Download Harvey EJ et all. Hormone changes affecting - Joan

Joan Temmerman
Nutrition 577: Nutritional Problems in the United States, Fall 2012
Review Questions: Obesity
100 points
1. (3 pts)
Discuss the use of BMI and waist circumference measurements in identifying obesity.
Obesity refers to excess body fat. BMI is an indirect indicator of excess fat, and is useful measurement to
classify people into various categories: underweight (BMI < 18.5, normal weight (BMI 18.5-24.9); overweight (BMI
25-29.9); class 1 obesity (BMI 30-34.9); class 2 obesity (BMI 35-39.9); class 3 obesity (BMI ≥ 40). Intra-abdominal
adiposity (visceral or central obesity) is associated with health risks, especially the spectrum of cardiometabolic
diseases.
a. 2 pts:
What are the cut-off values for each method? What are the strengths/weaknesses of each method?
Please see above for BMI classes. Waist circumference ≥ 35 inches is abnormal for women; ≥ 40 inches is
abnormal for men. BMI is an indirect measure of obesity and is easy to calculate but doesn’t take into account
body composition or the distribution of fat. An abnormal waist circumference indicates visceral adiposity and is
more predictive of health risk than BMI, but doesn’t provide information about body composition.
b. 1 pt:
What is the BMI of a man who is 6’2 and weighs 242 pounds? How would he be classified?
BMI = 242/(74)² X 703; = 242/5476 X 703; = 31.1; class 1 obesity
2. (9 pts)
a. 5 pts:
Epidemiology of obesity in the U.S.
How has the prevalence of overweight and obesity changed over the past several decades? What
groups are at greatest risk?
From 1960-1980 obesity rates were stable. There was a striking increase in obesity prevalence in the 1980’s and
1990’s. In men, a significant linear increase was seen from 2003-2008. In women, no significant increase occurred
from 1999-2008. Obesity prevalence varies significantly among ethnic and racial groups; the highest obesity rates
are in non-Hispanic blacks (both men and women) and in Mexican-American women. Obesity is especially
prevalent among ethnic/racial minority women of low SES. But in non-Hispanic black and Mexican-American men,
those with higher incomes are more likely to be obese than those with low income.
Between 1988–1994 and 2007–2008 the prevalence of obesity increased in adults at all income and education
levels. Currently the rates of increase are slowing, but the numbers remain high: in 2009-2010, morethan one-third
of U.S. adults (35.7%) were obese (CDC).
b. 4 pts:
What is meant by the terms “built environment” and “social environment?” Discuss specific
environmental factors that may have contributed to the current obesity epidemic.
The social environment refers to social factors that affect diet: individual knowledge, attitudes, and skills,
social support systems, cultural and societal norms, food assistance programs, socioeconomic factors, food
pricing, transportation, food and agricultural policies. The built environment includes physical factors that affect
diet such as sprawl vs. compactness, accessibility of stores, transportation, types of restaurants and retail food
outlets, neighborhood safety, recreational space (parks, walking and bike trails), adequate housing. In the
socioeconomic model, although individual behavior is important, the environment largely dictates individual
choices and behavior, including food choices. We live in a toxic, obesogenic environment, characterized by fast,
processed food high in energy but low in nutrition coupled with a sedentary lifestyle. The trend of shifting from
eating at home to eating out, and the abundance of cheap, tasty, processed food coincides with the increasing
prevalence of overweight & obesity in the US. Moreover, obesity rates are higher in minorities and economically
disadvantaged populations. The likely causes are differences in the built or social environments, not individual
differences. Consistent trends show poorer quality retail food environments in socioeconomically disadvantaged
neighborhoods.
3. (14 pts)
a. 2 pts:
Biology of Eating
Define the term “gut-brain axis” and explain its role in ingestion. (Be sure to identify the major nerve
that’s involved.)
