so she must rely on what she gets from her diet. Pregnant women who
are underweight at conception and delivery, as well as underweight women who do not
gain adequately during pregnancy, are at increased risk for LBW babies, premature babies
and delivery complications (Ehrenberg, et al., 2003; Viswanathan, et al., 2008; IOM, 2009).
For many women, it is difficult to gain the recommended amount of weight during
pregnancy. If necessary, counseling may need to be arranged, especially if women are
averse to gaining weight for social or personal reasons. They need to understand that
they have the greatest risk for poor outcome if they do not gain weight. Underweight
women need to be monitored more closely than any other group. (A section on Counseling is included later in this chapter.)
Consider the additional demands for calories, protein and nutrients that pregnancy
places on the body. An underweight woman has the smallest reserves, so failure to gain
indicates that inadequate nutrients are being consumed, depriving the fetus of essential
nutrients for growth and development.
WEIGHT GAIN RECOMMENDATIONS
OVERWEIGHT/OBESE
Unfortunately, as we have seen, the number of overweight and obese women in the US
keeps increasing, which is a major concern of healthcare professionals. It also has ramifications for women coming into pregnancy overweight or obese.
The IOM recommended weight gain for overweight women with a BMI between 25
and 29.9 is 15 to 25 lb — the same as the 1990 recommendation. The recommended rate of
gain is 0.6 lb per week, with a range of gain from 0.5 to 0.7 lb per week, which is slightly
lower than the 0.67 lb per week recommended in 1990. For obese women, with a BMI 30 or
higher, the total weight gain recommended is 11 to 20 lb, with a weekly gain the second and
third trimester of 0.5 lb, with a range of 0.4 to 0.6 lb.
There is discussion in the medical community over how much weight obese women
should gain. Some believe pregnant women need to gain 25 lb, no matter the prepregnant
weight; others believe a 15 lb gain is acceptable. Others say no gain may be appropriate.
Women who are overweight or obese prior to pregnancy and gain the IOM-recommended amount of weight, do not put on as much fat as women who are normal weight
or underweight prior to pregnancy (Lederman, et al., 1997). In fact, obese women who
gain 15 lb may put on no fat. Since it is lean tissue and not fat that is associated with
infant birth weight, it may not matter that these women do not gain any fat during
pregnancy (Lederman, et al., 1999).
Pre-pregnancy weight is the initial consideration. Is the woman only slightly
overweight, or does she fall into the obesity classification? Next, the quality of the diet
needs to be assessed. How much is she eating and is it nutritionally sound? Women can
eat an enormous quantity of food and still not meet their nutrient needs if the food is of
poor quality. The calories may be adequate but the nutrients may not be sufficient.
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87
In a severely obese woman with a diet that is nutritionally sound, providing
adequate calories, protein and nutrients, no weight gain or a small gain may be appropriate. In a woman who is not meeting her nutrient needs, some gain is desirable.
Women who are only slightly obese should still gain a minimum of 10 to 15 lb.
Many obese women have pre-pregnancy medical conditions that complicate the
pregnancy, e.g. hypertension, diabetes, pyelonephritis, and obstructive sleep apnea
(Cesario, 2003; IOM, 2009). Obesity during pregnancy can also cause complications such
as hiatal hernia, markedly elevated gastric emptying times, urinary tract infections,
excessive edema, pregnancy-induced hypertension, gestational diabetes, Caesarean
delivery, increased bleeding and wound complications. The chart below shows the
complication rates for various conditions in obese pregnant women (Naye, 1990).
Complications in Obese Women
Perinatal mortality rates(deaths/1000 births) for various risk factors
Pregnancy Risk Factor
Thin
Normal
Overweight
Maternal
Age <18 years
Age 35-50 years
Diabetes
Hypertensive disorders
Low weight gain
Smoking
7.8
1.4
1.2
4.9
12.9
18.4
7.0
4.8•
1.6
4.8
5.6•
21.0
3.6•
12.2•
1.4
5.2
10.0¶
22.3¶
10.5¶
23.4•
11.1•
10.9•
13.6
39.3•
Fetal
Preterm
Born 24-30 weeks
Born 31-37 weeks
Full term births
Major congenital defects
30.4
16.2
14.2
6.9
4.8
34.4¶
18.7¶
15.7
13.9•
7.8•
40.6•
22.7•
17.8¶
15.4•
8.6•
79.7•
46.2•
33.5•
41.2•
14.4•
37.3
48.3•
55.9•
120.9•
All cases
BMI: Thin = <20; Normal = 20-24; Overweight = 25-30; Obese = >30 kg/mm2
• = p < 0.001
¶ = p <0.05
Obese
(Naeye, 1990)
Some of the complications are due to the physiological changes of pregnancy
superimposed on the already-strained physiology of the woman. For instance, insulin
resistance, which normally increases during pregnancy, is further increased in obese
women (ADA, 2009). Compared to normal weight women, overweight pregnant
women have a two-fold increase in the risk for gestational diabetes which increases to
eight-fold if the pregnant woman is obese (Chu, et al., 2007).
Sexual & Reproductive Health
88
Some of the complications in overweight and obese women that can be lessened
with appropriate weight gain include: diabetes mellitus, hypertension, thromboembolism, caesarean delivery, macrosomia, preeclampsia, eclampsia and post-partum weight
retention (Baeten, et al., 2001; IOM, 2009), even if the woman has normal glucose tolerance (Jensen, et al., 2003).
Newborns of obese women have a higher perinatal morbidity and mortality rate
(ADA, 2009). Overweight women who gain less than 15 lb have a perinatal mortality
rate two times higher than overweight women gaining at least 15 lb (Naeye, 1979, 1990).
Regardless of weight gain, Naeye (1990) found that as maternal pre-gravid weight
increased — from thin to obese — perinatal mortality rates increased from 37 deaths per
1,000 births in thin women, to 121 deaths per 1,000 births in obese women.
The outcome of this research was duplicated by Baeten and coworkers (2001) who
found that the incidence of gestational diabetes, preeclampsia, eclampsia, macrosomia
and Caesarean delivery all increased with increasing pre-pregnancy weight. Unlike
Naeye, Baeten found no difference in the incidence of preterm deliveries, LBW babies
and SGA babies between weight groups.
It seems that the risk for SGA babies tends to decrease as the pre-pregnancy weight
of the mother increases, while the risk of LGA babies increases by 60 percent in obese
women, compared to women of normal pre-pregnancy weight (Ehrenberg, et al., 2004).
Congenital defects appear to increase with increasing pre-pregnancy weight. Naeye
(1990) showed increased perinatal deaths from congenital defects in his study. Prentice and
Goldberg (1996) conclude that there is a two-fold increase in the risk for NTD in obese
pregnant women (defined as BMI above 31) taking folic acid supplements. In a populationbased study, Watkins and colleagues (2003) found that maternal obesity, defined as a BMI 30
or higher, increased births to babies with spina bifida, omphalocele, heart defects and
multiple anomalies. There was an association between being overweight before pregnancy,
defined as a BMI of 25 to 29.9, with heart defects and multiple anomalies.
Complications that are increased in babies born to obese women include: macrosomia,
intrauterine growth retardation, stillbirths, congenital malformations, increased risk of
neural tube defects, increased risk of fetal death and higher rates of childhood obesity
(ACOG, 2005; Cesario, 2003; ADA, 2009).
Increasingly, women who have had bariatric surgery are becoming pregnant. While
the procedure may dramatically impact the pregnancy, many women who have had
bariatric surgery have had normal pregnancies with good outcomes (ACOG, 2005).
(Note: Chapter Eight will discuss bariatric surgery in more detail. The Nutrition
Dimension course Treating Severe Obesity is also recommended.)
A massive weight loss during pregnancy is to be avoided. Some obese women do
lose weight and have perfectly normal, healthy babies, but there are potential problems.
When the body loses weight, fat becomes a major source of energy. A by-product of fat
metabolism is ketones. As ketones build up in the blood, the acidity (pH) can change.
There is concern whether the ketones can affect the development of the fetal brain.
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89
Another problem is that fat cells of the body store drugs, toxins and other harmful
substances. If too many fat cells are broken down, and these harmful substances are
dumped into the blood, the fetus may be affected. While this is hard to determine or
prove beyond a doubt, it another reason for discouraging pregnant women — no matter
how obese — to lose much weight.
Counseling for overweight and obese pregnant women needs to be individualized.
The 2009 IOM weight gain guidelines are just that — guidelines. Ideally, women should try
to lose weight before they become pregnant. If they do not, pregnancy is a time when
women are very receptive to nutritional counseling, and this presents an opportunity
for improvement. An obese woman is more likely to want to change her diet during
pregnancy. Find ways to cut out calories that do not provide nutrients.
Amazingly, obese women can improve their diets, lose a small amount of weight and
produce a healthy baby. Even a small weight gain with a healthy diet can have a good
outcome.
COUNSELING PRINCIPLES
Pregnancy weight gain counseling isn't rocket science. Stick to these principles for
best results:
• Discuss a weight gain goal, set as a range;
• Help plan menus and snacks that will assist in meeting her weight gain goal;
• Describe where the weight that she gains goes;
• Discuss the importance of adequate gain for the health of mother and baby;
• Provide positive reinforcement for adequate gain; and
• Offer supportive resources to help her return to her pre-pregnancy weight after
the baby is born.
In an interesting study, Mumford, et al., (2008) found that women who were restrained eaters, dieters or weight cyclers had weight gains during pregnancy either
above or below IOM recommendations. Women who were normal, overweight or obese
gained more than recommended. Underweight women gained less than recommended.
WEIGHT GAIN IN ADOLESCENTS
Adolescence is a time of rapid physical growth. Nutrition needs increase significantly to support this growth and to promote and preserve nutrient stores. The extra
energy and nutrient demands of pregnancy place pregnant adolescents at nutrition risk.
The primary factor that increases nutrition risk is the amount of uncompleted
growth at the time of conception. The least physically mature pregnant teens (those who
are still growing) have not had time to store nutrients for their own body tissues and
systems because they use nutrients for growth and development. Do adolescents continue to grow during pregnancy? And if so, do the nutrition needs of the growing
pregnant teen compromise either the mother’s or baby’s needs? Numerous studies that
have been conducted provide some insights.
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90
Growth slows down after a young woman has had her first menstrual period, but
may continue for four more years. Therefore, menarche is a marker for completed
growth but not an absolute predictor.
Growth during pregnancy has been masked by a tendency of all pregnant women
to shrink during pregnancy (1/4 inch over 6 months). Therefore, some growth studies of
pregnant adolescents have measured leg lengths to determine growth. Larger increments of growth were observed in younger adolescents, 12 to 15 years, than in older
adolescents, 15 years and older (Scholl and Hediger, 1993).
Several studies have found that growing pregnant adolescents have babies with
lower birth weights than non-growing adolescents and pregnant adults. Scholl and
colleagues (1994) found that, after 28 weeks gestation, the still-growing pregnant teens
continued to accrue fat stores and gained more weight than non-growing teen mothers or
mature women. However, the still-growing mothers had infants with lower birth weights.
The weight gain distribution of pregnant adolescents differs from pregnant adults.
When pregnant adolescents gain the same amount as pregnant adults, the baby and
placenta are smaller in adolescents. Pregnant adolescents, particularly those at younger
ages, tend to gain more weight than do pregnant adults. This may be due to increased
fluid volume, because these younger pregnant adolescents also have smaller babies.
Pregnant adolescents also have a greater weight gain velocity from the beginning of
pregnancy (Hediger, et al., 1990).
Rees and coworkers (1992) found that adolescent mothers giving birth to infants
weighing 3000 to 4000 gm had a rate of gain that equaled the highest amount recommended in the NAS/IOM report. This suggests that restricting the natural gain of
adolescents to recommended rates may result in smaller than optimal gains. The provisional recommendations from the NAS/IOM report were to gain 0.36 to 0.53 kg/week.
The young women in this study gained 0.588 kg/week. The study concludes that
weight gain recommendations for adolescents may ultimately be higher than for adults.
However, in reviewing the literature, the Expert Work Group did not recommend
encouraging weight gain in the upper end of the range (Suitor, 1997).
Adolescents, especially the younger ones, tend to be underweight and do not like to
gain weight. Much of the aversion to weight gain has to do with peer pressure and not
wanting to be fat. Unfortunately, many teenage mothers are themselves not fully grown.
While many teens may gain inadequately, others gain excessively — more than 40
lb. In a study of adolescent weight gain, Howie, et al. (2003) found that 27 percent of all
adolescent mothers gained excessively compared to 18 percent of older women, across
all pre-pregnancy weights. In 2005, adolescents younger than 20 years were more likely
to gain excessively than women over 35 years (IOM, 2009).
It is important that teens gain adequately since they have additional risk factors
that can complicate pregnancy. Berenson, et al. (1997) found that pregnant girls under 18
were more likely to deliver babies weighing less than 2500 gm, as well as have babies
that were significantly lighter, if they gained 20 lb or less. Risk factors that contributed
to the inadequate weight gain in teens were: physical assault/battering during pregnancy, a sexually transmitted disease during pregnancy and an unplanned pregnancy.
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91
According to the 2009 IOM guidelines, there is insufficient evidence that the GWG
guidelines used for adults need to be modified for adolescents (IOM, 2009). The reason is
that younger girls would be in a lower BMI category than they would be using pediatric
growth charts. Therefore, the recommended weight gain would be higher than if the growth
charts were used. The committee decided this was okay, since younger girls need to gain
more weight than adults to have a baby the same size. They also felt that using growth
charts in obstetric practices would be difficult.
A study that investigated the pre-pregnancy weight classification of pregnant adolescents using the IOM criteria versus age- and sex-specific BMI charts for girls and adolescents, found that 23.5 percent of the pregnant adolescents were misclassified using IOM
criteria (Fernandez and Olson, 2008). Most of the misclassifications were girls at a healthy
weight or at risk of being overweight. The concern is that by recommending more GWG
than needed, these girls are at risk for post-partum weight retention. The authors recommend using the CDC age- and sex-specific BMI charts for pregnant adolescents.
TWIN AND MULTIPLE PREGNANCIES
In the US, less than 3 percent of all births are multiples, yet they account for 13
percent of all preterm births, 15 percent of all very preterm births, 21 percent of LBW
births and 25 percent of all VLBW births (Luke, 1999). From 1980 to 1998 the rate of triplet
and higher order births increased approximately 400 percent (MMWR, 2009).
Physiologically, the uterine circulation is greater in multiple pregnancies and the
levels of maternal hormones are higher, most likely to adjust to the physiological adaptations and weight gain with twins or multiples.
Little research exists on the weight gain recommendations for multiple pregnancies.
We know that many of the LBW twins and multiples experience shorter gestation periods,
because of the mother not being able to carry the babies to term. How much the shorter
gestation period has to do with weight gain is not clearly understood.
Luke (1996) studied 924 women who delivered twins. Mothers with ideal pregnancy outcomes (defined as 2500 to 2800 gm birth weight and gestation of 35 to 38
weeks), smoked significantly less and gained more weight. Weight gains of 35 lb or
more were significantly associated with an ideal outcome. To achieve at least a 35 lb
weight gain, women expecting twins should gain a minimum of 1 lb/week.
The 1990 IOM report recommends woman carrying twins has a weight gain of 35
to 45 lb, with a rate of gain of 1.5 lb per week during the second and third trimester.
Luke (1999) and the American Dietetic Association (2002) suggests that women
carrying twins eat 3500 kcal/day and gain 24 lb by 24 weeks and 40 to 45 lb at term.
Women carrying triplets should eat 4500 kcal/day and gain 36 lb by week 24. The
recommended total weight gain for triplets is 50 lb (Brown, 2000; JADA, 2002). These
calorie and weight gain recommendations are based on literature that suggests that
weight gain before 20 to 24 weeks is important in the ultimate outcome and birth
weight of multiples (Luke, 1999).
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92
Based on data from her studies, Luke and Hediger (2003) determined the optimal
rates of weight gain, for women pregnant with twins, based on pregravid weight. This
information is found in Appendix #5.
The 2009 IOM report states that like singleton pregnancies, pre-pregnancy BMI is a
factor in weight gain recommendations for the best outcomes in twin and multiple fetus
pregnancies. With a lack of good data to determine recommendations the committee
came out with provisional recommendations for all pre-pregnancy weight classes except
underweight women, as there was not enough data. The following are the new guidelines for weight gain for women with multiple fetuses:
• normal weight: 37 to 45 lb (17 to 25 kg)
• overweight: 31 to 50 lb (14 to 23 kg)
• obese: 25 to 42 lb (11 to 19 kg)
Weight gain in twin and multiple pregnancies is difficult, especially if a woman
does not know early in her pregnancy that she is carrying more than one fetus. She may
begin to gain weight more rapidly than if she had only one fetus, and so may begin to
restrict her intake to slow her rate of gain. Early diagnosis of twins and multiples is an
important part of adequate weight gain.
MONITORING WEIGHT GAIN
Weight gain is a good indicator of how a pregnancy is progressing. Monitoring
weight gain, and pegging it as insufficient or excessive, is difficult with just a list of
numbers. A Prenatal Weight Gain Grid is invaluable in monitoring weight gain.
To work with the Case Studies in this chapter, four weight gain grids, designed
using the 2009 IOM guidelines, are provided. One, for normal-weight women (shown
on the next page), has the upper, lower and mid-range of the recommended weight gain
plotted. The horizontal axis shows the week of gestation; the vertical axis is weight
gained or lost. The grids for underweight, overweight and obese women also have three
lines with the upper, lower and mid-range of recommended weight gain plotted.
(For use in your practice, Appendices #6 and #7 may be copied. Appendix #6 is a
weight gain grid for normal-weight women. Appendix #7 is a grid for any pre-pregnancy weight classification. In Appendix #7, the line for underweight women corresponds with the highest recommended weight gain — 40 lb. The line for normal weight
women is the mid-range of recommended gain — 30 lb, while the line for overweight
women corresponds to the minimum recommended gain — 15 lb. Creating a grid for all
pre-pregnancy weight classifications will simplify, for some, the need to have three or
four grids. You can also find weight gain grids online.)
To use the chart, a woman’s pre-pregnancy weight is put by the “0” on the vertical
(Weight Gain) axis. Weight gain (or loss) is plotted for each week of gestation, or when
the woman has her doctor’s appointments and is weighed.
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93
Normal Weight Prenatal Weight Gain Grid
45 (20.4)
Weight Gain in Pounds (kg)
40 (18.1)
35 (15.9)
30 (13.6)
25 (11.3)
20 (9.0)
15 (6.8)
10 (4.5)
5 (2.2)
0
1
4
7
10 13
16
19
22 25
28
31
34 37
40
Duration of Pregnancy (weeks)
Using the sample data below, determine the BMI then plot the weight gain on the
sample prenatal weight gain grid provided above.
• Jane weighs 125 lb and is 5'4" tall. Her BMI is approximately 21. That puts her in
the normal pre-pregnancy weight classification. At her first visit to the doctor, at 11
weeks gestation, she weighed 129 lb. As shown on the next page, Jane’s pre-pregnancy
weight of 125 lb goes on the weight gain axis next to “0.” Then find 11 weeks gestation
along the horizontal axis (weeks of gestation) and move up the line until you come to 4
lb (her gain so far during the pregnancy). Put a mark on the line at that point. The
weights for the entire pregnancy are plotted.
Pre-pregnancy weight: 125
Pre-pregnancy height: 5'4"
BMI_______________
% of Desirable Weight______________
Week 8: 127 lb
Week 12: 129 lb
Week 16: 133 lb
Week 20: 137 lb
Week 24: 143 lb
Week 26: 145 lb
Week 28: 147 lb
Week 30: 149 lb
Week 32: 153 lb
Week 34: 155 lb
Week 36: 155 lb
Week 37: 157 lb
Week 38: 158 lb
94
Sexual & Reproductive Health
Normal Weight Prenatal Weight Gain Grid
45 (20.4)
35 (15.9)
30 (13.6)
X
Jane's Weight Gain
25 (11.3)
Weight Gain in Pounds (kg)
40 (18.1)
20 (9.0)
X
X
X
X
15 (6.8)
X
10 (4.5)
Reference Woman's
Weight Gain Range
X
5 (2.2)
XX
X X
X
X
0
1
4
7
10 13
16
19
22 25
28
31
34 37
40
Duration of Pregnancy (weeks)
As you can see, Jane's weight gain was slightly above the upper limits of normal.
She began to gain rapidly around week 26, but tapered off so that her final gain was 30
lb. This is within the recommended range of 25 to 30 lb. If, however, her weight continued to rise rapidly, you would want to monitor her for hypertension or other problems.
Not all pregnancies follow the grid pattern; every woman gains differently. The
visual representation alerts the health practitioner to problems while they are still
possible to correct. (A chart outlining recommended weight gain and questions to help
uncover the reasons for inappropriate weight gain follows the Case Studies.)
It is important that the gain rate stays approximately parallel to grid lines — the
same slope, in other words. A slightly higher or lower gain is not cause for alarm if there
is a progressive increase in weight. Marked or persistent deviations should be investigated. Parker and Abrams (1992) concluded that weight gain grids do not indicate how
far a woman's gain pattern can deviate from the norm without causing a problem for
the pregnancy. Carmichael, et al., (1997) found that many women who had good pregnancy outcomes would have been suspected of being at risk for poor outcome on the
basis of their weight gain alone.
In some of the case studies to follow, the prenatal weight gain grid differs from the
ones previously shown, because each grid is based on the pre-pregnancy BMI of the
pregnant woman. The chart is plotted the same as the one shown above and is used the
same way, to monitor weight gain and compare the pattern of gain against the line.
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Sexual & Reproductive Health
CASE STUDY #1
Mary is 5'5" tall, with a pre-pregnancy weight of 105 lb. Her BMI is 17.5. Being
underweight, she would need to gain 28 to 40 lb.
In this case, the upper end of the recommended gain is appropriate, since she is
considerably underweight, not marginal.
Mary had nausea and vomiting in the first trimester. Her weights were:
Week 11: 101 lb
Week 20: 103.5 lb
Week 28: 105 lb
Week 16: 102 lb
Week 24: 104 lb
Week 32: 104 lb
The weights are plotted on a weight gain grid for underweight pre-pregnancy BMI
shown below.
By week 11, when Mary was seen by her doctor, she had lost 4 lb. This should have
set off alarms, since she was underweight to begin with.
By week 16 the nausea and vomiting were gone and were not contributing to
weight loss, so Mary did begin to regain some of her lost weight. But she gained slowly
and was never above her pre-pregnancy weight — she gained no weight during her
pregnancy, and had a spontaneous premature delivery of a stillborn baby.
The most common causes of this problem are a refusal to gain weight, a physical
problem interfering with weight gain, a psychological problem (one might investigate a
history of anorexia or bulimia) or lack of food because of socioeconomic conditions.
Underweight Prenatal Weight Gain Grid - Case Study #1
40 (18.1)
30 (13.6)
25 (11.3)
20 (9.0)
15 (6.8)
10 (4.5)
Spontaneous
Premature
Delivery
Mary's Weight Loss
5 (2.2)
0
Weight Gain in Pounds (kg)
35 (15.9)
X
-5 (-2.2)
1
4
7
10 13
X
16
X
19
X
22 25
X
28
Duration of Pregnancy (weeks)
X
31
34 37
40
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CASE STUDY #2
Debbie is 5'5", with a pre-pregnancy weight of 165 lb and her BMI is 27.5. Her
recommended gain is 15 to 25 lb, since she is overweight.
Her weights were: Week 14: 176; Week 18: 180; Week 22: 186; Week 26: 195; Week
30: 201; Week 34: 209, plotted below on a prenatal weight gain grid for overweight
women.
By Debbie’s first visit she had gained 11 lb. A diet history should have been done
immediately to determine the cause of the excess weight gain, with appropriate recommendations to slow the gain. Indeed, Debbie had slowed her weight gain by her next
visit, gaining only 4 lb. Then, at week 22, she had gained 6 more pounds — not excessive, but enough to look for dietary problems. At week 26, Debbie had a 7 lb gain,
recording a 13 lb gain in two visits.
At this point, if her diet history failed to account for the additional weight, water
retention should be suspected. She should be checked for preeclampsia, particularly if
the weight shoots up around week 22 to 30, when blood pressure is also likely to increase. Sometimes the weight gain is due to diet, sometimes not. The practitioner must
not prejudge a woman's eating habits.
If this excessive weight gain was due to diet, the goal would be to meet a more
acceptable pattern, as labeled “acceptable” on the prenatal weight gain grid. The goal is
to slow down the rate of the gain in the late second and third trimester, while maintaining adequate gain for the growth needs of the fetus.
Overweight Prenatal Weight Gain Grid - Case Study #2
45 (20.4)
X
Weight Gain in Pounds (kg)
40 (18.1)
35 (15.9)
30 (13.6)
25 (11.3)
20 (9.0)
Probable Preeclampsia
X
X
Debbie's
Weight Gain
X
15 (6.8)
X
X
10 (4.5)
5 (2.2)
0
1
4
7
10 13
16
19
22 25
28
Duration of Pregnancy (weeks)
31
34 37
40
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CASE STUDY #3
Ethel is 5'7" tall, with a pre-pregnancy weight of 118 lb and a BMI of 18.5. Her BMI
is just at the cutoff between normal and underweight. So we classify her as borderline,
and use either the upper limit of the normal pre-pregnancy weight, or the guidelines for
pre-pregnancy underweight. You can use either the underweight or normal weight
prenatal weight gain grids. Below and on the next page is Ethel's weight plotted using
both an prenatal weight gain grid for underweight women and one for normal weight
women so you can see how the weight gain pattern looks on both charts.
Ethel has nausea and vomiting during the first trimester, losing 5 lb by her first
visit to the doctor. She should be monitored to ensure proper gain. Her weights were:
Week 11: 113 lb
Week 26: 130 lb
Week 36: 144 lb
Week 15: 117 lb
Week 30: 133 lb
Week 38: 145 lb
Week 19: 122 lb
Week 32: 137 lb
Week 23: 126 lb
Week 34: 140 lb
After losing in the first trimester, Ethel made up the loss: she gained the lost 5 lb,
plus an additional 27 lb. Her total weight gain was in the mid-range for normal prepregnant weight and the lower end for prepregnant underweight women. This is an
acceptable weight gain.
Underweight Prenatal Weight Gain Grid - Case Study #3
40 (18.1)
Weight Gain in Pounds (kg)
35 (15.9)
30 (13.6)
X X
25 (11.3)
X
20 (9.0)
X
15 (6.8)
X
X
10 (4.5)
X
5 (2.2)
X
0
Ethel's Weight Gain
X
-5 (-2.2)
X
1
4
7
10 13
16
19
22 25
28
Duration of Pregnancy (weeks)
31
34 37
40
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Normal Weight Prenatal Weight Gain Grid - Case Study #3
45 (20.4)
35 (15.9)
30 (13.6)
25 (11.3)
Reference Woman's
Weight Gain Range
20 (9.0)
Weight Gain in Pounds (kg)
40 (18.1)
X X
X
X
15 (6.8)
X
X
10 (4.5)
X
5 (2.2)
X
0
Ethel's Weight Gain
X
X
-5 (-2.2)
1
4
7
10 13
16
19
22 25
28
31
34 37
40
Duration of Pregnancy (weeks)
CASE STUDY #4
Samantha is 5'6" and had a pre-pregnancy weight of 229 lb with a BMI of 37. That
puts her in the obese pre-pregnancy weight classification. By her first doctor visit, at
week 12, she had already lost 14 lb. Her weights, plotted on the next page, were:
Week 12: 215 lb
Week 28: 214 lb
Week 35: 218 lb
Week 16: 214 lb
Week 30: 214 lb
Week 36: 218 lb
Week 20: 214 lb
Week 32: 216 lb
Week 37: 219 lb
Week 24: 213 lb
Week 34: 216 lb
Week 38: 220 lb
Samantha lost a lot of weight early, then considerably slowed down her loss, and in
the third trimester regained some of the lost weight. While this is not an ideal situation,
it is acceptable for an obese woman, as long as the diet is nutritionally sound. The
concern is that she not go into ketosis, which may be harmful to the fetus.
When a lot of weight is lost early in the pregnancy, one way to indicate that is to
put the pregnancy weight on the weight gain axis next to the number of pounds that
were lost, and draw a line down to the zero weight mark at the proper week gestation,
as shown. The weight gained or lost during the rest of the pregnancy is counted from
the zero mark.
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Obese Prenatal Weight Gain Grid - Case Study #4
25 (11.3)
15 (6.8)
10 (4.5)
5 (2.2)
0
-5 (-2.2)
-10 (-4.5
Samantha's Weight Loss
Weight Gain in Pounds (kg)
20 (9.0)
-15 (-6.8)
X
X
X
X
X
X
X X
XX
XX
-20 (-9.0)
1
4
7
10 13
16
19
22 25
28
31
34 37
40
Duration of Pregnancy (weeks)
CASE STUDY #5
Casey is 5'6" tall and weighed 170 lb, with a BMI of 27.5. She is considered overweight. As you can see from the weight gain grid below, her weight gain pattern closely
follows the recommendations for an overweight pregnant woman.
.
Overweight Prenatal Weight Gain Grid - Case Study #5
35 (15.9)
25 (11.3)
Casey's Weight Gain
20 (9.0)
Weight Gain in Pounds (kg)
30 (13.6)
X
15 (6.8)
X
X
10 (4.5)
X
X
5 (2.2)
0
X
X
X
1
4
7
10 13
X
16
19
22 25
28
Duration of Pregnancy (weeks)
31
34 37
40
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100
The prenatal weight gain grids will help you determine if the amount and pattern
of weight gain is acceptable, excessive or inadequate. Proper weight gain is an important component of a successful pregnancy outcome. The chart below outlines what may
be an inadequate gain and questions to ask to help determine the cause of inappropriate
weight gain.
