Obesity

 

1. Describe the current rate of obeisty and apply it to morbidity.

2. Describe "Dyslipidemia" and explain why it is important to predicting outcome in obesity research.

3. Describe how specific genes in human obesity of body fat content has been obtained from studies.

 

Health Risks of Overweight and Obesity

Introduction

Overweight and obesity in the United States has increased markedly over the past decade. According to NHANES III data, approximately fifty-five percent of adults (or an estimated 97 million adults) in the United States are overweight or obese, a condition that substantially raises their risk of cardiovascular disease, certain types of cancer, and other diseases. Higher body weights are also associated with increases in all causes of mortality. Obese individuals may also suffer from social stigmatization and discrimination.

Overweight and obesity result from a complex interaction between genes and the environment characterized by long-term energy imbalance due to a sedentary lifestyle, excessive caloric consumption or both. They develop in a sociocultural environment characterized by mechanization, sedentary lifestyle, and ready access to abundant food. Attempts to prevent overweight and obesity are difficult to both study and achieve. Indeed, few research efforts have investigated either individual or community-based prevention strategies.

A substantial body of research, however, does exist on the health risks of overweight and obesity, and on methods for treatment. This report, which bases its recommendations primarily on published evidence, emphasizes the important role of primary care practitioners in evaluating all overweight and obese adults and promoting weight control through the use of multiple interventions and strategies tailored to particular patient needs.

While there is agreement about the health risks of overweight and obesity, there is less agreement about their management. Some have argued against treating obesity because of the difficulty in maintaining long-term weight loss and of potentially negative consequences of the frequently seen pattern of weight cycling in obese subjects. Others argue that the potential hazards of treatment do not outweigh the known hazards of being obese.

Overweight and obesity increase health risks from hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea and respiratory problems, and certain cancers.  Higher body weights are also associated with increases in all-cause mortality.

Morbidity

Above a BMI of 20 kg/m2, morbidity for a number of health conditions increases as BMI increases. Higher morbidity in association with overweight and obesity has been observed for hypertension, dyslipidemia, type 2, coronary heart disease (CHD), stroke, gallbladder disease, osteoarthritis, sleep and respiratory problems, and some types of cancer (endometrial, breast, prostate, and colon). Obesity is also associated with complications of pregnancy, menstrual irregularities, hirsutism, stress incontinence, and psychological disorders (depression).

The nature of obesity-related health risks is similar in all populations, although the specific level of risk associated with a given level of overweight or obesity may vary with race/ethnicity, and also with age, gender, and societal conditions. For example, the absolute risk of morbidity in chronic conditions such as CHD is highest in the aged population, while the relative risk of having CHD in obese versus nonobese individuals is highest in the middle adult years. A high prevalence of diabetes mellitus in association with obesity is observed consistently across races/ethnicities, while the relative prevalence of hypertension and CHD in obese versus nonobese populations varies between groups. 

The health risks of overweight and obesity are briefly described:

Hypertension

Data shows that the age-adjusted prevalence of high blood pressure increases progressively with higher levels of BMI in men and women.

Defined as mean systolic blood pressure  140mm Hg, mean diastolic as  90mm Hg or currently taking anti-hypertensive medication.

High blood pressure is defined as mean systolic blood pressure 140 mm Hg, or mean diastolic blood pressure   90 mm Hg, or currently taking anti-hypertensive medication. The prevalence of high blood pressure in adults with BMI  30 is 38.4 percent for men and 32.2 percent for women, respectively, compared with 18.2 percent for men and 16.5 percent for women with BMI < 25, a relative risk of 2.1 and 1.9 for men and women, respectively. The direct and independent association between blood pressure and BMI or weight has been shown in numerous cross-sectional studies, including the large international study of salt (INTERSALT) carried out in more than 10,000 men and women. INTERSALT reported that a 10 kg (22 lb) higher body weight is associated with 3.0 mm Hg higher systolic and 2.3 mm Hg higher diastolic blood pressure. These differences in blood pressure translate into an estimated 12 percent increased risk for CHD and 24 percent increased risk for stroke. Positive associations have also been shown in prospective studies.

Obesity and hypertension are comorbid risk factors for the development of cardiovascular disease. The pathophysiology underlying the development of hypertension associated with obesity includes sodium retention and associated increases in vascular resistance, blood volume, and cardiac output. These cardiovascular abnormalities associated with obesity are believed to be related to a combination of increased sodium retention, increased sympathetic nervous system activity, alterations of the renin-angiotensin system and insulin resistance. The precise mechanism whereby weight loss results in a decrease in blood pressure is unknown. However, it is known that weight loss is associated with a reduction in vascular resistance and total blood volume and cardiac output, an improvement in insulin resistance, a reduction in sypathetic nervous system activity, and suppression of the activity of the renin angiotensin aldosterone system.

Dyslipidemia manifested by:

High total cholesterol | High triglycerides | Low high-density lipoprotein cholesterol | Normal to elevated low-density lipoprotein cholesterol | Small, dense low-density lipoprotein particles

High total cholesterol

The relationship of the age-adjusted prevalence of high total cholesterol, defined as  240 mg/dL (6.21 mmol/L), to BMI is shown in Figure 3.

Figure 3. Age-Adjusted Prevalence of High Blood Cholesterol* According To Body Mass Index

Dyslipidemia manifested by:

High total cholesterol
The relationship of the age-adjusted prevalence of high total cholesterol, defined as greater than or equal to240 mg/dL (6.21 mmol/L), to BMI is shown in Figure 3.