Energy homeostasis, weight regulation and appetite are highly complex processes and involve multiple peripheral
and well as central (CNS) signals. The gut-brain axis includes the GI tract, the vagus nerve innervating the gut,
and the areas of the brain that respond to the vagal afferent signals. The arcuate nucleus in the hypothalamus is
the center for fuel sensing and appetite control. The gut-brain axis plays an essential role in the control of energy
intake and meal size: negative feedback reduces ingestion.
b. 2 pts:
According to Blom, what are some of the reasons why dietary protein is considered to be the most
satiating energy nutrient?
Protein is the most satiating macronutrient for several reasons. Protein has a thermogenic effect (it is not
stored and must be metabolized right away). Protein stabilizes blood glucose by stimulating gluconeogenesis.
Also, protein stimulates anorexigens ( GLP-1, GIP and CCK) which enhance satiety and decrease gastric
emptying. And finally, high protein decreases postprandial ghrelin secretion; because ghrelin is oregegenic and
stimulates hunger, decreasing ghrelin reduces appetite and intake.
c.
8 pts:
Discuss the roles of leptin, cholecystokinin, GLP-1 and ghrelin in regulating food intake. Be sure to
include the origin of each substance and identify the factors that influence their release.
-Cholecystokinin (CCK) is produced by the enteroendocrine I-cells of the proximal small intestine, and by enteric
nerves in the ileum and colon. CCK stimulates gallbladder contraction (bile release), and stimulates the pancreas
to release juice, enzymes and glucagon. Levels increase during and after a meal, reducing appetite. CCK is also
found in neurons in the brain, where it influences the perception of appetite. CCK suppresses appetite and
promotes satiety (anorexigenic).
-GLP-1 is also produced by the gut. GLP-1 is an incretin hormone; it enhances insulin secretion in response to
nutrients and enteral glucose. GlP-1 exerts a trophic effect on beta cells in the pancreas in response to meals.
GLP-1 also acts in the CNS to reduce food intake (anorexigen). GLP-1 also inhibits gastric emptying/GI motility,
and decreases glucagon secretion; lowering blood sugar levels after a meal. GLP-1 is important in glucoseenergy metabolism, and increases after bariatric surgery. Some of the newest medicines for diabetes are GLP-1
mimetics or receptor agonists.
-Leptin is produced by white adipose tissue. Levels increase with excess adipose tissue or overfeeding, and
decrease with reduced adipose tissue or starvation. Leptin decreases the urge to eat and also increases physical
activity to produce a negative energy balance. Leptin interacts with the arcuate nucleus in the hypothalamus, and
controls the level of stored body fat. Leptin resistance occurs with obesity: increased leptin levels fail to suppress
hunger. Very obese individuals have high leptin levels. Genetic disorders that cause low leptin levels respond
well to exogenous leptin, but administering leptin does not improve obesity (although there was hope in the past
that it could be the magic bullet).
-Ghrelin (produced by the stomach and duodenum) is the only orexigenic hormone. Ghrelin stimulates hunger
and food-seeking behavior, and promotes digestion. Ghrelin also interacts with the arcuate nucleus. Ghrelin
stimulates growth hormone secretion. Ghrelin levels increase between meals, and drop after eating and when
absorption begins.
d. 2 pts:
Discuss the effects of a) weight loss and b) a high protein meal on ghrelin secretion.
A high protein meal decreases postprandial ghrelin concentrations, producing satiety. Weight loss increases
ghrelin levels, stimulating appetite and a drive to regain.
4. (10 pts)
a. 3 pts
Fructose
What is high-fructose corn syrup, and how has its intake changed in the past ~ 40 yrs?
Fructose and glucose are monosaccharides. HFCS contains 42-55% sucrose, with the remainder glucose.
Since food processing (with added sugar) became common and widespread (since the 1970’s), sugar
consumption has increased, especially in fast food and soft drinks. Urbanization is associated with increased
fructose as a proportion of sugars (Gibson & Shepherd, Aliment Pharmacol Ther. 2005;21).
.
b. 3 pts
How might hormonal responses to fructose ingestion differ from the responses seen with ingestion of
other carbohydrates?
