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Obesity

COURSE

 Understand and Prevent Obesity

An estimated 97 million adults in the United States are overweight or obese. In European Union over 50% of both men and women were overweight, and roughly 23% of women and 20% of men were obese, a condition that substantially raises their risk of morbidity from hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea and respiratory problems, and endometrial, breast, prostate, and colon cancers.

(11) Concepts of Obesity

Africa Obesity and Health Chat

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Africa, Sub-Saharan

In parts of sub-Saharan Africa, there has been a tradition of some rulers being overweight or obese, a tradition that has continued through to the modern era. As well as this, the increasing affluence of some areas has led to a rise in the prevalence of obesity among the middle class, particularly westernized families.

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(33) Obesity

 Obesity and Globalization - Obesity is now the fifth highest risk factor for mortality in developed economies, which has major implications for health-care costs.

Obesity33

Obesity and Mortality

Majority of epidemiologic studies, mortality begins to increase with BMIs above 25 kg/m2. The increase in mortality generally tends to be modest until a BMI of 30 kg/m2 is reached.

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(34) Obesity

Our Supersized Kids

Obesity34

Weight Loss and Mortality

A number of studies of “generic weight loss” (cause of weight loss unknown), “weight cycling” (cycles of weight loss followed by weight regain), and mortality have been published. In most, but not all, of these studies, generic weight loss and weight cycling are associated with increases in mortality. None of these studies, however, differentiated between intentional and unintentional weight loss. With the exception of the studies below, very little is currently known about factors related to intentional and unintentional weight loss in the general population or about the relationship between weight loss intention and mortality.

Two studies of factors related to weight loss intention have been carried out in the general population: French and colleagues assessed correlates of intentional and unintentional weight loss of > 20 lb in the Iowa Women’s Health Study, a cohort study of approximately 29,000 women with a mean age of about 65 years; and Meltzer and Everhart analyzed data on 1-year self-reported weight change from approximately 9,000 participants in the nationally representative U.S. National Health Interview Survey, aged 45 years and above. The results of these two studies suggest the following:

  • In cross-sectional studies of weight loss recall, heavier persons are more likely to report intentional weight loss than unintentional weight loss, while the reverse is true for leaner persons;
  • Intentional and unintentional weight losses occur with similar frequency in the U.S. population and contribute similarly to long-term weight fluctuation;
  • The frequency of intentional weight loss is lower at older ages, while the frequency of unintentional weight loss is higher at older ages; and
  • Unintentional weight loss occurs more often in persons who report that their health status is poor, who use medications for chronic health conditions, and who smoke.

To date, only three studies have examined the relationship between intentional weight loss and mortality. Singh and colleagues published results from a 1-year randomized controlled trial of a “cardio protective diet” in East Indian patients hospitalized with recent myocardial infarction (mean age 50 years, mean BMI about 24 kg/m2 ). Although this study was not designed to specifically test the efficacy of intentional weight loss on lower mortality, the authors found that those who lost at least 0.5 kg (1.1 lb) had a 50 percent lower incidence of cardiac events and a 54 percent lower risk of overall mortality compared with counterparts who lost < 0.5 kg (1.1 lb). 317

Williamson and colleagues published a 12-year prospective observational study of weight loss and mortality that directly assessed weight loss intention. They analyzed data from 43,457 overweight (BMI > 27), never-smoking, white women ages 40 to 64 years. Mortality ratios were compared for women who intentionally lost weight with those for women who had no change in weight. In women with obesity-related comorbidities, intentional weight loss of any amount was associated with a statistically significant 20 percent reduction in all-cause mortality, primarily due to a significant 40 to 50 percent reduction in mortality from obesity-related cancers; diabetes-related mortality was also significantly reduced by 30 to 40 percent in those who intentionally lost weight. In women with no comorbidities, intentional weight loss was generally unrelated to mortality; however, after subdividing intentional weight loss by time interval, it was found that a loss of at least 20 lb that occurred within the previous year was associated with small to modest increases in mortality. The authors concluded that the association between intentional weight loss and longevity in middle age overweight women depends on health status. In addition, preliminary evidence suggests that intentional weight loss in middle-age overweight men may be associated with a similar reduction of diabetes-related mortality as was observed in the overweight women.

