Download High Fructose Corn Syrup and Childhood Obesity

THE UNIVERSITY OF NATURAL MEDICINE
HIGH FRUCTOSE CORN SYRUP AND CHILDHOOOD OBESITY IN THE UNITED
STATES: AN INVESTIGATION OF A CAUSAL RELATIONSHIP
DISSERTATION SUBMITTED TO
THE FACULTY OF THE DEPARTMENT OF NATURAL HEALTH SCIENCES
IN CANDIDACY FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY
BY
ANITA DEHLINGER DELPRETE
ALBUQUERQUE, NM
SEPTEMBER 2011
High Fructose Corn Syrup and Childhood Obesity
Copyright © 2011 by Anita Dehlinger DelPrete
All rights reserved.
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High Fructose Corn Syrup and Childhood Obesity
Dedicated to my grandmother Dr. Jean R. Dehlinger
who planted the first seed many years ago.
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High Fructose Corn Syrup and Childhood Obesity
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TABLE OF CONTENTS
Introduction
Chapter 1
Chapter 2
Chapter 3
Chapter 4
5
Obesity rates in the United States
Adiposity Determination
Trends and Prevalence
Pediatric Trends & Health Impacts
Economic Cost
8
15
19
29
Sugar Consumption and Metabolism
Proteins
Carbohydrates
Glucose and Fructose Metabolism
Glycolysis
Glycogen, Glycogenesis, de novo Lipogenesis
Metabolic Hormones
Lipids
Metabolic Regulatory Theories
Leptin
Metabolic Imbalances & Disorders
34
36
41
42
45
47
51
54
55
59
High Fructose Corn Syrup
Discovery, Use & Prevalence
Consumption Trends
Metabolism and Adiposity
Economic Benefits
Genetically Modified Foods (GMO/GE)
63
70
78
96
98
Other Contributing Factors
Portion size & Increased Caloric Intake
Physical Activity
Television, Computer & Video Games
Family Mealtime
Fast Food and Fat Consumption
Soda Consumption
Genetics
106
109
111
114
115
117
119
Conclusion
121
Appendix
128
End Notes
129
Bibliography
135
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Introduction
There is a global epidemic occurring and it is threatening to be one of the most
costly epidemics the world has experienced…obesity. Ten years ago the World Health
Organization (WHO) declared this epidemic to be “the biggest unrecognized public
health problem in the world”1 and sadly it has expanded since that declaration. The
health risk factors associated with obesity and excess adiposity have catapulted obesity
and overweight to one of the top health risk factors in the United States. According to the
Mayo Clinic (2011), these include are heart disease, stroke, cancer, type 2 diabetes,
chronic respiratory diseases, and accidents.2 Of these top health threats, six have been
directly associated with obesity and excessive adiposity which is precisely why health
professionals (adult and pediatric) are growing more concerned.
Current projections estimate that by 2030 half of all Americans will be obese, not
overweight but obese!3 This epidemic has traversed socio-economic, ethnic, racial,
gender, geographic and age boundaries and demarcations. While some groups or
classification of individuals may have a slightly higher preponderance of occurrence, no
population has escaped unscathed by this health crisis. According to the most recent
estimates of the Centers for Disease Control and Prevention (2011), 17% of all children
and adolescents in the United States are obese. Unfortunately, the CDC estimate does not
include those children who are overweight and/or borderline obese thus omitting a
significant population who may be at risk of developing the same health risks as those
who are classified “obese”. Some estimates report that an additional 25% of U.S.
children and adolescents are overweight.4 Thus cumulatively, these estimates suggest
that, at minimum, 42% of all U.S. children and adolescents are overweight or obese. The
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predominant questions for researchers is 1) what is/are causing these alarming rates of
overweight and obesity and 2) what can be done to stop and/or reverse these trends?
The impetus for deriving an answer to these pertinent questions is based in part
to averting future medical crises. Adverse health conditions that once only effected the
adult population are now manifesting in children and adolescents. Cardiovascular
disease, hypertension, high blood pressure, hyperlipidemia, type 2 diabetes, insulin
resistance, and sleep apnea, conditions that were once reserved to the “adult” population,
are becoming more prevalent among our youth. Increased prevalence of medical
conditions translates into increased medical cost and economic burden, especially for
those receiving government-funded medical care (Medicaid and Medicare). In 2000, the
economical cost associated with obesity in the United States was estimated to be $117
billion dollars.5
Interestingly, the surge of high fructose corn syrup (HFCS) consumption in the
United States parallels the child and adolescent overweight/obesity rates trajectory
spawning the investigation of a causal relationship between HFCS consumption and
obesity. Because of the prevalence of HFCS in beverages, soft drinks in particular,
several studies have investigated the role of carbonated beverages and obesity. However,
what has not been investigated is the cumulative dietary intake of HFCS consumed via
beverages (carbonated and non-carbonated juices) and food in relation to adiposity.
Similarly, certain aspects of HFCS and its metabolic processes, as well as glucose,
fructose and sucrose metabolism, have been investigated however, the sum total of all the
experimental “parts” (i.e. findings) have not been cumulatively analyzed. Because
HFCS contains fructose as well as glucose, several studies have researched metabolic and
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blood profile differences and/or similarities between the various sweeteners.6 Other
research has specifically investigated effects of HFCS consumption on weight gain and
fat mass7. Some studies have looked at HFCS consumption and satiety8 while others
have investigated effects on insulin, leptin and ghrelin levels.9 There has been research
on the efficacy of genetically modified foods as well.10 The relevance of this latter
research is that the vast majority of HFCS is derived from GMO/GE corn. Additionally,
HFCS has been shown to contain trace amounts of mercury11raising concerns as studies
have revealed toxic effects of mercury ingestion on the liver12 (the primary organ for
carbohydrate and fat metabolism), kidneys and brain tissue.
While seemingly unrelated, each experiment, each research investigation
provides information about a specific aspect of HFCS, but in order to determine the true
relationship between HFCS and obesity a critical analysis of all the information is
necessary. This research investigates the causal relationship between HFCS consumption
and excess adiposity and obesity among U.S. children and adolescents.
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CHAPT. 1- Obesity in the United States
ADIPOSITY DETERMINATION
In traditional “medical” terms, obesity is defined simply as an excess of body
fat,13 however, what defines “excessive” remains somewhat nebulous and often
subjective. Some contend that obesity falls into the classification of a non-communicable
disease (NCD)14 while others contend that obesity itself is not a “disease” but rather the
result of metabolic processes from which subsequent diseases may develop as a result of
being obese.15 The World Health Organization (WHO) includes harmful health
ramifications in their definition of obesity stating that obesity is “the condition of having
abnormal or excessive body fat accumulation that may impair health.”16 Some of these
deleterious health impairments will be discussed in detail later in this chapter. For
adults, excess adiposity is traditionally measured via a height-weight index known as the
Body Mass Index (BMI) [also known as the Quételet index named after creator and
statistician Lambert Adolphe Jacques Quételet] which is a ratio of weight in kilograms to
!"#$!! (!")
the square of height in meters, BMI= !!"#!! ! !; when converting BMI into pounds and
inches this calculation becomes
!"#$!! !" ! !"# 17
.
!!"#!! !" !
In the United States, an adult with a
BMI ≥ 25 (but < 30) is classified as “overweight”, a BMI ≥ 30 (but < 40) is “obese” and a
relatively new term of “super obese” applies to those with a BMI >40.18 However, in
their 2000 Report of Consultation regarding obesity, WHO further delineated levels of
obesity into three categories or sub-classifications: BMI 30-34.9 as Obese Class I, BMI
35-39.9 as Obese Class II and BMI ≥ 40 as Obese Class III.19 It should be noted that the
BMI index is not an exact measurement of adiposity, nor the only way to estimate or
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determine adiposity, but rather an agreed upon universal guideline of appropriate heightweight ratio and approximation of general adiposity.
One criticism of the BMI is that it generally has a low sensitivity and high
specificity in detecting excess adiposity.20 In clinical testing, sensitivity refers to the true
positive rate, that is, it reliably identifies all the individuals with a specific condition. For
example, if 100 people are tested for condition X and all 100 people actually have
condition X, but the test only identified 75 as having condition X then the test would
have a sensitivity of 75%. For 15 people the test showed a false negative; these
individuals thought that they were fine when in fact they had condition X. A test with a
low sensitivity is unreliable because is will fail to identify individuals who actually have
specific conditions. Conversely, specificity of a test refers to the number of false
positives. For example, if 100 people are screened for disease Y and only 75 actually
have that disease but all 100 test positive, the test has a low specificity rate. A test with a
low specificity is unreliable because it will give false positives. In this scenario, fifteen
people think they have disease Y when in fact they do not. Ideally, a test will have a high
sensitivity rate as well as a high specificity so as to accurately identify those individuals,
and only those individuals, with a specific condition.
Muscle tissue weighs more than adipose tissue (i.e. fat) therefore, it is possible
for a professional athlete with a low body fat percentage to score a high BMI based on
density of the muscle and smaller stature. A “real life” example of a specificity error
would be that a 5’6” male athlete weighing 173lbs., with a 29” waist and a true body fat
percentage of 10% would register a BMI of 28 thus falling into the upper end of the
“overweight” classification. Clearly, this individual is not overweight, yet because of his
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muscle density he falls into almost borderline “obese” category. Conversely, a sensitivity
error with respect to BMI would be a 5’9” female weighing 135 lbs. with a 36” waist who
registers a “normal” BMI of 20 yet has a true body fat percentage of 35%. Sole reliance
on the BMI index would indicate she is well within “normal” (which is often perceived as
“healthy”) limits. However, an elevated body fat percentage of 35% coupled with the
location of the excess adipose tissue, primarily the abdomen, potentially places her at risk
for developing adverse health conditions. Some researchers have coined the term
“metabolically obese but normal weight (MONW)”21 to classify individuals meeting this
criteria. While prevalence ranges between 5%-45% depending upon specific criteria and
BMI cut off, individuals who fall into this classification exhibit higher abdominal and
visceral adipose tissue, higher blood pressure, lower insulin sensitivity, higher risk for
developing NIDDM (type 2 diabetes) and cardiovascular disease (CVD).22
Another criticism of the BMI is that it does not identify individuals at risk for
developing adverse health conditions.23 While BMI is better at estimating subcutaneous
(a.k.a. peripheral) adipose tissue, waist circumference measurements are better at
estimating visceral (a.k.a. central) adipose tissue. Subcutaneous/peripheral fat is a soft,
pliable (or “mushy”) fat that lies just underneath the skin. Subcutaneous fat is
predominantly found in the lower trunk, hips, thighs and buttocks. In the trunk area it
lies outside on the abdominal wall and has no harmful [health] effects except to perhaps a
woman’s dream of wearing a size 2. Conversely, visceral/central fat lies deep inside the
abdomen surrounding vital organs such as the liver, kidneys, intestines, stomach, and
heart. Unlike subcutaneous fat, visceral fat is hard and associated with increased risk of
developing many adverse health conditions and diseases such as cardiovascular disease
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(CVD), high blood pressure, NIDDM (type 2 diabetes), arterial stiffening, colon cancer,
breast cancer, gallstones, sleep apnea and Alzheimer’s.24 In the previous example of the
5’9” female, her “normal” BMI rating masks the real health risk posed by her excess
abdominal fat. Clearly, BMI is not the most accurate method of determining adiposity
and the low sensitivity is a potential limitation25, nevertheless the BMI index is a
convenient, easy-to-interpret barometer for evaluating obesity26 and the most widely used
nationally and internationally.27
Because of studies linking visceral adipose to health risks and metabolic
disorders such as hyperlipidemia, hyperinsulinemia, glucose intolerance and insulin
resistance,28several health and medical professionals contend that waist circumference
measurements should additionally be used when calculating adiposity because of its
capability of estimating visceral adiposity. Savva et al. (2000) compared BMI, waist
circumference and waist-to-height ratio (WHtR) as predictors of cardiovascular disease
risk factors in children, specifically, high blood pressure, lipid and lipoprotein plasma
levels. Their findings concluded that waist circumference and WHtR measurements are
better predictors of the presence of cardiovascular risk factors than BMI. Results from
regression analysis revealed that waist circumference was the best predictor of all three
risk factors. Following waist circumference measurement, WHtR measurement was the
next best determinant while BMI was the least. Although BMI adequately predicts high
blood pressure, it fails to predict lipid and lipoprotein levels. Elevated blood lipid and
lipoprotein levels can evolve into hyperlipidemia and are considered to be significant
contributing risk factors for cardiovascular disease (CVD). A failure to predict these risk
factors could result in serious, and perhaps deadly, health consequences later on. Other
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studies similarly conclude that waist circumference is more efficient in predicting health
risks, specifically cardiovascular disease, stroke, elevated blood lipids, hypertension, and
metabolic disorders, than BMI.29
Another popular method of determining adiposity is the skinfold thickness
measurement. Skinfolds are compressed subcutaneous fat that can be measured by
calipers at designated areas, specifically, triceps, subscapular and suprailiac sites.30
Researchers conclude that skinfold thickness is predictive of overall adiposity, especially
in children and adolescents.31 However, some research suggests that skinfold thickness is
also a predictor of certain risk factors. In a cross sectional analysis of boys between the
ages of 10 and 15 years old, Morrison et al. (1999) concluded that overweight boys had
greater skinfolds, lower HDL, higher LDL and triglyceride levels, and higher blood
pressure (both systolic and diastolic). While non-invasive and a good barometer of
general adiposity, some contend that skinfold testing is no longer the most optimal form
of measurement due to potential increase for human error when taking the
measurements.32 It is impossible to ensure that every physician and healthcare personnel
taking these measurements will place the calipers in the exact location on every person
every time. There is simply a level of human variability that cannot be escaped.
A relatively recent addition to the adiposity determination assessment toolbox is
dual energy x-ray absorptionmetry (DXA). Traditionally used to determine bone density,
DXA has recently been used to determine adiposity by differentiating body weight into
bone mineral, lean soft tissue and fat soft tissue masses.33 While touted by some to be a
quick and accurate method of determining adiposity, it requires a full body x-ray scan
which subjects are not quite as enthusiastic about especially on young children. Add to
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that a cost of $25,000 - $30,000 per unit and it becomes less desirable.
The last method of determining adiposity discussed is hydrostatic weighting
(a.k.a. densitometry34). This is one of the most accurate methods of determining overall
adiposity however, like BMI it does not predict potential or existing health risk factors.
While the accuracy is within an impressive 1.5% according to Georgia State University’s
Department of Kinesiology and Health Body Composition (2011), 35 it is also one of the
most costly and least convenient forms of determining body fat percentage. It is based
upon Archimedes’ principle of water displacement and requires submersion in a
hydrostatic tank that is both expensive and difficult to find. From a clinical perspective
this is obviously a more preferable method of determining true adiposity because of the
accuracy, but unfortunately one that does not translate into real life applications.
Additionally, it does not delineate between visceral and peripheral adipose tissue which is
crucial when analyzing potential health risk factors.
Children have traditionally been measured using pediatric growth charts that
factor weight, length, age and head circumference, however, these were not standardized
until 1977, with modifications made in 1978 and 2000. This creates a challenge when
estimating child overweight and obesity rates and prevalence prior to 1977. In 1977, the
National Center for Health Statistics (HCHS) Growth Chart Task Force researched and
constructed the 1977 HCHS growth charts for children 2-18 years and alternative charts
for children birth to 36 months.36 These growth charts were based upon aggregate data
collected in the National Health Examination Survey (NHES) Cycle II and Cycle III, the
National Health and Nutrition Examination Survey (NHANES) 1971-74 for children ages
1-18 years, and data from the Fels Research Institute from 1929-1975. The NHANES is
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a national survey that began in the 1960’s. Survey data consists of interviews including
demographic, socioeconomic, dietary, and health-related questions as well as a physical
examination that includes medical, dental, physiological measurements and laboratory
tests. In 1978, these growth charts were modified to allow for standard deviation
calculations and were adopted for use by the World Health Organization (WHO). 37 One
admitted flaw of utilizing the Fels Institute’s longitudinal study data in creating the
standardized growth charts was its biased infant-toddler sample.38 While comprehensive
in duration (46 years), the Fels Institute data was a single longitudinal study of white,
middle class infants that were primarily formula fed and resided in the small geographic
town of Yellow Springs, Ohio, not exactly a representative sample of the United States.
Another limitation of the 1977 and 1978 growth charts is that they excluded extreme
percentile ranges and limited the ability to analyze and chart anything beyond the 5th and
97th percentiles which would include those children who were extremely underweight as
well as those who were extremely overweight/obese. Nevertheless, this data in
combination with the NHES and NHANES, became the predominant guidelines
regarding healthy growth/weight curves for children.
In 2000, an expert panel from the Centers for Disease Control and Prevention
convened to review and revise the standardized growth charts. The results were the 2000
CDC Growth Charts that included the addition of the age and gender specific Body Mass
Index (BMI) for children 2-20 years as well as addition of 3rd and 97th percentiles. A
criticism of the growth charts has been that they do not provide standards for growth
patterns of healthy children but rather are a set of approximated percentiles based upon
national survey data.39 Just because there is an identified trend does not necessarily mean
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it is a beneficial one, healthy one or one to aspire to. These critics maintain that these
trends should not translate into national health measurement standards. Several advisory
groups have recommended using BMI as a barometer for measuring adolescent adiposity.
40
The 2000 CDC Growth Charts classify children with a BMI ≥ 85th percentile as “at
risk of overweight” and those children with a BMI ≥ 95th percentile are classified as
“overweight”. However, in 2005, the Institute of Medicine issued a report that conveyed
the “seriousness, urgency and medical nature of childhood obesity, as well as the need to
take action.”41 One subsequent action step was the redefinition (or reclassification) of
children with a BMI ≥ 95th percentile as “obese” instead of “overweight”. Two years
later, a committee of pediatric and health experts not only endorsed the Institute of
Medicine’s recommendation, but further suggested that children with a BMI ≥ 85th
percentile (but < than 95th) be classified as “overweight” instead of “at risk of
overweight”. They noted that “at risk” is vague at best and inaccurate at worst. Because
there are no BMI references for children birth to 2 years of age, weight classification is
based on the weight-for-length/stature index. Children birth to two years with a weightfor-length > 95th percentile are currently considered “overweight”.42
OBESITY TRENDS & PREVALENCE
In a 2005 press release, the World Health Organization (WHO) estimated that
there were one billion people globally who were overweight and/or obese and that, if the
rate continued as current trends predicted, that number would grow to 1.5 billion people
by 2015.43 The world’s current estimated population is 6.8 billion, thus according to
WHO estimates currently one out of every seven people (14%) are overweight and/or
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obese.44 This is astonishing given that 1980 global obesity rates were 5% of men and 8%
of women. In roughly 30 years, rates almost tripled for men and doubled for women
globally. In the 2005 WHO estimates, over 75% of women over the age of thirty were
overweight in countries such as Egypt, Barbados, Malta, Mexico, Turkey, South Africa
and the United States. Similar rates for men were found in the nations of Germany,
Argentina, Greece, Kuwait, New Zealand, Samoa and the United Kingdom. A recent
report (2011) in the United Kingdom estimates that if current trends continue, by 2030
obesity rates among British men and women will be 40-48% and 35-43% respectively.
Similarly, they predict by that time 50% of all individuals in the United States will be
obese, not overweight, obese!45
In a 2007 meta-regression analysis of obesity in the United States, Drs. Youfa
Wang and May Beydoun from Johns Hopkins Bloomberg School of Public Health
predicted that by 2015, an alarming 75% of adults will be overweight and/or obese and
41% will be obese.46 These researchers analyzed trends and disparities among the
participants of the NHES and NHANES surveys with respect to gender, age, socioeconomic status (SES), geographical differences (urban vs. rural), race, ethnicity and
education however, for the purpose of this research further analysis of those findings
outside of age and gender disparities will be reserved for another time.
They compared data from the National Health Examination Survey (NHES I)
1960-1962 and the National Health and Nutrition Examination Surveys (NHANES) for
1971-1974 (NHANES I), 1976-1980 (NHANES II), 1988-1994 (NHANES III), 19992000 (NHANES) and 1999-2002 (NHANES). They defined overweight as having a BMI
of ≥ 25 and obesity as a BMI ≥ 30. At the time of NHES I (1960-1962); 49.5 % of men
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were overweight while 40.2% of women were overweight thus combined, 44.8% of men
and women over the age of 20 years were overweight. Those numbers increased slightly
by the NHANES II (1976-1980) to 52.9% for men and 42.0% for women for a
cumulative total of 47.4% for men and women. The most significant increases occurred
between the NHANES II (1976-1980) to the NHANES III (1988-1994), and the
NHANES III (1988-1994) to the NHANES (1999-2000) with an 8.6% increase and 8.5%
increase respectively. [Fig.1]
U.S. Adult Overweight Rates 1960-­‐2002 80.0% 70.0% 60.0% 50.0% Men 40.0% Women 30.0% Combined 20.0% 10.0% 0.0% NHES I NHANES I NHANES II NHANES III NHANES NHANES 1960-­‐1962 1971-­‐1974 1976-­‐1980 1988-­‐1994 1999-­‐2000 1999-­‐2002 Fig 1. U.S. Adult Overweight rates 1960-­‐2002. Data Source: Wang and Beydoun (2007) National Health Examination Survey (NHES I) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, NHANES 1999-­‐2002. Graphic created by author. Similar trends were found in the obesity category. The NHES I (1960-1962) data
reveal 13.3% of adults were obese; 10.7% of men were obese and 15.7% of women were
obese. Collectively (men and women), there was a slight increase to 14.6% by the
NHANES I (1971-1974), and another slight increase to 15.1% by the NHANES II (19761980). However, there was a substantial increase to 23.3% (an 8.5% increase) by the
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NHANES III (1988-1994) and another significant (7.6%) increase to 30.9% by the
NHANES (1999-2000). By 2000, 30% of all adults were not merely overweight but
obese. Interestingly, women across all surveys had a higher percentage in the obesity
category (BMI ≥ 30) than men, whereas men had a higher percentage in the overweight
category (BMI ≥ 25) category than women. [Fig.2]
Adult Obesity Rates 1960-­‐2002 40.0% 35.0% 30.0% 25.0% Men 20.0% Women 15.0% Combined 10.0% 5.0% 0.0% NHES I NHANES I NHANES II NHANES III NHANES NHANES 1960-­‐1962 1971-­‐1974 1976-­‐1980 1988-­‐1994 1999-­‐2000 1999-­‐2002 Fig 2. U.S. Adult Obesity rates 1960-­‐2002. Data Source: Wang and Beydoun (2007) National Health Examination Survey (NHES I) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, NHANES 1999-­‐2002. Graphic created by author. What was not analyzed and should be looked at in further studies is the
breakdown of these BMI ranges. For example, of the NHES I 13.3% obesity rates, were
the majority of individuals hovering around the 31-32 range or were they in the 40-45
range? Has the degree of adiposity increased as well as the prevalence? Similarly, is
there a greater prevalence of extreme or morbid obesity now than twenty, thirty or forty
years ago? Recently, morbid obesity has been added as a subcategory of obesity, this
refers to a BMI ≥ 40 and/or the individual is 100 pounds overweight. Unfortunately this
will be difficult to ascertain, as BMI specificity was not a category of the NHANES
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surveys.
The health implications of this global epidemic are alarming. Dr. Catherine
LeGalès Camus, WHO Assistant Director-General of Non-communicable Disease and
Mental Health, warns, “The sheer magnitude of the overweight and obesity problem is
staggering. The rapid increase of overweight and obesity in many low and middle
income countries foretells an overwhelming chronic disease burden in these countries in
the next 10 to 20 years, if action is not taken now.”47 Currently, WHO estimates that
over 2.6 million people die each year as a result of being overweight and/or obese.48
Sadly, this epidemic does not exclude some of the most vulnerable and least selfsufficient… our children.
PEDIATRIC OBESITY TRENDS & HEALTH IMPACTS
In 2010, an appalling WHO estimate stated that over 42 million children under
the age of five were overweight; of these, 35 million were children living in developing
nations.49 What used to be an isolated condition affecting the affluent, obesity has
traversed economic boundaries and proliferated the homes of the middle-class as well as
the poor and economically disadvantaged. Sharron Dalton, Associate Professor in the
Department of Nutrition, Food Studies and Public Health at New York University states,
“The forces of globalization have put these relatively cheap foods and drinks- high in
calories, low in nutrients-within reach of almost anyone, anywhere, giving childhood
obesity a foothold in even the poorest countries.”50 Dalton boldly contends that,
“childhood obesity is arguably the most pervasive and serious threat to children’s health
today.”51
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Obesity is associated with many significant health problems plaguing both adult
and pediatric populations. Sadly, what were once considered “adult” diseases and
disorders are becoming increasingly prevalent among children and adolescent
populations.
Obesity-related cardiovascular conditions now affecting children and
adolescents include cardiovascular disease (CVD),52 hypertension,53
hypercholesterolemia, and dyslipidemia.54 A study that has provided a wealth of
knowledge and clinical insight into cardiovascular disease and children is the Bogalusa
Heart Study.
Sponsored by the National Heart, Lung, and Blood Institute (NHLBI), the
Bogalusa Heart Study (1972-2002) was and is the longest biracial study of children
investigating the early natural history and etiology of cardiovascular disease and
hypertension.55 Conducted by Tulane University School of Medicine, the study consisted
of all children and young adults, approximately 22,000 subjects, residing in the town of
Bogalusa Louisiana.56 Data surveys were conducted in 1973-74, 1976-77, 1978-79, 198182, 1988-89 and 1988-2991 and consisted of anthropometric data (height, weight, length
of body segments and body segment masses), health history, hemoglobin, blood pressure,
serum lipids and lipoprotein levels, skinfold thickness, heat rate, salt intake, smoking,
alcohol use and dieting habits.57 Two parallel cohorts of children ages 7 to 9 years old
were identified, one in 1973 and the other in 1984, and reexamined throughout the
duration of the study into adulthood. The study clearly revealed that the etiology for
CVD, hypertension, and atherosclerosis begins in childhood. Freedman et al. (2004)
were specifically interested in data from the Bogalusa Heart Study surrounding the
relationship between BMI, skinfold measurements and adult adiposity. Analysis
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confirmed their presumptions that child BMI and triceps skinfold measurements are
positively associated with adiposity later in life. They also found skinfold measurement
to have a slightly stronger association with adult adiposity than did BMI, nevertheless
they concluded that both were reliant predictors of adiposity into adulthood.58
In addition to cardiovascular health risks, conditions such as non-insulindependent diabetes mellitus (NIDDM or type 2 diabetes mellitus), insulin resistance and
hyperinsulinemia are also prevalent among overweight and obese children. Endocrine
system health is also adversely affected, reproductive health (menstrual irregularities),59
mental health (depression, oppositional defiant disorder),60 musculoskeletal health61 and
sleep and respiratory health (sleep apnea, asthma)62 are other areas adversely affected by
excessive adiposity.
Since 1980, the number of overweight adolescents has tripled.63 Today, one in
three American children are overweight or at risk of becoming overweight and/or obese,
that is one third of the adolescent population. Dr. Cynthia Ogden and Margaret Carroll
(2010) analyzed the National Health Examination Surveys (NHES) and National Health
and Nutrition Examination Surveys (NHANES) with respect to pediatric and adolescent
obesity. Their findings were similar to those of Wang and Beydoun. Based on expert
committee recommendations and the 2000 CDC BMI-for-age-growth charts, Ogden and
Carroll’s obesity cutoff criteria were individuals who were ≥ 95th percentile of the sexspecific BMI-growth charts.64 Their analysis of the NHES II (1963-1965) & III (19661970) and NHANES I (1971-1974), NHANES II (1976-1980), NHANES III (1988-1994)
and NHANES 1999-2000, 2001-2002, 2003-2004, 2005-2006 and 2007-2008 concluded
that for children 2- 5 years of age obesity more than doubled between 1976-1980 and
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2007-2008 increasing from 5.0% to 10.4% respectively. Similarly, among children 6-11
years of age the rate tripled from 6.5% (1976-1980) to 19.6% (2007-2009). For
adolescents aged 12-19, the percentage of those that were obese tripled as well, from
5.0% (1976-1980) to 18.1% (2007-2008).65 [Fig. 3a & 3b]
Prevalence of Obesity among U.S. Children Percentage that are Obese 25.0 20.0 15.0 Total (2-­‐19 yrs.) 2-­‐5 yrs. 10.0 6-­‐11 yrs. 5.0 12-­‐19 yrs. 0.0 Fig 3a. Obesity rates among U.S. Children and adolescents. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. Percentage Prevalence of Obesity among U.S. Children 2-­‐19 years 18.0 16.0 14.0 12.0 10.0 8.0 6.0 4.0 2.0 0.0 1971-­‐1974 1976-­‐1980 1988-­‐1994 1999-­‐2000 2001-­‐2002 2003-­‐2004 2005-­‐2006 2007-­‐2008 NHANES NHANES NHANES NHANES NHANES NHANES NHANES NHANES Total (2-­‐19 yrs.) Fig 3b. Obesity rates among U.S. Children and adolescents. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. High Fructose Corn Syrup and Childhood Obesity
p. 23
They also discovered significant ethnic and gender disparities. In NHANES III
(1988-1994), there was not a significant difference between Mexican-American and nonHispanic White boys, 14.1% and 11.6% respectively (although some would argue
regarding health conditions 3% is significant enough). However, by NHANES 20072008 those rates has increased to 26.8% and 16.7% respectively; Mexican-American
boys had a 61% greater prevalence of obesity than non-Hispanic White boys. While not
highlighted in their analysis, the data also showed a significant increase in the prevalence
of obesity in non-Hispanic Black boys. In 1998-1994, non-Hispanic Black boys had the
lowest prevalence of obesity at 10.7% (compared to non-Hispanic White boys at 11.6 and
Mexican-American boys at 14.1%). However, by NHANES 2007-2008, while still
trailing behind Mexican-American boys (26.8%), non-Hispanic Black boys (19.8%) had
surpassed non-Hispanic White (16.7%) boys by three percentage points. [FIG. 4]
Among adolescent girls, the trend between Mexican-American girls and nonHispanic Black girls was reversed. In NHANES III (1988-1994), the prevalence of
obesity among adolescent girls was 8.9% among non-Hispanic White girls, 16.3% among
non-Hispanic Black girls, and 13.4% among Mexican-American girls. By NHANES
2007-2008, those rates had increased to 14.5%, 29.2% and 17.4% respectively. [FIG. 5]
The prevalence of obesity among non-Hispanic Black girls increased an alarming 80%
between 1988-1994 and 2007-2008. While there was an overall lower prevalence of
obesity among non-Hispanic White boys and girls, Mexican-American boys and nonHispanic Black girls had the highest prevalence of obesity among all ethnicities.
Between these two reporting periods, non-Hispanic White boys and Mexican-American
girls had the lowest percentage point increase, 5.1 and 4.0 respectively; non-Hispanic
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High Fructose Corn Syrup and Childhood Obesity
Black girls and Mexican-American boys had the highest percentage point increase of
12.9 and 12.7 respectively. [FIG 6] Given cultural and ethnic differences this data is
fascinating as it is usually presumed/assumed that trends occur within ethnicities
collectively. For example, Asians typically have smaller frames than Samoans. The
significant discrepancies of obesity prevalence between genders of the same ethnicity
warrants future research.
Prevalence of Obesity in U.S. boys 1988-­‐1994 and 2007-­‐2008 Prevalence of obesity 30 25 20 15 1988-­‐1994 10 2007-­‐2008 5 0 non-­‐Hispanic White boys non-­‐Hispanic Black boys Mexican American boys Fig 4. Percentage of obesity in U.S. boys between 1988-­‐1994 and 2007-­‐2008 categorized by ethnicity. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐
2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. p. 25
High Fructose Corn Syrup and Childhood Obesity
Percentage of obesity Prevalence of Obesity in U.S. girls 1988-­‐1994 and 2007-­‐2008 35 30 25 20 1988-­‐1994 15 2007-­‐2008 10 5 0 non-­‐Hispanic White girls non-­‐Hispanic Black girls Mexican American girls Fig 5. Percentage of obesity in U.S. girls between 1988-­‐1994 and 2007-­‐2008 categorized by ethnicity. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐
11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. Percentage Point increase of obesity prevalence between 1988-­‐1994 and 2007-­‐2008 Percentage points 14 12 10 8 Boys 6 Girls 4 2 0 non-­‐Hispanic white non-­‐Hispanic black Mexican American Fig 6. Percentage of increase of obesity in U.S. Children and adolescents between 1988-­‐1994 and 2007-­‐2008 categorized by ethnicity. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. It is estimated that one third of obese preschool children and half of obese
school-age children will become obese adults66 putting them at risk for developing
serious and sometimes fatal health conditions such as: asthma, cardiovascular disease
High Fructose Corn Syrup and Childhood Obesity
p. 26
(CVD), hyperlipidemia, high cholesterol, hypertension/high blood pressure, high
cholesterol, stroke, type 2 diabetes (NIDDM), musculoskeletal disorders such as
osteoarthritis, depression, anxiety, behavioral problems, menstrual irregularities, sleep
disorders and even certain cancers.67 In a follow up study of the Harvard Growth Study of
1922 to 1935, researchers from the USDA Human Nutrition Research Center on Aging at
Tufts University (Must et al., 1992) concluded that mortality from coronary heart disease,
atherosclerosis, stroke and colorectal cancer was greater among adult men who were
overweight adolescents. Similarly, women who were overweight adolescents were eight
times more likely to have difficulty with “activities of daily living” such as climbing
stairs and lifting and had a higher incidence of arthritis than women who were not
overweight in their adolescents.68 These health risks and subsequent financial costs will
be discussed later in detail.
Using multinomial logistic regression models of the Early Childhood
Longitudinal Study-Birth Cohort data [ECLS-B, a national study that provides data on
children’s status birth through kindergarten] for children 9 months of age and 2 years of
age, researchers Brian Moss and William Yeaton (2011) estimate that one third of
children in the United States were either at risk or obese at nine months age (31.9%) and
at two years of age (34.3%).69 Other studies have confirmed a positive correlation
between weight gain within the first few months of life and adult overweight and
obesity.70 In addition, some research reveals that the age at which excess adiposity begins
has a significant impact on adiposity in adolescence and adulthood bringing with it
subsequent health risks. 71 In a 2000 cohort study, Ekelund et al. analyzed a ten percent
sample of the 14,000 participants of the 1991-92 Avon Longitudinal Study of Pregnancy
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High Fructose Corn Syrup and Childhood Obesity
and Childhood (ALSPAC) to determine postnatal catch-up growth and its correlation
with obesity at five years old. Catch-up growth refers to a rapid growth rate (i.e. weight
gain) that occurs between the first and second year of life. Children who experienced
catch-up growth in either weight or length between the years of zero and two years of age
were heavier and taller at five years of age than other children who had not experienced
any “catch-up” growth. In addition, these children had a greater body mass index, higher
body fat percentage, higher total fat mass and higher central fat distribution (i.e. visceral
fat) than other children thus putting them at an increased risk of developing certain health
and metabolic risks later in adulthood and young adulthood.
A typically developing child will steadily gain body mass (i.e. weight) from birth
until the period of time between the ages of 4 to 7 years old. During this phase of
growth, adipose tissue (both size of and number of adipocytes) increases at a steady rate
and then levels out. At the 4 to 7 year benchmark, the rate of adipose tissue growth
diminishes but the height growth continues thus resulting in a sudden decline in weight
and body fat to a minimum set point. Upon reaching this set point the child will then
resume gaining weight into adulthood where it will [hopefully] stabilize at yet another set
point. The descending set point is called the “adiposity rebound” as it (adipose tissue
growth) suddenly but expectedly drops and then rebounds upward.72 [Illus.1]
Illus. 1 Author’s Schematic. Set point Set point of adiposity rebound Age of rebound: 1 2 3 4 5 6 7 8 9 1 0 High Fructose Corn Syrup and Childhood Obesity
p. 28
What is of great interest to researchers is when the rebound occurs. In a
longitudinal study of 151 children, Rolland-Cachera et al. (1984) found a positive
correlation between the age of adiposity rebound and degree of adiposity later in life.