After oral intake, glucose is transported to peripheral tissues for an energy source, and escapes first-pass
removal by the liver. Fructose, however, is removed mainly by the liver via the portal circulation, after absorption
into the bloodstream. After rapid uptake by the liver, fructose can be converted to triglycerides. Excess fructose
uptake by the liver is harmful and can lead to fatty liver and inflammation. Additional negative health effects of
high fructose intake (≥ 20%) include harmful changes in lipids (increased LDL and VLDL cholesterol and
triglycerides). A high fructose diet has been associated with visceral adiposity, dyslipidemia, and increased
insulin resistance (i.e. metabolic syndrome and elevated cardiovascular risk).
Unlike glucose, fructose doesn’t raise blood glucose and insulin levels.
c.
4 pts
Does this evidence support a physiologic role for fructose in the obesity epidemic? Are you
convinced? Why or why not?
Yes; the evidence indicates that dietary fructose is associated with metabolic syndrome, nonalcoholic liver
steatosis (NAFLD), dyslipidemia, inflammation, and visceral adiposity (obesity). Obesity is part of the cluster of
metabolic diseases; however I am unsure whether it is the cause or an effect of metabolic derangements.
HFCS was introduced into the US food supply during the early 1970s, and consumption increased until the late
1990s. The explosion of obesity, including childhood obesity began during this same time. I don’t think this was
coincidental, especially in light of the metabolic effects of HFCS.
5. (9 pts)
Secretory function of adipose tissue.
Discuss the biologic actions of adiponectin, resistin and free fatty acids that are released by
fat cells. What roles do they play in the development of obesity-related comorbidities?
Adipose tissue is an endocrine organ: it secretes adipokines, which are largely involved in insulin resistance,
chronic inflammation and the metabolic complications associated with obesity. Adiponectin is the exception; it is
protective against cardiovascular disease and is anti-inflammatory. Adipose tissue inflammation is characterized
by increased and activated macrophage infiltration. Such macrophages secrete harmful cytokines such as tissue
necrosis factor  (TNF), interleukins 1 and 6, and resistin.
Adiponectin is a protein secreted by adipocytes. It undergoes post-translational modifications necessary for
bioactivity, and is found in different isoforms in the circulation. Adiponectin is associated with a favorable
metabolic condition: it improves insulin sensitivity via increasing energy expenditure and fatty acid oxidation,
decreases macrophage infiltration of adipose tissue, reduces obesity-associated lipotoxicity and inflammation,
and increases endothelial nitric acid production for a vascular protective effect. Besides these peripheral actions,
adiponectin may help regulate energy homeostasis through a central effect. In obesity, adiponectin secretion is
significantly decreased
Resistin is a protein adipokine secreted by macrophages. One major site of action is on hepatic glucose
production. Resistin is involved in the development of insulin resistance, but may be less important than other
adipokines in humans.
Inflamed adipose tissue releases more free fatty acids (FFAs), which can accumulate in muscle and the liver,
producing insulin resistance. FFAs exert a lipotoxic effect. Visceral adiposity increases FFAs and delivers them
via the portal circulation to the liver.
6. (5 pts)
Why is visceral adiposity especially dangerous & what underlying mechanisms may account for this
added risk?
Visceral (intra-abdominal) obesity indicates that there is excess fat within the abdomen; this surrounds organs like
the liver and pancreas and bathes them in fat, which has toxic effects. Visceral fat, measured by waist circumference,
is one criteria of the metabolic syndrome. The cascades of inflammation and metabolic diseases are thought to
initiate from excess visceral/intra-abdominal fat. As above, visceral adiposity is very metabolically active, and
secretes adipoytokines involved in the inflammatory response. FFAs, also released from visceral fat, are lipotoxic and
linked to insulin resistance.
7. (10 pts)
a. 1 pts
Glycemic Index
What is the glycemic index and how is it measured?