The ongoing Swedish Obesity Study is a controlled trial of surgically induced weight loss and subsequent morbidity and mortality over a 10-year follow-up period (1,006 participants aged 37 to 57 years; initial BMI of 34 in men and 38in women). Although the study is not randomized (participants self-select for surgery), the controls (who receive a behavioral weight loss program) are computer-matched to surgical participants on a large number of potential confounders including weight. In a preliminary abstract,  the study reported the 2-year incidence rates. These results for disease and risk factor incidences suggest that 10-year mortality will ultimately be lower in the surgical intervention group. Definitive mortality results have not been reported to date.

 ENVIRONMENT

 The environment is a major determinant of overweight and obesity. Environmental influences on overweight and obesity are primarily related to food intake and physical activity behaviors. In countries like the United States, there is an overall abundance of palatable, calorie-dense food. In addition, aggressive and sophisticated food marketing in the mass media, supermarkets, and restaurants, and the large portions of food served outside the home, promote high calorie consumption. Many of our sociocultural traditions promote overeating and the preferential consumption of high calorie foods.

For many people, even when caloric intake isnot above the recommended level, the number of calories expended in physical activity is insufficient to offset consumption. Mechanization limits the necessity of physical activity required to function in society. Many people are entrenched in sedentary daily routines consisting of sitting at work, sitting in traffic, and sitting in front of a television or a computer monitor for most of their waking hours. In this obesity-promoting environment, individual attitudes and behaviors are critical in weight management. Many individuals may need extended treatment in clinical or community settings to enable them to cope with the complexities of long-term weight management, especially if there is a history of unsuccessful attempts at self-treatment. When the typical daily routine is so strongly biased towards promoting and perpetuating overweight and obesity, very high levels of knowledge, motivation, personal behavioral management skill, and lifestyle flexibility are required for an overweight or obesity-prone individual to avoid becoming overweight, or progressing to moderate or severe obesity.

Although there are undoubtedly some inter- and intrapopulation variations in the genetic predisposition to become overweight or obese, several lines of evidence suggest that genetic factors alone cannot explain the demographic and ethnic variations in overweight and obesity prevalence. For example, there is a difference in obesity prevalence among low- and high-income white women in industrialized societies. Other studies of populations, including migration studies, have shown an increase in average body weight in those who move from a traditional to a Westernized environment. Culturally determined attitudes about food, physical activity, and factors that vary with income, education, and occupation may increase the level of difficulty in weight management.

Body image concerns and other motivations for avoiding obesity or controlling weight within given limits also vary with ethnic background, age, socioeconomic status, and gender. Thus, the competence of practitioners in working with diverse sociocultural perspectives can be a critical factor in the success of obesity treatment.

 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 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 or 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.

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(35) Obesity

How being overweight or obese causes High Blood Pressure

Obesity35

WHY TREAT OVERWEIGHT AND OBESITY?

The recommendation to treat overweight and obesity is based not only on the previously presented evidence that shows overweight is associated with increased morbidity and mortality, but also on randomized controlled trial (RCT) evidence that weight loss reduces risk factors for disease. Thus, weight loss may help control diseases worsened by overweight and obesity and may also decrease the likelihood of developing these diseases. The evidence meeting the panel’s inclusion criteria is presented in the form of evidence statements with a corresponding rationale for each statement. Many of the RCTs examined by the panel included the use of pharmacotherapy for weight loss. When the panel began its deliberations in 1995, two weight loss drugs, fenfluramine and dexfenfluramine, were being used widely for long-term weight loss, i.e., 14 million prescriptions were given out over 11⁄2 years. However, as of September 1997, the Food and Drug Administration (FDA) requested the voluntary withdrawal of these drugs from the market due to a reported association between valvular heart disease and the use of dexfenfluramine and fenfluramine alone or combined with phentermine.

In November 1997, the FDA approved the drug sibutramine hydrochloride monohydrate for the management of obesity, including weight loss and maintenance of weight loss when used in conjunction with a reduced-calorie diet. Thus, at the present time only one weight loss drug is available for long-term weight loss. (Note: FDA approval for orlistat is pending a resolution of labeling issues and results of Phase III trials.)

However, due to rapidly evolving information regarding the use of pharmacotherapy for weight loss, the panel decided to present (below) their critique of those pharmacotherapy trials meeting their criteria for consideration.

Blood Pressure

To evaluate the effect of weight loss on blood pressure and hypertension, 76 articles reporting the results of RCTs were potentially eligible for inclusion. Sixty articles included lifestyle trials that studied diet and/or physical activity, and 16 articles were of pharmacotherapy trials. Dietary interventions included low-calorie diets and diets that promoted macronutrient composition changes, such as amount and type of dietary fat.