They determined that an early adiposity rebound (< 5.5 years old) is followed by a
“significantly higher” adiposity level later on than that of a later occurring adiposity
rebound (< 7 years old). The results from their 1984 study concluded that 1) children
obese at one year old who experience an early adiposity rebound will remain obese, 2)
children obese at one year old who experience a late adiposity rebound will eventually
join the “average” group, 3) children who are not obese at 1 year old who experience a
normal or delayed rebound will remain average or even a lower weight and 4) children
who are not obese at one year old who experience an early or “advanced” rebound will
reach their higher percentiles and their overweight will be detected later in their
adolescence. Whitaker et al. (1998) also demonstrated a clear correlation between early
adiposity rebound and higher BMI and obesity rate in young adulthood. They further
concluded that the increased risk of adult obesity associated with an early adiposity
rebound is independent of both the BMI at the time of the rebound and parent obesity.
This suggests that the age (time) that the rebound occurs is a better predictor and/or
bigger risk factor for adult overweight/obesity than the child’s BMI or even the parents’
weight status.
Researchers (Gordon-Larsen et al., 2009) examined the incidence and trends of
obesity among 12-21 year old adolescents during a 12-14 year period into their 20’s and
30’s. Data was obtained from the National Longitudinal Study of Adolescent Health and
High Fructose Corn Syrup and Childhood Obesity
p. 29
consisted of a sample size of nearly 21,000 youth. Gordon-Larsen et al. discovered that
13.3% of all adolescents were obese in 1996; by 2008, that number had surged to 36.1%.
In addition, 90% of those individuals who were obese as adolescents remained obese into
their 30’s.73 Studies have clearly shown a significant correlation between childhood
overweight/obesity and adult overweight/obesity. Simply, children who are overweight
and/or obese have a greater chance of remaining overweight into adulthood than do nonoverweight/obese children bringing with them substantial health and economic costs.
ECONOMIC COSTS OF OBESITY
Given the preponderance of medical conditions resulting from excess
adiposity, that often- if not always- require medical treatment, the economic burden of
obesity has become evident. In addition to the adverse health consequences, there are
also adverse economic consequences of the increasing obesity epidemic. The economic
burden of health care costs for the treatment of obesity-associated diseases is a tangential
epidemic whose rise and acceleration parallels the obesity trajectory. Unlike smoking or
alcohol consumption, there are very few studies that attempt to quantify the economic
costs associated with the obesity epidemic. In the 2000 Report of Consultation, the
World Health Organization (WHO) reported that the total economic cost of obesity is
comprised of three components: direct costs, opportunity costs and indirect costs. Direct
costs are defined as the cost to the individual as well as the cost to the service provider
treating the individual; in short, the medical costs. Opportunity costs refer to the social
and personal loss associated with obesity and obesity related diseases primarily resulting
from premature death and/or disability. Finally, indirect costs refer to the
High Fructose Corn Syrup and Childhood Obesity
p. 30
workplace/workforce loss due to diminished production resulting from absenteeism or
premature death. WHO’s analysis of global economic costs of obesity range from 2-7%
of total health care costs in developed nations.74 In 1992, Dr. Graham Colditz, an
epidemiologist and Associate Director for Prevention and Control at the Alvin J. Siteman
Cancer Center, Washington University School of Medicine and Barnes-Jewish Hospital,
analyzed the economic cost of obesity in the United States for the year 1986. Colditz and
his team used a prevalence-based “cost of illness” analysis to determine the total cost of
five prevalent obesity-related illnesses: non-insulin-dependent diabetes mellitus
(NIDDM- also known as type 2 diabetes), cardiovascular disease (CVD), gall bladder
disease, hypertension and cancer (colon and postmenopausal breast cancer specifically).
Prevalence-based cost of illness analysis identifies the costs incurred by an individual
with a particular illness within a specific time frame irrespective of the severity or “stage”
of the illness. This approach is appropriate for estimating the cost of an illness and/or
disease on an annual basis versus estimating costs over the lifetime (or duration) of the
illness/disease, the latter estimate approach is an incidence-based analysis.75
According to Colditz and his team, $11.3 billion dollars, or 57%, of all costs
associated with NIDDM were directly attributed to obesity. With respect to CVD, they
discovered that among the obese, 70% of CVD was directly attributable to obesity and
that 19% of the total costs of CVD were attributable to obesity, equating to $22.2 billion
dollars. Least expensive were the associated costs of cancer, hypertension and
gallbladder disease. They estimated that 23% of all breast cancers and 42% of all colon
cancers were attributable to obesity. The estimated cost of breast cancer that was
attributable to obesity accounted for 1.4% of all cancer costs and estimated cost of colon
High Fructose Corn Syrup and Childhood Obesity
p. 31
cancer attributable to obesity accounted for 1.1% of all cancer costs. Thus combined, the
2.5% of obesity-attributable cancer costs equaled $1.9 billion dollars. Hypertension and
gallbladder disease had economic costs of $1.5 billion and $2.4 billion respectively thus
bringing the cumulative cost of all five conditions to $39.3 billion dollars. In 1996, Wolf
and Colditz published revised estimates of economic costs of obesity and concluded that
approximately $68.8 billion dollars were spent on obesity-related diseases. 76 In just four
years, the costs of obesity related diseases increased $28.9 billion dollars; that is a 73.5%
increase in 48 months. Similar trends were found with adolescents specifically.
Drs. Guijing Wang and William Dietz (2002) analyzed the trend of obesity-related
diseases among youth (ages 6 to 17 years) and subsequent economic costs for the periods
1979-1981 and 1997-1999. Using data of the national Hospital Discharge Survey
(NHDS) collected by the National Center for Health Statistics, they analyzed the
incidence and hospitalization costs of obesity-related illnesses, specifically sleep apnea,
diabetes (NIDDM, type 2), obesity and gallbladder disease. Their research concluded
that both incidence of obesity related illness as well as the cost of treatment had increased
dramatically from 1979 to 1999.
The prevalence of NIDDM diabetes diagnoses increased from 1.43% (1979-1981)
to 2.36% (1997-1999), obesity diagnoses increased from 0.36% to 1.07%, sleep apnea
increased from 0.14% to 0.75% and gallbladder disease increased from 0.18% to 0.75%.
In addition to the increase in the number of diagnoses, the duration of hospitalization
increased as well. They estimated that the “total days of care” directly associated with
obesity increased from 152,000 in 1979-1981 to 310,000 in 1997-1999. They also
concluded that the percentage of total hospital costs for obesity related illnesses increased
High Fructose Corn Syrup and Childhood Obesity
p. 32
as well, from 0.43% (1979-1981) to 1.70% (1997-1999). These estimates translate into
an economic cost of approximately $35 million dollars during 1979-1981 and $127
million dollars in 1997-1999, a more than threefold increase of $92 million dollars.
Wang and Dietz suggest that their estimates err on the side of being fiscally
conservative for several reasons. First, they did not include the financial costs associated
with medication(s), follow up physician visits etc. in their analysis, only inpatient
hospitalization costs. Second, only four obesity-related diseases were included in the
sample (sleep apnea, diabetes, obesity and gallbladder disease); there are other obesityrelated diseases requiring treatment that were not included in their research. Finally and
perhaps most significantly, they only looked at children and adolescents with a primary
or secondary ICD-9 diagnosis of “obesity”, citing that many individuals with obesityrelated illnesses may not have obesity listed as a primary or secondary diagnosis thus
being left out of the sample despite the obvious associated medical costs. Woo et al.
(2009) also issued caution when estimating inpatient utilization through ICD-9 diagnosis
codes, specifically with “obesity diagnosis”. Out of a sample of 29,352 discharges, 5989
children between the ages of 2 and 20 years had a BMI of ≥ 95% yet only 512 (1.7%) had
a diagnosis of obesity. They determined that research only using obesity diagnosis (i.e.
ICD-9 codes) “may significantly underestimate the magnitude of utilization and
economic impact of inpatients with BMI ≥ 95th percentile”, concluding that “using
impatient diagnoses of obesity in children greatly underestimates the total health care
utilization by obese children and misidentifies patterns of specific inpatient care in this
population.”77
High Fructose Corn Syrup and Childhood Obesity
p. 33
CHAPT. 2- Sugar Intake and Metabolism
In order to understand how and why obesity rates are increasing we must first
understand the physiological process of metabolism and all the variables involved. Since
obesity is specifically related to adipose tissue (i.e. body fat), it is crucial to understand
how the body produces, utilizes and stores energy and what the mechanism(s) for storing
fat is. To answer these questions we must take a brief journey through the annals of
chemistry and human physiology and review the systems and processes involved in
digestion and metabolism. These two functions are symbiotic processes that are essential
for life and health.
The standardized definition of digestion is “the process of making food absorbable by
dissolving it and breaking it down into simpler chemical compounds that occurs in the
living body chiefly through the action of enzymes secreted into the alimentary canal.“78
At the risk of over simplification, foods are first digested (i.e. broken down into smaller
compounds) before they are metabolized for use throughout the body. Tortora et al.’s
physiology textbook defines metabolism as “an energy-balancing act between anabolic
(synthesis) and catabolic (degradative) reactions.”79 Anabolic reactions create (i.e. build)
complex molecules from simple substances conversely, catabolic reactions break down
complex molecules into simple ones. Catabolic reactions are necessary for energy
production as the breaking of bonds between molecules results in energy release in the
form of adenosine triphosphate (ATP). [This energy release will be discussed later in this
chapter.] As we look closer at the metabolic (i.e. anabolic and catabolic) processes that
occur during digestion, it will become evident that the foods we eat and beverages we
High Fructose Corn Syrup and Childhood Obesity
p. 34
drink determine our health and in some instances our mortality.
Humans derive energy from external food that is ingested then subsequently
digested. Food molecules are comprised of six nutrient categories and perform one of
three primary functions: 1) supply energy for life sustaining functions such as DNA
replication, nerve impulse conduction, active transport, protein synthesis and muscle
contraction; 2) synthesis of other molecules such as hormones, enzyme and muscle
proteins; and 3) storage of energy for future use. 80 The latter is the focus of attention for
this research. The six categories of nutrients are proteins, lipids (fats), carbohydrates,
vitamins, minerals and water. Although all of these nutrients are essential for life, since
carbohydrates and fats are directly involved in energy production and fat storage, they
will be the primary focus of this chapter. Proteins, lipids and carbohydrates are
catabolized in the gastrointestinal tract into their primary building blocks: amino acids,
fatty acids, glycerol, monoglycerides, and monosaccharides. Once in their primary form,
these compounds are then metabolized at a cellular level.
PROTEINS
Proteins are complex organic compounds containing carbon, hydrogen, oxygen,
nitrogen and in some cases, sulfur. They have a variety of functions in the body. Some
proteins have a structural function such as building and maintenance of muscle tissue,
connective tissue (collagen), and skin, hair and fingernails (keratin). Some proteins
provide a transportation function such as hemoglobin, a protein that is responsible for
transporting oxygen (O2) and carbon dioxide (CO2) in the blood. Then there are proteins
that have a regulatory function such as insulin and parathyroid hormones, or an
immunological function such as various antibodies.81 The primary building blocks of
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High Fructose Corn Syrup and Childhood Obesity
proteins are amino acids. For any kind of utilization in the body, proteins must be
catabolized into smaller peptides (dipeptides and tripeptides) and amino acids for
absorption to occur. When amino acids link together the attachment juncture, or the bond
adjoining them together, is called a peptide bond. When two amino acids combine the
result is a dipeptide molecule, when three amino acids combine the result is a tripeptide
molecule, and when four or more amino acids combine the result is a polypeptide
molecule. Dehydration synthesis is an anabolic process in which two molecules
combine to create a larger molecule, during this process a water molecule (H2O) is
released. In the example below, two amino acids undergo dehydration synthesis and
form a dipeptide molecule and a molecule of water. [Illus. 2]
Illus. 2 Author’s Schematic. Amino
Acid
Amino
Acid
Dehydration Synthesis
Dipeptide
H2 O
This process in reverse is the catabolic process of hydrolysis whereby water (H2O) [often
in tandem with enzymes] is utilized to break chemical bonds of molecules reducing them
into smaller molecules. Hydrolysis is the predominant process utilized in digestion.
Below is an illustration of hydrolysis of a dipeptide. [Illus.3]
Illus. 3 Author’s Schematic. Dipeptide
Hydrolysis (H 2O)
Amino
Acid
Amino
Acid
High Fructose Corn Syrup and Childhood Obesity
p. 36
When food is first chewed, salivary glands excrete saliva that contains the αamylase enzyme ptyalin and thus begins the digestive process. Once the masticated food
(protein) enters the stomach, the enzyme pepsin begins to breakdown the large protein
molecules into the smaller molecules: polypeptides, peptones and proteoses. As the
digestion process continues, these molecules enter the small intestine where they combine
with the pancreatic enzymes trypsin, chymotrypsin and carboxypoly-peptidase (a.k.a.
carboxypeptidase). These enzymes catabolize the polypeptides peptones, and proteoses
into smaller polypeptides and amino acids. These smaller molecules continue to travel
through the intestinal tract brushing up against the epithelial cells of the intestinal lumen.
Microvilli line intestinal epithelial cells comprising the “brush border” and contain the
digestive enzymes aminopolypeptidase and dipeptidase. As the polypeptides and amino
acids brush along these microvilli, the peptidase enzymes breakdown the polypeptides
into smaller dipeptides, tripeptides and amino acids. These dipeptides, tripeptides and
amino acids are then able to enter the epithelial cells where the final stage of digestion
occurs. Inside the cytosol of the epithelial cell, peptidases break down the dipeptides and
tripeptides into amino acids that are then able to enter the bloodstream for utilization. A
similar process occurs for the digestion and metabolism of carbohydrates.
CARBOHYDRATES
While carbohydrates have been demonized in recent years (spawning the low-carb,
no-carb diet craze), they are essential to life [for example, 2-deoxyribose is a
carbohydrate sugar that forms the backbone of deoxyribonucleic acid (DNA)] and
metabolic processes. A carbohydrate is an organic compound consisting of carbon,
hydrogen and oxygen molecules in with a hydrogen-carbon ration of 2:1. Carbohydrates
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High Fructose Corn Syrup and Childhood Obesity
are divided into three principle groups: monosaccharides (a.k.a. simple sugars),
disaccharides (two sugars), and polysaccharides (a.k.a. starches). While many
monosaccharides exist, the monosaccharides involved in metabolic processes that are of
great relevance to this research specifically are glucose and fructose (others include
galactose, ribose and deoxyribose). Disaccharides are two monosaccharides joined
together, again via dehydration synthesis, to comprise a larger sugar molecule and a
subsequent molecule of water. Just like the formation of dipeptides discussed earlier,
monosaccharides combine to form disaccharides. When the monosaccharides fructose
(C6H12O6) and glucose (C6H12O6) undergo dehydration synthesis the result is a
disaccharide sucrose (C12H22O11) molecule (table sugar) and a water (H2O) molecule.
[Illus. 4]
Illus. 4 Author’s Schematic. Fructose
C6H12O6
Glucose
C6H12O6
Dehydration Synthesis
Sucrose
C12H22O11
H2 O
Note that while fructose and glucose share the same number of carbon, hydrogen and
oxygen atoms, their structural composition is different thereby resulting in two different
molecules. The diagram below illustrates this slight, yet monumental difference. [Illus. 5]
Illus. 5 Author’s schematic of glucose and fructose molecules reference from Whitney et al. and Tortora et al. CH2OH
I
C
I
CH2OH
O
HO
O
H
H
H
I
I
I
I
C
C
H
HO I
C
C
I
OH
H
I
I CH2OH
I
I
H
I
I OH
C
C
HO
C
C
I
I
I
I
OH
H
H
OH
Glucose (C6H12O6)
Fructose (C6H12O6)
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High Fructose Corn Syrup and Childhood Obesity
We will discover later that these structural differences, while seemingly inconsequential,
yield significant differences in the body, especially with respect to metabolism and
energy production. The difference between these two molecules is an exemplary
example of how each and every individual molecule- down to the placement of individual
atoms- carries an important role in the cellular function of the body and the chemical
reactions that result.
Returning to disaccharides, sucrose, maltose and lactose are the most common
disaccharides in the body. Disaccharides are too large to pass through the cell membrane
wall and must be hydrolyzed into the monosaccharide form in order to be absorbed into
the blood stream. Again, hydrolysis is a catabolic reaction that utilizes water (H2O) to
break chemical bonds thereby releasing chemical energy in the form of single (simple)
sugars. Using the previous example, when a disaccharide sucrose molecule hydrolyzes,
the result is two monosaccharides: a fructose molecule and a glucose molecule. [Illus. 6]
Illus. 6 Author’s Schematic. Sucrose
C12H22O11
Hydrolysis (H 2O)
Fructose
C6H12O6
Glucose
C6H12O6
These monosaccharides are metabolized for cellular fuel, however the primary
monosaccharide unit is not the only unit of fuel. Polysaccharides are long chains of
monosaccharides linked together, and like disaccharides, polysaccharides must be broken
down into the primary monosaccharides for cellular absorption. These large
carbohydrates can contain from tens to hundreds of monosaccharides and their large
molecular shapes are ideal for storing energy. Glycogen is one such polysaccharide.
Glycogen is the most abundant polysaccharide in the body; comprised of many glucose
High Fructose Corn Syrup and Childhood Obesity
p. 39
molecules, glycogen is the body’s principle energy storage unit. Because of its role in
energy storage, glycogen’s metabolic process will be discussed in detail shortly.
DIGESTION & METABOLISM
As mentioned previously during the section on protein digestion, the first step of
digestion involves the salivary α-amylase enzyme ptyalin. Secreted by the parotid
glands, ptyalin breaks down food starches into disaccharides and other glucose polymers.
[A polymer is a molecule comprised of many molecules of similar structure called
monomers]. Because food remains in the oral cavity for a relatively short time (one to
three minutes depending upon how thorough the mastication is), only a small percentage
of the carbohydrates overall are broken down into disaccharides. Once swallowed, the
food bolus enters the stomach where it remains for approximately an hour mixing with
gastric secretions. The high acid pH of the stomach further digests the food and almost
40% of the starches are hydrolyzed into maltose and other glucose polymers by the time
the food substance is ready to exit the stomach. From the stomach, the food enters the
small intestine where it combines with the α-amylase pancreatic enzyme; this enzyme is
compositionally similar to salivary α-amylase but more potent. Within 30-40 minutes,
all of the starches have been hydrolyzed into disaccharides and other glucose polymers.
However, a disaccharide molecule is still too large to pass through the epithelial
membrane and must be broken down further into readily absorbable components,
specifically monosaccharides. The epithelial cells of the small intestine contain the
enzymes lactase, sucrase, maltase and α-dextrinase; these enzymes are all capable of
degrading disaccharides into their primary monosaccharide units. As the disaccharides
High Fructose Corn Syrup and Childhood Obesity
p. 40
brush against the epithelial cells lining the intestinal lumen, the enzymes hydrolyze the
disaccharides into primary monosaccharides. For example, the enzyme sucrase
hydrolyzes the disaccharide sucrose into the monosaccharides glucose and fructose.
These monosaccharides are absorbed into the capillary villi of the small intestine and
deposited into the liver via the hepatic portal vein where they are either used for
immediate energy or stored for future use.
While glucose and fructose are both monosaccharides and have the same
molecular/chemical formula, they are metabolized differently. In the epithelial cells of
the upper intestine, glucose is absorbed via active transport (technically, secondary active
transport of glucose) by a sodium-glucose co-transporter whereas fructose is absorbed
via facilitated diffusion further down in the duodenum and jejunum (lower intestines) by
way of a non-sodium dependent transporter process.82 It is believed that the carrier
glucose protein (i.e. transporter protein) has a receptor for a glucose molecule as well as a
sodium ion and that unless both receptors are simultaneously filled and activated the
transport process will not occur. Like glucose, fructose also requires a transporter carrier
(protein) to cross the cell membrane, however it does not require an additional sodium
ion for this diffusion to occur. Once inside the cell, glucose diffuses through the
basolateral membrane into the cytoplasm/extracellular fluid via facilitated diffusion and
is then released into the bloodstream. The difference in these transporter processes
affects the rate of absorption; in fact, fructose is absorbed half as rapidly as glucose is.
While both glucose and fructose require transporter proteins to facilitate diffusion across
the cell membrane, they differ in which protein is utilized. The transporter (carrier)
proteins are commonly referred to as the glucose transporter (GLUT) family. Several
High Fructose Corn Syrup and Childhood Obesity
p. 41
GLUT transport proteins, GLUT1-4, can transport glucose but only GLUT5 can transport
fructose. The difference in the GLUT transporters leads to another fundamental
difference between the two monosaccharides: unlike glucose, fructose does not stimulate
insulin secretion which some surmise is because insulin producing β cells in the pancreas
do not contain the GLUT-5 transporter protein or receptor.83 Insulin plays a significant
role in blood sugar regulation, fat metabolism and food intake (functions that will be
discussed later) so its stimulation or lack thereof is an essential component of
metabolism.
GLUCOSE VERSUS FRUCTOSE METABOLISM
In the liver, hepatic cells convert most of the fructose and galactose into glucose,
which comprises approximately 90-95% of all monosaccharides in the body. Because of
its role in the adenosine triphosphate (ATP) energy cycle, glucose is considered the
primary source of cellular fuel in the body and is essential for energy production. ATP, a
compound present in every cell, is comprised of adenine, ribose and three (tri) phosphate
radicals; the phosphate radical bonds are “high energy” and subsequently release a lot of
energy when they are broken (12,000 calories of energy to be exact84). From the
bloodstream, glucose enters into the cells via facilitated diffusion. Integral carrier
proteins within the cell wall bind with the glucose molecule and transport it from the
exterior of the cell into the interior of the cell. Once inside the cell, glucose undergoes a
ten step degradation processes (e.g. glycolysis) ultimately resulting in the release of ATP
(i.e. energy) and pyruvate molecules. Glycolysis (a.k.a. the glycolytic pathway) is how
energy is produced and released in the body; it literally means sugar breakdown (glyco =
High Fructose Corn Syrup and Childhood Obesity
p. 42
sugar and lysis = breakdown). It is the metabolic process by which a [six carbon] glucose
molecule is broken down into two [three carbon] pyruvate molecules releasing molecules
of ATP (energy) in the process. Once glucose enters the cell it is phosphorylated (it
combines with a phosphate group) into glucose 6-phosphate by the enzyme glucokinase.
Glucose 6-phosphate is then converted (or more accurately, rearranged) into fructose 6phosphate by phosphoglucoseisomerase. It is at this point of the glycolytic pathway that
free fructose can enter for metabolic degradation [to be discussed shortly]. The enzyme
phosphofructokinase then converts fructose 6-phosphate into fructose 1,6-biphosphate.
Fructose biphosphate aldolase splits fructose 1,6-biphosphate into two triose sugars:
dihydroxyacetone phosphate and glyceraldehyde 3-phosphate. These sugars are then
merged (or interconverted) by triosephosphate isomerase and dehydrated by
glyceraldehyde phosphate dehydrogenase to form 1,3-biphosphoglycerate. The enzyme
phosphoglycerate kinase converts 1,3-biphosphoglycerate into 3-phosphoglycerate and
forming and two ATP molecules (i.e. releases energy) in the process. 3phosphoglycerate is converted into 2-phosphoglycerate by phosphoglycerate mutase.
Enolase converts 2-phosphoglycerate into phosphoenolpyruvate that is then converted
into two pyruvate molecules by the enzyme pyruvate kinase. Additionally, two more
ATP molecules are released during this final step. If oxygen (O2) is present, pyruvate is
converted into acetyl coenzyme A (CoA) in the mitochondria of the cell and the Krebs
cycle (a.k.a. citric acid cycle, tricarboxylic cycle) begins. Thus the pyruvate molecule
links glycolysis (glucose metabolism) with the energy producing Krebs cycle. 85 [Illus. 7]
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High Fructose Corn Syrup and Childhood Obesity
Illus. 7 Author’s schematic of glycolysis reference from Whitney et al. and Tortora et al. Glucose Glucose 6-­‐
phosphate glucokinase Phosphoglucose isomerase Fructose 6-­‐
phosphate Fructose 1, 6-­‐
biphosphate Phosphofructo-­‐
kinase 1,3-­‐biphospho-­‐ glycerate phospho-­‐
glycerate kinase Glyceraldehyde-­‐ 3-­‐phosphate Triose phosphate isomerase ATP Dihydroxi-­‐
acetone phosphate Phospho-­‐
glycerate mutase 2-­‐phospho-­‐
glycerate Enolase Phosphoenol-­‐ pyruvate Pyruvate kinase Pyruvate (pyruvic acid) Mitochondria Krebs Cycle ATP Unlike glucose, fructose metabolism is independent of the phosphofructose kinase
regulatory pathway. Once inside the cell, fructose is phosphorylated into fructose-1
phosphate by the enzyme fructokinase. Just as biphosphate aldolase splits fructose 1,6biphosphate in glycogen synthesis, aldolase B splits fructose 1-phosphate into
glyceraldehyde and dihydroxyacetone phosphate. Glyceraldehyde has two separate
conversions: 1) the enzyme triokinase binds with glyceraldehyde to produce
glyceraldehyde 3-phosphate and 2) the enzyme glycerol dehydrogenase converts
glyceraldehyde into glycerol. [Illus. 8] Glycerol forms the backbone of phophsolipids
and triglycerides. 86
3-­‐phospho-­‐
glycerate Glyceraldehyde 3-­‐phosphate dehydrogenase Biphosphate aldolase p. 44
High Fructose Corn Syrup and Childhood Obesity
Illus. 8 Author’s schematic of glycolysis reference from Heinz et al. and Tortora et al. Fructose Fructokinase Fructose 1-­‐
phosphate Aldolase B Dihydroxi-­‐
acetone phosphate Triose phosphate isomerase Glyceraldehyde-­‐ 3-­‐phosphate Aldolase B s
kina
trio
e Glyceraldehyde glycerol dehydrongenase Glycerol glycerokinase Glycerol-­‐3-­‐P Fatty Acids esterfication Triglyceride (VLDL) These two processes (i.e. pathways) have been discussed in detail to emphasize the
complexity of the chemical reactions that occur continually in our bodies, and to illuminate
the importance of understanding what effect(s) chemical formulations [especially manmade] can have on these reactions.
Most dietary glucose passes through the liver and is metabolized into ATP, H20 and
CO2 in skeletal muscle cells as well as hepatic cells. Additionally, it is metabolized into
glycerol phosphate in fat cells for use in triglyceride synthesis. On the other hand,
High Fructose Corn Syrup and Childhood Obesity
p. 45
virtually all fructose is metabolized in the liver (hepatic cells) and results in the formation
of glycerol and fatty acids. Another significant difference between fructose and glucose
metabolism is the absence of ATP production either during the metabolism of fructose or
as an end product. Because fructose metabolism is not regulated by phosphofructose
kinase, its uptake by the liver and its metabolism into fatty acids is independent of
cellular ATP and citrate levels.87 These differences are why fructose consumption is of
great interest to metabolic scientists and researchers. While glucose and fructose share
the same chemical formula and some similar metabolic pathways, the entire process for
metabolism of these two monosaccharides is different. The question among researchers
is how significant is this difference?
Glycogen, Glycogenesis and de novo Lipogenesis
Whether glucose is utilized for immediate fuel or stored for future use depends
upon the needs and requirements of the body at that moment. For example, if energy is
required immediately, cells can oxidize glucose thereby releasing adenosine triphosphate
(ATP) energy for immediate use. If blood sugar levels are sufficient (or even elevated),
the liver converts excess glucose into the polysaccharide glycogen for storage via a
process called glycogenesis. Glycogen is basically a little storage pocket of energy
within the cell itself. If the glycogen stores within the cell are saturated, the liver
converts remaining glucose into fatty acids and glycerol, forming the long-term storage
lipid triglyceride. These triglycerides are then deposited into adipose tissue cells that
have a virtually unlimited storage capacity. This long-term storage unit is commonly
(and for many un-affectionately) known as “body fat”, and in large quantities results in
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obesity. This is how sugar, if not metabolized (burned) for energy, can ultimately be
converted into fat and why diets with a high sugar content [without a simultaneously high
caloric/energy expenditure] can lead to excessive weight gain and ultimately obesity as
well as metabolic disorders.
Glycogen is stored in the liver and skeletal muscle cells and is a considered “long
term” energy storage unit, versus adenosine triphosphate (ATP), which is “short term”
energy storage. When blood sugar levels drop excessively, the hepatic cells hydrolyze
glycogen back into glucose (a process called glycogenolysis) thereby releasing the
glucose molecules into the blood stream. While both skeletal muscle cells and liver cells
can store glycogen, only hepatic cells contain the enzyme glucose phosphatase necessary
to release glucose back into the blood.
As mentioned earlier, when the cellular glycogen storage units are saturated, liver
and fat cells can convert the remaining glucose into glycerol and fatty acids to form
triglycerides, a process called de novo lipogenesis (a.k.a. hepatic de novo lipogenesis,
lipogenesis, or DNL; lipo = fat and genesis = creation). Unlike glycogenesis, de novo
lipogenesis is a “one way street” in that fat cannot be hydrolyzed back into glucose for
utilization. Some studies have shown that overconsumption of carbohydrates can result
in anywhere from a two to threefold increase88 up to a six to tenfold increase89 of de novo
lipogenesis. In a study of long-term consumption of fructose and glucose on de novo
lipogenesis, dyslipidemia, insulin resistance and visceral adiposity, Stanhope et al. (2009)
discovered that hepatic de novo lipogenesis increased during prolonged fructose
consumption but remained unchanged during (and after) prolonged glucose
consumption.90 Test results confirmed that increased de novo lipogenesis generates fatty
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acids which are ultimately used in the formation of triglycerides. While both fructose-fed
and glucose-fed groups experienced weight gain (specifically, adipose tissue), they
differed in types and location of adipose tissue distribution. Their data suggests that
fructose consumption may “specifically promote” visceral adipose tissue development
whereas glucose consumption appears to favor development of subcutaneous adipose
tissue.
Metabolic Hormones: Glucagon & Insulin
Glucose metabolism and its conversion into glycogen and triglycerides for storage
has been discussed however, the blood glucose regulator insulin and its counterpart
glucagon have not. As referenced earlier, insulin is a hormone comprised of two amino
acid chains thus classified in the protein category. Insulin is just one of several hormones
secreted by the pancreas. The pancreas is comprised of two types or sections of tissue:
pancreatic acini, the exterior tissue which is responsible for secreting digestive enzymes
discussed earlier, and the islets of Langerhan’s, the more interior tissue that secretes
regulating hormones. Within the islets of Langerhan’s there are three major types of cells
cell classifications: alpha (α), beta (β) and delta (δ) cells. Alpha cells secrete glucagon,
the hormone responsible for increasing blood glucose levels; beta cells secrete insulin,
the hormone responsible for decreasing blood glucose levels; and delta cells secrete
somatostatin, a polypeptide which is able to suppress both insulin and glucagon release.
Glucagon is a large polypeptide with two primary functions in the liver: 1) breaking
down glycogen into glucose via glycogenolysis and 2) increasing gluconeogenesis, the
process of manufacturing glucose from amino acids, fats, and other substances that are
not carbohydrates. When blood glucose levels fall below normal, the pancreas secretes
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this hormone setting off a domino effect of chemical reactions resulting in the
degradation of stored liver glycogen. Once glycogen is catabolized into glucose, it is
released into the bloodstream and blood glucose levels rise. Gluconeogenesis occurs if
all of the glycogen in the liver has been expended and glucagon is still being secreted.
The hormone antithesis of glucagon is insulin. This unique polypeptide hormone
interacts with the three primary nutrients previously discussed: carbohydrates, proteins
and lipids. Glucagon is responsible for increasing blood glucose levels whereas insulin is
responsible for decreasing blood glucose levels. Insulin plays an essential role in
carbohydrate metabolism and utilization and/or storage of energy. Insulin causes excess
dietary carbohydrates that are not immediately used for energy to be converted and stored
as glycogen in the liver and smooth muscle cells. Insulin is also involved in protein
metabolism via its inhibitory effect on gluconeogenesis and is instrumental in lipid
metabolism and storage.
When large amounts of carbohydrates are consumed in a short period of time, the
result is an elevation of glucose circulating in the blood. As the body always seeks to
maintain homeostasis, this elevated blood glucose triggers the pancreas to release a surge
of insulin. When insulin is secreted, it circulates throughout the bloodstream until it
binds with target GLUT receptors imbedded within the membrane wall. Once these
target receptors are activated, the cells (such as muscle cells and adipose cells)
immediately become highly permeable to glucose. Glucose is then transported into the
interior of the cell via active transport and typical carbohydrate metabolic functions occur
and ATP energy is released. As large amounts of insulin are secreted, target receptors are
stimulated, membranes become permeable, and the excess glucose is removed from the
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blood as it is transported into the cells. Muscle cells metabolize or “burn” the energy
producing glucose via contraction of the muscle, i.e. exercise. If after several hours this
does not occur or if there is an excessive amount of glucose, then glucose is converted
into glycogen for storage in the hepatic and muscle cells for later use.
One of the primary functions of insulin is to facilitate the conversion of glucose to
glycogen in the liver. Insulin influences this process in three ways: 1) it inhibits the
hepatic enzyme phosphorylase that is, necessary for catabolizing glycogen into glucose,
2) it increases the enzymatic activity of glucokinase, the enzyme responsible for the
phosphorylation of glucose thereby essentially trapping the glucose in the cell
[preventing it from reentering the blood stream] and 3) it increases other enzymes
involved in glycogen synthesis, such as phosphofructokinase and glycogen synthase. The
relevance of this conversion process is that approximately two to three hours after a meal
blood glucose levels begin to drop and the body (i.e. cells) needs energy (glucose). When
this occurs the stored glycogen can be readily converted into glucose for immediate use.
The mechanism involved in the insulin-protein metabolism relationship is not as
well understood as with carbohydrate or lipid metabolism, however insulin does
positively influence protein integrity. That is, preservation of proteins. Scientists have
discovered that insulin decreases the rate at which amino acids are released from the
muscle cells thereby inhibiting protein catabolism. 91 Insulin also inhibits protein
degradation by hindering gluconeogenesis thus preserving amino acids that would have
otherwise been catabolized and converted into glucose. Without the presence of insulin,
protein degradation occurs and catabolized amino acids are released into the blood and
ultimately excreted via urine. One of the most dangerous effects of diabetes mellitus is
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this dumping and excretion of protein that can lead to muscle wasting if not arrested.
In addition to decreasing blood glucose levels, increasing hepatic glycogen levels
and inhibiting protein degradation, insulin is intricately involved in lipid metabolism and
storage. If the body is busy pulling excess glucose from the blood to utilize for energy it
means that it is not catabolizing stored adipose tissue for energy production. Not only
does insulin, in essence, preserve current adipose (fat), it also promotes future adipose
deposits. As previously discussed, insulin secretion results in a surge of glucose to
entering cells, primarily hepatic and smooth muscle cells. If both cells and cellular
glycogen stores are saturated, glucose is then converted into fatty acids that are then
stored as triglycerides in adipose cells. It has been discovered that insulin has an
inhibitory effect on lipoprotein lipase, an enzyme residing in the capillary epithelial wall
of the liver and adipose tissue that hydrolyzes triglycerides into glycerol and fatty acids.
Thus, insulin actually promotes stored adipose preservation. In the absence of insulin,
lipoprotein lipase is activated and hydrolysis of triglycerides occurs resulting in surge of
fatty acids and glycerol molecules in the blood stream. The liver will convert some of
these excess fatty acids into cholesterol and phospholipids that are also released into the
bloodstream. This high blood lipid content can lead to a plaque build up (or thickening)
of the arterial wall ultimately resulting in atherosclerosis. This condition can seriously
impede healthy blood flow and greatly increase the risk of heart attack or stroke.
Research within the last few decades has also discovered that insulin affects leptin release
[discussed in detail shortly] and can acutely increase plasma leptin levels.92
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LIPIDS
Lipids are a group of organic compounds containing hydrogen, carbon and oxygen
but unlike carbohydrates they do not contain a 2:1 hydrogen to oxygen ratio. Because
there is a lower O2 content, there are fewer polar covalent bonds thus resulting in
insolubility in polar solvents such as water. Hence the origin of the adage oil and water
don’t mix. Since they do not flow freely in high water content blood, lipids often
combine with proteins, specifically lipoproteins, for efficient transport throughout the
bloodstream. Lipids are essential to healthy function and have several sub-classifications
or sub-categories: triglycerides (a.k.a. triacylglycerols), phospholipids (lipids that contain
phosphorus), steroids (most notable, cholesterol), lipoproteins, eicosanoids and other
lipid substances including vitamins E and K.