Glycemic index (GI) classifies dietary carbohydrates (CHO) based on how 50 grams of a given food affects
blood glucose over 2 hours. The standard is glucose, with a GI of 100%; GI is the percentage of the area under
the curve relative to 50 grams glucose (a portion of white bread). High GI foods are those with a GI > 70; medium
GI = 56-69, and ≤ 55 is low GI.
b. 1 pts
What is the difference between a food’s glycemic index and its glycemic load? (In other words,
what additional information does the glycemic load consider?)
The glycemic load (GL) is the GI multiplied by the number of CHO grams in the portion of food eaten divided by
100. GL takes into account the quantity and the quality of CHO in a food; it measures the overall effect on glucose
levels. For example, I cup of cooked carrots provides about 10 g CHO, and the GI is 49. So the GL is 4.9. GI 110 = low GI; 11-19 = medium; ≥ 20 is high GL.
c. 6 pts
Briefly discuss some of the strengths and shortcomings of the glycemic index. Name 2 foods with a
high and 2 foods with a low glycemic index.
Diets with high GI and GL are associated with increased insulin resistance, elevated triglycerides, and
decreased HDL. Several studies have reported higher resting energy expenditure as well as lower triglycerides
and less insulin resistance after a lower GL diet (Bray). However, GI is affected by the other foods consumed
with CHO, especially fat, protein and fiber (synergy and the food matrix), as well as previous meal composition,
physical activity, and the glucose tolerance of the individual. Therefore the total glucose effect is not so simple.
Potatoes and watermelon are high GI foods. Milk and oatmeal are low GI foods.
d. 2 pts
Do you think that educating clients about the glycemic index would contribute to weight loss? Explain.
The GI concept is somewhat controversial. I think patients with diabetes or pre-diabetes may benefit from a
lower GI diet. Using the GI or the GL may improve diabetic control beyond just CHO counting. Some patients
(especially those with insulin resistance) may benefit more from a low GI diet for weight loss than a standard low
fat diet. Ultimately it’s about personal preference.
8.
(12 pts)
Atkins and other low-CHO diets
a) 4 pts
Describe the general features of the Atkins and South Beach diets (you may use the internet to
gain more info, but don’t just copy what you find).
Atkins diet is a low carbohydrate diet, starting at 20 grams of CHO daily and increasing toward 50 g. daily (810% of calories from CHO). It is high in protein (32-34%) and high in fat (58%). It has been criticized about
being high in saturated fat. The Zone diet is 40 % CHO, 30% fat, and 30% protein, and emphasizes
monounsaturated fats and omega-3 fatty acids. It is less extreme in CHO and fat components than Atkins,
and promotes healthier fats..
b) 4 pts
Briefly discuss the advantages and disadvantages of high-protein/low-carbohydrate diets versus
conventional low-fat/high-carbohydrate diets for weight loss.
At 6 months, there is greater weight loss with an Atkins (very low CHO) diet compared to a conventional diet,
However, after 1 year, there aren’t significant changes in weight loss produced by different diets. So reduced
calorie diets produce clinically significant weight loss regardless of the macronutrient composition (Dansinger
ML et al, JAMA 2005;293(1):43-51). Dietary CHO drives insulin production, so I recommend considering a
CHO-restricted diet to patients with diabetes. Also, CHO restriction can lower triglycerides and raise HDL.
High CHO can raise triglycerides more than fat does. Consuming higher protein has a thermogenic effect,
increases satiety, results in more deposition of lean body mass, produces greater weight loss and enhances
weight maintenance..
c) 4 pts
Would you be comfortable recommending either (or both) of these diets to a
client? Why or why not?
The best diet is that which is sustainable, so personal preference should be the guiding factor. I would
recommend whatever approach is a better personal fit. However, a low CHO diet is more effective at
reducing inflammation than a low-fat diet, and increasing protein has benefits. I would maximize my clients
nutritional preferences with the most beneficial sources. In general I would counsel patients to avoid a diet
high in refined CHO and saturated and trans fats. Instead choose lean sources of protein, and emphasize
complex CHO, including whole grains, fruit and vegetables, and low-fat dairy products. Use primarily
unsaturated fats, especially monounsaturated, and omega-3 FAs. Ultimately, a healthy lifestyle emphasizing
good nutrition and regular activity is the most effective approach
9.
