obesity

Definition

Obesity is an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight. Obesity is associated with increased risk of illness, disability, and death.

Description

Obesity traditionally has been defined as a weight at least 20% above the weight corresponding to the lowest death rate for individuals of a specific height, gender, and age (ideal weight). Twenty to forty percent over ideal weight is considered mildly obese; 40–100% over ideal weight is considered moderately obese; and 100% over ideal weight is considered severely, or morbidly, obese. More recent guidelines for obesity use a measurment called BMI (body mass index) which is the individual's weight multiplied by 703 and then divided by twice the height in inches. BMI of 25.9–29 is considered overweight; BMI over 30 is considered obese. Measurements and comparisons of waist and hip circumference can also provide some information regarding risk factors associated with weight. The higher the ratio, the greater the chance for weight-associated complications. Calipers can be used to measure skin-fold thickness to determine whether tissue is muscle (lean) or adipose tissue (fat).

Much concern has been generated about the increasing incidence of obesity among Americans. Some studies have noted an increase from 12% to 18% occurring between 1991 and 1998. Other studies have actually estimated that a full 50% of all Americans are overweight. The World Health Organization terms obesity a worldwide epidemic, and the diseases which can occur due to obesity are becoming increasingly prevalent.

Excessive weight can result in many serious, potentially life-threatening health problems, including hypertension, Type II diabetes mellitus (non-insulin dependent diabetes), increased risk for coronary disease, increased unexplained heart attack, hyperlipidemia, infertility, and a higher prevalence of colon, prostate, endometrial, and, possibly, breast cancer. Approximately 300, 000 deaths a year are attributed to obesity, prompting leaders in public health, such as former Surgeon General C. Everett Koop, M.D., to label obesity "the second leading cause of preventable deaths in the United States."

— Rosalyn Carson-DeWitt

For more information on obesity, visit Britannica.com.

The presence of excess body fat. The great prevalence of this condition, its severe consequences for physical and mental health, and the difficulty of treating it make the prevention of obesity a major public health priority.

Obesity is most often defined in terms of body weight relative to height, since both height and weight are easily measured. Obesity is considered to begin at a weight-for-height that is 20–30% above desirable weight, with this desirable weight taken as the midpoint of ranges of weight associated with the greatest longevity in studies of life-insured individuals. In population surveys, obesity is defined as a body weight that meets or exceeds the 85th percentile of the Body Mass Index (BMI), an index of weight-for-height that correlates well with body fat content. See also Adipose tissue.

The prevalence of obesity increases with age, is higher in women than men, and is highest among the poor and minority groups. Obesity increases the likelihood of high blood cholesterol, high blood pressure, and diabetes, and therefore of the diseases for which such conditions are risk factors—coronary heart disease, stroke, and kidney disease. It also increases the likelihood of gallbladder disease and cancers of the breast and uterus. Thus, obesity increases overall mortality rates, and it does so in proportion to the degree and duration of overweight. Individuals who become obese at the earliest ages are at highest risk of premature mortality. Distribution of excess fat to the upper body rather than the lower body may also increase risk.

The causes of most cases of obesity are poorly understood. At the simplest level, obesity results from an excess of energy (caloric) intake over expenditure, but this statement does not explain why some individuals can eat as much as they like without gaining weight while others remain overweight despite constant dieting. Studies of genetically obese animals and those with damage to the part of the brain called the hypothalamus suggest that individuals may balance body weight around a “setpoint” that is maintained—without conscious control—by variations in metabolic rate in response to caloric intake. Variations in the prevalence of obesity among population groups suggest a genetic basis for the condition. The complexity of body-weight regulatory mechanisms suggests that obesity is not due to a single cause but, like other chronic diseases, is multifactorial in origin. Specific inherited differences that might influence setpoints include differences in nearly every anatomic, neurologic, and biochemical factor known to affect food intake and utilization, energy metabolism, and energy expenditure. See also Energy metabolism; Metabolic disorders.

Because the causes of obesity are incompletely understood, it is difficult to formulate effective treatment strategies. Studies suggest that programs combining diet and exercise help obese individuals lose more weight and maintain losses longer than either program does separately. See also Food; Nutrition.

Obesity is most commonly defined as a condition of weighing at least 20% over ideal body weight, where ideal body weight is determined in the US by the 1959 or 1983 Metropolitan Life Insurance Company Tables. Like many aspects of obesity, use of life insurance tables as the sole indicator remains controversial. These insurance charts do not take into account the changes in ideal weight with age or provide information on body fat distribution; nor do they base measurements on all ethnic groups and those of the lower socioeconomic classes. To counter such biases, obesity can be determined by body mass index (which relates weight to height) and the percentage of body fat.

The causes of obesity continue to be debated and studied. Though it has long been considered the simple result of too little exercise and too much eating, new research suggests there may also be some hereditary influence, and particularly that the genetic tendency for obesity may be correlated to the mother's weight. Relatively unusual causes include adult-onset diabetes, deficient thyroid hormone secretion, and, very rarely, tumours of the adrenal gland, pancreas, or pituitary gland. Unexplained abnormal function of the brain's appetite control centre may also play a role. Researchers are particularly concerned about the increasing number of children and adolescents who are overweight in the US and Europe.

Obesity may cause a variety of health complications. Most clearly, overweight has an adverse effect on life expectancy. In general, the greater the degree of overweight, the higher the mortality or excess death rate. Obesity may be associated with elevated blood cholesterol, and has been linked to hypertension, diabetes, cancer, coronary artery heart disease, degenerative arthritis, gall stones, sleep disorders, and depression.

For many the ‘psychological burden’ of being obese in Western cultures, which prize slenderness, particularly in women, is an additional adverse effect. Prior to the nineteenth century, overweight and fatness stood as a sign of health and prosperity, and conveyed social esteem. By the mid and late nineteenth century, a new ethos emerged which championed slenderness as a sign of both beauty and physical health. By the early twentieth century, on the other hand, obesity became associated with laziness, gluttony, and the lower classes. As Keith Walden has written, ‘females who stayed slim demonstrated that they had the money and sense to buy nutritious foods and eat balanced meals, and that they had the time to exercise. They did not have menial jobs which required substantial brawn to perform.’ In twenty-first-century Western culture, especially for whites, and the middle and upper classes, the abhorrence of fat and obesity continues. As Anne Beller describes it, fat is suicidal: a sin at best and at worst a sort of felony. Yet for many African Americans and Hispanics, as well as other ethnic groups, a larger body still holds positive social value.

Suggested treatments for obesity range from a plethora of rarely successful fad diets to medical procedures such as stapling the stomach to reduce intake or shortening the intestines to curtail absorption. The most tried and true method remains adjustment of the energy balance — decreasing caloric intake while increasing energy usage. Vigorous exercise not only ‘burns’ nutrient stores but is also shown in some situations to increase metabolic rate for up to 15 hours after activity. Those with a hereditary tendency toward obesity find it more difficult to lose weight, due to a lower resting metabolic rate and possible complications in appetite regulation. In this regard, and in evolutionary terms, a tendency toward obesity can actually have survival value — a lower metabolic rate and a substantial fat store would allow one to live longer in times of famine. But in the contemporary West, where food is relatively plentiful and slenderness highly prized, it works to one's disadvantage.

— Margaret A. Lowe

Bibliography

• Beller, A. S. Fat and thin: a natural history of obesity. Farrar, Straus and Giroux, New York.
• Walden, K. (1985). The road to Fat City: an interpretation of the development of weight consciousness in Western society. Historical reflections, 12, 331-73

See also body composition; dieting; energy balance; weight.

Excessive accumulation of body fat. A body mass index above 30 is considered to be obesity (and above 40 gross obesity). The desirable range of BMI for optimum life expectancy is 20-25; between 25 and 30 is considered to be overweight rather than obesity. People more than 50% above desirable weight are twice as likely to die prematurely as those within the desirable weight range.

Obesity is due to the excessive storage of fat in the body, particularly under the skin and around certain internal organs. In 1985, 34 million Americans were obese. Of British adults surveyed in 1991, 13 per cent of men and 15 per cent of women were obese; double the percentage of people who were obese in 1981. A 1995 survey indicates that these figures are continuing to rise. Obesity can be caused by diseases, such as certain cancers, gall-bladder diseases, and hormonal imbalances, but these causes are rare. Many obese people suggest that their condition is due to underactive thyroid glands, but this accounts for less than one in a thousand cases. Most obesity results from eating too much and not exercising enough. This results in a positive energy balance, more energy is consumed than expended. For every 3500 Calories consumed above requirements, approximately one pound of fat is stored in the body.

Obesity is difficult to define quantitatively without knowing how much fat is normal for a given person. Nevertheless, it is generally agreed that the proportion of fat in the body should not exceed 20-25 per cent in men and 28-30 per cent in women. Many medical authorities use body mass as an indicator (see body mass index); people with a body mass index exceeding 30 are considered obese. However, obesity is not the same as being overweight. A very muscular person may be heavy but still have a very low fat content. Heavy body-builders often have less than 10 per cent body fat. There are two main types of obesity: childhood onset obesity and adult onset obesity.