Physical activity, when included, was used to help promote increased energy expenditure.

These trials did not always control for other dietary factors that lower blood pressure, such as dietary salt, and the degree to which those taking the blood pressure measurements were blinded to the patient’s change in weight.

Of the 35 lifestyle RCT articles deemed acceptable, 16 included hypertensive patients, and 19 were conducted in individuals with normal or high-normal blood pressure.

Lifestyle Trials in Hypertensive Patients

Evidence Statement: Weight loss produced by lifestyle modifications reduces blood pressure in overweight hypertensive patients.

Evidence Category A. Rationale: A 1987 meta-analysis 381 covering five of the acceptable studies in hypertensive patients concluded that weight loss accomplished by dietary interventions significantly lowered blood pressure. In hypertensive patients, 10 kg (22 lb) of weight loss was associated with an average reduction of 7 mm Hg systolic and 3 mm Hg diastolic blood pressure compared with controls.

Since publication of this meta-analysis in 1987, almost all relevant studies have reported that weight loss reduces blood pressure or the need for medication in hypertensive patients:

The Trial of Antihypertensive Interventions and Management (TAIM), conducted in hypertensive individuals not taking medication for 6 months, reported that, compared with controls, a mean net weight reduction of 4.7 kg (10.4 lb) reduced systolic and diastolic blood pressure by 2.8 mm Hg and 2.5 mm Hg, respectively; the effects on blood pressure were equivalent to drug therapy among those participants who lost 4.5 kg (9.9 lb) or more.

One study in older (age 60 to 80 years) hypertensive adults whose blood pressure medication was withdrawn (Trial of Nonpharmacologic Interventions in the Elderly, TONE) showed that after 2 years, mean net weight loss of nearly 4 kg (9 lb) resulted in more participants free of trial endpoints (occurrence of high blood pressure, resumption of blood pressure medication, or occurrence of a cardiovascular-clinical complication [39.2 percent versus 26.2 percent]).

Furthermore, blood pressure control was similar for men and women and for African-Americans and whites.

In other studies of primarily middle-aged hypertensive adults, compared with controls, weight loss significantly reduced a return to hypertension medication at 1 year and at 4 to 5 years.

The Multiple Risk Factor Intervention Trial, which recruited 12,866 high-risk men, 30 percent of whom had hypertension, delivered an integrated intervention addressing several lifestyle behaviors and included weight loss as an important component. Significant reductions in systolic and diastolic blood pressure were found over 6 years compared with the usual care group and were directly related to weight loss: 1 kg (2.2 lb) of weight loss was associated with a reduction of 0.4 mm Hg systolic and 0.3 mm Hg diastolic blood pressure in men not taking antihypertensive medications. The effect was slightly lower for men taking antihypertensive medications.

Only one RCT conducted in hypertensive patients reported no significant change in blood pressure despite weight loss of 3.3 kg (7.3 lb).

Another study conducted in hypertensive individuals suggested that weight loss reduced blood pressure only when sodium intake was also reduced. This finding was not consistent with a prior study of hypertensive patients and has not been corroborated in subsequent larger trials conducted in nonhypertensive individuals.

Lifestyle Trials in Nonhypertensive Individuals

Evidence Statement: Weight loss produced by lifestyle modifications reduces blood pressure in overweight nonhypertensive individuals.

Evidence Category A. Rationale: A semi quantitative review covering four of the acceptable studies in nonhypertensive individuals concluded that weight loss through dietary interventions significantly lowered blood pressure. In nonhypertensives, excluding one outlier trial that showed very large reductions in blood pressure, 372 1 kg (2.2 lb) of weight loss was associated with a reduction of 0.45 mm Hg in both systolic and diastolic blood pressure. Since this review, published in 1991, almost all relevant studies have reported that weight loss reduces blood pressure in nonhypertensive individuals.

