Obesity

Published on 02/03/2015 by admin

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Last modified 02/03/2015

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CHAPTER 7

Obesity

1. Define the terms “overweight” and “obesity.”

2. Does fat distribution affect the assessment of risk in an overweight or obese patient?

3. Explain the role of waist circumference in risk stratification.

4. How is waist circumference measured?

5. What adverse health consequences are associated with obesity?

Obesity is clearly associated with diabetes, hypertension, hyperlipidemia, coronary artery disease, degenerative arthritis, gallbladder disease, and cancer of the endometrium, breast, prostate, and colon. It has also been associated with urinary incontinence, gastroesophageal reflux, infertility, sleep apnea, and congestive heart failure. The incidence of these conditions rises steadily as body weight increases (Figs. 7-1 and 7-2). Risks increase with even modest weight gain. Health risks are magnified with advancing age and a positive family history of obesity-related diseases.

6. Summarize the economic consequences of obesity.

7. What are the psychological complications of obesity?

8. How common is obesity?

Obesity has reached epidemic proportions in the United States. The National Health and Nutrition Examination Survey (NHANES) conducted by the federal government uses direct measures of height and weight in a representative sample of Americans to estimate the prevalence of obesity. The prevalence of obesity increased significantly during the 1980s and 1990s but has now leveled off. The latest data from the NHANES showed that in 2009 to 2010, 35.7% of adults in the United States had a BMI greater than 30 kg/m2. This rate of obesity has not changed significantly from those in 2003 through 2008. The prevalence of overweight (BMI > 25 kg/m2) was found to be 68.8%. The prevalence of severe obesity (BMI > 40 kg/m2) was 6.3% in the latest dataset. In children and adolescents aged 2 to 19 years, the prevalence of obesity was found to be 16.9%, not changed from 2007 to 2008 prevalences.

9. What caused the dramatic rise in the prevalence of obesity in the 1980s and 1990s?

10. Describe the current model for obesity as a chronic disease.

Obesity is now viewed as a chronic, often progressive metabolic disease much like diabetes or hypertension. This view requires a conceptual shift from the previous widely held belief that obesity is simply a cosmetic or behavioral problem. Development of obesity requires a period of positive energy balance during which energy intake exceeds energy expenditure. Maintaining energy balance is one of the most important survival mechanisms of any organism. A sustained negative imbalance between energy intake and expenditure is potentially life-threatening within a relatively short time. To maintain energy balance, the organism must assess energy stores within the body; assess the nutrient content of the diet; determine whether the body is in negative energy or nutrient balance; and adjust hormone levels, energy expenditure, nutrient movement, and ingestive behavior in response to these assessments.

11. Do abnormal genes cause obesity?

Obesity is clearly more common in people who have family members who are also obese. Genetics appears to be responsible for 30% to 60% of the variance in weight in most populations. The problem of human obesity, however, involves an interaction between genetic susceptibility and environmental triggers. The genes that we possess to regulate body weight evolved somewhere between 200,000 and 1 million years ago, at which time the environmental factors controlling nutrient acquisition and habitual physical activity were dramatically different. A number of single gene defects have been identified that cause severe childhood obesity. These include mutations in the leptin gene, leptin receptor, the MC4R gene, brain-derived neurotrophic factor (BDNF), and SIM-1. However, these mutations are quite rare, explaining less than 8% of severe early-onset obesity. Genome-wide association studies have identified more than 20 genes that are associated with common forms of human obesity. The most common of these is the FTO gene. The allele of this gene that is associated with weight gain is present in 15% of humans. However, the weight gain associated with this high-risk allele is only 3 kg. Thus, common human obesity appears to be the result of alterations in a large number of genes, each having relatively small effects (polygenic).

12. What is leptin?

13. Does leptin deficiency cause human obesity?

14. Explain how the melanocortin system is involved in weight regulation.

Alpha-melanocortin (alpha-melanocyte–stimulating hormone [α-MSH]) is one of the hormone products of the POMC gene. This neuropeptide acts in the hypothalamus on melanocortin receptors, particularly the MC4-R subtype, to regulate body weight. By stimulating the MC4-R, α-MSH inhibits food intake, whereas the natural antagonist, Agouti-related peptide (AGRP), which is also made in the hypothalamus, stimulates food intake. MC4-R agonists have been developed. Although these drugs decrease food intake and reduce body weight in obese rodents, they have not been found to be useful as single agents in obese humans. The failure of these drugs and others that work through hypothalamic regulatory pathways to produce significant weight loss in obese humans has raised questions about the role of these systems in common forms of human obesity.

15. What is ghrelin?

16. Does a decrease in energy expenditure play a role in the development of obesity?

17. What are the components of energy expenditure?

image Basal metabolic rate (BMR): The amount of energy needed to maintain body homeostasis by maintaining body temperature, maintaining cardiopulmonary integrity, and maintaining electrolyte stability.

image Thermic effect of food: A relatively small component (5% to 10%) that represents the energy cost associated with the assimilation of a meal.

image Physical activity energy expenditure (PAEE): This is the most variable component. It can account for as little as 10% to 20% of total energy expenditure in people who are sedentary or as much as 60% to 80% of total energy expenditure in training athletes. PAEE increases with planned physical activity or with activities of daily living, such as stair climbing and even fidgeting. The unconscious component of physical activity has been termed non-exercise activity thermogenesis (NEAT) and may be a regulated parameter.

18. Explain the concept of energy balance.

19. Are there other factors involved in the increase in the prevalence of obesity?

Over the past 10 years, investigators have identified a range of novel environmental factors that may be related to the increase in obesity seen over the past 40 years. One area that has received a good deal of attention is reduced sleep time. It is clear that on average Americans are sleeping less than they did 50 years ago. Epidemiologic studies have shown that shortened sleep time is associated with obesity, and experimental studies have shown that sleep restriction is associated with insulin resistance, increased appetite, and a change in fat oxidation. Medication use is another factor that may be involved in promoting obesity. Widely used medications that promote weight gain include newer antipsychotic medications, sulfonylureas, insulin, thiazolidinediones, and progesterone-containing birth control medications. Other novel factors that are potentially involved include the aging of the population as well as increases in the number of ethnic minorities in the United States, the use of climate control systems in houses and public buildings (mice housed in thermoneutral environments weigh more than mice housed at lower temperatures), and environmental toxins (some studies suggest that adipose tissue increases in response to environmental toxins in an effort to sequester them).

20. What options are available for treating the obese patient?

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