Childhood onset obesity may develop because of hormonal imbalances or some other illness, but it is usually caused by overeating when young. This results in the production of an abnormally high number of adipocytes, cells specialized for fat storage. Adults who were obese as children tend to retain a high number of adipocytes, even if they are thin and have a low fat diet. The high number of adipocytes means that a large storage space is always available for fat. Thus adults who suffered childhood onset obesity are generally predisposed to obesity.

Adult onset obesity occurs when a person becomes obese for the first time after reaching adulthood. He or she usually has a normal number of adipocytes but each one is enlarged with fat. Slimming leads to the fat cells returning to normal size. Adults who have suffered adult onset obesity usually find it much easier to control their weight than adults who were obese as children.

Obesity is a major health hazard. Obese people are predisposed to a number of diseases, including diabetes, high blood pressure, and cardiovascular diseases. Some medical experts suggest that life expectancy decreases by approximately 1 per cent for each pound of excess fat carried by an individual between the ages of 45 and 50.

A bodily condition marked by excessive generalized deposition and storage of fat.

Definition

Obesity is an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight. Obesity is associated with increased risk of illness, disability, and death.

The branch of medicine that deals with the study and treatment of obesity is known as bariatrics. As obesity has become a major health problem in the United States, bariatrics has become a separate medical and surgical specialty.

Description

Obesity traditionally has been defined as body weight at least 20% above the weight corresponding to the lowest death rate for individuals of a specific height, sex, and age (designated as the ideal weight). Twenty to forty percent over ideal weight is considered mildly obese; 40–100% over ideal weight is considered moderately obese; and 100% over ideal weight is considered severely, or morbidly, obese. According to some estimates, approximately 25% of the United States population can be considered obese, 4 million of whom are morbidly obese. Other studies state that over 50% of American adults are obese, based on body mass index (BMI) measurements. Excessive weight can result in many serious, and potentially deadly, health problems, including hypertension, Type II diabetes mellitus (non-insulin dependent diabetes), increased risk for coronary disease, increased unexplained heart attack, hyperlipidemia, infertility, and a higher prevalence of colon, prostate, endometrial, and possibly, breast cancer. Approximately 300,000 deaths a year are attributed to obesity, prompting leaders in public health, such as former Surgeon General C. Everett Koop to label obesity "the second leading cause of preventable deaths in the United States."

Causes & Symptoms

The mechanism for excessive weight gain is clear—more calories are consumed than the body burns, and the excess calories are stored as fat (adipose) tissue. However, the exact cause is not as clear and likely arises from a complex combination of factors. Genetic factors significantly influence how the body regulates appetite and the rate at which it turns food into energy (metabolic rate). Studies of adoptees confirm this relationship. The majority of adoptees followed a pattern of weight gain that more closely resembled that of their birth parents than their adoptive parents. A genetic predisposition to weight gain, however, does not automatically mean that a person will be obese. Eating habits and patterns of physical activity also play a significant role in the amount of weight a person gains.

Some recent studies have indicated that the amount of fat in a person's diet may have a greater impact on weight than the number of calories the food contains. Carbohydrates like cereals, breads, fruits and vegetables, and protein (fish, lean meat, turkey breast, skim milk) are converted to fuel almost as soon as they are consumed. Most fat calories are immediately stored in fat cells, which add to the body's weight and girth as they expand and multiply. There is continuing research on the theory that fat is metabolized as fuel and energy and that only excess carbohydrates are converted to stored fat. Current evidence shows that weight gain comes mostly from total calories consumed, rather than from the amount of carbohydrates. A study published in 2002 found that low-fat diets are no more effective in weight reduction programs than low-calorie diets. At any rate, a sedentary life-style, particularly prevalent in affluent societies like the United States, can contribute to weight gain. Psychological factors, such as depression and low self-esteem may, in some cases, also play a role in weight gain.

At what stage of life a person becomes obese can effect his or her ability to lose weight. In childhood, excess calories are converted into new fat cells (hyperplastic obesity), while excess calories consumed in adulthood only serve to expand existing fat cells (hypertrophic obesity). Since dieting and exercise can only reduce the size of fat cells, not eliminate them, persons who were obese as children can have great difficulty losing weight, since they may have up to five times as many fat cells as someone who became overweight as an adult.

Obesity can also be a side effect of certain disorders and conditions, including:

• Cushing's syndrome, a disorder involving the excessive release of the hormone cortisol

• hypothyroidism, a condition caused by an underactive thyroid gland
• neurologic disturbances, such as damage to the hypothalamus, a structure located deep within the brain that helps regulate appetite
• consumption of certain drugs, such as steroids, antipsychotic medications, or antidepressants

The major symptoms of obesity are excessive weight gain and the presence of large amounts of fatty tissue. Obesity can also give rise to several secondary conditions, including:

• arthritis and other orthopedic problems, such as lower back pain
• heartburn
• high cholesterol levels
• high blood pressure
• menstrual irregularities or cessation of menstruation (amenorhhea)
• shortness of breath that can be incapacitating
• skin disorders, arising from the bacterial breakdown of sweat and cellular material in thick folds of skin or from increased friction between folds

Diagnosis

Dignosis of obesity is made by observation and by comparing the patient's weight to ideal weight charts. Many doctors and obesity researchers refer to the body mass index (BMI), which uses a height-weight relationship to calculate an individual's ideal weight and personal risk of developing obesity-related health problems. Physicians may also obtain direct measurements of an individual's body fat content by using calipers to measure skin-fold thickness at the back of the upper arm and other sites. The most accurate means of measuring body fat content involves immersing a person in water and measuring relative displacement; however, this method is very impractical and is usually only used in scientific studies requiring very specific assessments. Women whose body fat exceeds 30% and men whose body fat exceeds 25% are generally considered obese.

Doctors may also note how a person carries excess weight on his or her body. Studies have shown that this factor may indicate whether or not an individual has a predisposition to develop certain diseases or conditions that may accompany obesity. "Apple-shaped" individuals who store most of their weight around the waist and abdomen are at greater risk for cancer, heart disease, stroke, and diabetes than "pear-shaped" people whose extra pounds settle primarily in their hips and thighs.

Treatment

Treatment of obesity depends primarily on the degree of a person's overweight and his or her overall health. However, to be successful, any treatment must affect life-long behavioral changes rather than short-term weight loss. "Yo-yo" dieting, in which weight is repeatedly lost and regained, has been shown to increase a person's likelihood of developing fatal health problems than if the weight had been lost gradually or not lost at all. Behavior-focused treatment should concentrate on:

• What a person eats and how much. This aspect may involve keeping a food diary and developing a better understanding of the nutritional value and fat content of foods. It may also involve changing grocery shopping habits (e.g. buying only what is on a prepared list and going only on a certain day), timing of meals (to prevent feelings of hunger, a person may plan frequent small meals), and actually slowing down the rate at which a person eats.
• How a person responds to food. This may involve understanding what psychological issues underlie a person's eating habits. For example, one person may binge eat when under stress, while another may always use food as a reward. In recognizing these psychological triggers, an individual can develop alternate coping mechanisms that do not focus on food.
• How people spend their time. Making activity and exercise an integral part of everyday life is a key to achieving and maintaining weight loss. Starting slowly and building endurance keeps individuals from becoming discouraged. Varying routines and trying new activities also keeps interest high.

For most who are mildly obese, these behavior modifications entail lifestyle changes they can make independently while being supervised by a family physician. Other mildly obese persons may seek the help of a commercial weight loss program (e.g. Weight Watchers). The effectiveness of these programs is difficult to assess, since programs vary widely, dropout rates are high, and few employ members of the medical community. However, programs that emphasize realistic goals, gradual progress, sensible eating, and exercise can be very helpful and are recommended by many doctors. Programs that promise instant weight loss or feature severely restricted diets are not effective and, in some cases, can be dangerous.

For individuals who are moderately obese, medically supervised behavior modification and weight loss are required. While doctors will put most moderately obese patients on a balanced low-calorie diet (1200–1500 calories a day), they may recommend that certain individuals follow a very low-calorie liquid protein diet (400–700 calories) for as long as three months. This therapy, however, should not be confused with commercial liquid-protein diets or commercial weight-loss shakes and drinks. Doctors tailor these diets to specific patients, monitor patients carefully, and use them for only a short period of time. In addition to reducing the amount and type of calories consumed by the patient, doctors will recommend professional therapists or psychiatrists who can help the individual effectively change his or her behavior in regard to eating.

The Chinese herb ephedra (Ephedra sinica, or ma huang), combined with exercise and a low-fat diet in physician-supervised weight-loss programs, can cause at least a temporary increase in weight loss. However, the large doses of ephedra required to achieve the desired result can also cause:

• anxiety
• heart arrhythmias
• heart attack
• high blood pressure
• insomnia
• irritability
• nervousness
• seizures
• strokes
• death

Ephedra should not be used by anyone with a history of diabetes, heart disease, or thyroid problems. It is not recommended for long-term use, and can cause serious medical or psychiatric problems if used too long. An article that appeared in the Journal of the American Medical Association in early 2003 advised against the use of ephedra.