Triglycerides are the most abundant lipid in the body and are known as “neutral
fats”. They are the body’s most highly concentrated source of energy and are the primary
unit for energy storage in adipose tissue. Triglycerides are comprised of a glycerol
molecule and three fatty acids (hence tri-glycerides). Depending upon bonds between
fatty acids, triglycerides can form saturated, mono-unsaturated or polyunsaturated fats.
Phospholipids form cell membranes and are found in high concentrations in nerves
and brain tissue. They are comprised of a polar “head” and two non-polar “tails”; the
non-polar tails line up touching ends and the polar heads face outwards. This formation
creates the membrane for every cell; healthy cells must have healthy membranes and
these membranes are comprised of lipids. Each steroid (cholesterol, vitamin D, sex
hormones and bile salts) has a different function in the body. Cholesterol comprises cell
membranes and is an essential precursor to vitamin D, bile salts and hormones. Vitamin
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High Fructose Corn Syrup and Childhood Obesity
D is necessary for bone growth and repair as well as calcium regulation. Bile salts are
essential for digestion and emulsification of fat for absorption; in addition, they are
necessary for absorption of fat-soluble vitamins A, E, D and K. The sex hormones
estrogens, progesterone and testosterone are lipids that regulate and stimulate
reproductive organs and are essential for healthy function. Lipoproteins (discussed in
detail later in this chapter) are lipid-protein molecules that help transport lipids to the
liver and adipose tissue for storage as well transport cholesterol to cells and remove any
excess from the blood. Eicosanoids are lipid substances that are involved in an array of
processes from blood clotting and inflammation to stomach acid secretion and smooth
muscle contraction of the intestinal tract. As one can see, lipids are an integral part of
the body’s healthy functioning
The first step of the digestion of dietary fats is the emulsification process whereby
larger fat globules are broken into smaller ones so that enzymes can begin to break down
their surfaces. Bile salts and lecithin, both found in the liver, are required and responsible
for successful fat emulsification. The polar parts of bile salts and lecithin attach to the
polar portions of the on the surface of the fat globule dissolving the surface layer making
the molecule fragile and easily fragmented during peristalsis of the bowels. Once the
smaller, more fragile molecules enter the small intestine, pancreatic enzyme lipase breaks
down the emulsified fat molecules into fatty acids and two monoglycerides. [Illus. 6]
Illus. 6 Author’s Schematic FAT
Bile & Peristalsis
Emulsified
Fat
Pancreatic Lipase
FATTY
ACIDS
Monoglyceride Monoglyceride High Fructose Corn Syrup and Childhood Obesity
p. 53
Outside of the cell, monoglycerides and fatty acids are dissolved in the bile acid
and diffuse into the cellular fluids via the microvilli of the brush border; from there they
then diffuse through the intestinal epithelial membrane into the endoplasmic reticulum.
Once inside the endoplasmic reticulum of the cell, the fatty acids and monoglycerides
essentially re-combine to form “new” triglycerides. These new triglycerides aggregate
with cholesterol, phospholipids, β-lipoprotein to form a chylomicron. Chylomicrons are
then transported into the lymph system. 80-90 percent of all digested fat is metabolized
and absorbed this way and transported into the blood via chylomicrons and the lymphatic
system. Once all of the chylomicrons have been removed from the blood, the remaining
lipids in the blood plasma are in the form of lipoproteins. Lipoproteins are smaller than
chylomicrons but have a similar composition; they too contain cholesterol, phospholipids,
triglycerides and protein.
The function of lipoproteins is to transport various lipid components in the blood;
some transport cholesterol while others transport triglycerides. Lipoproteins are broken
into several classifications: Low Density Lipoproteins (LDL), Very Low Density
Lipoproteins (VLDL), and High Density Lipoproteins (HDL). Compositionally, LDLs
have a higher cholesterol level (55%) and lower triglyceride (20%) and protein (25%)
levels. LDLs deliver cholesterol to various cells in the body, smooth muscle fibers in
arteries for example. VLDLs have higher triglyceride levels (65%) and lower cholesterol
(25%) & protein (10%) levels. VLDLs transport triglycerides to the fat cells in adipose
tissue for long-term storage. After depositing the triglycerides they are then converted
into LDLs. Of the lipoproteins, HDLs contain the lowest level of cholesterol (13%), the
highest level of protein (50%), and a moderate level of triglycerides (37%). The function
High Fructose Corn Syrup and Childhood Obesity
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of HDLs is to remove excess cholesterol from body cells and transport it to the liver for
elimination. This street sweeper function has earned them the name of “good
cholesterol” as they help clean the blood and prevent accumulation of cholesterol on the
arterial walls (a.k.a. the infamous “plaque”).
METABOLIC THEORIES
Over the years, several theories regarding metabolism and metabolic regulatory
pathways have emerged. While each have a different locus of control, they all include
the interaction of neurological pathways in the brain. The hypothalamus is the portion of
the brain that, among other activities of the central nervous system, is responsible for
regulating homeostasis. The principle functions of the hypothalamus are: control the
autonomic nervous system (ANS), regulate body temperature, regulate food intake,
regulate thirst, plays a role modulating the circadian rhythm (i.e. 24 hour sleep-awake
cycle), and is also associated with emotions of rage and aggression. The hypothalamus is
divided into four primary regions housing twelve neuron clusters. The two neuron
clusters actively engaged in caloric intake are: the lateral hypothalamic cluster (a.k.a. the
feeding/hunger center) and the ventromedial nuclei (a.k.a. the satiety center). Stimulation
of the lateral hypothalamic cluster causes animals (including humans) to eat heartily,
whereas stimulation of the ventromedial nuclei causes a cessation of food intake.
Scientists have studied the intricacies of the hypothalamus and its various functions
for decades; yet ironically, in the same year (1953) two different theories regarding the
hypothalamic regulation of energy consumption and expenditure emerged: the glucostatic
theory and the lipostatic theory. According to the glucostatic theory, changes in blood
glucose concentrations are detected by glucoreceptors in the hypothalamus and affect
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energy intake (i.e. food consumption). An increase in blood glucose concentrations
results in increased feelings of satiety resulting in a cessation of consumption.
Conversely, a decrease in blood glucose concentrations diminishes the activity in the
hypothalamus [specifically the ventromedial nuclei] which in turn shuts down or inhibits
the satiety center thereby causing/spurring the individual to eat.93
The lipostatic theory regarding food intake regulation centers around lipid
metabolism rather than sugar (glucose) metabolism. The lipostatic theory posits that
hormones and other metabolic products resulting from fat metabolism (metabolic
byproducts so to speak) circulating in the blood signal the hypothalamus indicating how
much adipose tissue is in the body. It was hypothesized that in an effort to maintain the
body’s adiposity (i.e. maintain the same level of body fat) these substances inhibit the
satiety center in the hypothalamus resulting in a continuation of consumption. 94 During
this same period, geneticists were also investigating the role of genes and genetic markers
with respect to satiety, adiposity and energy expenditure lending to complex theories
regarding intricate neural networks, pathways and feedback loops. Leptin was one of
those discovered markers whose role in metabolic functions specific to food intake and
energy expenditure is still being investigated.
Leptin
Leptin (synonymously referred to in scientific literature as the “ob gene protein
product”, “ob protein” or “ob product”) is a hormone protein predominantly produced in
adipocytes of white fat tissue95 that, although not completely understood, is thought to be
a lipostatic signal “that contributes to body weight regulation through modulating feeding
behavior and/or energy expenditure”.96 In short, this hormone protein helps regulate
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and/or inhibit food intake, increase energy expenditure (burning of fatty acids) and
subsequently reduce body fat. In 1950, while studying the genetic make up of
excessively voracious, obese mice, Dr. Margaret Dickie of The Jackson Laboratory
discovered the obese (ob) mouse gene. Dr. Dickie found that severely obese mice were
homozygous for a single gene mutation (named ob) increasing in weight until they were
nearly four times the size of a normal mouse.97 Homozygous ob/ob (also known as ob or
Lepob 98) mice have a mutation in the gene for the protein leptin 99; this mutation prevents
the ob/ob mouse from manufacturing leptin. Ob/ob mice are also hyperphagic (unable to
stop eating) and exhibit the diabetes-like syndromes of hyperglycemia, glucose
intolerance, elevated plasma levels and impaired wound healing.100 Shortly thereafter in
1966, Dr. Douglas Coleman (also of The Jackson Laboratory) initiated several
experiments building upon Dr. Dickie’s research. In 1972, he discovered the
homozygous db/db mutation (also known as db, Leprdb or the diabetes mutation101) and
postulated that the db/db mouse has a genetic defect in its satiety center. Db/db mice
have a mutation in the leptin receptor (LEP-R) resulting in elevated levels of leptin in
their blood. The LEP-R receptors are located in the gut as well as muscle tissue however,
the highest concentration lies within the ventromedial hypothalamus. In addition to being
obese, the mice are also polyphagic, polydipsic, polyuric, exhibit hyperplasia of the islet
β cells (pancreatic), hyperinsulinemia and exhibit impaired wound healing.102 According
to reports, Dr. Coleman’s theories eventually led to the successful cloning of the genes
behind the ob and db mutations by researchers at The Rockefeller University in the mid
1990s.
Dr. Jefferey Friedman and his colleagues at The Rockefeller University are credited
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with discovering the protein hormone leptin while investigating the positional cloning
(i.e. DNA sequencing) of the mouse ob gene and its human counterpart in 1994.103 Leptin
deficiency has been directly associated with obesity (and other neuroendocrine
anomalies) in both mice and humans.104 Campfield et al. (1995) discovered that when
injected with leptin, ob/ob mice reduced food intake and body weight however, this
reaction did not occur with db/db mice leading them to surmise that leptin acts directly on
neural networks that control feeding and energy balance.105 Although how remained an
unknown.
In 2004, Dr. Friedman reported that experiments with human subjects revealed that
weight gain resulted from increased circulating plasma leptin levels. Conversely, both
obese and lean subjects lost adipose tissue when plasma leptin levels were decreased.106
Although not completely understood, scientists have concluded that leptin interacts with
neural receptors in the central nervous system, specifically in the hypothalamus, in some
sort of a negative feedback loop.
With respect to satiety and food regulation, researchers have since discovered that
leptin specifically influences two neurons located in the arcuate nucleus of the
hypothalamus: neuropeptide Y (NPY) and pro-opiomelanocortin (POMC). Leptin
suppresses the activity of NPY neurons while it simultaneously enhances the activity of
POMC neurons.107 NPY neurons affect feeding behavior, specifically by stimulating
appetite and food intake (as well as other roles not relevant to this paper) whereas POMC
suppresses appetite and food intake.108 Dr. Shirley Pinto and her colleagues at The
Rockefeller University discovered that leptin alters the number of neural connections that
either excite or inhibit NPY and POMC by altering the synaptic inputs of these
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neurons.109 So leptin plays a key role in when and how much an individual consumes.
Leptin also influences glucose metabolism, which in turn, influences adipose production
and storage. Studies have also shown that in mice leptin can influence hepatic glucose
production by increasing gluconeogenesis while simultaneously decreasing
glycogenoloysis.110 Thus, leptin increases the manufacturing of glucose from amino
acids, fats, and other substances that are not carbohydrates while decreasing the
hydrolysis of stored glycogen into glucose. This means the stored glycogen that is not
hydrolyzed into glucose for utilization will eventually be converted into fat. Liu et al.
(1989) concluded that, “it is likely that these metabolic effects of leptin participate to the
regulation of hepatic glucose metabolism under physiological conditions.”111
In a human case study by Dr. I. Sadaf Farooqi and his colleagues (1999), a
morbidly obese nine-year-old girl with congenital leptin deficiency (a condition marked
by the inability to sense being full112) was injected with recombinant methionyl leptin
subcutaneously once a day for 12 months. At the onset of this trial, the young girl’s
weight registered in the 99.9th percentile weighing 94.4 kg (208 lbs.) at a height of 140
cm (4’8”). Of the 94.4 kg (208 lbs.), 55.9 kg (123 lbs.) of her weight was fat; almost
60% of her body was adipose tissue. After 12 months of therapy her total weight loss
was 16.4 kg (36 lbs.) of which adipose tissue (i.e. body fat) comprised 15.6 kg (34 lbs.).
During the trial, her energy expenditure remained constant thus the weight loss,
specifically the loss of adipose tissue, was directly attributed to the introduction of leptin
into her system.113 In a 2002 follow up study, Farooqi et al. reported similar findings
with three other children who also had congenital leptin deficiency.114 One caveat to Dr.
Farooqi’s studies is that all the individuals had the ob genetic mutation, the real question
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is would he yield the same results in obese individuals without the genetic anomaly?
Emilsson et al. (1997) suggest that leptin may have an effect on pancreatic β-cells
inhibiting insulin secretion.115 This is important because maintaining proper blood
glucose levels is a continuous regulatory process essential to health and function.
Adverse conditions such as hypoglycemia, diabetes mellitus (NIDDM), hyperlipidemia,
insulin resistance and obesity can result from chronic irregularities.
METABOLIC IMBALANCES & DISORDERS
Hypoglycemia
Low blood glucose levels mark a condition called hypoglycemia. In hypoglycemic
individuals, often copious amounts of insulin are secreted by the pancreas resulting in a
rapid cellular uptake of blood glucose. This rapid cellular uptake of glucose results in a
rapid decrease of glucose circulating in the bloodstream. When blood glucose levels drop
precipitously, the adrenal glands secrete epinephrine, cortisol and other stress hormones
that stimulate the release of stored glycogen. Common symptoms of hypoglycemia are
weakness, dizziness, increased heart rate, hunger, anxiety and sweating. These symptoms
do not result so much from the drop in blood glucose but rather from the surge of stress
hormones released. Nevertheless, this condition is serious and if untreated can result in
more deleterious effects such as mental disorientation, convulsions and even shock.116
Insulin Resistance
The insulin resistance syndrome (a.k.a. Syndrome X, metabolic syndrome X and
Reaven Syndrome117) has traditionally been used to describe a clustering of metabolic
abnormalities that originally included glucose intolerance, insulin-stimulated glucose
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uptake, hyperinsulinemia, hypertension, dyslipidemia marked by high triglycerides (TG)
and low HDLs, but has recently (2002) expanded to include small, dense LDLs, increased
uric acid concentrations, decreased levels of adiponectin (a hormone protein with similar
functions as leptin) and increased levels of plasminogen activator inhibitor 1 (inhibits the
activators which break down blood clots).118 In layman’s terms it is simply as the name
implies, the body becomes resistant to insulin. After prolonged and excessive sugar
consumption the adipose and muscle tissue cells become saturated with glucose
molecules. To prevent further overload, the cells reduce the number of active insulin
receptors by locking/inactivating them, a mechanism that although identified is still not
wholly understood. The pancreas then secretes even more insulin in an attempt to
override the cells’ resistance, a condition called hyperinsulinemia. In response to the
surge of insulin, the cells “lock” more insulin receptors and the cycle continues. Any
glucose circulating throughout the bloodstream is diverted into adipose tissue for longterm storage but if those cells are saturated the glucose remains circulating in the
bloodstream which can ultimately lead to NIDDM (type 2 diabetes).119 In an analysis of
fructose, weight gain and the insulin resistance syndrome, Sharon Elliott and her
colleagues (2002) purport, that while a considerable amount of research still needs to be
done particularly with human subjects, elevated fructose consumption is clearly a
contributor “to nearly all the classic manifestations of the insulin resistance syndrome”
including hyperinsulinemia, hyperlipidemia, hypertension, and impaired glucose
tolerance.
Diabetes Mellitus
Perhaps the most serious condition associated with an insulin imbalance is the
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metabolic disorder (which some argue is a “disease”) diabetes mellitus, a.k.a. diabetes.
Diabetes is classified into two types: Type 1 Diabetes, also known as insulin-dependent
diabetes mellitus (IDDM) or “juvenile diabetes” and Type 2 Diabetes, commonly
referred to as non-insulin-dependent diabetes mellitus (NIDDM) or “adult onset”.120
Type 1 diabetes most often occurs in young children and is s classified as an autoimmune
disorder wherein the immune system destroys the beta cells in the pancreas thus insulin is
never produced. For these individuals, insulin must be administered via injection to
ensure proper blood glucose levels. Approximately 5-10 percent of all diabetics have
type 1 diabetes which leaves an astounding 85-90 percent that fall in the latter category.
Type 2 diabetes (non-insulin-dependent diabetes mellitus or NIDDM) is a metabolic
disorder as opposed to an autoimmune disorder. In type 2 diabetes, the pancreas is able
to secrete insulin but the target cell receptors are less responsive to the insulin. This
decreased cellular sensitivity to insulin results in an inability to remove excess sugar from
the bloodstream. The primary difference between the two classifications of diabetes
mellitus is that type 1 diabetics have significantly decreased levels of insulin whereas
type 2 diabetics have normal to high levels of insulin but their cell receptors are resistant
to it. Another significant difference is that type 2 diabetes is environmentally induced
resulting in diminished metabolic function, whereas type 1 diabetes is predominantly
genetically/biologically induced, the individual is born with a physiological malfunction
of the pancreatic beta cells resulting in an inability to produce insulin. Although recent
research has shown that environmental factors also can also contribute to the onset of
type 1 diabetes as well. 121 Approximately 80-90 percent of type 2 (NIDDM) diabetics
are obese and it is the excess adiposity (and consumption of certain foods resulting in that
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excess adiposity) that has caused the diabetic condition to emerge. Regardless of the
category, type 1 and type 2 diabetes share the same fundamental markers: 1) high blood
glucose levels (300-1200 mg/dl), 2) abnormal fat metabolism and 3) protein wasting all
of which are dangerous and, if not arrested, can become deadly.
Hyperlipidemia
Hyperlipidemia, as the name implies, is the condition of excessive blood lipids
(hyper = over, excessive and lipid = fat), also known as dyslipidemia,
hypercholesterolemia, or hyperlipoproteinemia. Excess blood lipids (cholesterol)
circulating in the blood can begin to line (or coat) the arterial walls eventually
diminishing, and in some cases blocking altogether, essential blood flow. Often this
condition is linked to diabetes and is a significant risk factor for cardiovascular disease
and stroke due to the influence on arterial plaque buildup.
A common denominator of all these conditions is that their origin ultimately
begins at phase I: mastication. High sugar foods translate into high sugar blood. These
are the most prevalent metabolic disorders that can result from metabolic imbalances and
erratic blood glucose levels. While not an exhaustive list, they provide a glimpse as to
how serious excess adiposity can become.
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CHAPT. 3- High Fructose Corn Syrup
HISTORY & ORIGINS: HOW AND WHY HFCS WAS MADE
The chemical conversion of glucose to fructose [that is converting a glucose
molecule into a fructose molecule via induced chemical reactions], known as the Lobry
de Bruyn-Alberda van Ekenstein transformation, was first discovered in 1885 by Cornelis
Adriaan Lobry van Troostenburg de Bruyn and Willem Alberda van Ekenstein.122
Twentieth century scientists continued to experiment with various chemical reactions and
hopeful conversions. However, some incommodities of the chemical process are that it
produces non-metabolized substances (byproducts), yields less than 40% fructose and has
reduced sweetness and notable “off flavors”.123 Because of these disadvantages,
scientists began experimenting with other catalytic facilitators, namely enzymes.
In 1957, Richard Marshall and Earl Kooi discovered the enzymatic conversion of
glucose into fructose using xylose isomerase (a.k.a. D-Glucose/xylose isomerase, Dxylose ketol isomerase; glucose isomerase124). In their endeavor to disprove the
prevailing hypothesis that xylose isomerase was unable to act on aldoses besides Dxylose specifically, they discovered that not only was the enzyme able to act on other
aldoses (such as D-glucose), but that under specific conditions, it would actually
transform/convert glucose into fructose.125 They placed 90 g. of D-glucose in 500 ml of
arsenate (similar to phosphate) buffer containing 2.5 mmole of magnesium chloride
(MgCl2) and 5.0 g. of lyophilized (freeze-dried), xylose rich Pseudomonas hydrophila
cells and allowed the solution to rest in a sealed container for 48 hours. After the
incubation process, they discovered the solution yielded 29.2 g of D-fructose. They
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concluded that, “present evidence warrants only speculation on the metabolic
significance of the isomerization of other sugars by this enzyme” and suggested future
investigation of other “d-glucose isomerizing activity in other microorganism, and on the
substrate specificity of the enzyme”.126 Japan’s Dr. Yoshiyuki Takasaki was one such
scientist to pursue that investigation.
For years, Dr. Takasaki studied sugar-isomerizing enzymes for Japan’s Agency of
Industrial Science and Technology, Ministry of International Trade and Industry.127 In
his research on Production and Utilization of Glucose Isomerase from Streptomyces sp
(1966), Takasaki noted that a few problems existed for the commercial use of glucose
isomerase enzymes, most notably the cost of cultivating the enzyme. 128 He discovered a
method for cultivating the enzyme from “cell-free extracts of a strain of Streptomyces sp.
isolated from soil”.129 This was a monumental (and subsequently profitable) discovery as
the enzyme was now able to be cultivated in a more economic medium, soil. Later,
Takasaki (1971) discovered the amount of fructose yielded was dependent upon the
sugar-borate ratio. He was able to convert 88-90% of glucose into fructose with a 1:1
sugar-borate ratio and a 7.5 pH, substantially more than Marshall and Kooi’s 40%.130 The
volume of yielded fructose was yet another significant step in the journey to commercial
mass production and thus he is credited with creating the industrialized process of
manufacturing high fructose corn syrup (HFCS).
The production of HFCS has three primary enzymatic “steps”: liquefaction,
saccharification and isomerization.131 (Illus. 7 chronicles this process) First, starch must
be extracted from the corn. Corn is soaked in hot water (approx. 140°) with sulfites,
caustic soda and hydrochloric acid for two days until the kernel swells and break into
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four components: germ, starch, hull and protein. 132 The starch of the corn is composed
of the glucose-containing polysaccharides amylose and amylopectin (disaccharide and
polysaccharide) and requires significant heat and additional enzymes to hydrolyze into
the simple sugar glucose. Once the starch is extracted, the enzyme α-amylase (extracted
from Bacillus spp.133) is added and hydrolyzes the polysaccharides into shorter chained
dextrins and oligosaccharides [liquefaction step]. A second enzyme
glucoamylase/amyloglucosidase (extracted from the Apergillus fungi 134) is added and
hydrolyzes the dextrins and oligosaccharides into the simple sugar glucose
[saccharification step]. The result of these two enzymatic steps is glucose syrup,
commonly known as corn syrup. The third step, isomerization, is the most complex (and
costly) step which converts the glucose into fructose via enzymatic hydrolysis and liquid
chromotography. The use of glucose isomerase (also called D-glucose ketisomerase or
D-zylose ketoisomerase) is more intricate than the two previous enzymes. Whereas αamylase and glucoamylase are added directed to the mixture, in the isomerization step the
mixture (i.e. glucose syrup) is passed over a support structure containing glucose
isomerase (hence the glucose is stationary and “immobilized”). The immobilized glucose
isomerase is reused until most of the enzymatic activity is exhausted. The result of this
isomerization step is a liquid containing 90% fructose and 10% glucose, commonly
referred to as HFCS-90 or industrial HFCS. HFCS-90 is then blended with glucose
syrup to produce HFCS-55 (55% fructose 45% glucose) and HFCS-42 (42% fructose and
58% glucose).
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High Fructose Corn Syrup and Childhood Obesity
Illus. 7 High Fructose Corn Syrup (HFCS) enzymatic production process-­‐ author’s schematic. oligosaccharides Corn [wet milled] Corn Starch glucose isomerase & HFCS 90 (industrial) (enzyme) chromatography step HFCS 55 α-­‐amylase (enzyme)
Glucose (corn syrup) (dextrins & maltodextrins) glucoamylase/ amyloglucosidase (enzyme) HFCS 42 The wet milling process has recently drawn attention as there are growing concerns
surrounding the use of mercury grade caustic soda (a.k.a. sodium hydroxide or lye) as a
primary medium during this phase of processing. “Caustic soda” is a mercury cell chloralkali product known for its catalytic properties and widely used in manufacturing
processes. From a health and nutritional perspective, these products are concerning
because the process of making them requires electrolysis of sodium chloride via a
mercury cell and mercury is extremely toxic.135As with most chemical processes, there is
a transfer of compounds that occurs which is not necessarily desirable but often deemed
acceptable by the manufacturer. However, the problem occurs when the substance
transferred is a known toxin. In an investigation of measured mercury concentrations in
food, Renee Dufault and her colleagues (2009) discovered that in a 2005 field test of
twenty samples of HFCS (both 42 and 55), 45% contained mercury ranging from 0.00 to
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0.570 µg mercury/g HFCS. They estimated that that the average mercury exposure from
HFCS could range from zero to 28.4 µg.136 A now recognized toxin, mercury is able to
enter the endothelial cells of the blood-brain and placenta barriers (hence the FDA
warning pregnant women to refrain from eating seafood which often contains mercury
and other PCBs). Gradually, mercury can accumulate in the kidneys, liver and brain
tissue affecting both the central nervous system as well as key metabolic processes.137
According to Dr. Choong Yong Ung (2010), within 24 hours of ingestion or
inhalation, mercury is absorbed into the gastrointestinal tract, metabolized and distributed
throughout the body via red blood cells.138 Furthermore, Ung et al.’s research into
mercury-induced hepatotoxicity revealed that mercury can cause liver damage via
oxidative stress and cell death, as well as deregulating kinases (such as glucokinase)
responsible for gluconeogenesis and adipogenesis that “may eventually lead to
syndromes such as mitochondrial dysfunction, endocrine disruption and metabolic
disorders.”139 (italics added)
DISCOVERY, USE AND PREVALENCE
Due to the high fructose content and subsequent sweetness, HFCS-55 is used in
beverages such as carbonated drinks, energy drinks and fruit juices. Because it does not
crystalize like its sucrose counterpart, it makes it the ideal sweetener for beverages from a
manufacturing standpoint as well as a distribution standpoint (i.e. crystallization will not
occur once it is sitting on a shelf). HFCS-42 is not as sweet as HFCS-55 and therefore is
used in baked good, processed foods, condiments, dairy products such as yogurt,
pudding, and ice cream, sherbet and other frozen deserts. Some processed foods such as
desert items could probably get away with using HFCS-55 however, very few people (if
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any) would want their macaroni and cheese or hotdog to taste as sweet as a Coke or
Pepsi.
Outside of the growing organic movement, whether food product or beverage,
HFCS has been the predominant sweetener used in the food and beverage industry in the
United States for the last 25 to 30 years. On a relative sweetness scale with sucrose (table
sugar) equaling 100, glucose has a sweetness of 70-80, fructose has a sweetness of 140,
and HFCS ranges from 120-160 (depending upon fructose concentration).140 The
intensity of sweetness is of great financial significance to food and beverage
manufacturers. Ounce per ounce, HFCS is sweeter than sucrose (cane/beet sugar) and
that means less of it is needed to achieve the same (if not higher) level of sweetness as
sucrose. Once people are accustomed to a certain level of sweetness it is difficult for
them to reduce it. The same behavior occurs with sodium chloride (table salt), people
become accustomed, or more accurately desensitized, to high levels of sodium (table salt
not naturally occurring sodium) added to food and thus when it is diminished or removed
from the food it tastes “bland”.
ECONOMIC EFFECTS
While Marshall and Kooi are credited with the discovery of enzymatic conversion,
Takasaki is often credited with the evolution and industrialization of this process for the
purpose of mass production. According to Bhosale et al., Clinton Corn Processing
Company introduced the production of glucose isomerization (GI) “on an industrial
scale” in 1967, however, GI was not officially commercially available in the United
States until 1974.141 By 1980, almost all starch-processing companies were utilizing GI
technology and it still commands the largest market share in the food industry to date. It
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can be concluded from earlier discussion of Takasaki’s research that the economic cost
benefits were a motivational factor ushering in the technological advances for mass
production of HFCS. Serendipitously, at the same time that Takasaki and his team were
perfecting GI for mass production, the price of corn commodities was dropping
precipitously.142 According to Heather Schoonover and Mark Muller of the Institute for
Agriculture and Trade Policy (IATP) (2006), for manufacturers, HFCS was and is an
economical sugar substitute because, “Sugar is one of the few commodities for which a
government price support program still exists. To ensure fair price for farmers and to
maintain a domestic source, sugar prices are kept above a minimum price floor,
guaranteeing that sugar prices cannot fall below the cost of production. Replacing sugar
with a corn product, therefore, can represent a substantial cost savings to food
manufacturers.”143
In 1970, HFCS represented less than 1% of caloric sweeteners in the United States.
Today, it comprises over 40% of all sugar consumption in the U.S. and is a $2.6 billion
dollar industry.144 Using the U.S. Department of Agriculture food consumption tables
from 1967 to 2000, Bray et al. (2004) analyzed food consumption patterns in the United
States and discovered the consumption of HFCS increased more than 1000% between
1970 and 1990, “far exceeding the changes in intake of any other food or food group”.145
HFCS is the primary sweetener in both manufactured food and beverages, including but
not limited to: carbonated beverages, fruit juices, cereals, breads, cookies, biscuits, jams
& jellies, yogurt, ice cream, frozen deserts, canned foods, spaghetti sauce, lunch meat,
pizza and salad dressing.146 HFCS-42 was introduced into the U.S. market in 1967 for
use in foods (i.e. baked goods) as the sweetness was not enough to trump the flavor of the
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food itself. The sweeter HFCS-55 followed ten years later in 1977, replacing sugar (cane
and beet sugar) and becoming the predominant sweetener used in beverages.147 By 2000,
HFCS-55 constituted 61% of all HFCS produced. There are several reasons HFCS has
replaced sugar in the food and beverage manufacturing industry: 1) HFCS is cheaper than
sucrose- 32 cents per pound versus 52 cents per pound, 2) HFCS is a liquid and therefore
easier to transport and use in beverages, 3) HFCS (both 42 and 55) is sweeter than
sucrose, 4) HFCS has a higher solubility than sucrose and 5) HFCS is acidic, containing
preservative properties and therefore maintains a longer shelf life under certain
conditions.148
CONSUMPTION TRENDS
In their analysis of consumption, prices and expenditures in the United States,
Judith Putnam and Jane Allshouse (1999) analyzed per capita consumption of major food
commodities in the United States over a twenty-seven year period, 1970-1997. Between
1982 and 1997, per capita consumption of sugar, primarily sucrose (been and cane sugar)
and HFCS, increased 34 pounds (roughly 28%) to a record average of 154 pounds per
annum, per person. That equates to 53 teaspoons of sugar per person, per day. A
teaspoon of table sugar yields 16 calories thus and additional 53 teaspoons of sugar a day
equates to an additional 848 calories a day. This is approximately half of the daily
caloric requirements of most adults [based upon 1500 kcal/day for women and 2000
kcal/day for men149].
Putnam and Allshouse discovered that not only was there a significant increase in
total sugar consumption, but also in types of sugar consumed. In 1970, sucrose was the
primary sugar sweetener used in the food and beverage industry yielding 83% of the
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High Fructose Corn Syrup and Childhood Obesity
market share for calorie consumption, however, by 1997 that percentage had plummeted
to 43%. Conversely, HFCS’s total share of use and consumption rose from 16% (1970)
to 56% (1997) [Figure 5]. Not surprisingly, per person-per pound consumption of
sucrose and HFCS follow the same trajectory. In 1970, annual per capita use of sucrose
was 102 lbs., by 1997 that number had decreased to 60 lbs. per person. However,
individual consumption of HFCS per annum skyrocketed from 0.5 lbs. in 1970 to 62.4
lbs. per person in 1997 [Figure 6]
100% Percentage of Sucrose and HFCS used as primary caloric sweetener in the U.S. 83% 80% 56% 60% 43% 40% 16% 20% 0% 1970 Sucrose HFCS 1997 Figure 5. The percentage of Sucrose and HFCS as primary caloric sweetener in the U.S. Resource: Putnam and Allshouse, 1999: Data Source from UDSA Economic Research Service. Statistical Bulletin No. 965. Graphic created by author. p. 72
High Fructose Corn Syrup and Childhood Obesity
Use of Sucrose and HFCS per pound per person 120 102 100 80 62.4 60 60 40 20 0.5 0 1970 Sucrose HFCS 1997 Figure 6 Use of Sucrose and HFCS per pound per person. Resource: Putnam and Allshouse, 1999: D ata Source from UDSA Economic Research Service. Statistical Bulletin No. 965,. Graphic created by author. Further analysis of the USDA Economic Research Service (ERS) data tables (tables
30, 51 & 52) reveal interesting trends, especially when cross-referenced with obesity
trends. Sucrose (table sugar) consumption experienced its sharpest decline between 1970
and 1986 decreasing from 72.5 lbs./yr. to 42.8 lbs./yr. respectively. Conversely, HFCS
experienced its sharpest rise in consumption within that same period from 0.4 lb./yr. to
32.3 lbs./yr. After 1986, HFCS consumption increased steadily until peaking at 44.2
lbs./yr. in 2002 while sucrose consumption rose only fractionally. [FIG 7] In 2003,
consumption for both sucrose and HFCS was at 43.4 lbs., however, from that point
forward sucrose consumption increased slightly while HFCS consumption decreased.
Since the majority of HFCS (61%) is earmarked for beverages, some suggest that the
increased availability of bottled water and diet drinks explains the HFCS consumption
decrease. Hodan Wells and Jean Buzby (2008), from the USDA Economic Research
Service (ERS), report that between 2000 and 2005 bottled water consumption increased
from 16.7 gallons per person to 25.4 gallons. In addition, consumption of diet beverages
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High Fructose Corn Syrup and Childhood Obesity
increased 16 percent during that same time.150
Sucrose (Table Sugar) vs. HFCS ConsumpPon 80.0 Pounds per person 70.0 60.0 50.0 40.0 30.0 20.0 Sucrose lb/yr HFCS lb/yr 10.0 0.0 Fig 7. Sucrose (Table Sugar) and HFCS Consumption 1970-­‐2010. Data Source: USDA ERS Briefing Room: Sugar and Sweeteners: Data Tables 51 (2011). Graphic created by author. United States Department of Agriculture (USDA) economists Stephen Haley, Jane
Reed, Biing-Hwan Lin and Annetta Cook (2005) analyzed the distribution of sweetener
consumption in the U.S. by demographic and product characteristics between 1994 and
1996. Data analyzed consisted of food intake surveys conducted by the USDA
Agricultural Research Service (ARS) which tracks household and individual food
consumption in the United States. Total data sample consisted of 20,862 individuals:
15,303 adults in the 1994-1996 Continuing Survey of Food Intakes by Individuals
(CSFII) and 5,559 children birth to nine years of age in the child-oriented 1998 CSFII.
For the purpose of their analysis, sweetener consumption was divided into several
categories: 1) sugar (defined as refined cane and beet sugar), 2) corn sweetener (defined
as corn syrup and HFCS), 3) others (inclusive of honey, maple syrup, maple sugar,
sorghum syrup and molasses) and 4) total sweeteners (all categories combined).151 With
respect to socio-economic status of sweetener consumption, their findings are a bit
surprising. CSFII household income brackets were based on Federal poverty guidelines:
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“low income” was defined as 130% or less of the poverty level, “middle income” was
131-350% of the poverty level and 350% and over the poverty level defined “high
income”. Low-income households had the lowest per pound, per capita consumption of
sweeteners totaling 99 lbs./year; 42.7 lbs. of sugar, 54.2 lbs. corn sweetener and 2.1 lbs.
other. Middle-income households had the highest per capita consumption at 105.8
lbs./year; 47.8 lbs. of sugar, 57.5 lbs. of corn sweetener and 0.5 lb. other. High-income
households were a hair behind middle-income households with a total sweetener
consumption of 102.1 lbs./year; 46.7 lbs. of sugar, 54.5 lbs. of corn sweetener and 0.9
other. According to their estimates, low-income household sugar consumption was 8.0%
less than the national average. In addition, they conclude that refined sugar consumption
(cane and beet) is more positively correlated with increasing levels of income than corn
sweetener (HFCS) consumption.152 That is to say that low income households consumed
more HFCS than refined [cane and beet] sugar. Not altogether surprising given the
relative cheapness of prepackaged, fast foods and “junk” foods. In the U.S. food and
beverage industry, the least expensive foods are unfortunately most often the highest in
sugar (specifically HFCS) and fat and lowest in nutrients. Their assertion would seem to
support the contention suggesting lower socio-economic households consume cheap,
manufactured foods due to their inability to pay for the more costly fresh fruits,
vegetables and whole grains.