Advice from health care professionals is important. When surveyed, 2,237 women
reported on their pre-pregnancy weight, advice on how much weight to gain and how
much they actually gained during pregnancy (Cogswell, et al., 1999). Twenty seven
percent said they had been given no advice on how much weight to gain, 14 percent
were advised to gain less than IOM recommendations and 22 percent were advised to
gain more than IOM recommendations. Advised and target weight gains were strongly
associated with actual weight gain.
The next chapter will cover the types of foods necessary to ensure adequate calories and proper nutrition.
Weight Gain Problems
Inadequate gain BMI ≥18.5: gain less than 2.2 lb/month 2nd & 3rd trimester
Inadequate gain BMI <18.5: individualize
Inadequate gain obese women: less than 1 lb 2nd & 3rd trimester
Excessive gain: gain more than 6.5 lb/month 2nd & 3rd trimester for all weight
classifications
Source: Nutrition During Pregnancy, National Academy of Sciences, 1990; JADA, 2002)
Problems: What to ask
Weight Gain Too Slow
• Are measurement & recording accurate?
• Is the overall pattern acceptable?
• Does she have nausea and vomiting?
• Was there edema on a previous visit that's
resolved?
• Does she have money & access to food?
• Is she resisting weight gain?
• Does she have an eating disorder?
• Does she understand the relationship of
weight gain to the infant's health?
• Is she: Smoking? Drinking? Using drugs?
• Does she have any medical problems?
• Is she exercising & not eating enough?
Weight Gain Too Fast
• Are measurement & recording accurate?
• Is the pattern acceptable?
• Does she have edema? Is the weight
water?
• Is she carrying twins? Triplets?
• Does she have gestational diabetes?
• Has she decreased her activity & not her
food intake?
• Has her food intake increased
dramatically?
• Is she eating high-fat & sugar foods?
• Is she overeating? Is she bored? Depressed? Stressed?
• Has she been counseled about gain?
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101
Chapter Seven
Diet Assessment for Pregnancy
The last three chapters of this course discuss the relationship of nutrition to the
outcome of pregnancy. To ensure a good diet, nutritional requirements must be translated into dietary needs — what foods, and how much of those foods, will meet nutritional needs. As a professional, it is important to know not only what a pregnant
woman should be eating, but also how to determine the adequacy of her diet.
This chapter will explain the components of a good diet. It contains diet-assessment tools which have been proven useful in determining the nutritional adequacy of a
pregnant woman’s diet. Professionals are encouraged to copy them from the Appendices for use with their clients.
DIETARY GUIDELINES
There is no right way or wrong way to eat during pregnancy, as long as nutritional
needs are met. A diet needs to address the cultural, economic and lifestyle needs of the
pregnant woman. Urging a woman to eat a diet that is not personalized dramatically
increases the chance of noncompliance. With creativity and patience, a nutritionally
sound diet can be achieved for all women. Remember, both the amounts of nutrients
and the timing are important. During the first trimester, vitamins and minerals are more
important than calories, particularly zinc, folic acid, vitamins B6 and B12. The need for
calories, iron and calcium increases in the second and third trimester.
Adequate weight gain is the best way to monitor caloric intake. Regardless of
other, more specific recommendations, if a woman is not gaining enough weight, her
caloric intake should be increased — using healthy foods and limiting empty-calorie
foods, of course.
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102
MYPYRAMID FOR MOMS
The USDA Food Guide Pyramid, now called MyPyramid, is designed to individualize the amount of food, based on an individual’s age, gender and activity. It can be
found at: <www.mypyramid.gov>
When it first came out it was not applicable for pregnant and lactating women.
Now, there is an interactive section — MyPryamid for Moms — for pregnancy an
breastfeeding that is quite extensive and interactive.
A pregnant woman can get an individualized meal plan based on her age, height,
weight, due date, pre-pregnancy weight (BMI) and activity level. This information is
entered into a calculator on the site, and a meal plan appears on the screen. The meal
plan is broken down into trimesters, with a daily caloric level and amount of food to eat
in five food groups. The calorie level and amount of food in the foods groups changes
each trimester. Note that the amount of food to eat in each group is given in household
measures — ounces and cups — and not the number of servings per day. The food
groups are the same as MyPyramid for the general population.
Let's look at what you get when using MyPryamid for Moms. For our example we
will use a 27-year-old pregnant woman, due in seven months. Her height is 5'5", with a
pre-pregnancy weight of 165 lb. She does 30 to 60 minutes of activity daily. Below is an
individualized chart from MyPyramid for Moms based on the information we entered.
A more detailed chart can be found in Appendix #9A.
MyPyramid for Moms
Your calorie needs may be more or less than the average. Check with your health care
provider to make sure you are gaining weight appropriately. To learn more about weight gain
during pregnancy, click here. To see how your food choices compare to your Plan go to the
MyPyramid Menu Planner.
The calories and amounts of food you need change with each trimester of pregnancy.
Your Plans are based on 2400, 2800, and 2800 calorie food intake patterns. They may show
different amounts of food for different months, to meet your changing nutritional needs.
Changing the amount of calories you eat each trimester also helps you gain weight at the
correct rate.
1st
Trimester
8 oz
2nd
Trimester
10 oz
3rd
Trimester
10 oz
Vegetables
3 cups
3 1/2cups
3 1/2 cups
Fruits
2 cups
2 1/2 cups
2 1/2 cups
Milk
3 cups
3 cups
3 cups
Meat & Beans
6 1/2 oz
7 oz
7 oz
Grains*
*Aim for making at least half of grains whole grains.
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Once the meal plan is in place, another section, MyPyramid Menu Planner for Moms,
lets the woman enter what she is eating into the calculator and compares it to what is in
her meal plan. There are numerous reports she can print out to see how well she is
eating on a daily or weekly basis. In addition, there is a report that shows ways to
improve her diet, information on specific foods and which foods to include in her diet
to help her reach her goals.
Another section offers information sheets and tips on various nutrition topics. As
you become familiar with the site, you will find there are many layers to it and lots of
very valuable information.
MyPyramid uses the concept of leader nutrients — foods within each group that
provide specific nutrients. By eating enough food from each group, a person’s daily
nutrient needs are sure to be met. As we discuss each food group, the leader nutrients
are also listed in the chart pertaining to that food group.
The chart below summarizes general dietary recommendations for pregnant
women. It is in household measures to be consistent with MyPyramid. Each food group,
and recommendations, will be discussed below. The amount of fiber per serving is also
included. Appendix #8 lists healthy choices of nutrient-dense foods from each food
group to meet the dietary recommendations during pregnancy.
Dietary Guidelines for Pregnancy
Food Group
Recommended #
of servings daily*
Total Fiber per
serving
Meat & Meat Alternatives¶
6-8 ounces
0-9
Milk, Yogurt & Cheese
3 - 4 cups
0
Fruits
2 - 3 cups
3-5
Vegetables
3 - 4 cups
3-5
Breads & Cereals
6 - 11 ounces
2-3
Fat, Oils & Sweets
Based on needs
0
*Individualize based on weight gain needs and nutritional status of the mother. More foods from the “fats, oils and
sweets” group can be used if nutrient intake is adequate and caloric intake is inadequate and may contain some fiber.
¶Refers to the meat, poultry, fish, dry beans, eggs & nuts group. Plant sources contain fiber; animal sources do not.
CALORIES
The caloric content of diets will vary, based on individual choices. Eating the minimum
number of servings from each food group does not assure the correct caloric intake. Intakes
can vary by as much as 1800 kcal/day, from 1200 to 3000 kcal/day, based on food choices.
Some women will need to increase the amount eaten in each food group to gain an
adequate amount of weight, while others will need to alter the types of foods they
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104
consume to avoid an excessive weight gain. Individualizing these dietary recommendations based on the likes, dislikes and needs of your clients will help them succeed in
planning and implementing the proper pregnancy diet.
Of course, it cannot be said too often: “empty” calories are of little or no benefit to
either the mother or fetus. If, however, adequate nutrition is being obtained, foods from
the fats, oils and sweets group can add needed calories if used sparingly.
MEAT/MEAT ALTERNATIVES
The meat and meat-alternatives group provides sources of protein, iron, niacin,
thiamin, vitamins B6 and B12, folic acid, magnesium and zinc. The recommended amount
to eat is 6 to 8 oz a day. The chart below lists some foods in this group and the nutrients
provided. Remember to caution about consumption of fish, as discussed in Chapter Four.
Meat, Poultry, Fish, Dry Beans, Eggs & Nuts
Nutrients
Protein, iron, riboflavin, niacin,
vitamins B6 & B12, phosphorus, zinc
Food
Meat, fish, poultry
Canned tuna, salmon
Eggs, Hot dogs, Luncheon meats
Protein, iron, thiamin, folic acid,
vitamins B6 & E, phosphorus,
magnesium, zinc, fiber
Peanut butter, Nuts
Dried beans, peas, lentils, cooked Tofu
Recommendation: 6-8 ounces/day
(eat at least 1 source of plant foods daily to decrease fat and cholesterol
and to increase fiber)
It does not matter if the protein source is animal or plant; the nutrients will be
adequate if the recommended amounts are eaten. If the diet is higher in animal protein,
the fat and cholesterol content is higher. For this reason, it is best to choose at least one
plant source of protein a day, as plant proteins have quite a bit more fiber. Legumes
contain 9 gm of fiber per serving.
Most pregnant women get adequate protein in their diets; low-income women are
most at risk due to an overall lack of food. Vegetarians can get enough protein in their diet
and usually do, although vegans, who eat no animal products whatsoever, must be more
careful in planning a diet adequate in protein and include plant protein sources daily.
Iron absorption differs between diets containing mostly animal vs. mostly plant
foods. The iron in animal protein is in the heme form, which is better absorbed than the
non-heme form in plants. Vegetarians, therefore, may have enough dietary iron, but the
Sexual & Reproductive Health
105
amount absorbed may be inadequate, since the phytates in plant foods bind the nonheme iron. Eating iron and vitamin C -rich foods together increases iron absorption.
DAIRY GROUP
Milk and milk products are major sources of calcium, riboflavin, protein, vitamin
B12 and magnesium. The recommendation is three to four cups per day.
The chart below lists the leader nutrients in this food group. To decrease the fat
content of the diet, low-fat (1 percent) or non-fat milk dairy products are preferred over
whole milk products. If however, the pregnant woman has an inadequate weight gain and
she likes dairy products, the extra calories from whole or 2 percent milk may help her gain
weight and can be encouraged. The need of the fetus for adequate calories supersedes the
long-term consideration of cholesterol limitation.
Milk, Yogurt & Cheese
Nutrients
Food
Calcium, Vitamin D,
Riboflavin, Protein,
Magnesium, Vitamins: A,
E, B6, B12
Milk: Whole, 2%, 1%, non-fat
Reconstituted skim or evaporated, buttermilk
Cheese, Cheese spread
Cottage cheese, Cream soup
Ice cream, Pudding & custard, Yogurt
Recommendation: 3-4 cups/day • Use low-fat or nonfat milk dairy products
If a woman is lactose-intolerant, options are available to her to make sure she gets
enough calcium. Fermented milk products such as yogurt, kefir, buttermilk, cottage
cheese and cheese may be tolerated, even though milk is not. If the intolerance is doserelated, small amounts may not cause diarrhea, gas, cramping, etc.
Foods other than dairy products provide calcium, as shown on the next page. The
amount of calcium in foods equivalent to one 8 oz glass of milk is provided by: 8 oz (2
cups) of tofu, 2/3 cup of tofu processed with calcium, 1.5 cups of dark green leafy vegetables, or 3/4 cup of amaranth (a grain), 10 oz fortified rice milk or 1 to 1.5 oz of soy
cheese. Other good sources of calcium are almonds, sesame seeds, canned salmon and
sardines (including the bones).
Foods with calcium added are now available: orange juice, breakfast cereals, yogurt, Wonder Bread®, milk, cheese etc. The added calcium dramatically increases the
calcium content of the foods that have naturally occurring calcium and adds a source of
calcium to foods that do not usually contain calcium. For example, the calcium in milk
may increase from 300 mg/cup to 600 mg/cup. You need to read the label to find out
exactly how much calcium is added and the total amount per serving. The milk in
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106
deluxe coffee drinks (preferably decaffeinated) can add up to quite a bit of calcium.
Organic milk may or may not have vitamin D added, so read the label.
An alternative for individuals with a lactose intolerance, as discussed in Chapter
Five is the lactase enzyme, Lactaid® .
If all else fails, a calcium supplement can be taken to ensure adequate calcium intake,
with calcium carbonate the preferable form. Tums®, an antacid, is inexpensive calcium
carbonate, but remember that calcium can interfere with iron absorption. Also, pregnant
women should not drink unpasteurized milk as it may have bacteria harmful to pregnancy.
Calcium Content of Foods
Serving Size Calcium, mg
Dairy
Milk, whole, non-fat, low-fat 8 oz
Lactaid milk™
8 oz
Yogurt, low-fat
8 oz
low-fat fruited
8 oz
Buttermilk
8 oz
Cottage cheese
1/4 C.
Cheddar cheese
1 oz
Swiss cheese
1 oz
Parmesan cheese
1 Tbsp.
Ice cream
1/2 C.
Frozen yogurt
1/2 C.
Sour cream
2 Tbsp.
Cream cheese
1 oz
Pudding, vanilla
1 C.
Legume Products
Soymilk, unfortified
Soymilk, fortified
Soy cheese
Tofu, not processed
w/calcium
Tofu, processed w/calcium
Green soybeans
Soy beans
Navy beans
290
300
415
345
316
167
210
272
100
88
100
34
23
298
8 oz
10
8 oz 200-500
1 oz 200-300
3.5 oz
1/2 C.
1/2 C.
1/2 C.
1/2 C.
150
258
131
86
64
Serving Size Calcium, mg
Grains, Seeds & Nuts
Rice milk, fortified
Amaranth
Farina
Sunflower seeds
Sesame seeds
Almonds
Tahini
8 oz
1 C.
1 C.
1 oz
2 Tbsp.
1/2 C.
2 Tbsp.
240
275
147
20
160
160
128
Vegetables and Fruit
Kale
1/2 C.
Turnip greens
1/2 C.
Collard greens
1/2 C.
Bok choy
1/2 C.
Mustard greens
1/2 C.
Broccoli
1/2 C.
Figs
5 medium
90
99
74
79
75
70
135
Seafood
Sardines, canned w/bones 3.5 oz
Salmon, canned w/bones 3.5 oz
370
200
Other
Blackstrap molasses
Calcium-fortified OJ
140
240
1 Tbsp.
6 oz
FRUIT/VEGETABLE GROUPS
The major nutrients in the fruit and vegetable food group are: vitamins A, C, folic
acid and fiber. We also know that fruits and vegetables are high in antioxidants. The
recommended amount to eat per day is two to three cups of fruits and three to four
cups for vegetables. Fruits are preferred over fruit juice, although one serving of juice
per day is acceptable. The charts below list the foods that are good sources of each
nutrient and the amount considered a serving.
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107
The color of the fruit or vegetable is a giveaway to the major nutrient found in it.
Dark green vegetables are the best source of folic acid, while containing some vitamin
C. The yellow and orange fruits and vegetables contain vitamin A or its plant version,
beta-carotene. The citrus fruits are the major source of vitamin C. It is recommended to
eat a variety of colors of fruits and vegetables, including one dark green and one deep
orange fruit or vegetable daily.
Since folic acid and vitamin C are water-soluble, they are destroyed by heat and
water. Boiling will destroy 60 to 90 percent of these vitamins. Recommend foods that
contain folic acid and vitamin C be eaten in their raw state.
Fruits & Vegetables
FRUITS
Nutrients
Food
Vitamins A & C
Fiber, Folic acid
Potassium
Citrus fruits/juices
Cantaloupe, Strawberries
Tangerines, Banana, Apricots
Canned fruits, dried fruits
Recommendation: 2 - 3 cups/day
Emphasize fruit over juice; one good source of vitamin C /day
VEGETABLES
Nutrients
Food
Vitamin C, Fiber
Broccoli, cabbage, Peppers/tomatoes
Folic acid, Vitamin A
Magnesium, Iron
Broccoli, asparagus, Brussels sprouts
Greens: spinach, beet, mustard, turnip
Dark leafy lettuce
Fiber, various vitamins
and minerals
Carrots, artichokes, eggplant, cucumber, squash,
acorn squash, beets, cauliflower etc
Recommendation: 3 - 4 cups/day
Eat a variety of colors of vegetables to ensure good nutrient intake
There are many other fruits and vegetables not listed in the charts above. That does
not mean women are not supposed to eat them, only that they are not as good sources
of vitamins A, C and folic acid. Use the remaining fruits and vegetables to fill the daily
recommended amount of vegetables.
Not only do fruits and vegetables provide vitamins and minerals, they are an
excellent source of fiber, both dietary and functional fiber, containing 3 to 5 gm of total
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fiber per serving. During pregnancy, with increased constipation, the more fiber included in the diet the better — especially dietary fiber which increases fecal bulk.
BREADS/CEREALS GROUP
Breads, cereals, rice and pasta contain good sources of thiamin, niacin, iron and
zinc. As with fruits and vegetables, foods in this group contain fiber. The type of breads
and cereals chosen dramatically affects fiber content of the diet. Whole grain products
are a much better source of fiber than white or processed grain products.
The chart below lists the types and amounts of foods considered a bread serving.
Breads & Cereals
Nutrients
Thiamin, Niacin
Iron, Riboflavin
Phosphorus, Fiber
Food
Bread
Hot cereals, grains (oats, rye, barley, millet, amaranth, etc.)
Ready-to-eat cereals
Macaroni, noodles, spaghetti, rice, cooked
Cornbread, Roll, muffin, biscuit, tortilla
Crackers, Bun, bagel, English muffin
Recommendation: 7-11 ounces/day
Make half your servings whole grains, as they are higher in fiber
and magnesium, zinc, folic acid, vitamins B6 and E
A minimum of 7 oz per day is recommended from the breads and cereals group,
with 4 oz being whole grain products. Increasing the amount eaten to 8 to 11 oz per day
is a good way to increase nutrient-dense calories for weight gain and for fiber.
Each ounce of breads and cereals contains an average of 2 to 3 gm of total fiber. If
the bread or cereal is whole grain with seeds and nuts, it may contain more fiber. If a
woman consumes 8 oz per day of breads and cereals, she can consume 16 to 24 gm of
fiber a day, getting close to her recommended intake of 28 gm per day. Of all the food
groups, this one is most likely to be adequate.
FATS, OILS AND SWEETS
An additional category is the fats, oils and sweets group, which includes foods that
are sources of sugar, fat, salt, alcohol or other foods as shown on the next page. These
foods are not totally off limits. The goal is to eat the recommended amount from the
other groups first, then add these foods to reach the desired calorie level. If you do
consume these foods, concentrate on the plant oils and nuts and fish as they are the
healthiest fats and oils.
109
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Excesses of fat, cholesterol and sodium, and a deficiency of fiber, are possible even
if someone eats from each of the food groups every day. To avoid this problem, become
familiar with the types of food in each group that contain sugar, fat and sodium and
those that are high in fiber.
The food groups most likely to be inadequate in the diet are milk and milk products and fruits and vegetables, indicating inadequate intakes in calcium, magnesium
and folic acid. Other nutrients that have been found to be low in the diets of pregnant
women include: calories, vitamin B6, zinc, copper and iron.
Fats, Oils & Sweets
Includes foods that are:
• high in sugar, fat, salt, cholesterol, alcohol and/or caffeine
• high in calories and/or low in nutrients
• not essential or necessary in the diet
Sugar
Cake, pie, cookies, donuts,
sweet rolls, candy, soft
drinks, jelly, syrup, desserts, sugar, honey
Fat
Salt
margarine, oils,
salad dressing,
cream, butter,
cream cheese,
gravy, sauces
Potato and corn chips,
pretzels, pickles, olives,
bouillon, soy sauce, steak
sauce, salt, seasoned salt,
canned goods, luncheon
meats, cured ham
This concept of "food groups" is not perfect, but it is a start. MyPyramid emphasizes
grains, fruits and vegetables in an effort to help people reduce dietary cholesterol and fat
and increase total fiber. Non-dairy sources of calcium (e.g., grains) are emphasized since the
recommendation for milk is decreased to three servings/day. Plant proteins are encouraged.
A good resource for nutritional information is the March of Dimes website:
<www.Marchofdimes.com>
FEEDBACK FORM
If a woman has not used a food group or exchange system to keep track of her
intake, it may be confusing for her at first. To help her plan her diet and keep track of
what she is eating, a feedback form is useful (sample on the next page). This form
provides spaces to write in the total amount of food from each food group she should
have in one day.
To determine how much a pregnant woman should eat, you or the client can get
this information from MyPyramid for Moms individualized meal plan then transfer it
to the feedback form. Or you can create the meal plan yourself.
To keep track of what she eats, the woman checks off a box within the food group.
Each box indicates either 1 oz or 1 cup, based on the food group. At the end of the day
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she counts how much of each food group she has eaten, writes that in the column
provided, and compares it to what is recommended for her, in the adjacent column. At
the end of the day, the pregnant woman knows how her diet compares to what is recommended.
A feedback form is a consciousness raising tool, helping make women aware of
what they are eating compared to what they should be eating. Appendix #9 is a sample of
a food plan from MyPyramid for Moms. A blank Feedback form, called "A Daily Food
Guide" is included in Appendix #9A; it can be duplicated for use with your clients.
Sample Feedback Form For Daily Food Guide
FOOD GROUP
Meat/Protein*
Animal
x
x
x
x
Plant
Milk
x
x
Fruits
x
x
Vegetables
x
x
x
x
x
Breads/Cereals
x
x
x
x
x
Whole grain
x
x
x
x
x
Fats, oils, sweets
x
x
x
Vit. A,C (fruit/veg)
x
x
I ate:
My total
should be:
(4)
_____
(3)
_____
4
_____
2
_____
0
_____
1
_____
3
_____
3
_____
2
_____
3
_____
1
_____
4
_____
3
_____
3
_____
7
_____
8
_____
5
_____
**
_____
3
_____
**
_____
Record the amount of food that you ate today in each food group. Each box equals either one ounce
or one cup, based on the food group. The total amount eaten in each group should equal or exceed
what you are allowed in your personal meal plan, developed for you by your nutrition counselor or
MyPyramid.
*The amount eaten in these groups is counted by the recommended sub-groups and the total for the
group is in parentheses. Example: meat/protein total recommended is 3, shown in parentheses, with
2 servings of animal and one serving of plant food recomended.
**The number of servings in this group is based on your caloric needs and varies from day to day.
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ASSESSING THE DIET
How do you determine if the diet is adequate? The best way is a diet assessment
using some form of diet history. A 24-hour recall, asking the woman to list everything
she ate or drank for the prior 24 hours, is a good method, but it has drawbacks: it’s time
consuming, the portion sizes recorded are usually not accurate, the period used is
probably not typical. Also, many people can't remember what they ate.
(Often, people want to “do right” and will make their diet look better. Any method
that relies on memory and honesty is subject to this problem, so the counselor must
impress upon her that accuracy is essential for proper assessment, and that no judgment
or blaming will take place.)
A food frequency chart is another diet history method that asks the number of
times per week that foods are consumed. No serving sizes are requested, so it’s hard to
get exact amounts of nutrients consumed. Also, the specific foods (such as the types of
fruits or vegetables) may or may not be requested. It is helpful to examine the completed food frequency form with the client to find out if the fruits and vegetables are
high in vitamins A and/or C, if the meat eaten is fried or broiled, if the breads are whole
grain or white and if the dairy products eaten are whole, low-fat or non-fat.
What the food frequency form does give is an idea of the individual’s pattern of
eating. The types of foods typically consumed gives an indication of missing groups of
foods, inadequate consumption of groups of foods or excesses of “other” foods. Because
diets tend to fall into patterns over time, this information is valuable — more so, in my
opinion, than the details of a 24-hour recall.
Depending upon your clientele, this form may be more appropriate to use since it
is easier to fill out than a 24-hour recall. A sample food frequency form is included in
Appendix #10. To use this form, the patient puts a check mark in the column that best
represents the number of times per week that a food is eaten. At the bottom of the page
the totals are tallied.
The diet history shown on the next page, Diet Assessment #1, is an example of a
completed food frequency record. In the sample, the meat total includes beef, pork,
ham, hamburger, hot dogs and luncheon meats; breads and cereals includes breakfast
cereals, grains, breads, rolls, biscuits, tortillas and crackers. Sample weekly totals have
been completed for you.
Once the weekly totals are completed, add up the totals for each food group, and
divide the total by seven to get an idea of the average number of servings eaten each
day, then compare it to the recommended number of servings for that food group.
According to the Healthy Eating Index-2005 (USDA, CNPP, 2008), the food groups
most likely to be adequate are Grains and Meat/Beans. Far below the maximum were
dark green and orange vegetables, legumes and whole grains. So when completing your
assessment, pay close attention to the groups that tend to be lacking in American diets.
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DIET ASSESSMENT #1
The average number of times a week a food is eaten for Diet Assessment #1 is:
Meat, poultry, fish, dry beans, eggs & nuts =
meat
7
poultry
3
fish
0
legumes
1
eggs
1
12 times/week
12 times/week ÷ 7 days/week = 1.7 times/day on average
This is below the recommended 6-8 ounces/day.
Milk, yogurt & cheese =
dairy products
5 servings/week
5 times/week ÷ 7 days/week = .71 times/day
This is below the recommended 3-4 cups/day.
Fruits =
fruits
4
4 times/week ÷ 7 = .57 times/day
This is below the recommended 2 to 3 cups/day
Vegetables =
vegetables
7
7 times/week ÷ 7 = 1 time/day
This is below the recommended 3 to 4 cups/day.
Breads, cereals, rice & pasta =
breads/cereals
26
rice and pasta
6_
32 times/week
32 times/week ÷ 7 = 4.5 times/day
This is below the recommended 7 to 11 ounces/day.
The fats, oils and sweets group is represented by sodas, alcohol, cakes, pies, chips,
ice cream, candy and fats. In Diet Assessment #1 the weekly number of times fat is
eaten is 21 (3 per day), and 32 times “junk” foods are eaten, over 4.5 times/day.
The food frequency form gives us the following information to assess this diet:
The diet is low in meat and meat alternatives, milk products, fruits, vegetables,
breads and cereals. Protein, calcium, vitamin C, folic acid, vitamin A, B vitamins, iron,
magnesium and fiber are possibly inadequate, while fat and sugar are high. Calories are
probably adequate due to the high consumption of calorie-dense “junk food.”
It is obvious that there are problems with the diet. Many of the desirable foods
checked are in the infrequent columns, particularly milk and milk products and fruits
and vegetables. Undesirable “junk” foods, with a lot of calories, fat and sugar, are in the
more frequently used columns. In short, it is the opposite of what is recommended.
If you do not have time to add up the weekly totals for each type of food, just
scanning the form and looking where the Xs fall can give you valuable information. For
desirable foods, the Xs should be in the columns on the left. For undesirable foods, the
Xs should be in the columns indicating infrequent use, on the right. Dividing the form
into food groups and scanning for the Xs gives a quick assessment of the diet that can
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113
be shown immediately to the client in an informal interview. It is a good visual representation, and even the least motivated client can be implored to “move those Xs over.”
The pregnant woman eating this diet needs nutritional counseling. Recommendations would include increasing protein, milk and milk products, breads and cereals and
fruits and vegetables, while decreasing the other foods. This will increase intake of
nutrients and decrease calories (helpful if she is gaining weight excessively).
Diet Assessment #1
Please check the column that shows how often you eat the following foods. Check only one column for each
food. Your answers will be used for educational purposes.
2-4
times
a day
Beef, pork, ham, hamburger
Luncheon meats, hot dogs
Chicken, turkey, poultry
Fish, seafood
Eggs
Dried peas or beans (legumes)
Peanut butter
Nuts
Cereals (dry or cooked)
Grains
Breads, rolls, biscuits
Tortillas
Crackers
Pasta, noodles, spaghetti, macaroni
Milk
Cheese
Yogurt, pudding, custard
Fruits
Fruit juices
Vegetables
Water
Added fat
Coffee, tea, cocoa
Sodas, fruit flavored drinks
Alcohol: beer, wine, whiskey
Candy, sweets
Cakes, pies, cookies, donuts, sweet rolls
Potato chips, pretzels, corn/tortilla chips
Ice cream
Weekly Totals:
7
Meat __________________
3
Poultry ________________
0
Fish ___________________
1
Legumes _______________
1
Eggs __________________
26
Bread & Cereals _________
6
Rice & Pasta ____________
Once
daily
2-4
times
a week
Once
weekly
Hardly
ever or
never
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
4
7
Fruits & Juices* ___________
Cakes, pies ____________
7
7
Vegetables* _______________
Chips ________________
5
1
Dairy products ____________
Ice cream _____________
7
7
Water ____________________
Candy ________________
7
21
Sodas ___________________
Fats __________________
3
53
Alcohol __________________
Other ________________
*Ask types to determine if they are high in vitamins A or C
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The key to successful nutritional counseling is to find specific changes to recommend, within the client's budget and cultural constraints. It is better if the patient can
come up with the suggestions for diet changes as she is more likely to follow the diet.