Diuretic herbs, which increase urine production, can cause short-term weight loss but cannot help patients achieve lasting weight control. The body responds to heightened urine output by increasing thirst to replace lost fluids, and patients who use diuretics for an extended period of time eventually start retaining water again anyway. In moderate doses, psyllium, a mucilaginous herb available in bulk-forming laxatives like Metamucil, absorbs fluid and makes patients feel as if they have eaten enough. Red peppers and mustard help patients lose weight more quickly by accelerating the metabolic rate. They also make people more thirsty, so they crave water instead of food. Walnuts contain serotonin, the brain chemical that tells the body it has eaten enough. Dandelion (Taraxacum officinale) can raise metabolism and counter a desire for sugary foods.

The amino acid 5-hydroxytryptophan, or 5-HTP, which is extracted from the seeds of the Griffonia simplicifolia plant, is thought to increase serotonin levels in the brain. Serotonin is a neurotransmitter, or brain chemical, that regulates mood and thus can be linked to mood-related eating behaviors. When physical and mental stress reduces serotonin levels in the body, 5-HTP may be helpful in regulating mood by boosting serotonin levels. Individuals should consult with their healthcare professional before taking 5-HTP, as the amino acid may interact with other medications and can have potentially serious side effects.

Acupressure and acupuncture can also suppress food cravings. Visualization and meditation can create and reinforce a positive self-image that enhances the patient's determination to lose weight. By improving physical strength, mental concentration, and emotional serenity, yoga can provide the same benefits. Also, patients who play soft, slow music during meals often find that they eat less food but enjoy it more.

Eating the correct ratio of protein, carbohydrates, and good-quality fats can help in weight loss via enhancement of metabolism. Support groups and self-help groups such as Overeaters Anonymous and TOPS (Taking Off Pounds Sensibly) that are informed about healthy, nutritious, and balanced diets can offer an individual the support he or she needs to maintain this type of eating regimen.

Allopathic Treatment

For individuals who are severely obese, dietary changes and behavior modification may be accompanied by surgery to reduce or bypass portions of the stomach or small intestine. The risks of obesity surgery have declined in recent years, but it is still only performed on patients for whom other strategies have failed and whose obesity seriously threatens their health. Other surgical procedures are not recommended, including liposuction, a purely cosmetic procedure in which a suction device is used to remove fat from beneath the skin, and jaw wiring, which can damage gums and teeth and cause painful muscle spasms.

A newer approach to weight loss is the development of functional foods, which are food products that incorporate natural compounds shown to help in weight loss programs. These compounds include carbohydrates with a low glycemic index, which help to suppress appetite; green tea extract, which increases the body's energy expenditure; and chromium, which encourages the body to burn stored fat rather than lean muscle tissue. Functional food products are currently undergoing clinical testing.

Appetite suppressant drugs are sometimes prescribed to aid in weight loss. These drugs work by increasing levels of serotonin or catecholamine, which are brain chemicals that control moods and feelings of fullness. Appetite suppressants, though, are not considered truly effective, since most of the weight lost while taking them is usually regained after stopping. Also, suppressants containing amphetamines can be potentially abused by patients. While most of the immediate side effects of these drugs are harmless, the long-term effects in many cases, are unknown. Two drugs, dexfenfluramine hydrochloride (Redux) and fenfluramine (Pondimin) as well as a combination fenfluramine-phentermine (Fen/Phen) drug, were taken off the market when they were shown to cause potentially fatal heart defects. In 1999, the United States Food and Drug Administration (FDA) approved a new prescription weight loss drug, Orlistat. Unlike other anti-obesity drugs that act as appetite suppressants, Orlistat encourages weight loss by inhibiting the body's ability to absorb dietary fat. The drug can cause side effects of abdominal cramping, gas, and diarrhea.

Other weight-loss medications available with a doctor's prescription include:

• Sibutramine (Meridia)
• Diethylpropion (Tenuate, Tenuate Dospan)
• Mazindol (Mazanor, Sanorex)
• Phendimetrazine (Bontril, Prelu-2)
• Phentermine (Adipex-P, Fastin, Ionamin, Oby-Cap)

Phenylpropanolamine (Acutrim, Dextarim) is the only nonprescription weight-loss drug approved by the FDA. These over-the-counter diet aids can boost weight loss by 5%. Combined with diet and exercise and used only with a doctor's approval, prescription anti-obesity medications enable some patients to lose 10% more weight than they otherwise would. Most patients regain lost weight after discontinuing use of either prescription medications or nonprescription weight-loss products.

Prescription medications or over-the-counter weight loss products can cause:

• constipation
• dry mouth
• headache
• irritability
• nausea
• nervousness
• sweating

None of the weight loss drugs should be used by patients taking monoamine oxidate inhibitors (MAO inhibitors).

Doctors sometimes prescribe fluoxetine (Prozac), an antidepressant that can increase weight loss by about 10%. Weight loss may be temporary and side effects of this medication include diarrhea, fatigue, insomnia, nausea, and thirst. Weight loss drugs currently being developed or tested include ones that can prevent fat absorption or digestion, reduce the desire for food and prompt the body to burn calories more quickly, and regulate the activity of substances that control eating habits and stimulate overeating.

Expected Results

As many as 85% of dieters who do not exercise on a regular basis regain their lost weight within two years. In five years, the figure rises to 90%. Repeatedly losing and regaining weight (yo-yo dieting) encourages the body to store fat and may increase a patient's risk of developing heart disease. The primary factor in achieving and maintaining weight loss is a lifelong commitment to regular exercise and sensible eating habits.

Prevention

Obesity experts suggest that a key to preventing excess weight gain is monitoring fat consumption rather than counting calories, and the National Cholesterol Education Program maintains that only 30% of calories should be derived from fat. Only one-third of those calories should be contained in saturated fats (the kind of fat found in high concentrations in meat, poultry, and dairy products). Because most people eat more than they think they do, keeping a detailed food diary is a useful way to assess eating habits. Eating three balanced, moderate-portion meals a day—with the main meal at mid-day—is a more effective way to prevent obesity than fasting or crash diets. Exercise increases the metabolic rate by creating muscle, which burns more calories than fat. When regular exercise is combined with regular, healthful meals, calories continue to burn at an accelerated rate for several hours. Finally, encouraging healthful habits in children is a key to preventing childhood obesity and the health problems that follow in adulthood.

New Directions in Obesity Treatment

The rapid rise in the incidence of obesity in the United States since 1990 has prompted researchers to look for new treatments. One approach involves the application of antidiabetes drugs to the treatment of obesity. Metformin (Glucophage), a drug that was approved by the Food and Dug Administration (FDA) in 1994 for the treatment of type 2 diabetes, shows promise in treating obesity associated with insulin resistance.

Another field of obesity research is the study of hormones, particularly leptin, which is produced by fat cells in the body, and ghrelin, which is secreted by cells in the lining of the stomach. Both hormones are known to affect appetite and the body's energy balance. Leptin is also related to reproductive function, while ghrelin stimulates the pituitary gland to release growth hormone. Further studies of these two hormones may lead to the development of new medications to control appetite and food intake.

A third approach to obesity treatment involves research into the social factors that encourage or reinforce weight gain in humans. Researchers are looking at such issues as the advertising and marketing of food products; media stereotypes of obesity; the development of eating disorders in adolescents and adults; and similar questions.

Resources

Books

Ackerman, Norman. 5-HTP: The Natural Way to Overcome Depression, Obesity, and Insomnia. New York: Bantam Books, 1999.

Flancbaum, Louis, MD, with Erica Manfred and Deborah Biskin. The Doctor's Guide to Weight Loss Surgery. West Hurley, NY: Fredonia Communications, 2001.

Harris, Dan R., ed. Diet and Nutrition Sourcebook. Detroit, MI: Omnigraphics, 1996.

"Nutritional Disorders: Obesity." Section 1, Chapter 5 in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers, MD, and Robert Berkow, MD. Whitehouse Station, NJ: Merck Research Laboratories, 1999.

Periodicals

Aronne, L. J., and K. R. Segal. "Weight Gain in the Treatment of Mood Disorders." Journal of Clinical Psychiatry 64 (2003 Supplement 8): 22–29.

Bell, S. J., and G. K. Goodrick. "A Functional Food Product for the Management of Weight." Critical Reviews in Food Science and Nutrition 42 (March 2002): 163–178.

Brudnak, M. A. "Weight-Loss Drugs and Supplements: Are There Safer Alternatives?" Medical Hypotheses 58 (January 2002): 28–33.

Colquitt, J., A. Clegg, M. Sidhu, and P. Royle. "Surgery for Morbid Obesity." Cochrane Database Systems Review 2003: CD003641.