(8 pts)
Calcium
a) 4 pts
Discuss the role of calcium and dairy products in weight loss. What intracellular mechanisms are
hypothesized to be involved? Be sure to discuss the potential role of 1,25-(OH)2 vitamin D.
Dietary calcium plays an important role in metabolism and energy regulation; there is an inverse relationship
between calcium intake, weight, and body fat. Increasing calcium intake increases fat oxidation, shifting body
composition to more skeletal muscle and less body fat. The distribution of fat is positively affected by high
calcium intake as well, with more fat lost from the abdominal area. Increasing calcium while restricting
calories augments weight loss and fat loss. The source of calcium is important as well; dairy products
produce 50-70% greater fat loss during energy restriction, compared to calcium supplements.
Intracellular calcium regulates adipocyte metabolism. Calcitrophic hormones such as parathyroid hormone
and 1,25(OH)2 vitamin D regulate intracellular calcium. Higher calcium intake suppresses these hormones,
which could positively affect thermogenesis and shift energy from adipose tissue to muscle. 1,25 (OH)2
vitamin D inhibits uncoupling protein 2 (UCP2) expression, therefore suppressing lipolysis and increasing
adipocyte fat storage. In mice, a high calcium diet suppresses 1,25(OH)2 vitamin inhibition of UCP2.
Consequently adipocyte UCP2 expression increases lipolysis and thermogenesis.
b) 4 pts
Briefly discuss at least 2 hypotheses that might explain why dairy intake may be associated with
a more powerful weight-loss effect than calcium alone.
Dairy products exert the greatest results compared to inorganic calcium such as supplements. One reason
may be the high whey content. Whey is rich in bioactive compounds; whey slows lipogenesis, accelerates
lipolysis, and partition nutrients from adipose tissue to skeletal muscle. Moreover, whey proteins display
angiotensin-converting enzyme (ACE) activity. Adipocytes have a renin-angiotensin system (RAS) which may
regulate lipid metabolism. Inhibition of this adipocyte RAS could explain how dairy products reduce obesity.
Protein has very beneficial qualities: it produces the greatest satiety of any macronutrient, it has a
thermogenic effect (protein requires more energy to be metabolized), it improves glucose regulation, weight
loss, and weight maintenance. Additionally increasing protein lowers triglycerides and preserves lean body
mass. Dairy products, and especially whey protein, are a rich source of essential and branched amino acids.
It has been suggested that leucine, a branched chain amino acid abundant in whey protein, may exert a large
anabolic effect on skeletal muscle.
All of the above may explain why dairy products produce significantly greater effects on fat loss and fat
distribution than fortifying or supplementing calcium.
10.
(10 pts)
Metabolic Syndrome
a) 2 pt
List the 5 (or 6, according to Minich & Bland) criteria used to diagnose metabolic syndrome.
The metabolic syndrome (metS) describes a cluster of cardiometabolic conditions that increase the risk of
T2DM and CVD. It includes abdominal obesity (measured by an abnormal waist circumference), elevated
blood pressure, hyperglycemia, dyslipidemia (elevated triglycerides, low HDL), as well as signs of thrombosis
and inflammation. Fatty liver is thought to be part of the constellation. There are different definitions of metS;
for example, ATP-III and WHO have different criteria for diagnosing it. But generally, 3 out of 5 criteria are
necessary to make the diagnosis.
b) 5 pts
Discuss the advantages and disadvantages of a low-fat diet in treatment of persons with
metabolic syndrome. What kinds of fats would you advocate? Explain your rationale.