At each BMI level, the prevalence of high blood cholesterol is greater in women than in men. In a smaller sample, higher body weight is associated with higher levels of total serum cholesterol in both men and women at levels of BMI > 25. Several large longitudinal studies also provide evidence that overweight, obesity, and weight gain are associated with increased cholesterol levels. In women, the incidence of hypercholesterolemia also increases with increasing BMI. In addition, the pattern of fat distribution appears to affect cholesterol levels independently of total weight. Total cholesterol levels are usually higher in persons with predominant abdominal obesity, defined as a waist-to-hip circumference ratio of  greater than or equal to0.8 for women and  greater than or equal to1.0 for men.

High triglycerides

The strong association of triglyceride levels with BMI has been shown in both cross-sectional and longitudinal studies, for both sexes and all age groups. In three adult age groups, namely, 20 to 44 years, 45 to 59 years, and 60 to 74 years, higher levels of BMI, ranging from 21 or less to more than 30, have been associated with increasing triglyceride levels; the difference in triglycerides ranged from 61 to 65 mg/dL (0.68 to 0.74 mmol/L) in women and 62 to 118 mg/dL (0.70 to 1.33 mmol/L) in men).

Low high-density lipoprotein cholesterol

HDL-cholesterol levels at all ages and weights are lower in men than in women. Although low HDL-cholesterol in this study was defined as < 35 mg/dL (0.91 mmol/L) in men and < 45 mg/dL (1.16 mmol/L) in women, the panel accepts the definition of low HDL-cholesterol as 35 mg/dL for men and women used by the National Cholesterol Education Program's Second Report of the Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II Report). Cross-sectional studies have reported that HDL-cholesterol levels are lower in men and women with higher BMI. Longitudinal studies have found that changes in BMI are associated with changes in HDL-cholesterol. A BMI change of 1 unit is associated with an HDL-cholesterol change of 1.1 mg/dL for young adult men and an HDL-cholesterol change of 0.69 mg/dL for young adult women.

*Defined as 35 mg/dL in men and 45 mg/dL in women.

Normal to elevated low-density lipoprotein cholesterol

The link between total serum cholesterol and CHD is largely due to low-density lipoprotein (LDL). A high-risk LDL-cholesterol is defined as a serum concentration of greater than or equal to160 mg/dL. This lipoprotein is the predominant atherogenic lipoprotein and is therefore the primary target of cholesterol-lowering therapy. Cross-sectional data suggest that LDL-cholesterol levels are higher by 10 to 20 mg/dL in relation to a 10- unit difference in BMI, from levels of 20 to 30 kg/m2. According to extensive epidemiological data, a 10 mg/dL rise in LDL-cholesterol corresponds to approximately a 10 percent increase in CHD risk over a period of 5 to 10 years.

Small, dense low-density lipoprotein particles

Few large-scale epidemiological data are available on small, dense LDL particles. Clinical studies have shown that small, dense LDL particles are particularly atherogenic and tend to be present in greater proportion in hypertriglyceridemic patients with insulin resistance syndrome associated with abdominal obesity.

 At each BMI level, the prevalence of high blood cholesterol is greater in women than in men. In a smaller sample, higher body weight is associated with higher levels of total serum cholesterol in both men and women at levels of BMI > 25. Several large longitudinal studies also provide evidence that overweight, obesity, and weight gain are associated with increased cholesterol levels. In women, the incidence of hypercholesterolemia also increases with increasing BMI. In addition, the pattern of fat distribution appears to affect cholesterol levels independently of total weight. Total cholesterol levels are usually higher in persons with predominant abdominal obesity, defined as a waist-to-hip circumference ratio of   0.8 for women and   1.0 for men.

High triglycerides

The strong association of triglyceride levels with BMI has been shown in both cross-sectional and longitudinal studies, for both sexes and all age groups. In three adult age groups, namely, 20 to 44 years, 45 to 59 years, and 60 to 74 years, higher levels of BMI, ranging from 21 or less to more than 30, have been associated with increasing triglyceride levels; the difference in triglycerides ranged from 61 to 65 mg/dL (0.68 to 0.74 mmol/L) in women (134) and 62 to 118 mg/dL (0.70 to 1.33 mmol/L) in men.

HDL-cholesterol levels at all ages and weights are lower in men than in women. Although low HDL-cholesterol in this study was defined as < 35 mg/dL (0.91 mmol/L) in men and < 45 mg/dL (1.16 mmol/L) in women, the panel accepts the definition of low HDL-cholesterol as 35 mg/dL for men and women used by the National Cholesterol Education Program's Second Report of the Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II Report). Cross-sectional studies have reported that HDL-cholesterol levels are lower in men and women with higher BMI. Longitudinal studies have found that changes in BMI are associated with changes in HDL-cholesterol. A BMI change of 1 unit is associated with an HDL-cholesterol change of 1.1 mg/dL for young adult men and an HDL-cholesterol change of 0.69 mg/dL for young adult women.

Normal to elevated low-density lipoprotein cholesterol

The link between total serum cholesterol and CHD is largely due to low-density lipoprotein (LDL). A high-risk LDL-cholesterol is defined as a serum concentration of  160 mg/dL. This lipoprotein is the predominant atherogenic lipoprotein and is therefore the primary target of cholesterol-lowering therapy. Cross-sectional data suggest that LDL-cholesterol levels are higher by 10 to 20 mg/dL in relation to a 10- unit difference in BMI, from levels of 20 to 30 kg/m2. According to extensive epidemiological data, a 10 mg/dL rise in LDL-cholesterol corresponds to approximately a 10 percent increase in CHD risk over a period of 5 to 10 years.

Small, dense low-density lipoprotein particles

Few large-scale epidemiological data are available on small, dense LDL particles. Clinical studies have shown that small, dense LDL particles are particularly atherogenic and tend to be present in greater proportion in hypertriglyceridemic patients with insulin resistance syndrome associated with abdominal obesity.