Espelund, U., T. K. Hansen, H. Orskov, and J. Frystyk. "Assessment of Ghrelin." APMIS Supplementum 109 (2003): 140–145.

Hundal, R. S., and S. E. Inzucchi. "Metformin: New Understandings, New Uses." Drugs 63 (2003): 1879–1894.

Pirozzo, S., C. Summerbell, C. Cameron, and P. Glasziou. "Advice on Low-Fat Diets for Obesity (Cochrane Review)." Cochrane Database Systems Review 2002: CD003640.

Schurgin, S., and R. D. Siegel. "Pharmacotherapy of Obesity: An Update." Nutrition in Clinical Care 6 (January-April 2003): 27–37.

Shekelle, P. G., M. L. Hardy, S. C. Morton, et al. "Efficacy and Safety of Ephedra and Ephedrine for Weight Loss and Athletic Performance: A Meta-Analysis." Journal of the American Medical Association 289 (March 26, 2003): 1537–1545.

Tataranni, P. A. "Treatment of Obesity: Should We Target the Individual or Society?" Current Pharmaceutical Design 9 (2003): 1151–1163.

Veniant, M. M., and C. P. LeBel. "Leptin: From Animals to Humans." Current Pharmaceutical Design 9 (2003): 811–818.

Organizations

American Dietetic Association. (800) 877-1600. .

American Obesity Association (AOA). 1250 24th Street NW, Suite 300, Washington, DC 20037. (202) 776-7711 or (800) 98-OBESE. .

American Society of Bariatric Physicians. 5453 East Evans Place, Denver, CO 80222-5234. (303) 770-2526. .

American Society for Bariatric Surgery. 7328 West University Avenue, Suite F, Gainesville, FL 32607. (352) 331-4900. .

North American Association for the Study of Obesity. 8630 Fenton St., Suite 412, Silver Spring, MD, 20910. (301) 563-6526. .

Overeaters Anonymous. P.O. Box 44020, Rio Rancho, New Mexico, 87174-4020. (505) 891-2664. .

Weight-control Information Network (WIN). 1 WIN Way, Bethesda, MD 20892-3665. (202) 828-1025 or (877) 946-4627.

[Article by: Paula Ford-Martin; Rebecca J. Frey, PhD]

Definition

Obesity is an abnormal accumulation of body fat, usually 20 percent or more over an individual's ideal body weight. Obesity is associated with increased risk of illness, disability, and death.

The branch of medicine that deals with the study and treatment of obesity is known as bariatrics. As obesity has become a major health problem in the United States, bariatrics has become a separate medical and surgical specialty.

Description

Childhood obesity is in the early 2000s a significant health problem in the United States. Obese children and adolescents are at increased risk for developing diabetes, hypertension, coronary artery disease, sleep apnea, orthopedic problems, and psychosocial disorders.

Obesity involves excessive weight gain and fat accumulation. For children and adolescents, obesity is defined in terms of body mass index (BMI) percentile. BMI is a formula that considers an individual's height and weight to determine body fat and health risk, and it is used differently for children and adolescents than it is for adults. In adults, BMI often misrepresents obesity because it does not consider healthy weight from muscle tissue; therefore, body fat percentage is considered a more accurate method for determining obesity in adults. In children and adolescents, because body fat changes as they mature, BMI is gender- and age-specific and plotted on gender-specific growth charts to determine BMI-forage. Curved lines on the chart (percentiles) are used by healthcare professionals to identify children and adolescents at risk for overweight and obesity. Children and adolescents with a BMI-for-age in the 85th to 95th percentile are considered overweight and at risk for obesity, and those with a BMI-for-age greater than the 95th percentile are considered obese.

Demographics

According to the American Obesity Association and the Centers for Disease Control and Prevention, 30.3 percent of children aged six to 11 years are overweight and 15.3 percent are obese, and 30.4 percent of adolescents aged 12 to 19 years are overweight and 15.5 percent are obese. From 1980 to 2004, the prevalence of obesity among children quadrupled, and the prevalence of obesity in adolescents more than doubled. Overweight and obesity is more prevalent in boys (32.7%) than girls (27.8%). Obesity is more common in African American, Hispanic American, and Native American children and adolescents, than among Caucasians of the same ages.

Causes and Symptoms

Although obesity can be a side effect of certain hormonal disorders or use of certain medications, the primary cause of obesity in children and adolescents is excess calorie consumption coupled with a sedentary lifestyle. Children and adolescents living in the twenty-first century are the most inactive generation ever. The majority of schools no longer offer daily physical education classes; and active leisure activities, such as bicycle riding, have been replaced by sedentary activities, such as television watching and playing computer games. Studies have documented dramatic changes in childhood food consumption from the 1970s to 2004. Fast foods and foods eaten at other restaurants have increased by 300 percent since 1977, and soft drink consumption has also increased significantly. In addition, standard meal portion sizes and snacking have increased.

Obesity is the result of a complex interaction of genetics and environmental factors. Genetics influence how the body regulates appetite and metabolism, while certain environmental factors encourage excess calorie consumption. The body requires a certain amount of energy for basic metabolism and to support additional physical activity. When calories consumed from food and beverages equal calories expended during physical activity, body weight is maintained. When calories consumed exceed calories expended, weight gain results. To gain one pound, 3,500 additional calories must be consumed. In American society, excess calories are easily consumed just by drinking soft drinks and eating "supersized" fast food meals. A sedentary lifestyle results in far fewer calories being burned daily.

The major symptoms of obesity are excessive weight gain and the presence of large amounts of fatty tissue. Obesity can cause a number of other conditions, including type 2 diabetes, hypertension, high cholesterol, joint pain, asthma, hypothyroidism, and gallstones. Type 2 diabetes, previously referred to as adult-onset diabetes, has increased dramatically in children, and this increase has been directly linked to obesity.

When to Call the Doctor

Overweight and obese children should be evaluated by a physician for diabetes, hypertension, high cholesterol, and other medical conditions that are influenced by excessive weight gain. Primary care physicians can be consulted for weight management counseling to help children lose weight.

Diagnosis

Obesity in children and adolescents is diagnosed using the BMI-for-age formula described above, which is used to define obesity. Comorbid conditions, such as diabetes and high cholesterol, are diagnosed using medical laboratory tests.

Treatment

As of 2004, no weight loss drugs were approved for use in children, although some drugs used to treat obesity are approved for use in adolescents age 16 years and older. A few drugs are under investigation for use in children. Although no drugs are specifically approved for pediatric weight loss, some physicians may prescribe them "off-label." Because the side effects of these medications in children are unknown, children should not use adult weight loss drugs.

For extremely obese adolescents, surgical procedures—called bariatric surgery—may be performed, but only rarely. These procedures involve significant surgical alteration of the digestive tract and require substantial modification of diet after the surgery to much less than 1,000 calories per day. The long-term effects on growth and development from severe postoperative calorie restriction are not unknown, and weight loss surgery should only be performed on adolescents as a last resort.

The most effective treatment for obese children and adolescents is behavior and lifestyle modification under the guidance of a physician or weight management specialist experienced in dealing with children and adolescents. Behavior and lifestyle modification involves the following:

• assessment of child's and family's eating habits
• implementation of a regular, safe exercise program and increasing active leisure activities
• limiting television viewing and other sedentary activities
• setting reasonable goals and monitoring goal achievement using positive, non-food-related incentives
• counseling regarding how to keep a food/activity diary to track progress
• extensive support by involving entire family and/or joining a weight loss group of peers

Alternative Treatment

Alternatives for weight loss involve the use of ephedra-containing drugs or herbal preparation or the use of diuretics and laxatives. Both of these practices are unsafe, especially for children and adolescents. Because ephedra can cause severe cardiac side effects, the Food and Drug Administration has issued warnings against its use. Diuretics and laxatives can result in severe dehydration and improper absorption of nutrients.

Acupressure and acupuncture can suppress food cravings. Visualization and meditation can create and reinforce a positive self-image that enhances the patient's determination to lose weight. By improving physical strength, mental concentration, and emotional serenity, yoga can provide the same benefits.

Given the drastic increase in childhood obesity, special summer programs and therapeutic schools have been formed to help children lose weight. Summer camp programs that focus on healthy eating and exercise habits are available for overweight and obese children. In addition, in early 2004, the first alternative school for overweight and obese children, which operates like other private and charter schools, but with a focus on healthy weight loss and maintenance, was established.

Prognosis

Obese and overweight children and adolescents are more likely to be obese or overweight as adults. According to the American Obesity Association, obese children aged 10 to 13 have a 70 percent chance of remaining obese for the rest of their lives. Obese individuals are at increased risk for many other diseases and early death. Behavior and lifestyle modification programs involving positive goal-setting, increased exercise, and group support can help children and adolescents successfully and safely lose weight.