Among Hispanic, non-Hispanic Black and non-Hispanic White ethnicities, nonHispanic Black individuals had the highest per capita consumption of sweeteners
consuming 45.0 lbs. of sugar, 58.2 lbs. of corn sweeteners and 3.1 lbs. other for a total
consumption of 106.3 lbs./year. Hispanic individuals had the lowest consumption of
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sweeteners overall but the biggest differentiation between sugar and corn sweetener
consumption. Their total consumption was 94.1 lbs./year comprised of 38.2 lbs. of sugar,
55.5 lbs. of corn sweetener and 0.4 lb. of other. Non-Hispanic White individuals had the
second highest total consumption of sweeteners at 105.4 lbs./year. They had the highest
consumption of sugar at 48.6 lbs./year followed by 56.1 lbs. of corn sweetener and 0.7
other.
With respect to age variances, age categories were designated as follows: 2-11
years, 12-19 years, 20-39 years, 40-59 years and ≥ 60 years. Between genders, males
consumed more sweeteners in all categories. Average male consumption was 119.8 lbs.
of sweetener categorized into 51.8 lbs. of sugar, 66.4 lbs. of corn sweetener and 1.6 lbs.
of other. Average female consumption was a total of 86.9 lbs. of sweetener broken down
into 41.2 lbs. of sugar, 45.3 lbs. of corn sweetener and 0.4 lb. of other. What is
interesting about this data (although not terribly surprising) is that in both gender
categories, the highest total sweetener consumption occurred in individuals ages 12-19
years old. Furthermore, 12-19 year old males and females had the highest consumption
of corn sweetener among all age categories 58% for males and 57% for females. Males
(12-19 yrs.) consumed 159.8 lbs. of sweetener per year (40 lbs. more than the combined
average of all ages 2-60 and over); 65.7 lbs. of sugar, 93.0 lbs. of corn sweetener and 1.0
lb. other. Similarly, females (12-19 yrs.) consumed a total of 114.2 lbs. of sweetener;
49.5 lbs. of sugar, 64.6 lbs. of corn sweetener and 0.2 lb. other. [FIG 8]
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High Fructose Corn Syrup and Childhood Obesity
Pounds Per Person Sweetener ConsumpPon among U.S. Adults (1994-­‐1996) and children 12-­‐19 years (1998) 100 90 80 70 60 50 40 30 20 10 0 Sugar (cane & beet) Corn Sweetener (HFCS & corn syrup) Males-­‐ all Males 12-­‐19 ages yrs. Females-­‐ all Females ages 12-­‐19 yrs. Fig 8. U.S Sweetener consumption for adults and children per pound per person. Data Source: USDA ERS –Haley et al. 2005 Graphic created by author. With this level of consumption it is of no surprise that obesity and overweight rates have
increased dramatically among children and adolescents.
A pertinent question arising out
of this data is: is it the increase in cumulative sugar consumption that is responsible for
the significant increase in child (and adult) adiposity or is it the type of sugar consumed
that is the decisive variable? At first glance, common sense would say certainly, more
sugar consumed = more calories = more fat, but sometimes things are not always as they
appear at face value.
When comparing the U.S. consumption rates of HFCS (USDA ERS 2011)
alongside the obesity rates of U.S. children and adolescents (Ogden et al. 2010) the
growth curves have striking similarities. [Fig 9] The period between 1972 and 1988
marks the most significant increase for both HFCS consumption and obesity rates. In
1972, the annual consumption of HFCS was 0.8 lb. per person and by 1988 that number
catapulted to 34.9 lb. per person. Similarly, the percentage of U.S. children 2-19 years of
age who were obese in 1972 was 5.0%, by 1988 that number had doubled to 10.0%.
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High Fructose Corn Syrup and Childhood Obesity
After 1988, both HFCS consumption and obesity rates continued to increase. HFCS
consumption peaked in 1999 with an annual per capita consumption of 45.4 lbs. and then
began a slow descent; currently the annual per capita rate of consumption is 35.1 lbs. per
person.153 Obesity rates, however, continued to climb until peaking in 2003, at which
point 17.1% of children and adolescents 2-19 yrs. old were obese. What is most alarming
about the obesity rates is that these numbers do not include children who were
overweight, only children who were categorized as obese. As mentioned earlier in the
discussion of BMI, and individual can be one or two pounds away from a label (or
diagnosis) of “obese” yet are still extremely overweight and at risk for severe health
complications.
U.S. HFCS ConsumpPon and Child Obesity Rates 50.0 45.0 40.0 35.0 HFCS consumpgon per lb/per person 30.0 25.0 20.0 Percentage of children 2-­‐19 yrs. Obese 15.0 10.0 5.0 0.0 1972 1978 1988 1999 2001 2003 2007 Fig 9. U.S. HFCS Consumption 1970-­‐2010 and U.S. Child and Adolescent obesity rates 1972-­‐2007). Data Sources: USDA ERS B riefing Room: Sugar and Sweeteners: Data Tables ( 2011) and Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. This continued increase in obesity rates despite a decrease in HFCS consumption is not
necessarily surprising because the consumption of HFCS was still extremely high.
Obesity rates peaked in 2003 at 17.1% and at that time per capita HFCS consumption had
only decreased 2 lbs. down to 43.4 lbs. (from its peak at 45.4 lbs. in 1999). The data
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from 1972 to 1999 appears to be a “slam dunk” for the HFCS-obesity correlation theory,
however data from 1999 to 2003 appears to negate that supposition. What must be taken
into account is the compound interest effect with respect to physiological processes. As
discussed in chapter 2, metabolic processes involved in glucose and fructose are very
complex. If a child was overweight (not obese thus not registering in the data) in 2001
and maintained (but did not increase) a high refined carbohydrate diet (one common
among fast food and prepackaged foods), it is quite possible that physiologically by 2003
all of his/her glycogen stores were saturated resulting in all calories not immediately
utilized being converted directly into triglycerides and stored as additional fat. In this
scenario, if a child reduced soda consumption (which contains HFCS) from three a day to
one a day, while that would be a significant reduction in HFCS consumption,
physiologically that may still be too much sugar for his/her body to utilize. What is
surprising about the data is the consumption pattern of sucrose and HFCS between 20032007 compared to obesity rates. According to the data tables (table 51), sucrose
consumption began to increase during this period while HFCS consumption and obesity
rates both decreased. Some experts contend that HFCS is not responsible for the
[alarming] rise in obesity rates, claiming that the metabolic processes between sucrose,
glucose, fructose and high fructose corn syrup are not significantly different.154
METABOLISM AND ADIPOSITY
Several studies have looked at differences between glucose and fructose
consumption and their relationship with metabolic processes. 155 However, the majority of
studies investigate and measure the differences between sugars consumed via liquid
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only156 and do not take into account differentiation of sugars present in food. For
example, in one experiment [that included food] the breakfast consisted of a bagel and
cream cheese.157 While a registered dietician designed the meal, what is not known (or
perhaps what is not stated in the reports) is whether or not the bagel contained any
additional sugars such as HFCS or sucrose. Hypothetically, if a bagel contained 2 g. of
HFCS and test subjects were given a liquid beverage containing 10 g. of sucrose then
total sugar consumption for that meal would be 12 g. with a breakdown of 2 g. of HFCS
and 10 g. of sucrose. Conversely, if the subjects were given a beverage containing 10 g.
of HFCS then while the total sugar consumption would be a constant 12 g., the
differentiation would be 12 g. of HFCS and 0 g. sucrose. Over time this could result in
significant metabolic differences. Nevertheless, the research performed thus far has shed
some light on metabolic differences and/or similarities between the various sugars, and
spawned further questions.
In a comparison study of dietary fructose and glucose on circulating insulin, leptin
and ghrelin levels, Dr. Karen Teff of the University of Pennsylvania School of Medicine
and her colleagues (2004) discovered that dietary fructose reduces circulating insulin and
leptin but increases ghrelin and triglycerides.158 Their subjects were twelve normal
weight women ages 19-33 each with a BMI within “normal” ranges. Experimental
testing consisted of two 48-hour periods a month apart. For one two day period, the
subjects were only allowed to consume meals whose simple-sugar carbohydrates were
derived from fructose (HFr), namely in the form of a fructose-sweetened beverage; an
additional liter of water was consumed throughout the day. Conversely, during the
second 48-hour period, meals consisted of simple-sugar carbohydrates derived from
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High Fructose Corn Syrup and Childhood Obesity
glucose (HGl) in the form of a glucose-sweetened beverage; an additional liter of water
was consumed throughout the day. The research team administered each meal and each
sweetened beverage consumed. Blood samples were taken thirty minutes after each meal
as well as at other hourly intervals throughout the day for the purpose of analyzing the
following plasma concentrations: glucose, insulin, leptin, ghrelin, GIP (gastric inhibitory
polypeptide, an endocrine hormone now believed to induce insulin secretion and also
effect fatty acid metabolism through stimulation of lipoprotein lipase159), GLP-1
(glucagon-like peptide-1, a hormone that induces insulin secretion while suppressing
glucagon secretion and also appears to restore the glucose sensitivity of pancreatic βcells160), triglycerides (TG) and free fatty acids (FFA). As anticipated by the team,
plasma glucose levels were lower after HFr meals compared to HGl meals. There was a
significant decrease of 65% (± 5%) in insulin levels after HFr meals compared with HGl
meals; in addition, insulin secretion continued to be blunted throughout the day by
approximately 49% (± 5%) during the days of HFr consumption. There was a slight
difference between HGl meals and HFr meals with respect to plasma leptin levels.
As
with insulin there was a significant difference in ghrelin levels. On the HGl days, plasma
ghrelin decreased by 30-35% after each meal; conversely, the suppression of ghrelin after
HFr meals was deemed “not significant”. Interestingly, it was what occurred during the
duration of the day (i.e. non-meal times) that caught researchers attention. During the
evening and early morning hours (i.e. fasting state; 11:00pm-3:00am), on HGl days,
ghrelin concentrations did not increase above baseline however, on HFr days, plasma
ghrelin levels were elevated above baseline. GIP levels were similar in the fasting state
(i.e. 11:00pm-3:00am) for both HGl and HFr days. However, GIP concentrations
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increased more rapidly after HGl meals (within 30 minutes of consumption) than HFr
meals (within 60 minutes of consumption). In addition, overall plasma GIP levels
remained higher throughout the day on HGl days than on HFr days. While there was not
much differentiation between peak levels of GLP-1 after HGl meals versus HFr meals,
the GLP-1 levels remained elevated for a longer period of time (120 minutes) after HFr
meals than HGl meals. Plasma TG (triglyceride) levels increased (i.e. spiked) more
rapidly 4-5 hours after a HFr breakfast than after a HGl breakfast, in addition the TG
peak was higher with the HFr meal than the HGl meal. Plasma TG levels also remained
elevated throughout the 24 hour period on the HFr days whereas TG levels decreased
after peaks and remained below baseline levels during the night on HGl days. During the
morning prior to breakfast (9:00 am), plasma TG levels were markedly higher (approx.
35%) on HFr days than on HGl days. Plasma FFA levels were similar for both HFr days
and HGl days and they concluded that the differences were not statistically significant
and would not be expected to influence insulin sensitivity. Their results indicate that
consumption of HFr meals and beverages results in lower circulating plasma leptin and
insulin concentrations and higher ghrelin and triglyceride levels than consumption of HGl
meals and beverages. [Ghrelin is a hormone produced by the oxyntic glands of the
stomach that stimulates hunger161 as well as protects against chronic stress induced
depression, anxiety162 and enhances cognition163. Like glucagon is the counterpart of
insulin, ghrelin is considered to be the counterpart of leptin, in fact, ghrelin rivals NPY
for potency in stimulating appetite.164] Teff et al. surmise that because insulin, leptin and
ghrelin are participants with the central nervous system (CNS) regarding long-term
regulation of energy, prolonged consumption of diets high in fructose could lead to
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weight gain and obesity. In addition, due to the elevated plasma TG levels upon
consumption of fructose, chronic consumption of fructose could also contribute to CVD
and atherogenesis.165
In a short-term study investigating endocrine and metabolic profiles after
consumption of different sugars, Stanhope et al. (2008) examined differences between
HFCS and sucrose when compared to glucose and fructose consumption. The format was
a somewhat similar to Teff et al. however the duration was shorter (24 hours versus 48
hours) and the participants were a mixed gender sample of 18 men and 16 women. Like
Teff et al.’s study, subjects were given prepared meals with an accompanying beverage
that was sweetened with either HFCS, sucrose, fructose or glucose. Their analysis
centered on the differences and/or similarities in blood profiles for the 24-hour testing
period. They reported no significant differences between HFCS and sucrose in plasma
glucose, leptin, ghrelin, TG or FFA concentrations.166 Insulin was slightly “but
significantly” increased with sucrose consumption versus HFCS consumption, however
the team deemed this increase to be age related as there was no reported significant
increase in subjects > 35 years old but only in subjects < 35 years old. While they
reported that plasma profiles during sucrose and HFCS consumption “were not different”,
their data tables state that plasma TG level during HFCS consumption was 1,043.5 mg/dL
whereas levels were 738.7 mg/dL during sucrose consumption, that’s 304.8 mg/dL
difference which may not be statistically “significant” but is certainly relevant, especially
over prolonged accumulation. Melanson et al. (2007) also report no significant
differences in blood glucose, insulin, leptin levels or appetite upon consumption of HFCS
or sucrose.167 However, this too was a short-term (48 hour) study and the team concluded
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that further research was needed to see if similar results would occur in a longer study.
Studies like these are often the foundation for those who contend that HFCS is
metabolically equivalent to sucrose and that it is the recipient of unwarranted criticism and
“bad press”. However, obesity is not result of short-term consumption but rather longterm over indulgence therefore, emphasis within the scientific community should be on
long-term studies.
Overall, there are very few studies isolating metabolic differences and/or
similarities between HFCS and sucrose. A major contention of HFCS supporters such as
White et al. (2010) is that HFCS is compositionally similar to sucrose (more so than to
straight fructose or straight glucose) and that the majority of studies examine the
metabolic differences between glucose and fructose168 rather than between HFCS and
sucrose.169 This is a valid contention. In fact, research investigating metabolic
differences and/or similarities between sucrose and HFCS is extremely limited and longterm studies are almost non-existent. The majority of research designs have been
conducted within a 24-48 hour testing period which might be sufficient for analysis of
short-term effects on blood and metabolic profiles, but certainly is not sufficient to
project any potential (or probable) long-term effects or adverse health ramifications.
One of the few long-term studies with human subjects conducted thus far was by a team
of researchers from the Department of Nutrition at The University of California- Davis
who observed the effects of fructose consumption on blood lipid profiles during a tenweek period. Swarbrick et al. (2008) concluded that long-term consumption of diets high
in fructose could potentially increase the risk of developing CVD.170 While their
conclusion sounds robust, their sample consisted of seven overweight and/or obese, post-
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menopausal women and thus is neither a substantial nor representative sample for
conclusions to necessarily be projected onto the general public. However, as with other
studies investigating the effects of fructose consumption, their results clearly indicate that
fructose consumption significantly increases TG levels.171
Dr. White and his colleagues (2010) reported that it is the American Medical
Association’s (AMA) position that HFCS “does not appear to contribute” to obesity more
than any other sweetener. They also reported that the American Dietetic Association
(ADA) “have concluded that high-fructose corn syrup is not a unique cause of
obesity.”172 Both reports, the AMA’s Report 3 of The Council on Sciences and Public
Health: The Effects of High Fructose Syrup (2008) and the ADA’s Position on the
American Dietetic Association: Use of Nutritive and Nonnutritive Sweeteners, have been
thoroughly examined (and re-examined) yet those specific quotes remain elusive. The
AMA’s report actually concluded that, “because the composition of HFCS and sucrose
are so similar, particularly on absorption by the body, it appears unlikely that HFCS
contributes more to obesity or other conditions than sucrose. Nevertheless, few studies
have evaluated the potentially differential effect of various sweeteners, particularly as
they relate to health conditions such as obesity, which develop over relatively long
periods of time.”173(italics added) The council did not definitively conclude HFCS was
“not” a cause of obesity, nor that it was not a significant cause, only that the available
evidence was insufficient at that time to specifically restrict the use of HFCS or to require
the use of a warning label on food products containing HFCS.174 Furthermore, in their
Executive Summary, the Council on Science and Public Health also stated that, “only a
few small, short-term experimental studies have compared the effects of HFCS to sucrose
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and most involved some form of industry support. Epidemiological studies on HFCS and
health outcomes are unavailable, beyond ecological studies, because nutrient databases
do not contain information on the HFCS content of foods and have only limited data on
added sugars in general.”175 (italics added) In addition, they recommended more
“independent research” (e.g. research sans ties-financial or otherwise- to the food &
beverage manufacturing industry) as well as long-term and epidemiological studies on
the health effects of HFCS. With respect to the American Dietetic Association (ADA),
again latitude may have been exercised by White et al.’s interpretation of the ADA’s
position. In the ADA’s 2004 Report White et al. cited, the context behind the ADA’s
position was/is that sweeteners (whether fructose, sucrose, or HFCS) “by themselves” are
not the sole reason for obesity or weight gain. The report does not state that sweeteners
were not a contributing factor to obesity…only that they were not the sole factor,
“existing evidence does not support the claim that diets high in nutritive sweeteners by
themselves have caused and increase in obesity rates or other conditions.”176 This position
was reached based on findings from David Lineback and Julie Jones’ (2003) summary
report of the 2002 Sugars and Health Workshop.177 The context behind their (Lineback
and Jones) report of findings was regarding the scarcity of research available overall, not
simply the scarcity of scientific research implicating HFCS and they concluded, “this is
not to say that sugars may not be involved in other health issues cited, particularly when
their overconsumption results in an energy imbalance with resulting weight gain, but that
currently evidence is not sufficient to validate a direct causative role for sugars
consumption.”178 They also reported that a major limitation of data collection regarding
specific sugar intake, as well as cumulative sugar intake, is that it is currently not possible
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to “analytically distinguish” between added sugars and naturally occurring sugars.179 For
example, with Kraft Brand’s Capri Sun Grape Juice, there is no delineation between
naturally occurring fructose contained in the grape and pear juices and added HFCS, all
that is reported is the cumulative sugar content of 16 grams.180 Similarly, an apple pie
from McDonald’s contains 13 grams of sugar and contains: high fructose corn syrup,
sugar, dextrose and brown sugar.181 Aside from the notation that it contains less than 2%
of dextrose and brown sugar the remaining composition is unknown. Does it contain 11
grams of HFCS and 2 grams of sugar (i.e. sucrose) or does it contain 4 grams of HFCS
and 8 grams of sugar? For those investigating a potential correlation between sugar
consumption and obesity and specifically whether or not one sugar (such as HFCS)
increases adiposity over another sugar, this unknown is extremely relevant.
In another article espousing the “misconceptions about high-fructose corn syrup”,
Dr. White (2009) boldly proclaims that with respect to metabolic differences between
sucrose and HFCS, “in the relatively few studies in which the 2 have been compared, no
differences in metabolic markers of obesity or measures of satiety were observed.”182
Some noteworthy thoughts: first, the references cited were all short-term studies (24-48
hours) with one study having a testing period less than five hours. Second, “no
differences” is perhaps another liberal inference as one of the cited studies revealed a 300
point difference in plasma TG levels183 (perhaps statistically insignificant but a difference
nonetheless) while another study regarding uric acid levels concluded “the implication
for HFCS from these results is far from clear.”184 Finally, he claims that the markers of
serum glucose, insulin, ghrelin, triacyglycerols (triglycerides), uric acid, satiety and
hunger were all comparable between sucrose and HFCS.185 However, these results were
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again after short-term trials, some only several hours in duration; hardly sufficient time to
make such a declarative conclusion with respect to HFCS and a condition that develops
over time such as obesity. It is also of some consideration that Dr. White, a well known
biochemist (some contend an expert in the field) who has published several papers in the
defense of HFCS as well as authored two reference books on enzymes, proteins and
peptides, is the president and founder of White Technical Research, an international
consulting firm for the food and beverage industry and proudly proclaims his affiliation
with the Corn Refiners Association, a national association representing the corn refining
(i.e. wet milling) industry.186 These associations cast a shadow on the purity or nonbiased nature of his assertions.
Four years after the ADA’s position cited by White et al. and in the same year the
AMA issued their report of finding regarding HFCS (note: findings that were based upon
scientific research only published through December 2007), a team of researchers
conducted one of the few studies regarding sugar consumption and adiposity specifically
(also one of the few with a lengthier duration). In a long-tern study involving SpragueDawley rats, scientists from the University of West Virginia (Light et al., 2008) were
interested in adiposity with respect to consumption of fructose, glucose, sucrose and
HFCS-55 sweetened beverages. They accurately noted that while several animal studies
have investigated the differences between glucose and fructose consumption with respect
to adiposity, there lacks voluminous research comparing HFCS alongside fructose and
glucose. They also pointed out an important research design element: dosage of
sweetener used. They contend that previous animal studies used high doses of sweetener
that were “unlikely to be physiologically relevant to the amount of sugar consumed by
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humans”.187
In their eight-week study, they specifically used a dose of sweetener comparable
to the amount that is found in a typical soft drink. Forty-four female Sprague-Dawley
rats were divided into five groups of 8-9 rats each. All rats consumed the same solid food
but different liquid solutions. Liquid solutions were either plain distilled water or water
sweetened with glucose, fructose, sucrose or HFCS-55. The concentration of added
sweetener was 13% w/v (weight/volume), again the equivalent of sweetener found in an
average soft drink. For eight weeks the rats were allowed to access food and liquid ad
libitum (at their leisure). Rats given the glucose-sweetened solution consumed the
greatest amount of liquid totaling 5154 mL, they were followed by rats given the sucrosesweetened solution consuming a total of 3403 mL. Fructose and HFCS-55 solution rats
followed and were relatively close in consumption volume at 2267 mL and 2795 mL
respectively. Those consuming the distilled water had the lowest liquid consumption at
1844 mL but had the highest food consumption at 968 g. Conversely, the glucose group,
while consuming the most liquid, had the lowest food intake at 597 g. The reduction of
solid food consumption could be attributed to the increased caloric consumption gained
via the liquid glucose solution and vice versa for those drinking the water. Results for
total caloric consumption is as follows: water = 3678 kcal, glucose = 4719 kcal, sucrose =
4247, fructose = 4224 kcal and HFCS-55 = 4140 kcal. Again, those consuming the
glucose solution consumed the most calories, water consumed the least (not surprisingly)
and sucrose, fructose and HFCS-55 had relatively similar total caloric consumption. If
one stopped analysis at this juncture these findings would certainly support White et al.
and others’ contention that HFCS and sucrose are metabolically identical. However, the
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body weight and body composition results prove contrary and are quite damaging to the
champions of HFCS. Surprisingly, rats drinking the glucose-sweetened solution had the
least amount of total weight gain at 174 g. accompanied by 7.9 g. of gonadal adipose
tissue and 3.1 g. of retroperitoneal (abdominal) adipose tissue. Rats drinking water had
the second least amount of weight gain at 176 g., but had least amount of gonadal and
retroperitoneal adipose tissue at 6.3 g. and 2.9 g. respectively. Sucrose solution rats had a
total weight gain of 186 g. with gonadal and retroperitoneal adipose tissue being 9.8 g
and 4.2 g. respectively. Fructose solution rats experienced a 195 g. increase in weight
with gonadal adipose and retroperitoneal adipose tissue at 9.5 g and 4.0 g. respectively.
The group with the highest total weight gain, as well as highest amount of adipose tissue,
was the group fed the HFCS-55 solution. These rats increased body weight by 198 g. (24
g. more than the glucose group and 12 g. more than the sucrose group); in addition,
gonadal adipose was an 11.6 g. and retroperitoneal adipose was 5.0 g. While Light et al.
contend that these differences are not statistically significant they do conclude that the
type of sweetener added does, in fact, influence body weight and fat mass.188 However, it
is this author’s contention that these differences might very well become statistically
significant over a prolonged period of time, 52 weeks for example. While not
highlighted, their data indicates that the liver of the HFCS group weighed more (8.1 g.)
than those in the water, glucose, sucrose or fructose group (6.4 g., 7.0 g., 7.4 g., and 7.6
g. respectively). The liver is a key regulator of both glucose and fat metabolism (and
storage) therefore this increase could become a significant factor in a prolonged study.
Since HFCS-55 has replaced sucrose in the food and beverage industry as the preferred
sweetener, the liver weight differentiation between the groups (HFCS and sucrose in
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particular) could be very important regarding human metabolism, adiposity and other
physiological conditions. Sometimes one point is a significant difference. For example,
in human blood analysis, (according to the 2010 standards of the American Diabetes
Association) an A1C rage of 5.7-6.4% classifies and individual as “increased risk” for
diabetes and anything over 6.5% is a diagnosis of diabetes.189 In this example, a tenth of
a percentage, which is usually deemed statistically insignificant, is quite significant. Light
et al.’s data clearly shows that rats consuming HFCS-55 for eight weeks not only
weighed more than the sucrose solution group (12 g. more), but also had more adipose
tissue as well, 16.6 g. and 14.0 g. (combined gonadal and retroperitoneal) respectively. If
there is no significant metabolic difference between sucrose and HFCS as proponents of
HFCS suggest then what is the explanation for the increased adiposity in the HFCS
group?
A valid criticism of the HFCS-Obesity correlation theory is that the total
consumption (HFCS and sucrose sugars combined) has increased over the years and
adiposity is an outcome of energy consumption versus energy expenditure. Again, more
energy (kcal) consumed than energy (kcal) expended results in accumulation of stored
adipose tissue (fat). Thus critics contend that it is the total consumption that is the
pivotal component in the purported correlation between sugar consumption and increased
adiposity and not the individual type of sugar, specifically, HFCS.190 According to the
USDA ERS data tables (2011), with an exception of a slight dip in 1975, total sugar
consumption per capita has increased steadily at an approximate rate of 1-2 lbs. per year
from 1970 until 1999; total consumption increasing from 72.9 lbs./yr. to 92.6 lbs./yr.
respectively. From 1999 to 2010 there has been a steady decrease again, averaging 1-2
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lbs. per year to a present rate of 82.1 lbs./yr. per capita in 2010. While overall sugar
consumption increased, the most shocking finding is the differentiation in the types of
sugars that were being consumed. There is an inverse relationship between sucrose
consumption and HFCS consumption, which given the substitution of HFCS for sucrose
in the food and beverage industry is not surprising. As mentioned earlier, in 1970 per
capita sucrose consumption was 72.5 lbs./yr. while HFCS was a mere 0.5 lb./yr. per
capita. As sucrose consumption decreased steadily, HFCS consumption increased
peaking at 45.5 lbs./yr. in 1999. Between 2000-2002, both held relatively steady with
minor fluctuation of less than half a pound and by 2003 total consumption was split
evenly among them at 43.4 lbs./yr. After 2003, sucrose consumption began a slight
increase to 47.0 lbs. in 2010 and conversely, HFCS consumption began decreasing to
35.1 lbs. in the same year and most notably so did obesity rates. The period between
1978 and 1988 becomes interesting when adding the variable of child obesity rates.
As discussed previously, in 1972 the rate of child and adolescent obesity was 5.0%
and consumption of HFCS was a paltry 0.8 lb./yr., meanwhile the consumption of
sucrose was at 72.8 lbs./yr.191 By 1978, sucrose consumption decreased almost ten
pounds to 63.5 lbs./yr., HFCS consumption increased slightly to 3.5 lbs./yr., and child
obesity rates were at 5.5%. A decade later, sucrose consumption had decreased to 44.2
lbs./yr. and conversely, HFCS consumption had increased to 34.9 lbs./yr. at the same
time obesity rates had doubled. Between 1978 and 1988, total sugar consumption
increased 6.3 lbs./yr. but the breakdown of sugar consumption is interesting. In ten years
sucrose consumption decreased 20.9 lbs. while HFCS consumption increased 27.2 lbs.
and again, obesity rates doubled. Another significant period occurs between 2003 and
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2007. In 2003, child obesity rates peaked at 17.1% but by 2007 those rates had decreased
to 15.5%. During this time total sugar consumption decreased from 86.8 lbs. (2003) to
83.7 lbs. (2007) similarly, HFCS consumption decreased from 43.4 lbs. to 40.1 lbs. but
sucrose consumption increased negligibly from 43.4 lbs. to 43.6 lbs. At first glance this
appears to confirm the contention that it is the quantity of sugar consumed that is the
smoking gun with respect to adiposity and not the quality (type) of sugar ingested.
However, you will recall from the previous section that studies have shown that there are
metabolic differences between different sugars, even between HFCS and sucrose.
Certainly, the quantity of any food substance ingested plays a role in overall weight as
well as lean muscle tissue to adipose tissue ratio. However once cannot dismiss the type
of substance either, 300 calories in a chicken breast is not metabolically equivalent 300
calories of chocolate cake or 300 calories of carrots.
If there is no significant metabolic difference [with respect to adiposity] between
sucrose and HFCS, then one would expect to find obesity rates consuming sucrose to be
similar to obesity rates consuming HFCS however, the data does not reveal that.
Between 1978 and 1988 sucrose consumption decreased (65.1 lb. to 44.2 lbs.
respectively) but obesity rates increased (5.5% to 10.0% respectively). During this same
time period HFCS consumption experienced its greatest surge from 7.7 lbs. to 34.9 lbs.
Opposition would contend that the rise in obesity during 1978-1988, despite the decrease
of sucrose consumption, was directly attributed to an overall increase in total sugar
consumption but that theory does not explain the period between 2003 and 2007. Again,
between 2003 and 2007 sucrose consumption increased but HFCS consumption and
adolescent obesity rates both decreased. [Fig 10]
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High Fructose Corn Syrup and Childhood Obesity
Another weakness of the “cumulative sugar consumption” hypothesis is the time
period between 1999 and 2003. During this time, obesity rates steadily increased from
13.9 % (1999) to 17.1% (2003) yet total sugar consumption decreased from 92.6 lbs. to
86.8 lbs. In addition, both sucrose and HFCS consumption decreased from 45.4 lbs. and
47.2 lbs. (1999) to 43.4 lbs. and 43.4 lbs. (2003) suggesting there were other variables
that were also influential factors.
U.S. Sucrose ConsumpPon, HFCS ConsumpPon and Child Obesity Rates 80.0 70.0 60.0 HFCS consumpgon per lb./
per person 50.0 Percentage of children 2-­‐19 yrs. Obese 40.0 30.0 Sucrose consumpgon lb./
person 20.0 10.0 0.0 1972 1978 1988 1999 2001 2003 2007 Fig 10. U.S. HFCS and Sucrose Consumption 1970-­‐2010 and U.S. Child and Adolescent obesity rates 1972-­‐2007). Data Sources: USDA ERS Briefing Room: Sugar and Sweeteners: Data Tables (2011) and Ogden et al. (2010) National Health Examination Surveys II (ages 6-­‐11) III (ages 12-­‐17) and National Health and Nutrition Surveys (NHANES) I-­‐III and NHANES 1999-­‐2000, 2001-­‐2001, 2003-­‐2004, 2005-­‐2006, 2007-­‐2008. Graphic created by author. An admitted weakness of utilizing the USDA Data Tables for analysis of sucrose
consumption, HFCS consumption and child obesity rates is that while the obesity rates
are specific to children and adolescents, the sugar and HFCS consumption data is
cumulative of the U.S. population which means adults are included in that data sample. It
is highly improbable that a three or five year-old child consumed 78.2 lbs. of sugar
(sucrose) in 1972 or 45.4 lbs. of HFCS in 1999. However, it is also just as unlikely that
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the same three or five year old child purchased and prepared the food he/she ate.
Obviously, the parents/caretakers are responsible for ensuring that their child eats. It
stands to reason that if the parent/caretaker is consuming large quantities sugar-laden
foods that those same foods are being fed to their children. Nevertheless, the data does
suggest a correlation between consumption of HFCS and increased adiposity among
children and adolescents.
Daily per capita total carbohydrate consumption rose 27% from 386 grams (1970)
to 491 grams (1994). Putnam and Allshouse attribute this increase to the increased use of
grains and sweeteners, as carbohydrates from sugars also increased 21% during the same
period (from 152 grams to 184 grams.). Between 1977-1994, consumption of grain
products such as pizza and lasagna (pasta) increased 115%; snack foods such as pretzels,
popcorn, crackers, and corn chips rose 200%; and consumption of “ready to eat” cereals
increased 60%. It should be noted that most all of these popular grain products often
contain added sugar in the form of HFCS (HFCS-42 specifically). However, while
overall consumption of grain products increased, they assert that whole grain
consumption remained below the ADA recommended daily allowance.
Overall caloric intake increased 500 calories (15%) between 1970 and 1994.
Again, at the risk of being repetitive, all calories are not metabolically and
physiologically the same. While they may contain [and release] the same kcal energy
unit, the other physiological responses outside of ATP production can vary. The same
500 kcal from protein such as a chicken breast will not yield the same physiological
response in the body as 500 kcal of sugar. Protein consumption remained consistent at
eleven percent (11%) of total calories consumed but what is of great interest are their
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findings that while the proportion of calories yielded from carbohydrates increased (47%
to 51%), the proportion of calories derived from fats decreased (42% to 38%). This data
is contrary to those who hypothesize that obesity is not related to the increase of sugar
intake but rather an increase in overall dietary fat consumption.192 Dr. Walter C. Willett
(1998) of the Department of Nutrition, Harvard School of Public Health and professor of
medicine at Harvard Medical School, expressed concerns regarding the low-fat diet craze
in the 1990s, specifically that substituting carbohydrates for dietary fat consumption
could induce serious metabolic abnormalities [such as hyperlipidemia and
hypertricglceridemia] within a sedentary population that also exhibited a prevalence of
insulin resistance.
In an ecological study of dietary fat intake and its relationship to [excess] adiposity,
Dr. Willett concluded that dietary fat was not the “primary cause” of obesity. For
example, at the time of the study approximately 60% of South Africans were overweight
yet less than 22% of their caloric intake was from dietary fats, he found similar findings
in Saudi Arabia. He concluded that “compensatory mechanisms” within the body occur
such that in the long-term, fat consumption within the rate of 18-40% appears to have a
minimal effect on overall adiposity.193 Subsequently, limiting or removing it from one’s
diet, contrary to popular hypotheses of that time, did not result in shedding of unwanted
pounds (fat). However, some studies have contradicted Dr. Willett’s conclusion.
Gazzaniga and Burns (1993) examined the relationship between diet composition and
body fatness in preadolescent children (9-11 yrs.) and discovered that dietary fat
consumption, specifically saturated fats, were significantly correlated to body fat
percentage (BF%). In obese subjects, a greater portion of caloric intake was derived from
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dietary fats and significantly less in carbohydrates than in non-obese subjects.
Additionally, obese children expended more energy per day than did non-obese children.
Gazzaniga and Burns surmised this increased energy expenditure resulted from the
additional body weight that was being carried; in short, it requires more energy to move a
larger mass. They concluded that a diet higher in fat and lower in carbohydrates may
contribute to obesity in preadolescent children. A significant limitation of this study is
that data was extrapolated from a 24-hour recall survey completed by the parents so
human error is a factor. Additionally, their data reveals that obese subjects consumed
more calories overall than did the non-obese subjects (9384 kcal versus 7056 kcal
respectively194) , another variable that could be a contributor to their adiposity.