Type 2 Diabetes

The increased risk of diabetes as weight increases has been shown by prospective studies in Norway, the United States, Sweden, and Israel. More recently, the Nurses' Health Study, using data based on self-reported weights, found that the risk of developing type 2 diabetes increases as BMI increases from a BMI as low as 22. Since women in particular tend to under-report weight, the actual BMI values associated with these risks are likely to be higher than the Nurses' Health Study data would suggest. An association between type 2 diabetes and increasing relative weight is also observed in populations at high risk for obesity and diabetes, such as in American Indians.

In recent studies, the development of type 2 diabetes has been found to be associated with weight gain after age 18 in both men and women. The relative risk of diabetes increases by approximately 25 percent for each additional unit of BMI over 22 kg/m2. Additionally, in a prospective study representative of the U.S. population, it was recently estimated that 27 percent of new cases of diabetes were attributable to weight gain in adulthood of 5 kg (11 lb) or more. Both cross-sectional and longitudinal studies show that abdominal obesity is a major risk factor for type 2 diabetes.

Coronary Heart Disease

Observational studies have shown that overweight, obesity, and excess abdominal fat are directly related to cardiovascular risk factors, including high levels of total cholesterol, LDL-cholesterol, triglycerides, blood pressure, fibrinogen, and insulin, and low levels of HDL-cholesterol. Plasminogen activator inhibitor-1 causing impaired fibrinolytic activity is elevated in persons with abdominal obesity. Overweight, obesity, and abdominal fat are also associated with increased morbidity and mortality from CHD.

Recent studies have shown that the risks of nonfatal myocardial infarction and CHD death increase with increasing levels of BMI. Risks are lowest in men and women with BMIs of 22 or less and increase with even modest elevations of BMI. In the Nurses' Health Study, which controlled for age, smoking, parental history of CHD, menopausal status, and hormone use, relative risks for CHD were twice as high at BMIs of 25 to 28.9, and more than three times as high at BMIs of 29 or greater, compared with BMIs of less than 21. Weight gains of 5 to 8 kg 17.6 lb) increased CHD risk (nonfatal myocardial infarction and CHD death) by 25 percent, and weight gains of 20 kg (44 lb) or more increased risk more than 2.5 times in comparison with women whose weight was stable within a range of 5 kg (11 lb). In British men, CHD incidence increased at BMIs above 22 and an increase of 1 BMI unit was associated with a 10 percent increase in the rate of coronary events. Similar relationships between increasing BMI and CHD risk have been shown in Finnish, Swedish, Japanese, and U.S. populations.

A relationship between obesity and CHD has not always been found. Two reasons may account for this: the first is an inappropriate controlling for cholesterol, blood pressure, diabetes, and other risk factors in statistical analysis and the second is that there was an inadequate controlling for the confounding effect of cigarette smoking on weight. People who smoke often have a lower body weight but more CHD.

Congestive Heart Failure

Overweight and obesity have been identified as important and independent risk factors for congestive heart failure (CHF) in a number of studies, including the Framingham Heart Study. CHF is a frequent complication of severe obesity and a major cause of death; duration of the obesity is a strong predictor of CHF. Since hypertension and type 2 diabetes are positively associated with increasing weight, the coexistence of these conditions facilitates the development of CHF. Data from the Bogalusa Heart Study demonstrate that excess weight may lead to acquisition of left ventricular mass beyond that expected from normal growth.

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension or underlying heart disease. Ventricular dilatation and eccentric hypertrophy may result from elevated total blood volume and high cardiac output. Diastolic dysfunction from eccentric hypertrophy and systolic dysfunction from excessive wall stress result in so-called "obesity cardiomyopathy". The sleep apnea/obesity hyperventilation syndrome occurs in 5 percent of severely obese individuals, and is potentially life-threatening. Extreme hypoxemia induced by obstructive sleep apnea syndrome may result in heart failure in the absence of cardiac dysfunction.

Stroke

The relationship of cerebrovascular disease to obesity and overweight has not been as well studied as the relationship to CHD. A report from the Framingham Heart Study suggested that overweight might contribute to the risk of stroke, independent of the known association of hypertension and diabetes with stroke.

More recently published reports are based on larger samples and delineate the importance of stroke subtypes in assessing these relationships. They also attempt to capture all stroke events, whether fatal or nonfatal. These studies suggest distinct risk factors for ischemic stroke as compared to hemorrhagic stroke, and found overweight to be associated with the former, but not the latter. This may explain why studies that use only fatal stroke outcomes (and thus overrepresent hemorrhagic strokes) show only weak relationships between overweight and stroke.

These recent prospective studies demonstrate that the risk of stroke shows a graded increase as BMI rises. For example, ischemic stroke risk is 75 percent higher in women with BMI > 27, and 137 percent higher in women with a BMI > 32, compared with women having a BMI < 21.

Gallstones

The risk of gallstones increases with adult weight. Risk of either gallstones or cholecystectomy is as high as 20 per 1,000 women per year when BMI is above 40, compared with 3 per 1,000 among women with BMI < 24.

The prevalence of gallstone disease among women increased from 9.4 percent in the first quartile of BMI to 25.5 percent in the fourth quartile of BMI. Among men, the prevalence of gallstone disease increased from 4.6 percent in the first quartile of BMI to 10.8 percent in the fourth quartile of BMI.

Osteoarthritis

Individuals who are overweight or obese increase their risk for the development of osteoarthritis.  The association between increased weight and the risk for development of knee osteoarthritis is stronger in women than in men.  In a study of twin middle-aged women, it was estimated that for every kilogram increase of weight, the risk of developing osteoarthritis increases by 9 to 13 percent. The twins with knee osteoarthritis were generally 3 to 5 kg (6.6 to 11 lb) heavier than the co-twins with no disease.  An increase in weight is significantly associated with increased pain in weight-bearing joints. There is no evidence that the development of osteoarthritis leads to the subsequent onset of obesity.  A decrease in BMI of 2 units or more during a 10-year period decreased the odds for developing knee osteoarthritis by more than 50 percent; weight gain was associated with a slight increase in risk.