Too often counselors tell clients what they think is best for them and lose sight of many
other possibilities and options for these clients.
DIET ASSESSMENT #2
Diet Assessment #2
Please check the column that shows how often you eat the following foods. Check only one column for each
food. Your answers will be used for educational purposes.
2-4
times
a day
Beef, pork, ham, hamburger
Luncheon meats, hot dogs
Chicken, turkey, poultry
Fish, seafood
Eggs
Dried peas or beans (legumes)
Peanut butter
Nuts
Cereals (dry or cooked)
Grains
Breads, rolls, biscuits
Tortillas
Crackers
Pasta, noodles, spaghetti, macaroni
Milk
Cheese
Yogurt, pudding, custard
Fruits
Fruit juices
Vegetables
Water
Added fat
Coffee, tea, cocoa
Sodas, fruit flavored drinks
Alcohol: beer, wine, whiskey
Candy, sweets
Cakes, pies, cookies, donuts, sweet rolls
Potato chips, pretzels, corn/tortilla chips
Ice cream
Weekly Totals:
Meat __________________
8
Poultry ________________
4
1
Fish ___________________
7
Legumes _______________
1
Eggs __________________
31
Bread & Cereals _________
5
Rice & Pasta ____________
Once
daily
2-4
times
a week
Once
weekly
Hardly
ever or
never
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
Fruits & Juices* ___________
Cakes, pies ____________
0
7
Vegetables* _______________
Chips ________________
7
15
7
3
Dairy products ____________
Ice cream _____________
7
3
Water ____________________
Candy ________________
18
20
Sodas ___________________
Fats __________________
4
49
Alcohol __________________
Other ________________
*Ask types to determine if they are high in vitamins A or C
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Looking only at the position of the Xs indicates milk/milk products and fruits and
vegetables are low and the “other” foods are too high. For instance, All of the foods in
the meat/beans/protein category are eaten two to four times a week or once a week,
with the exception of legumes, which are eaten daily. Milk and milk products are consumed two to four times a week and cheese once a day. Fruits and vegetables are in the
"hardly ever or never" column.
The average number of times a day that foods are eaten are:
meat, poultry, fish, dry beans, eggs & nuts – 3
milk, yogurt & cheese – 1
fruits and vegetables – 1
breads, cereals, rice & pasta – 5.1
other – 7
fats – 2.9
This woman is not getting enough milk products, breads and cereals and fruits and
vegetables. Her meat and meat alternate intake is adequate. Too much “junk food” is
consumed. She is eating chips two to four times a day, so her sodium intake may be
high, especially if she uses high-sodium meats and canned foods. Other dietary problems include too much fat and too little fiber.
DIET ASSESSMENT #3
Let’s evaluate one more diet, Assessment #3, charted on the following page. Try
analyzing it before reading the evaluation that follows.
This diet is the best of all we’ve evaluated. The average number of times/day from
each group:
meat, poultry, fish, dry beans, eggs & nuts – 2.6
milk, yogurt & cheese – 4.7
fruits and vegetables – 5.6
breads, cereals, rice & pasta – 8.2
other – 0.43
fats – 1
There is little to recommend to improve this diet. Even though protein seems a little
low, with the amount of dairy products and breads and cereals in the diet, it is most likely
adequate. Check the types of foods consumed to make sure the fat content is not too high.
Also check to see if the bread and cereals are whole grain, contributing to the fiber intake. If
weight gain is adequate, indicating adequate caloric intake, then this diet is fine.
Sexual & Reproductive Health
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Diet Assessment #3
Please check the column that shows how often you eat the following foods. Check only one column for each
food. Your answers will be used for educational purposes.
2-4
times
a day
Beef, pork, ham, hamburger
Luncheon meats, hot dogs
Chicken, turkey, poultry
Fish, seafood
Eggs
Dried peas or beans (legumes)
Peanut butter
Nuts
Cereals (dry or cooked)
Grains
Breads, rolls, biscuits
Tortillas
Crackers
Pasta, noodles, spaghetti, macaroni
Milk
Cheese
Yogurt, pudding, custard
Fruits
Fruit juices
Vegetables
Water
Added fat
Coffee, tea, cocoa
Sodas, fruit flavored drinks
Alcohol: beer, wine, whiskey
Candy, sweets
Cakes, pies, cookies, donuts, sweet rolls
Potato chips, pretzels, corn/tortilla chips
Ice cream
Weekly Totals:
1
Meat __________________
4
Poultry ________________
3
Fish ___________________
7
Legumes _______________
3
Eggs __________________
48
Bread & Cereals _________
10
Rice & Pasta ____________
Once
daily
2-4
times
a week
Once
weekly
Hardly
ever or
never
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
18
0
Fruits & Juices* ___________
Cakes, pies ____________
21
1
Vegetables* _______________
Chips ________________
33
1
Dairy products ____________
Ice cream _____________
18
0
Water ____________________
Candy ________________
0
7
Sodas ___________________
Fats __________________
1
3
Alcohol __________________
Other ________________
*Ask types to determine if they are high in vitamins A or C
EATING PATTERN
It has been suggested that the optimal eating pattern for women is three meals and
two snacks per day (IOM, 1990). Siega-Riz et al. (2001) found that pregnant women who
ate fewer than three meals and two snacks had a 30 percent higher risk for delivering
preterm babies. In addition, women who went for longer than 13 hours a day without
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eating had a three-fold greater risk of delivering preterm babies, less than 34 weeks
gestation, than pregnant women who ate within 13 hours in a day.
The mechanism behind this finding appears to be related to the neuropeptide
corticotropin-releasing hormone (CRH). Hermann et al. (2001) found that fasting (or not
eating food) for more than 13 hours increased maternal CRH levels compared to not
eating for less than 13 hours. The researchers also found an inverse relationship between maternal CRH levels and gestational age at delivery. This may explain why
pregnant women who eat infrequently may give birth to more preterm babies. It may be
prudent to recommend that pregnant women eat fairly often during the day and have a
snack at bedtime.
Hobel and colleagues (2003) review the relationship between psychosocial and
nutritional stress on poor pregnancy outcome and explain in detail the relationship
between food intake and poor pregnancy outcome.
SUMMARY
It should be obvious by now that although there are specific dietary recommendations for pregnant women, a nutrition counselor has the ability to fine-tune those recommendations to meet the specific needs of his or her clients. Tools to assist in the
evaluation of a diet and to assist a woman follow her diet are integral parts of helping
women eat optimally while pregnant. For motivated clients, encourage them to use the
MyPyramid site, as it contain lots of good information that you know if reliable.
Keep the following questions in mind as you assess the diet of your clients:
• Which nutrient needs are being met?
• Which food practices should be reinforced?
• What aspects of the food practices most need improvement?
• Which practices should be discouraged or eliminated?
These questions can help guide your interactions with your client. Too often as
counselors we try to make too many changes in the diet all at once. It may be that a
client can only change one, two or three behaviors. Which ones will have the most
impact? Once those are determined, work on those, then go on to others if possible.
Other concerns that determine if a client can meet her nutritional needs concern
her financial and social situation as well as cultural and ethnic practices.
You can counsel a client all you want, but if she cannot buy, store or prepare food,
what good will it do? You need to know if she has money for food, can get to the store,
has a refrigerator, stove and/or oven. Do not be timid or feel like you are prying if you
have to ask uncomfortable questions. How you phrase questions may determine how
honest a response you get. The chart on the next page lists food programs for lowincome women that will supplement their diet.
Cultural and ethnic food practices must also be considered when counseling clients
about dietary practices. With an increasingly varied ethnic population, understanding
the food preferences and social aspects of food can increase the likelihood that your
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suggestions for improving the nutritional quality of the diet will be followed. Also,
many women are now vegetarians and should be reassured that they can meet all their
nutritional needs but may need to include a wider range of foods or an increase amount
of certain foods.
Most importantly, be practical. Look for ways to improve diets that are easy to
follow, do not take a lot of time, and fit into the lifestyle of your client.
Nutrition Services & Programs for Pregnant Women
Commodity Supplemental Food Program (CSFP): Services and benefits: Monthly
canned or packaged foods & opportunities for nutrition education. Eligibility:
Household income <185% of federal poverty level. Website:
www.fns.usda.gov/fdd/programs/csfp
Expanded Food and Nutrition Education Program (EFNEP): Services and benefits:
Provides individual & group education & training on food & nutrition & getting the
most for your food dollar. Many programs also offer a special series for pregnant
teens. Eligibility: Households w/children under 19 years of age w/income <125%
of federal poverty level are eligible if found to be at nutritional risk.
Supplemental Nutrition Assistance Program (formerly the Food Stamp Program):
Services and benefits: Food vouchers, cards, or checks to purchase foods at
participating grocery stores. Eligibility: Households w/low income & w/resources
(aside from income) of <$2000. Formal application must be made to a local public
assistance or social services agency. Website: www.fns.usda.gov/snap
Special Supplemental Nutrition Program for Women, Infants, and Children (WIC):
Services and benefits: Monthly food packages, nutrition education, & referrals for
health care and other services. Eligibility: Household income less than 185% of
federal poverty level & be certified to be at nutritional risk. Website:
www.fns.usda.gov/wic
Other sources of nutrition services and information in the community may exist.
Some of these services may be provided for a minimal charge or even for free
while other services are billed just like other medical appointments. Look for these
services in the community:
• Public health nutritionists in city, county or state health departments
• Nutrition specialists with Agricultural Extension Service Programs associated with
state universities
• Dietitians employed at local community hospitals, medical clinics, health centers,
and in private practice.
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Chapter Eight:
Special Diet Problems,
Supplementation & Exercise
Monitoring the pregnant woman's dietary intake throughout her pregnancy is
an important component of a successful outcome. Special dietary issues may appear
during pregnancy that were not evident in an initial screening or early in the pregnancy.
The chart below lists several problems associated with inadequate intake.
Special Dietary Problems
• Food security - limited access to food (low income)
• Food safety
• Avoidance of foods
– intolerance, fads, cultural practice
• Adherence to vegan diet
• Substance abuse
– alcohol, tobacco, illicit drugs
• Restricted weight gain
• Pica
• Attitude, feelings about pregnancy
• Lifestyle precludes adequate nutrient intake
• Nausea, vomiting, constipation, heartburn, leg cramps
• Herbal and alternative products
• Clinical information indicating nutritional risk:
– over- or underweight
– anemia
– bariatric surgery
– multiple gestation
– adolescence – health issues
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WEIGHT GAIN
When evaluating the diets of pregnant women, be on the lookout for any weight
gain problem. One of the most common symptoms is gaining too much weight — any
gain in excess of 6.5 lb per month is too much, especially in repeat pregnancies. A
woman who weighed 120 lb at the beginning of her first pregnancy may find herself at
160 lb at the end of her second or third.
These women need help to find ways to cut calories, but not nutrients. Finding
and eliminating hidden fat in the diet decreases calories without changing nutrient
composition. Typical sources of excess or hidden fats are: meat, whole milk, salad
dressings, mayonnaise, butter, margarine, crackers, fried foods, nuts, meats, marinades,
sauces and gravies etc. Appendix #8, “Healthy Food Choices,” can help women choose
foods that have more nutrients and fewer calories.
The opposite problem is gaining too little weight — less than 2.2 lb per month.
Inadequate gain is an indication of insufficient calories and nutrients. While excess gain
can be a problem for the mother, inadequate gain is more a problem for the fetus.
Solutions need to be found so the mother can increase her intake.
Usually, non-fat and low-fat dairy products are recommended for pregnant
women. In the case of inadequate weight gain, the rule may need to be broken — whole
milk dairy products are recommended as a source of extra calories. After delivery, the
woman can switch back to low-fat dairy products.
A good suggestion is to mix up a pitcher of a nutrient-packed beverage that can be
sipped throughout the day. An example is a milk shake with added egg (cooked), yogurt
and fruit. Adding instant breakfast preparations to milk is another option. Using fruit juice
as the base is preferable for some women. The idea is to find something that can be made
easily and ingested throughout the day, and which is high in nutritive value. Be imaginative! But with the continuous carbohydrate ingestion, be careful about dental decay.
If a woman is having problems with her weight gain, she should be screened for
an eating disorder such as anorexia nervosa or bulimia or a problem with food that will
prevent her from gaining adequate weight and increase her risk for a LBW or SGA baby
(Conti, et al., 1998). These diseases affect a woman's dietary intake and her ability to
gain weight while pregnant. If this is the case, the woman may need more help than
you can give her and a referral to a psychologist or clinic may be necessary.
Also consider that inadequate weight gain may be linked to disordered eating that
may not be a typical eating disorder. Fairburn et al. (1992) found that 80 percent of
women have aversions to food that do not interfere with adequate weight gain in
pregnancy, while 53 percent have cravings for specific foods. In this study of 100
women, three had a clinically diagnosed eating disorder that was non-specific. In these
three cases the women had an easier time gaining weight early in the pregnancy and
more difficulty later on, probably fearful of not losing the weight once the pregnancy
was over. There was no relationship in this study between eating disorders and poor
pregnancy outcome. This was a small, voluntary study and may not have included
women with more serious eating disorders
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The chart below lists symptoms that might indicate an eating disorder is present. A
more complete discussion of eating disorders can be found in Nutrition Dimension
courses: Diet, Weight Control & Eating Disorders and Treating Eating Disorders.
Prenatal Screening for Eating Disorders
Anorexia Nervosa
• weighs less than 85% of desirable prepregnancy weight
• no weight gain
• history of poor appetite or large
weight loss
• unrealistic expectations for
weight during pregnancy
Bulimia
• history of large weight fluctuations
• nausea/vomiting whether pregnant or
not
• history of binge/purge behavior
• awareness of bulimia in self or others
• laxative or diuretic abuse
• fixation with body shape/weight
• oral health screening
Adapted from “Nutrition During Pregnancy and the Postpartum Period”, Calif Dept of Health, 1990.
NAUSEA AND VOMITING
Some weight gain problems are worsened by nausea and vomiting which can
make the woman reluctant to eat or affect absorption of nutrients.
Nausea and vomiting affect half of all pregnant women, usually beginning early in
the pregnancy and disappearing by week 12, but these symptoms can last until week
20. Nausea and vomiting may be difficult to treat, since hormonal changes are usually
presumed to be the cause. Other theories as to the cause of nausea and vomiting include: lower blood sodium; alterations in brain chemoreceptors; altered metabolism;
slower emptying of the stomach and heightened senses.
Increased estrogen causes a sensitivity to smells, called hyperolfaction, not experienced in nonpregnant women. These smells may be to food or to items found in a
women's normal environment, such as cleaning chemicals, dogs, mold, coffee, garbage,
perfume, soaps etc. Many pregnant women cite sensitivity to smells as the trigger to
their problems. Hyperolfaction may be a cue to pregnant women to seek cleaner, quieter, and more temperate environments (Erick, 1995). It may also explain why some
women experience relief from their nausea when hospitalized but find that the nausea
recurs once they are back in their usual environments.
While the symptoms of nausea and vomiting range from unpleasant to life-threatening, there are remedies that work, although highly individualized. With good detective work and an open mind, solutions can be found for most women. Appendix #13
lists some solutions for nausea and vomiting. An excellent reference is Miriam Erick's
book, No More Morning Sickness, A Survival Guide For Pregnant Women, or her client
education resource: Take Two Crackers and Call Me in the Morning! Brookline, MA:
Grinnen-Barrett Publishing, 1995.
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A newer reference by Miriam Erick is Managing Morning Sickness: A Survival Guide
for Pregnant Women. Bull Publishing, 2004. Another book that may be helpful is by
Elizabeth Kaledin, The Morning Sickness Companion. St Martins, Griffen & Thomas
Dunne Books, 2003.
A woman with a severe or prolonged nausea and vomiting problem should have her
weight gain monitored closely. In many normal weight or overweight women, a slight
weight loss in the first trimester is rapidly made up once the problem disappears. Women
most at risk are those who are underweight at onset, have severe or prolonged nausea and
vomiting, lose weight during the first trimester, and don’t regain or gain adequately thereafter.
Potassium lost through vomiting can be replaced by eating foods rich in potassium, such as bananas, oranges, prunes, potatoes, cantaloupe and legumes. At least one
serving per day of a potassium-rich food will replace losses. Since food intake (and
consequently nutrient intake) is down at this time, women should take a multi-vitamin
and mineral supplement.
Severe and prolonged nausea and vomiting can progress to hyperemesis
gravidarum (HG), a condition affecting 0.5 to 1 percent of all pregnant women (Leduc,
1997). HG usually begins before the 20th week of gestation with intractable vomiting,
severe enough to cause weight loss, dehydration, electrolyte imbalance, ketonuria and
acid-base imbalances. These can all lead to hospitalization and the need for nutrition
support — tubefeeding or total parenteral nutrition. In some women, adequate treatment can prevent the need for nutrition support, but in others it may not (Erick, 1997).
It is important to try to keep food in the stomach. An empty stomach increases
nausea and vomiting, making it harder for the woman to eat. Once the vomiting begins,
it may be difficult to stop. Eating smaller meals that are rich in easily digestible carbohydrates, at more frequent intervals, and avoiding any foods that increase the symptoms
are good tips. However, some women may crave different types of foods, such as those
that are sweet, salty, crunchy, bitter, sour, mushy, hard, spicy, hot, cold, thin or thick.
The goal is to gain adequate weight, with the healthiest diet possible. If there is an
aversion to healthy foods, getting calories in, no matter the source, is critical even if it
means eating “junk” foods. A woman can supplement vitamins and minerals, but not
calories. Erick (1995) says that one of the solutions that works best for some of her
patients is potato chips and lemonade!
Women who are troubled with nausea and vomiting are at risk of damaging the
enamel on their teeth because the acid in the vomit can soften dental enamel. The best
advice is to have them rinse their mouths out with 1 cup of water mixed with 1/2 teaspoon of baking soda, to neutralize the acid.
Vitamin B6 is sometimes prescribed for nausea and vomiting, but caution should be
used when taking this vitamin. The RDA is 2.2 mg/day, but women are often advised to
take up to 50 to 100 mg/day. At that level, vitamin B6 acts like a drug. Side effects in
women — especially peripheral nerve damage— have been documented at 100 mg/day,
and it is likely that the fetus is affected, too, although this has not been proven. Avoid
megadosing with vitamin B6.
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Ginger, a folk remedy, has been used for centuries to alleviate nausea during pregnancy. In 2004, a study from Australia found that ginger, early in pregnancy, is as effective
as vitamin B6 in reducing nausea and vomiting in pregnant women and is safe to use
(Smith, et al., 2004). Other studies have reviewed the literature and found that ginger does
appear safe for pregnant women (Boone and Shields, 2005; Borrelli, et al., 2005).
HEARTBURN AND CONSTIPATION
Heartburn is caused by the relaxation of the cardio-esophageal sphincter, allowing
stomach acid to be regurgitated into the esophagus. This condition is worse late in the
pregnancy, and is most noticeable when a woman is lying down or bending over. To
prevent the problem or decrease the symptoms, it is best to avoid high-fat meals, since
they delay gastric emptying.
Highly seasoned foods or foods that increase gastric acidity can cause a problem
and should be avoided. A more complete list of solutions can be found in Appendix #11.
If antacids are used, calcium in the antacid may interfere with iron absorption. To minimize this problem, take antacids on an empty stomach and at a different time than iron.
Constipation is another common problem in pregnancy. The causes can be many —
decreased peristalsis of the GI tract, inadequate intake of fiber and fluids, stress, medications and calcium and iron supplementation. To help with this problem you may
recommend increasing dietary fiber and fluid, increasing exercise or taking a commercially available laxative, such as Metamucil®. See Appendix #11.
LEG CRAMPS
Leg cramps, affecting 15 to 30 percent of all pregnant women, are most common
during the second half of pregnancy and usually occur at night. Causation is unknown,
but an imbalance of calcium, phosphorus and magnesium, with elevated serum phosphorus levels and decreased serum calcium and magnesium, is suspected.
Inadequate calcium and magnesium intake, and excessive phosphorus intake, may
be the cause. Limiting foods high in phosphorus — animal foods, dairy products, carbonated beverages and phosphate-containing supplements — should help balance
dietary calcium and phosphorus. Conversely, eating magnesium-rich foods — legumes,
dark green leafy vegetables and whole grain products — will elevate serum magnesium.
Several studies have shown that supplementing pregnant women affected by leg
cramps with non-phosphate-containing calcium salts increases total serum calcium
levels and improves leg cramps. This clinical correlation is far from perfect since other
controlled and double-blind studies have failed to indicate a correlation between leg
cramps and either intake of dairy products or type of calcium supplement used.
The most effective treatment for leg cramps is to discourage women from pointing
their toes during sleep or stretching. Gentle flexing of the feet will provide relief for
many women. If dietary intake of calcium is <600 mg, a supplement is recommended
for general dietary adequacy. However, the supplement may not provide relief from the
leg cramps. A list of solutions for leg cramps can be found in Appendix #11.
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NON-NUTRITIVE SWEETENERS
The FDA has approved five non-nutritive sweeteners as food additives: saccharin,
aspartame, acesulfame-K (potassium), sucralose and neotame. The position paper
Position of the American Dietetic Association: Use of Nutritive and Nonnutritive Sweetners
(JADA, 2004) is an excellent review of the topic and the individual nonnutritive
sweetners. In regard to pregnancy, the authors conclude:
In summary, the studies on the effects of nonnutritive sweeteners on reproductive abilities in females and males, as well as on the developing fetus
have been reviewed and these sweeteners deemed safe by numerous regulatory bodies and expert communities around the world. Thus, the consumption of acesulfame potassium, aspartame, saccharin, sucralose and
neotame within acceptable daily intakes is safe during pregnancy.
• Saccharin (Sweet 'N Low® or Sugar Twin®) crosses the placenta and is distributed to fetal tissues, so there has been concern about its safety. However, the National
Toxicology Program of the National Institutes of Health and the California Environmental Protection Agency recommended that saccharin no longer be classified as a carcinogen (JADA, 2004). The amount of saccharin can not exceed: 12 mg/fluid ounce in a
beverage, 20 mg in packaged amounts and 30 mg/serving in processed foods (JADA,
2004).
• Aspartame, (Nutra-sweet,® Equal®) is made from two amino acids, aspartic acid
and phenylalanine. Some infants have a metabolic defect, phenylketonuria (PKU),
preventing them from metabolizing phenylalanine. Concern exists whether a fetus
with PKU can be harmed by the mother ingesting too much aspartame. In studies
looking at fetal transfer of the metabolites of aspartame, it was found that if placental
transfer did occur, it was not clinically significant (JADA, 2004). The FDA has established an Acceptable Daily Intake (ADI) of 50 mg/kg body weight/day (JADA, 2004).
According to a review of all the available data on aspartame, Magnuson and
colleagues (2007) concluded that aspartame is safe at the current levels of consumption, which averages 4.9 mg/kg body weight/day, with high users consuming 13.3
mg/kg body weight/day, nowhere near the ADI.
• Acesulfame-K, known as Sunett® or Sweet One® is 200 times sweeter than
sucrose, can withstand high cooking/baking temperatures, does not provide any energy
and is not metabolized by the body. Little acesulfame-K is used in foods due to its
intense sweetness; it is often used in combination with other sweeteners. The ADI
established by the FDA is 15 mg/kg body weight per day (JADA, 2004).
• Sucralose, known as Splenda®, is 600 times sweeter than sucrose, provides no
energy, is not well absorbed by the body and is stable when exposed to high heat.
Sucralose has been deemed safe in humans after the FDA reviewed 110 studies in humans
and animals (JADA, 2004). The ADI is 5 mg/kg body weight per day (JADA, 2004).
• Neotame is another approved nonnutritive sweetener, 13,000 times sweeter than
sucrose. At high doses, there is no apparent effect on pregnant women and their fetus.
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The FDA has established an ADI of 2 mg/kg body weight per day (JADA, 2004).
• Stevia, the newest nonnutritive sweetener approved for use in the US, is derived
from the leaves of a South American herb (Stevia rebaudiana). It has taken a long time for
FDA approval. In 1991, FDA banned stevia as an “unsafe food additive.” When the 1994
Diet Supplement, Health and Education Act was passed, the FDA had no choice but
allow stevia be sold as a supplement, since it was from an herb. Use was limited, as
most of the available products had a bitter taste.
In 2008, the FDA approved two stevia sweetners, Truvia® and SweetLeaf.® Only 95
percent pure steviol glycosides (sweet extracts from the stevia plant) are approved for
use in food and beverages and these do not have the bitter taste. Truvia will be used in
drinks manufactured by Coca-cola. SweetLeaf is from Wisdom Natural Brands of
Phoenix, AZ. You can also find stevia in health food stores. The ADI of stevia is 2 mg/kg
body weight/day (Damarck, 2009).
Research done on animals has proven stevia safe. However there is very little
research on pregnant women. Since the FDA approval of stevia products is relatively
new, it will be interesting to see what information will become available about its effect
on pregnant women and if the recommendations for use in pregnancy will change.
While nonnutritive sweetners are safe, moderation of sugar substitutes is suggested for any pregnant woman. Beverages containing nonnutritive sweeteners should
not replace beverages with important nutrients.
CAFFEINE
Caffeine is a central nervous system stimulant. It can cause insomnia, nervousness,
irritability, anxiety and disturbances in heart rate and rhythm. Caffeine also acts on the
kidney to produce diuresis. Caffeine does cross the placenta, and so has the potential to
affect the fetus, which cannot metabolize caffeine effectively. In pregnant women, the
liver is slower to detoxify caffeine, so it stays in the blood longer, increasing the potential of placental transfer to the fetus.
Unfortunately, the studies published to date conflict with one another. Two 1993
JAMA studies also came to contradictory conclusions on the effects of caffeine on outcome of pregnancy. Some studies have found decreased birth weights, increased number of LBW babies and increased spontaneous abortions. One showed that high levels
(over 600 mg/day) can cause spontaneous abortion and premature births, but other
variables such as smoking were not taken into account.
Other studies add to the debate. Fenster, et al., (1998) linked increased risk of
spontaneous abortion with caffeine intake, while Klebanoff, et al., (1999) found that only
extremely high levels of caffeine increase the risk for spontaneous abortions. Signorello
and McLaughlin (2004), in a review of the literature, concluded the evidence was equivocal
that caffeine intake increased spontaneous abortions.
Another study, based on hundreds of telephone interviews, found no association
between caffeine intake and preterm delivery (Pastore and Savitz, 1995). Caffeine intake
was estimated from coffee, tea, colas, and non-cola caffeinated soft drinks. In a review of
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the literature to date, Golding (1995) found no association between caffeine consumption
and congenital malformations or preterm delivery. Two studies published in 2006 found
no relationship between caffeine intake and congenital anomalies (Browne, 2006) and
the risk of preterm delivery (Chiaffarino, et al, 2006).
Hinds and colleagues (1996) had similar conclusions to Golding when reviewing
the effects of caffeine on pregnancy outcome variables. She concluded that:
...heavy caffeine use, >300 mg/day, is associated with small reductions in
infant birth weight. However, overwhelming evidence indicated that caffeine is not a human teratogen and that caffeine appears to have no effect
on preterm labor and delivery.
The CARE Study Group (2008) did find that caffeine consumption throughout pregnancy was associated with decreased birth weight. This was true when caffeine consumption was greater than 300 mg/day compared with less than 100 mg/day.
Giannelli, et al., (2003) found that a caffeine intake above 300 mg/day increased the risk
for miscarriage. Wisborg (2003) concluded that “Drinking coffee during pregnancy is
associated with an increased risk of stillbirth but not with sudden infant death.”
Women consuming 0 to 3 cups of coffee per day did not have more stillbirths.
Pregnant women consuming 4 to 7 cups per day had an 80 percent increase, and women
consuming more than 8 cups per day had a 300 percent increase in stillbirths.
Weng (2008) found that women who consumed 200 mg or more per day of caffeine
had twice the chance of having a miscarriage as women who did not consume any
caffeine. However, Savitz and colleagues (2008) did not find any increase in miscarriages, in women who drank between 200 and 350 mg of caffeine a day.
The best recommendation at present is to reduce caffeine intake to the equivalent
found in two cups of coffee, approximately 150 to 300 mg of caffeine. The March of Dimes
recommends no more than 200 mg of caffeine, the amount found in 12 oz of coffee.
The chart on the following page lists the caffeine content of selected beverages and
drugs. Note serving sizes: A 16 oz cup of coffee is actually 2 cups, not 1. Many energy drinks
that contain caffeine are 12 oz or more, not 8 oz.
Changing habits is not easy. If a woman needs one vice, caffeine intake appears the
least likely to do harm, certainly less than drinking alcohol or smoking cigarettes. It may
be easier on the mother to have a cup of coffee a day, than to worry about it or give it up.
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Caffeine Content of Selected Items
Item
Coffee (5 oz cup)
Brewed, drip
Brewed, percolator
Instant
Decaffeinated
Starbucks, tall
Cappuccino, short
Tea (8 oz cup)
Regular bag
Regular loose
Instant
Iced
Tea, bottled
Chocolate
Milk chocolate
Dark chocolate
mg/serving
60-180 cup
40-170/cup
30-120/cup
3/cup
375/12 oz
35/8 oz
46/cup
40/cup
30/cup
70/cup
15/12 oz
1-15/oz
5-35/oz
Item
Beverages
Coca Cola
Pepsi
Diet Rite
Dr. Pepper
Mountain Dew
Tab
Chocolate milk
Hot chocolate/cocoa
Drugs
Aspirin
Excedrin, Anacin
No-Doz
Vivarin
Cafergot
Darvon
mg/serving
65/12 oz
62/12 oz
33/12 oz
61/12 oz
55/12 oz
45/12 oz
2-7/8 oz
6-42/cup
32/pill
60/pill
100/pill
200/pill
100/pill
32/pill
BARIATRIC SURGERY
The number of women having bariatric surgery is increasing dramatically — 13,365
in 1998 to approximately 72,177 in 2002 (IOM, 2009). Therefore the number of women
becoming pregnant who have had this type of surgery is increasing.