The Trials of Hypertension Prevention Phase 1 (TOHP I) and Phase 2 (TOHP II) are among the larger, well-designed randomized trials, having follow-up rates exceeding 90 percent. They followed the participants for 18 months and 3 to 4 years. The sample size of the weight loss intervention arms ranged from approximately 300 (TOHP I) to 600 (TOHP II). The populations were diverse, consisting of 30 to 35 percent women and 15 to 18 percent African-Americans, and were recruited from 10 centers in TOHP I and 9 centers in TOHP II. Results from both TOHP I and TOHP II demonstrated that weight loss reduced blood pressure and the incidence of hypertension. Compared with controls, in both trials 10 kg (22 lb) of weight loss was associated with a reduction of 7 mm Hg systolic and 5 to 6 mm Hg diastolic blood pressure at 18 months. At 36 months, systolic and diastolic blood pressure was reduced by 6 and 4 mmHg, respectively, for every 10 kg of weight loss.

In addition, weight loss reduced the incidence of hypertension at 18 months by 20 to 50 percent and at 3 years by 19 percent. Secondary analyses from TOHP I and analyses under way from TOHP II demonstrated that the greater the weight loss the greater the blood pressure reduction, and as long as weight loss was maintained, blood pressure remained reduced. One study that focused on older African-American diabetics showed that weight loss of 2.4 kg (5.3 lb) at 6 months resulted in a reduction of 3.9 and 4.0 mm Hg systolic and diastolic blood pressure. Only one study in nonhypertensive individuals showed inconsistent results, where weight reduction decreased systolic (significant) and diastolic (nonsignificant) blood pressure at 12 months in women but not in men. Another study showed short-term (3 months) blood pressure reduction but no longer-term (9 months) blood pressure reduction despite maintenance of weight loss of 9 kg (19.8 lb).

Pharmacotherapy Trials

Evidence Statement: Weight loss produced by most weight loss medications (except for sibutramine) and adjuvant lifestyle modifications is accompanied by reductions in blood pressure.

Evidence Category B. To determine the effects of pharmacological therapy on weight loss and subsequent changes in blood pressure levels, 10 RCT articles were examined. Weight loss studies using pharmacotherapy were conducted predominantly in white women and assumed that dietary changes were uniform in the active drug and placebo groups. All of these studies had a placebo-control group for which dietary recommendations for weight loss were provided; weight loss also occurred in the placebo group. No studies examined whether weight loss using pharmacotherapy results in blood pressure reductions similar to weight loss produced by diet therapy, nor were the results compared with a pure control group with no weight loss. In addition, none of the studies that examined the effect of pharmacotherapy on blood pressure controlled for weight loss. In general, the use of phentermine, fenfluramine, and dexfenfluramine resulted in similar or better weight loss than that seen in the control or placebo group, and reductions in systolic and diastolic blood pressure were concomitantly similar to or better than those observed in the diet plus placebo group. However, one study on dexfenfluramine showed increased blood pressure compared to controls, even though weight loss was greater with dexfenfluramine than with placebo. Another study showed blood pressure lowering consistent with weight reduction produced by dexfenfluramine in women with upper-body obesity, but not in women with lower-body obesity. In a combined summary of data on orlistat presented at he FDA Endocrinologic and Metabolic Drugs Advisory Committee Meeting (held in Bethesda, Maryland, in May 1997), only a small decrease in systolic (approximately 2 mm Hg) and diastolic (approximately 1 mm Hg) blood pressure was observed compared to the placebo. In a study of sibutramine, a net weight loss at 3 months of approximately 2 kg (4.4 lb) did not result in lower blood pressure compared with placebo controls. Eleven double-blind placebo-controlled trials lasting from 12 to 52 weeks showed that sibutramine is associated with mean increases in systolic blood pressure of 1 to 3 mm Hg, in diastolic pressure of 1 to 2 mm Hg, and mean increases in pulse rate of 3 to 5 beats per minute relative to placebo. In hypertensive obese patients, the mean change in blood pressure was the same in the sibutramine group and the placebo group; both dropped. Systolic pressure decreased 5.4 mm Hg in the sibutramine groupand 5.8 mm Hg in the placebo group, while the diastolic drop was 5.9 mm Hg and 3.7 mm Hg, respectively. At the FDA recommended doses, 45 percent of patients had an increase, 35 percent had a decrease, and 20 percent had no change in blood pressure.

 

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(36) Obesity

World Health Organization - OBESITY

How Fat Kills

Obesity36

What is the “normal”weight of a person? How is it determined?