A randomized controlled trial of 6 months' duration examined the effect of weight loss on clinical improvement in patients with osteoarthritis. Patients taking phentermine had an average weight loss of 12.6 percent after 6 months while the control group had an average weight loss of 9.2 percent. There was improvement in pain-free range of motion and a decrease in analgesic use in association with weight loss; patients with knee disease showed a stronger association than those with hip disease. Similarly, improvement of joint pain was observed in individuals who had undergone gastric stapling, resulting in an average weight loss of 45 kg (99 lb).

Sleep Apnea

Obesity, particularly upper body obesity, is a risk factor for sleep apnea and has been shown to be related to its severity.  The major pathophysiologic consequences of severe sleep apnea include arterial hypoxemia, recurrent arousals from sleep, increased sympathetic tone, pulmonary and systemic hypertension, and cardiac arrhythmias. Most people with sleep apnea have a BMI > 30.  Large neck girth in both men and women who snore is highly predictive of sleep apnea. In general, men whose neck circumference is 17 inches or greater and women whose neck circumference is 16 inches or greater are at higher risk for sleep apnea.

Colon Cancer

Many studies have found a positive relation between obesity and colon cancer in men but a weaker association in women.  More recent data from the Nurses' Health Study suggest that the relationship between obesity and colon cancer in women may be similar to that seen in men. Twice as many women with a BMI of > 29 kg/m2 had distal colon cancer as women with a BMI < 21 kg/m2. In men, the relationship between obesity and total colon cancer was weaker than that for distal colon cancer.

Other data from the Nurses' Health Study show a substantially stronger relationship between waist-to-hip ratio and the prevalence of colon polyps on sigmoidoscopy, than with BMI alone. Even among leaner women, a high waist-to-hip ratio is also associated with significantly increased risk of colon polyps.

Breast Cancer

Epidemiologic studies consistently show that obesity is directly related to mortality from breast cancer, predominantly in postmenopausal women, but inversely related to the incidence of premenopausal breast cancer. Ten or more years after menopause, the premenopausal "benefit" of obesity has dissipated. Among postmenopausal women, peripheral fat is the primary source of estrogens, the major modifiable risk factor for postmenopausal breast cancer.

This crossover in the relationship of obesity with breast cancer, pre- and postmenopausally, complicates prevention messages for this common female cancer. Recent data from the Nurses'Health Study, however, show that adult weight gain is positively related to risk of postmenopausal breast cancer. This relation is seen most clearly among women who do not use postmenopausal hormones. A gain of more than 20 lb from age 18 to midlife doubles a woman's risk of breast cancer. Even modest weight gains are positively related to risk of postmenopausal cancer.

Obesity and Women's Reproductive Health

Menstrual Function and Fertility

Obesity in premenopausal women is associated with menstrual irregularity and amenorrhea.  As part of the Nurses' Health Study, a case control study suggested that the greater the BMI at age 18 years, even at levels lower than those considered obese, the greater the risk of subsequent ovulatory infertility. The most prominent condition associated with abdominal obesity is polycystic ovarian syndrome, a combination of infertility, menstrual disturbances, hirsutism, abdominal hyperandrogenism, and anovulation. This syndrome is strongly associated with hyperinsulinemia and insulin resistance.

Pregnancy

Pregnancy can result in excessive weight gain and retention. The 1988 National Maternal and Infant Survey observed that 41.6 percent of women reported retaining  9 lb of their gained weight during pregnancy, with 33.8 percent reporting  14 lb of retained weight gain.  The retained weight gain associated with pregnancy was corroborated by the study of Coronary Artery Risk Development in Young Adults (CARDIA). As a result of their first pregnancy, both black and white young women had a sustained weight gain of 2 to 3 kg (4.4 to 6.6 lb) of body weight.

Another study on a national cohort of women followed for 10 years reported that weight gain associated with childbearing ranged from 1.7 kg (3.7 lb) for those having one live birth during the study to 2.2 kg (4.9 lb) for those having three. In addition, higher prepregnancy weights have been shown to increase the risk of late fetal deaths.

Obesity during pregnancy is associated with increased morbidity for both the mother and the child. A tenfold increase in the prevalence of hypertension and a 10 percent incidence of gestational diabetes have been reported in obese pregnant women.  Obesity also is associated with difficulties in managing labor and delivery, leading to a higher rate of induction and primary Caesarean section.  Risks associated with anesthesia are higher in obese women, as there is greater tendency toward hypoxemia and greater technical difficulty in administering local or general anesthesia. Finally, obesity during pregnancy is associated with an increased risk of congenital malformations, particularly of neural tube defects.

A certain amount of weight gain during pregnancy is desirable. The fetus itself, expanded blood volume, uterine enlargement, breast tissue growth, and other products of conception generate an estimated 13 to 17 lb of extra weight. Weight gain beyond this, however, is predominantly maternal adipose tissue. It is this fat tissue that, in large measure, accounts for the postpartum retention of weight gained during pregnancy. In turn, this retention reflects a postpartum energy balance that does not lead to catabolism of the gained adipose tissue. In part, this may reflect reduced energy expenditure through decreased physical activity, even while caring for young children, but it may also reflect retention of the pattern of increased caloric intake acquired during pregnancy.

One difficulty in developing recommendations of optimal weight gain during pregnancy relates to the health of the infants. A balance must be achieved between high-birth-weight infants who may pose problems during delivery and who may face a higher rate of Caesarean sections and low-birth-weight infants who face a higher infant mortality rate.  However, data from the Pregnancy Nutrition Surveillance System from CDC showed that very overweight women would benefit from a reduced weight gain during pregnancy to help reduce the risk for high-birth-weight infants.