Prevention

Obesity can be prevented by instilling healthy eating and regular exercise habits in children at an early age. Minimizing and structuring daily time for sedentary activities like television viewing and encouraging outdoor activities such as bicycle riding, walking, running, and active play, and active indoor activities such as dancing can help increase physical activity. Dietary modifications to help prevent obesity include limiting soft drink and fast food consumption, monitoring food portion sizes, and providing a well-balanced diet.

Nutritional Concerns

Nutrition is a primary factor for weight management of obese children and adolescents. Poor nutrition and dietary habits can lead to weight gain and obesity. Dietary modification is important for helping children lose weight and prevent obesity.

The following nutritional guidelines can help in the management of obesity:

• Limit soft drink consumption to one per day or less. One 12-ounce can of soda has 120 calories or more. Often, children and adolescents consume "super-size" sodas that may contain up to 1,000 calories.
• Limit fast food restaurant visits to one per week, and choose healthy options like grilled chicken and smaller sized portions of high-calorie items.
• Monitor food serving sizes.
• Increase consumption of fruits, vegetables, high-fiber foods, and whole-grain foods.
• Be aware that "low-fat" foods often substitute sugar for fat, and calories may actually be the same as the regular or high-fat version.

Parental Concerns

Parents of obese children and adolescents should be concerned for their current and future health, since obesity can result in diabetes, hypertension, and coronary artery disease. Losing weight can be very difficult for obese children, and parental support is essential for success. Because children model behavior after their parents, obesity often affects both parents and children. Parents should strive to have healthy eating habits and exercise regularly to be effective role models for their children. Making healthy eating and exercise a family priority is better for everyone and helps reinforce positive changes in behavior for the obese child.

Obese children and adolescents are more susceptible to eating disorders, negative self-esteem and body image, and depression due to peer influences. Counseling, peer group therapy, and family therapy may be required to support lifestyle modifications for obese children and adolescents.

Resources

Books

Burniat, Walter, et al. Child and Adolescent Obesity: Causes and Consequences, Prevention and Management. Cambridge, UK: Cambridge University Press, 2002.

Kiess, Wieland, et al. Obesity in Childhood and Adolescence. Basel, Switzerland: S. Karger AG, 2004.

Periodicals

Eissa, M. A. H., and K. B. Gunner. "Evaluation and Management of Obesity in Children and Adolescents." Journal of Pediatric Health Care 18(March 2004): 35–38.

Manson J. E., et al. "The Escalating Pandemics of Obesity and Sedentary Lifestyle." Archives of Internal Medicine 164(February 9, 2004): 249–258.

McWhorter, J. W., et al. "The Obese Child: Motivation as a Tool for Exercise." Journal of Pediatric Health Care 17(February 2003): 11–17.

Ritter, J. "Obese Teens Turn to Surgery of Last Resort." Chicago Sun-Times, March 29, 2004.

St-Onge M. P., et al. "Changes in Childhood Food Consumption Patterns: A Cause for Concern in Light of Increasing Body Weights." American Journal of Clinical Nutrition 78(December 2003): 1068–73.

Organizations

American Dietetic Association. Web site: www.eatright.org.

American Obesity Association (AOA). 1250 24th Street NW, Suite 300, Washington, DC 20037. Web site: www.obesity.org.

American Society of Bariatric Physicians. 5453 East Evans Place, Denver, CO 80222–5234. Web site: www.asbp.org.

American Society for Bariatric Surgery. 7328 West University Avenue, Suite F, Gainesville, FL 32607. Web site: www.asbs.org.

National Institute of Diabetes and Digestive and KidneyDiseases. 31 Center Drive, USC2560, Building 31, Room 9A-04, Bethesda, MD 20892–2560. Web site: www.niddk.nih/gov.

Shape Up America! Web site: www.shapeup.org/.

Web Sites

"BMI for Children and Teens." Centers for Disease Control and Prevention, 2004. Available online at www.cdc.gov/nccdphp/dnpa/bmi/bmi-for-age.htm (accessed October 26, 2004).

"Fitness for Your Child." IDEA Health and Fitness Association. Available online at www.ideafit.com/articles/fitness_child.asp (accessed October 26, 2004).

"Obesity in Youth." American Obesity Association. Available online at www.obesity.org/subs/fastfacts/obesity_youth.shtml (accessed October 26, 2004)

Other

Childhood Assessment Calculator. Available online at www.shapeup.org/oap/entry.php (accessed October 26, 2004).

[Article by: Jennifer E. Sisk, MA]

The storage of excessive amounts of fat, particularly under the skin and around certain internal organs. Obesity usually results from a positive energy balance and not having a balanced diet. Obesity is a well-recognized predisposing factor for a number of diseases, including diabetes mellitus, hypertension, and other cardiovascular diseases. Some medical experts estimate that life expectancy decreases by approximately 1% for each pound (about 450 g) of excess fat carried by an person of 45-50 years of age. Obesity is difficult to define quantitatively, but it is generally accepted that anyone who has a body mass index (BMI) greater than 30 is obese. According to this definition, it is possible to be obese without being over-weight. Conversely, muscular athletes may be over-weight without being obese.

Obesity is defined as having a body mass index (BMI), which is the relationship of mass to height, of 30 or more, or a weight of about 30 pounds over the maximum desirable for the individual's height. Those at least 100 pounds over their ideal weight are regarded as morbidly obese.

Obesity as a health problem was first discussed by Thomas Short (1690?–1772) in A Discourse Concerning the Causes and Effects of Corpulency. Together with A Method for Its Prevention and Cure (London, 1727). In 1829, the English physician William Wadd (1776–1829) published his Comments on Corpulency, Lineaments of Leanness, Mems on Diet and Dietetics. In 1863, Dr. William Banting (1779–1878) proposed his special "Banting diet" as a treatment for obesity. So-called Bantingism, a diet low in sugar and oily foods, swept across England, making it the first fad diet craze of national proportions. Largely compilations of unscientific speculations and opinions, these early works were supplanted by more systematic studies coming primarily from Germany and France throughout the latter half of the nineteenth century.

The United States did not come into the forefront of obesity research until Hugo Rony's Obesity and Leanness (1940). By the 1950s, the National Institutes of Health served as a catalyst for new investigations into the causes and nature of obesity, launching a new era in evaluating this potentially life-threatening condition. Researchers in the early twenty-first century understand obesity as a complex condition that can be approached from one of four different perspectives: behavioral/psychological aspects; physiological factors; cellular bases in the functions of fat cells; and genetic and molecular factors.

This last aspect came to scientists attention in the late twentieth century. In 1992, a specific gene responsible for obesity in mice was discovered and two others were identified shortly thereafter. Since this pathbreaking work, a number of genes thought to be responsible for predisposing humans to obesity have been uncovered. With the advent of new genetically targeted pharmaceuticals, the prospect of developing a "magic bullet" for people in this category might be on the horizon.

Still, the principal cause of obesity for most Americans is a combination of overeating and sedentary lifestyle. The Centers for Disease Control and Prevention (CDC) has kept data on obesity since 1985 through its Behavioral Risk Factor Surveillance System (BRFSS). The BRFSS reveals an alarming rise in overweight Americans. In 1985, no state had an obese population of 20 percent or more; in 1997, three states reported in that category; by 2000, a staggering 22 states had an obese population of 20 percent or greater. Of even more concern was the rising obesity rate among American children. The CDC reported skyrocketing obesity rates among children ages 12 to 17, from about 4 percent in 1963 to 11 percent by 1994.

As of 2000, 19.8 percent of the total U.S. population was obese. The prevalence of Americans (estimated as high as 47 million) with a metabolic syndrome (high blood pressure, high cholesterol, and high blood sugar and triglycerides) associated with obesity underscored a national need for stricter dietary regimens and more consistent exercise.

Bibliography

Bray, George A., Claude Bouchard, and W. P. T. James, eds. Handbook of Obesity. New York: Marcel Dekker, 1998.

Centers for Disease Control and Prevention. "Health Topic: Obesity/Overweight." Updated 30 May 2002. Available from http://www.cdc.gov/health/obesity.htm.

Pool, Robert. Fat: Fighting the Obesity Epidemic. New York: Oxford University Press, 2001.

Obesity and overweight now affect more than 50 percent of adult Americans. Diabetes mellitus, hypertension, heart disease, gallbladder disease, and some forms of cancer result from obesity. Whether these diseases are yet present or not, the obese individual should be encouraged to lose weight by appropriate methods to reduce the future likelihood that they will develop. Methods of weight loss include diet, nutritional education, self-help groups, and behavioral change. Under some circumstances drugs or surgery may be considered.

Definition and Measurement of Obesity

Obesity and overweight are best defined using the body mass index (BMI). This index is determined by dividing body weight in kilograms by the square of the height in meters: BMI = W/H². The normal rate for BMI is 18.5 to 25. A BMI between 25 and 30 kg/m² is defined as over-weight and a BMI above 30 kg/m² is defined as obesity (Table 1). Visceral fat can be used as an index of central adiposity. An increase in visceral fat reflects central obesity and increases health risks. The waist circumference is used to assess the amount of visceral obesity. A waist circumference in men of 40 inches (102 cm) or more, and in women, of 35 inches (88 cm) or more, is the threshold for defining central obesity (Table 1).