Putnam and Allshouse also discovered that types of fats consumed changed as well
as the percentage/proportion of the overall caloric constitution. In 1970, animal fat
comprised 35% of dietary fat consumption while other fats and oils (primarily vegetable
oils) comprised 43%. By 1994, animal fat had decreased to 25% of all fat consumption
and other fats and oils rose to 52%. The increase in “other fats and oils” category was
most likely due to a significant increase in consumption of fast foods, snack-foods, salad
dressings and other foods laden with hydrogenated vegetable oils. For salad dressings
and cooking oils alone per capita consumption almost doubled between 1970 and 1997
from 15 to 29 pounds per person per year. 195
ECONOMIC BENEFITS
Some contend that the increase in sugar consumption and hydrogenated oil
consumption is inversely proportional to the decrease in price of crop/raw material for
manufacturers, specifically corn, soybean and wheat. The Institute for Agriculture and
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Trade Policy (IATP) asserts (2006):
“The problem with the extensive use of these cheap commodities in food
products is that they fall into the very dietary categories that have been
linked to obesity: added sugars and fats. U.S. farm policies driving
down the price of these commodities make added sugars and fats some
of the cheapest food substances to produce. High fructose corn syrup
and hydrogenated vegetable oils- products that did not even exist a few
generations ago but now are hard to avoid- have proliferated thanks to
artificially cheap corn and soybeans.
Whether by intention or not,
current farm policy has directed food industry investment into producing
low-cost, processed foods high in added fats and sugars.”196
An example of this influence is Kraft Brand’s recent switch from cane sugar
(sucrose) to HFCS in their popular children’s juice line Capri Sun. Due to the economic
cost of sugar (cane and beet) they have now converted to using HFCS to sweeten these
beverages. While they contend that the change was made “to help better manage costs
for consumers in today’s difficult economic environment”197there is no doubt they are
preserving the welfare of their own profit margin as well. Government support for
producing grain, corn and soybean (the latter two commonly referred to as oilseed crops)
takes many forms: money invested in universities and corporations for specific crop
research, direct subsidy payments to farmers to produce specific crops (to offset the
low/set crop prices), as well as agreements for future crop exports.198 These subsidies
indirectly affect the cattle/livestock industry as well since the majority of U.S. livestock
are grain-fed instead of a healthier and more natural grass-fed. The IATP contends that
by keeping crop prices for feed grains so low, the U.S. farm policy has created an unfair
market advantage favoring large, industrialized livestock production over “diversified
sustainable” (i.e. mixed crop and livestock) livestock production. Sadly, produce crops
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(i.e. fruits and vegetables) on the other hand receive far less government support.
According to the IATP, it is this lack of support that creates a riskier economic
environment for produce farmers. Although fresh produce carries a higher price point,
the lack of support for growing these crops “makes growing vegetables a much riskier
proposition”.199
GENETICALLY MODIFIED FOODS (GMO/GE)
One of the largest areas of research today, estimated at $40 to $100 billion
dollars,200 is biotechnology and genetic engineering specifically, genetically modified
organisms (GMO, GM or genetically engineered, GE) crops. In an effort to increase crop
production and ultimately profitability, scientists have genetically modified crops to be
resistant to pesticides, fungi, bacteria and insects. To genetically modify a crop, scientists
splice together one or more genes into the crop’s genome using viral promoters,
transcription terminators, reporter genes and antibiotic resistant marker genes.201
Bacterium, fungi, and viruses are used as catalysts to graft in the desired gene product to
the host. The problem is that despite the industry driven propaganda, little scientific
research exists regarding the safety and efficacy of these GM products. Dr. Arpad
Pusztai and his colleague, Dr. Stanley W.B. Ewen, from the Rowett Research Institute
(RRI) in Scotland secured a multi-million dollar grant to investigate the impact, if any, on
genetically modified potatoes on animal and human health.202Once a staunch supporter of
GMO, his findings not only changed his stance but also eventually resulted in his
indefinite suspension at the institute and termination of research funding. After working
for RRI for 36 years and publishing almost 300 papers and nine books, Dr. Pusztai was
“removed from service, his research papers were seized, and his data confiscated”203 in
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retaliation for comments made during a 1998 interview regarding his findings on the
effects of GM foods relative to their safety. Prior to splicing with the genetic marker
(gene product), Pusztai and Ewen first isolated the gene product (i.e. protein) lectin from
the snowdrop plant to determine its toxicity and/or effect on absorption of a normal diet
within the intestinal tract. Even at high doses, adding lectin by itself (administered via an
eyedropper) to normal (i.e. non-GM) food did not exhibit any adverse effects; the rats
were not harmed. However, this was not the case for rats fed GM “pest resistant”
potatoes spliced with lectin and the Cauliflower Mosaic Virus (CaMv). The rats fed GM
potatoes where the lectin had been added genetically via splicing suffered damaged
organs, intestinal tract and immune system.204 They concluded that the splicing process
somehow “destabilized the potato genome”205and those elements which made the potato
resistant to insects (i.e. substances that were toxic to the insect) were also making the
potato toxic. Furthermore, they discovered that the splicing process itself was
unpredictable. Their results revealed that genetic differences can occur between sibling
batches of GM foods despite being derived from the same root-stock and subjected to
indistinguishable conditions. It was assumed that these offspring batches would contain
an identical genetic composition however, Pusztai and Ewen’s nearly three year
experiment proved contrariwise. The GM batches were not the same. When discussing
the strains of GM spliced potatoes Dr. Pusztai recounts,
“We had two successful lines, both coming from the same genetic
transformation of the parent line at the same time. They were going
through the same laboratory tests and were growing in the fields for two
years down in the South of England. And when we looked at the two lines,
we found that against our expectations they were different. They were
different compositionally. For example, one of the lines contained exactly
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the same amount of protein as the parent line but the other line, even
though it was as successful in protecting the plant against aphids
nematodes, it contained 20 percent less protein. Now this was a totally
unpredictable effect.”206
This unpredictability was most troublesome to the scientists and they realized that more
research was needed before deeming GE products as safe for human consumption, “We
don’t eat a lot of these things in GM foods that are now being sold. So it should be in our
interest to get it properly tested.”207 Mae-Wan Ho et al. (2000) reported that post-Pusztai
research has discovered that the CaMv promoter is susceptible to horizontal transfer (i.e.
it participates and potentially instigates unintended rearrangement of genetic coding) and
recombination hot spots (areas where the DNA break and then repair)208 thus contributing
to significant instability within the line. In addition, it has the potential for insertion
mutagenesis, insertion carcinogenesis and reactivation of dormant viruses or to create
new viruses in species it is transferred to.209 Dr. Ho, a geneticist, and her colleagues
recommend that “all transgenic crops containing CaMv 35S or similar promoters which
are recombinogenic should be immediately withdrawn from commercial production or
open field trials. All products derived from such crops containing transgenic DNA
should also be immediately withdrawn from sale and from use for human consumption
and animal feed.”210 Not surprisingly, this recommendation has met its share of criticism.
In many countries, lack of sufficient research regarding the safety and efficacy of
genetically modified foods has resulted in stringent restrictions and even moratoriums on
production. The United Kingdom (UK) has placed a moratorium on all GE foods
pending research on the environmental and human health effects. In 1997, Austria
banned the use of Bt corn. In 1999, Greece banned seven GE crops (including corn),
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Italy banned GE corn and oil byproducts and Brazil banned the cultivation of GE soybean
and are now exporting GE-free soybeans.
Germany banned the cultivation of GE corn
in 2000. Norway banned all GE foods and food manufacturers in Switzerland have
banned all GE ingredients. Japan has mandated testing on potential health risks of GE
foods and its two largest breweries have banned the use of all U.S. GE/GMO corn.211
Sadly, the U.S. is nowhere to be found in the list. Why? The answer is as disturbing as
Pusztai and Ewen’s results.
FDA APPROVAL
In 1992, in response to numerous inquiries regarding the safety and regulatory
oversight of foods produced through genetic modification such as recombinant DNA
techniques (i.e. gene splicing and cell fusion), the U.S. Food and Drug Administration
(FDA) issued a policy statement essentially deeming genetically modified foods to be
“functionally and physiologically equivalent” to normal, non-modified foods and
therefore fall under the GRAS (generally recognized as safe) purview as per sections
201(s) and 409 of the 1958 Federal Food, Drug and Cosmetic (FD&C) Act.212 According
to 201(s) of this Act, “any substance that is intentionally added to food is a food additive,
that is subject to premarket review and approval by FDA, unless the substance is
generally recognized, among qualified experts, as having been adequately shown to be
safe under the conditions of its intended use.”213 (italics added) Substances (foods, food
additives, chemicals etc.) that are recognized as GRAS do not require a formal premarket
review by the FDA. Instead, the process is voluntary. Manufacturers are encouraged,
although not mandated, to seek the FDA for guidance and “consultation”. Again, this
process is not mandated and somewhat akin to telling a ten year old child it would be nice
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if they cleaned their room before watching TV but did not require them to. The GRAS
label is a very broad and somewhat nebulous term, particularly when applied to
genetically modified foods. According to the FDA, foods that are derived from new plant
varieties, despite how they are derived, “are not routinely subjected to scientific tests for
safety”.214 It is the “how” that is becoming a point of contention for many scientists,
consumers and regulating authorities. Proponents (from both private corporations as well
as government agencies) of genetic engineering contend that modifying the genetic code
of a food, such as introducing a protein from another food or plant, does not change the
constitution of the item and thus the original properties of that food are still intact and
thus safe. Because the food as a whole was not altered it is considered safe as the FDA
“has not found it necessary to conduct, prior to marketing, routine safety reviews of
whole foods derived from plants.”215 In the example of Puzstai’s potatoes, 20% less
protein is not a constitutional change because it is still by definition a potato. To add
further confusion to the GMO/GE safety and efficacy debate is the FDA’s stance that
food is deemed “adulterated” (and thereby rendered harmful and unlawful) if it “bears or
contains an added poisonous or deleterious substance that may render the food injurious
to health.”216(italics added) By FDA standards, GMO/GE foods do not have “added”
substances requiring pre-market research and approval. Apparently, microorganisms,
viruses, bacterium etc. added to a food substance via DNA recombinant techniques is not
really “added”, so there appears to be somewhat of a tap dance over terminology and
definitions. Additionally, there remains no guidance on the process by which these
substances, harmful or not, are added. As seen in Pusztai’s and Ewen’s research, the
recombinant process itself was unpredictable. In addition, there are no long-term studies
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to prove or disprove the safety of these new biotechnological processes, nor the safety of
the resulting food product. Even scientists within the FDA have expressed concerns
regarding product versus process. In response to the 1992 Statement of Policy, Dr. Linda
Kahl (FDA compliance officer) stated in a memorandum to the FDA Biotechnology
Coordinator, “the document is trying to force an ultimate conclusion that there is no
difference between foods modified by genetic engineering and foods modified by
traditional breeding practices. This is because of the mandate to regulate the product, not
the process.”217 In 2001, the FDA stated that they no longer felt the “voluntary
consultation process” for genetically modified foods was sufficient to ensure the safety of
foods into the U.S. commerce supply.218 However, to date no definitive actions or
regulations have been implemented and the process remains voluntary.
GMO/GE PROCESSING: WHY THE CONCERN
The relevance (and importance) of understanding GE/GMO crops with respect to
HFCS is that virtually all of the corn used to produce HFCS is GE/GMO corn. A
popular strain of GE/GMO corn used in the U.S. is Bt-corn. It is derived from the soil
bacterium Bacillus thuringiensis (Bt) which has a delta endotoxin that is toxic to
caterpillars, specifically during the larvae stage. Industry scientists claim that the Bt delta
endotoxin is selective, “generally not harming insects in other orders”219and because of
this selectivity they deem it safe for humans and other animals. However, Pusztai’s
research has shown, it is not necessarily the gene product used that is harmful but rather
the recombinant DNA splicing process itself. In an examination of the possible
toxicological effects of three GM corn varieties on mammalian and human health, French
researchers Joël Spiroux de Vendômois and his colleagues (2009) discovered toxic,
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adverse reactions affecting the liver, kidneys as well as the heart, adrenal glands, and
spleen in subjects fed GMO grain.220 de Vendômois et al. performed a comparative
analysis of three popular commercialized GM corn specifically, NK 603, MON 810 and
MON 863 (all manufactured by the Monsanto Corporation). NK 603 (Monsanto’s
Roundup Ready® Corn line) was created to be resistant to the pesticide Roundup®,
whereas MON 810 and MON 863 both contain Bt endotoxins. The data analyzed were
the pre-approval research trails (one per GMO product) Monsanto submitted to the FDA
that, resulting from a lawsuit, were obtained and made public by Greenpeace attorneys in
Denmark and Germany (MON 810 and MON 863) as well as the Swedish Board of
Agriculture (NK 603).221 According to de Vendômois et al., the sample size for each
clinical trial consisted of 200 male and 200 female Sprague-Dawley rats for a total of 400
test subjects, yet only ten were randomly selected and measured at the 5th and 14th week
mark. They rightly conclude that this extremely minute sample size of ten rats measured
only twice in 14 weeks was (and is) “insufficient to ensure an acceptable degree of power
to the statistical analysis performed and submitted by Monsanto.” In addition, they
discovered that Monsanto’s statistical analysis ignored gender differences and skewed
actual results in favor of not detecting a substantial effect by approximately 70%.222
Utilizing Monsanto’s own data they performed sex-specific analysis via the Shapiro test,
Bartlett test, Welch method, Kruskal-Wallis rank sum test as well as an ANOVA per sex,
per variable for each GMO. Results were substantially different from that reported to the
FDA.223
Male rats fed NK 603 were more sensitive than the counterpart female rats and had
relatively higher liver weights (11% increase at the end of the trial) than the non-NK 603
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group. These rats (male and female) also exhibited “statistically significant” urine ionic
disturbances and kidney deficiencies that suggested potential renal leakage. MON 863
rats also exhibited diminished renal function however, in the MON 863 group renal
disturbances were specifically attributed to increased creatinine levels the development of
chronic interstitial nephropathy. In addition, female rats fed MON 863 exhibited
“statistically significant” differences in serum glucose and triglyceride levels (up to 40%
increase and a physiological state “indicative of a pre-diabetic profile”), elevated
creatinine, elevated blood urea nitrogen levels, increased liver weight and increased body
weight overall (3.7%). Males on the other hand experienced a decrease (7%) in kidney
weight as well as a chronic nephropathy and an overall decrease in body weight (3.3%).
MON 810 rats (male and female) displayed significant disturbances within the liver as
well as elevated blood urea nitrogen, increased adrenal gland, kidney and spleen weights.
Just as Pusztai (and others) has espoused the necessity of further testing, de Vendômois et
al. conclude that because these GMO/GE substances are not naturally occurring and
subsequently have not been a staple within the human diet (not until the last 10-12 years),
it is essential that long-term studies be performed as “the consequences for those who
consume them, especially over long time periods are currently unknown.” 224 The United
Nation’s Food and Agriculture Organization (2000) acknowledged the lack of studies
regarding long-term effects from consumption of GMO foods and recommended
monitoring changes in nutrient levels in foods derived from GMO products as well as
assessment of the nutritional status of the consumer population.225
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CHAPT. 4- Other Contributing Factors to Childhood Obesity
PORTION SIZE & INCREASE IN CALORIC INTAKE
Analysis of patterns and trends of U.S. food portion sizes reveals that portion size,
both inside and outside of the home, has increased substantially since the 1970s.226
Young and Nestle (2002), from the Department of Nutrition and Food Studies at NYU,
report that per capita caloric intake contained 500 more calories in 1996 than in 1977
(similar to findings of Putnam and Allshouse). In addition, 1996 portion sizes exceeded
both USDA and FDA standards; cookies exceeded USDA standards by 700%, pasta
exceeded by 480%, muffins by 333% and steaks and bagels trailed at 224% and 195%
respectively.227 In the 1950’s there was one size of french fries (which is now considered
“small”) offered by McDonald’s whereas now, there is small, medium, large and extralarge (a.k.a. “supersized”). Interestingly, these increases are not unilateral across the
globe. In 1999, an extra-large soda at McDonald’s in Rome, London and Dublin was the
equivalent of a large in the U.S. Similarly, a large order of french fries in the U.K.
yielded 446 calories per serving versus 610 calories per serving for the same “size” in the
U.S.
Their data indicates that the upward trend towards larger portion sizes began in the
1970, increased sharply in the 1980s, and has continued the ascent into the 1990s.
Researchers Samara Nielsen and Barry Popkin from the University of North Carolina
(Chapel Hill) found similar trends as well. They analyzed 63,380 surveys from the
National Food Consumption Survey 1977 (NFCS77), Continuing Survey of Food Intake
for Individuals 1989 and 1996 (CFSII89 and CFSII96) collectively and concluded that
portion sizes served inside and outside of the home increased between 1977 and 1996.
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Their findings regarding the increase of portion sizes within the home suggests that new
patterns of behavior have also occurred. In addition to the increased consumption of high
density, low nutrient foods (e.g. fast foods and prepared foods), families (children and
adults) are simply consuming more. Researchers Fisher et al. (2003) further contend that
larger portion sizes “may constitute an obesigenic environmental influence” for
preschoolers.228 They discovered preschoolers consumed more calories when given largeportion lunches irrespective of their level of hunger. Furthermore, they observed that
when given the larger portioned meal, the average bite size was larger as well. The larger
bite size was not determined to be sex specific only meal size specific, that being the
average bite size was smaller during the normal, age appropriate sized meals. They also
observed that children who ate more when served the large portion also had greater
intakes even in the absence of hunger. This observation would suggest that consumption
was not solely biological (i.e. a physiological response to the hunger-satiety feedback
mechanism) but behavioral as well.
Adults are also prone to consuming larger portions,229 subsequently consuming
more calories, irrespective of hunger.230 In a study investigating the relationship between
the size of a pre-packaged snack and caloric intake, researchers Rolls et al. (2003)
discovered that additional caloric consumption was correlational to the size of the
packaged snack. On five separate days 60 adults (34 women and 26 men) were served a
package of potato chips as an afternoon snack, three hours prior to dinner. Snack sizes
varied each day: 28 g., 42 g., 85 g., 128 g., or 170 g. Researchers discovered that
subjects consumed the contents of the larger package (170 g.) just as readily as the
smaller package (28 g.) and that during dinner caloric intake was not modified to offset
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the additional calories consumed at snack-time.231 Clearly, hunger and satiety are not the
only variables governing consumption.
Nielsen and Popkin suggest that growth in the food industry sector, variety of new
products, an increase in people eating out, aggressive marketing as well as price
competition among manufacturers are possible contributors for this increase. Today,
corporations spend between $10 to $15 billion dollars annually on child/youth-targeted
advertising including brand licensing, product placement, contests, promotions, in-school
marketing, video games, mobile marketing (cell phone, ipod® etc.) and social networking
sites (Facebook®, Twitter® etc.), compared to just $100 million in 1983. 232 Contrary to
what one might think, this demographic (children and adolescents) constitutes a large
segment of consumers, a $200 billion dollar segment according to some estimates, of
which the majority is spent on candy, snack food, soda and cereal.233 WHO contends
evidence suggests that “the heavy marketing of these foods and beverages” to young
children bears some responsibility in the prevalence of obesity among children.234
The increase of portion size has resulted in an increase of overall caloric
consumption.235 However, studies also suggest that it is not portion size alone that is
responsible for excessive caloric intake but a combination of large portions of highdensity foods.236 High-density (a.k.a. energy density) food refers to the amount of energy
in a given weight of food and is dependent upon water, protein, carbohydrate and fat
content.237 For example, a salad is considered “low-density” due to the high fiber, high
water and low fat and low calorie (kcal) content, as the name implies it is less dense.
Conversely, a cheeseburger or Snicker’s bar is high-density due to the high fat, high
sugar, low water and low fiber content. Compositionally, these latter foods are
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comprised of high k/cal compounds resulting in an overall high(er) k/cal yield.
Obviously, a pound of lettuce and a pound of cheese are not caloric equivalents despite
registering the same weight on a scale. Consequently, consumption of these highdensity/high-energy foods results in a higher caloric intake.238 Sadly, data reveals that as
consumption of high-density foods has risen, consumption of high fiber fruits and
vegetables has declined.239 Pediatricians and nutrition experts are rightfully concerned
that this decline has resulted in insufficient levels of vital nutrients such as iron, folate,
calcium and vitamin A.240 The cumulative effect of years of insufficient nutrient intake
can result in significant adverse health conditions.
DECREASED PHYSICAL ACTIVITY, INCREASED TELEVISION & COMPUTER USAGE
Physical Activity
With respect to excess adiposity and obesity, diet and exercise are
inextricably intertwined. When caloric consumption exceeds caloric expenditure the
body converts the excess energy (calories) into fat. Physical activity is a cornerstone
foundation for health and wellbeing of both adults and children. Physical activity
strengthens the immune system, increases bone density, improves mental health and self
esteem, reduces stress, increases energy and protects against diseases/conditions such as
CVD, hyperlipidemia, hypertension, insulin resistance, certain cancers (breast, pancreatic
and colon) and osteoporosis.241 In addition, physical activity helps maintain a healthy
body weight and can reduce excess adiposity.242 In a 12 month randomized trial of 201
overweight, sedentary women researchers (Jakicic, et al. 2003) discovered that both
moderate and vigorous levels of exercise yield weight loss (8% to 10% of body weight
respectively) and improved cardiovascular fitness.243 This benefit applies to children as
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well. A 29.6- week study of 292 elementary school students in Songhkla, Thailand
suggests that a long-term school-based exercise program can prevent weight gain and
may facilitate a “remission” of obesity in children. 244
In 2003, the Youth Risk Surveillance Survey (YRSS) reported that 62.6% of
students (ninth through 12th grade) nationwide met the recommended standards of
physical activity (≥ 20 minutes of rigorous activity ≥ 3 days/week) and 24.7% met the
standards for moderate physical activity (≥ 20 minutes of rigorous activity ≥ 3
days/week). Only 11.5% of youth did not engage in any type of physical activity, sadly
that number doubled (23.1%) by the 2009 Youth Risk Surveillance Survey.245 By 2009,
18.4% of students participated in ≥ 60 minutes of rigorous physical activity ≥ 7
days/week and 37.0% participated in ≥ 60 minutes of rigorous physical activity ≥ 5
days/week. Standards and definitions of physical activity were modified between 2003
and 2009 thus making definitive conclusions between the two data samples difficult to
draw and allowing only for observational estimates. Nevertheless, in 2003 87.3% of
students engaged in rigorous and moderate physical activity (categories combined)
whereas 55.4% of students in 2009 engaged in rigorous physical activity (again,
categories combined). Again, it is impossible to make a direct and completely accurate
comparison between the two sets of data because of dissimilar variables.
First, there is a significant difference between 20 minutes of exercise ≥ 3 days a
week and ≥ 60 minutes of rigorous physical activity ≥ 7 days/week. If there are only
three categories of reported physical activity to chose from (7 days a week, 5 days a week
or no activity) as in the 2009 survey, hypothetically there could be a significant number
of students who participated in rigorous exercise two to three days a week or who
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exercise daily but for only 30 minutes not 60 and therefore did not fall into any
recognized category. Second, the 2003 “insufficient moderate physical activity”
category was removed in the 2009 survey. What is not known is whether or not that was
combined with the “no rigorous physical activity during the week” category. The 2003
survey reported “moderate” and “insufficient” exercise whereas the 2009 survey only
reported “rigorous”. If the categories were combined it might explain the increase in “no
rigorous physical activity” in 2009 especially taking into consideration the increase in
participation of physical education class (PE). In 2003, 55.7% of students reported
attending ≥ 1 day of PE and 28.4% reported attending ≥ 5 days of PE. By 2009, those
numbers had increased to 56.4% and 33.3 % respectively. Albeit not statistically
significant, it is an increase and somewhat surprisingly, not a decrease.
Television, Computers and Video Games
The YRSS surveys also reported daily television and computer usage. In 2003,
28.4% of students reported watching ≥ 3 hours of television per day. That number
decreased slightly in 2009 to 32.8% however, reported computer usage was 24.9% ≥ 3
hours per day. The 2003 survey did not collect data regarding computer usage (again,
dissimilarities between the 2003 & 2009 survey data) therefore any conclusion is purely
speculative. Despite the inconsistencies in data collected the 2003 and 2009 Youth Risk
Surveillance Surveys, these reports provide an overview of national trends in the
adolescent population. Television and computer usage are both sedentary activities
requiring minimal energy expenditure. There are no studies on other sedentary activities
such as board games and reading as they relate to overweight and obesity. However,
prior to the “computer age” obesity and overweight was not as pervasive prompting
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researchers to investigate a possible connection between the two.
As of 1999, video games accounted for over 30% of the toy market in the United
States with approximately 97% of teenagers (12-17) playing either on a computer,
console, portable (hand held) unit or via the internet.246 Dr. Jean-Philippe Chaput, from
the Department of Pediatrics at the University of Ottawa, and his colleagues (2011)
discovered that during one hour of playing video games, energy expenditure was
significantly higher however, ad libitum energy intake (i.e. consumption) was
significantly increased during the resting state post-playtime.247As with other studies
regarding television viewing,248Chaput et al. discovered that post-play consumption was
not associated with appetite or hunger. There is some mildly good news regarding video
games and that is the emergence of “active” video games. These are video games that
require users to move their body to elicit a desired response on the monitor and game
genres range from sports and races to dance and yoga. Dr. Elaine Biddiss and Jennifer
Irwin (2010) found that active video games can facilitate light to moderate physical
activity in some cases increasing energy expenditure 100% and elevating heart rate
20%.249 Maddison et al. also discovered that active video games have a positive
influence on BMI and body fat composition in overweight and obese children, namely
reducing both.250 While this activity may not compare to activity expended during
participation in real athletic events, it is certainly a move (no pun intended) in the right
direction.
There appears to be a direct relationship between hours of television watched and
adiposity.251 In analysis of the California Teen Longitudinal Survey of 1993 and 1996,
Kaur et al. found that children who watched television ≥ 2 hours a day were twice a likely
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to be overweight in the 1996 follow up study than those who watched < 2 hours a day.252
Similarly, an earlier study by Dietz and Gortmaker (1985) found that every one hour of
television viewing resulted in a 2% increase in prevalence of obesity among 12-17 year
olds.253 Dr. Ross Anderson et al. (1998) from Johns Hopkins School of Medicine
investigated the correlation between television and BMI specifically. They discovered
that children who watched television ≥ 2 hours a day had higher BMIs and greater body
fat than children who watched < 2 hours a day.254 They also surmised that repeated
exposure to food commercials prompt children to increase consumption regardless of
hunger or lack thereof, ultimately resulting in weight gain. A recent study (2011) found
that children who engage in high levels of television viewing are more responsive to
advertising geared towards food than non-food (e.g. toys).255 Additionally, “high
viewing” children migrated towards high-density, high carbohydrate and high fat food
selections even after watching commercials marketing toys, whereas the “low viewing”
children did not. Temple et al. (2007) found that television watching increased the time
spent eating, the amount consumed and caloric intake.256 There also appears to be an
inverse relationship to television at mealtime and consumption of whole grains, fruits,
and vegetables. Children from families that have the television on during two or more
meals a day consume less grains, green and yellow vegetables, non-fried potatoes, beans
and nuts than children from families who do not watch television during mealtime.257
This intertwines with another proposed contributor to child obesity: the reduction (and for
some families cessation) of traditional “family meal time”.
High Fructose Corn Syrup and Childhood Obesity
p.114
REMOVAL OF TRADITIONAL FAMILY MEALTIME
Family mealtime has been positively associated with adolescents making healthy
food choices, diminished consumption of fried foods, diminished frequency of eating
disorders, increased family connectedness and improved adolescent mental health.258
Family dinners are positively correlated with children eating breakfast as well as higher
consumption of fruits, vegetables and whole grains.259 Consistent family mealtime is also
positively correlated with healthy child and adolescent body weight. Children and
adolescents who never report eating family meals are significantly more likely to become
overweight and/or obese.260Despite the benefits of family meals, sadly, the prevalence of
regular family mealtime appears to be diminishing.
In 1991, only 27% of adolescents (12-17 years old) ate dinner with their family
every day, 47% ate with them 4 to 6 days a week and 27% ate together 1-3 days a week.
261
The percentage of younger children (< 12 years old) who eat as a family every day is
slightly better at 41%-to 45% but still abysmally small especially given the role it appears
to have with proper nutrient intake. In a comparative study of 16,862 children (9-14
years old) who ate dinner as a family never/some days, most days or every day, Gillman
et al. (2000) observed that children who ate meals with their family daily consumed more
vegetables and fruits (twice as much) and less fried foods and soda.262 These youth also
had a higher intake of essential nutrients such as calcium, iron, vitamin C, folate and
fiber. Furthermore, they consumed less saturated fat, trans fat and high glycemic foods.
What is interesting about their data is that children who ate meals with their family daily
consumed more calories than those in the never/some category (9294.6 k/cal. and 8677.2
k/cal. respectively), however they had a lower BMI than those who ate never/some days.
High Fructose Corn Syrup and Childhood Obesity
p.115
Surprisingly, children who ate family meals daily had slightly less physical activity than
those who never or some times ate with the family. To summarize, children who ate
meals with family daily consumed more calories, more nutrients, and had less physical
activity than children who never or some times ate family meals, yet they had a lower
BMI. This suggests that what is consumed plays a key role in weight and adiposity in
children and adolescents.
FAST FOOD & FAT CONSUMPTION
Changes in fast food consumption patterns also play a role in obesity and share
similar trajectories. Contrary to most expectations, dietary fat consumption has
decreased among children and adolescents over the last 20 to 30 years.263 In an analysis
of food intake trends from 1965-1996, Cavadini et al. (2000) discovered a significant, and
somewhat surprising, dietary “shift” among U.S. adolescents (ages 11 to 18 years). In an
analysis of 12,498 Nationwide Food Nutrition Surveys (NFCS), researchers discovered
that total energy intake among adolescents decreased between 1965 and 1996 as did the
proportion of energy derived from fat. In 1965, the percentage of total energy (caloric)
intake derived from fat was 38.7%. This proportion decreased steadily until 1996 when it
accounted for only 32.7% of total intake. Similarly, the consumption of saturated fats
followed similar trends falling from 15% (1965) to 11.6% (1996). [Fig 11] According to
their analysis, there was a 17% decrease of overall energy intake during this 30 year
period which they acknowledge seems “counter intuitive” given the rise in adolescent
overweight and obesity.
p.116
High Fructose Corn Syrup and Childhood Obesity
Percentage of Total Intake Percentage of Total Energy Intake Among U.S. Adolescents 1965-­‐1996 60 50 40 Total Fat 30 Saturated 20 Carbohydrate 10 0 1965 1977 1989-­‐91 1994-­‐96 Fig. 11 Percentage of Total Energy Intake among U.S. Adolescents 1965 to 1996. Data Source: Nationwide Food Consumption Surveys (NFCS) Cavadini et al. 2000. Graphic created by author. While this study suggests dietary fats are not positively correlated with obesity it
could be that, as with sugars, it is the type of dietary fat that is most influential. As with
the rise of HFCS, the use of hydrogenated oils (a.k.a. trans fatty acids) in the food
industry surged during the 1980’s and 1990’s. Approximately 40% of all processed
foods in the United States contain trans fatty acids.264 According to some estimates,
hydrogenated oils comprised 4-7% of U.S. caloric fat content by 1990.265 While attractive
to the food industry because of its long shelf life duration and stability during high
temperature deep-frying,266 trans fatty acids have been associated with cardiovascular
disease, high cholesterol, systemic inflammation, insulin resistance, visceral adiposity,
and type 2 diabetes.267 Additionally, partially hydrogenated soybean oils have been
shown to increase blood glucose levels, insulin and LDL levels.268 In fact, the adverse
health affects associated with trans fatty acids led to the FDA requiring manufacturers to
list trans fat content on all food labels as of January 2006.269 While the labeling is
required and can certainly be found on national fast food restaurant chain websites, most
High Fructose Corn Syrup and Childhood Obesity
p.117
foods consumed in fast food restaurants do not have food labels printed on the wrapper or
cardboard container.
St.-Onge et al. (2003) reports a significant increase in fast food consumption among
children and adolescents over the last 20 to 30 years. Between 1977 and 1989, fast food
consumption among adolescents 12-18 years old increased from 6.5% to 16.7%, and had
reached 19.3% by 1994.270 While overall fat consumption had decreased, studies indicate
that individuals (children and adults) who consume fast foods on a regular basis consume
more calories, more fat, more sugar and less fruits and vegetables than individuals who
do not eat fast food.271 Fast food is laden with added sugars and fats and thus combined
increase the energy content (calories) significantly. In a three-year study, Duffey et al.
(2007) concluded that fast food consumption has a positive association with BMI. The
greater the fast food consumption the higher the corresponding BMI.272
SODA CONSUMPTION
Not surprisingly, there has likewise been a dramatic increase in the consumption of
carbonated beverages during emergence of HFCS into the food and beverage market. In
1986, approximately 28 gallons of non-diet, carbonated beverages were consumed
annually per person, by 1997 that number grew to 41 gallons per person. The 2009
YSSR Surveys found that 29.2% of students drank ≥ 1 soda per day. The average soda
contains 30-40 g. of sugar (primarily from HFCS-55) averaging approximately 150
calories. At the minimum rate of one soda per day that is an additional 1050 k/cal.
(calories) per week and 54,600 k/cal. per year. Studies have associated sugar-sweetened
beverages with obesity in children.273 However, in a review of children’s beverage
High Fructose Corn Syrup and Childhood Obesity
p.118
consumption from 1987-1998, researchers Park et al. (2002) discovered that carbonated
beverage consumption actually decreased from 1987-88 to 1997-98 from 84% to 72%
respectively.274 In 2000, soda consumption accounted for one third of all added sugar
intake in the U.S. diet.275 In an investigation of the effects of HFCS sweetened soda on
body weight and food intake, Todoff and Alleva (2001) found that after three weeks of
HFCS consumption both male and female subjects gained weight (females significantly
and males to a lesser, but still measureable, extent).276 Other studies have concluded that
consumption of sugar-sweetened beverages is associated with increased BMI and obesity
in children and adolescents.277 However, a long-term study investigating beverage
consumption and BMI in children (Blum et al. 2005) had results researchers were not
anticipating.
Consumption of regular soda, diet soda, milk, 100% juice, or other sweetened
beverages (sports drinks, kool-ade etc.) in 166 children (grades 3rd-6th) over a two-year
period was examined. Researchers discovered that children who were overweight and/or
who had gained weight during the two-year period had a significantly higher
consumption of diet soda than normal weight subjects.278 In fact, diet soda was the only
beverage associated with increased BMI. Blum et al. concluded that the mechanism
behind the increased BMI and diet soda consumption remained unclear [positing that
perhaps the overweight subjects increased their consumption of diet soda in an attempt to
lose weight] and suggested that further longitudinal studies were needed. A common
question that arises when discussing the role of soft drinks and obesity/adiposity is
whether it is the beverage itself that is responsible for the purported weight gain or
whether it is the increase of total caloric consumption that is the real culprit? Again,
High Fructose Corn Syrup and Childhood Obesity
p.119
there is evidence on both sides. Some studies show a clear correlation between soft drink
consumption and adiposity279 while others show no correlation at all.280 Others suggest
that increase in overall caloric consumption is responsible and sugar-sweetened
beverages, specifically soft drinks, should not be singled out.281
ROLE OF GENETICS
To paraphrase Dr. Dean Ornish when asked about the role of genetics and obesity,
indeed overweight children frequently have parents who are also overweight but so are
the family dog and cat.282 Some researchers investigating monozygotic twins have
implied that body weight and composition are influenced by genetic factors283 while
others contend that genetic factors appear to influence and affect the body’s response to
external factors (i.e. environmental factors)284and that expression of a specific genotype
is dependent upon the environment.285 As seen in the discussion on leptin, genes and
genetic coding certainly participate in human physiology and metabolic processes,
however a genetic predisposition to a condition does not definitively guarantee an
expression of that condition. The environmental conditions must support, if not
catalyze, the emergence of that condition. For example, dry wood has a predisposition
to burn when ignited, dry wood soaked in gasoline has a greater predisposition to burn
when ignited but without the catalyst of fire, neither scenario will result in burning
wood. The environmental factor of fire must be present for the ignition to occur.