The 1990 Institute of Medicine report made recommendations concerning maternal weight gain. It recommended that each woman have her BMI measured and recorded at the time of entry into prenatal care. For women with a BMI of less than 20, the target weight gain should be 0.5 kg (1.1 lb) of weight gain per week during the second and third trimester. For a woman whose BMI is greater than 26, the weight gain target is 0.3 kg (0.7 lb) per week during the last two trimesters. 

Women who are overweight or obese at the onset of pregnancy are advised to gain less total weight during the pregnancy.

Psychosocial Aspects of Overweight and Obesity

Social Stigmatization | Psychopathology and Obesity | Binge Eating Disorder | Body Image

Social Stigmatization

In American and other Westernized societies there are powerful messages that people, especially women, should be thin, and that to be fat is a sign of poor self-control.  Negative attitudes about the obese have been reported in children and adults, in health care professionals, and in the overweight themselves.

People's negative attitudes toward the obese often translate into discrimination in employment opportunities, college acceptance, less financial aid from their parents in paying for college, job earnings, rental availabilities, and opportunities for marriage.

Much of the research on the social stigma of obesity has suffered from methodological limitations. For example, a number of the early studies relied on line drawings rather than more lifelike representations of obese people and on checklists that forced one to make YES or NO choices. More important, there has been a lack of research that has looked at the impact of obesity in the context of other variables, such as physical attractiveness, the situational context, and the degree of obesity.  In addition, social stigma toward the obese has primarily been assessed among white individuals.

There is some evidence that members of other racial and ethnic groups are less harsh in their evaluation of obese persons. One study assessed 213 Puerto Rican immigrants to the United States, and found a wide range of acceptable weights among them. Crandall found that Mexican students were significantly less concerned about their own weight and were more accepting of other obese people than were U.S. students.

In addition, the degree of acceptance of obesity among people of lower education and income has not been well studied. Thus, these data are very incomplete with respect to racial and ethnic groups other than whites.

Psychopathology and Obesity

Research relating obesity to psychological disorders and emotional distress is based on community studies and clinical studies of patients seeking treatment. In general, community-based studies in the United States have not found significant differences in psychological status between the obese and nonobese.  However, several recent European studies in general populations do suggest a relationship between obesity and emotional problems.Thus, it may be premature to state that there is no association between obesity and psychopathology or emotional distress in the general population. More focused, hypothesis-driven, and long-term studies are needed.

Overweight people seeking weight loss treatment may, in clinic settings, show emotional disturbances.  In a review of dieting and depression, there was a high incidence of emotional illness symptoms in outpatients treated for obesity.  However, several factors influenced these emotional responses, including childhood onset versus adult onset of obesity (those with childhood onset obesity appear more vulnerable).  Another study that compared different eating disorder groups found that obese patients seeking treatment showed considerable psychopathology, most prominently mild to severe depression. Sixty-two percent of the obese group seeking treatment showed clinically significant elevations on the depression subscale of the Minnesota Multiphasic Personality Inventory, and 37 percent of this same group showed a score of 20 or higher (indicating clinical depression) on the Beck Depression Inventory. Focusing on depression was considered an important component of the weight loss program. 

Another study compared obese people who had not sought treatment to an obese group that had sought treatment in a professional, hospital-based program, and to normal weight controls. Again, obese individuals seeking treatment reported more psychopathology and binge eating compared to the other groups. Both obese groups reported more symptoms of distress than did normal weight controls. The authors suggest that the obese population is not a homogenous group, and thus, may not respond in the same way to standardized treatment programs. In particular, obese individuals seeking treatment in clinic settings are more likely than obese individuals not seeking treatment and normal controls to report more psychopathology and binge eating.

Binge Eating Disorder

Binge eating disorder (BED) is characterized by eating larger amounts of food than most people would eat in a discrete time period (e.g., 2 hours) with a sense of lack of control during these episodes.  It is estimated to occur in 20 to 50 percent of individuals who seek specialized obesity treatment.  In community-based samples, the prevalence is estimated to be approximately 2 percent.

Comparisons have been made between BED and bulimia nervosa (BN), an eating disorder characterized by recurrent and persistent binge eating, accompanied by the regular use of behaviors such as vomiting, fasting, or using laxatives. Studies comparing normal-weight individuals who have BN with obese BED individuals have found that obese binge eaters are less likely to demonstrate dietary restraint and show few if any adverse reactions to moderate or severe dieting. Most obese binge eaters do not engage in inappropriate compensatory behaviors such as purging.

Compared with BN, the demographic distribution of BED is broader with respect to age, gender, and race, while data suggest that BED is as common in African-American women as in white women.The difference between BED and BN is dramatic regarding gender. Very few men have BN, whereas the distribution is close to equal in BED.

Compared to obese nonbingers, obese individuals with BED tend to be heavier, report greater psychological distress, and are more likely to have experienced a psychiatric illness (especially affective disorders). They also report an earlier onset of obesity and a greater percentage of their lifetime on a diet.

Some studies have shown histories of greater weight fluctuation or weight cycling in obese binge eaters compared with nonbingers, but others have not. These individuals are also more likely than nonbinging obese people to drop out of behavioral weight loss programs, and to regain weight more quickly.

Critics of behavioral treatment of obesity have argued that caloric restriction may cause or contribute to the episodes of binge eating and BN.  Three studies have tested this hypothesis.  Neither moderate nor severe caloric restriction exacerbated binge eating. All three studies showed that weight control treatment featuring caloric restriction significantly reduced the frequency of binge eating in these patients.