The normal (perhaps a better term is “healthy”) weight for an individual is actually a function of age, gender, and height. Charts published by the U.S. Centers for Disease Control (CDC) represent the weights and heights for American children. Most of these charts show the healthy weight for a child, although some are actual measurements of weights of children in the United States and represent the “real” weights but not necessarily healthy weights.  A complete set of charts from the CDC is available at: http://www.cdc.gov/growthcharts

Online calculators are also available to do the math for you. This calculator will take your child’s gender, age, height, and weight and give you the percentile that he or she is now and what the “ideal” body weight should be: http://pediatrics.about.com/cs/growthcharts2/l/bl_ibw_calc.htm

The data in the charts are arranged by age and gender and are placed into “percentiles.” A percentile is the percentage of the population that weighs a given amount or less.

Many authorities feel that on the average, Americans are too heavy.

 If height matters, then how do you account for height in finding a normal or healthy weight?

Yes, height matters. The charts and calculator previously noted account for height. An easy way to find the healthy weight for your child has been developed and takes into account both weight and height. It is called the body mass index (BMI). The calculation is a bit complex. It is figured by taking the weight in kilograms (kg) divided by the height in meters squared (m2). This works easily in the metric system but is a little more complicated in the pounds/inches American system.

The formula is as follows:

BMI = 105X703/61X61=73,815/3,721=19.8

An easier way to find this is by using an already created calculator.  The BMI is not in and of itself a measure of fat in the body. Other, more complicated ways of doing that, including measuring skin-fold thickness, are available. Nonetheless, the BMI for most people is a very good tool for evaluating excess weight.

Terms:

Body mass index (BMI) - A number calculated from height and weight that is used to determine whether a person is in the “normal” weight, underweight, overweight, or obese range.

Fat - See also lipids. One gram of fat contains and produces nine calories of energy. As an adjective and colloquially, it refers to being overweight or obese.

I heard that waist circumference is important. What does it mean if my child has a large waist size?

Excessive abdominal (stomach, belly) fat has a worse health prognosis than fat distributed elsewhere on the body. A male with a waistline over 40 inches or a nonpregnant female with a waist of more than 35 inches is at a higher risk of developing such medical conditions as diabetes mellitus, elevated cholesterol and triglycerides, hypertension, and coronary artery (heart) disease.

Thus, it is not just the weight that matters, but also the weight distribution. Weight around the waist is worse than excess pounds in, say, the legs. Metabolic syndrome is a condition that is sometimes seen in adults. This is cluster of risk factors for heart disease and stroke and includes the following:

• Excess abdominal fat

• Abnormal blood lipids (fats), including high triglycerides, decreased high-density lipoprotein (HDL) cholesterol, and elevated low-density lipoprotein (LDL) cholesterol

• Insulin resistance/high blood sugar

• High blood pressure

• Elevated markers of inflammation such as blood C-reactive protein

The key problems with the metabolic syndrome are obesity and insulin resistance. It is estimated that 50 million people in the United States have this syndrome, which the American Heart Association defines as follows:

• Waistline: men ≥ 40 inches (102 cm) and women ≥ 35 inches (88 cm)

• Elevated triglycerides ≥ 150 mg/dL

• Reduced HDL (“good”) cholesterol: men < 40 mg/dL and women < 50 mg/dL

• High blood pressure ≥ 130/85 mm Hg

• Elevated fasting blood glucose ≥ 100 mg/dL

Key to treating this is prevention of obesity in children. After a person has this syndrome, the goals are to lose weight, treat the elevated blood pressure and sugar, increase exercise, and go on a diet low in saturated and trans fats and cholesterol.

Terms:

Diabetes mellitus - A complex disease of small blood vessels and glucose metabolism. It is manifested by elevated levels of sugar (glucose) in the blood. Long-term adverse consequences include kidney failure, cataracts, poor circulation leading to heart attacks, strokes, leg ulcers, and other serious problems.

Cholesterol - A fat (lipid) that is an essential part of the membranes of cells. It is made by the body as well as ingested with food. It is a steroid and is necessary for life, but an excess can produce atherosclerosis leading to vascular and other diseases including heart attacks and strokes.

Triglycerides - Lipids or fats composed of three molecules of fatty acid attached to one molecule of glycerol. Elevated levels have been associated with the development of serious medical diseases.

Hypertension - An elevation of the pressures in the heart and arteries, which can lead to severe disease including heart attacks and strokes. Also called high blood pressure.

Coronary artery (heart) disease - A disease of the arteries of the heart in which the deposition of plaque (cholesterol, calcium, and other compounds) progressively blocks the flow of blood to the heart, which can lead to chest pain (angina pectoris) and myocardial infarction (heart attack).

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