“Biological” and “environmental” have often been theoretical rivals. In psychology,
there are those who contend behavior is determined by environmental factors and those
who contend it is determined by innate biological factors. Similarly, the debate
continues regarding the origins of overweight and obesity and the truth most likely lies
High Fructose Corn Syrup and Childhood Obesity
p.120
somewhere in the middle. Children learn from and imitate their parents’ behavior. Just
as healthy eating patterns are established by parents286 so are unhealthy eating patterns.
Most children are overweight and obese because they consume the same foods that their
parents eat and employ the same behaviors that their parents employ. For example,
researchers at Harvard’s School of Medicine (Gilman et al. 2009) have found a
significant association between parental smoking and smoking initiation among
adolescents 12-17 years old.287 The reality is that in today’s society it is much easier
(and sadly encouraged) to cast blame for being overweight/obese on “genetics” than to
take responsibility for one’s own inability to exercise restraint and self-control.
p.121
High Fructose Corn Syrup and Childhood Obesity
CONCLUSION
The obesity epidemic in the United States is reaching critical mass (no pun
intended) and a solution must be found. If nothing is done to arrest this epidemic or at
the very least, slow down the rate of acceleration, the impending health and economic
costs could be cataclysmic. Obesity has been directly associated with a cornucopia of
adverse health conditions including, but not limited to, CVD, hyperlipidemia, cancer,
breathing impairments, sleep disorders, high blood pressure, insulin resistance, NIDDM
(type 2 diabetes) and psychological problems.288
There are additional tangential health concerns potentially associated with mercury
byproducts that have been detected in HFCS. Laboratory tests have clearly detected
trace, yet significant, amounts of mercury in HFCS produced in the United States. Aside
from hepatic and renal toxicity, mercury has been the center of much debate regarding a
possible association (and some would contend causal relationship) with birth defects and
learning disabilities such as Autism, Autism Spectrum Disorder (ASD) and Attention
Deficit Hyperactivity Disorder (ADHD).289 Dufault et al. (2009) found a striking
similarity between HFCS consumption rates and annual growth rates of ASD in
California. While no direct causal relationship was determined, they rightly concluded
that mercury contamination could be a contributing factor and that significant research is
needed in this area of neurodevelopment. In an analysis of blood mercury levels and
diagnosis of autism, Drs. Catherine DeSoto and Robert Hitlan (2007) found a
“statistically significant” relationship between blood mercury levels and the diagnosis of
ASD.290 In another prospective study of mercury toxicity and autism, Geier and Geier
High Fructose Corn Syrup and Childhood Obesity
p.122
(2007) found that over 50% of individuals diagnosed with ASD had mercury toxicity
biomarkers (specifically coproporphy, pentacarboyxyprophyrin and precoproporphyrin)
that were more than two standard deviations above the mean than their non-ASD
siblings.291 While there may not yet be a definitive causal relationship between HFCS
and learning disabilities such as ASD and ADHD, there is little evidence vindicating it
either. Clearly, this is an area of research that needs further investigation, especially in
light of potential en utero fetal toxicity.
The goal of this research was to determine whether or not high fructose corn syrup
(HFCS) is responsible, either in whole or in part, for the current obesity epidemic
plaguing children in the United States. To claim that HFCS is the sole contributor and/or
cause of child overweight and obesity would be synonymous with claiming cigarette
smoking is the only cause of lung cancer or driving while intoxicated is the only cause of
automobile accidents. However, is it just as erroneous to claim that cigarette smoking
does not contribute to lung cancer or that driving while intoxicated does not result in
automobile accidents, and the same applies for HFCS and obesity. While there are
several aggregate contributors to the overweight and obesity epidemic, such as decrease
in physical activity, increased use and prevalence of television, computers and electronic
media etc., increase in portion sizes and prevalence of prepared, packaged and “fast”
foods, research shows that HFCS is clearly a contributing factor and, in the eyes of this
author, one of the most significant ones.
There have been many studies investigating metabolic differences and/or
similarities between various sweeteners: glucose, fructose, sucrose and HFCS. However,
the majority are short-term studies often 24-48 hours in duration. While short-term
High Fructose Corn Syrup and Childhood Obesity
p.123
metabolic profile results are valuable, they are not applicable for determining long-term
physiological responses and metabolic profiles. They are woefully insufficient in
predicting long term adiposity as confirmed by Light et al.’s research. Results from this
eight-week study revealed a significant difference in adiposity between subjects that
consumed HFCS and those that consumed sucrose, glucose and fructose. Not only did
the HFCS subjects have an overall higher weight gain and greater abdominal fat increase,
their livers weighed significantly more than all the other subjects… even more than the
sucrose “equivalent” group. A healthy liver is essential for proper metabolism, fat
emulsification and energy production/storage. Light et al.’s study clearly shows that long
term HFCS consumption has an adverse affect on the liver and similar studies with
human subjects are desperately needed. However, champions of HFCS and industry
supporters have altogether ignored studies like Light et al. choosing rather to focus on
short-term blood profile results in defense of their pro-HFCS stance. If the liver is
overloaded or worse, damaged, normal metabolic processes will be impeded. Studies
have shown that mercury and recombinant DNA splicing both adversely affect the liver
(as well as other organs). Mercury is known to cause hepatotoxicity292 and trace, yet
cumulatively significant, amounts have been detected in HFCS. Add to this equation the
fact that the majority of HFCS is produced from genetically modified corn and GMO/GE
corn has toxic effects on the liver.293 In addition, like Light et al.’s rats fed HFCS, rats
fed GMO/GE corn experienced liver weight gain (11% in 14 weeks).294 When these three
aspects of HFCS are looked at collectively, the case against HFCS becomes even more
damaging.
The real question that many would prefer to remain the proverbial “white elephant”
p.124
High Fructose Corn Syrup and Childhood Obesity
is what do we do about it? As with many policy decisions, this will most likely be a
function of economics. To ban the use of HFCS in foods and beverages would have a
significant financial impact to food and beverage manufacturers, as profit margins would
shrink. This, of course, would be passed along to the consumer (as seen in the case with
Capri Sun) with most likely higher prices and smaller portions, the days of “super size
me” would come to an abrupt end (which is not altogether an adverse side effect). There
could also be a potential impact on commercial farmers. Although a large portion of corn
is used for grain-feed, a significant portion is used to make HFCS. It is unknown whether
or not other industries (biofuels for example) would absorb the utilization. If not, there
could be a potential surplus of corn especially given the more stringent regulations other
nations have regarding use of GE/GMO corn imported from the U.S.
There is of course, the separate matter of the use of GE/GMO corn and the
unknown, yet potential, adverse health ramifications to humans. Again, this will most
likely be a decision of economics rather than consumer health. Powerful corporations
such as Monsanto, ConAgra and Calgene, Inc. have invested tens of billions of dollars
into R & D and are not likely to let the return on their “investment” dissipate, and
certainly not without a lengthy and costly fight. Add to this equation other special
interest groups (the Corn Growers Association for example) and federal bureaucracies
(FDA, EPA and UDSA) and the removal of HFCS from the U.S. food supply becomes all
the more unlikely. Nevertheless, unlikely not does mean unnecessary.
For years,
radium was touted as containing beneficial properties and curative powers and was a
common additive in products such as toothpaste, hair creams, salves and even food
items.295 However, it has since been discovered that this wonder compound is poisonous
High Fructose Corn Syrup and Childhood Obesity
p.125
and exposure, much less ingestion, results in serious and often deadly effects.
There is of course the issue of current and future economic costs of obesity-related
health issues. The economic impact of the treatment of obesity-related diseases and
disorders is astounding and one that, given the current economic climate, cannot be
sustained indefinitely. At some point the money will run out.
At this juncture, the most viable solution appears to be grassroots education for
both children and adults. It is not the role of government to mandate what individuals eat
or do not eat, but it is their role to provide accurate information particularly regarding
dangerous and/or toxic substances in our food supply. In the United States there are
many examples of consumer education changing consumer trends. While corporations
(such as biotech companies, pharmaceutical companies, food and beverage manufacturers
etc.) protectively guard their profits they know that at the end of the day the customer is
always right. If consumers don’t buy the product they change the product. In the 1980’s
when Coca- Cola changed their formula sales decreased so significantly that they had to
revert to the original formula. The growing “organic” movement is another example of
consumer driven manufacturing. Consumers are demanding that stores carry organic
products and what was once only found at health food stores and local farmer’s markets
is now widely accessible in superstores such as Target, Costco, Kroger and Walmart.
Even manufactures have changed what they provide due to consumer pressure and desire
to maintain their profit margin.
In addition to consumer education, the FDA should require manufacturers to list
the amount of HFCS contained in the food/beverage just as the 2006 ruling requires trans
fats to be listed. Currently, if a food/beverage contains HFCS it must be listed as an
High Fructose Corn Syrup and Childhood Obesity
p.126
ingredient but that does not give the consumer information as to how much is contained
in the food/beverage. There should also be careful consideration given to developing a
national database for analysis of food composition with respect to types of sugars and
types of fats. This would enable researchers to accurately analyze caloric and nutrient
trends.
There clearly needs to be more specific, long-term studies regarding HFCS and
metabolic processes. As shown, the majority of the experiments to date are short term
(24 to 48 hours) and with small sample sizes. Additionally, large scale, independent
studies regarding GMO/GE foods and the effects of long-term ingestion are needed. The
current studies are scarce, insufficient and often industry driven. There is too little
information and too many unknowns (and what is known is extremely disturbing). With
respect to adiposity and obesity, more research should specifically examine the effect
GMO/GE foods have on the liver and hepatic enzymes as well as potential effects on
regulatory hormones such as insulin, leptin and ghrelin. The rats fed MON 863 who
exhibited a “pre-diabetic profile” are a clear example of why this needs further
examination as this could have significant implications for human health.
In short, there is no “smoking gun”, no magic bullet that the “blame” can be cast
upon. Multiple facets contribute to and fuel this epidemic. This means that each factor
must be carefully examined and dealt with accordingly. Those in the food and beverage
industry often shift the focus towards the lack of physical activity and we, as a society,
certainly need to look at ways to address this significant decline. Physical activity burns
calories. To maintain a healthy body weight, energy expenditure should mirror energy
consumption. However, that does not mean that we should ignore and fail to address
High Fructose Corn Syrup and Childhood Obesity
other contributing factors such as portion size, hydrogenated oils or, as this author
contends, the utilization of HFCS as the primary food and beverage sweetener.
p.127
p.128
High Fructose Corn Syrup and Childhood Obesity
APPENDIX
Table 1. MMWR Youth Risk Behavior Surveillance Summaries-­‐ United States 2003 and 2009 2003 2009 Participated in rigorous physical activity -­‐ 7 days/week n/a 18.4% Participated in rigorous physical activity -­‐ 5 days/week n/a 37.0% Participated in rigorous physical activity ≥ 3 days/week 62.6% n/a Participated in moderate physical activity ≥ 5 days/week 24.7% n/a Insufficient moderate physical activity -­‐7 days/week 33.4% n/a No rigorous physical activity during the week 11.5% 23.1% 1 day a week or more 55.7% 56.4% 5 days a week or more 28.4% 33.3% n/a 24.9% 38.2% 32.8% n/a 29.2% Milk Consumption-­‐ drank ≥ 3 glasses of milk per day 17.0% 14.5% male 22.7% 19.8% female 11.2% 8.7% n/a 13.8% 22.0% 22.3% 12.0% Physical Activity * P.E. Class Attendance Computer use ≥ 3 hours per day ** Television use ≥ 3 hours per day Dietary Behaviors Soda Consumption-­‐ drank ≥ 1 soda per day *** Ate vegetables ≥ 3 times a day Ate fruits and vegetables ≥ 5 times a day Obesity, Overweight and Weight Control Obese Overweight 13.5% Described themselves as overweight 29.6% 27.7% Trying to lose weight 43.8% 44.4% Had exercised to lose weight and/or prevent weight gain Had restricted food consumption to lose weight and/or prevent weight gain 57.1% 61.5% 42.2% 39.5% 15.8% * The 2003 and 2009 Youth Risk Behavior Surveillance Surveys differ in data collected and reported for Physical Activity. In 2003, the three designated categories were: Sufficient Rigorous Physical Activity (e.g., running, swimming, soccer, cycling etc. for ≥20 minutes for ≥ 3 days/week), Sufficient Moderate Physical Activity (walking, skating, pushing lawnmower, mopping floors etc. for ≥30 minutes ≥5 days/week) and Insufficient Amount of Physical Activity. The 2009 survey designations: Physically active at least 60 minutes 7 days/week (activity that elevated heart rate and made them breath hard), Physically Active at least 60 minutes 5 days/week (activity that elevated heart rate and made them breath hard) and Did not participate in at least 60 minutes of activity on any day. ** Computer usage was not measured in the 2 003 survey. *** Soda consumption was not measured in the 2003 survey. High Fructose Corn Syrup and Childhood Obesity
p.129
End Notes
1
(World Health Organization (WHO), 2000)
(The Mayo Clinic, 2011) (The Mayo Clinic, 2011)
3
(UK Daily Mail, 2011)
4
(Dehghani, 2005)
5
(U.S. Department of Health & Human Services)
6
(Rodin, 1988) (Elliott, 2002) (Crapo, 1982) (Light, 2009) (Swarbrick, 2008) (Stanhope K. H., 2008)
(Stanhope K. G., 2008) (Jurgens, 2005)
7
(Light, 2009)
8
(Soenen, 2007) (Monsivais, 2007) (Melanson K. A., 2008)
9
(Melanson K. Z., 2007) (Teff, 2004)
10
(Pusztai A. , 2001) (Pusztai D. A., 2000) (de Vendomois, 2009) (Ho M.-W. R., 2000) (Ho M.-W. R.,
1999)
11
(Dufault R. L., 2009) (Dufault R. S., 2009)
12
(Wadaan, 2009) (Ung, 2010) (Donaldson, 1978)
13
(Krebs, 2007)
14
(World Health Organization (WHO), 2000)
15
(Dalton, 2004)
16
(World Health Organization, 2011)
17
(Whitney, 1998)
18
(Centers for Disease Control and Prevention, 2011)
19
(World Health Organization (WHO), 2000)
20
(Bedogni, 2003) (Reilly, 2000) (Lazarus, 1996) (Sarria, 2001) (Ellis, 1999)
21
(Conus, 2004) (Conus F. R.-L., 2007)
22
(Conus F. R.-L., 2007) (Conus F. A.-L.-O.-P.-L., 2004)
23
(Krebs, 2007)
24
(Ferreira, 2004) (Schouten, 2011) (Gosnell, 2007) (World Health Organization (WHO), 2000)
25
(Reilly, 2000)
26
(Savva SC, 2000)
27
(World Health Organization, 2011)
28
(Williams, 1997) (Goran M. G., 1999) (Sjostrom, 1992) (Goodpaster, 2000) (World Health Organization
(WHO), 2000)
29
(Maffeis, 2001) (Gower, 1999) (Larsson, 1984) (Freedman D. D., 2009)
30
(Krebs, 2007)
31
(Gower, 1999) (Addo, 2010)
32
(Krebs, 2007)
33
(Goran M. I., 1998)
34
(Goran M. I., 1998)
35
(Georgia State University Department of Kineseology and Health)
36
(Kuczmarski, 2000) (National Center for Health Statistics, 1977)
37
(Kuczmarski, 2000)
38
(National Center for Health Statistics, 1977) (Kuczmarski, 2000)
39
(Krebs, 2007)
40
(Himes J.H., 1994; Hedley A.A., 2004; Guo S.S., 2002; Gower, 1999; Maffeis, 2001; Savva SC, 2000;
St. Onge, 2003; Paeratakul S, 2003; Young, 2002; Bowman S. G., 2004) (Krebs, 2007) (Elliott, 2002)
41
(Krebs, 2007)
42
(Centers for Disease Control and Prevention, 2011) (Centers for Disease Control and Prevention, 2011)
43
(World Health Organization, 2005)
44
(Associated Press, 2011)
45
(UK Daily Mail, 2011)
46
(Wang Y. B., 2007)
47
(World Health Organization, 2005)
48
(World Health Organization, 2010)
49
(World Health Organization, 2010)
50
(Dalton, 2004)
2
High Fructose Corn Syrup and Childhood Obesity
p.130
51
(Dalton, 2004)
(Crowely, 2010) (Meyer, 2006)
53
(Chiolero, 2007) (Boyd, 2005)
54
(Gidding, 1995)
55
(U.S. National Institute of Health, 2006)
56
(Gidding, 1995) (Tulane University School of Medicine, 2011)
57
(U.S. National Institute of Health, 2006)
58
(Freedman D. K., 2005)
59
(Richards, 1985)
60
(Mustillo, 2003) (Woo, 2009)
61
(Dietz W. G., 1982)
62
(Carroll, 2007) (Goldsobel, 2008) (Belamarich, 2000)
63
(U.S. Department of Health & Human Services)
64
(Ogden, 2010)
65
(Ogden, 2010)
66
(Wang Y. B., 2007)
67
(Van Cleave, 2005) (U.S. Department of Health & Human Services) (U.S. National Library of Medicine
National Institutes of Health) (Wang G. D., 2002) (Miller, 2004) (Ogden C, 2010) (Krebs, 2007)
(Langreth, 2009)
68
(Must A, 1992)
69
(Moss, 2011)
70
(Stettler N. S., 2005)
71
(Ekelund, 2006) (Stettler N. K., 2003)
72
(Whitaker R. P., 1998)
73
(Gordon-Larsen, 2010)
74
(World Health Organization (WHO), 2000)
75
(Centers for Disease Control and Prevention, 2011) (Colditz, 1992)
76
(Wolf A. C., 1994)
77
(Woo, 2009)
78
(Merriam-Webster, 2011)
79
(Tortora, 1993)
80
(Tortora, 1993)
81
(Guyton, 1991)
82
(Bray G. N., 2004) (Whitney, 1998) (Guyton, 1991)
83
(Bray G. N., 2004)
84
(Guyton, 1991)
85
(Tortora, 1993) (Whitney, 1998) (Parker, 2010)
86
(Tortora, 1993) (MedBio, 2011) (Heinz, 1968)
87
(Stanhope K. S., 2009)
88
(McDevitt, 2001)
89
(Schwartz, 1995)
90
(Stanhope K. S., 2009)
91
(Guyton, 1991)
92
(Saad, 1998) (Bray G. N., 2004) (Farooqi S. K., 2001)
93
(Tortora, 1993)
94
(Guyton, 1991) (Tortora, 1993)
95
(Gautron, 2011)
96
(Saad, 1998)
97
(Dickie, 1946)
98
(The Jackson Laboratory, 2011)
99
(The Jackson Laboratory, 2011)
100
(The Jackson Laboratory, 2011)
101
(The Jackson Laboratory, 2011)
102
(The Jackson Laboratory, 2011)
103
(Zhang, 1994)
52
High Fructose Corn Syrup and Childhood Obesity
p.131
104
(Farooqi I. J., 1999) (Zhang, 1994) (Maffei, 1995) (Frederich, 1995) (Pelleymounter, 1995) (Halaas,
1995) (Campfield, 1995)
105
(Campfield, 1995)
106
(Friedman, 2002)
107
(Howard Hughes Medical Institute, 2004)
108
(Millington, 2007)
109
(Perl, 2004)
110
(Liu L. K., 1998)
111
(Liu L. K., 1998)
112
(Medical Research Council, 2011)
113
(Farooqi I. J., 1999)
114
(Farooqui, 2002)
115
(Emilsson, 1997)
116
(Murray, 2003) (Tortora, 1993)
117
(Grundy, 1998)
118
(Elliott, 2002)
119
(Schwarzbein, 1999)
120
(Tortora, 1993)
121
(Murray, 2003)
122
(Bhosale, 1996) (Wikipedia, 2011)
123
(Bhosale, 1996)
124
(Bhosale, 1996)
125
(Marshall, 1957)
126
(Marshall, 1957)
127
(Takasaki, 1971) (Takasaki, 1972) (Takasaki, 1966)
128
(Takasaki, 1966)
129
(Takasaki, 1966) (Takasaki, Formation of Glucose Isomerase by Streptomyces sp., 1973)
130
(Takasaki, 1971)
131
(Lamot, 1983) (Bhosale, 1996)
132
(U.S. Department of Agriculture (USDA), 2011)
133
(Parker, 2010)
134
(Parker, 2010)
135
(Dufault R. L., 2009)
136
(Dufault R. L., 2009)
137
(Wadaan, 2009)
138
(Ung, 2010)
139
(Ung, 2010)
140
(Elmhurst College, 2011) (OUKosher, 2011)
141
(Bhosale, 1996)
142
(Parker, 2010)
143
(Schoonover, 2006)
144
(Haley S. R.-H., 2005)
145
(Bray G. N., 2004)
146
(Putnam, 1999) (Parker, 2010)
147
(U.S. Department of Agriculture (USDA), 2011)
148
(Schoonover, 2006)
149
(Whitney, 1998)
150
(Wells, 2008)
151
(Haley S. R.-H., 2005)
152
(Haley S. R.-H., 2005)
153
(U.S. Department of Agriculture (USDA), 2011)
154
(White J. , 2009) (White J. , 2010)
155
(Crapo, 1982) (Angelopoulos, 2009) (Swarbrick, 2008) (Stanhope K. G., 2008) (Stanhope K. H., 2008)
(Melanson K. A., 2008) (Petersen, 2001) (Jurgens, 2005) (Elliott, 2002)
156
(Stanhope K. G., 2008) (Stanhope K. H., 2008) (Light, 2009; Bowman S. G., 2004) (Rodin, 1988)
High Fructose Corn Syrup and Childhood Obesity
p.132
157
(Teff, 2004)
(Teff, 2004)
159
(WIkipedia, 2011)
160
(Wikipedia, 2011)
161
(Cummings, 2001)
162
(Lutter, 2008)
163
(Atcha, 2009)
164
(Cummings, 2001)
165
(Teff, 2004)
166
(Stanhope K. G., 2008)
167
(Melanson K. Z., 2007)
168
(Jurgens, 2005) (Elliott, 2002) (White J. 2008) (White J. F., 2010)
169
(White J., 2008) (White J., 2009)
170
(Swarbrick, 2008)
171
(Swarbrick, 2008)
172
(White J. F., 2010)
173
(White J. F., 2010)
174
(Council on Science and Public Health, 2008)
175
(Council on Science and Public Health, 2008)
176
(American Dietetic Association, 2004)
177
(American Dietetic Association, 2004) (Lineback, 2003)
178
(Lineback, 2003)
179
(Lineback, 2003)
180
(Kraft Brands, 2011)
181
(McDonalds, 2011)
182
(White J. , 2009)
183
(Melanson K. Z., 2007)
184
(Angelopoulos, 2009)
185
(White J. , 2009)
186
(White J. , 2010)
187
(Light, 2009)
188
(Light, 2009)
189
(American Diabetes Association, 2010)
190
(White J. F., 2010)
191
(U.S. Department of Agriculture (USDA), 2011)
192
(Bray G. P., 1998) (Lineback, 2003)
193
(Willett, Is dietray fat a major determinant of body fat?, 1998) (Willett, Dietary fat and obesity: and
unconvincing relation, 1998)
194
(Gazzinga, 1993)
195
(Putnam, 1999)
196
(Schoonover, 2006)
197
(Kraft Brands, 2011)
198
(Schoonover, 2006)
199
(Schoonover, 2006)
200
(Farrell, 1987)
201
(Pusztai A. , 2001)
202
(Cummins, 2000)
203
(Pusztai D. A., 2000)
204
(Cummins, 2000) (Pusztai D. A., 2000)
205
(Pusztai D. A., 2000)
206
(Pusztai D. A., 2000)
207
(Pusztai D. A., 2000)
208
(Ho M.-W. R., 2000)
209
(Ho M.-W. R., 1999) (Ho M.-W. R., 2000)
210
(Ho M.-W. R., 1999)
158
High Fructose Corn Syrup and Childhood Obesity
p.133
211
(Cummins, 2000)
(U.S. Food and Drug Administration (FDA), 1992)
213
(Food and Drug Administration (FDA), 1958)
214
(U.S. Food and Drug Administration (FDA), 1992)
215
(U.S. Food and Drug Administration (FDA), 1992)
216
(U.S. Food and Drug Administration (FDA), 1992)
217
(Alliance for Bio-Integrity, 2001)
218
(U.S. Department of Health & Human Services, 2001)
219
(University of Kentucky College of Agriculture, 2003)
220
(de Vendomois, 2009)
221
(de Vendomois, 2009)
222
(de Vendomois, 2009)
223
(U.S. Food and Drug Association (FDA), 2000)
224
(de Vendomois, 2009)
225
(Food and Agriculture Organization of the United Nations, 2000)
226
(Nielsen, 2003) (Young, 2002)
227
(Young, 2002)
228
(Fisher, 2003)
229
(McConahy, 2002)
230
(Rolls B. R., 2004)
231
(Rolls B. R., 2004)
232
(Linn, 2008)
233
(Linn, 2008)
234
(World Health Organization (WHO), 2003)
235
(Rolls B. M., 2002) (McConahy, 2002) (Rolls B. R., 2004) (Fisher, 2003) (Nielsen, 2003) (Young,
2002)
236
(Kral, 2004) (Rolls B. R., 2006)
237
(Krebs, 2007)
238
(Kral, 2004)
239
(Cavadini, 2000) (St. Onge, 2003) (Enns, 2003) (Enns, 2002) (Paeratakul S, 2003)
240
(Cavadini, 2000)
241
(Ornish, 2001) (Ruiz, 2006) (Ulrich, 1996) (McTiernan, 2003) (Michaud, 2001) (Rizzo, 2008)
242
(Rising, 1994) (Mo-suwan, 1998) (Jakicic, 2003) (Rizzo, 2008)
243
(Jakicic, 2003)
244
(Mo-suwan, 1998)
245
(Grunbaum, 2003) (Eaton, 2009)
246
(Chaput, 2011)
247
(Chaput, 2011)
248
(Temple, 2007)
249
(Biddiss, 2010)
250
(Maddison, 2011)
251
(Kaur, 2003) (Dietz W. G., 1985) (Andersen, 1998) (Dennison B. E., 2002) (Dennison B. E., 2002)
(Matheson, 2004) (Matheson, 2004)
252
(Kaur, 2003)
253
(Dietz W. G., 1985)
254
(Andersen, 1998)
255
(Boyland, 2011)
256
(Temple, 2007)
257
(Coon, 2001)
258
(Sen, 2006) (Neumark-Sztainer, 2004) (Gillman M. R.-S., 2000) (Fulkerson, 2009)
259
(Videon, 2002) (Neumark-Sztainer, 2004)
260
(Fulkerson, 2009) (Taveras, 2005)
261
(Gillman M. R.-S., 2000)
262
(Gillman M. R.-S., 2000)
212
High Fructose Corn Syrup and Childhood Obesity
p.134
263
(Enns, 2003) (Enns, 2002) (Cavadini, 2000) (St. Onge, 2003) (Willett, Is dietray fat a major determinant
of body fat?, 1998)
264
(Choi, 2008)
265
(Harvard School of Public Health, 2011)
266
(Mozaffarian, 2006)
267
(Mozaffiarian, 2010)
268
(Vega-Lopez, 2006)
269
(Choi, 2008) (U.S. Department of Health and Human Services, 2011)
270
(St. Onge, 2003)
271
(Paeratakul S, 2003) (Enns,, 2003) (Enns, 2002)
272
(Duffey K. G.-L., 2007)
273
(Ludwig, 2001)
274
(Park, 2002)
275
(Guthrie, 2000)
276
(Tordoff, 1990)
277
(Ludwig, 2001) (Gillis, 2003)
278
(Blum, 2005)
279
(Bray G. N., 2004) (Tordoff, 1990) (Ludwig, 2001)
280
(Gillis, 2003) (Forshee R. S., 2001)
281
(Forshee R. S., 2007) (White J. , 2010) (White J. , 2008) (Murray R. F., 2005)
282
(Ornish, 2001)
283
(Bouchard, 1990) (O'Rahilly, 2006) (Butte, 2006)
284
(Grundy, 1998)
285
(Butte, 2006)
286
(Sen, 2006)
287
(Gilman, 2009)
288
(Boyd, 2005) (Chiolero, 2007) (Meyer, 2006) (Freedman D. D., 2009) (Hannon, 2005) (Carroll, 2007)
(Waring., 2008) (Mustillo, 2003) (Taylor, 2006) (Elliott, 2002)
289
(Geier, 2007) (Cheuk, 2006) (Bradstreed, 2003) (Dufault R. S., 2009)
290
(DeSoto, 2007)
291
(Geier, 2007)
292
(Ung, 2010)
293
(de Vendomois, 2009)
294
(de Vendomois, 2009)
295
(The National Museum of Nuclear Science & History, 2011)
High Fructose Corn Syrup and Childhood Obesity
p.135
Bibliography 1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Addo, O.Y., Himes, J.H. "Reference curves for triceps and subscapular skinfold thicknesses in US children and adolescents." The American Journal of Clinical Nutrition 91 (2010): 635-­‐642. Ahima, Rexford S. "Digging deeper into obesity." The Journal of Clinical Investigation 121, no. 6 (2011): 2076-­‐2079. Alliance for Bio-­‐Integrity. "FDA Docs." Alliance for Bio-­‐Integrity. 2001. http://www.biointegrity.org/FDAdocs/01/index.html (accessed August 2011). American Academy of Pediatrics-­‐ Committee on Nutrition. "Prevention of Pediatric Overweight and Obesity." Pediatrics 112, no. 2 (2003): 424-­‐430. American Diabetes Association. "Summary of Revisions for the 2010 Clinical Practice Recommendations." Diabetes Care 33, no. Suppl. 1 (2010): S3. American Dietetic Association. "Position of the Amerian Dietetic Association: Use of Nutritive and Nonnutritive Sweeteners." Journal of The American Dietetic Association 104, no. 2 (2004): 255-­‐269. Andersen, R.E., Crespo, C.J., Barlett, S., Cheskin, L.J., Pratt, M. "Relationship of Physical Acitivity and Television Watching With Body Weight and Level of Fatness Among Children." Journal of the American Medical Association (JAMA) 297, no. 12 (1998): 938-­‐942. Angelopoulos, T.J., Lowndes, J., Zukley, L., Melanson, K.J., Nguyen, V., Huffman, A., Rippe, J.M. "The Effeect of High-­‐Fructose Corn Syrup Consumption on Triglycerides and Uric Acid." The Journal of Nutrition 139, no. suppl (2009): 1242S-­‐1245S. Associated Press. "Study: Global obesity rates double since 1980." The Washington Times, Februrary 3, 2011. Atcha, Z., Chen, W.S., Ong, A.B., Wong, F.K., Neo, A., Browne, E.R., Witherington, J., Pemberton, D.J. "Cognitive enhancing effects of ghrelin receptor agonists." Psychopharmacology (Berl) 206, no. 3 (2009): 415-­‐427. Barlow, S.E., Dietz, W.H. "Obesity Evaluation and Treatment: Expert Committee Recommendations." Pediatrics 102, no. 3 (1998): e29-­‐e39. Barone, J.G., Hanson, C., DaJusta, D.G., Gioia, K., England, S.J., Schneider, D. "Nocturnal Enuresis and Overweight Are Associated With Obstructive Sleep Apnea." Pediatrics 124, no. 1 (2008): e53-­‐e59. Bedogni, G., Lughetti, L., Ferrari, M., Malavolti, M., Poli, M., Bernasconi. S., Battistini, N. "Sensitivity and specificity of body mass index and skinfold thincknesses in detecting excess adiposity in children aged 8-­‐12 years." Annals of Human Biology 30, no. 2 (2003): 132-­‐139. Belamarich, P.F., Luder, E., Kattan, M., Mitchell, H., Islam, S., Lynn, H., Crain, E.F. "Do Obese Inner-­‐City Children With Asthma Have More Symptoms Than Nonobese Children With Asthma?" Pediatrics 106, no. 6 (2000): 1436. Benson, L., Baer, H.J., Kaelber, D.C. "Trends in the Diagnosis of Overweight and Obesity in Children and Adolescents: 1999-­‐2007." Pediatrics 123, no. 1 (2009): e153-­‐e158. Berg, F.M. Underage and Overweight: America's Childhood Obesity Crisis-­‐ What Every Family Needs to Know. New York, NY: Hatherleigh Press, 2004. Bhosale, S.H., Rao, M.B., Deshpande, V.V. "Molecular and Industrial Aspects of Glucose Isomerase." Microbiological Reviews 60, no. 2 (1996): 280-­‐300. Biddiss, E., Irwin, Jennifer. "Active Video Games to Promote Physical Activity in Children and Youth." Archives of Pediatric and Adolescent Medicine 164, no. 7 (2010): 664-­‐672. Blum, J.W., Jacobsen, D.J., Donnelly, J.E. "Beverage Consumption Patterns in Elementary School Aged Children across a Two Year Period." Journal of the American College of Nutrition 24, no. 2 (200): 93-­‐98. Bouchard, C., Tremblay, A., Despres, J-­‐P., Nadeau, A., Lupien, P.J., Theriault, G., Dussault, J., Moorjani, S., Pinault, S., Fournier, G. "The Response to Long-­‐Term Overfeeding in Identical Twins." The New England Journal of Medicine 322, no. 21 (1990): 1477-­‐1482. High Fructose Corn Syrup and Childhood Obesity
p.136
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