Body Image

Body image is defined as the perception of one's own body size and appearance and the emotional response to this perception. Inaccurate perception of body size or proportion and negative emotional reactions to size perceptions contribute to poor body image. Obese individuals, especially women, tend to overestimate their body size.

People at greater risk for a poor body image are binge eaters, women, those who were obese during adolescence or with early onset of obesity, and those with emotional disturbances. It is no surprise, then, that in some groups of obese persons, these individuals are more dissatisfied and preoccupied with their physical appearance, and avoid more social situations due to their appearance.

Body image dissatisfaction and the desire to improve physical appearance often drives individuals to seek weight loss. However, obese persons seeking weight reduction must come to terms with real limits in their biological and behavioral capacities to lose weight. Otherwise, weight loss attempts may only intensify the sense of failure and struggle that is already present among many obese individuals. For this reason, psychosocial interventions which incorporate strategies to improve body image may be helpful for those who want to lose weight and are very concerned about their physical appearance. A review of body image interventions in obese persons can be found in Rosen.

Body image perceptions of individuals in various ethnic and racial groups may be different, on average, from those of the mainstream culture. There may be a similar range of attitudes but on a different scale; for example, it may take a much greater degree of overweight to elicit negative reactions. Differences in body image and weight-related concerns between black and white girls and women have been observed.  In general, black girls and women report less social pressure to be slim, fewer incidences of weight-related discrimination, less weight and body dissatisfaction, and greater acceptance of overweight than their white counterparts.

Genetic Influence in the Development of Overweight and Obesity

Obesity is a complex multifactorial chronic disease developing from interactive influences of numerous factors—social, behavioral, physiological, metabolic, cellular, and molecular. Genetic influences are difficult to elucidate and identification of the genes is not easily achieved in familial or pedigree studies. Furthermore, whatever the influence the genotype has on the etiology of obesity, it is generally attenuated or exacerbated by nongenetic factors.

A large number of twin, adoption, and family studies have explored the level of heritability of obesity; that is, the fraction of the population variation in a trait (e.g., BMI) that can be explained by genetic transmission. Recent studies of individuals with a wide range of BMIs, together with information obtained on their parents, siblings, and spouses, suggest that about 25 to 40 percent of the individual differences in body mass or body fat may depend on genetic factors.  However, studies with identical twins reared apart suggest that the genetic contribution to BMI may be higher, i.e., about 70 percent.  There are several other studies of monozygotic twins reared apart that yielded remarkably consistent results. Some of the reasons behind the different results obtained from twin versus family studies have been reported.  The relative risk of obesity for first-degree relatives of overweight, moderately obese, or severely obese persons in comparison to the population prevalence of the condition reaches about 2 for overweight, 3 to 4 for moderate obesity, and 5 and more for more severe obesity.

Support for a role of specific genes in human obesity of body fat content has been obtained from studies of Mendelian disorders with obesity as one of the clinical features, single-gene rodent models, quantitative trait loci from crossbreeding experiments, association studies, and linkage studies. From the research currently available, several genes seem to have the capacity to cause obesity or to increase the likelihood of becoming obese.  The rodent obesity gene for leptin, a natural appetite-suppressant hormone, has been cloned as has been its receptor.  In addition, other single gene mutants have been cloned.  However, their relationship to human disease has not been established, except for one study describing two subjects with a leptin mutation.  This suggests that for most cases of human obesity, susceptibility genotypes may result from variations of several genes.

Severely or morbidly obese persons are, on the average, about 10 to 12 BMI units heavier than their parents and siblings. Several studies have reported that a single major gene for high body mass was transmitted from the parents to their children. The trend implies that a major recessive gene, accounting for about 20 to 25 percent of the variance, is influenced by age and has a frequency of about 0.2 to 0.3.  However, no gene(s) has (have) yet been identified. Evidence from several studies has shown that some persons are more susceptible to either weight gain or weight loss than others.  It is important for the practitioner to recognize that the phenomenon of weight gain cannot always be attributed to lack of adherence to prescribed treatment regimens.

Treatment Guidelines

The presence of overweight and obesity in a patient is of medical concern because it increases the risk for several diseases, particularly cardiovascular diseases (CVDs) and diabetes mellitus and it increases all-cause mortality. Treatment of the overweight and obese patient is a two-step process: assessment and management. Assessment requires determination of the degree of obesity and absolute risk status. Management includes both weight control or reducing excess body weight and maintaining that weight loss as well as instituting other measures to control associated risk factors. The aim of this guideline is to provide useful advice on how to achieve weight reduction and maintenance of a lower body weight. It is also important to note that prevention of further weight gain can be a goal for some patients.  Obesity is a chronic disease, and both the patient and the practitioner need to understand that successful treatment requires a life-long effort.

Assessment and Classification

When assessing a patient as a candidate for weight loss therapy, consider the patient's body mass index (BMI), waist circumference, and overall risk status. Consideration also needs to be given to the patient's motivation to lose weight.

Assessment of Weight and Body Fat

Two measures important for assessing overweight and total body fat content are determining body mass index (BMI) and measuring waist circumference.

Body Mass Index: The BMI, which describes relative weight for height, is significantly correlated with total body fat content. The BMI should be used to assess overweight and obesity and to monitor changes in body weight. In addition, measurements of body weight alone can be used to determine efficacy of weight loss therapy. 

BMI is calculated as weight (kg)/height squared (m2). To estimate BMI using pounds and inches, use: [weight (pounds)/height (inches)] x 703. Weight classifications by BMI, selected for use in this report, are shown in the table below.