Prevalence of Overweight

More females than males are overweight at any age. The frequency of overweight increases with age to reach a peak at forty-five to fifty-four years in men and at age fifty-five to sixty-four in women. The National Health and Nutrition Examination Survey (NHANES) conducted by the U.S. government (published in 1993) found a BMI of 25 or more in 59.4 percent of men age twenty years or older and in 50.7 percent of women over the age of twenty years. The prevalence of obesity (BMI 30 or more) was 19.5 percent in men and 25.0 percent in women. The incidence of obesity continues to increase dramatically in the United States and elsewhere. A number of factors including age, sex, and physical inactivity influence the amount of body fat.

At birth, the human infant contains about 12 percent body fat. During the first years of life, body fat rises rapidly to reach a peak of about 25 percent by six months of age and then declines to 18 percent over the next ten years. At puberty, there is a significant increase in the percentage of body fat in females and a decrease in males. By age eighteen, males have approximately 15 to 18 percent body fat, and females have 25 to 28 percent. Between ages twenty and fifty, the fat content of males approximately doubles and that of females increases by about 50 percent. Total body weight, however, rises by only 10 to 15 percent: fat now accounts for a larger part of the body weight and lean body mass decreases.

Table 1

Risks Related to Obesity

As the BMI increases, there is a curvilinear rise in excess mortality. This excess mortality rises more rapidly when the BMI is above 30 kg/m². A BMI over 40 kg/m² is associated with a further increase in overall risk and for the risk of sudden death. The principal causes of the excess mortality associated with overweight include hypertension, stroke, and other cardiovascular diseases, diabetes mellitus, certain cancers, reproductive disorders, gall-bladder disease, and sudden death.

The insulin-resistant state or metabolic syndrome is strongly associated with visceral fat. It may include consequences such as glucose intolerance or type 2 diabetes mellitus, hypertension, polycystic ovarian syndrome, dyslipidemia (the state of abnormal—either higher or lower—values for blood fats), and other disorders. These are often responsive to weight loss, especially when this is achieved early and the loss is maintained.

Development of Obesity

Several mechanisms lead to obesity, including neuroendocrine imbalances, particular drugs, diet, reduced energy expenditure, and genetic factors that lead to certain syndromes and predisposition to obesity. Obesity can follow damage to the hypothalamus in the brain, but this is rare. Cushing's disease is somewhat more common and can result in obesity. Treatment should be directed at the cause of the increased formation of adrenal corticosteroids.

Treatment of diabetics with insulin, sulfonylureas, or thiazolidinediones (but not metformin) can increase hunger and food intake, resulting in weight gain. Treatment with some antidepressants, anti-epileptics, and neuroleptics can also increase body weight, as can cyproheptadine (a serotonin antagonist that produces weight gain), probably through effects on the monoamines (including norepinephrine, epinephrine, dopamine, histamine, and serotonin) in the central nervous system.

Eating a high-fat diet and excessive consumption of sugar-sweetened beverages and the prevalence of abundant varieties of food in cafeterias or supermarkets are dietary factors in the development of obesity. Reduced energy expenditure relative to energy intake is another major component. Energy expenditure can be divided into four parts.

An inactive individual at rest burns between 800 and 900 kilocalories during a twenty-four hour period. This rate is lower in females than in males, and declines with age, and could account for much of the increase in fat stores if food intake does not decline similarly. The effect of physical exercise on metabolism is variable but on average is responsible for about one-third of the daily energy expenditure. From a therapeutic point of view this component of energy expenditure is most easily manipulated. Dietary thermogenesis is the energy expenditure that follows the ingestion of a meal. Heat produced by eating may dissipate up to 10 percent of the ingested calories. These thermic effects of food are one type of metabolic "inefficiency" in the body, that is, where dietary calories are not available for "useful" work. In the obese, the thermic effects of food are reduced particularly in individuals with impaired glucose tolerance or diabetes. Acute over-or underfeeding will produce corresponding shifts in overall metabolism, which can be as large as 15 to 20 percent.

Genetic factors can produce some types of obesity that are easily recognized. Among these types of obesity are: (1) the Bardet-Biel syndrome, characterized by retinal degeneration, mental retardation, obesity, polydactyly, and hypogonadism; (2) the Alstrom syndrome, characterized by pigmentary retinopathy, nerve deafness, obesity, and diabetes mellitus; (3) Carpenter syndrome, characterized by acrocephaly (abnormalities in the facial and head bones), mental retardation, hypogonadism, obesity, and preaxial syndactyly (extra fingers or toes on one hand or foot); (4) the Cohen syndrome, characterized by mental retardation, obesity, hypotonia (reduced tone of the muscles, resulting in a "floppy" muscle mass), and characteristic facies (an appearance of the face that is typical of specific genetic diseases); (5) the Prader-Willi syndrome, characterized by hypotonia, mental retardation, hypogonadism, and obesity; and (6) the pro-opiomelanocortin (POMC) syndrome, characterized by defective production of POMC that is recognized as a red-headed fat child with a low plasma cortisol (a value that is below the normal range).

If both parents are obese, about 80 percent of their offspring will be obese. If only one parent is obese, the likelihood of obesity in the offspring falls to less than 10 percent. Studies with identical twins suggest that inheritance accounts for about 70 percent and environmental factors (diet, physical inactivity, or both) account for 30 percent of the variation in body weight. Deficiency of the gene leptin and deficiency of the leptin receptor are rare, but are associated with massive human obesity. Absence of convertase I has also been associated with obesity in one family. The most common defects associated with massive obesity are abnormalities in the melanocortin receptor system—up to 4 percent of massively obese people may have this type of defect.

Evaluation of the Obese Patient

A medical evaluation should include the expected medical history, family history, personal and social history, and review of the systems of the body with a particular focus on the medications that can cause weight gain. A physical examination should include an assessment of the patient's height, weight, waist circumference, blood pressure, and level of health risk due to obesity. Laboratory tests should include a lipid panel, glucose level, chemistry panel for hepatic (liver) function and uric acid, thyroid function testing, and, if indicated a cortisol level.

Evaluating Risk Using the Body Mass Index (BMI)

Individuals with a normal BMI (20–25 kg/m²) have little or no risk from obesity. Any individual in this weight range who wishes to lose weight for cosmetic reasons should do so only with conservative methods. Individuals with a BMI of greater than 25 to 29.9 kg/m² are in the low-risk group for developing heart disease, hypertension, gallbladder disease, and diabetes mellitus associated with obesity. They too should be encouraged to use low-risk treatments, such as caloric restriction and exercise. Individuals with a BMI of 27 to 30 kg/m² or more who have diseases related to obesity may use adjunctive pharmacotherapy for weight loss.

Individuals with a BMI of 30 to 40 kg/m², have moderate risk for developing diseases associated with obesity. Diet, drugs, and exercise would all appear to be appropriate forms of treatment. Individuals with significant degrees of excess weight often find exercise difficult. However, exercise is very important in helping to maintain weight loss. The use of weight loss medications, as an adjunct to treatment, may also be useful in this group. Individuals who have a BMI above 40 kg/m² have a high risk of developing diseases associated with their obesity. Moderate to severe restriction of calories is the first line of treatment, but for some of these patients surgery may be advisable.

Treatment of Obesity

Any diet must reduce an individual's caloric intake below daily caloric expenditure if it is to be successful. This requires an assessment of caloric requirements, by estimating caloric expenditure from desirable weight tables; for men, multiply desirable weight by 30 to 35 kilocalories/kilogram, (14–16 kilocalories/lb.); for women, multiply desirable weight by 25 to 30 kilocalories/kilogram (12–14 kilocalories/lb.). After assessing caloric requirements, a reasonable calorie deficit can be prescribed. A caloric deficit of 500 kilocalories/day (3,500 kilocalories/week) will produce the loss of approximately one lb. (0.45 kilograms) of fat tissue each week. Table 2 gives a list of diets divided into different levels of energy.

The very low calorie diet (below 800 kilocalories) was developed to facilitate the rate of weight loss since lower energy intake should lead to greater energy deficit. In free living people, however, diets with 400 kilocalories/day have not produced greater weight loss than those with 800 kilocalories/day, suggesting either that they are harder to adhere to or that there is an adaptation in energy expenditure. In either case, these diets should only be used under appropriate medical supervision.

Table 2

Types of diets. There are several types of diets with more than 800 kilocalories/day that usually have more than 1,200 kilocalories/day. They can be divided into several categories. These categories are based on the relative proportion of macronutrients included in the diet and whether they use special foods. For all diets it must be true that they reduce the calorie intake to produce a negative energy balance. Low-carbohydrate diets are touted because they produce ketosis (a state of increased ketones associated with diabetes and fasting) and allow you to eat all of the protein and fat you want. This ends up reducing total calorie intake to about 1,500 kilocalories/day. Since these diets generally have carbohydrate levels below 50 g./day they are ketogenic and can be monitored clinically by the appearance of ketones in the urine. They vary in the level of fiber that is employed. The Atkins diet has low fiber levels, the Sugar Busters diet higher fiber levels.