A traditional low-fat diet may be high in refined CHO and worsen metS. The type of fat makes a difference:
saturated fat worsens metS by increasing triglycerides and blood pressure. Trans fat lowers HDL (which is
protective). Monounsaturated fat has a positive metabolic effect via improving insulin sensitivity. The omega3 fatty acids DHA and EPA lower triglycerides and have a cardioprotective effect. I recommend restriction of
unsaturated and trans fats, and an emphasis on unsaturated fats, especially monounsaturated, and omega-3
fatty acids. However, fat is the most energy dense, and the amount of energy from fat needs to be
considered.
c) 3 pts
Discuss at least 1 phytochemical that may influence insulin signaling and, therefore, metabolic
syndrome. Be sure to identify its dietary source(s) & indicate whether the evidence is convincing.
Whole, unprocessed plant foods, such as fruit and vegetables (F & V), are a rich source of phytochemicals.
Richly pigmented F & V are an especially good source. Many large observational studies have consistently
shown that increased F & V consumption correlates with deceased incidence of metS, T2DM, and CVD.
Conversely, lower F & V intake is associated with a greater incidence of metS, and obesity and metS have
risen to parallel with the trend of low F & V consumption in the US. Olive oil, which is a monounsaturated fat,
improves insulin sensitivity. Virgin olive oil is particularly high in phytochemicals. Resveratrol, a red wine
polyphenol, has demonstrated antioxidant, vascular, and metabolic protective effects in many studies.
Cinnamon, ginseng, and hops (a climbing vine), are some additional sources of phytochemicals that positively
impact insulin signaling and metS. There is compelling evidence that clearly shows the effect of food-based
phytochemicals on metS.
11.
(6 pts)
Diet and Physical Activity
a) 3 pts
What is a reasonable, “achievable” weight loss goal for obese persons?
5-10% weight loss is considered clinically significant because this produces many clinical health
improvements. Modest weight loss of 5-10% improves every feature of the metabolic syndrome.
b) 3 pts
Briefly discuss at least 2 benefits of physical activity as a component of weight-loss programs. Is
exercise alone an effective intervention? What role can exercise play in maintaining weight loss?
Exercise has many positive health benefits, even without weight loss. For example, regular activity improves
insulin sensitivity for 48-72 hours afterwards. Exercise lowers the risk of cardiovascular disease and all-cause
premature mortality, increases bone density. Exercise lowers blood pressure, LDL and triglycerides, and
raises HDL. Physical activity (PA) ameliorates depression and enhances cognitive functioning.
Weight loss decreases the resting metabolic rate (RMR) but exercise attenuates this: resistance exercise
increases muscle mass, which increases RMR.
Calorie deficit plays the primary role in weight loss: exercise alone is less effective than calorie restriction with
exercise. Although reducing calories exerts a more powerful effect, establishing an exercise routine during
weight loss is invaluable. Regular activity is critical for maintaining weight loss, and is the main predictor of
long-term success (Wadden TA, Butryn ML, Wilson C. Gastroenterology 2007;132). Members of the National
Weight Control Registry show that a high level of activity is the main determinant of sustained success
12.
(4 pts)
Obesity Medications
Briefly discuss the mechanisms through which 2 obesity medications (Orlistat, phentermine,
other) contribute to weight loss. What are important drawbacks to each medication? Would you
recommend the use of meds for clients who need to lose weight? Why or why not?
Orlistat (Xenical/Alli) is a selective pancreatic lipase inhibitor. Orlistat works by blocking the absorption of
fat; it does not have any effect on appetite. It is very safe and approved for longterm use, but only modestly
effective. Side effects (oily fecal spotting or incontinence, flatulence, malabsorption of vitamins) are related to
excess dietary fat. Orlistat is available over-the-counter in a lower dose as Alli.
Phentermine in a β phenylethylamine (sympathmimetic amine similar to amphetamines). It is noradrenergic
and decreases hunger and appetite (anorectant). Side effects include hypertension, tachycardia,
nervousness, irritability, dry mouth, constipation, restlessness, and sleep disturbance. It is a stimulant, and is
approved for short term therapy only, however, many bariatricians use it long term as well. Phentermine is
more effective that Orlistat. However, appetite suppressants are indicated only as adjuvant therapy; the
comprehensive approach must include regular activity as well as healthy nutrition for any success. I do
prescribe phentermine in some cases.