Table IV-1: Classification of Overweight and Obesity by BMI*

 

Obesity Class

BMI (kg/m2)

Underweight 

 

<18.5

Normal

 

18.5-24.9

Overweight

 

25.0-29.9

Obesity

I

30.0-34.9

 

II

35.0-39.9

Extreme Obesity

III

greater than or equal to40

* Pregnant women who, on the basis of their prepregnant weight, would be classified as obese may encounter certain obstetrical risks. However, the inappropriateness of weight reduction during pregnancy is well recognized (Thomas, 1995). Hence, this guideline specifically excludes pregnant women.

Waist Circumference: The presence of excess fat in the abdomen out of proportion to total body fat is an independent predictor of risk factors and morbidity. Waist circumference is positively correlated with abdominal fat content. It provides a clinically acceptable measurement for assessing a patient's abdominal fat content before and during weight loss treatment.  The waist circumference at which there is an increased relative risk is defined as follows:


High Risk

Men: >102 cm ( >40 in.)

Women: >88 cm ( >35 in.)

The BMI is calculated as follows:
BMI=weight (kg)/height squared (m2)
To estimate BMI from pounds and inches use:
[weight (pounds)/height (inches)2] x 703=
(1 lb=0.4536 kg)
(1 in=2.54 cm=0.0254 m)

Evaluation and Treatment Strategy

When physicians encounter patients in the clinical setting, the opportunity exists for identifying overweight and obesity and accompanying risk factors and for initiating treatment for both the weight and the risk factors, as well as chronic diseases such as CVD and type 2 diabetes. When assessing a patient for treatment of overweight and obesity, consider the patient's weight, waist circumference, and the presence of risk factors. The strategy for the evaluation and treatment of overweight patients is presented in the Treatment Algorithm. This algorithm applies only to the assessment for overweight and obesity and subsequent decisions based on that assessment. It does not reflect any initial overall testing for other conditions and diseases that the physician may wish to do. Approaches to therapy for cholesterol disorders and hypertension are described in ATP II and JNC VI, respectively. In overweight patients, control of cardiovascular risk factors deserves equal emphasis as weight loss therapy. Reductions of risk factors will reduce the risk for cardiovascular disease whether or not efforts at weight loss are successful. The panel recognizes that the assessment for overweight and obesity may take place as part of an overall health assessment; however, for clarity, the algorithm focuses only on the evaluation and treatment of overweight and obesity. Each step (designated by a box) in the process is reviewed when you go to the Treatment Algorithm and click on the various boxes.

Management of Weight Loss

The initial goal of weight loss therapy is to reduce body weight by approximately 10 percent from baseline. If this goal is achieved, further weight loss can be attempted, if indicated through further evaluation. A reasonable timeline for a 10 percent reduction in body weight is 6 months of therapy.

After 6 months, the rate of weight loss usually declines and weight plateaus because of less energy expenditure at the lower weight. Lost weight usually will be regained unless a weight maintenance program consisting of dietary therapy, physical activity, and behavior therapy is continued indefinitely. After 6 months of weight loss treatment, efforts to maintain weight loss should be put in place. If more weight loss is needed, another attempt at weight reduction can be made. This will require further adjustment of the diet and physical activity prescriptions.

For patients unable to achieve significant weight reduction, prevention of further weight gain is an important goal; such patients may also need to participate in a weight management program. Priority should be given to reducing saturated fat to enhance lowering of LDL-cholesterol levels. Frequent contacts with the practitioner during dietary therapy help to promote weight loss and weight maintenance at a lower weight.

An increase in physical activity is an important component of weight loss therapy, although it will not lead to substantially greater weight loss over 6 months. Most weight loss occurs because of decreased caloric intake. Sustained physical activity is most helpful in the prevention of weight regain. In addition, it has a benefit in reducing cardiovascular and diabetes risks beyond that produced by weight reduction alone. For most obese patients, exercise should be initiated slowly, and the intensity should be increased gradually. The exercise can be done all at one time or intermittently over the day.

Goals of Weight Loss and Management

The general goals of weight loss and management are:

To reduce body weight.
To maintain a lower body weight over the long term.
To prevent further weight gain.
Specific targets for each of these goals can be considered.

Depending on the degree of overweight and the presence of other diseases or risk factors, a patient should be advised to either reduce body weight or prevent further weight gain. All patients with a BMI of 30 or those with a BMI of 25 to 29.9 kg/m2 (or a high waist circumference) and two or more risk factors should attempt to lose weight. However, it is important to ask the patient whether they want to lose weight. Patients with a BMI of 25 to 29.9 kg/m2 with one or no risk factors should work on maintaining their current weight and prevent further weight gain. The justification for offering these overweight patients the option of maintaining (rather than losing) weight is that their health risk, while higher than that of persons with a BMI of <25, is only moderately increased.

Evidence indicates that a moderate weight loss can be maintained over time if some form of therapy continues. It is better to maintain a moderate weight loss over a prolonged period than to regain from a marked weight loss.

Weight Loss

Target Levels for Weight Loss | Rate of Weight Loss
Target Levels for Weight Loss

The initial target goal of weight loss therapy for overweight patients is to decrease body weight by about 10 percent. If this target can be achieved, consideration can be given to the next step of further weight loss. 

Evidence Statement: Overweight and obese patients in well-designed programs can achieve a weight loss of as much as 10 percent of baseline weight, a weight loss that can be maintained for a sustained period of time (1 year or longer). Evidence Category A.

Rationale: The rationale for this initial goal is that even moderate weight loss, i.e., 10 percent of initial body weight, can significantly decrease the severity of obesity-associated risk factors. It can also set the stage for further weight loss, if indicated. Available evidence indicates that an average weight loss of 8 percent can be achieved in 6 months; however, since the observed average 8 percent includes people who do not lose weight, an individual goal of 10 percent is reasonable. This degree of weight loss can be achieved and is realistic, and moderate weight loss can be maintained over time. It is better to maintain a moderate weight loss over a prolonged period than to regain from a marked weight loss. The latter is counterproductive in terms of time, costs, and self-esteem. Patients generally will wish to lose more weight than 10 percent, and will need to be counseled and persuaded of the appropriateness of this initial goal.  Further weight loss can be considered after this initial goal is achieved and maintained for 6 months.