Low-fat diets recommend fat intake in the range of 10 to 20 percent of calories. The higher carbohydrate increases fiber intake. These diets were developed in a setting designed to reverse the atherosclerotic plaques associated with risks for heart disease, but because of the high fiber content they were often associated with weight loss. Moderate fat levels with higher carbohydrates are characteristic of many widely recommended "healthy diets." For weight loss, the New York Health Department recommends the Prudent Diet, which has stood the test of time.

The portion-controlled diet makes use of prepared foods that have a narrow range of calories. This includes liquid or powdered drinks as well as frozen or canned entrees that have about 300 kilocalories/meal. These can be combined conveniently and thus removes the problem of counting calories from the individual. A number of popular diets focus on a single food, and although nutritionally unbalanced, they are simple to follow and the monotony of single items tends to limit food intake.

Food Guide Pyramid. The Food Guide Pyramid provides an approach to evaluating the quality of your diet. At the bottom of the pyramid are the grains, beans, and starchy vegetables that provide vitamins, minerals, fiber, and energy; six or more servings are recommended. On the next level are the vegetables (3–5 servings) and the fruits (3–4 servings). On the third level are the meats, fish, poultry, and nuts (2–3 servings) along with the milk and yogurt (2–3 servings). At the top are the fats, sweets, and alcohol. Reducing the number of servings proportionally will provide you with a calorie-reduced diet. Most important for the dieter, however, is to sharply reduce the fats and sugar at the top of the pyramid and to reduce or eliminate alcoholic beverages. Not only do alcoholic beverages have calories, their consumption tends to reduce the individual's control in selecting the quality and quantity of foods to eat.

Changing behavioral patterns of eating. The basic principles of behavioral approaches for obesity can be summarized under the ABCs of eating.

• The A stands for antecedent. If one looks at eating as the response to events in the environment, then the antecedent events are those that trigger eating.
• The B stands for the behavior of eating. This includes among other things the place, the rate, and the frequency with which an individual eats. If the act of eating can be focused at one place with one plate and place setting it can help to provide control over eating.
• The C is the consequence of the eating. The feelings an individual has about eating can be altered, and rewards for changing eating patterns can be instituted.

Exercise and physical activity. The only part of energy expenditure that is amenable to significant manipulation is physical activity. During sleep, the lowest level of activity, approximately 0.8 kilocalories/minute is consumed. Thus, if an individual sleeps for an entire 24 hours, approximately 1,150 calories will be expended. Reclining increases this level to approximately 1.0-1.4 kilocalories/minute. Obese and diabetic patients should be encouraged to increase their physical activity for two reasons: First, it consumes calories, but second, and more important, exercise increases glucose utilization and may improve insulin sensitivity.

Drug treatment of obesity. Only a few drugs have been approved by the Food and Drug Administration for treatment of obesity. Studies following individuals who have used these drugs for two years have been published for sibutramine (Meridia) and orlistat (Xenical). Weight-loss drugs should be reserved for patients with moderate-or high-risk obesity (BMI >30 kg/m²) or a BMI above 27 if they have other significant diseases related to obesity. They should be considered for the patient who has failed to lose weight with other methods. Herbal products containing ephedra and an herbal source of caffeine can also produce weight loss when used in accordance with the package instructions.

Surgery. Gastric operations reduce the size of or bypass the stomach, but should be reserved for people with a BMI above 40 or when recommended by a physician.

The Obese Child

Estimates of the prevalence of obesity in children range from 3 to 15 percent. This figure has been rising more rapidly than in the rest of the population. The appearance of obesity in childhood and particularly adolescence is important because it most often persists into adult life. It may be a precursor to the appearance of type 2 diabetes in adolescents. The possibility of treatment should be considered for children who are above the seventy-fifth percentile of weight for height, and might be encouraged for those who are above the ninety-fifth percentile of weight for height. The treatment of prepubertal children should probably involve both parents and child since at this age the principal control of food availability is in the hands of the parents. For adolescents, however, it may be better to separate patient and parents, since the interaction between these groups may be part of the problem. Where growth has not reached its fullest extent, dietary restriction should attempt to reduce further weight gain. Severe caloric restriction and the use of appetite-suppressing drugs may slow height growth. For both children and adolescents, involvement in a regular exercise program is probably the first line of treatment.

Bibliography

Bessesen, D. H., and R. Kushner. Evaluation and Management of Obesity. Center for Obesity Research and Education. Philadelphia: Hanley and Belfus, 2002.

Bray, George A. Contemporary Diagnosis and Management of Obesity. Newtown, Pa.: Handbooks in Health Care, 1998.

National Heart, Lung, and Blood Institute (NHLBI). ClinicalGuidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Bethesda, Md., 1998.

Yanovski, J., and S. Z. Yanovski. "Obesity." New England Journal of Medicine 346, no. 8 (21 February 2002): 591–602.

—George Bray

Quotes:

"Outside every fat man there was an even fatter man trying to close in." - Kingsley Amis

"I don't weigh a pound over one hundred and eighty and, what's more, I never did." - Fatty Arbuckle

"The obese is in a total delirium. For he is not only large, of a size opposed to normal morphology: he is larger than large. He no longer makes sense in some distinctive opposition, but in his excess, his redundancy." - Jean Baudrillard

"Every day the fat woman dies a series of small deaths." - Shelley Bovey

"I don't mind that I'm fat. You still get the same money." - Marlon Brando

"Imprisoned in every fat man, a thin one is wildly signaling to be let out." - Cyril Connolly

See more famous quotes about Obesity

The popular psychological interpretation of obesity is lack of self-esteem and overindulgence in fear and denial; layers of protection to insulate the dreamer from involvement or action; hopelessness and helplessness to express power and authority; fear that rejection will be the only reward for effort. Other possible meanings are the "fat cat" who ate the mouse, being full of oneself, or fattening up the livestock (for slaughter). (See also Fat).

Obesity
Classification and external resources
Silhouettes and waist circumferences representing normal, overweight, and obese
ICD-10	E66.
ICD-9	278
OMIM	601665
DiseasesDB	9099
MedlinePlus	003101
eMedicine	med/1653
MeSH	C23.888.144.699.500

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health, leading to reduced life expectancy and/or increased health problems.^[1][2] Body mass index (BMI), a measurement which compares weight and height, defines people as overweight (pre-obese) when their BMI is between 25 kg/m² and 30 kg/m², and obese when it is greater than 30 kg/m².^[3]

Obesity increases the likelihood of various diseases, particularly heart disease, type 2 diabetes, breathing difficulties during sleep, certain types of cancer, and osteoarthritis.^[2] Obesity is most commonly caused by a combination of excessive dietary calories, lack of physical activity, and genetic susceptibility, although a few cases are caused solely by genes, endocrine disorders, medications or psychiatric illness. Evidence to support the view that some obese people eat little yet gain weight due to a slow metabolism is limited; on average obese people have a greater energy expenditure than their thin counterparts due to the energy required to maintain an increased body mass.^[4][5]

The primary treatment for obesity is dieting and physical exercise. To supplement this, or in case of failure, anti-obesity drugs may be taken to reduce appetite or inhibit fat absorption. In severe cases, surgery is performed or an intragastric balloon is placed to reduce stomach volume and/or bowel length, leading to earlier satiation and reduced ability to absorb nutrients from food.^[6][7]

Obesity is a leading preventable cause of death worldwide, with increasing prevalence in adults and children, and authorities view it as one of the most serious public health problems of the 21st century.^[8] Obesity is stigmatized in the modern Western world, though it has been perceived as a symbol of wealth and fertility at other times in history, and still is in many parts of Africa.^[2][9]

Contents 1 Classification 2 Effects on health 2.1 Mortality 2.2 Morbidity 2.3 Obesity survival paradox 3 Causes 3.1 Diet 3.2 Sedentary lifestyle 3.3 Genetics 3.4 Medical and psychiatric illness 3.5 Social determinants 3.6 Infectious agents 4 Pathophysiology 5 Management 5.1 Dieting 5.2 Exercise 5.3 Weight loss programs 5.4 Medication 5.5 Surgery 5.6 Clinical protocols 6 Epidemiology 7 Public health 8 Economic impact 9 History and culture 9.1 Etymology 9.2 Historical trends 9.3 The arts 9.4 Size acceptance and the obesity controversy 10 Childhood obesity 11 In other animals 12 References 13 Further reading 14 External links

Classification

Main article: Classification of obesity

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health.^[1] It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.^[10][11] BMI is closely related to both percentage body fat and total body fat.^[12]

An obese male with a body mass index of 46 kg/m²: weight 146 kg (322 lb), height 177 cm (5 ft 10 in)

In children a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as an absolute number but in relation to a historical normal group, such that obesity is a BMI greater than the 95th percentile.^[13] The reference data that these percentiles are based on are from 1963 to 1994, and thus have not been affected by the recent increases in weight.^[14]

BMI	Classification
< 18.5	underweight
18.5–24.9	normal weight
25.0–29.9	overweight
30.0–34.9	class I obesity
35.0–39.9	class II obesity
≥ 40.0	class III obesity

BMI is calculated by dividing the subject's mass by the square of his or her height, typically expressed either in metric or US "customary" units:

Metric: BMI = kilograms / meters²

US customary and imperial: BMI = lb * 703 / in²

where lb is the subject's weight in pounds and in is the subject's height in inches.