Several months ago, the FDA approved 2 new medications for long term therapy, in conjunction with a
balanced diet and exercise. Qsymia is a controlled release of phentermine and topiramate (topiramate is
thought to affect both appetite suppression and satiety enhancement). Qsymia produces about 10% weight
loss. Belviq (lorcaserin) is a selective serontonin 2C receptor agomist (serotonin is a neurotransmitter that
modulates fat and calorie intake and controls hunger). Belviq is less effective, producing about 3-3.7% weight
loss.
Obesity is a chronic disease with a strong biochemical and hormonal basis, and obesity treatment requires a
longitudinal chronic care model. Medications can be a useful adjunct for obese patients, and should be part of
the armamentarium. Long term pharmacotherapy use may be necessary, just as for other chronic conditions.
The newer medications, especially Qysmia, appear promising.
EXTRA CREDIT (3 pts):
Discuss the role of gastric bypass surgery in weight loss. What does the procedure involve?
Which patients are good candidates? What are important side effects? What are expected
results?
http://www.mayoclinic.com/health/gastric-bypass/HQ01465
Roux-en-Y gastric bypass (RYGB) is the most common bariatric surgery in the US, and is considered the gold
standard. It is usually done laparoscopically and is both restrictive and malabsorptive. Bariatric surgery is viewed
as the most effective treatment for long term weight loss and maintenance, as well as treatment of T2DM. The
average weight loss after RYGB is loss of 60% of excess body weight. About 80% of patients with T2DM will have
resolution (almost 100% if T2DM is present less than 10 years) Bariatric surgery is a major procedure and
involves permanent, lifelong changes.
To qualify for surgery, patients must have a BMI ≥40 (severe obesity), or a BMI ≥ 35 with a serious comorbidity
related to obesity, such as T2DM, hypertertension, obstructive sleep apnea, cardiovascular disease. Patients are
typically between 18 and 65). Patients must be willing to make longitudinal and permanent lifestyle changes, and
comply with dietary recommendations, long term vitamin supplementation, and indefinite follow up. Most
insurance companies require an extensive psychiatric evaluation before surgery. Surgeons require smoking
cessation, and many require some weight loss before surgery to reduce liver size. A large liver makes the
procedures more difficult, and is the main reason that surgery is converted from a laparoscopic to an open
procedure.
Roux-en-Y gastric bypass
(A)
Stomach before bariatric surgery. (B) Stomach after Roux-en-Y
gastric bypass procedure; food is redirected to the middle portion of
the small intestine, limiting absorption of calories.
(Source: American Family Physician - April 15, 2006)
.
The upper stomach is transected, creating a 15 ml pouch (restrictive component). The upper jejunum is transected,
and the distal end anastomosed to the gastric pouch, creating the alimentary (roux) limb. The proximal end of the
transected jejunum (the biliopancreatic limb) is anastomosed to the side of the alimentary (roux) limb ~100 cm distal
to the gastrojejunostomy, creating a common channnel, where food meets the bile and pancreatic juices. Part of the
small intestine is bypassed, creating the malabsorptive component. RYGB results in about 60% excess body weight
loss, and resolution of diabetes in 80% of patients. It has a metabolic effect: blood glucose stabilizes almost
immediately, even before weight loss, due to favorable changes in gut and other hormones that are important in
energy homeostasis and whose expression is altered by metabolic surgery (ghrelin, GLP-1, PYY1–36, GIP, insulin,
leptin and adiponectin). Alterations in the gut hormones ghrelin, PYY, GLP-1 and GIP seem to underlie glucose
homeostasis. They decrease appetite and reset weight set point to a lower level.
Patients who incorporate permanent lifestyle changes, and who view surgery as a tool and part of a comprehensive
approach are the best candidates. Patients must be compliant and follow lifelong vitamin supplementation and
surveillance, otherwise they are likely to become deficient in iron, B12, calcium, vitamin D, and protein. Post-op
patients can’t eat large volumes of food, or tolerate refined carbohydrates. They need to emphasize protein intake and
separate food from liquids.