Pregnancy after bariatric surgery appears safe, with no significant differences in the
complications between women who have had gastric bypass surgery and those who
have not (WHRNP, 2004). In a study of 298 women who gave birth after bariatric surgery,
the authors found an increase in Cesarean delivery (Sheiner, et al., 2004). A newer study
suggests that the health risks of pregnancy are decreased in women who have had
bariatric surgery, compared to women who are obese (Roye, et al., 2008). This study did
not find any increased risk to fetal outcome.
Guelinckx, et al., (2009) did find improved fertility and reduced risk of gestational
diabetes, hypertensive disorders of pregnancy and macrosomia in pregnant women after
surgery compared to morbidly obese pregnant women. However, there was an increase
in intrauterine growth restriction and the potential for nutritional deficiencies that could
affect both mother and infant.
Women who have had an adjustable gastric banding procedure are at risk of unexpectedly becoming pregnant after weight loss following surgery.
To achieve a successful pregnancy after bariatric surgery, there are nutritional issues
that must be addressed, such as type of procedure, length of time since surgery, previous
pregnancies and any complications or adverse outcomes, age and any comorbid conditions.
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Vertical-banded gastroplasty (VBG) and other gastric restriction surgeries known
as “restrictive surgeries” were approved by the FDA for use in the US in 2001. The goal
of restrictive surgeries is to reduce the size of the stomach and to slow gastric emptying.
The effect is to physically limit the volume and rate of food intake by reducing the
stomach to a small pouch, usually 30 ml in size but sometimes as small as 15 mL.
The Roux-en-Y gastric bypass surgery (RYGB), which is more popular, reduces the
size of the stomach and bypasses the duodenum and proximal jejunum by attaching the
jejunum directly to the small pouch created in the stomach. The effect is to physically
limit the volume and rate of food intake, as well as to limit the absorptive capacity of
the small intestine.
These changes in anatomy substantially impact food and nutrient intake. RYGB is
known as a malabsorptive/restrictive procedure. The restriction is a result of a very
small stomach pouch (less than 20 mL). The degree of malabsorption depends on the
length of the intestine that is bypassed. At a minimum, the duodenum and upper
jejunum are circumvented.
The period of rapid weight loss following bariatric surgery — up to six months after
surgery — is the worst time for a woman to become pregnant and is the most challenging nutritionally. Once weight loss has slowed and intake has stabilized —usually 12 to
16 months post-surgery — it is much safer to become pregnant.
If you are assessing or counseling a pregnant woman after bariatric surgery, you
must determine the following:
• Adequacy of the diet. Is the woman getting adequate calories, protein, fluid,
vitamins and minerals? With the reduced stomach size, she may need to eat six
to eight times per day. It is essential she eat protein foods with high biological
value protein, since the volume of food she can eat is decreased.
• Adequate weight gain. Is the woman gaining appropriately? This can be tricky,
as she may still be losing weight, but eating sufficiently for herself and her baby.
Close supervision of weight gain or loss compared to her intake is essential.
• Malabsorption of vitamins and minerals. If the woman had a RYGB, she will
most likely malabsorb iron, vitamin B12, vitamin D, calcium and folate (IOM,
2009). It is essential to evaluate her nutritional status with lab work to see if she
is deficient and needs additional supplements. A routine vitamin and mineral
supplement is essential as well.
The bottom line is that women who have had bariatric surgery can deliver normal,
healthy babies, without complications, but they must pay close attention to their diet,
under the supervision of a dietitian or other health professional.
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FOOD SAFETY
Pregnant women are considered to be at increased risk for food-borne disease.
During pregnancy, plasma levels of immunosuppressive hormones increase — particularly during the third trimester — to enable the maternal immune system to coexist with
the fetus. This can put both the mother and fetus at risk. Organisms that pregnant
women are most susceptible to are listed in the chart below. Tips for keeping food safe
are found on the following page.
Some of the organisms, Listeria in particular, can be deadly to the mother and fetus.
Listeria has also been found in deli meats and hot dogs, so these should be well heated
before eating. Other organisms such as Campylobacter, Staphylococcus, and Salmonella
cause severe gastrointestinal problems, including dehydration and blood volume
depletion, which are dangerous to the fetus. Toxoplasma, a parasite, can be found in
under cooked meat and unwashed fruits and vegetables.
Taking proper precautions with food purchasing, handling, preparation and storage can help prevent food-borne illness. The chart on the following page offers suggestions. Additionally, wash all fruits and vegetables under running water, avoid cleaning
cat litter boxes (if you have to, wear gloves), and if gardening, wear gloves. Information
is also available at: <www.womenshealth.gov.> and
<www.mypyramid.govmypyramid/moms/food_safety.html>
Food-borne Bacteria
BACTERIA
Salmonella
(>2,000 types)
Campylobacter jejuni
Yersinia enterocolitica
Listeria monocytogenes
Vibrio sp.
Staphylococcus aureus
Clostridium perfringens
Clostridium botulinum
Escherichia coli 0157:H7
FOOD SOURCE
Mostly foods of animal origin: meat, poultry, dairy, raw milk,
eggs
Raw milk, meats, clams, eggs
Chocolate milk, tofu, ice cream
Soft cheese, coleslaw, celery, raw milk, lettuce, seafood, deli meats
Raw seafood
Meat & dairy products, fish, poultry, cream sauces & salads,
puddings, custards, cream-filled bakery items
Meat & poultry products
Canned food, luncheon meats, lobster, smoked fish, ham
Raw or rare ground beef, unpasteurized milk
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Keeping Food Safe
Shopping
Cold
Storage
Thawing
Food
Preparation
Serving Food
& Handling
Leftovers
Listeria
• Don't buy cans or jars with dents, cracks or bulging lids.
• Don't buy broken boxes or packages.
• Don't buy raw cheese or milk and unpasteurized juice ;do not use
raw eggs or products with raw eggs and do not use raw sprouts.
• Keep perishable food cold.
• Refrigerate perishable food as soon as you get it home.
• Store canned goods in cool, dry place for use within 1 year. Never
put above stove, under sink or in a garage or damp basement.
• Don't thaw on counter. Bacteria grow quickly at room temperature.
• Thaw food in refrigerator the night before or in microwave just
before cooking.
• Keep work area clean and cook thoroughly.
• Wash hands, utensils and cutting boards in hot soapy water before
preparing food and after handling raw meat or poultry.
• Cook meat to at least 160° F. (Poultry juices run clear; fish flakes
with fork).
• Cook ground beef to well-done (brown). Do not serve pink ground beef.
Use a thermometer to check the temperature of ground beef.
• Never leave food at room temperature over 2 hours.
• Promptly refrigerate food after meals; don't let it sit out. Divide
food into small containers for quick cooling in refrigerator.
• Remove stuffing from poultry. Refrigerate separately.
• For buffets, keep cold food on ice or use small serving dishes and
replenish from the refrigerator.
• For hot foods, use a heating dish or reheat small servings from
refrigerator and replenish buffet.
• Can grow at refrigeration temperatures of 40°F or below.
• Use all perishable precooked or ready-to-eat items as soon as possible.
• Clean the refrigerator regularly.
• Use a refrigerator thermometer to keep temperature 40°F or below.
• Do not eat hot dogs, luncheon meats, deli meats unless reheated until
steaming hot. Do not eat semi-soft cheeses, patés, meat spreads, raw
milk or refrigerated smoked seafood (unless the seafood is cooked).
USDA; Food Safety Inspection Service: www.fsis.usda.gov/index.htm
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HERBS
Herbal teas and other herbal remedies have been part of folk medicine for centuries.
Some people turn to herbal teas to reduce their caffeine intake. Many herbal teas may be
safe but some have been demonstrated to have potentially harmful side effects such as
diarrhea, vomiting, depressed breathing and even miscarriage. Potentially dangerous
herbs include lobelia, sassafras, coltsfoot, comfrey, and pennyroyal (Tyler, 1993).
To be safe, pregnant women should choose only herbal teas containing ingredients
ordinarily found in their diets (orange rind and cinnamon would be better choices, for
example, than chamomile or hibiscus). Encourage them to buy name brand products
that are packaged in filter tea bags; these companies have histories of quality control. To
avoid displacing more nutritious beverages, herbal tea consumption should be limited
to two 8 oz servings per day (Lesan, 1990).
A note of caution about the use of herbal products during pregnancy: Many
women feel that herbs are natural products and therefore safe during pregnancy while
drugs are not. This is not the case. Herbs affect the physiology of the body and may not
be safe for pregnant women. Also, since herbs are regulated as dietary supplements,
therefore they are not tested for safety or efficacy.
Foote and Rengers (2000) review the safety of herbs during pregnancy and clearly
show problems with their use. Pennyroyal is an abortive agent and comfrey contains a
hepatotoxic substance. Both of these herbs have been proven unsafe for pregnancy.
The American Herbal Products Association (AHPA) has a Botanical Safety Handbook,
which offers safety criteria classifications, including "not to be used during pregnancy."
Included are herbs such as black cohosh, chasteberry, dong quai, ephedra, feverfew,
goldenseal and kava-kava. Appendix #15 lists herbs considered not appropriate for use
during pregnancy, and provides other resources for information on herbs.
The National Institutes of Health, has a National Center for Complementary and
Alternative Medicine and is a great resource on herbs. The url is: nccam.nih.gov.
Unless proven safe, herbs should not be used during pregnancy. For a complete
discussion of herbs, see the Nutrition Dimension course Herbal Supplements.
ADOLESCENT PREGNANCY
Pregnant adolescents have had a higher incidence of infant mortality and low birth
weight babies than older pregnant women. A combination of increased nutrient needs
and lifestyle factors affecting nutrient intake accounts for an increase in poor pregnancy
outcome. The mother's age, in itself, is not a determining factor.
Adolescents who conceive soon after menarche may still be growing, but they have
babies similar in weight to those borne by adults (IOM, 2009). If a pregnant adolescent
has a second pregnancy, the baby weighs less (IOM, 2009). It appears that the fat being
mobilized in the pregnant teen goes to her growth, not her baby (IOM, 2009).
What earlier weight gain guidelines for adolescents failed to take into account was
that many pregnant teens gain more weight compared to older pregnant adults (Howie,
et al., 2003). The concern is that the increased weight gain, like adults, does lower the
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incidence of LBW, but can also lead to an increase in macrosomic babies, postpartum
weight retention, and obesity later in life.
This concern was born out by Nielsen, et al., (2006) who showed that when 815
African American adolescents increased their GWG from below to within the 1990 IOM
guidelines, outcomes were improved. Any additional weight gain was not beneficial,
especially if the adolescent was overweight or obese prior to pregnancy. The 2009 IOM
report does not recommend a modification of gestational weight gain guidelines for
females below 20 years of age, but states:
Adolescents who follow adult BMI cutoff points will likely be categorized
in a lighter group and thus advised to gain more; however, younger adolescents often need to gain more to improve birth outcomes.
Weight gain should be monitored closely. The nutrients most often lacking in their
diets are calcium, iron, zinc, vitamins A, D, B6, riboflavin, folic acid and total energy.
Many of these deficiencies are a result of poor eating habits.
The most challenging aspect of managing pregnant teens is lifestyle. Factors that
can interfere with adequate nutrient intake include substance abuse, erratic eating
habits, fad diets, peer pressure, income, access to food, living situation, etc. The chart
below summarizes nutrition-related risk factors for adolescents.
Working with pregnant teens often means becoming a combination of psychologist, mother-surrogate and best pal, not an absolute authority. Many teens will change
their eating habits when shown the importance to the fetus, but iron and calories may
remain inadequate. Dietary changes must be done within the context of their everyday
lives and fit with their lifestyles. Pregnant adolescents, like other adolescents, tend to
eat what is available and convenient. The nutritious foods they need are not always
easily available to them at places and times when they do eat. It is also important to
realize that pregnant adolescents often lack a stable and continuous food supply.
Nutrition Risk Factors for Adolescents
• Low prepregnancy weight for height
• Indications of malnutrition
• Inadequate pregnancy weight gain
• Excessive prepregnancy weight (indication of poor eating habits)
• Anemia
• Unhealthy lifestyle
» substance abuse
» eating disorders
» poor dietary habits
» smoking
• Pica, food intolerances, allergies, fad diets, increased snacking
• Decreased food preparation skills and limited access to food prep facilities
• Unfavorable reproductive history
• Chronic diseases
• Socioeconomic factors affecting intake; no stable access to food; peer pressure
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Prenatal Supplements
High-risk Women
• Adolescent
• Heavy cigarette smoking
• Alcohol or substance abuse
• Inadequate dietary folic acid
• Iron deficiency anemia
• Vegetarian, especially vegans
• Bariatric surgery
• Poor quality diet
• Under 25 and not consuming
adequate calcium
• Lactose-intolerant
• Multiple fetuses
Nutrient
Vitamin B6
Vitamin C
Vitamin D*
Vitamin E
Folic acid
Amount
2 mg
50 mg
200 IU
15 IU
400 mcg
Guidelines for Use
• Contain nutrients in amounts shown
below
• Begin in the second trimester
• Free of artificial colorings
• Take between meals or at bedtime
• Vegans (complete vegetarians) may
need 400 IU vitamin D &
2 mcg B12
• Bariatric surgery may increase need
for supplements, based on lab tests
Nutrient
Iron (ferrous)
Zinc
Copper
Calcium
Magnesium
Amount
30 mg
15 mg
2 mg
250 mg
100-320 mg
*Women living above the 35º lattitude — Boston, San Franscisco, Chicago — will need up
to 800-1,000 IU additional Vitamin D.
SUPPLEMENTATION
Most pregnant women are prescribed vitamin supplements by their doctor. Not all
prenatal vitamins are alike; levels of nutrients vary. The most important nutrients to be
supplemented are iron, folic acid, vitamin B6, vitamin D (cholecalciferol), vitamin E,
pantothenic acid, calcium, magnesium, zinc, copper, and possibly selenium.
Not all physicians recommend vitamin and mineral supplements. If the diet is
adequate, only folic acid, iron and vitamin D are recommended. However, women in a
high-risk group, listed in the chart above, may be recommended supplements along
with the recommendations for a prenatal supplement. All other nutrients should be
included at or near 100 percent of the RDA for pregnant women.
The importance of supplementing in low-income women was shown by Scholl et
al., (1997). The risk for preterm and very preterm deliveries was reduced two- to fourfold when low-income urban women took a vitamin and mineral supplement in the first
and second trimester. The risk for LBW and very LBW births was reduced six- and
seven-fold when these women supplemented the first and second trimester. The authors
conclude that supplementation in this group has the potential to decrease morbidity
and mortality in infants.
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Hasan, et al., (2009) found that the use of any vitamin supplement early in pregnancy was associated with a decreased risk of miscarriage, but note that this may also
be due to healthier behaviors in the women who supplement.
Problems can arise from improper supplementation. Minerals interact with one
another, decreasing absorption and/or serum levels. Zinc, copper, iron, calcium, and
magnesium all are known to interact; there are other possible interactions, not yet
proven, such as zinc with folate, and vitamin E with iron.
If several nutrients must be supplemented, the safest course is to recommend a
multivitamin and mineral, with additional calcium and iron if necessary. (How to
supplement has been covered in previous chapters.) Megadoses should be avoided
during pregnancy, particularly vitamin A, as it can harm the fetus.
Accutane®, a drug used to treat acne, is a vitamin A retinoid analog. Use of this drug
during pregnancy can cause severe birth defects. Similarly, megadoses of preformed
vitamin A (which is fat-soluble and stored in the body) should be avoided entirely.
Supplementing with many nutrients increases the chances of interactions. It is
preferable to space supplements out throughout the day. Unfortunately, since many
women have trouble remembering to take supplements, the risk of accidental overdosing increases. One multi-vitamin supplement is better than many individual supplements. There is a tip sheet on supplements during pregnancy at <Mypyramid.gov>
Other nutritional supplements, such as protein powder, instant breakfasts or other
food supplements, may be necessary for an undernourished woman. If biochemical,
anthropometric and clinical data indicate poor nutritional status or malnutrition, start
some form of nutritional therapy right away. If in doubt, start. Treating with food
supplements cannot do much harm; the potential benefit far outweighs any risk.
PICA
Pica is a pathological craving for foods or non-food substances. Despite research,
the etiology of pica remains a mystery. Numerous theories have been proposed that
include nutritional, psychological, cultural, pharmacological and disease as the cause.
In some cultures it is expected that pregnant women eat various substances. Clay, corn
starch, laundry starch, ice, dirt and baking soda are the most common non-food substances eaten by women in the US.
In an interesting observational report of 300 postpartum women in a hospital
serving low-income women, Cooksey (1995) found that 194 of them (65 percent) ate one
or more pica substances during pregnancy. Of those with pica, 152 ate ice or freezer
frost by itself or along with other substances. Substances eaten included dirt, clay,
cigarette ashes, ice, freezer frost, flour, baking powder, cornstarch and powdered milk.
One woman ate three to four 8 lb bags of crushed ice daily; another ate 5 quarts of
freezer frost while another ate two cans of baking powder daily.
In addition to pica, Cooksey found 40 of 280 women (14 percent) having olfactory
cravings — cravings to smell specific substances. Substances women craved included
gasoline, bleach, ammonia, aerosol air freshener, aerosol disinfectant, pine oil cleaning
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solution, rubbing alcohol, nail polish remover, powder cleanser, chalk, body powder,
concrete chips and powder detergent. These olfactory cravings occurred separate from
or in conjunction with pica. Cooksey speculated that a change in a pregnant woman's
sense of smell might account for some of the olfactory cravings.
Estimates of the incidence of pica vary from 10 percent to 68 percent; the number
practicing pica has apparently been constant since the 1970s, according to Horner, et al.,
(1991). The women with the highest incidence are African Americans who live in rural
areas and have a family history of pica. In a rural, socioeconomically disadvantaged
area, Corbett (2003) found that 38 percent of the pregnant women in two rural clinics
practiced pica. The incidence was highest in African American women. The material
consumed was similar to that found in other studies: dirt, clay and starch.
Magnesium carbonate ingestion was reported as well. This practice seems to be
either unique to this population or not reported elsewhere. Magnesium carbonate is sold
in a block, about the size of a 35-mm film box. It can be bought on either side of the USMexico border, where it is sold in pharmacies to be used for heartburn or as a laxative.
Pregnant women consuming a number of “bricks” a day ingest too much magnesium,
which potentially could be harmful. No studies have been done to look at this issue.
Pica can interfere with nutritional status by decreasing the amount of nutritious
foods eaten and by reducing the bioavailability of minerals, especially iron, zinc, magnesium and potassium (Danford, 1982). The most common side effects of pica include
anemia and toxemia, with zinc deficiency seen in dirt and clay eaters. It may be that
eating specific foods or other substances causes the deficiency or that an iron or other
deficiency causes the pica (Danford, 1982).
Hemoglobin levels have been found to be lower in women with pica than those
without, but birth weight does not seem to be affected (Rainville, 1998). Other complications may be due to the substance eaten, and include hypertension, bezoars, intestinal
perforations, maternal bowel obstruction, achlorhydria, dental injury, constipation and
hemolytic anemia.
Clay, laundry starch or cornstarch bind iron and other minerals, making them
unavailable for absorption. If enough non-food substances replace calories, nutrient
intake will decrease. Ice and freezer frost, also commonly ingested, can cause a decrease
in total food intake, leading to inadequate weight gain in extreme cases. Some substances can be toxic and teratogenic to the fetus.
Culture and tradition seem to play a big part in pica. Old wives’ tales extol the
benefits to the baby of eating clay daily. I've heard women tell stories of family members
insisting that they eat clay, even keeping it in the refrigerator for them, and how women
from the rural South who have relocated to another part of the country have clay sent to
them from home. When women move away from the culture or society that accepts pica
as a normal part of pregnancy, the food behavior usually disappears, indicating that it
is, indeed, a social phenomenon rather than a dietary or physiological condition.
If a woman had pica, and anemia results, treat the anemia, then counsel her to try
to decrease the non-food consumption. It is only necessary to stop the behavior if the
item consumed is dangerous, like sink cleaner, or if it interferes with adequate caloric
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intake and weight gain. Decreasing the behavior is more achievable. For some women it
is easier to substitute an acceptable food for the non-food item. For others, chewing
gum or another non-food activity works.
Screening all pregnant women for pica is important to determine those women
who can do potential harm to themselves and the unborn baby. Many women may want
to be asked but will not bring it up themselves, thinking it is “crazy.” Ask
nonjudgmental questions like, “Many women eat things like clay, starch, or baking soda
when they are pregnant. Do you?” If the answer is yes, explore how much they eat and
then screen for nutritional deficiencies.
VEGETARIAN DIETS
Well-planned vegan and lacto-ovo-vegetarian diet can meet nutritional needs
during pregnancy (JADA, 2003). Nutritional care of pregnant women who are lacto-ovovegetarian differs little from that of nonvegetarians. A vegan diet requires more careful
planning to include a variety of foods. Pregnant vegans who eat a limited variety of
foods place themselves at nutritional risk and jeopardize their baby's future health.
Lacto-ovo-vegetarians should give special attention to intakes of iron, folic acid,
vitamin D and zinc during pregnancy (JADA, 2003). In addition, pregnant vegetarians
should include fish for the Ω-3 DHA. If they do not, then they need to include good
sources of alpha-linolenic acid, such as flax seed, canola oil, soybean oil or walnuts.
Dietary planning for vegans should emphasize consuming adequate calories and
foods rich in the problem nutrients — iron, folic acid, vitamin D, calcium, zinc, vitamin
B12 and protein. The diet of pregnant vegans should be supplemented with a reliable
source of vitamin B12 and also vitamin D if exposure to the sun is limited. Supplements
of folic acid are also advised as well as a multi-vitamin and mineral supplement.
Although certain vegetarian diets can be healthy, the food choices of some vegetarians may not be so healthy. Vegetarian diets that are haphazard or monotonous will not
provide proper nutrition.
In a recent companion paper to the ADA position statement on vegetarian diets
(2003), Messina and colleagues present a Vegetarian Food Guide Pyramid that can easily be
used by vegans and lacto-ovo-vegetarians. The pyramid emphasizes calcium-rich
choices in each food group. Food groups used in the guide are grains; legumes, nuts
and other protein-rich foods; vegetables; fruits; and fats. Appendix #16 shows the
Vegetarian Food Guide Pyramid along with modifications for pregnancy.
EXERCISE
Exercising alleviates many discomforts of pregnancy: backaches, fatigue, indigestion,
swelling, leg cramps and hemorrhoids; may help sleep better, improve posture and help
prevent or treat gestational diabetes. Exercising also prepares the muscles used in giving
birth. The benefits of regular exercise of moderate to somewhat hard levels of intensity
include: reduced fat deposition and retention, shorter and less complicated labors, higher
energy levels during and after pregnancy and quicker postpartum recovery.
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The medical community is moving from a somewhat restrictive attitude concerning exercise during pregnancy to one that is much more liberal. In 2002, the American
College of Obstetricians and Gynecologists (ACOG) published exercise guidelines for
pregnancy, which state that if not contraindicated, exercise during pregnancy, in a wide
range of recreational activities, appears to be safe, such as walking, swimming, bicycling
and aerobics (low-impact and water are preferred). Strength training is recommended
as it may help prevent some of the aches and pains common in pregnancy and make
your muscles stronger.
The absolutely contraindicated activities during pregnancy include scuba diving
and water-skiing; other activities that should be avoided include downhill skiing, highaltitude sports, hockey, gymnastics and horseback riding (Hyatt, et al., 2003).
Information on pregnancy and exercise is available on the ACOG website:
<www.acog.org/publications/patient_education/bp119.cfm>
There is a synergy between nutrition and exercising. The body seems to utilize
nutrients better when a woman exercises. The emotional and psychological sense of
well-being is an added benefit. A woman who feels better during her pregnancy is more
likely to take better care of herself. The chart below summarizes exercise during pregnancy (Dewey and McCrory, 1994; Hyatt, et al., 2003; USDA 2005).
Exercise During Pregnancy
• Incorporate 30 minutes or more of moderate-intensity physical activity on
most, if not all, days of the week.
• Engage in activities that you enjoy, are safe, are not compromised by a
change in balance and center of gravity and can be modified as the pregnancy progresses. These can be either weightbearing or non-weightbearing.
• Avoid activities with a high risk of falling or abdominal trauma.
• The frequency and duration of the exercise should be tailored to your needs
and your level of fitness.
• Increase frequency and intensity very gradually if inactive prior to pregnancy.
• Avoid exercising in the supine position after the first trimester.
• Avoid exercising in hot, humid environments.
• Maintain maternal core temperature below 38° C.
• Drink liquids before , during and after exercise to ensure adequate hydration.
• Avoid exercising when fatigued and take frequent rest periods to minimize
potential fetal stress.
• Warm up for 5 - 10 minutes with light exercise and stretch your muscles. At
the end of your exercise, cool down for 5-10 minutes, including stretching.
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Physical changes to the body during pregnancy need to be taken into consideration
when designing an exercise program. The increases in hormones cause a slackening of
abdominal muscles and relaxation of joints. Undue stress on these areas of the body
should be avoided.
The positive aspect of exercising is that common problems can be alleviated. In pregnancy, the increase in the size and weight of the uterus pulls the spine into an exaggerated
curve. Muscles in the lower back then tense, causing backache. The neck gets tense from
slumped shoulders. Improper weight distribution causes leg and foot exhaustion. Exercising, maintaining correct posture and strengthening selective muscles can decrease pregnancy discomfort. Numerous exercise courses for pregnant women are available.
By the end of pregnancy, maternal oxygen consumption is 16 to 32 percent above
nonpregnant norms. During exercise, cardiovascular adjustments are made that include
a reduction in uterine blood flow, concentration of hemoglobin and hematocrit and
increased oxygen extraction from blood. Even though less blood flows to the uterus, it
appears that oxygen consumption by the fetus remains constant. Thus, there is an
increase in the percentage of oxygen that is transported to the fetus.
Measurements of fetal response to exercise have found that it is not in distress —
exercising does not seem to harm it. There is one exception, however: an increase in
maternal body temperature can harm the fetus. This means that exercise should be
moderate, and saunas, hot tubs and steam baths should be avoided. Clothing that
“breathes” will help keep body temperature down.
Studies show lower birth weights of babies born to women who exercised before
pregnancy. The lower birth weight may by an indication that caloric intake is not adequate to meet the demands of both pregnancy and exercise. Therefore, a pregnant
woman who exercises regularly and fairly heavily, may need to increase calories above
the recommended additional 300 per day.
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Chapter Nine:
Medical Complications
Major medical complications of pregnancy include hypertensive disorders of
pregnancy and diabetes.
Hypertensive disorders are the most common medical complications of pregnancy
and include chronic hypertension, gestational hypertension, and preeclampsia.
Chronic hypertension is found in 1 to 5 percent of pregnant women. The diagnosis
is based a history of hypertension before pregnancy or an elevation in blood pressure to
at least 140/90 mm Hg before 20 weeks gestation (Sibai, et al., 1995). These women are
at increased risk for preeclampsia, abruptio placentae and morbidity and mortality of
the fetus. Treatment includes drugs to control blood pressure. While diuretics and
dietary salt restrictions are prescribed, their use is highly controversial as it can further
restrict plasma volume expansion.
Gestational hypertension (also known as pregnancy-induced hypertension or PIH)
is defined as an elevation in blood pressure after 20 weeks gestation in women who did
not have elevated blood pressure prior to pregnancy. In these women, the pregnancy
outcome is excellent without drugs. The increase in blood pressure may be an early sign
of preeclampsia, may indicate chronic hypertension or be a transient increase only
during pregnancy.
Preeclampsia is by far the most serious hypertensive disorder of pregnancy, with
the potential for serious complications and an estimated 7 to 8 percent of all pregnant
women suffer from it (JADA, 2002). Preeclampsia is defined as the development of
increased peripheral vascular resistance, reduced cardiac output, reduced plasma
volume, and decreased glomerular filtration rate with retention of salt and water
(Newman and Fullerton, 1990; Roberts, et al., 2003; Hawfield and Freedman, 2009). By
the 14th week of gestation there are changes in the vascular system, before the onset of
other clinical symptoms — hypertension, edema and proteinuria — which occur after
the 20th week gestation.
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In normal pregnancies, peripheral vascular resistance decreases as plasma volume
expands. In preeclampsia, plasma volume does not expand appropriately and peripheral vascular resistance does not decrease. The result is decreased cardiac output and
plasma volume, coupled with higher peripheral vascular resistance which reduces
perfusion of the placenta, kidneys, liver and brain. The circulation and exchange of
nutrients between the mother and fetus is impaired. The fetus can suffer intrauterine
growth retardation from a lack of oxygen and nutrients. If placental insufficiency is
severe enough, fetal hypoxia is possible.