Bowman, S.A., Gortmaker, S.L., Ebbeling, C.B., Pereira, M.S., Ludwig, D.S. "Effects of Fast-­‐Food Consumption on Energy Intake and Diet Quality Among Children in a National Household Survey." Pediatrics 113, no. 1 (2004): 112-­‐118. Bowman, S.L., Vinyard, B.T. "Fast Food Consumption of US Adults: Impact on Energy and Nutrient Intakes and Overweight Status." Journal of the American College of Nutrition 23, no. 2 (2004): 163-­‐168. Boyd, G.S., Koenigsberg, J., Falkner, B., Gidding, S., Hassink, S. "Effect of Obesity and High Blood Pressure on Plasma Lipid Levels in Children." Pediatrics 116, no. 2 (2005): 442-­‐446. Boyland, E.J., Harrold, J.A., Kirkham, T.C., Corker, C., Cuddy, J., Evens, d., Dovey, T.M., Lawton, C.L., Blundell, J.E., Halford, J.C.G. "Food Commercials Increase Preference for Energy-­‐Dense Foods, Particularly in Children Who Watch More Television." Pediatrics 128, no. 1 (2011): e93-­‐e100. Bradstreet, J., Geier, D.A., Kartzinel, J.J. Adams, J.B., Geier, M.R. "A Case-­‐Control Study of Mercury Burden in Children with Autistic Spectrum Disorders." Journal of American Physicians and Surgeons 8, no. 3 (2003): 76-­‐79. Bray, G.A., Nielsen, J.S., Popkin, B.M. "Consumption of high-­‐fructose corn syrup in beverages may play a role in the epidemic of obesity." American Society for Clinical Nutrition 79 (2004): 537-­‐543. Bray, G.A., Popkin, B.M. "Dietary fat intake does affect obesity." The American Journal of Clinical Nutrition 68 (1998): 1157-­‐1173. Broussard, B.A., Johnson, A., Himes, J.H., Story, M., Fitchner, R., Hauck F., Carter, K.B, Hayes, J., Frohlich, K., Gray, N., Valway, S., Gohdes, D. "Prevalence of obesity in American Indians and Alaska Natives." American Society for Clinical Nutrition 53 (suppl) (1991): 1535S-­‐1542S. Broyles, S., Katzmarzyk, P.T., Sathanur, R.S., Chen, W., Bouchard, C., Freedman, D.S.., Berenson, G.S. "The Pediatric Obesity Epidemic Continues Unabated in Bogalusa, Louisiana." Pediatrics 125, no. 5 (2010): 900-­‐905. Buchholz, T. "Fast food is not the primary cause of obesity." In Fast Food, by At Issue, 17-­‐27. New York, NY: Greenhaven Press, 2005. Buchs, A.E., Sasson, S., Joost, H.G., Cerasi, E. "Characterization of GLUT5 Domains Responsible for Fructose Transport." Endocrinology 139, no. 3 (1998): 827-­‐831. Butte, N.F., Cai, G., Cole, S.A., Comuzzle, A.G. "Viva la Familia Study: genetic and environmental contributions to childhood obesity and its comorbidites in the Hispanic population." The American Journal of Clinical Nutrition 84 (2006): 646-­‐654. Campfield, L.A., Smith, F.J., Guisez, Y., Devos, R., Burn, P. "Recominant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks." Science 269, no. 5223 (1995): 546-­‐549. Caprio, S., Genel, M. "Confronting the Epidemic of Childhood Obesity." Pediatrics 115, no. 2 (2004): 494-­‐495. Caprio, S., Hyman, L.D., McCarthy, S., Lange, R., Bronson, M., Tamborlane, W.V. "Fat distribution and cardiovascular risk factors in obese adolescent girls: importance of the intraabdominal fat depot." The Amerian Journal of Clinical Nutrition 64 (1996): 12-­‐17. Carroll, C.L., Pertonella, S., Raykov, N. Smith, S.R., Zuckler, A.R. "Childhood Overweight Increases Hospital Admission Rates for Asthma." Pediatrics 120, no. 4 (2007): 734-­‐740. Cavadini, C., Siega-­‐Riz, A.M., Popkin, B.M. "US adolescent food intake trends from 1965-­‐
1996." Archives of Disease in Children 83, no. 1 (2000): 18-­‐24. Centers for Disease Control and Prevention. About BMI for Children and Teens. http://www.cdc.gov/healthyweight/assessing/bmi/childrens bmi/about childrens bmi.html (accessed January 2011). —. Consequences. http://www.cdc.gov/obesity/childhood/consequences.html. (accessed January 2011). —. Consequences. http://www.cdc.gov/obesity/childhood/consequences.html. (accessed January 2011). —. Contributing Factors. http://www.cdc.gov/obesity/childhood/causes.html. (accessed Janurary 2011). High Fructose Corn Syrup and Childhood Obesity
p.137
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
—. Defining Childhood Overweight and Obesity. http://www.cdc.gov/obesity/childhood/defining.html. (accessed January 2011). —. Economic Evaluation-­‐ Glossary of Terms. June 2011. http://www.cdc.gov/dhdsp/programs/nhdsp_program/economic_evaluation/docs/Econo
mic_Evaluation_Glossary.pdf (accessed June 2011). —. Overview of CDC Growth Charts. 2011. http://www.cdc.gov/nccdphp/dnpa/growthcharts (accessed April 2011). —. Overweight and Obesity. 2011. http://www.cdc.gov/obesity/defining.html (accessed 2011). —. Tips for Parents-­‐ Ideas to Help Children Maintain a Healthy Weight. http://cdc.gov/healthyweight/children/index.html (accessed Janurary 2011). Chaput, J-­‐P., Visby, T., Nyby, S., Klingenberg, L., Gregersen, N.T., Tremblay, A., Astruup, A., Sjodin.A. "Video game playing increases food intake in adolescents: a randomized crossover study." American Journal of Clinical Nutrition 93 (2011): 1196-­‐1203. Cheuk, D.K., Wong, V. "Attention-­‐deficit hyperactivity disorder and blood mercury level: a case-­‐control study in Chinese children." Neruopediatrics 37, no. 4 (2006): 234-­‐240. Chiolero, A., Bovet, P., Paradis, G., Paccaud, F. "Has Blood Pressure Increased in Children in Response to the Obesity Epidemic?" Pediatrics 119, no. 3 (2007): 544-­‐553. Choi, E. "Trans Fat Regulation: A Legislatvie Remedy for America's Heartache." Southern California Interdisciplinary Law Journal 17 (2008): 509-­‐544. Colditz, Graham A. "Economic costs of obesity." The American Journal of Clinical Nutrition 55 (1992): 503s-­‐507s. College of Natural Resources-­‐Department of Nutritional Sciences and Toxicology. "Department of Nutritional Sciences and Toxicology." College of Natural Resources University of California, Berkeley. http://nature.berkeley.edu/departments/nut/undergrad_class/nst106/NST_lect05 (accessed June 28, 2011). Collins, Tracy Brown. Fast Food. New York, NY: Greenhaven Press, 2005. Collison, K.S., Saleh, S.M. Bakheet, R.H., Al-­‐Rabiah, R.K., Inglis, A.L., Makhou, n.J., Maqbool, Z.M., Zaidi, M.Z., Al-­‐Johi, M.A., Al-­‐Mohanna, F.A. "Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS-­‐55." Obesity 17, no. 11 (2009): 2003-­‐2013. Commitee on Nutrition. "Prevention of Pediatric Overweight and Obesity." Pediatrics 112, no. 2 (2003): 424-­‐430. Committe on Nutrition. "The Use and Misuse of Fruit Juice in Pediatrics." Pediatrics 107, no. 5 (2002): 1210-­‐1213. Conus, F., Alison, D.B., Rabasa-­‐Lhoret, R., St-­‐Onge, M., St-­‐Pierre, D.H., Tremblay-­‐Lebeau, A., Poehlman, E.T. "Metabolic and behavioral characteristics of metabolically obese but normal-­‐
weight women." Journal of Clinical Endocrinology and Metabolism 28, no. 10 (2004): 5013-­‐
5020. Conus, F., Rabasa-­‐Lhoret, R., Peronnet, F. "Characteristics of metabolically obese normal-­‐
weight (MONW) subjects." Applied Physiology, Nutrition, and Metabolism 32, no. 1 (2007): 4-­‐
12. Cook, S., Auinger, P., Huang, T.T-­‐K. "Growth Curves for Cardio-­‐Metabolic Risk Factors in Children and Adolescents." The Journal of Pediatrics 155(3) , no. (suppl) (2009): S6.e15-­‐
S6.e26. Coon, K.A., Goldberg, J., Rogers, B.L., Tucker, K.L. "Relationship Between Use of Television During Meals and Children's Food Consumption Trends." Pediatrics 107, no. 1.e7 (2001): 1-­‐9. Council on Science and Public Health. "The Health Effects of High Fructose Syrup." No.3, The Council on Science and Public Health, The American Medical Association, Chicago, 2008. Crapo, P.A., Scarlett, J.A., Kolterman, O.G. "Comparison of the metabolic responses to fructose and sucrose sweetened foods." The American Journal of Clinical Nutrition 36 (1982): 256-­‐
261. High Fructose Corn Syrup and Childhood Obesity
p.138
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
Crowely, D.I., Khoury, P.R., Ubrina, E.M., Ippisch, H.M., Kimball, T.R. "Cardiovascular Impact of the Pediatric Obesity Epidemic: Higher Left Ventricular Mass is Related to Higher Body Mass Index." The Journal of Pediatrics 158, no. 5 (2010): 700-­‐714. Cummings, D.E., Purnell, J.Q., Frayo, S., Schmidova, K., Wisse, B.E., Weigle, D.S. "A Preprandial Rise in Plasma Ghrelin Levels Suggests a Role in Meal Initiation in Humans." Diabetes 50 (2001): 1714-­‐1719. Cummins, R., Williston, B. Genetically Engineered Food A Self-­‐Defense Guide for Consumers. New York, NY: Marlowe & Company, 2000. Dalton, S. Our Overweight Children What Parents, Schools, and Communities Can Do To Control the Fatness Epidemic. Berkeley, CA: University of California Press, 2004. Davidson College. "Biology Department." Davidson College. 2004. http://www.bio.davidson.edu/people/kabern/seminar/2004/GMbios/CW.html (accessed August 2011). de Vendomois, JS., Roullier, F., Cellier, D., Seralini, G.E. "A Comparison of the Effects of Three GM Corn Varieties on Mammalian Health." International Journal of Biological Sciences 5, no. 7 (2009): 706-­‐726. Dehghani, M., Akhtar-­‐Danesh, N., Merchant, AT. "Childhood Obesity, prevalence and prevention." 2005. http://www.nutritionj.com/content/4/1/24 (accessed January 2011). Dennison, B.A., Erb, T.A., Jenkins, P.L. "Television Viewing and Television in Bedroom Associated With Overweight Risk Among Low-­‐Income Preschool Children." Pediatrics 109, no. 6 (2002): 1028-­‐1035. Dennison, B.A., Rockwell, H.L., Nichols, M.J., Jenkins, P. "Children's Growth Parameters Vary by Type of Fruit Juice Consumed." Journal of the American College of Nutrition 18, no. 4 (1999): 346-­‐352. DeSoto, M.C., Hitlan, R.T. "Blood Levels of Mercury Are Related to Diagnosis of Autism: A Reanalyis of an Important Data Set." Journal of Child Neurology 22, no. 11 (2007): 1308-­‐
1311. Diamond, M., Hopson, J. Magic Trees of the Mind. New York, NY: Penguin Putnam, Inc., 1998. Dickie, M.M, Woolley, G.W. "Obese, a new mutation in the house mouse." Journal of Heredity 37 (1946): 365-­‐368. Dietz, W.H., Gortmaker, S.L. "Do We Fatten Our Children at the Television Set? Obesity and Televison Viewing in Children and Adolescents." Pediatrics 75, no. 5 (1985): 807-­‐812. Dietz, W.H., Gross, W.L., Kirkpatrick, J.A. "Blount disease (tibia vara): Another skeletal disorder associated with childhood obesity." The Journal of Pediatrics 101, no. 5 (1982): 735-­‐
737. Dietz, Wiliam H. "Period of Risk in Childhood for the Development of Adult Obesity-­‐ What Do We Need to Learn?" The Journal of Nutrition 127 (1997): 1884S-­‐1886S. Donaldson, M.L., Gubler, C.J. "Biochemical effects of mercury poisoning in rats." The American Journal of Clinical Nutrition 31 (1978): 859-­‐864. Dufault, R., LeBlanc. B., Schnoll, R., Cornett, C., Schweitzer, L., Wallinga, D., Hightower, J., Patrick, L., Lukiw W.J. "Mercury from chlor-­‐alkali plants: measured concentrations in food product sugar." Environmental Health 8, no. 2 (2009): 1-­‐6. Dufault, R., Schnoll, R., Lukiw, WJ., LeBlanc, B., Cornett, C., Patrick, L., Wallinga, D., Gilbert, SG., Crider, R. "Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children." Behavioral Brain and Functions 5, no. 1 (2009): 44-­‐58. Duffey, K.J., Gordon-­‐Larsen, P., Jacobs Jr., D.R., Williams, D., Popkin, B.M. "Differential associations of fast food and restaurant food consumption with 3-­‐y change in body mass index: the Coronary Artery Risk Development in Young Adults Study." The American Journal of Clinical Nutrition 85 (2007): 201-­‐208. Duffey, K.J., Popkin, B.M. "High-­‐fructose corn syrup: is this what’s for dinner?" The American Journal of Clinical Nutrition 88, no. (suppl) (2008): 1722S-­‐1732S. Eaton, D.K, Kann, L., Kinchen, S., Shanklin, S., Ross, J., Hawkins, J., Harris, W.A., Lowry, R., McManus, T., Chyen, D., Lim, C., Whittle, L, Brener, N.D., Wechler, H. Youth Risk Behavior Survelliance -­‐ United States 2009. MMWR Surveillance Summaries, Centers for Disease High Fructose Corn Syrup and Childhood Obesity
p.139
84.
85.
86.
87.
88.
89.
90.
91.
92.
93.
94.
95.
96.
97.
98.
99.
100.
101.
Control and Prevention, Department of Health and Human Services, Atlanta: Office of Surveillance, Epidemiology, and Laboratory Services, Centers for Disease Control and Prevention, 2009, 148. Ekelund, U., Ong, K., Linne, Y., Neovius, M., Brage, S., Dunger ,D.B., Wareham, N.J., Rossner, S. "Upward weight percentile crossing in infancy and early childhood independently predicts fat mass in young adults: the Stockholm Weight Development Study (SWEDES)." The American Journal of Clinical Nutrition 83 (2006): 324-­‐330. Elliott, S.S., Keim, N.L., Stern, J.S., Teff, K., Havel, P.J. "Fructose, weight gain, and the insulin resistance syndrome." The American Journal of Clinical Nutrition 76, no. 5 (2002): 911-­‐922. Ellis, K.J., Abrams, S.A., Wong, W.W. "Monitoring Childhood Obesity: Assessment of the Weight/Height Index." American Journal of Epidemiology 150, no. 9 (1999): 939-­‐946. Elmhurst College. Chemistry Department. 2011. http://www.elmhurst.edu/~chm/vchembook/549sweet.html (accessed July 9, 2011). Emilsson, Y., Liu, Y.L., Cawthorne, M.A., Morton, N.M., Davenport, M. "Expression of the functional leptin receptor mRNA iin pancreatic islets and direct inhibitory action of letptin on insulin secretion." Diabetes 46, no. 2 (1997): 313-­‐316. Encyclopaedia Britannica . Encyclopaedia Britannica Online. http://britannica.com/EBchecked/topic/231001/germanate (accessed July 6, 2011). Enns, C.W., Mickle, S.J., Goldman, J.D. "Trends in Food and Nutrient Intakes by Adolescents in the United States." Family Economics and Nutrition Review 12, no. 2 (2003): 15-­‐27. Enns, C.W., Mickle, S.J., Goldman, J.D. "Trends in Food and Nutrient Intakes by Children in the United States." Family Economics and Nutrition Review 14, no. 2 (2002): 56-­‐66. Farooqi, I.S., Jebb, S.A., Langmack, G., Lawrence, E., Cheetham, C.H., Prentice, A.M., Hughes, I.A., McCamish, M.A., O'Rahilly, S. "Effects of Recombinant Leptin Therapy in a Child with Congenital Leptin Deficiency." New England Journal of Medicine 341, no. 12 (1999): 879-­‐884. Farooqi, S., Keog, J.M., Kamath, S., Jones, S., Gibson, W.T., Trussell, T., Jebb, S.A., Lip, G.H.Y., O'Rahilly, S.O. "Metabolism: Partial leptin deficiency and human adiposity." Nature 414 (2001): 34-­‐35. Farooqui, I.S., Matarese, G., Lord, G.M., Keogh, J.M., Lawrence, E., Agwu, C., Sanna, V., Jebb, S.A., Perna, F., Fontana, S., Lechler, R.I., DePaoli, A.M., O'Rahilly, S. "Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency." The Journal of Clinical Investigation 110, no. 8 (2002): 1093-­‐
1103. Farrell, Kenneth R. Communicating Biotechnology. Agriculture and Natural Resources, University of California -­‐Davis, Davis: California Agriculture, 1987. Ferreira, I., Snjider, M.B., twisk, J.W., van Mechelen, W., Kemper, H.C., Seidell, J.C., Stehouwer, C.D. "Central fat mass versus peripheral fat and lean mass: opposite (adverse versus favorable) associations with arterial stiffness? The Amsterdam Growth and Health Longitudinal Study." Journal of Endocrinology and Metabolism 89, no. 6 (2004): 2632-­‐2639. Fields, S. "The Fat of the Land: Do Agriculture Subsidies Foster Poor Health?" Environmental Health Perspectives 112, no. 14 (2004): 112-­‐114. Fisher, J.O., Rolls, B.J., Birch, L.L. "Children's bit size and intake of an entree are greater with large portions than with age-­‐appropriate or self-­‐selected portions." The American Journal of Clinical Nutrition 77 (2003): 1164-­‐1170. Food and Agriculture Organization of the United Nations. Safety aspects of genetically modified foods of plant origin. Food and Agriculture Organization, United Nations, Geneva: World Health Organization, 2000. Food and Drug Administration (FDA). Federal Food, Drug and Cosmetic Act. Food and Drug Administration, U.S. Department of Health and Human Services, Washington, DC: U.S. Department of Health and Human Services, 1958. —. "Genetically Engineered Foods." Statement of James H. Maryanski Ph.D before the Subcommitte on Basic Research House Commitee on Science. Washington, DC: U.S. Departmet of Health and Human Services, 1999. 4. High Fructose Corn Syrup and Childhood Obesity
p.140
102.
103.
104.
105.
106.
107.
108.
109.
110.
111.
112.
113.
114.
115.
116.
117.
118.
119.
120.
Forshee, R.A., Storey, M.L. "The Role of Added Sugars in the Diet Quality of Children and Adolescents." Journal of the American College of Nutrition 20, no. 1 (2001): 32-­‐43. Forshee, R.A., Storey, M.L., Allison, D.B., Klinsmann, W.H., Lineback, D.R., Miller, S.A., Nicklas, T.A., Weaver, G.A., White, J.S. "A Critical Examination of the Evidence Relating High Fructose Corn Syrup and Weight Gain." Critical Reviews in Food Science Nutrition 47, no. 6 (2007): 561-­‐582. Frederich, R.C., Hamann, A., Anderson, S., Lollmann, B., Lowell, B.B., Flier, J.S. "Leptin levels reflect body lipid content in mice: Evidence for diet-­‐induced resistance to leptin action." Nature Medicine 1, no. 12 (1995): 1311-­‐1314. Freedman, D.S., Dietz, W.H., Srinivasan, S.R., Berenson, G.S. "Risk Factors and Adult Body Mass Index Among Overweight Children: The Bogalusa Heart Study." Pediatrics 123, no. 3 (2009): 750-­‐757. Freedman, D.S., Khan, L.K.., Serdula, M.K., Dietz, W.H., Srinivasan, S.R., Berenson, G.S. "The Relation of Childhood BMI to Adult Adiposity: The Bogalusa Heart Study." Pediatrics 115, no. 1 (2005): 22-­‐27. Freedman, DS., Khan, LK., Deitz, WH., Srinivasant, SR., Berenson, GS. "Relationship of Childhood Obesity to Coronary Heart Disease Risk Factors in Adulthood: The Bogalusa Heart Study." Pediatrics 108, no. 3 (2001): 712-­‐718. Friedman, Jeffrey M. "The Function of Leptin in Nutrition, Weight and Physiology." Nutrition Reviews 60 , no. suppl s10 (2002): S1-­‐S14. Fulkerson, J.A., Kubik, M.Y., Story, M., Lytle, L., Arcan, C. "Are There Nutritional and Other Benefits Associated with Family Meals Among At-­‐Risk Youth?" Journal of Adolescent Health 45, no. 4 (2009): 389-­‐395. Gautron, L., Elmquist, J.K. "Sixteen years and counting: an update on leptin in energy balance." The Journal of Clinical Investigation 121, no. 6 (2011): 2087-­‐2079. Gazzinga, J.M., Burns, T.L. "Relationship between diet composition and body fatness, with adjustment for resting energy expenditure and physical activity, in preadolescent children." The American Journal of Clinical Nutrition 58 (1993): 21-­‐28. Geier, D.A., Geier, M.R. "A Prospective Study of Mercry Toxicity Biomarkers in Autistic Spectrum Disorders." Journal of Toxicology and Envrionmental Health, Part A 70 (2007): 1723-­‐1730. Georgia State University Department of Kineseology and Health. Body Composition. http://www2.gsu.edu/~wwwfit/bodycomp.html (accessed 2011). Gidding, S.S., Bao, W., Srinivasan, S.R., Berenson, G.S. "Effects of secular trends in obesity on coronary risk factors in children: The Bogalusa Heart Study." The Journal of Pediatrics 127, no. 6 (1995): 868-­‐874. Gillis, L.J., Bar-­‐Or, O. "Food Away from Home, Sugar-­‐Sweetened Drink Consumption and Juvenile Obesity." Journal of the American College of Nutrition 22, no. 6 (2003): 539-­‐545. Gillman, M.W., Rifas-­‐Shiman, S.L., Frazier, L., Rockett, H.R.H., Camargo, C.A., Field, A.E., Berkey, C.S., Colditz, G.A. "Family Dinner and Diet Quality Among Older Children and Adolescents." Archives of Family Medicine 9 (2000): 235-­‐240. Gillman, M.W., Rifas-­‐Shiman, S.L., Frazier, L., Rockett, H.R.H., Camargo, C.A., Field, A.E., Berkey, C.A., Colditz, G.Q. "Family Dinner and Diet Quality Among Older Children and Adolescents." Archives of Family Medicine 9 (2000): 235-­‐240. Gilman, S.E., Rende, R., Boergers, J., Abrams, D.B., Buka, S.L., Clark, M.A., Colby, S.M., Hitsman, B., Kazura, A.N., Lipsitt, L.P., Lloyd-­‐Richardson, E.E., Rogers, M.L., Stanton, C.A., Stroud, L.R., Niaura, R.S. "Parental Smoking and Adolescent Smoking Initiation: An Intergenerational Perspective on Tobacco Control." Pediatrics 123, no. 2 (2009): e274-­‐e281. Goldsobel, Alan B. "Relationship of Body Mass Index With Asthma Indicators in Head Start Children." Pediatrics 122, no. Supplement 4 (2008): S208. Goodpaster, B.H., Thaete, F.L., Kelley, D.E. "Thigh adipose tissue distribution is associated with insulin resistance in obesity and in type 2 diabetes mellitus." Amercian Clinical Journal of Nutrition 71 (2000): 885-­‐892. High Fructose Corn Syrup and Childhood Obesity
p.141
121.
122.
123.
124.
125.
126.
127.
128.
129.
130.
131.
132.
133.
134.
135.
136.
137.
138.
139.
140.
141.
Goran, M., Gower, B. "Relation between visceral fat and disease risk in children and adolescents." The American Journal of Clinical Nutrition 70, no. (suppl) (1999): 149S-­‐156S. Goran, Michael I. "Measurement Issues Related to Studies of Childhood Obesity: Assessment of Body Composition, Body Fat Distribution, Physical Activity and Food Intake." Pediatrics 101, no. supplement (1998): 505-­‐518. Gordon-­‐Larsen, P, The, N.S., Adair, L.S. "Longitudinal Trends in Obesity in the United States From Adolescence to the Third Decade of Life." Obesity 19, no. 9 (2010): 1801-­‐1804. Gosnell, Mariana. "Killer Fat." Discover Magazine. February 28, 2007. http://discovermagazine.com/2007/feb/visceral-­‐fat (accessed August 2011). Gower, B.A., Nagy, T.R., Goran, M.I. "Visceral Fat, Insulin Sensitivity, and Lipids in Prepubertal Children." Diabetes 48 (1999): 1515-­‐1521. Gross, L.S., Li, L., Ford, E.S., Liu, S. "Increased consumption of refined carboydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment." The American Journal of Clinical Nutrition 79, no. 5 (2004): 774-­‐779. Grunbaum, J., Kann, L., Kinchen, S., Ross, J., Hawkins, J., Lowry, R., Harris, W., McManus, T., Chyen, D., Collins, J. Youth Risk Behavior Surveillance -­‐ United States 2003. MMWR Surveillance Summaries No. SS-­‐5, Centers for Disease Control and Prevention, Department of Health and Human Services, Atlanta: Office of Surveillance, Epidemiology, and Laboratory Services, Centers for Disease Control and Prevention, 2003, 106. Grundy, Scott M. "Multifactorial causation of obesity: implications for prevention." The American Journal of Clinical Nutrition 67, no. suppl (1998): 563S-­‐572S. Guo S.S., Wu W., Chumlea C, Roche A.R. "Predicting overweight and obesity in adulthood from body mass index values in childhood and adolescence." The American Journal of Clinical Nutrition 76 (2002): 653-­‐658. Guthrie, J.F., Morton, J.F. "Food sources of added sweetners in the diets of Americans." Journal of the American Dietetic Association 100 (2000): 43-­‐51. Gutin, B., Ramsey, L., Barbeau, P., Cannady, W., Ferguson, M., Litaker, M. Owens, S. "Plasma leptin concentrations in obese children: changes during 4-­‐mo periods with and without physical training." The American Journal of Clinical Nutrition 69 (1999): 388-­‐394. Guyton, AC. Textbook of Medical Physiology (Eight Edition). Pennsylvania, PA: W.B. Saunders Company, 1991. Halaas, J.L., Gajwala, K.S., Maffei, M., Cohen, S.L.. Chait, B.T., Rabinowitz, D., Lallone, R.L., Burley, S.K., Friedman, J.M. "Weight-­‐reducing effects on the plasma protein encoded by the obese gene." Science 269, no. 5223 (1995): 543-­‐546. Haley, S., Reed, J., Lin, B-­‐H., Cook, A. "Sweetener Consumption in the United States: Distribution by Demographic and Product Characteristics." Economic Research Service, United States Department of Agriculture, Washington D.C., 2005. Haley, S.L. "Sugar and Sweeteners/SSS-­‐223." Economic Research Service/USDA. May 1998. http://www.ers.usda.gov/briefing/sugar/sugarpdf/SSS223sugarhfcsprodcosts.pdf (accessed June 30, 2011). Hannon, T.S., Rao, G, Arlanian, S.A. "Childhood Obesity and Type 2 Diabetes Mellitus." Pediatrics 116, no. 2 (2005): 473-­‐480. Harvard School of Public Health. "The Nutrition Source." Harvard School of Public Health. 2011. http://www.hsph.harvard.edu/nutritionsource/nutrition-­‐news/transfats (accessed September 2011). Hedley A.A., Ogden C.L., Johnson C.L., Carrol J.M., Curtin L.R., Flegal K.M. "Prevalence of Overweight and Obesity Among US Children, Adolescents and Adults, 1999-­‐2002." Journal of the American Medical Association (JAMA) 291, no. 23 (2004): 2847-­‐2850. Heinz, F., Lamprecht, W., Kirsch, J. "Enzymes of fructose metabolism in human liver." The Journal of Clinical Investigation 47, no. 8 (1968): 1826-­‐1832. Hendel, A. Fat Families Thin Families. Dallas, TX: Benbella Books, 2008. Himes J.H., Dietz, W.H. "Guidelines for overweight in adolescent preventive services: recommendations from an expert committee: the Expert Committee on Clinical Guidelines High Fructose Corn Syrup and Childhood Obesity
p.142
142.
143.
144.
145.
146.
147.
148.
149.
150.
151.
152.
153.
154.
155.
156.
157.
158.
for Overweight in Adolescent Preventive Services." The American Journal of Clinical Nutrition 59 (1994): 307-­‐316. Ho, M-­‐W., Ryan, A., Cummins. "Hazards of transgenic plants containing the cauliflower mosaic viral promotor." Microbial Ecology in Health and Disease 12 (2000): 6-­‐11. Ho, M-­‐W., Ryan, A., Cummins, J. "Cauliflower Mosaic Viral Promoter-­‐ A Recipe for Disaster." The Institute of Science in Society (ISIS). 1999. http://www.i-­‐sis.org.uk/camvrecdis.php (accessed August 2011). Hortobagyi, T., Israel, R.G., O"Brien, K. F. "Sensitivity and specificity of the Quetelet index to assess obesity in men and women." The European Journal of Clinical Nutrition 48, no. 5 (1994): 369-­‐375. Howard Hughes Medical Institute. Research News. April 2004. www.hhmi.org/news/pdf/friedman5.pdf (accessed July 2011). Huang, W.l., Ramsey, K.M., Marcheva, B., Bass J. "Circadian rhythms, sleep, and metabolism." The Journal of Clinical Investigation 121, no. 6 (2011): 2133-­‐2141. Jakicic, J.M., Marcus, B.H., Gallagher, K.I., Napolitano, M., Lang, W. "Effect of Exercise Duration and Intensity on Weight Loss in Overweight, Sedentary Women." Journal of the American Medical Association (JAMA) 290, no. 10 (2003): 1323-­‐1330. Janssen, I., Katzmarzyk, T.P., Srinivasan, S.R., Chen, W., Malina, R.M., Bouchard, C., Berenson, G.S. "Utility of Childhood BMI in the Prediction of Adulthood Disease: Comparison of National and International References." Obesity Research 13, no. 6 (2005): 1106-­‐1115. Juhola, J., Magnussen, C.G., Viikari, J.S. A., Kahonen, M., Hutri-­‐Kahonen, N., Jula, A., Lehtimaki, T., Akerblom, H.K., Pietikainen, M., Laitinen, T., Jokinen, E., Taittonen, L., Raitakari, O.T., Juonala, M. "Ageing brain abnormalities in young obese patients with type 2 diabetes: a cause for concern." The Journal of Pediatrics, April 2011: 1-­‐7. Juhola, J., Magnussen, C.G., Viikari, J.S.A., Kahonen, M., Hutri-­‐Kahonen, N, Jula, A., Lehtimaki, T., Akerblom, H.K., Pietikainen, M., Laitinen, T., Jokinen, El., Taittonen, L., Raitakari, O.T., Juonala, M. "Tracking of Serum Lipid Levels, Blood Pressure, and Body Mass Index from Childhood to Adulthood: The Cardiovascular Risk in Young Finns Study." The Journal of Pediatrics 03 (April 2011): 1-­‐7. Jurgens, H., Haass, W., Castaneda T.R., Schurmann, A., Koebnick, C., Dombrowski, F., Otto, B., Nawrocki, A.R., Scherer, P.E., Spranger, J., Ristow, M., Joost., H-­‐G., Havel, P.J., Tschop, M.H. "Cosuming Fructose-­‐sweetened Beverages Increases Body Adiposity in Mice." Obesity Research 13, no. 7 (July 2005): 1146-­‐1156. Kappes, S.M., Schmidt, J.S., Lee, S.-­‐Y. "Mouthfeel Detection Threshold and Instrumental Viscosity of Sucrose and High Fructose Corn Syrup Solutions." Journal of Food Science 71, no. 2 (suppl) (2006): S597-­‐S602. Kaur, H., Choi, W., Mayo, M.S., Harris, K.J. "Duration of television watching is associated with increased body mass index." The Journal of Pediatrics 143, no. 4 (2003): 506-­‐511. Kennedy, G.C. "The Role of Depot Fat in the Hypothalamic Control of Food Intake in the Rat." Proceedings of the Royal Society of London. Series B, Biological Sciences (The Royal Society) 140, no. 901 (1953): 578-­‐592. Kraft Brands. Capri Sun Mom's. 2011. http://www.kraftbrands.com/CaprisunMoms/faq.aspx (accessed August 2011). Kral, T.VE, Roe, L.S., Rolls, B.J. "Combined effects of energy density and portion size on energy intake in women." The American Journal of Clinical Nutrition 79 (2004): 962-­‐968. Krebs, N.F., Himes, J.H., Jacobson, D., Nicklas, T.A., Guidlay, P., Styne, D. "Assessment of child and adolescent overweight and obesity." Pediatrics 120, no. (suppl 4) (2007): S193-­‐S228. Kuczmarski, R.J., Ogden, C.L., Grummer-­‐Strawn, L.M., Flegal, K.M., Guo, S.S., Wei, R., Mei, Z., Curtin, L.R., Roche, A.F., Johnson, C.L. CDC Growth Charts: United States. Advance Data 314, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention/National Center for Health Statistics, Atlanta: U.S. Department of Health and Human Services, 2000, 1-­‐27. High Fructose Corn Syrup and Childhood Obesity
p.143
159.
160.
161.
162.
163.
164.
165.
166.
167.
168.
169.
170.
171.
172.
173.
174.
175.
176.
Lagstrom, H., Hakanen, M., Niinikoski, H., Viikari, J., Ronnemaa, T., Saarinen, M., Pahkala, K., Simell, O. "Growth Patterns and Obesity Development in Overweight or Normal-­‐Weight 13-­‐
Year-­‐Old Adolescents: The STRIP Study." Pediatrics 122, no. 4 (2007): e876-­‐e883. Lamot, E. "The indusrial production of isoglucose." Antoine van Leeuwenhoek 49 (1983): 88-­‐
89. Langreth, R. "Most Expensive Diseases." Forbes. 2009. http://www.forbes.com/2009/12/14/most-­‐expensive-­‐diseases-­‐lifestyle-­‐health-­‐costs-­‐
treatments print.html (accessed May 2011). Larsson, B., Svardsudd, K., Welin, L., Wilhelmsen, L., Bjorntorp, P. and Tibblin, G. "Abdominal adipose tissue distribution, obesity and risk of cardiovascular disease and death: 13 year follow up of participants in a study of men born in 1913." British Medical Journal 288, no. 6428 (1984): 1401-­‐1404. Lazarus, R., Baur, L., Webb, K., Blyth, F. "Body mass index in screening for adiposity in children and adolescents: systematic evaluation using receiver operating characteristic curves." The American Journal of Clinical Nutrition 63 (1996): 500-­‐506. Levy E., Levy, P., Le Pen, C., Basdevant, A. "The economic cost of obseity: the French situation." Inernational Journal of Obesity Related Metabolic Disorders 19, no. 11 (1995): 788-­‐
792. Li, S., Zhao, J.H., Luan, J., Langenberg, C., Luben, R.N., Khaw, K.T., Wareham, N.J., Loos, R.J.F. "Genetic predisposition to obesity leads to increased risk of type 2 diabetes." Diabetologia 54 (2011): 776-­‐782. Light, H.R., Tsanzi, E., Gigliotti, J., Morgan, K., Tou, J.C. The Type of Caloric Sweetener Added to Water Influences Weight Gain, Fat Mass, and Reproduction in Growing Sprague-­‐Dawley Female Rats. Division of Animal and Nutritional Sciences, West Virginia University, Morgantown: West Virginia University, 2009. Lineback, D.R., Jones, J.M. "Sugars and Health Workshop: summary and conclusions." The American Journal of Clinical Nutrition 78, no. suppl (2003): 893S-­‐897S. Linn, S., Novosat, C.L. "Calories for Sale: Food Marketing to Children in the Twenty-­‐First Centruy." The ANNALS of the American Academy of Political and Social Science 618 (2008): 133-­‐155. Liu, L., Karkanais, G.B., Morales, J.C., Hawkins, M., Barzilai, N., Wang, J., Rossetti, L. "Intracerebroventricular Leptin Regulates Hepatic but Not Peripheral Glucose Fluxes." The Journal of Biological Chemistry 273, no. 47 (1998): 31160-­‐31167. Liu, Mihn. Leptin: A Piece of the Obesity Pie. August 2004. http://www.scq.ubc.ca/leptin-­‐a-­‐
piece-­‐of-­‐the-­‐obesity-­‐pie/ (accessed August 2011). Ludwig, K.S., Peterson, K.F., Gortmaker, S.L. "Relation between consumption of sugar-­‐
sweetened drinks and childhood obesity: a prospective, observational analysis." The Lancet 357 (2001): 505-­‐508. Lutter, M., Sataka, I., Osborne-­‐Lawrence, S., Rovinsky, S.A., Anderson, J.G., Jung, S., Birnbaum, S., Yanagisawa, M., Elmquist, J.K., Nestler, E.J., Zigman, J.M. "The orexigenic hormone ghrelin defends against depressive symptoms of chronic stress." Nature Neruoscience 11, no. 7 (2008): 752-­‐753. Maddison, R., Foley, L., Mhurchu, C.N., Jian, Y., Jull, A., Prapavessis, H., Hohepa, M., Rodgers, A. "Effects of active video games on body composition: a randomized controlled trail." The American Journal of Clinical Nutrition 94, no. 1 (2011): 156-­‐163. Maffei, M., Halaas, J., Ravussin, E., Pratley, R.E., Lee, G.h., Zhang, Y., Fei, H., Kim. S., Lallone, R., Ranganathan, S., Kern, P.A., Friedman, J.M. "Leptin levels in human and rodent: Measurement of plasma leptin and ob RNA in obese and weight-­‐reduced subjects." Nature Medicine 1, no. 11 (1995): 1155-­‐1161. Maffeis, C., Pietrobelli, A., Grezzani A., Provera, S., Tato, L. "Waist Circumference and Cardiovascular Risk Factors in Prepubertal Children." Obesity Research 9, no. 3 (2001): 179-­‐
187. Mallory, G.B., Fiser, D.H., Jackson, R. "Sleep-­‐associated breathing disorders in morbidly obese children and adolescents." Journal of Pediatrics 115, no. 6 (1989): 892-­‐897. High Fructose Corn Syrup and Childhood Obesity
p.144
177.
178.
179.
180.
181.
182.
183.
184.
185.
186.
187.
188.
189.
190.
191.
192.
193.
194.
195.
196.
197.