.
Additional Resources used:
Gropper SS and Smith JL, eds. Advanced Nutrition and Human Metabolism. 6th edition. Belmont, CA: Wadsworth, Cengage Learning, 2012.
Centers for Disease Control and Prevention. Overweight and Obesity; Adult Obesity Facts. Accessed Sept. 16, 2012 at:
http://www.cdc.gov/obesity/data/adult.html
Wadden TA, Butryn ML, Wilson C. Lifestyle modification for the management of obesity. Gastroenterology 2007;132:2226-2238.
Dansinger ML et al. Comparison of the Atkins, Ornish, Weight Watchers and Zone Diets for Weight Loss and Heart Disease Risk Reduction (A
Randomized Trial). JAMA. 2005; 293(!):43-53.
Sacks FM et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med 2009;360(9):859-873.
Gibson PR, Shepherd SJ. Personal view: food for thought--western lifestyle and susceptibility to Crohn's disease. The FODMAP hypothesis.
Aliment Pharmacol Ther. 2005;21(12):1399-409.
Harvey EJ et all. Hormone changes affecting energy homeostasis after metabolic surgery. Mt Sinai J Med 2010;77(5):446-465.
Kohli R, Stefater MA, Inge TH. Molecular insights from bariatric surgery. Rev Endocr Metab Disord. 2011 Feb.
Singh GK, Siahpush M, Kogan MD. Neighborhood socioeconomic conditions, built environments, and childhood obesity. Health Aff (Millwood)
2010:29(3):503-512.
Neil K. Mehta, MSc and Virginia W. Chang, MD, PhD. Weight Status and Restaurant Availability: A Multilevel Analysis. Am J Prev Med. 2008
February ; 34(2): 127–133
Assigned resources used:
Yanovski SZ, Yanovski JA. Drug Therapy: Obesity. N Engl Med. 2002;356(8):591-602.
Ford PB, Dzewaltowski DA. Disparities in obesity prevalence due to variation in the retail food environment: three testable hypotheses. Nutr Rev.
2008;66(4):216-228.
Flegal KM, Carroll MD, Ogden CL, Curtain LR. Prevalence and trends in obesity among US adults, 1999-2008. JAMA 2010;303(3):235-241.
Scwartz GJ. Biology of eating behavior in obesity. Obes Res. 2004;12:S102-S106.
Blom WAM, Lluch A etal. Effect of a high-protein breakfast on the postprandial ghrelin response. Am J Clin Nutr. 2006;83:211-220.
Clinical Nutrition Updates: Atkins diet revisited. Arbor Clinical Nutrition Updates 2005;203:1-3.
Schaefer EJ, Gleason JA, Dansinger ML. Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr.2009;139:1257S1262S.
Rasouli N, Kern PA. Adipocytokines and the metabolic complications of obesity. J Clin Endocrinol Metab. 2008;93(11):S64-S73.
Minich DM, Bland JS. Dietary management of the metabolic syndrome beyond macronutrients. Nutr Rev.2008;66(8):429-444.
Poddar KH, Hosig KW et al. Low-fat dairy intake and body weight and composition changes in college students. J Am Diet Assoc. 2009;109(8):
1433-8.
Zemel MB, Miller SL. Dietary calcium and dairy modulation of adiposity and obesity risk. Nutr Rev. 2004;62(4):125-131.
Keim NL, Blanton CA, Kretsch MJ. America’s obesity epidemic: Measuring physical activity to promote an active lifestyle. J Am Diet
Assoc.2004;104:1398-1409.
Bray. Lifestyle and pharmacological approaches to weight loss: Efficacy and safety. J Clin Endocrinol Metab. 2008;93(11):S81-S88.
Healthy People 2010 and 2020. Accessed Sept. 11 2012 at: http://www.healthypeople.gov/2020/default.aspx