Endothelial dysfunction (vasospasm, altered vascular permeability, altered fatty
acid composition) may explain the hyperlipemia, antioxidant deficiency, coagulation
defects, ischemia and infarctions of the uterus and placenta seen in preeclampsia (Sibai,
et al., 1995, Williams, et al., 1995; Mutter and Karumanchi, 2008).
The placenta plays an important role in the development of preeclampsia, especially the endothelial dysfunction. Certain anti-angiogenic soluble proteins produced by
the placenta are increased, interfering with the pro-angiogenic proteins responsible for
the growth of new or existing blood vessels and the proper functioning of the placenta
(Mutter and Karumanchi, 2008; Hawfield and Freedman, 2009).
What causes the increased production of these anti-angiogenic proteins is not
known. However, the increase in these proteins occurs before the clinical symptoms of
preeclampsia and could be used as a tool to identify the disease before the clinical
symptoms appear. Risk factors and complications are shown below.
Preeclampsia Risks and Complications
Risk Factors (General)
• Nulliparous under 20 or over 35
• Diabetes/insulin resistance
• Chronic hypertension
• Hyperhomocysteinemia
• Previous pregnancies
• Lower socioeconomic class
• Lack of education
• Poor nutrition
• Deficient prenatal care
• Emotional stress
• BMI (obesity)
• Vitamin D deficiency
• Darker skin
Complications — Maternal
• Convulsions
• Cerebral hemorrhage
• Abruptio placentae
• Pulmonary edema
• Renal failure
• Liver failure
• Death
Complications — Fetal
• Severe growth retardation
• Hypoxia
• Prematurity
• Death
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The risk of preeclampsia increases with increased BMI (O'Brien, et al., 2003). Specifically, for each 5 to 7 kg/m2 increase in BMI, the risk of preeclampsia doubled.
The cause of preeclampsia has been and still is hotly debated. Since the incidence
of the disorder is higher in malnourished women and in women with fewer financial and
educational resources, nutritional links to the disease have been investigated.
Proposed theories as to the cause of preeclampsia include:
• changes in the production and/or ratio of various prostaglandins that increase
vasoconstriction and decrease vasodilation;
• the relationship of dietary calcium and blood pressure;
• inadequate amounts of omega-3 fatty acids;
• increased oxidative stress with inadequate antioxidants (vitamins C and E,
selenium) (Zhang, et al., 2002; Chappell, et al., 2002; Scholl, et al., 2005);
• alterations in placental and endothelial growth factors and their receptors
(Polliotti, et al., 2003; Hawfield and Freedman, 2009 );
• inflammation;
• cytokine production; and
• elevated homocysteine (Roberts, et al., 2003)
More recently, a maternal deficiency of vitamin D is being investigated as an independent risk factor for preeclampsia (Bodnar, et al., 2007). To date, no certain cause has
been determined. However, the last 5 to 10 years has seen the focus of research turn to
oxidative stress as a primary factor in preeclampsia and the role of specific nutrients in
the prevention of preeclampsia.
CALCIUM, MAGNESIUM AND PREECLAMPSIA
Hypertension has traditionally been linked to excessive dietary sodium and treatment
was a low-sodium diet and diuretics. However, in pregnant women this worsens the condition. Research has shown that in some individuals, low serum calcium contributes to elevated blood pressure, and in pregnant women is linked to preeclampsia.
Guatemala, with rampant malnutrition, has low levels of preeclampsia. In theory, this
should not be the case, since malnutrition seems to increase the rate of preeclampsia. Upon
further investigation, we find that Guatemalan women are malnourished, with calorie,
protein and nutrient deprivation, but they have adequate levels of calcium. Tortillas, a staple
in their diet, are soaked in calcium-rich lime. Therefore, calcium is one of the few nutrients
in adequate supply in the diet of Guatemalans. The same is true in Ethiopia, where a grossly
inadequate diet nevertheless contains adequate calcium, and preeclampsia is low.
Belizian and Villar (1980) believe that dietary calcium prevents preeclampsia by maintaining serum calcium levels, which stabilizes blood pressure. Remember, 80 percent of all
calcium is required in the third trimester, when there tends to be an elevation in blood pressure.
It’s possible that sufficient calcium in the diet can prevent the rise in blood pressure.
Bucher, et al., (1996) looked at 14 published studies on the relationship of calcium
supplementation during pregnancy on blood pressure, preeclampsia and pregnancy out-
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come. He found that the data supported the conclusion that calcium supplementation
during pregnancy reduces systolic and diastolic blood pressure and preeclampsia.
Carroli and colleagues (1994) reviewed six clinical trials and found that calcium supplementation reduced the risk of all types of hypertension in pregnancy by 50 percent and
reduced the incidence of preeclampsia between 45 and 74 percent.
Other studies have looked at the relationship of calcium intake to preeclampsia and
suggest that increased calcium intake reduces the incidence of preeclampsia. Ito, et al., (1994)
found that 10.9 percent of women supplemented with calcium developed preeclampsia
versus 16.9 percent of those not given calcium. Purwar, et al., (1996) found a decrease in the
incidence of preeclampsia in women supplemented with 2 gm of elemental calcium a day.
In the placebo group 29.03 percent of the women developed preeclampsia versus 8.24
percent in the calcium-supplemented group. On the other hand, Sanchez-Ramos, et al.,
(1995) found no change in the incidence of preeclampsia in women supplemented with
2 gm of calcium per day.
A total of 13 clinical trials and four meta-analyses have investigated the relationship of calcium, blood pressure and preeclampsia and suggest that calcium supplementation reduces the incidence of preeclampsia. Many of these studies were conducted in
other countries on women with a much lower calcium intake than women in the US.
The designs of these studies varied, making it difficult to compare their results.
To clarify the relationship, a clinical intervention trial by the National Institute of
Health, Calcium for Preeclampsia Prevention (CPEP) was conducted at five university
US medical centers (Levine, et al., 1997) to determine if supplementing women with 2
gm of calcium a day reduced the incidence of preeclampsia. A total of 4,589 women
between 13 and 21 weeks gestation were randomly assigned to the control group or the
experimental group. The study concluded that calcium supplementation did not reduce
the incidence or severity of preeclampsia, nor did it reduce the incidence of gestational
hypertension. These results were true for women with the lowest mean daily calcium
intake of 422 mg/day, similar to women in developing countries.
It is important to put the results of this study in perspective. While calcium supplementation itself does not prevent preeclampsia, adequate calcium during pregnancy is still
essential for the developing fetus. In some pregnant women, increasing dietary calcium or
supplementing the diet may in fact reduce blood pressure during pregnancy (Roberts, 1997).
In a review of studies, Ritchie and King (2000) also concluded that at present there
is not enough evidence to recommend routine calcium supplements to reduce blood
pressure, but that certain populations may benefit, such as pregnant teens, women at
risk for PIH and women with inadequate calcium intake.
Hofmeyr, et al., (2006) reviewed 12 studies of calcium supplementation and hypertensive disorders of pregnancy, finding that calcium supplementation reduced the risk
of preeclampsia by almost one-half. The reduced risk was greatest for women at highest
risk of preeclampsia and with the lowest intake of calcium. These results contradict
earlier studies showing no effect of calcium supplementation, and opens the question of
whether supplementation replaces a deficient nutrient, or is a therapeutic treatment.
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Altered serum magnesium levels have also been implicated in the development of
preeclampsia, as many preeclamptic women have hypomagnesemia. Magnesium
activates numerous enzymes, including those involved in membrane transport and
integrity, muscle contraction, vasodilation and vasoconstriction, and blood coagulation.
Generally, magnesium inhibits smooth muscle contraction (heart, arteries and uterus),
promoting vasodilation.
Hypomagnesemia is associated with increased blood pressure and increased
peripheral vascular resistance. The ratio of prostacyclins (vasodilators) to thromboxanes
(vasoconstrictors) is profoundly altered in women with low serum magnesium. (See
below for a more complete discussion of prostaglandins and preeclampsia).
In the US, the average intake of magnesium is 250 mg/day. The DRI for pregnant
women is 350 to 400 mg/day (based on age). Too much dietary protein, calcium, phosphorus or vitamin D can increase the need for magnesium, as more magnesium is lost in
the urine. To prevent the possibility of hypomagnesemia contributing to preeclampsia,
make sure the diet contains a minimum of 320 mg of magnesium per day by including
whole grains, peanut butter, dark green vegetables and soy products.
PROSTAGLANDINS AND PREECLAMPSIA
Fatty acids are the precursors of prostaglandins, substances that regulate many
functions of the body, such as platelet production, stickiness of platelets and their ability
to clot, constriction and dilation of arteries and immune functions. The fatty acids we eat
become part of the membrane of each and every cell.
The development of preeclampsia may be a problem in the ratio of two prostaglandins — prostacyclin and thromboxane, as shown below. Prostacyclin I2 (PGI2) is a potent
vasodilator produced by the endothelial cells of the vascular bed (arteries, veins).
Beginning early in pregnancy, there is an increase in prostacyclin synthesis. Thromboxane A2 (TXA2), a potent vasoconstrictor produced by platelets from Ω-6 fatty acids, also
increases during pregnancy. There is a balance between these two prostaglandins that
prevents too much or too little vasoconstriction or vasodilation.
Prostaglandins & Preeclampsia
Prostacyclin I2
• Vasodilator
• Synthesis increases in normal
pregnancies
• Synthesis does not increase
normally in preeclamptic women
Thromboxane A2
• Vasoconstrictor
• Increases platelet production
• Increases blood clotting
• Synthesis increases in normal
pregnancies
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Pregnant women who develop preeclampsia have a much smaller increase in
prostacyclin production than other pregnant women, while the TXA2 production continues to increase (Fitzgerald, et al., 1987a, 1987b; Baker, et al., 1996; Walsh, 2004). The
decreased prostacyclin production can be measured as early as 11 weeks gestation,
preceding the clinical signs of preeclampsia.
The decreased PGI2 may indirectly cause the symptoms of preeclampsia, either by
altering the sensitivity of tissues to other vasoactive compounds or by altering the ratio
of PGI2 to TXA2 in favor of vasoconstriction. Increased vasoconstriction makes the heart
work harder pumping blood, thus increasing blood pressure.
Platelets from preeclamptic women have more unsaturated fatty acids incorporated into the cell membrane than normal pregnant women (Garzetti, et al., 1993). This
is significant since TXA2 is produced from unsaturated Ω-6 fatty acids. An abundance of
these fatty acids will cause an increased production of the vasoconstricting TXA2, which
may cause or exacerbate rises in blood pressure seen in preeclampsia.
In an attempt to find ways to alter the ratio of PGI2 to TXA2 that would increase
vasodilation, the use of low-dose aspirin was investigated. Wallenburg et al. (1986) and
Beaufils et al. (1985) were able to block the chronic formation of TXA2, preventing
preeclampsia, with relatively low doses of aspirin, which blocks the cyclooxygenase
enzyme necessary to convert fatty acids to TXA2.
Later studies have had mixed results. Hauth et al. (1993) and Sibai et al. (1993)
found a reduced occurrence of preeclampsia in women taking 60 mg of aspirin. A larger,
multi-center trial Collaborative Low-dose Aspirin Study in Pregnancy (CLASP), found
an insignificant reduction in the incidence of preeclampsia. Aspirin did, however,
significantly reduce the likelihood of a preterm delivery. It should also be noted that in
these studies the compliance rate for aspirin was low, and could have altered the study
results (Walsh, 2004). In a newer study, Vainio and colleagues (2004) showed that pregnant women with pregnancy-induced hypertension had an abnormal ratio of prostacyclin to thromboxane, which was normalized on low dose aspirin.
The Ω-3 fatty acid content of cells may influence the risk for preeclampsia. Williams and coworkers (1995) measured the polyunsaturated fatty acids in the erythrocytes
(red blood cells) of 22 preeclamptic women and 40 pregnant women with a normal
pregnancy. They found that women with the lowest levels of Ω-3 fatty acids were 7.6
times more likely to have preeclampsia compared to those women with the highest
levels of Ω-3 fatty acids. A 15 percent increase in the ratio of Ω-3 to Ω-6 fatty acids
decreased the risk of preeclampsia by 46 percent.
Velzing-Aarts and colleagues (1999) found a significant decrease in the long chain
Ω-3 content of the umbilical veins and arteries of preeclamptic women, 21 and 23 percent lower than the control women. Platelet long chain Ω-3 fatty acids were marginally
lower in the preeclamptic women.
A very interesting finding from the Velzing-Aarts study was that other fatty acids
were also out of balance. Women consuming adequate amounts of Ω-6 fatty acids had
lower amounts of the long chain Ω-6 fatty acids and higher amounts of long chain Ω-9
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fatty acids (monounsaturated) than control women. This points to the possibility that
preeclamptic women have abnormal transplacental transfer of long chain PUFA, leading to the abnormal ratios that favor production of the vasoconstrictive TXA2, and/or
inadequate intake of Ω-3 fatty acids. The only way to increase cellular levels of Ω-3 fatty
acids is to consume more in your diet. Chapter Three and Appendix #14 list dietary
sources. The chart below summarizes the benefits of Ω-3 fatty acids.
Ω-3 Fatty Acids & Preeclampsia
Effect of Ω-3s:
• Improves PGI2 to TXA2 ratio
• Decreases TXA2 production
• Increases TXA3 production
• Increases dilation of vessels
• Appears to be beneficial in
preeclampsia
How to increase cellular Ω-3s
• Average 300 to 400 mg of fish oils
daily (fish 3 times a week)
or
• Average 500 to 1500 mg of vegetable
sources daily by using canola oil,
green vegetables
OXIDATIVE STRESS AND PREECLAMPSIA
Oxidative stress is an imbalance between prooxidants and antioxidants, with either
an increase in production of prooxidants — free radicals or reactive oxygen species — or
a decrease in antioxidants, leading to cellular damage.
In pregnancy, the placenta is the main source of free radical production and antioxidant synthesis. In preeclampsia, the balance is upset, with more free radicals than
antioxidants, leading to systemic oxidative stress (Perkins, 2006).
Prooxidants are biologically active molecules that function as vasoconstrictors, as
well as triggering platelet production which leads to formation of microthrombi (mini
blood clots). The end result is a decreased perfusion of the placenta and other organs,
and decreased circulating plasma volume (Roberts, et al, 2003).
To investigate the impact of oxidative stress on preeclampsia, Scholl and colleagues
(2005) measured urinary levels of isoprostane 8-iso-prostaglandin F2α — a metabolite
that indicates oxidative damage to lipids and measured the overall antioxidant power
of the pregnant women. The study found a five-fold increase in preeclampsia with
increased isoprostane excretion and a three-fold decrease in preeclampsia with increased antioxidant power. These changes were found before clinical symptoms of
preeclampsia were present. Increased isoprostane excretion was related to diet, specifically fat intake and included energy-adjusted fat, polyunsaturated fat and PUFA — Ω-3
and Ω-6. No dietary link to antioxidant power was found, which may be a function of
the small study size.
Lipids, especially PUFA, are easily oxidized. As the amount increases in the diet, so
does the need for antioxidants, which may explain the finding of the link between
dietary fats and increased oxidative stress.
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Nutrients that are under clinical investigation for their role in preventing or promoting
preeclampsia include: vitamins C, E, D, selenium, zinc, copper, glutathione, fats and Ω-3
fatty acids. Presently, the results of studies investigating vitamin C and vitamin E have been
equivocal. In a Cochrane Database Review, the authors found that antioxidant supplementation reduced the risk of preeclampsia (Rumbold, et al., 2005). Other studies have found that
supplementation with vitamins C and E does not prevent preeclampsia (Rumbold, 2006)
and increased the number of low birthweight babies (Poston, et al., 2006).
• Vitamin D. Low vitamin D levels may be involved in preeclampsia, since the physiological alterations in preeclampsia by be directly or indirectly affected by vitamin D and
include: placental implantation, abnormal angiogenesis, excessive inflammation, immune
dysfunction and hypertension (Bodnar, et al., 2007; Vills, et al., 2009).
Pregnant women with lower serum vitamin D concentrations early in their pregnancies were found more likely to develop preeclampsia with a serum vitamin D level 15
percent lower than controls. In the US there is a high frequency of women who are overtly
vitamin D deficient or vitamin D insufficient (Bodnar, et al., 2007). In Norway, Haugen et al.,
(2009) found that pregnant women who supplemented 400 to 600 IU/day (10 to 15 mcg)
had a 27 percent lower incidence of preeclampsia than pregnant women who did not
supplement vitamin D. A multivitamin and mineral supplement may also decrease the
incidence of preeclampsia (Bodnar, et al, 2006; Catov, et al., 2008)
At the present time there is no definitive cause of preeclampsia. Until there is, the
best advice is to eat a varied diet, including foods that are rich in vitamins, minerals and
phytochemicals (plant foods) to ensure adequate antioxidant intake and supplement
with a multi-vitamin and mineral and vitamin D.
• Treatment. As mentioned, treating preeclampsia with sodium restriction and
diuretics can do more harm than good. Even with edema present, the plasma volume of
a preeclamptic is less than that of a pregnant woman without the disease. Life-threatening complications for both the mother and fetus can result from the use of diuretics.
They are not indicated for preeclampsia. In fact, strict salt restriction can reduce the
intake of fat, protein, and calcium: it also tends to reduce the energy intake, limits
maternal weight gain and reduces maternal fat stores (vanBuul, et al., 1995).
The best treatment is simple enough: a balanced diet, prenatal vitamin supplement,
decreased activity, frequent monitoring of blood pressure and urine, and bed rest with
the patient positioned on her left side, which decreases the pressure of the baby on vital
organs and promotes diuresis. This positioning can lower blood pressure without any
other intervention. In addition, adequate amounts of Ω-3 fatty acids, calcium, vitamins
C, E and D, and plant foods rich in antioxidants are recommended.
DIABETES
Insulin was discovered in 1921 and made available for treatment of diabetics
shortly thereafter. Before that, few diabetics could conceive. If they did, the perinatal
mortality rate was high: it has been estimated at 42 percent.
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If diabetes is diagnosed and treated, the rate of maternal complications approaches
that of the normal population. Perinatal mortality has decreased as well. New research
shows that the better the glucose control during pregnancy, the better the outcome.
Untreated diabetes can have devastating consequences, shown in the chart below.
Risk factors that require further testing are: family history of diabetes; previous poor
outcome of pregnancy — stillbirth, prematurity, malformed infant, macrosomia (over 9
to 10 lb at birth) perinatal death; hypertension; hydramnios in present pregnancy;
obesity; over age 35; and glycosuria. Tolstoi and Josimovich (1999) have an excellent
review of the etiology and management of gestational diabetes.
Complications of Diabetes
Maternal
Fetal
• Changing insulin requirements
• Preeclampsia
• Polyhydramnios (more than 2000 mL
amniotic fluid at birth)
• Postpartum hemorrhage
• Progression of retinopathy
• Progression of nephropathy
• Stillbirths and neonatal deaths
• Macrosomia
• Prematurity
• Traumatic deliveries
• Hypoglycemia
• Polycythemia
• Jaundice
• Respiratory distress syndrome
• Congenital anomalies
• Hypocalcemia
• Pathophysiology. Pregnancy, by itself, alters metabolism. The main energy
source that is utilized by the fetus is glucose. (Amino acids are supplied to the fetus for
some energy, but mostly for protein needs.) The mother’s metabolism makes adjustments to provide for the needs of the fetus as well as supplying her own needs. To do
that, the mother begins to burn fat as her source of energy.
The changes in metabolism, discussed in detail in Chapter Four, are: lower fasting
blood glucose (10 to 20 mg/dL less than nonpregnant women); increased free fatty acids
(which are higher during normal pregnancy); elevated plasma ketones; lower plasma
insulin; increased insulin resistance; and increased plasma cholesterol and triglycerides.
Two to three times as much insulin is needed during pregnancy. This insulin
resistance is a result of the hormones produced for pregnancy (estrogen and progesterone). Another hormone, human placental lactogen (HPL), is a potent insulin antagonist.
HPL enhances fat mobilization and reduces maternal glucose utilization and protein
degradation so the fetus has a plentiful supply of glucose and amino acids. Insulinase,
produced by the placenta, degrades insulin, reducing its supply even further.
Diabetes causes additional metabolic abnormalities in pregnancy. In the mother,
there is a relative insulin deficiency, due to resistance of the tissues, decreased production and degradation of insulin. Elevations in plasma glucose, free fatty acids, triglycerides and branched-chain amino acids result from the insulin deficiency.
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If the diabetes is uncontrolled during pregnancy, the metabolic abnormalities can
potentially cause serious harm to the mother and the fetus. Alterations in fetal metabolism as a result of maternal diabetes include an increase in the amount of energy fuels
available, and hyperinsulinemia, the cause of macrosomia. Screening for diabetes is
extremely important to prevent complications.
ONSET PRIOR TO PREGNANCY
Women with carbohydrate intolerance during pregnancy are divided into two
classifications: those previously diagnosed with diabetes mellitus (pregestational diabetics) and those with no prior knowledge of carbohydrate intolerance (gestational
diabetics). Approximately 0.2 to 0.3 percent of all pregnancies include pregestational
diabetes requiring insulin; 2 to 3 percent are women with gestational diabetes.
In the nonpregnant adult, distinguishing between Type 1 (insulin-dependent)
diabetes mellitus or Type 2 (non-insulin-dependent) diabetes mellitus is important
because it affects treatment. This is not necessarily true for pregnant women, as treatment for Type 1 and 2 pregestational diabetics who become pregnant is similar. Most
Type 2 women require insulin when pregnant. The distinction for pregnant diabetics is
whether or not they are using insulin, which dramatically alters nutritional treatment.
GESTATIONAL DIABETES
Gestational diabetes (GDM), also called gestational carbohydrate intolerance (GCI),
is a carbohydrate intolerance of variable severity with onset or first recognition during
the present pregnancy. This definition applies whether or not insulin is used and
whether or not the carbohydrate intolerance persists after the pregnancy is over. Ninety
percent of pregnant diabetics have gestational diabetes.
Research indicates that 35 percent of all women who develop gestational diabetes
had no previously identifiable risk factors, so it was recommended that all pregnant
women be screened. Now, women who meet all the following criteria do not need to be
screened: under age 25; normal pre-pregnancy body weight; no first-degree relative
with diabetes; are not Hispanic, Native American, Asian American or African American;
no history of abnormal glucose tolerance and no history of poor obstetrical outcome. A
woman with risk factors should be tested during her initial prenatal visit. Others should
be screened for gestational diabetes between weeks 24 and 28, when it usually appears.
There are two approaches to screening for GDM (Diabetes Care, 2009). Initial screening is the oral administration of 50 gm of glucose. The test is considered positive if the
blood sugar is either above 140 mg/dL after 1 hour and catches about 80 percent of
women with GDM. Or the test can be considered positive if the blood sugar is above
130 mg/dL after 1 hour and catches about 90 percent of women with GDM.
If the first screening is abnormal, a three-hour oral glucose tolerance test (OGTT)
with 100 gm of glucose should be done. Diabetes is diagnosed if two or more values in
the chart on the following page are elevated, even if the fasting level is normal (Am.
Diabetes Assoc., 2009).
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Once diagnosed, the treatment goal is to prevent hyperglycemia, defined as fasting
plasma glucose equal to or above 95 mg/dL, and either one-hour postprandial plasma
glucose equal to or below 140 mg/dL, or two-hour postprandial plasma glucose equal
to or below 120 mg/dL (Am. Diabetes Assoc, 2009). Diet manipulation has been the
treatment for most gestational diabetics. Practitioners have been treating gestational
diabetics with insulin if hyperglycemia persists.
Gestational Diabetes Diagnosis
Plasma Glucose
Fasting
1 Hour
2 Hour
3 Hour
100 gm test
95 mg/dl
180 mg/dl
155 mg/dl
140 mg/dl
5.3 mmol/L
10.0 mmol/L
8.6 mmol/L
7.8 mmol/L
Diabetes Care 32 (supp ): S13, 2009
NUTRITIONAL MANAGEMENT
DIABETIC PREGNANCIES
The American Diabetes Assn. publishes guidelines for the management of diabetes
in Diabetes Care (online at: <http://care.diabetesjournals.org/>). The latest recommendations were published in 2006, with an update in 2009. The overall recommendations
that are related to pregnancy are to base your treatments on nutritional assessment of
the individual and set up a nutrition plan that will meet the following goals:
• Individualize medical nutrition therapy (MNT) based on pre-pregnancy weight
and height to provide adequate energy and nutrients to meet the needs of
pregnancy and to be consistent with established blood glucose goals.
• Avoid ketonemia from ketoacidosis or starvation.
• Focus your MNT for gestational diabetes on food choices for appropriate weight
gain, normoglycemia, and absence of ketosis.
• Restrict calories for obese women (BMI above 30). A 30 to 33 percent calorie
restriction to 25 kcal/kg actual weight per day and restriction of carbohydrate to 35
to 40 percent of calories is recommended.
• Maintain as near normal blood glucose levels as possible, adding insulin if diet alone
does not control hyperglycemia.
As you can see, these guidelines do not prescribe how to divide calories among carbohydrate, protein and fat. That is left to the skill of the practitioner. In addition, gestational
diabetics need to test their blood sugars, even if they are not taking insulin. That is the only
way to individualize the diet and determine if they need further intervention.
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As a place to start, I will present a management strategy that has worked for many
pregnant diabetics. The goals and guidelines for nutritional treatment of diabetic pregnancies used here were developed by either “Sweet Success"™ a program developed by
the Calif. Diabetes and Pregnancy Program of the Calif. Dept. of Health Services, or the
Joslin (Mass.) Diabetes Center (2005). The goals are:
• Normal weight gain, based on prepregnant weight and IBW;
• Caloric intake of 25 to 30 kcal/kg of pre-pregnancy IBW during the first and
early second trimester;
• Caloric intake of 25 to 35 kcal/kg of pre-pregnancy IBW during the late second
and third trimester;
Diet for Gestational Diabetes
• First and early second trimester: 25-30 kcal/kg ideal body weight
• Late second and third trimester: 25-35 kcal/kg ideal body weight
• Blood sugar control: ≤95 mg/dLfasting
≤140 mg/dL 1 hour postprandial
≤120 mg/dL 2 hours postprandial
• Limit simple sugars, sweets, refined, highly processed carbohydrates.
• Emphasize complex carbohydrates, high fiber foods.
• Eat 3 meals and 2 to 4 snacks. Space snacks and meals >2 hours apart.
• Common carbohydrate guidelines: 2 carbohydrate choices (30 gm) at
breakfast, 3-4 choices (45 to 60 gm) at lunch and evening meal, and 1-2
choices (15 to 30 gm) for snacks.
• Limit snacks if they consistently elevate blood sugar levels.
• Add protein to meals,snacks to provide calories and satisfy appetite
Recommendations include: avoid all simple sugars, sweets and refined carbohydrates; limit carbohydrate at each meal; and emphasize complex carbohydrates and
fiber. Notice that fat and protein intake is higher than usually recommended.
Since carbohydrate intake is lower due to carbohydrate intolerance and insulin
resistance, the percentage of fat and protein increases. To prevent excess weight gain,
recommend lean meats and non-fat or low-fat dairy products. The calories and carbohydrates should be distributed over three meals and snacks. Some protein should be
included at meals and snacks to prevent postprandial excessive glucose.
When designing a diet for gestational diabetics keep in mind that insulin resistance
is greater early in the morning. Breakfast should contain no more than 15 to 30 gm of
carbohydrate. Carbohydrates that are quickly absorbed, such as fruit, fruit juices, bagels, potatoes and highly refined and processed cereals, are not desirable. Use slowerabsorbable complex carbohydrates: high-fiber foods, whole grain breads, cereal, crackers, brown rice, pasta, legumes and vegetables.
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If hyperglycemia persists in the morning, consider eliminating all fruit, juices and
milk at breakfast.
As the pregnancy progresses, hormonal influences increase glucose intolerance.
The amount and types of carbohydrate tolerated at 28 weeks may not be tolerated at 35
weeks, and the diet should be adjusted accordingly. Also, exercise should be encouraged to help with the insulin resistance and blood sugar control (Tolstoi and Josimovich,
1999; Franz, et al., 2002.).
Don’t be held back by culturally and socially acceptable foods for breakfast. If it works, use
it. The chart on the previous page summarizes dietary recommendations for gestational diabetics.
Dietary intervention for gestational diabetics decreases maternal and fetal complications
and perinatal mortality. Patients must be educated and followed to maximize compliance and minimize complications, but the effort is worthwhile.
If insulin is required to treat gestational diabetes, nutritional management will be
different than described above, based on the insulin regime. Snacks must be added to
prevent hypoglycemia and liberalization of carbohydrate intake is possible.
NUTRITIONAL MANAGEMENT
PREGESTATIONAL DIABETES
Women with pregestational diabetes are harder to manage during pregnancy. As
the pregnancy progresses, insulin resistance and carbohydrate intolerance increase,
changing insulin requirements and dietary needs. These diabetics need constant monitoring and support as insulin needs change frequently and nausea and vomiting may
complicate management.
Oral hypoglycemic agents are small molecules that readily cross the placenta and
are not recommended for use by pregnant women. Insulin, a large molecule that will
not cross the placenta, is the treatment of choice for pregnant diabetic women.
The goal for treatment is maintaining the hemoglobin A1c one percent above normal
(Am Diabetes Assoc, 2003a). The recommended weight gain, rate of gain and caloric
needs for a pregestational diabetic are the same as the non-diabetic pregnant woman.
Nutritional recommendations are summarized in the chart on the next page. Remember,
these guidelines are a place to start, but each diet needs to be individualized.