Recommendation: The initial goal of weight loss therapy should be to reduce body weight by approximatety 10 percent from baseline. With success, further weight loss can be attempted, if indicated through further assessment.

Rate of Weight Loss

A reasonable time line for weight loss is to achieve a 10 percent reduction in body weight over 6 months of therapy. For overweight patients with BMIs in the typical range of 27 to 35, a decrease of 300 to 500 kcal/day will result in weight losses of about 1/2 to 1 lb/week and a 10 percent weight loss in 6 months. For more severely obese patients with BMIs  35, deficits of up to 500 to 1,000 kcal/day will lead to weight losses of about 1 to 2 lb/week and a 10 percent weight loss in 6 months.

Evidence Statement: Weight loss at the rate of 1 to 2 lb/week (calorie deficit of 500 to 1,000 kcal/day) commonly occurs for up to 6 months, at which point weight loss begins to plateau unless a more restrictive regimen is implemented.

Rationale: To achieve significant weight loss, an energy deficit must be created and maintained. Weight can be lost at a rate of 1 to 2 lb/week with a calorie deficit of 500 to 1,000 kcal/day. After 6 months, this caloric deficit theoretically should result in a loss of 26 to 52 lb. However, the average amount of weight lost actually observed over this time period usually is in the range of 20 to 25 lb. A greater rate of weight loss does not yield a better result at the end of 1 year.  It is difficult for most patients to continue to lose weight after a period of 6 months due to changes in resting metabolic rates and difficulty in adhering to treatment strategies, although some can do so. To continue to lose weight, diet and physical activity goals need to be revised to create an energy deficit at the lower weight, since energy requirements decrease as weight is decreased. To achieve additional weight loss, the patient must further decrease calories and/or increase physical activity. Many studies show that rapid weight reduction almost always is followed by regaining of weight. Moreover, with rapid weight reduction, there is an increased risk for gallstones and, possibly, electrolyte abnormalities.

Recommendation: Weight loss should be about 1 to 2 lb/week for a period of 6 months with the subsequent strategy based on the amount of weight lost.

Exclusion from Weight Loss Therapy

Patients in whom weight loss therapy is not appropriate include most pregnant or lactating women, those with serious psychiatric illness, and patients who have a variety of serious illnesses in whom caloric restriction might exacerbate the illness.

Special Considerations

Adapting Weight Loss Programs To Meet the Needs of Diverse Patient Populations

Standard obesity treatment approaches should be tailored to the needs of patients. It is, however, difficult to determine from the literature how often this occurs and whether it makes weight loss programs more effective. Very few published reports of such adapted programs can be identified, particularly when a distinction is made from reports that include or focus on special populations but do not report any particular steps taken to modify the intervention for these populations. In addition, it is impossible to compare directly the amount of weight lost using specially adapted programs with that achieved when more standard approaches are used. Studies reporting these programs are sometimes pilot studies or descriptive reports. Where randomized controlled trials or quasi-experiments are available, they usually do not include an internal comparison with a program involving no adaptations. 

Large individual variation exists within any social or cultural group; furthermore, there is substantial overlap among subcultures within the larger society. There is, therefore, no "cookbook" or standardized set of rules to optimize weight reduction with a given type of patient. A theoretical and qualitative analysis of cultural appropriateness in obesity treatment programs has been conducted, and it provides some guidance for incorporating patient characteristics and perspectives when designing and delivering weight loss programs.  For example:

I. Adapt the setting and staffing to the patient population. The setting should:

be physically accessible to the patient;
have features likely to be familiar to the patient;
be free of negative psychosocial connotations;
be devoid of aspects that create a large social distance among patients or between patient and practitioner; and
promote active patient participation and high patient self-esteem and self-efficacy.

The staff should be culturally self-aware and culturally competent in working with persons of diverse cultural backgrounds and income or educational levels. For example, cultural adaptation of programs has been approached with the assumption that community centers may be preferable to hospitals or medical offices as venues for conducting lifestyle weight reduction programs. Or, some programs have included peer educators as a possible way of helping to overcome background and social class differences by providing a bridge of knowledge, experience, and perspective between patients and practitioners.

II. List assumptions about the type of patient for whom the program will be best suited and evaluate the extent to which these assumptions are appropriate for prospective patients. Where appropriate, modify the program to avoid the need for certain assumptions. Consider patients':

preexisting knowledge base;
day-to-day routine;
discretionary time;
financial resources and living situation;
cultural preferences for types of food and activity.
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For example, redesign printed materials to be suitable for patients with low literacy skills or poor vision. Offer dietary and physical activity recommendations that will be feasible for low-income patients living in inner-city areas with limited access to supermarkets or with high crime rates.

III. Consider how the obesity treatment program fits in other aspects of the health care and self-care of the patient(s), and integrate other aspects where appropriate. For example, for those patients with diabetes, information about weight reduction should be aligned with other diabetes management advice.

IV. Expect and allow for program modifications based on patient feedback and preferences. Program appropriateness can be increased when patients can express their needs and preferences, and the program is then adapted to those needs and preferences. This is especially applicable when practitioners have limited common experience with patients.

In recent years, a fat acceptance, nondieting advocacy group has developed. This has emerged from concerns about weight cycling and its possible adverse effects on morbidity and mortality. However, recent evidence suggests that intentional weight loss is not associated with increased morbidity and mortality. For this reason, the guidelines have been made explicit on the importance of intervention for weight loss and maintenance in the appropriate patient groups.