Marshall, R.O., Kooi, E.R. "Enzymatic Conversion of D-­‐Glucose to D-­‐Fructose." Science 125, no. 3249 (1957): 648-­‐649. Martindale, D. "Fast Food May Be Addictive." In Fast Food, by At Issue, edited by Tracy Brown Collins, 10-­‐15. New York, NY: Greenhaven Press, 20005. Matheson, D.M, Killen, J.D., Wang, Y., Varady, A., Robinson, T.N. "Children's food consumption during television viewing." The American Journal of Clinical Nutrition 79 (2004): 1088-­‐1094. Mayes, Peter A. "Intermediary metabolism of fructose." The American Journal of Clinical Nutrition 58, no. suppl. (1993): 754S-­‐765S. McConahy, K.L., Smiciklas-­‐Wright, H., Birch, L.L., Mitchell, D.C., Picciano, M.F. "Food Portions are positiviely related to energy intake and body weight in early childhood." The Journal of Pediatrics 140, no. 3 (2002): 340-­‐347. McCormick, D.P., Sarpong, K., Jordan, L., Ray, L.A., Jain, S. "Infant Obesity: Are We Ready to Make this Diagnosis?" Journal of Pediatrics 157, no. 1 (2010): 15-­‐19. McDevitt, R.M., Bott, S.J., Harding, M., Coward, W.A., Bluck, L.J., Prentice, A.M. "De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women." The American Journal of Clinical Nutrition 74, no. 6 (2001): 737-­‐746. McDonalds. Nutrition Exchange. 2011. http://nutrition.mcdonalds.com/nutritionexchange/itemDetailInfo.do?itemID=10005 (accessed August 2011). McTiernan, A., Kooperber, C., White, E., Wilcox, S., Coates, R., Adams-­‐Campbell, L.L., Woods, N., Ockene, J. "Recreational Physical Activity and the Risk of Breast Cancer in Postmenopausal Women." Journal of the American Medical Association (JAMA) 290, no. 10 (2003): 1323-­‐1377. MedBio. Carbohydrate Metabolism. 2011. http://www.medbio.info/Horn/Time%201-­‐
2/carbohydrate_metabolism.htm (accessed 2011). Medical Research Council. "Obesity." Medical Research Council. 2011. http://www.mrc.ac.uk/Achievementsimpact/Storiesofimpact/Obesity/index.htm (accessed July 2011). Melanson, K.J., Angelopoulos, T.J., Nguyen, V., Buckley, L., Lowness, J., Rippe, J.M. "High-­‐
fructose corn syrup, energy intake, and appetite regulation." The American Journal of Clinical Nutrition 88, no. (suppl) (2008): 178S-­‐144S. Melanson, K.J., Zukely, L., Lowndes, J., Nguyen, V., Angelopoulos, T.J., Rippe, J.M. "Effects of high-­‐fructose corn syrup anad sucrose consumption on ciruculating glucose, insulin, leptin, and ghrelin on appetite in normal-­‐weight women." Nutrition 23, no. 2 (2007): 103-­‐112. Merriam-­‐Webster. Digestion. 2011. http://www.merriam-­‐webster.com/dictionary/digestion (accessed March 2011). Meyer, A.A., Kundt, G., Steiner, M., Schuff-­‐Werner, P., Kienast, W. "Impaired Flow-­‐Mediated Vasodilation, Carotid Artery Intima-­‐Media Thickening, and Elevated Endothelial Plasma Markers in Obese Children: The Impact of Cardiovascular Risk Factors." Pediatrics 117, no. 5 (2006): 1560-­‐1567. Michaud, D.S, Giovannucci, E., Willett, W.C., Colditz, G.A., Stampfer, M.J., Fuchs, C.S. "Physical Activity, Obesity, Height and the Risk of Pancreatic Cancer." Journal of the American Medical Association (JAMA) 286, no. 8 (2001): 921-­‐929. Miller, J., Rosenbloom, A., Silverstein, J. "Childhood Obesity. " Journal of Endocrinology and Metabolism 89 (2004): 4211-­‐4218. Millington, George W.M. "The role of proopiomelanocortin (POMC) neurones in feeding behavior." Nutrition & Metabolism 4, no. 18 (2007): 1-­‐16. Moeller, S.M., Fryhofer, S.A., Osbahr, A.J., Rabinowitz, C.B. "The Effects of High Fructose Syrup." Journal of the American College of Nutrition 28, no. 6 (2009): 619-­‐626. Monsivais, P., Perrigue, M.M., Drewnowski, A. "Sugars and satiety: does the type of sweetener make a difference." American Journal of Clinical Nutrition 86 (2007): 116-­‐123. Moran, TH. "Fructose and Satiety." The Journal of Nutrition 139, no. (suppl) (2009): 1253S-­‐
1256S. High Fructose Corn Syrup and Childhood Obesity
p.145
198.
199.
200.
201.
202.
203.
204.
205.
206.
207.
208.
209.
210.
211.
212.
213.
214.
215.
216.
217.
218.
219.
220.
Morrison, J.A., Barton, B.A., Biro, F.M., Daniels, S.R., Sprecher, D.L. "Overweight, fat patterning, and cardiovascular disease risk factors in black and white boys." The Journal of Pediatrics 135 (1999): 451-­‐457. Moss, B.G., Yeaton, W.H. "Young Children's Weight Trajectories and Associated Risk Factors: Results From the Early Childhood Longitudinal Study-­‐Birth Cohort." American Journal of Health Promotion 25, no. 3 (2011): 190-­‐198. Mo-­‐suwan, L., Prongprapai, S., Junjana, C., Puetpaiboon, A. "Effects of a conrolled trial of a school-­‐based exercise program on the obesity indexes of preschool children." The American Journal of Clinical Nutrition 68 (1998): 1006-­‐1011. Mozaffarian, D., Katan, M.B., Ascherio, A., Stampher, M.J., Willett, W.C. "Trans Fatty Acids and Cardiovascular Disease." The New England Journal of Medicine 354 (2006): 1601-­‐1613. Mozaffiarian, D., Stamplfer, M.J. "Removing industrial trans fat from food." BMJ 340 (2010): c1826. Mueller, W.M., Gregoire, F.M., Stanhope, K.L., Mobbs, C.V., Mizuno, T.M., Warden, C.H., Stern, J.S., Havel, P.J. "Evidence That Glucose Metabolism Regulates Leptin Secretion from Cultured Rat Adipocytes." Endocrinology 139, no. 2 (1998): 551-­‐558. Murphy, R., Tura, A., Clark, PM., Holst, JJ., Mari, A., Hattersley, AT. "Glukokinase, the pancreatic glucose sensor, is not the gut glucose sensor." Diabetologia 52 (2009): 154-­‐159. Murray, M. , Lyon, M. How to Prevent and Treat Diabetes with Natural Medicine. New York, NY: Penquin Group, Inc., 2003. Murray, R., Frankowski, B., Taras, H. "Are soft drinks a scapegoat for childhood obesity?" The Journal of Pediatrics 146 (2005): 586-­‐590. Must A, Jacques FP, Dallal GE, Bajema CJ, Dietz WH. "Long-­‐Term Morbidity and Mortality of Overweight Adolescents." The New England Jouranal of Medicine 5 (1992): 1350-­‐1355. Mustillo, S., Worthman, C., Erkanli, A., Keeler, G., Angold, A., Costello, EJ. "Obesity and Psychiatric Disorder: Developmental Trajectories." Pediatrics 111, no. 4 (2003): 851-­‐859. National Center for Health Statistics. NCHS Growth Curves for Children Birth -­‐ 18 Years United States. Number 165 , U.S. Department of Health, Education, and Welfare, Hyattsville: DHEW Publication No, (PHS) 78-­‐1650, 1977, 1-­‐80. Neumark-­‐Sztainer, D., Wall, M., Story, M., Fulkerson, J.A. "Are family meal patterns associated with disordered eating behaviors among adolescents?" Journal of Adolescent Health 35 (2004): 350-­‐359. Nielsen, S.J., Popkin, B.M. "Patterns and Trends in Food Portion Sizes 1977-­‐1998." Journal of the American Medical Association (JAMA) 289, no. 4 (2003): 450-­‐453. Nolan, J.J. "Ageing brain abnormalities in young obese patients with type 2 diatebes: a cause for concern." Diabetologia 53, no. 11 (2010): 2273-­‐2275. Ogden C, Carroll M, Curtin L, Lamb M, Flegal K. "Prevalence of High Body Mass Index in US Children and Adolescents, 2007-­‐2008." Journal of the American Medical Association (JAMA) 303, no. 3 (2010): 242-­‐249. Ogden, C., Carroll, M. "Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-­‐1965 Through 2007-­‐2008." Centers for Disease Control National Center for Health Statistics, 2010. O’Brien, R. The Unhealthy Truth. New York, NY: Broadway Books, 2009. Okie, S. Fed Up! Winning the War Against Childhood Obesity. Washington DC: Joseph Henry Press, 2005. Ong, K.K.L., Ahmed, M.L., Emmett, P.M., Preece, M.A., Dunger, D.B., and the Avon Longitudinal Study of Pregnancy and Childhood Study Team. "Association between postnatal catch-­‐up growth and obesity in childhood: a prospective cohort study." British Medical Journal 320 (2000): 967-­‐971. O'Rahilly, S., Farooqi, I.S. "Genetics of Obesity." Philosophical Transactions of the Royal Society London B Biological Sciences 361 (2006): 1095-­‐1105. Ornish, Dean. Eat More, Weigh Less. New York, NY: Harper Collins Publishers, 2001. OUKosher. High Fructose Corn Syrup. 2011. http://www.oukosher.org/index.php/articles/single print/2489 (accessed July 2011). High Fructose Corn Syrup and Childhood Obesity
p.146
221.
222.
223.
224.
225.
226.
227.
228.
229.
230.
231.
232.
233.
234.
235.
236.
237.
238.
239.
Paeratakul S, Ferdinand DP, Champagne CM, Ryan DH, Bray GA. "Fast food consumption among US adults and children: Dietary and nutrient intake profile." Journal of American Dietic Association 103, no. 10 (2003): 1332-­‐1338. Park, Y.K., Meier, E.R., Bianchi, P., Song, W.O. "Trends in Children's Consumption of Beverages: 1987-­‐1998." Family Economics and Nutrition Review 14, no. 2 (2002): 69-­‐79. Parker, K., Salas, M., Nwosu, V.C. "High fructose corn syrup: Production, use and public health concerns." Biotechnology and Molecular Biology Review 5, no. 5 (2010): 71-­‐78. Pelleymounter, M.A., Cullen, M.J., Baker, M.B., Hecht, R., Winters, D., Boone, T., Collins, F. "Effects of the obese gene product on body weight regulation in ob/ob mice." Science 269, no. 5223 (28 1995): 540-­‐543. Perea-­‐Martinez, A., Carbajal, R.L., Rodriguez, H.R., Zarco, R.J., Barrios, F.R., Loredo, A.A. "Association of Comorbidity with Obesity in Mexican Children and Adolescents." Pediatrics 121, no. supplement (2008): S149-­‐S150. Pereira, M.A., Kartashov, A.I., Ebbeling, C.B., Van-­‐Horn, L., Slattery, M.L., Jacobs Jr., D.R., Ludwig, D.S. "Fast-­‐food habits, weight gain, and insulin resistance (the CARDIA study): 15 year prospective analysis." Lancet 365 (2005): 36-­‐42. Perl, Rebecca. "How leptin rewires the brain." The Rockefeller University Scientist. May 14, 2004. http://www.rockerfeller.edu/pubinfo/news notes/rus 051404 c.php (accessed July 2011). Petersen, K.F., Laurent, D., Yu, C., Cline, Q.W., Shulman, G.I. "Stimulating Effects of Low-­‐Dose Fructose on Insulin-­‐Stimulated Hepatic Glycogen Synthesis in Humans." Diabetes Journal (American Diabetes Association) 50, no. 6 (2001): 1263-­‐1268. Press, Associated. "Study: Global obesity rates double since 1980." The Washington Times, February 3, 2011: 2. Pusztai, Arpad. "Genetically Modified Foods: Are They a Risk to Human/Animal Health." American Institute of Biological Sciences. 2001. http://www.actionbioscience.org/biotech/pusztai.html (accessed January 2011). Pusztai, Dr. Arpad, interview by R. Frontline (India) Rmiiandzan. Interview with Arpad Pusztai (November 10, 2000). Putnam, J.J., Allshouse, J.E. "Food Consumption, Prices, and Expenditures, 1970-­‐1997." Statistical Bulletin No.965, Food and Rural Economics Division, Economic Research Service, U.S. Department of Agriculture, Washington, DC, 1999, 1-­‐189. Redondo, MJ., Yu, L., Hawa, M., Mackenzie, T., Pyke, DA., Eisenbarth, GS., Leslie, RDG. "Heterogeneity of Type I diabetes: analysis of monozygotic twins in Great Britian and the United States." Dibetologia 44 (2000): 345-­‐362. Reilly, J.J., Dorosty, A.R., Emmett, P.M., and The ALSPCA Study Team. "Identification of the obese child: adequacy of the body mass index for clinica practice and epidemiology." International Journal of Obesity 24 (2000): 1623-­‐1627. Richards, G.E., Cavallo, A., Meyer III, W.J., Prince, M.J., Peters, E.J., Stuart, C.A., Smith, E.R. "Obesity, acanthosis nigiricans, insulin resistance, and hyperandrogenemia: Pediatric perspective and natural history." Journal of Pediatrics 107, no. 6 (1985): 893-­‐897. Rising, R., Harper, I.T., Fontvielle, A.M., Ferraro, R.T., Spraul, M., Ravussin, E. "Determinants of total daily energy expenditure: variability in physical activity." The American Journal of Clinical Nutrition 59 (1994): 800-­‐804. Rizzo, N.S., Ruiz, J.R., Oja, L., Veidebaum T., Sjostrom. "Associations between physcial activity, body fat, and insulin resistance (homeostatis model assesment) in adolescents: the European Youth Heart Study." The American Journal of Clinical Nutrition 87 (2008): 586-­‐592. Rodin, J., Reed, D., Jamner, L. "Metabolic effects of fructose and glucose: implications for food intake." The American Journal of Clinical Nutrition 47 (1988): 683-­‐698. Rolland-­‐Cachera, MF., Deheeger, M., Bellisle, F., Sempe, M., Guilloud-­‐Bataille, M., Patois, E. "Adiposity rebound in children: a simple indicator for predicting obesity." The American Journal of Clinical Nutrition 39 (1984): 129-­‐135. High Fructose Corn Syrup and Childhood Obesity
p.147
240.
241.
242.
243.
244.
245.
246.
247.
248.
249.
250.
251.
252.
253.
254.
255.
256.
257.
258.
259.
Rolls, B.J., Morris, E.L., Roe, L.S. "Portion size of food affects energy intake in normal-­‐weight and overweight men and women." The American Journal of Clinical Nutrition 76 (2002): 1207-­‐1213. Rolls, B.J., Roe, L.S., Kral, T.V.E., Meengs, J.S., Wall, D.E. "Increasing the portion size of a packaged snack increases energy intake in men and women." Appetite 42, no. 1 (2004): 63-­‐
69. Rolls, B.J., Roe, L.S., Meengs, J.S. "Reductions in portion size and energy density of foods are additive and lead to sustained decreases in energy intake." The American Journal of Clinical Nutrition 83 (2006): 11-­‐17. Ruiz, J.R., Rizzo, N.S., Hurtig-­‐Wennlof, A., Ortega, F.B., Warnburg, J., Sjostrom, M. "Relations of total physical activity and intensity to fitness and fatness in children: the European Youth Heart Study." The American Journal of Clinical Nutrition 84 (2006): 299-­‐303. Saad, M.R., Khan, A., Sharma, A., Michael, R., Riad-­‐Gabriel, M.G., Boyadjian, R., Jinagouda, S.D., Steil, G.M., and Kamdar, V. "Physiological Insulinemia Acutely Modulates Plasma Leptin." Diabetes Journal 47 (1998): 544-­‐549. Sarria, A., Moreno, L.A., Garcia-­‐Llop, L.A., Fleta, J., Morellon, M.P. and Bueno, M. "Body mass index, triceps skinfold and waist circumference in screening for adiposity in make children and adolescents." Acta Paedicatrica 90, no. 4 (2001): 387-­‐392. Savva, S.C., Tornaritis, M., Savva, M.E., Kourides, Y., Panagi, A., Silikiotou, N., Georgiou, C., Kafatos A. "Waist circumference and waist-­‐to-­‐height ratio are better predictors of cardiovascular disease risk factors in children than body mass index." International Journal of Obesity 24 (2000): 1453-­‐1458. Schlicker, S.A., Borra, S.T., Regan, C. "The Weight and Fitness Status of United States Children." Nutrition Reviews 52, no. 1 (1994): 11-­‐17. Schlosser, E. Fast Food Nation. New York, NY: First Perennial, 2002. Schoonover, H., Muller, M. "Food without Thought: How U.S. Farm Policy Contributes to Obesity." Institute for Agriculture and Trade Policy, Minneapolis, 2006, 1-­‐14. Schouten, F., Twisk, J.W., de Boer, M.R., Stehouwer, C.D., Serne, E.H., Smulders, Y.M., Ferreira, I. "Increases in central fat mass and decreases in periheral fat mass are associated with accelerated arterial stiffening in healthy adults: the Amsterdam Growth and Health Longitudinal Study." The American Journal of Clinical Nutrition 94 (2011): 40-­‐48. Schwartz, J-­‐M., Neese, R.A., Turner, S., Dare, D., Hellerstein, M.K. "Short-­‐Term Alterations in Carbohydrate Energy Intake in Humans." Journal of Clinical Investigation 96 (1995): 2735-­‐
2743. Schwarzbein, D., Deville, N. The Schwartzbein Principle: The truth about losing weight, being healthy and feeling younger. Deerfield Beach, FL: Health Communications, Inc., 1999. Sen, Bisakha. "Frequency of Family Dinner and Adolescent Body Weight Status: Evidence from the National Longitudinal Survey of Youth, 1997." Obesity 14, no. 11 (2006): 2266-­‐
2276. Shabecoff, P., Shabecoff, A. Poisoned Profits The Toxic Assault on Our Children. New York, NY: Random House, 2008. Shibli, R., Akons, Rubin, L., Akons, H., Shaoul, R. "Morbidity of Overweight (>85th Percentile) in the First 2 Years of Life." Pediatrics 122, no. 2 (2008): 267-­‐272. Shields, M., Carroll, MD., Ogden, CL. "Adult Obesity Prevalence in Canada and the United States." US Department of Health and Human Services-­‐ Centers for Disease Control and Prevention, Atlanta, GA, 2011, 1-­‐8. Singhal, A., Farooqi, I.S., O'Rahilly, S., Cole, T.J., Fewtrell, M., Lucas, A. "Early nutrition and leptin concentrations in later life." The American Journal of Clinical Nutrition 75 (2002): 993-­‐
999. Sjostrom, Lars. "Morbidity of severely obese subjects." The American Journal of Clinical Nutrition 55 (1992): 508S-­‐515S. Skinner, A.C., Mayer, M.L., Fower, K., Weinberger, M. "Heath Status and Health Care Expenditures in a Nationally Representative Sample: How Do Overweight and Healthy-­‐
Weight Children Compare?" Pediatrics 121, no. 2 (2008): e269-­‐e277. High Fructose Corn Syrup and Childhood Obesity
p.148
260.
261.
262.
263.
264.
265.
266.
267.
268.
269.
270.
271.
272.
273.
274.
275.
276.
277.
Soenen, S., Westerp-­‐Plantenga, M.S. "No differences in satiety or energy intake after high -­‐
fructose corn syrup, sucrose, or milk preloads." The American Journal of Clinical Nutrition 86 (2007): 1586-­‐1594. Soot, C., White, J.H. "School Health Initiatives and Childhood Obesity: BMI Screening and Reporting." Policy, Politics, & Nursing Practice 11, no. 2 (2010): 108-­‐114. St. Onge, M.P., Keller, K.L., Heymsfield, S.B. "Changes in childhood food consumption patterns: a cause for concern in light of increasing body weights." The American Journal of Clinical Nutrition 78 (2003): 1068-­‐1073. Stanhope, K.L., Griffen, S.C., Bair, B.R., Swarbrick, M.M., Keim, N.L., Havel, P.J. "Twenty-­‐four-­‐
hours endocrine and metabolic profiles following consumption of high-­‐fructose corn syrup-­‐, sucrose-­‐, fructose-­‐, and glucose-­‐sweetnened beverages with meals." The American Journal of Clinical Nutrition 87, no. 5 (2008): 1194-­‐1203. Stanhope, K.L., Havel, P.J. "Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrsoe or high-­‐fructose corn syrup." The American Journal of Clinical Nutrition 88, no. (suppl) (2008): 1733S-­‐1737S. Stanhope, K.L., Schwartz, J.M., Keim, N.L., Griffen, S.C., Bremer, A.A., Graham, J.L., Hatcher, B., Cox, C.L., Dyachenko, A., Zhang, W., McGahan, J.P., Seibert, A., Krauss, R.M., Chiu, S., Schaefer, E.J., Ai, Masumi, A., Otokozawa, S., Nakajima, K., Nakano, T., Beysen, C., Hellerstein, M.K., Berglund, L., Havel, P.J. "Consuming fructose-­‐sweetened, not glucose-­‐sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans." The Journal of Clinical Investigation 119, no. 5 (2009): 1322-­‐1334. Steinberger, J., Moran, A., Hong, C-­‐P, Jacobs, D.R., Sinaiko, A.R. "Adiposity in childhood predicts obesity and insulin resistance in young adulthood." The Journal of Pediatrics 138, no. 4 (2001): 469-­‐473. Stettler, N., Kumanyika, S.K., Katz, S.H., Zemel, B.S., Stallings, V.A. "Rapid weight gain during infancy and obesity in young adulthood in a cohort of African Americans." The American Journal of Clinical Nutrition 77 (2003): 1374-­‐1380. Stettler, N., Stallings, V.A., Troxel, A.B., Zhao, J., Schinnar, R., Nelson, S.E., Ziegler, E.E., Strom, B.L. "Weight Gain in the First Week of Life and Overweight in Adulthood: A Cohort Study of European American Subjects Fed Infant Formula." Circulation 111, no. 15 (2005): 1897-­‐
1903. Stoll, Andrew. The Omega-­‐3 connection. New York, NY: Simon & Schuster, 2001. Swarbrick, M.M., Stanhope, K.L, Elliott, S.S., Graham, J.L., Christiansen, M.P., Griffen, S.C., Keim, N.L., Havel, P.J. "Consumption of fructose-­‐sweetened beverages for 10 weeks increases postprandial tricylglycerol and apolipoprotein-­‐B conentrations in overweight and obese women." British Journal of Nutrition 100, no. 5 (2008): 947-­‐952. Takasaki, Yoshiyuki. "Effect of Borate on Glucose-­‐fructose Isomerization Catalyzed by Glucose Isomerase." Agriculture Biological Chemistry Journal 35, no. 9 (1971): 1371-­‐1375. Takasaki, Yoshiyuki. "Formation of Glucose Isomerase by Streptomyces sp." Agriculture Biological Chemistry Journal 38, no. 3 (1973): 667-­‐668. Takasaki, Yoshiyuki. "On the Separation of Sugars." Agriculture Biological Chemistry Journal 36, no. 13 (1972): 2575-­‐2577. Takasaki, Yoshiyuki. "Production and Utilization of Glucose Isoerase from Strptomyces sp." Agriculture Biological Chemistry Journal 30, no. 12 (1966): 1247-­‐1253. Taveras, E.M., Rifas-­‐Shiman, S.L., Berkey, C.S., Rockett, H.R.H., Field, A.E., Frazier, A.L., Colditz, G.A., Gillman, M.W. "Family Dinner and Adolescent Overweight." Obesity Research 13, no. 5 (2005): 900-­‐906. Taylor, E.D., Theim, K.R., Mirch, M.C., Ghorbani, S., Tanofsky-­‐Kraff, M., Adler-­‐Wailes, D.C., Brady, S., Reynolds, J.C., Calis, K.A., Yanovski, J.A. "Orthopedic Complications of Overweight in Children and Adolescents." Pediatrics, 117 2006. Teff, K.L., Elliott, S.S., Tschop, M., Keiffer, T.J., Rader, D., Heiman, M., Townsend, R.R., Keim, N.L., D'Alessio, D., Havel, P.J. "Dietary Fructose Reduces Circulating Insulin and Leptin. Attenuates Postprandial Suppression of Ghrelin and Increases Triglycerides in Women." The Journal of Clinical Endocrinology & Metabolism 89, no. 6 (2004): 2963-­‐2972. High Fructose Corn Syrup and Childhood Obesity
p.149
278.
279.
280.
281.
282.
283.
284.
285.
286.
287.
288.
289.
290.
291.
292.
293.
294.
295.
296.
297.
298.
Temple, J.L., Giacomelli, A.M., Kent, K.M., Roemmich, J.N., Epstein, L.H. "Television watching increases motivated responding for food and energy intake in children." The American Journal of Clinical Nutrition 85 (2007): 355-­‐361. The Jackson Laboratory. Mice Database. 2011. http://jaxmice.jax.org/strain/000642.html (accessed August 2011). —. Research Highlights. 2011. http://www.jax.org/milestones/researchhighlights.html (accessed July 2011). The Mayo Clinic. Men's health: Preventing the top 7 threats. February 5, 2011. http://www.mayoclinic.com/health/mens-­‐health/MC00013 (accessed September 5, 2011). —. Women's Health: Preventing the top 7 threats. February 5, 2011. http://www.mayoclinic.com/health/womens-­‐health/MC00014 (accessed September 5, 2011). The National Museum of Nuclear Science & History. Albuquerque, NM, 2011. Thompson, D.R., Obarzanek, E., Franko, De., Barton, B.A., Morrison, J., Biro, F.M., Daniels, S.R., Striegel-­‐Moore, R.H. "Childhood Overweight and Cardiovascular Diseaase Risk Factors: The National Heart, Lung, and Blood Institute Growth and Health Study." The Journal of Pediatrics 150 (2007): 18-­‐25. Tordoff, M.G., Alleva, A.M. "Effect of drinking soda sweetened with aspartame or high-­‐
fructose corn syrup on food intake and body weight." The American Journal of Clinical Nutrition 51 (1990): 963-­‐969. Tortora, G., Grabowski, S.R. Principles of Anantomy and Physiology (Seventh Edition). New York, NY: Harper Collins College Publishers, 1993. Tulane University School of Medicine. The Bogalusa Heart Study. 2011. http://tulane.edu/som/cardiohealth/index.cfm (accessed September 2011). U.S. Department of Agriculture (USDA). Agriculture Research Service. 2011. http://www.ars.usda.gov/is/AR/archive/dec97/corn1297.htm?pf=1 (accessed July 2011). —. Economic Research Service. 2011. http://www.ers.usda.gov/Briefing/Sugar/Data.htm (accessed July 13, 2011). U.S. Department of Health & Human Services. Childhood Obesity. http://aspse.hhs.gov/health/reports/child obesity (accessed January 2011). —. "View Rule 66 FR 4706." Food and Drug Administration. January 18, 2001. http://www.reginfo.gov/public/do/eAgendgaViewRule (accessed August 2011). U.S. Department of Health and Human Services. Trans Fat Now Listed with Saturated Fat and Cholesterol on the Nutrition Facts Label. June 24, 2011. http://www.fda.gov/food/labelingnutrition/ConsumerInformation/ucm109832.htm (accessed September 2011). U.S. Food and Drug Administration (FDA). Statement of Policy-­‐ Foods Derived from New Plan Varieties. Docket No. 92N-­‐0139, Food and Drug Administration, U.S. Department of Health and Human Services, Washington, DC: U.S. Department of Health and Human Services, 1992, 36. U.S. Food and Drug Administration (FDA). "Nutrition Basics Help Fight Child Obesity." 2011. U.S. Food and Drug Association (FDA). Biotechnology Consultation Note to the File BNF No. 000071. October 9, 2000. http://www.fda.gov/Food/Biotechnology/Submissions/ucm155788.htm (accessed August 2011). U.S. National Institute of Health. Bogalusa Heart Study. January 26, 2006. http://clinicaltrials.gov/ct2/show/NCT00005129 (accessed September 2011). U.S. National Library of Medicine National Institutes of Health. In U.S., Obesity Afflicts Even Some of the Tiniest Tots. http://www.nlm.nih.gove/medlineplus/new/fullstory_107215.html. (accessed January 2011). UK Daily Mail. "News: HALF of U.S. population will be obese by 2030 experts predict." UK Daily Mail. August 28, 2011. http://www.dailymail.co.uk/news/article-­‐2030563/HALF-­‐U-­‐S-­‐
population-­‐obese-­‐2030-­‐experts-­‐predict.html (accessed August 2011). High Fructose Corn Syrup and Childhood Obesity
p.150
299.
300.
301.
302.
303.
304.
305.
306.
307.
308.
309.
310.
311.
312.
313.
314.
315.
316.
317.
318.
319.
Ulrich, C.M. Georgious, C.C., Snow-­‐Harter, C.M., Gillis. "Bone mineral density in mother-­‐
daughter pairs: relations to lifetime exercise, lifetime milk consumption, and calcium supplements." The American Journal for Clinical Nutrition 63 (1996): 72-­‐79. Ung, C.Y., Lam, S.H., Hlaing, M.M., Winata, C.L., Korzh, S., Mathavan, S., Gong, Z. "Mercury-­‐
induced hepatotoxicity in zebrafish: in vivo mechanistic insights from transcriptome analysis, phenotype anchoring and targeted gene expression validation." BMC Genomics 11, no. 212 (2010): 1-­‐16. University of Kentucky College of Agriculture. "Bt-­‐Corn: What is it and how it works." College of Agriculture, The University of Kentucky, Lexington, 2003. Van Cleave, J., Gortmaker, SL., Perrin, JM. "Dynamics of Obesity and Chronic Health Conditions Among Children and Youth. ." Journal of the American Medical Association (JAMA) 303, no. 7 (2005): 623-­‐630. Vega-­‐Lopez, S., Ausman, L.M., Jalbert, S.M., Erkkila, A.T., Lichtenstein, A.H. "Palm and partially hydrogenated soybean oils adversely alter lipoprotein profiles compared with soybean and canola oils in moderately hyperlipidemic subjects." The American Journal of Clinical Nutrition 84 (2006): 54-­‐62. Videon, T.M, Manning, C.K. "Influences on adolescent eating patterns: the importance of family meals." Journal of Adolescent Health 32, no. 5 (2002): 365-­‐373. Viner, R.M., Cole, T.J. "Television Viewing in Early Childhood Predicts Adult Body Mass Index.” The Journal of Pediatrics 147, no. 4 (2005): 429-­‐435. Wadaan, Mohamad A.M. "Effects of Mercury Exposure on Blood Chemistry and Liver Histopathology of Male Rats." Journal of Pharmacology and Toxicology 4, no. 3 (2009): 126-­‐
131. Wallinga, D., Sorensen, J., Mottle, P., Yablon, B. "Not So Sweet: Missing Mercury and High Fructose Corn Syrup." The Institute for Agriculture and Trade Policy., Minneapolis, MN, 2009. Wang, GW., Dietz, WH. "Economic Burden of Obesity in Youths Aged 6 to 17 Years: 1979-­‐
1999." Pediatrics 109, no. 5 (2002): e81-­‐e86. Wang, Y., Beydoun, M. "The Obesity Epidemic in the United States-­‐ Gender, Age, Socioeconomic, Racial/Ethnic, and Geographic Characteristics: A systematic Review and Meta-­‐Regression Analysis." Epidemiologic Reviews 29 (2007): 6-­‐28. Waring., M.E., Kapane, K.L. "Overweight in Children and Adolescents in Relation to Attention-­‐
Deficit/Hyperactivity Disorder: Results From a National Sample." Pediatrics 122, no. 1 (2008): e1-­‐e6. Wells, H.F., Buzby, J.C. "High-­‐Fructose Corn Syrup Usage May Be Leveling Off." Economic Research Service, United States Department of Agriculture, Washington, D.C., 2008. Whitaker, R.C., Pepe, M.S., Wright, J.A., Seidel, K.D., Dietz, W.H. "Early Adiposity Rebound and the Risk of Adult Obesity." Pediatrics 101, no. 3 (1998): e5-­‐e11. White, J.S. Clarifying Added Sugar Myths. February 2010. www.foodprocessing.com/articles/2010/john_white_sweetener.html (accessed August 2011). White, J.S. "Misconceptions about High-­‐Fructose Corn Syrup: Is it Uniquely Responsible for Obesity, Reactive Dicarbonyl Compounds, and Advanced Glycation Endproducts? ." The Journal of Nutrition 139, no. (suppl) (2009): 1219S-­‐1227S. White, J.S. "Straight talk about high-­‐fructose corn syrup: what is and what it ain’t." The American Journal of Clinical Nutrition 88, no. (suppl) (2008): 1716S-­‐1721S. White, J.S., Foreyt, J.P., Melanson, K.J., Angelopoulos, T.J. "High-­‐Fructose Corn Syrup: Controversies and Common Sense." American Journal of Lifestyle Medicine, 2010: 515-­‐520. Whitney, E. N., Cataldo, C.B., Rolfes, S.R. Understanding Normal and Clinical Nutrition-­‐ Fifth Edition. Belmont, CA: Wasdwoth Publishing Company, 1998. Wikipedia. Gastric inhibitory polypeptide. July 2011. http://en.wikipedia.org/wiki/Gastric_inhibitory_polypeptide (accessed August 2011 ). —. Glucagon-­‐like peptide-­‐1. July 2011. http://en.wikipedia.org/wiki/Glucagon-­‐like_peptide-­‐1 (accessed August 2011). High Fructose Corn Syrup and Childhood Obesity
p.151
320.
321.
322.
323.
324.
325.
326.
327.
328.
329.
330.
331.
332.
333.
Wikipedia. Lobry–de Bruyn–van Ekenstein transformation. February 2011. http://en.wikipedia.org/wiki/Lobry–de_Bruyn–van_Ekenstein_transformation (accessed July 6, 2011). Willett, Walter C. "Dietary fat and obesity: and unconvincing relation." The American Journal of Clinical Nutrition 68 (1998): 1149-­‐1150. Willett, Walter C. "Is dietray fat a major determinant of body fat?" The American Journal of Clinical Nutrition 67, no. suppl (1998): 556S-­‐512S. Williams, M.J, Hunter, G.R., Kekes-­‐Szabo, T., Snyder, S., Treuth, M.S. "Regional fat distribution in women and risk of cardiovascular diseae." The American Journal of Clinical Nutrition 65 (1997): 855-­‐860. Wolf, A.M., Colditz, G.A. "The Cost of Obesity: The US Perspective." Pharmacoeconomics 5 (1994): 34-­‐37. Wolf, PA., Bridges, JR., Wicklund, R. "Application of Agonist-­‐Receptor Modeling to the Sweetness Synergy between High Fructose Corn Syrup and Sucralose, and between High-­‐
Potency Sweeteners." Journal of Food Science 75, no. 2 (2010): S95-­‐S102. Woo, J.G., Zeller, M. H., Wilson, K., Inge, T. "Obeisty Identified by Discharge ICD-­‐9 Codes Underestimates the True Prevalence of Obesity in Hospitalized Children." Journal of Pediatrics 154 (2009): 327-­‐331. World Health Organization (WHO). Diet, Nutrition and the Prevention of Chronic Diseases. WHO Technical Report Series 916, Joint WHO/FAO Expert Consultation, World Health Organization (WHO), Geneva : World Health Organization, 2003, 95. World Health Organization (WHO). OBESITY: PREVENTING AND MANAGING THE GLOBAL EPIDEMIC. Report of a WHO consultation, Geneva, Switzerland: World Health Organization, 2000, 1-­‐253. World Health Organization (WHO). Global Strategy on Diet, Physical Activity and Health. 2010. http://www.who.int/dietphysicalactivity/childhood/en (accessed April 2011). —. Media Center-­‐ Obesity and Overweight. March 2011. http://www.who.int.mediacentre/factsheets/fs311/en/index.html. (accessed April 2011). —. WHO Media Center. September 25, 2005. http://www.who.int/mediacenter/news/releases/2005/pr44/en (accessed April 2011). Young, L.R., Nestle, M. "The Contribution of Expanding Portion Sizes to the US Obesity Epidemic." American Journal of Public Health 92 (2002): 246-­‐249. Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold. L., Friedman, J.M. "Positional cloning of the human mouse obese gene and its human homologue." Nature 272 (1994): 425-­‐432.