The recommended percentage of calories from carbohydrate is: breakfast, 10 to 15
percent; morning snack, 10 percent; lunch, 20 to 25 percent; afternoon snack, 15 percent;
dinner, 25 percent; bedtime snack, 15 percent.
Carbohydrates must be adequate to prevent ketosis — approximately 175 gm/day.
Because these women are taking insulin to control blood glucose, dietary carbohydrate
can be as high as 50 to 55 percent of total calories. Emphasis should be placed on complex carbohydrates and soluble fiber. Simple sugars should be restricted and the use of
highly processed breakfast cereals discouraged. Fresh fruit should be encouraged
instead of fruit juices.
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Diet for Pregestational Diabetes
Nutritional Recommendations
• First and early second trimester: 25-30 kcal/kg ideal body weight
• Late second and third trimester: 25-35 kcal/kg ideal body weight
• Distribution of total calories:
45-50% carbohydrate
20-25% protein
30-35% fat
• Distribute calories between 3 meals and 3 snacks to cover insulin.
• All food must be eaten to cover insulin.
• Avoid simple sugars.
• Achieve normoglycemia. Maintain blood sugars: ≤105 mg/dl fasting; ≤155
mg/dl one hour postprandial and ≤130 mg/dl two hours postprandial.
• Avoid ketosis. May need to check for ketones.
• Avoid excessive weight gain. Choose low-fat, high fiber foods.
Protein requirements are calculated at 0.8 gm/kg with an additional 25 gm/day,
approximately 20 to 25 percent of total calories. The fat content of the diet is 30 to 35
percent of total calories, less than 10 percent saturated fat, with an emphasis on the use
of monounsaturated and polyunsaturated fats. Calories, carbohydrates, fat and protein
are evenly distributed throughout the day to cover insulin needs, divided into three
meals and two to three snacks.
Any pregnant woman with pregestational diabetes should have a Registered
Dietitian or Certified Diabetes Educator design a diet specifically for her. Each diet
prescription is individualized according to the specific needs of the pregnant woman,
including pre-pregnancy weight, insulin regime, exercise plan and dietary likes and
dislikes. Follow-up must be provided, especially late in pregnancy when insulin resistance is greatest. Home monitoring of blood glucose is a necessary part of treatment.
Insulin needs can change constantly, due to the pregnancy hormones.
In late pregnancy, glucose levels rise dramatically after a meal. This may necessitate increasing the number of doses of regular insulin, rather than increasing the total
amount of insulin in one or two doses a day. Home monitoring assists the health professionals in determining the proper amount and type of insulin required. It is important
to check blood sugars a minimum of four times a day: fasting, before a meal, after a
meal and at bedtime. Some clinics test women as many as seven times a day. Don't
forget to recommend exercise, as it will help control blood sugar levels.
PREGNANCY, HIV AND AIDS
When the AIDS epidemic began over 25 years ago, women had a one in four
chance of passing the virus to their child. Now, in developed countries, that rate has
dropped from 25 percent to 1.5 percent, a stunning achievement (Nielsen, 2006). Even
with the best treatment, transmission does occur, but not very often.
Two major concerns about HIV-infected women becoming pregnant are the effect
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of pregnancy on the disease, and transmission of the virus to the fetus. Hocke, et al.,
(1995) showed that pregnancy did not cause a progression of HIV. In the US, pregnancy
does not appear to affect viral load or progression of HIV (ADA, 2002).
Transmission (referred to as vertical transmission) of the HIV virus from mother to
child can occur by two routes during pregnancy: intrauterine (in utero); or intrapartum
(at delivery). Women who have not had any drug treatment during pregnancy can still
receive treatment during delivery, which was found to decrease the transmission to the
child (Nielsen, 2006; Public Health Service Task Force, 2006).
A landmark study, the AIDS Clinical Trial Group (ACTG), showed that transmission from mother to fetus could be reduced by two-thirds by treating HIV-infected
pregnant women with 100 mg zidovudine (INN) (also called azidothymidine (AZT) and
(ZDV), tradenamed Retrovir® ), five times a day during the pregnancy initiated at 14 to
34 weeks, with IV zidovudine during labor, and oral zidovudine given to the child for
six weeks after birth (Connor, et al., 1994). Without drug treatment the transmission rate
is between 15 and 40 percent; with treatment the transmission rate can go as low as 1.5
percent (ADA, 2002; Public Health Service Task Force, 2006; Nielsen, 2006 ). Adding
protease inhibitors to the drug treatment may be able to reduce the transmission rate
even lower to 0.9 percent (Morris, et al., 2005).
A number of studies now suggest that the viral load may be a predictor of which
women are more likely to transmit the HIV. Dickover, et al., (1996) showed that at
delivery the number of HIV RNA copies was strikingly different between women who
transmitted the virus to their fetus and those who did not. No woman who had fewer
than 20,000 copies of HIV RNA transmitted the virus. All women with more than 80,000
copies of HIV RNA did transmit the virus to their fetuses. Of 22 women who took
zidovudine and reduced viral load from an average of 43,043 RNA copies/mL to 4,238
copies/mL at delivery, none transmitted the virus.
Landesman and colleagues (1996) showed that, at delivery, women with membranes ruptured for more than four hours had increased maternal-fetal HIV transmission. C-sections reduce the rate of HIV transmission from mother to fetus and are now
offered to HIV-positive women. While C-sections do significantly decrease transmission
of HIV to the child, they do not eliminate the risk entirely.
Now researchers are trying to determine if there is a link between certain
antiretroviral drugs and LBW and preterm deliveries. At the present time, there is no
definitive answer (Public Health Service Task Force, 2006). According to Peckham and
Newell (2000), nutrition intervention does not reduce transmission of HIV, but there
does seem to be benefit from nutrition intervention on increasing maternal well-being,
pregnancy outcome and infant health.
Breast milk can serve as a means of transmitting HIV virus from mother to baby
(ADA, 2002). After reports that 22 infants were infected from breast milk, Ruff, et al.,
(1994) found HIV-1 DNA in 70 percent of breast milk specimens from HIV-positive
women up to four days after delivery, declining to approximately 50 percent at six to 12
months postpartum. Some HIV-positive women had no detectable levels in breast milk.
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Studies are now looking at ways to decrease transmission of HIV in breast milk, especially in developing countries. The use of antiretrovirals may help decrease transmission via breast milk (Nielsen, 2006).
The Public Health Service Task Force (PHSTF) has published recommendations for
use of antiretroviral drugs in pregnancy to reduce perinatal HIV transmission: these are
available on the Internet (PHSTF, 2006). The gold standard of antiretroviral drug
therapy in HIV/AIDS is a combination of drugs that includes protease inhibitors. The
PHSTF states: “Pregnancy should not preclude the use of optimal therapeutic regimes.
However, recommendations regarding the choice of antiretroviral drugs for treatment of
infected pregnant women are subject to unique considerations.”
The considerations include changes in dosing, the effect of the drug on the pregnant woman and the short- and long-term effects on the fetus and the newborn.
The most commonly used antiretroviral in pregnancy is zidovudine, and many
physicians and researchers believe it should be included in the drug regime. Some
women may already be on antiretrovirals when they discover they are pregnant, which
may require that they stop for a while. Other women may not be on them and present
for treatment early or late in their pregnancy. So treatment options for antiretrovirals
will depend on each woman's situation and her reaction to the drugs used.
A list of antiretrovirals and pregnancy-related information can be found in the
PHSTF document (2006) and the Canadian Consensus guidelines for the care of HIV-positive
pregnant women: putting recommendations into practice (Burdge et al., 2003).
Currently, there are no special nutritional recommendations for pregnant women
with HIV. It is important that they be well fed to prevent any nutritional deterioration of
their immune system and to provide adequate nutrients to the fetus. Use of higher
levels of supplementation may also be warranted, as we know that HIV-infected nonpregnant individuals have higher nutrient needs and incidence of vitamin deficiencies.
In addition, pregnancy itself causes changes in cell-mediated immunity, characterized
by a decrease in CD4 T cells and decreasing the ratio of CD4 : CD8 T cells, which is also
a characteristic of AIDS. Inadequate diet can further depress immunity. Nutrients of
concern are protein, calories, zinc, vitamin B6, folic acid, vitamin C and iron.
The drugs women are taking during pregnancy have may side effects, including
anemia, nausea and vomiting, aminotransferase elevations (increased liver enzymes)
and hyperglycemia. Many of these side effects need nutrition intervention.
Also, remember to talk with these women about GI upsets that may limit food
intake; proper food handling, as they are immunocompromised; any problems with
chewing due to dental problems; sores in their mouth from candidiasis, or other swallowing problems Solutions to these problems can dramatically increase intake and lead
to a healthier pregnancy.
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Chapter Ten:
Alcohol, Tobacco & Other Drugs
Consumption of alcohol during pregnancy can affect the outcome of pregnancy.
Both the amount of alcohol consumed and the timing of consumption affect the fetus,
resulting in congenital anomalies and/or growth retardation. The exact mechanism
causing the adverse outcome is unknown. Approximately 13 percent of pregnant
women consume alcohol, with three percent drinking heavily or binge drinking
(Bertrand, et al, 2004).
Alcohol is detoxified by the liver. Ethanol is broken down to acetaldehyde, then to
acetic acid, and eventually to carbon dioxide and water, as shown below.
The liver can only detoxify so much alcohol at a time; it takes five to six hours to
detoxify the alcohol in 4 oz of whiskey or 2.5 pints of beer. If more alcohol is present than
the liver can detoxify, it will continually circulate until the liver is able to detoxify it.
Alcohol Detoxification
Mother
ingests
alcohol
Alcohol
Fetus
Fetus
Fetus
Liver
Acetaldehyde
Acetic Acid
CO2 + H2O
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Food slows down the absorption of alcohol into the blood. Anyone who has had a
drink on an empty stomach knows the effects of alcohol are felt more quickly than with
food. Slowing down alcohol absorption into the blood gives the liver more time to
detoxify it, so that there is less circulating in the blood. The alcohol concentration of the
blood is determined by how much alcohol is consumed, the period of time in which it is
consumed and whether emptying time is slowed by food.
Alcohol crosses the placenta and concentrates in fetal tissues. How much alcohol and/
or metabolites are necessary to damage the fetus is not known. The less alcohol is consumed during pregnancy, the less that crosses the placenta, and consequently the less
risk to the fetus. Complications of alcohol use and abuse during pregnancy have been
linked to reduced birth weight, prematurity, stillbirth, miscarriage, increased perinatal
morbidity and mortality, increased incidence of malformations, functional disturbances,
mental retardation, behavioral and developmental delays and abnormalities, and fetal
alcohol syndrome (FAS).
FETAL ALCOHOL SYNDROME
One thousand to 6,000 babies are born with FAS each year (Bertrand, et al., 2004),
Infants born with FAS have developmental deficiencies in major organs (especially the
heart and brain) and psychomotor disturbances. Many are mentally retarded, with
neurological impairment, a small head, poor coordination, hyperactivity and irritability.
Growth impairment and facial alterations include decreased head circumference, a
flattened nose, small upper lip and eyes set close together. Other congenital anomalies
may also be present. Amounts of alcohol insufficient to cause FAS may still result in
growth problems, sometimes called fetal alcohol effect.
Alcohol consumption may explain the abnormalities seen in infants born to mothers abusing alcohol, as indicated in the chart below.
Effects of Alcohol on Development By Trimester
First Trimester
Second Trimester
Third Trimester
Hyperplasia
Rapid cell division
Organs/tissues develop:
CNS, heart, eyes,
arms, legs, ears, teeth,
palate, external
genitalia
Hyperplasia
Hypertrophy
Organs/tissues continue
to develop: ears, CNS,
eyes, teeth, external
genitalia
Brain begins to develop
Hypertrophy
Fetus grows rapidly
Rapid bone growth and
mineralization
Brain develops
Organs/tissues continue
to develop: eyes, CNS,
external genitalia
Effects of alcohol
Major morphological
abnormalities
Abnormalities of FAS seen
in organs/tissues
Physiological defects
Minor morphological
abnormalities
Growth impaired
Physiological defects
Minor morphological
abnormalities
Growth impaired
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The central nervous system is most affected from weeks 2 to 6; the heart from 2.5 to
5.5 weeks; and ocular development from 3.5 to 7 weeks. The defects seen in FAS affect
organs whose development is mostly completed by the 10th to 12th week of gestation.
The organs affected in FAS develop so early that many women may not realize
they are pregnant in time to stop consuming alcohol. Tragically, great damage may be
done to the fetus before the mother has an opportunity to prevent it.
Alcohol consumption later in pregnancy may not have the same effects as early in
pregnancy. In a study conducted by Rosett et al. (1983), women who drank heavily
throughout pregnancy had a higher incidence of intrauterine growth retardation (IUGR)
and congenital anomalies. Rare and moderate drinkers throughout pregnancy had no
difference from the control group.
Women who reduced heavy drinking before the third trimester had offspring
whose growth was similar to rare and moderate drinkers but with a higher frequency of
abnormalities, similar to the heavy drinkers throughout pregnancy. It appears that
drinking in the later stages of pregnancy interferes with growth, while drinking early in
pregnancy affects organ development.
Some of the adverse effects of alcohol on pregnancy outcome may result from
altered dietary intake and impaired metabolism, absorption and utilization of nutrients.
Women who abuse alcohol have reduced intake of many nutrients, including calories,
protein, essential fats and vitamins and minerals.
Intestinal transport of amino acids, calcium and some vitamins is altered with
alcohol. The liver, busy detoxifying alcohol, may have impaired metabolism of nutrients. Reduced serum levels of zinc have been documented in pregnant women at delivery (McClain and Su, 1983).
Alcohol may also impair placental transport of some nutrients. Other metabolic
changes include decreased Vitamin A storage in the liver (Leo and Kieber, 1982) and
impaired uptake and utilization of folate (Halsted, et al., 1971). Thiamin malabsorption
may also occur. As discussed earlier, deficiencies or inadequacies in specific nutrients
can cause adverse outcomes of pregnancy. It is possible that, in some women, the effects
of alcohol are mediated by changes in nutrient intake and/or utilization.
How much alcohol can cause damage? We know that drinking more than four
drinks per day throughout pregnancy can cause FAS. In addition, heavy alcohol consumption increases the risk of mental retardation and learning disabilities (ADA, 2002). One or
two drinks, timed just right, may be enough to cause less severe complications, such as
impaired fetal growth, lower Apgar scores and reduced fertility in women (ADA, 2002).
The Centers for Disease Control estimates that there are three times the number of
babies born with alcohol-related damage, referred to as fetal alcohol effects (FAE) than
with FAS. These children have some but not all, of the physical or mental defects of FAS
(Institute of Medicine, 1996).
There is no safe level of drinking during pregnancy. While four or five drinks a day
causes FAS, drinking moderately or even lightly can cause fetal alcohol effects, which causes
physical and/or mental defects. Light drinking, such as one or two drinks a week, in some
studies has shown behavioral and learning problems (March of Dimes, 2006).
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In an interesting study, Baer, et al., (2003) investigated the relationship of alcohol
consumption by parents during pregnancy and the drinking habits of their children at
age 21. Family history of alcohol intake, maternal smoking, caffeine and drug use were
all measured. The authors found that 14 percent of women who drank heavily during
pregnancy (five or more drinks per day on more than one occasion) had offspring with
alcohol problems. Only 4.5 percent of children of women who drank infrequently or not
at all had drinking problems. The authors concluded that prenatal exposure to alcohol is
a risk factor for development of drinking problems.
There is widespread awareness of the risks of drinking alcohol during pregnancy.
But some women drink, regardless of the potential consequences, and some who drink
deliver normal children. Nevertheless, abstinence is the only absolutely safe recommendation. Women who are pregnant or trying to get pregnant should be counseled to
avoid alcohol altogether as any alcohol will increase risk to the fetus.
SMOKING
Cigarette smoking adversely effects pregnancy outcome. Studies show maternal
smoking retards fetal growth. A smoker is twice as likely to deliver a low birth weight
(LBW) baby (USDHHS, 2004). There is also an increased risk of preterm delivery and
perinatal mortality (ADA, 2002). The good news is that in general, smoking during
pregnancy declined from 19.5 percent in 1989 to 11 percent in 2004 (USDHHS, 2004). If
all pregnant women stopped smoking, there would be an estimated 11 percent reduction in stillbirths and a 5 percent reduction in newborn deaths (USDDHS, 2004).
A large Danish study with over 2,000 singleton pregnancies found that smoking
was the most important risk factor for intrauterine growth retardation (Nordentoft, et
al., 1996). The effects of daily drinking, poor maternal school education, and poor social
support variables were insignificant in the final risk model.
The effect of cigarette smoking is dose-related: as the number of cigarettes smoked
increases, birth weight decreases. There is also a possibility that cigarette smoking is
teratogenic. Maternal pre-pregnancy weight and prenatal weight gain may mediate the
effects of cigarette smoking on birth weight.
Hellerstedt et al. (1997) found that no level of gestational weight gain in obese
women will eliminate the effects of cigarette smoking on birth weight. In this study
Hellerstedt compared the weight gain of normal weight and obese smokers and nonsmokers, to the IOM recommendations, and the birthweight of their babies. For obese
women, whatever their weight gain, the risk for LBW and small for gestational age
(SGA) babies was five times higher in smokers than nonsmokers. In normal weight
women, there was no increased risk for LBW babies, but the risk for SGA births was
significantly elevated in the smokers compared to the nonsmokers.
The cause of the growth retardation may be the direct effect of toxic substances
such as cyanide and carbon monoxide in tobacco smoke. It may also be caused by the
vasoconstricting effects of nicotine or a decreased placental zinc to cadmium ratio or a
decrease in uteroplacental blood flow.
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159
Cigarette Smoking & Pregnancy
Cigarette smoke (5% carbon monoxide (CO))
Hb has higher affinity for CO than oxygen
Hb + CO = carboxyhemoglobin (COHb)
Hb bound to CO releases oxygen at lower partial pressure
Decreases oxygen-carrying capacity of the blood
Chronic hypoxia of maternal and fetal tissues
Maternal
Increases in:
• Ventilation
• Cardiac output
• Hgb/Hct
Fetal
• Increase in Hgb/Hct
• Decrease in O2 use
• Redistribution of
blood
Placental
• Increased size &
surface area
• Increased vascularity
• Decreased diffusion
distance
Another possibility is that the mother is not eating enough food to compensate for
the decreased efficiency of metabolism caused by carbon monoxide and the increased
metabolic rate caused by nicotine.
Cigarette smoke contains more than 2,000 compounds, with 5 percent carbon
monoxide (CO). Hemoglobin (Hb) has 210 times greater affinity for CO than for oxygen.
Hb and CO form carboxyhemoglobin (COHb), which is incapable of transporting
oxygen. Increased CoHb decreases the oxygen-carrying capacity of the blood and
results in hypoxia to maternal, fetal and placental tissues, as seen in the chart above.
Tobacco smoke has other dangers. Cyanide is detoxified in the body. One of three
possible routes of detoxification involves vitamin B12. Thus, using vitamin B12 to
detoxify cyanide lowers serum B12 which has been implicated in premature delivery,
IUGR, anemia and smaller babies. All of these problems have been identified in women
who smoke cigarettes during pregnancy.
Other nutrients found to be lower in the serum of smokers are beta carotene,
vitamin C, folic acid and some amino acids. Pregnant smokers may require increased
amounts of these nutrients. The vitamin C requirement may double for heavy smokers
(≥ 20 cigarettes/day). A prenatal supplement, with perhaps an additional 200 mg of
Vitamin C for pregnant smokers, is indicated if their diet is otherwise adequate.
The effects of smoking are reversible if the habit is given up during pregnancy. The
sooner the woman quits, the better for birth weight. If a woman quits smoking in her
Sexual & Reproductive Health
160
first trimester, she is no more likely to have a low birthweight baby than a non-smoker.
Ideally, no woman should smoke while pregnant. If she does, try to get her to cut down
as much as possible or refer her to a smoking cessation program.
Unfortunately, just telling some pregnant woman that their babies may weigh 150
to 350 gm less will not convince them to stop or cut back. It is often effective to approach the subject from the standpoint of the direct effect on the fetus. Every time a
pregnant woman puffs on a cigarette, so does the fetus, as evidenced by a momentary
stop in fetal heartbeat. The fetal heart rate may also increase. This can be easily demonstrated to her with a stethoscope. TV ads portraying a fetus puffing on a cigarette are
particularly striking, as well.
Nutrition can only go so far in reducing the risks of smoking. Typically, a smoker
will be less than conscientious about her diet and may use another substance — caffeine
or alcohol. If you can't get her to quit or cut down, work on the diet issues and recommend a multivitamin supplement, since smoking puts her in a high-risk category.
Remember, risks are cumulative. If a mother smokes and drinks, the effect on the fetus
will be more pronounced than if she does only one.
DRUGS
Studying the effect of drugs on fetuses is difficult. Animal studies are not reliable
indicators of teratogenicity due to species differences; short-term studies do not always
detect defects that emerge later. The defects resulting from exposure to drugs are dependent to a large extent on gestational timing, and to a lesser extent on drug dosage,
which in itself is difficult to determine in pregnancy.
Physiological changes of pregnancy alter drug metabolism. Pregnancy causes
decreased gastric tone and motility, decreased hydrochloric acid in the first two trimesters (increasing during the third trimester), decreased albumin-binding capacity of
drugs (so more “free” drugs circulate) and increased excretion of drugs by the kidneys
(due to increased renal perfusion and filtration), which may accelerate clearance of
drugs from the body. Faster drug clearance may decrease effectiveness of the drugs.
Drugs are transferred across the placenta by simple diffusion, which is dependent
upon the chemical properties of the drug and the concentration of free drugs. The
longer the blood level of a drug is maintained, the greater the chance it will cross the
placenta. The larger the dose, the greater the concentration. While a drug taken in small
doses might not cross the placenta, in a large dose, it may well do so.
Drugs can act as teratogens by causing abortions, malformations, altered fetal
growth, functional deficits, carcinogenesis or mutagenesis. There are many pathways a
drug can take to be a teratogen:
• Inhibition of certain important enzymes;
• Mutation of genes;
• Changes in cell membrane integrity;
• Competition for protein binding sites;
• Interactions with other drugs/teratogens.
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The timing of drug exposure is crucial. During the first 10 weeks of gestation
(during hyperplasia), the developing organ systems are highly susceptible to drugs.
Later, during hypertrophy, growth problems can occur, but organs are still susceptible to
interference from drugs.
Drugs can affect pregnancy in other ways. Aspirin and other salicylates can prolong pregnancy and increase blood loss at delivery. Aspirin inhibits the production of a
prostaglandin that initiates uterine contraction, delaying labor. Aspirin adversely affects
platelet function by blocking the cyclooxygenase enzyme necessary for the production
of thromboxane that regulates platelet function.
A good resource for information on teratogens during pregnancy and lactation is
the Organization of Teratology Information Specialists (OTIS) and their web site:
<www.OTISpregnancy.org>
MEDICATION DURING PREGNANCY
During pregnancy, 62 percent of pregnant women take at least one drug; 25 percent
take an opiate and 13 percent take a psychotropic drug (Cheney, 2003). Over-the-counter
drugs are also commonly used by pregnant women (Black, et al., 2003).
Many pregnant women must take medication to control a disease or disorder, such
as asthma, hypertension, lupus, arthritis, seizures or other disorders. Failure to take the
medication may put both the mother and the baby at risk. However, taking the medication
has its own risks.
Unfortunately, it is difficult to do research on medications during pregnancy. You
can't do studies that potentially harm a baby. Therefore most studies of pregnant
women are retrospective, unless women must take medication and you can study them
prospectively during their pregnancy.
For instance, severe asthma during pregnancy has the potential to be a life-threatening event for both the mother and fetus. Complications from asthma during pregnancy include low birth weight infants, fetal hypoxia and intrauterine growth retardation (Cheney, et al., 2003). Drugs are a necessity to control this disease, yet there is only
one published study on asthma medications during pregnancy (Schatz, et al., 2001).
Many women have successfully used asthma medications during pregnancy. A registry
for pregnant women using asthma medication does exist (Meadows, 2001). The purpose
of this and other registries is to collect and pool data on the course of pregnancies and
outcomes in women using medications.
Fluoxetin (Prozac®) has been used by pregnant women to treat depression for over
10 years without teratogenic effects (Cheney, et al., 2003). While short-term side effects
have not been seen, long-term effects on offspring are unknown.
Common over-the-counter medications that appear safe include acetaminophen,
chlorpheniramine, kaolin and pectin. Other medications, such as histamine H2-receptor
blockers, pseudoephedrine and atropine/diphenoxylate should be used with caution
(Black, et al., 2003).
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To help clinicians prescribe medications to pregnant women, the FDA has established Pregnancy Categories A, B, C, D, and X.
• Category A consists of the safest drugs. These drugs have no proven harm to the
fetus in the first trimester (or later trimesters) in controlled studies.
• Category B refers to drugs that have been tested on animals and found safe, but
there are no human studies yet. Basically, more information is needed.
• Category C drugs have adverse effects on fetal animals, but no information is
available on humans.
• Category D is reserved for drugs that have been found to have human fetal risks,
but the benefits may outweigh the risks. These drugs may be used when the life
of the mother is at risk and there is no alternative but to use the drug.
• Category X is for drugs that are proven harmful to the fetus and the risk of using
the drug clearly outweighs any benefit.
Using this information may be a bit more difficult than it appears. For example,
Acyclovir® has been used in the treatment of HIV/AIDS for 10 years and is considered
“safe.” It is designated Category C. A much newer drug also used to treat HIV/AIDS,
Famciclovir,® is designated Category B. In addition, many feel this labeling system is an
oversimplification. Many drugs labeled Category C (no data on pregnancy) may in fact
be as harmful as, or more harmful than, a drug labeled Category X. The FDA is working
on a new drug labeling system for pregnancy that would replace the letter categories. It
is still being developed.
Before taking any drugs, including over-the-counter drugs, a pregnant woman
should consult with a pharmacist or her prenatal care provider and carefully weigh the
risks and benefits. Is the drug absolutely necessary? If so, it may be more harmful not to
take it. If the drug is not necessary, it may be better to wait.
Other questions to ask are:
• Is there an alternate drug that may be less harmful?
• Is there a particular time during the pregnancy I should not take this drug?
• Do you know the correct dose during pregnancy?
STREET DRUGS
It is difficult to get an accurate count of the number of pregnant women using drugs
such as cocaine, heroin, amphetamines, morphine, methadone, benzodiazepines, barbiturates and marijuana. Screening is difficult and is not routine. In the 1980s and 1990s, an
epidemic of “crack babies” in urban areas attests to the scope of the problem.
Problems in pregnancy may be related to the direct effect of the drug on the fetus
or an indirect effect related to maternal self-neglect — inadequate nutrient intake,
malnutrition, poor health, poor hygiene, smoking or poor prenatal care. When determining the effects of drugs on pregnancy outcome, it is not always easy to separate the
effects of the drugs themselves from the poor care the mother takes of herself during
pregnancy. The chart on the following page summarizes the potential complications for
the mother and the fetus/infant from the use of street drugs.
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Complications from Drug Use
Maternal
Fetal/Infant
Spontaneous abortion or intrauterine death
Preeclampsia and abruptio placentae
Malnutrition
Placental insufficiency
Premature labor
Uterine irritability and meconium staining
Congenital infection
Increased perinatal mortality — neonatal
deaths, stillbirths
Birth asphyxia
Cerebral hemorrhage
Growth retardation
Hypoglycemia
Irritability
Myocardial infarction
Necrotizing enterocolitis
Precipitous delivery
Prematurity
Congenital anomalies
Increased incidence of SIDS
Intrauterine growth retardation
Cocaine — in whatever form — is a central nervous system stimulant, causing
increased heart rate, hypertension and vasoconstriction. Reductions in uterine blood
flow secondary to the vasoconstriction may cause fetal hypoxia and reduced nutrient
supply to the fetus, resulting in many of the complications seen in babies born to mothers using cocaine, such as growth retardation — reduced birth weight, length, head
circumference and microcephaly. Other complications include congenital malformations, CNS abnormalities, neurodevelopmental defects, sudden infant death syndrome
(SIDS) and feeding intolerance. Feeding problems may be due to physiological and
structural problems or may result from the neurodevelopmental defects causing poor
organizational responses and poor visual attention.
Marijuana use in pregnant women has been investigated. The active ingredient in
marijuana is Δ9-tetrahydrocannabinol (THC), which is fat-soluble and crosses the
placenta. Therefore, the exposure to the fetus may be prolonged. Smoking marijuana
causes increases in carboxyhemoglobin, which may decrease oxygen delivery to the
fetus (as discussed in the section on tobacco smoke), impairing growth.
Women who have smoked a lot of marijuana in the past may also place infants at
risk, especially if they have a poor food intake. As fat stores are mobilized, the active
ingredient, THC, is released from the fat stores into the blood and across the placenta.
It is difficult to make specific recommendations for nutrition intervention in pregnant women using street drugs, since little is known about the nutrition-related effects
of these drugs. Drug abuse is endemic in our society and the use of nutrition and diet to
aid recovery is coming into the forefront.
When interviewing a pregnant women, it is important to screen for the use of
drugs, and specifically mention alcohol, as many women do not consider this a drug.
The National Center for Education in Maternal and Child Health (1997) publishes
Screening for Substance Abuse During Pregnancy: Improving Care, Improving Health. This
document contains information and tools on how to screen pregnant women for alcohol
Sexual & Reproductive Health
164
and drugs as well as how to ask questions in a manner that is more likely to get a
truthful response. The screening tools in the document are very short and easy to use.
The publication can be downloaded from
<www.mchlibrary.info/pubs/pdfs/subabuse.pdf>
Many other publications, screening tools and articles are available on the
NCEMCH library relating to maternal and child health issues.
Another resource is the ACOG (American College of Obstetricians and Gynecologists) prevention tool kit: Drinking and Reproductive Health: A Fetal Alcohol Spectrum
Disorders Prevention Tool Kit. It can be downloaded at:
<www.acog.org/departments/healthissues/FASDToolKit.pdf>
It is important to assist all women in following the nutrition guidelines presented in
this course as best they can, and possibly increasing their intake due to the poor nutritional status coming into pregnancy. However, women worrying about money for their
next fix, women hung over from an alcohol binge, or women who have indulged in
hallucinogens for years may not be too concerned about their diet or too interested in
hearing about “rules.” Refer them to appropriate resources for recovery.
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165
Case Study
Please read through the following case study and answer the questions from the material
provided. A discussion of the case follows. (If you anticipate sharing this coursebook, please do
not write in the book. Photocopy the pages and work on the copies.)
“Rita” (the name is fictitious) was referred to the clinic to see a dietitian. Her doctor
is concerned about her rapid weight gain and feels she should go on a weight reduction
diet. Since she is close to term, he feels that too much weight may make labor and
delivery more difficult.
The following information is in Rita’s chart:
Name: Rita
Height: 5'4"
Age: 36
Pre-pregnancy weight: 145 lb
FAMILY HISTORY
Mother - elevated blood pressure
PATIENT’S HISTORY
Rheumatic fever as a child
Heart murmur as a child
Anemia - diagnosed 2 years ago
No alcohol or cigarette use
Onset of menses - 12 years of age
Birth control: OCAs (stopped one year ago)
IUD, no history of infection
OBSTETRICAL HISTORY
Gravida 3, Para 2
2001 - Birth to 6 lb, 1 oz female, no complications
2002 - Birth to 7 lb, 5 oz male, water retention 25th week
PRESENT PREGNANCY
Pre-pregnancy weight: 145 lb
Present weight: 182 at 35 weeks gestation
Hgb:
10.3 then 11.5
Sexual & Reproductive Health
WEIGHTS
Pre-pregnancy:
10 Weeks:
19 Weeks
21 Weeks
24 Weeks
29 Weeks
35 Weeks
166
145
157
160
168
176
182
182
24-HOUR RECALL DIET HISTORY (This is her entire intake for the 24-hour period.)
5:30 pm
Roast beef
2 oz
Green beans
1/4 cup
Baked potato
1 medium
Butter
2 tsp
Cookies
5 - 10
Apple
2 medium
SOCIOECONOMIC INFORMATION
Married, husband at home; 2 children at home, 1 male, 1 female
Income less than $550 per week
12th grade education level
Complete the following, using the information provided above:
1. Plot Rita’s weight gain on the weight gain grid provided on the next page.
2. Assess Rita for any nutritional risks and write those below.
3. Determine how much weight Rita should gain and the rate of gain.
4. Make dietary recommendations to be sent to her physician, giving your rationale for
these recommendations.
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167
Prenatal Weight Gain Grid
Name: ___________________________________________
60
58
Date: _________________ Weeks Gestation: ____________
56
Age: _________________ Height: ____________________
54
Prepregnant Weight: ________________________________
52
50
Desirable Weight: __________________________________
48
% Weight for Height: _____________ BMI: _____________
46
Weight Classification: _______________________________
44
Weight Gain Recommendation: ________________________
42
40
38
36
34
32
30
28
26
en
m
24
wo
t
h
22
en
ig
om
we
r
w
20
ht
de
un
eig
w
r
18
fo
al
rm
o
n
16
en
for
wom
t
h
14
eig
erw
v
o
12
for
men
o
w
10
bese
for o
8
6
4
2
0
-2
-4
0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42
Weeks Gestation
Weight in Pounds
60
58
56
54
52
50
48
46
44
42
40
38
36
34
32
30
28
26
24
22
20
18
16
14
12
10
8
6
4
2
0
-2
-4
Sexual & Reproductive Health
168
CASE STUDY DISCUSSION
“Rita” is 36 years old. Her previous pregnancies are unremarkable, with the exception of water retention with her last child. Her first child was not low birth weight, but
was small. She had rheumatic fever as a child. With a heart murmur, one could suspect
that there could be some heart damage. There is a family history of elevated blood
pressure on her mother’s side. Her low income could signal financial problems that
influence her diet and food availability.
With this pregnancy she was anemic, although her hemoglobin increased. Her
weight gain was satisfactory during the 1st trimester and early in the 2nd. Her weight
gain increased dramatically in the second half of pregnancy, beginning around the 20th
week and ending the 29th week. In 6 weeks, Rita gained 16 lb, an excessive amount.
Her diet history shows inadequacy in all nutrients. The caloric intake is approximately 800 to 850 kcal, which could not produce the rapid weight gain. Is she misrepresenting her diet history or has she radically altered her diet because her doctor was
upset with her dramatic weight gain? Since Rita’s weight gain is not due to diet, it must
be water gain. With Rita’s history of water retention during her last pregnancy, rheumatic fever and her mother’s history of elevated blood pressure, her weight gain could
be from preeclampsia.
She was evaluated and diagnosed with preeclampsia.
Treatment for Rita is to decrease activity and eat well. Rita’s diet must be improved. Calories, protein and nutrients must be increased. Rita’s weight gain was due to
water, masking a poor weight gain due to an inadequate diet. Calories are important,
particularly since it is the 3rd trimester and the fetus is growing rapidly.
A prenatal supplement is called for, with the inadequate diet and the anemia
earlier in pregnancy. The nutrients most important at this late stage in the pregnancy are
calories and protein for growth; calcium for blood pressure regulation and fetal skeletal
growth; iron for blood losses at delivery; magnesium for vasodilation and other vitamins and minerals at recommended levels. Also consider increasing her long chain fatty
acids (DHA) to ensure proper brain and eye development. If she is unable to eat foods
high in Ω-3 fatty acids, you can supplement with fish oil capsules or dietary flax seed
oil.
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169
© 2009, Nutrition Dimension, Inc.
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Appendix #1
183
Risk Factors Affecting Pregnancy Outcome
Use as a checklist with prenatal clients to determine nutritional risks
Prepregnancy weight status
_____ underweight
_____ overweight
Rate of weight gain
_____ inadequate
_____ excessive
Biochemical indices
_____ low hemoglobin
_____ low hematocrit
_____ high blood sugar
_____ proteinuria
Conditions associated with nutritional risk
_____ adolescence
_____ 5 or more previous pregnancies
_____ 12 months or less between delivery and
conception
_____ breastfeeding during pregnancy
_____ multiple pregnancy
_____ hyperemesis gravidarum
_____ preeclampsia
_____ gestational diabetes
Diabetes (before pregnancy):
_____ Type 1 (non-insulin dependent)
_____ Type 2 (insulin dependent)
© 2009, Nutrition Dimension, Inc.
Current medical/obstetrical complications
_____ hypertension
_____ diabetes
_____ heart disease
_____ renal disease
_____ liver disease
_____ cancer
_____ bariatric surgery
_____ other medical condition(s)
Other factors
_____ low income
_____ substance abuse
_____ alcohol use
_____ caffeine intake
_____ smoking
_____ medications (over-the-counter)
_____ prescription medications
_____ excessive vitamin/mineral supplements
_____ eating disorder
_____ pica
_____ psychological problems
_____ cultural food issues
_____ frequency of food intake
Inadequate intake of:
_____ meat and meat alternates
_____ milk and milk products
_____ breads and cereals
_____ vitamin A fruits and vegetables
_____ vitamin C fruits and vegetables
_____ other fruits and vegetables
Diet inadequate in:
_____ protein
_____ calories
_____ folic acid
_____ zinc
_____ vitamin B6
_____ vitamin B12
_____vitamin C
_____vitamin A
_____calcium
_____magnesium
_____ fiber
_____ Ω-3 fatty acids
Diet excessive in:
_____ calories
_____ fat
_____ sodium
Remember, how you ask a question is important if you want an honest answer. Nutrition
During Pregnancy and Lactation, National Academy Press, 1992, is an excellent reference. It has
many good ways to ask questions that are nonjudgmental.
Appendix #2
184
Recommended Dietary Allowances
Vitamins¶
© 2009, Nutrition Dimension, Inc.
FUNCTIONS
Pregnancy
RDA
Tolerable Intake
Levels (UL)1
VITAMIN C
Tooth & bone formation, healthy gums,
collagen, immunity, anti-oxidant
THIAMIN (B1)
Energy production; growth and functioning of
nerve tissue, memory and emotional stability
1.4 mg
Unknown
RIBOFLAVIN (B2)
Energy production, synthesis of fats and
amino acids; cell growth
1.4 mg
Unknown
NIACIN
Energy production, synthesis & breakdown
of fats, carbohydrates and proteins; synthesis of cholesterol, red blood 'cells + others
18 mg
35 mg
VITAMIN B6
Synthesis and breakdown of amino acids;
multiplication of cells; production of RBCs,
immune cells, neurotransmitters
1.9 mg
FOLATE
DNA, RNA synthesis, new cell growth, red
blood cells
VITAMIN B12
Growth, red blood cells, nervous system,
detox smog & tobacco smoke
VITAMIN A
Vision, skin, immunity, resistance to infection, antioxidant, cancer prevention
VITAMIN D
Formation of bones, teeth and cartilage; aids
absorption of calcium & phosphorus
VITAMIN E
(alpha-tocopherol)
Antioxidant – protects unsaturated fats in
cells from damage
VITAMIN K
Formation of blood clotting factors
BIOTIN
Coenzyme for metabolic reactions
30 μg*
CHOLINE
Structural interity of cell membranes; cell
signaling; lipid & cholesterol transport and
metabolism
450 mg*
PANTOTHENIC ACID
Component of coenzyme A and fatty acid
metabolism
≤ 18 yrs 80 mg
19-50 yrs 85 mg
2000 mg
≤ 18 yrs 80 mg
19-50 yrs 100 mg
600 μg DFE
1000 μg
2.6 μg
Unknown
≤ 18 yrs 750 μg
19-50 yrs 770 μg
5 μg*
(200 IU)
15 mg
≤ 18 yrs 75 μg*
19-50 yrs 90 μg*
6 mg*
¶ Note: Values are RDA unless followed by an asterisk. An asterisk denotes an AI value.
* AI (Adequate Intake) value, not RDA
1 Reference: IOM, Dietary Reference Intakes, National Academy Press 1997, 1998, 2000, 2001, 2002
Above
20,000 I.U.
50 μg
1000 μg
Unknown
Unknown
3.5 gm
Unknown
Appendix #3
185
Recommended Dietary Allowances
Minerals¶
FUNCTIONS
Tolerable Intake
Levels (UL)1
CALCIUM
Formation of bones and teeth; nerve impulses;
activating/relaxing smooth muscles; blood
clotting
IRON
Part of red blood cells; carries oxygen within the
body; involved in energy production, immunity
MAGNESIUM
Energy production; muscle relaxation; nerve
transmission; heart functions; dental health
SODIUM
Involved in nerve impulse, muscle action, water
and acid-base balance
none
Unknown
POTASSIUM
Involved in water balance, regulating muscle
actions, starting glycogen and protein synthesis
none
18 gm
ZINC
Essential for DNA, RNA, protein synthesis, skin
growth, wound healing, immune function, taste
COPPER
© 2009, Nutrition Dimension, Inc.
Pregnancy
RDA
Red blood cell formation; energy production;
immunity; protective wrapping around nerves;
aids formation of bone and collagen
≤18 yrs 1300 mg*
19-50 yrs 1000 mg*
2,500 mg
≤18 yrs 27 mg
19-50 yrs 27 mg
45 mg
≤18 yrs 400 mg
19-30 yrs 350 mg
31-50 yrs 360 mg
350 mg of
supplemental mg
≤18 yrs 13 mg
19-50 yrs 11 mg
1000 ug
≤ 18 yrs 34 mg
19-50 yrs 40 mg
≤ 18 yrs 8 mg
19-50 yrs 10 mg
60 μg
400 μg
≤18 yrs 29 μg*
19-50 yrs 30 μg*
Unknown
SELENIUM
Antioxidant; protects against free radicals;
enhances vitamin E
CHROMIUM
Component of glucose tolerance factor (GTF)
which helps get glucose into the cell; indirectly
affects level of fats in the blood
MANGANESE
Metabolism of amino acids, DNA, RNA, fatty
acids, cholesterol; formation of bones, teeth
2 mg*
≤ 18 yrs 9 mg
19-50 yrs 11 mg
IODINE
Regulates metabolism
220 μg
FLUORIDE
Inhibit and reverse dental caries
3 mg*
≤ 18 yrs 900 μg
19-50 yrs 1,100 μg
10 mg
PHOSPHORUS
Component of membranes; buffers; storage and
transfer of energy; activation of catalytic proteins
MOLYBDENUM
Enzyne cofactor
≤18 yrs 1,250 mg
19-50 yrs 700 mg
50 μg
¶ Note: Values are RDA unless followed by an asterisk. An asterisk denotes an AI value.
* AI (Adequate Intake) value, not RDA
1 Reference: IOM, Dietary Reference Intakes, National Academy Press 1997, 1998, 2000, 2001, 2002
UL for minerals: Boron 20 mg/day; Vanadium 1.8 mg/day; Nickel 1 mg/day
3.5 gm
≤ 18 yrs 1.7 mg
19-50 yrs 2 mg
Appendix #3A
186
Recommended Dietary Allowances
Macronutrients
Functions
ENERGY
Essential for the body's functions:
respiration, circulation, metabolism,
body temperature etc.
PROTEIN
Part of every cell: Necessary for
growth, maintenance of tissue and
tissue repair; horomone production;
immune function; fluid-electrolyte
balance; ace-base balance; tranport of
nutrients; energy; and blood clotting
FATTY ACIDS
Ω-3 alpha-linolenic acid
Ω-6 linoleic acid
General: Part of cell membranes;
prostaglandins: immunity, inflammation, blood clotting
Ω-3 (DHA): Development of fetal
nervous system and retina.
Pregnancy
RDA
≤18 years:(calories)
1st trimester: 2368
2nd trimester: 2708
3rd trimester: 2820
19-50 years: (calories)
1st trimester: 2403
2nd trimester: 2743
3rd trimester: 2855
1.1 gm/kg/day
or
Dietary Fiber: Increases fecal bulk,
aids laxation and ameliorates constipation.
Functional Fiber: delays gastric
emptying; increases sensation of
fulness; may reduce prostprandial
blood glucose; reduce serum cholesterol levels
© 2009, Nutrition Dimension, Inc.
CARBOHYDRATES
Provide energy to the cells, especially
the brain.
Simple sugars: monosaccharides,
disaccharides
Complex carbohydrates: polysaccharides (starches, grains etc)
Carbohydrates, protein
fats and alcohol all
provide energy
Meat, fish, poultry, eggs,
cheese, dairy products,
legumes, grains, rice,
soy, seeds, vegetables
0.8 gm/kg/day + 25 gm/day
13 gm*
1.4 gm*
Optimal ratio: 1 to 5 Ω-3 to Ω-6
FIBER
Food Sources
28 gm
(Total Fiber)
Total Fiber = Dietary fiber and
Functional fiber
Ω-3 fatty acids:
Fish, canola oil, flaxseed,
English walnuts, soybeans,
soybean oil
Ω-6 fatty acids:
Meat, dairy products, eggs,
vegetable oils (sunflower,
corn, safflower)
Dietary Fiber: Part of the
plant structure. Found in
bran, grains, vegetables,
legumes, nuts, seeds
Functional Fiber:Isolated or
extracted from plant
source includes: gums,
pectins, oligosaccharides.
Found in grains, vegetables, plant foods
175 gm/day
¶ Note: Values are RDA unless followed by an asterisk. An asterisk denotes an AI value.
* AI (Adequate Intake) value, not RDA
1 Reference: IOM, Dietary Reference Intakes, National Academy Press 2002
Simple sugars: table sugar,
lactose, fructose
Complex: grains, starches
found in breads, pasta,
cereals, legumes
187
Appendix #4
Body Mass Index Chart
Height (inches)
Weight
(lbs)
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
17.3
18.4
19.5
20.6
21.7
22.7
23.8
24.9
16.7
17.8
18.8
19.9
20.9
22.0
23.0
24.1
16.2
17.2
18.2
19.2
20.2
21.2
22.2
23.2
15.6
16.6
17.6
18.6
19.5
20.5
21.5
22.5
14.2
15.1
16.0
16.8
17.7
18.6
19.5
20.4
13.7
14.6
15.5
16.3
17.2
18.0
18.9
19.8
13.3
14.2
15.0
15.8
16.7
17.5
18.3
19.2
12.9
13.7
14.5
15.3
16.2
17.0
17.8
18.6
12.5
13.3
14.1
14.9
15.7
16.5
17.2
18.0
12.2
12.9
13.7
14.5
15.2
16.0
16.7
17.5
11.8
12.6
13.3
14.0
14.8
15.5
16.3
17.0
26.0
27.1
28.2
29.2
30.3
31.4
32.5
33.6
34.7
35.7
36.8
37.9
39.0
40.1
41.2
42.2
43.3
44.4
45.5
46.6
47.6
48.7
49.8
50.9
52.0
25.1
26.1
27.2
28.2
29.3
30.3
31.4
32.5
33.5
34.5
35.6
36.6
37.7
38.7
39.7
40.8
41.8
42.9
43.9
45.0
46.0
47.1
48.1
49.2
50.2
24.3
25.3
26.3
27.3
28.3
29.3
30.3
31.3
32.3
33.4
34.4
35.4
36.4
37.4
38.4
39.4
40.4
41.4
42.5
43.5
44.5
45.5
46.5
47.5
48.5
23.5
24.4
25.4
26.4
27.4
28.3
29.3
30.3
31.3
32.3
33.2
34.2
35.2
36.2
37.1
38.1
39.1
40.1
41.0
42.0
43.0
44.0
45.0
45.9
46.9
22.0
22.9
23.8
24.7
25.6
26.5
27.5
28.4
29.3
30.2
31.1
32.0
33.0
33.9
34.8
35.7
36.6
37.5
38.4
39.4
40.3
41.2
42.1
43.0
43.9
21.3
22.2
23.0
23.9
24.8
25.7
26.6
27.5
28.4
29.3
30.1
31.0
31.9
32.8
33.7
34.6
35.5
36.2
37.2
38.1
39.0
39.0
40.8
41.7
42.6
20.6
21.5
22.3
23.2
24.1
24.9
25.8
26.6
27.5
28.3
29.2
30.1
30.9
31.8
32.6
33.5
34.4
35.2
36.1
36.9
37.8
38.7
39.5
40.4
41.2
20.0
20.8
21.7
22.5
23.3
24.2
25.0
25.8
26.6
27.5
28.3
29.1
30.0
30.8
31.6
32.5
33.3
34.1
35.0
35.8
36.6
37.5
38.3
39.1
40.0
19.4
20.2
21.0
21.8
22.6
23.4
24.2
25.0
25.8
26.7
27.5
28.3
29.1
29.9
30.7
31.5
32.3
33.1
33.9
34.7
35.5
36.3
37.2
38.0
38.8
18.8
19.6
20.4
21.2
21.9
22.7
23.5
24.3
25.1
25.9
26.6
27.4
28.2
29.0
29.8
30.6
31.4
32.1
32.9
33.7
34.5
35.3
36.1
36.8
37.6
18.3
19.0
19.8
20.5
21.3
22.1
22.8
23.6
24.3
25.1
25.9
26.6
27.4
28.2
28.9
29.7
30.4
31.2
32.0
32.7
33.5
34.2
35.0
35.8
36.5
17.7
18.5
19.2
20.0
20.7
21.4
22.2
22.9
23.6
24.4
25.1
25.9
26.6
27.3
28.1
28.8
29.6
30.3
31.0
31.8
32.5
33.3
34.0
34.7
35.5
245
250
255
260
55.0
56.1
57.2
58.3
53.1
54.1
55.2
56.3
51.3
52.3
53.3
54.4
49.5
50.5
51.5
52.6
47.9
48.9
49.8
50.8
15.1
16.1
17.0
18.0
18.9
19.9
20.8
21.7
22.7
23.6
24.6
25.5
26.5
27.4
28.4
29.3
30.3
31.2
32.1
33.1
34.0
35.0
35.9
36.9
37.8
38.8
39.7
40.7
41.6
42.6
43.5
44.4
45.4
46.3
47.3
48.2
49.2
14.6
15.6
16.5
17.4
18.3
19.2
20.1
21.1
120
125
130
135
140
145
150
155
160
165
170
175
180
185
190
195
200
205
210
215
220
225
230
235
240
18.0
19.1
20.2
21.3
22.4
23.6
24.7
25.8
26.9
28.0
29.2
30.3
31.4
32.5
33.7
34.8
35.9
37.0
38.1
39.3
40.4
41.5
42.6
43.8
44.9
46.0
47.1
48.2
49.4
50.5
51.6
52.7
53.9
44.9
45.8
46.7
47.6
43.4
44.3
45.2
46.1
42.1
43.0
43.8
44.7
40.8
41.6
42.5
43.3
39.6
40.4
41.2
42.0
38.4
39.2
40.0
40.8
37.3
38.0
38.8
39.6
36.2
37.0
37.7
38.4
11.5
12.2
12.9
13.6
14.4
15.1
15.8
16.5
17.2
18.0
18.7
19.4
20.1
20.8
21.5
22.3
23.0
23.7
24.4
25.1
25.9
26.6
27.3
28.0
28.7
29.4
30.2
30.9
31.6.
32.3
33.0
33.7
34.5
35.2
35.9
36.6
37.3
© 2009, Nutrition Dimension, Inc.
80
85
90
95
100
105
110
115
BMI =
weight (kg)
height (M)2
(Convert pounds to kilograms by dividing by
2.2. Example: 143 lbs. divided by 2.2 = 65 kg)
Source: NAS, Nutrition
During Pregnancy, 1990.
Appendix #5
188
Optimal Weight Gain for Twin Pregnancies
Rates of Weight Gain (pounds/week)
Prepregnancy BMI
0-20 Weeks
20-28 Weeks
28 Weeks to delivery
Underweight:
BMI <19.8
1.25 - 1.75
1.50 - 1.75
1.25
Normal:
BMI 19.8 - 26.0
1.0 - 1.50
1.25 - 1.75
1.0
Overweight:
BMI 26 - 29
1.0 - 1.25
1.0 - 1.50
1.0
Obese:
BMI >29
0.75 - 1.0
0.75 - 1.25
0.75
© 2009, Nutrition Dimension, Inc.
Cumulative Weight Gain (pounds)
Prepregnancy BMI
0-20 Weeks
20-28 Weeks
28 Weeks to delivery
Underweight:
BMI <19.8
25 - 35
37 - 49
50 - 62
Normal:
BMI 19.8 - 26.0
20 - 30
30 - 44
37- 54
Overweight:
BMI 26 - 29
20 - 25
28 - 37
31 - 50
Obese:
BMI >29
15 - 20
21 - 30
25 - 42
Adapted from Luke B, Hediger ML, Nugent C, et al. Body mass index specific-weight gains associated with optimal
birthweights in twin pregnancies. J Repro Med. 48:217-224, 2003.
Weight Gain During Pregnancy: Reexamining the Guidelines, IOM and NRC, National Academies Press, 2009.
Appendix #6
189
Prenatal Weight Gain Grid
Normal Prepregnancy Weight
© 2009, Nutrition Dimension, Inc.
60
58
Date: _________________ Weeks Gestation: ____________
56
Age: _________________ Height: ____________________
54
Prepregnant Weight: ________________________________
52
50
Desirable Weight: __________________________________
48
% Weight for Height: _____________ BMI: _____________
46
Weight Classification: _______________________________
44
Weight Gain Recommendation: ________________________
42
40
38
36
34
32
30
28
26
24
22
20
18
16
14
12
10
8
6
4
2
0
-2
-4
0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42
Weight in Pounds
Name: ___________________________________________
Weeks Gestation
IOM, Weight Gain During Pregnancy, Reexamining the guidelines, 2009.
Appendix #7
190
© 2009, Nutrition Dimension, Inc.
Prenatal Weight Gain Grid
Name: ___________________________________________
60
58
Date: _________________ Weeks Gestation: ____________
56
Age: _________________ Height: ____________________
54
Prepregnant Weight: ________________________________
52
50
Desirable Weight: __________________________________
48
% Weight for Height: _____________ BMI: _____________
46
Weight Classification: _______________________________
44
Weight Gain Recommendation: ________________________
42
40
38
36
34
32
30
28
26
en
24
om
tw
h
22
en
ig
om
we
r
w
20
ht
de
un
eig
w
r
18
fo
al
rm
o
n
16
n
for
ome
w
t
14
eigh
erw
v
o
12
for
men
o
w
10
bese
for o
8
6
4
2
0
-2
-4
0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42
Weight in Pounds
60
58
56
54
52
50
48
46
44
42
40
38
36
34
32
30
28
26
24
22
20
18
16
14
12
10
8
6
4
2
0
-2
-4
Weeks Gestation
IOM, Weight Gain During Pregnancy, Reexamining the guidelines, 2009.
191
Appendix #8
Healthy Food Choices
Milk &
Milk Products
3-4 cups/day
Meat &
Meat Alternates
6-8 oz/day
Fruits
2-3 cups/day
Vegetables
3-4 cups/day
© 2009, Nutrition Dimension, Inc.
Breads & Cereals
7-11 ounces/day
SMARTEST CHOICES
USE SPARINGLY
Nonfat milk
Lowfat milk (1%)
Buttermilk
Plain lowfat yogurt
Skimmed milk cheese
Low fat cottage cheese
Nonfat milk mozarella,
ricotta, farmer's, feta cheese
Whole milk
Reduced fat (2%)
Fruit-flavored yogurt
Cream
Cream soups
Regular cheese
Creamed cottage cheese
Beef: flank, round, lean cuts
Pork: leg, ham (smoked)
Lamb: leg, sirloin, shank
Fish: tuna (in water), fish
Lean luncheon meat
Poultry: chicken, turkey (breast)
Cornish hen (no skin)
Dried beans, peas (kidney,
lima, soy, lentils, navy)
Tofu
Nuts, seeds, peanut butter*
Rib roast, chuck, brisket
Bacon, ribs, loin
Tuna in oil
Cold cuts, hot dogs, sausage
Capon, duck, goose
Fried meats
Fresh fruit, unsweetened
canned fruit & juice
Canned syrup, sweetened
juice, nectars, juice
drinks
Fresh, frozen or canned
vegetables
Avocadoes, olives
Unsweetened dry or cooked
cereal
Whole grain or enriched
bread
Rice, pastas, noodles
Tortillas
Potatoes
Bread sticks, whole grain
crackers, rice cakes
Bagels
Graham crackers
Sugar- or honey-coated,
granola
Sweet rolls, pastries,
coffeecake, croissants
Fried rice, fettucini
Tortilla chips
French fried, creamed, chips
Snack crackers
* Use with moderation. Contain high amount of fat (unsaturated), but can add lots of calories.
© 2009, Nutrition Dimension, Inc.
Appendix #9
192
Appendix #9A
193
Daily Food Guide Feedback Form
Food Group
Recommended amount per day
(in ounces and cups)
Meat & Meat Alternates
_______________
Milk & Milk Products
_______________
Fruits
_______________
Vegetables
_______________
Breads & Cereals
_______________
Fats, Oils & Sweets
_______________
Specific Recommendations
FEEDBACK FORM
Food Group
I ate:
My total
should be:
_____
_____
Animal
_____
_____
Plant
_____
_____
Milk
_____
_____
Fruits*
_____
_____
_____
_____
_____
_____
_____
_____
Breads/Cereals*
_____
_____
Whole grain
_____
_____
_____
_____
Meat/Protein*
Vit. A, C fruit
Vegetables*
Vit. A, C vegetable
Fats, Oils & Sweets**
© 2009, Nutrition Dimension, Inc.
Amount Eaten
Record the amount of food that you ate today in each food group. Each box equals either one ounce or one cup,
based on the food group. The total amount eaten in each group should equal or exceed what you are allowed in your
personal meal plan, developed for you by your nutrition counselor.
*The amount eaten in these groups is counted by totaling the recommended sub-groups along with the main group.
**The number of servings in this group is based on your caloric needs and varies from day to day.
Appendix #10
194
Food Frequency Form
Please check the column that shows how often you eat the following foods.
Check only one column for each food.
Name___________________________
Date____________________________
2-4
Times
a Day
Once
Daily
2-4
Times
a Week
Once
Weekly
Hardly
Ever or
Never
© 2009, Nutrition Dimension, Inc.
Beef, pork, ham, hamburger
Luncheon meats, hot dogs
Chicken, turkey, poultry
Fish, seafood
Eggs
Dried peas or beans (legumes)
Peanut butter
Nuts
Cereals (dry or cooked)
Grains
Breads, rolls, biscuits
Tortillas
Crackers
Rice
Pasta, noodles, spaghetti, macaroni
Milk
Cheese
Yogurt, pudding, custard
Fruits
Fruit juices
Vegetables
Water
Added Fat
Coffee, tea, cocoa
Sodas, fruit flavored drinks
Alcohol: beer, wine, whiskey
Candy, sweets
Cakes, pies, cookies, donuts, sweet rolls
Potato chips, pretzels, corn/tortilla chips
Ice cream
WEEKLY TOTALS:
Meat ___________________
Poultry __________________
Fish ____________________
Legumes ________________
Eggs ___________________
Breads & cereal ___________
Rice & pasta _____________
Fruits & juices* ___________
Vegetables* ______________
Dairy products ____________
Water ___________________
Sodas __________________
Alcohol _________________
Cakes, pies ______________
Chips ___________________
Ice cream ________________
Candy __________________
Fats ____________________
Other ___________________
*Ask types to determine if they are high in vitamin A or C
Appendix #11
195
Solutions to Common Pregnancy Problems
PROBLEM
Inadequate
Weight Gain
Heartburn
© 2009, Nutrition Dimension, Inc.
Constipation
Leg Cramps
SOLUTION
• Exercising and not eating enough - add food and calories to your diet
• Nausea and vomiting - see Appendix #13
• Afraid to gain weight - talk with a professional to help you gain the weight you need
• Increase to the maximum the servings of foods from the Food Guide Pyramid
• To increase calories in your diet: eat foods with more fat; eat small meals more often;
drink high-calorie, nutritious beverages such as yogurt smoothies, milkshakes, juice
drinks; eat sweets and high-calorie desserts once all your requirements for nutritious
foods are met
• Have your diet analyzed to determine what you may be missing if you are unable to
increase your food intake
• Keep food or beverages nearby at all times to eat or drink throughout the day
• Set a timer to remind yourself to eat
• Eat 4-6 times a day instead of 3 meals a day
• Avoid getting too full
• Drink liquids between meals if you feel too full
• Avoid greasy, highly seasoned food and coffee and cigarettes
• Wear clothing that is loose around the waist
• Do not lie down immediately after a meal
• Sleep and rest with your head slightly elevated
• Sip water, milk or juice when you have heartburn
• Take a walk, sit up, or sit quietly and breathe deeply when you have heartburn
• Use antacids that do not contain aluminum
• Eat high fiber foods: fruits, vegetables, whole grain, dried peas and beans, nuts
• Eat oatmeal, applesauce, legumes and barley to soften the stool
• Drink plenty of water, six 8 oz glasses per day
• Exercise daily to stimulate your intestines
• Iron supplements can cause constipation. Determine if you can decrease your dose. If not,
take with prune juice
• Use bulk-producing laxatives, such as Metamucil or Effersyllium, as they are not absorbed
into the body
• Raise your feet on a stool during bowel movements to reduce straining
• Check with your doctor before using any over-the-counter laxatives as there may be
ingredients harmful to your baby
• Eat foods high in calcium: milk, yogurt, cheese, pudding, sardines, canned salmon, tofu,
almonds, baked beans, tortillas treated with lime, broccoli, amaranth
• Eat foods high in magnesium: avocado, beans (garbanzo, kidney, navy, pinto, soy), broccoli,
greens, bran or whole wheat cereal, peanuts, peanut butter, tofu, whole wheat bread, whole
wheat muffins, sesame butter (tahini) and lima beans
• Avoid excess phosphate in animal products such as meat and milk and in carbonated
beverages (soda) and processed foods
• Supplement calcium (600 mg) and magnesium (320 mg) if diet is inadequate
• Do not use calcium phosphate as a supplement
Appendix #12
196
Folate Content of Selected Foods
© 2009, Nutrition Dimension, Inc.
Food
Common Measure
Folate (mcg)
Beverages
Orange juice
Pineapple juice
Tomato juice
Peach Nectar
Apple juice
4 fl oz
4 fl oz
4 fl oz
4 fl oz
4 fl oz
55
30
25
2
0.5
Fruits
Avocado
Orange
Papaya
Blackberries
Raspberries
Grapefruit
Canteloupe or strawberries
Banana
Pear
Pineapple, canned
Peaches, canned
Grapes or watermelon
Apple
1/2 medium
1 medium
1 cup
1 cup
1 cup
1 medium
1 cup
1 medium
1 medium
1 cup
1 cup
1 cup
1 medium
60
40
53
49
32
24
27
22
15
12
8
4
0.5
Legumes (dried peas & beans)
Lentils, cooked
Pinto beans, cooked
Lima beans, baby, cooked
Black beans, cooked
Kidney beans, cooked
Navy beans, cooked
Split peas, cooked
Miso, fermented soybeans
Tempeh
Tofu, raw, firm
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
358
294
273
25
229
163
127
91
86
74
Vegetables
Spinach, cooked
Asparagus, cooked
Green peas, cooked
Broccoli, cooked
Lettuce, raw
Green beans, cooked
Squash, zucchini
Corn on the cob
Sweet potato, cooked
Potato, baked
Carrots, raw
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 ear
1 cup
1 medium
1 medium
262
190
94
78
75
41
30
38
35
22
10
Dairy Products, Eggs & Margarine
Milk, all kinds
Egg, whole
Ricotta cheese
Yogurt, plain, nonfat
Cheese, cottage
Cheese, parmesan, grated
8 fl oz
1 medium
1 cup
1 cup
1 cup
1 cup
15
23
32
28
30
8
Fish/Seafood
Crab or mussels, cooked
Tuna, canned
Most other fish
1 cup
1/2 cup
4-6 oz
65
4
5-15
Food
Common Measure
Folate (mcg)
Meat and Poultry
Liver, chicken, cooked
Liver, beef or pork, cooked
Chicken giblets, cooked
Beef or pork, cooked
Frankfurter
Chicken or turkey, cooked
Turkey, cooked
Sausage
Bacon
1 cup
1 oz
1 cup
1 oz
1
1 oz
1 oz
1
1 slice
1077
62
545
2
2
2
2
0.5
0.3
Breads/Crackers¶
Roll, hard
English muffin
Bread (various kinds)
Roll, hamburger
Muffin
Bagel
Tortilla, corn
Cornbread
Crackers (various kinds)
1
1
1 slice
1
1
1
1
1 2"x2" square
1
40
20
8-16
15
15
13
6
5
0.3-1
Cereals (non-sugar coated)
Total
Product 19
Grape-nuts
All-Bran
Raisin Bran
Bran Chex
Wheaties
Rice Krispies
Oat Bran
Oatmeal, cooked
Malt-o-Meal, cooked
Cheerios
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
466
466
402
301
130-201
143
102
100
48
9
5
5
Pasta & Grains
Wheat germ, crude
Brewers yeast, dry
Amaranth, uncooked
Quinoa, dry
Flour, rye, dark
Cornmeal, dry*
Flour, wheat & whole grain*
Flour, white*
Millet, cooked
Rice, wild, cooked
Bulgur, cooked
Couscous, cooked
Barley, pearled, cooked
Spaghetti, cooked*
Macaroni, cooked*
Rice, brown/white, cooked
1 cup
1 Tbsp
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
1 cup
324
313
95
83
77
66/220
53/64
32/192
46
43
33
27
26
17/98
10/95
8/6
Snack Foods
Chocolate chip cookie
Danish pastry
Cake donut
Apple pie
1
1
1
1 slice
7
43
21
37
¶Some of these products are made from enriched flour, some are not. The folic acid content will vary based on the type of flour
used.
* These foods have two values. The first value is for an unenriched version of the product the second is for the enriched version of
the product; which has folic acid added.
Appendix #13
197
Handling Nausea & Vomiting During Pregnancy
The Problem
Many women experience nausea and vomiting with their pregnancy. For some women the problem is minor
and stops by the 12th to 20th week of pregnancy. Other women experience more severe problems that do
not go away and continue to get worse. Outlined here are strategies to deal with the problem and to prevent
problems from occurring. Remember, the physical and hormonal changes of pregnancy are causing the
nausea/vomiting and it will go away.
How To Get Started
Identify what may trigger your nausea. Some examples include:
• smells — food, cooking food, coffee, perfume, soap, animals, mold, etc.
• motion — abrupt movements, rocking, jarring, bumpy rides, etc.
• tastes — specific foods such as meat, fried foods, spicy foods
• fatigue
Keep a journal to help identify problem areas for you. You will often find that a solution appears to you once
you know what the problem is. Include the following in your journal or log:
• time of day
• activity
• noise
• trigger (if you can identify it)
• food eaten
• food desired
• beverages, including water
• how you felt
• notes for yourself
Determining What to Eat
There is no right way or wrong way to eat if you are battling nausea and vomiting.The goal is to eat foods
and drink beverages that stay down. Always ask yourself what you want to eat or what sounds good to you,
and then eat it. Foods can have a variety of characteristics that may help you identify what you want to eat:
• flavor — sweet, sour, bitter, salty, spicy, bland
• consistency — thin, thick, lumpy, smooth, hard
• texture — crunchy, soft
• temperature — hot, cold, room temperature
© 2009, Nutrition Dimension, Inc.
Figure out if certain foods work for you at certain times of the day or under certain circumstances. There are
no rules or restrictions for what works. If you want potato chips for breakfast, eat them! Try to let go of your
preconceptions to find solutions.
Preventing Problems
If your nausea does not go away, do the following:
1. Take a multivitamin and mineral supplement to provide nutrients you are not getting in your diet.
2. See a Registered Dietitian (RD) who can analyze your diet and intake and help you with it.
3. Monitor your weight and weight gain. This is the biggest problem that can affect the fetus. The RD or
your health care provider will monitor your weight as well to determine if there is a problem.
4. Dehydration can be a problem with poor fluid intake and vomiting. Try to find beverages that you can
tolerate. If you are experiencing problems, see your health care provider.
Appendix #14
198
Sources of Omega-3 Fatty Acids
100 gm (3.5 oz) portion sizes
© 2009, Nutrition Dimension, Inc.
Food
Total Fat
(gm)
Total
saturated
(gm)
Total
Total
monounsaturated polyunsaturated
(gm)
(gm)
18:3
(gm)
20:5†
(gm)
22:6†
(gm)
Cholesterol
(mg)
Anchovy, european
Bluefish
Catfish, channel
Cod, Atantic
Eel, european
Flounder, unspecified
Halibut, Pacific
Herring, Pacific
Mackerel, Atlantic
Ocean perch
Pollock
Sablefish
Salmon, chinook
Salmon, pink
Snapper, red
Swordfish
Trout, rainbow
Tuna, albacore
Whitefish, lake
Crab, Dungeness
Crayfish
Lobster, northern
Shrimp, unspecified
Clam, littleneck
Mussel, blue
Oyster, Pacific
Scallop, Atlantic
Squid, unspecified
4.8
6.5
4.3
.7
18.8
1.0
2.3
13.9
13.9
1.6
1.0
15.3
10.4
3.4
1.2
2.1
3.4
4.9
6.0
1.0
1.4
.9
1.1
.8
2.2
2.3
.8
1.1
1.3
1.4
1.0
.1
3.5
.2
.3
3.3
3.6
.3
.1
3.2
2.5
.6
.2
.6
.6
1.2
.9
.1
.3
.2
.2
.1
.4
.5
.1
.3
1.2
2.9
1.6
.1
10.9
.3
.8
6.9
5.4
.6
.1
8.1
4.5
2.1
.2
.8
1.0
1.2
2.0
.2
.4
.2
.1
.1
.5
.4
.1
.1
1.6
1.6
1.0
.3
1.4
.3
.7
2.4
3.7
.5
.5
2.0
2.1
1.7
.4
.2
1.2
1.8
2.2
.3
.3
.2
.4
.1
.6
.9
.3
.4
—
—
Tr
Tr
.7
Tr
.1
.1
.1
Tr
—
.1
.1
.2
Tr
—
.1
.2
.2
—
Tr
—
Tr
Tr
Tr
Tr
Tr
Tr
0.5
.4
.1
.1
.1
.1
.1
1.0
.9
.1
.1
.7
.8
.3
Tr
.1
.1
.3
.3
.2
.1
.1
.2
Tr
.2
.4
.1
.1
0.9
.8
.2
.2
.1
.1
.3
.7
1.6
.1
.4
.7
.6
.5
.2
.1
.4
1.0
1.0
.1
Tr
.1
.1
Tr
.3
.2
.1
.2
—
59
58
43
108
46
32
77
80
42
71
49
—
—
—
39
57
54
60
59
158
95
147
—
38
—
37
—
Beef, roast
Chicken, raw, white*
Pork, fresh, ham
Linseed oil
Canola oil
Soybean oil
Salad dressing**
Salad dressing**
Margarine**
Avocados
Beans, dry
Lentils
Soybeans, dry
Walnuts, English
Broccoli
Spinach
23.0
1.7
20.8
100.0
100.0
100.0
35.7
79.4
60.8
17.3
1.5
1.2
21.3
61.9
.4
.4
10.0
.4
7.5
9.4
6.8
14.4
6.0
11.8
14.1
2.6
.2
.2
3.1
5.6
Tr
Tr
10.8
.4
9.7
20.2
55.5
23.3
8.3
22.7
26.0
11.2
.1
.2
4.4
14.2
Tr
Tr
.9
.4
2.2
66.0
33.3
57.9
19.8
41.3
18.1
2.0
.9
.5
12.3
39.1
.2
.1
0.3
Tr
.2
53.3
11.1
6.8
2.5
4.2
1.6
.1
.6
.1
1.6
6.8
.1
.1
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
73
58
74
0
0
0
0
59
0
0
0
0
0
0
0
0
†Plants and meats do not contain 20:5 and 22:6 fatty acids — means no data available. Tr=<0.05 grams per 100 grams of food.
*Chicken is white meat, raw, without the skin.
**The amount of fat and Ω-3 fats is dependent upon the ingredients in these products. Salad dressings and margarine do not
contribute significantly to the Ω-3 content of the American diet.
Source: Table on the content of Ω-3 fatty acids and other fat components in selected foods, USDA, Nutrition Research Data
Branch, Human Nutrition Information Service, HNIS/PT-103, 1986.
Appendix #15
199
Medicinal Herbs Considered Not Appropriate
for Use During Pregnancy or Lactation
Agnus Castus
Asafoetida
Bogbean
Broom
Calamus
Chamomile, Roman
Cola
Cornsilk
Dong Quai
Eupatorium
Foxglove
Germander
Ground Ivy
Heliotropium
Horsetail
Juniper
Mandrake
Melilot
Nettle
Petasites
Pokeroot
Queen's Delight
Rhubarb
Senna
Squill
Uva-Ursi
Wormwood
Aloes
Aristolochia
Boldo
Buchu
Calendula
Chaparral
Coltsfoot
Crotalaria
Dogbane
Euphorbia
Frangula
Ginseng
Eleuthero
Groundsel
Hops
Horseradish
Life Root
Maté
Mistletoe
Osha
Plantain
Poplar
Ragwort
Rue
Shepherd's Purse
St. John's Wort
Vervain
Yarrow
Angelica
Avens
Boneset
Buckthorn
Cascara
Cohosh, Black
Comfrey
Damiana
Ephedra
Fenugreek
Fucus
Ginseng, Panax
Guarana
Horehound, Black
Hydrocotyle
Licorice
Male Fern
Motherwort
Passionflower
Pleurisy Root
Prickly Ash
Raspberry
Sassafras
Skunk Cabbage
Tansy
Wild Carrot
Yellow Dock
Apricot Kernel
Blue Flag
Borage
Burdock
Chamomile, German
Cohosh, Blue
Cottonroot
Devil's Claw
Eucalyptus
Feverfew
Gentian
Goldenseal
Hawthorne
Horehound, White
Jamaican Dogwood
Lobelia
Meadowsweet
Myrrh
Pennyroyal
Podophyllum
Pulsatilla
Red Clover
Scullcap
Stephania
Tonka Bean
Willow
Yohimbe
© 2009, Nutrition Dimension, Inc.
Exclusion from this list should not be construed as a recommendation for safety. Unless proven safe, herbs should not be used
during pregnancy. Foote J and Rengers B. Nutrition in Complementary Care. A Dietetic Practice group of the ADA. Volume 2(2). Winter, 2000.
Additional Resources about Herbs:
Alternative Medicine Foundation:
American Botanical Council:
Consumer Healthcare Products Association:
Consumerlab.com:
Council for Responsible Nutrition:
Herb Research Foundation:
National Center for Complementary and Alternative Medicine:
National Institutes of Health: Office of Dietary Supplements:
Supplement Watch:
United States Pharmacopoeia:
www.amfoundation.org
www.herbalgram.org
www.chpa-info.org
www.consumerlab.com
www.crnusa.org
www.herbs.org
http://nccam.nih.gov
http://dietary-supplements.info.nih.gov
www.supplementwatch.com
www.usp.org
Appendix #16
200
Vegetarian Food Pyramid
Fats:
2 servings
Legumes,
nuts & other
protein-rich foods:
5 servings
Grains:
6 servings
Medium fruit, 1
Cut up or cooked fruit,
1/2 cup (125 mL);
Fruit juice, 1/2 cup (125 mL);
Dried fruit, 1/4 cup (60 mL)
Cooked vegetables, 1/2 cup (125 mL);
Raw vegetables, 1 cup (250 mL);
Vegetable juice, 1/2 cup (125 mL)
m-
ric
hf
ood
s: 8
Bok
cho
c
mus ollards, y, broc
coli,
tard
Chin
g
1 cu reens, ese cabb kale
or
p(
ag
r
Forti
fied aw 2 cup 250 mL okra coo e, ,
toma
ked,
s (50 ), or
Cow
to ju
s mi
1/2
ice 1 0 mL);
lk
c
/ 2 cu
Tem up (125 or yog
p (1
pe
u
m
Alm
25 m
ond h or cal L); Che rt or for
s
L)
1/2 esame t s 1/4 cu cium-se ese 3/4 tified s
o
t
a
p
o
y
t
cup
h
(125 ini, 2 tb (60 mL ofu 1/2 c z (21 gm milk,
up
sp
);
)
mL)
; So (30 mL Almond (125 m ;
ynut
L
s 1/4 ); Cooke butter o );
r
d
1 oz
cup
(60 soybean
(28
mL)
gm)
s
calc
ium
-for
tifie
d br
eakf
ast
cere
al
Vegetables:
4 servings
lciu
Fort
if
juice ied
1
(125 / 2 cup
m
Figs L);
,5
Fruits:
2 servings
Ca
fruit
oil,
margarine,
or mayonnaise,
1 tsp (5mL)
ser
vin
gs
Cooked beans, peas, or lentils, 1/2 cup (125 mL);
Tofu or tempeh, 1/2 cup (125 mL);
Nut or seed butter, 2 tbsp (30 mL);
Nuts, 1/4 cup (60 mL);
Meat analog, 1 oz (28 gm);
Egg 1
Bread, 1 slice;
Cooked grain or cereal, 1/2 cup (125 mL);
Cooked grain or cereal, 1/2 cup (125 mL);
Ready-to-eat cereal, 1 oz (28 gm)
Modification to the Food Guide Pyramid
During pregnancy include the following:*
B12 - rich foods
4 servings
Beans/nuts/seeds/ eggs
7 servings
Calcium-rich foods
8 servings
*The number of servings in each group is the minimum amount needed. The minimum number of servings from other groups
is not different from the Vegetarian Food Guide above. Additional foods can be chosen from any of the groups in the
Vegetarian Food Guide to meet energy needs.
© 2009, Nutrition Dimension, Inc.
Recommendations for Pregnant Vegetarians
Pregnant lacto-ovo-vegetarians:
• Emphasize dietary iron, folate, vitamin D and zinc
• Daily iron and folic acid supplement
Pregnant vegans:
• Emphasize calories, iron, folic acid, vitamin D, calcim, zinc, vitamin B12 and protein
• Daily iron and folic acid supplement and vitamin D if sunlight exposure is limited
• Reliable source of vitamin B12 daily
Examination
201
NW109
Answer each question by checking the correct answer online or filling the circle corresponding to the correct answer on the answer sheet. There is one best answer for each question. If you want a record of your
answers, photocopy the answer sheet or record your choices on another piece of paper. Do not detach the
examination from the book. This exam has 40 questions.
1. The onset of the symptoms of PMS occurs:
a. at the beginning of the menstrual cycle
b. at the end of the menstrual cycle
c. 7 to 14 days prior to menstruation
d. 21 days prior to menstruation
e. 2 to 3 days prior to ovulation
2. Which of the following nutrients has solid evidence that supplementation can reduce symptoms of
PMS, including water retention, mood changes and food cravings?
a. magnesium b. evening primrose oil
c. complex carbohydrates
d. calcium
e. vitamin B6
3. Which active ingredient in the herb chasteberry improves fluid retention in PMS?
a. opiods
b. estrogen-like substance
c. progesterone-like substance
d. β-endorphins
e. flavonoids
4. Norethisterone, an older progestogen, and levonorgestrel, found in OCA have what effect on serum
lipids?
a. increase total cholesterol and HDL cholesterol
b. decrease total cholesterol and increase free fatty acids
c. decrease total cholesterol and free fatty acids
d. increase LDL cholesterol and decrease HDL cholesterol
e. have no measurable effect
© 2009, Nutrition Dimension/Gannett Education, Inc.
5. The hormone dose in oral contraceptives is higher now than when first introduced.
a. True b. False 6. Two nutrients whose requirement increases while using oral contraceptives are:
a. calcium and folic acid
b. vitamin A and B6
c. vitamin B6 and folic acid
d. iron and zinc
e. vitamin D and selenium
Exam, cont’d
202
NW109
7. Women using oral contraceptives have a lower risk for venous thromboembolytic disease, including
deep vein thrombosis and pulmonary embolism, than women who are pregnant.
a. True b. False
8. Of the following supplemental levels of vitamin B6, which is considered safe?
a. no level is safe
b. 100 mg
c. 250 mg
d 500 mg
e. 600 mg
9. The most important controllable factors determining the perinatal mortality rate are:
a. prenatal care and adequate nutrition
b. giving birth in a hospital and vitamin supplements
c. sophisticated medical equipment and hospital births
d. socioeconomic status and adequate nutrition
e. education level and attitude
10. A mother, underweight prior to pregnancy, who does not gain adequately during pregnancy, will
deliver an infant who is at higher risk for:
a. macrosomia, coronary heart disease and cancer
b. low birth weight, coronary heart disease and diabetes
c. macrosomia, diabetes and autoimmune disease
d. hypertension, cancer and heart failure
© 2009, Nutrition Dimension/Gannett Education, Inc.
11. The plasma volume expands during pregnancy by 20 to 100 percent. Why is this plasma volume
expansion critical?
a. to ensure an adequate supply of white blood cells
b. for adequate perfusion of the placenta
c. for digestion and absorption of nutrients
d. to ensure adequate hormonal production
e. to form the baby’s blood supply
12. Which of the following metabolic changes occur during pregnancy?
a. shift to glucose as a primary energy source for the mother
b. shift to the use of fat as a primary energy source for the mother
c. decreased sensitivity of maternal tissues to insulin
d. a and c
e. b and c
13. Which nutrient(s) does the fetus use as its primary energy source?
a. fat b. protein c. glucose d. a, b, and c e. a and b
Exam, cont’d
203
NW109
14. Which nutrients are transported across the placenta against a concentration gradient, allowing the
mother to become deficient if her intake is inadequate?
a. calcium, B6, zinc b. amino acids, calcium, iron, DHA
c. zinc, iron, folic acid, DHA
d. iron, folic acid, B6
e. all minerals
15. What recommendation would you give to a pregnant woman who wants to eat fish to meet her Ω-3
fatty acid requirement?
a. Eat two servings per week of fish that are low in mercury, such as salmon, shrimp and light tuna.
b. Eat two servings per week of fish that are low in mercury, such as shark and swordfish.
c. Eat one serving of fish a day or intake is inadequate to meet the needs of the mother and fetus.
d. Do not eat any fish, as all fish is unsafe to eat.
16. If a pregnant woman has edema, she should always limit her salt intake.
a. True
b. False
17. Which nutrients are critical during the first trimester of pregnancy?
a. magnesium and folate
b. iron and zinc
c. zinc and folate
d. calcium and zinc
e. copper and iron
18. NC is 19 years old, in her 16th week of pregnancy and smokes 1.5 packs of cigarettes a day. At the
clinic her hemoglobin is 10.3 gm/dl and her hematocrit is 31 percent. Is she anemic?
a. No
b. Yes
© 2009, Nutrition Dimension/Gannett Education, Inc.
19. Which of the following was the main reason for the publication of new weight gain guidelines in 2009
by the Institute of Medicine:
a. The amount of weight gain necessary for a healthy pregnancy had been too low.
b. An increase in small-for-gestational age babies indicating women were not gaining enough weight during pregnancy.
c. The complications of pregnancy were increasing due to improper weight gain recommendations.
d. Women are now gaining too much weight during pregnancy, having large-for-gestational age babies and retaining excess weight.
20. A pregnant woman who is underweight at conception should gain how many pounds? a. 15 to 22 b. 20 to 29
c. 25 to 34
d. 28 to 40
e. as much as possible
Exam, cont’d
204
NW109
21. CR is 5'7" and weighed 115 lb prior to pregnancy. At the end of her second trimester CR had gained a
total of 12 lb — 5 lb her first trimester and 7 lb the second trimester. Which of the following statements
best reflects her weight gain so far?
a. the weight gained both trimesters is adequate
b. not enough weight was gained during the first trimester
c. the weight gain during the second trimester was inadequate
d. the weight gained both trimesters is inadequate
22. Excessive weight gain, above IOM recommendations, increases maternal body fat and can lead to what
potential problem?
a. increased risk for large for gestational age babies
b. decreased heart rate
c. glucose intolerance in the fetus
d. excess water retention
e. it doesn't matter how much a woman gains, the more the better
23. It is impossible for a pregnant vegetarian to get adequate nutrients from the diet:
a. True
b. False
24. If an obese women with a BMI of 39 prior to pregnancy gains only two pounds by the beginning of the
third trimester, what do you recommend?
a. that she immediately gains at least a pound a week.
b. that she gains at least 15 pounds in the third trimester
c. that she gains as much weight as the fetus will weigh
d. do not worry about weight gain if her diet is adequate in calories, protein and other nutrients
e. that she increases her intake to at least six meals a day so she begins to gain weight
© 2009, Nutrition Dimension/Gannett Education, Inc.
25. Which of the following foods has the same amount of calcium as an 8 oz glass of milk?
a. 2 cups tofu
b. 1 cup amaranth c. 1.5 cups dark green leafy vegetables
d. all of the above e. none of the above
26. Which of the following food groups are most likely to be inadequate in the diet of pregnant women?
a. fruits, meats and meat alternates
b. vegetables, fats, oils & sweets
c. milk & milk products, fruits & vegetables
d. milk & milk products, breads & cereals
e. meat and meat alternates, breads & cereals
27. Which of the following is recommended to prevent heartburn during pregnancy?
a. avoid high-fat meals
b. avoid spicy foods
c. don't lie down after eating
d. a, b and c
Exam, cont’d
205
NW109
28. Exercising during pregnancy causes what physiological alteration?
a. decreased respiration
b. decreased uterine blood flow with less oxygen supply to the fetus
c. increased kidney filtration
d. decreased uterine blood flow and no change in oxygen to the fetus
e. increased incidence of anemia
29. Which of the following nutrients may interfere with each other when supplemented?
a. protein and vitamin C
b. vitamin B12 and calcium c. iron and zinc
d. zinc and vitamin C
30. Iron supplementation is necessary for all pregnant women during the first trimester.
a. True
b. False
31. How much supplemental vitamin D is safe for pregnant women?
a. 200 IU
b. 800 IU
c. 2,000 IU
d. 5,000 IU
e. 10,000 IU
32. Which of the following is NOT a clinical symptom of preeclampsia?
a. elevated blood pressure
b. elevated cholesterol level
c. protein in the urine
d. edema
e. all are symptoms
© 2009, Nutrition Dimension/Gannett Education, Inc.
33. A client of your develops preeclampsia. Which of the following nutrients should you make sure are
in her diet in adequate amounts?
a. Ω-6 fatty acids, vitamin C and vitamin E
b. Ω-3 fatty acids, vitamin D and plant foods
c. Ω-6 fatty acids and plant foods
d. Ω-3 fatty acids, dairy foods and protein
34. Although you must individualize the diet of a pregnant diabetic woman, what percentage of calories from carbohydrate appear to give the best glucose control for gestational diabetic women?
a. 35 to 40 percent
b. 40 to 45 percent
c. 45 to 50 percent
d. 50 to 55 percent
e. 55 to 60 percent
Exam, cont’d
206
NW109
35. Gestational diabetes is characterized by which of the following metabolic changes?
a. increased insulin resistance
b. decreased total cholesterol
c. decreased serum ketones
d. decreased insulin resistance
e. high blood pressure
36. Maternal smoking during pregnancy has what effect on the outcome of pregnancy?
a. none
b. low birth weight babies c. malformed babies
d. neural tube defects
e. nicotine withdrawal
37. Smokers have lower serum levels and may need to supplement:
a. vitamin C
b. folic acid
c. zinc d. a and b
e. b and c
38. Zidovudine can decrease transmission of the HIV virus from mother to fetus by how much?
a. 2/3
b. 1/2 c. 1/3 d. 1/4 e. 1/8
© 2009, Nutrition Dimension/Gannett Education, Inc.
39. The best recommendation we can make to pregnant women regarding caffeine intake during pregnancy is to reduce caffeine intake to two cups of coffee a day or the equivalent amount of caffeine —
150 mg to 300 mg per day.
a. True
b. False
40. Which of the following physiological changes of pregnancy alter drug metabolism?
a. decreased gastric tone and motility
b. decreased hydrochloric acid secretion
c. decreased albumin-binding capacity of drugs
d. increased excretion of drugs by kidneys
e. all of the above