The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000, provide the values listed in the table at right.^[3]

Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaks down "class III" obesity into further categories whose exact values are still disputed.^[15]

• Any BMI ≥ 35 or 40 is severe obesity
• A BMI of ≥ 35 or 40–44.9 or 49.9 is morbid obesity
• A BMI of ≥ 45 or 50 is super obese

As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; the Japanese have defined obesity as any BMI greater than 25^[16] while China uses a BMI of greater than 28.^[17]

Effects on health

Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, and osteoarthritis.^[2] As a result, obesity has been found to reduce life expectancy.^[2]

Mortality

Relative risk of death for men in United States by BMI.[18]

Relative risk of death for women in United States by BMI.[18]

Obesity is one of the leading preventable causes of death worldwide.^[8][19][20] Large-scale American and European studies have found that mortality risk is lowest at a BMI of 22.5–25 kg/m^2[21] in non-smokers and at 24–27 kg/m² in current smokers, with risk increasing along with changes in either direction.^[22][23] A BMI above 32 has been associated with a doubled mortality rate among women over a 16-year period.^[24] In the United States obesity is estimated to cause an excess 111,909 to 365,000 death per year,^[2][20] while 1 million (7.7%) of deaths in the European Union are attributed to excess weight.^[25][26] On average, obesity reduces life expectancy by six to seven years:^[2][27] a BMI of 30–35 reduces life expectancy by two to four years,^[21] while severe obesity (BMI > 40) reduces life expectancy by 10 years.^[21]

Morbidity

Main article: Obesity associated morbidity

Obesity increases the risk of many physical and mental conditions. These comorbidities are most commonly shown in metabolic syndrome,^[2] a combination of medical disorders which includes: diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels.^[28]

Complications are either directly caused by obesity or indirectly related through mechanisms sharing a common cause such as a poor diet or a sedentary lifestyle. The strength of the link between obesity and specific conditions varies. One of the strongest is the link with type 2 diabetes. Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.^[29]

Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (such as osteoarthritis, obstructive sleep apnea, social stigmatization) and those due to the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).^[2][30] Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state, increasing the risk of thrombosis.^[30]

Medical field	Condition	Medical field	Condition
Cardiology	ischemic heart disease:[31] angina and myocardial infarction congestive heart failure[2] high blood pressure[2] abnormal cholesterol levels[2] deep vein thrombosis and pulmonary embolism[32]	Dermatology	stretch marks[33] acanthosis nigricans[33] lymphedema[33] cellulitis[33] hirsutism[33] intertrigo[34]
Endocrinology and Reproductive medicine	diabetes mellitus[2] polycystic ovarian syndrome[2] menstrual disorders[2] infertility[2][35] complications during pregnancy[2][35] birth defects[2] intrauterine fetal death[35]	Gastrointestinal	gastroesophageal reflux disease[2][36] fatty liver disease[2] cholelithiasis (gallstones)[2]
Neurology	stroke[2] meralgia paresthetica[37] migraines[38] carpal tunnel syndrome[39] dementia[40] idiopathic intracranial hypertension[41]	Oncology[42]	breast, ovarian esophageal, colorectal liver, pancreatic gallbladder, stomach endometrial, cervical prostate, kidney non-Hodgkin's lymphoma, multiple myeloma
Psychiatry	depression in women[2] social stigmatization[2]	Respirology	obstructive sleep apnea[2][43] obesity hypoventilation syndrome[2][43] asthma[2][43] increased complications during general anaesthesia[2][5]
Rheumatology and Orthopedics	gout[44] poor mobility[45] osteoarthritis[2] low back pain[46]	Urology and Nephrology	erectile dysfunction[47] urinary incontinence[48] chronic renal failure[49] hypogonadism[50]

Obesity survival paradox

See also: Obesity paradox

Although the negative health consequences of obesity in the general population are well supported by the available evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, a phenomenon known as the obesity survival paradox.^[51] The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,^[51] and has subsequently been found in those with heart failure and peripheral artery disease (PAD).^[52]

In people with heart failure, those with a BMI between 30.0–34.9 had lower mortality than those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.^[53] Similar findings have been made in other types of heart disease. People with class I obesity and heart disease do not have greater rates of further heart problems than people of normal weight who also have heart disease. In people with greater degrees of obesity, however, risk of further events is increased.^[54][55] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.^[56] One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.^[57] Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD the benefit of obesity no longer exists.^[52]

Causes

At an individual level, a combination of excessive caloric intake and a lack of physical activity is thought to explain most cases of obesity.^[58] A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness.^[59] In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet,^[60] increased reliance on cars, and mechanized manufacturing.^[61][62]

A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors (environmental pollutants that interfere with lipid metabolism), (3) decreased variability in ambient temperature, (4) decreased rates of smoking, because smoking suppresses appetite, (5) increased use of medications that can cause weight gain (e.g., atypical antipsychotics), (6) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to obesity in children), (8) epigenetic risk factors passed on generationally, (9) natural selection for higher BMI, and (10) assortative mating leading to increased concentration of obesity risk factors (this would not necessarily increase the number of obese people, but would increase the average population weight).^[63] While there is substantial evidence supporting the influence of these mechanisms on the increased prevalence of obesity, the evidence is still inconclusive, and the authors state that these are probably less influential than the ones discussed in the previous paragraph.

Diet

Main article: Diet and obesity

Map of dietary energy availability per person per day in 1961 (kcal/person/day)[64]      no data      <1600      1600–1800      1800–2000      2000–2200      2200–2400      2400–2600      2600–2800      2800–3000      3000–3200      3200–3400      3400–3600      >3600

Map of dietary energy availability per person per day in 2001–2003 (kcal/person/day)[65]      no data      <1600      1600–1800      1800–2000      2000–2200      2200–2400      2400–2600      2600–2800      2800–3000      3000–3200      3200–3400      3400–3600      >3600

Average per capita energy consumption of the world from 1961 to 2002^[64]

The per capita dietary energy supply varies markedly between different regions and countries. It has also changed significantly over time.^[64] From the early 1970s to the late 1990s the average calories available per person per day (the amount of food bought) has increased in all parts of the world except Eastern Europe. The United States had the highest availability with 3,654 calories per person in 1996.^[64] This increased further in 2003 to 3,754.^[64] During the late 1990s Europeans had 3,394 calories per person, in the developing areas of Asia there were 2,648 calories per person, and in sub-Saharan Africa people had 2,176 calories per person.^[64][66]

The widespread availability of nutritional guidelines^[67] has done little to address the problems of overeating and poor dietary choice.^[68] From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.^[69] During the same period, an increase occurred in the average amount of calories consumed. For women, the average increase was 335 calories per day (1,542 calories in 1971 and 1,877 calories in 2004), while for men the average increase was 168 calories per day (2,450 calories in 1971 and 2,618 calories in 2004). Most of these extra calories came from an increase in carbohydrate consumption rather than fat consumption.^[70] The primary source of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily calories in young adults in America.^[71] Consumption of sweetened drinks is believed to be contributing to the rising rates of obesity.^[72][73]

As societies become increasingly reliant on energy-dense, big-portion, fast-food meals, the association between fast-food consumption and obesity becomes more concerning.^[74] In the United States consumption of fast-food meals tripled and calorie intake from these meals quadrupled between 1977 and 1995.^[75]

Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.^[76]

Obese people consistently under-report their food consumption as compared to people of normal weight.^[77] This is supported both by test of people carried out in a calorimeter rooms^[78] and by direct observation.

Sedentary lifestyle

See also: Exercise trends

A sedentary lifestyle plays a significant role in obesity.^[79] Worldwide there has been a large shift towards less physically demanding work,^[80][81][82] and currently at least 60% of the world's population gets insufficient exercise.^[81] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.^[80][81][82] In children there appears to be declines in levels of physical activity due to less walking and physical education.^[83] World trends in active leisure time physical activity are less clear. The World Health Organization indicates that people worldwide are taking up less active recreational pursuits, while a study from Finland^[84] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.^[85]

In both children and adults there is an association between television viewing time and the risk of obesity.^[86][87][88] A 2008 meta-analysis found that 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.^[89]

Genetics

Main article: Genetics of obesity

A 1680 painting by Juan Carreno de Miranda of a girl presumed to have Prader-Willi syndrome^[90]

Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient calories are present. As of 2006 more than 41 of these sites have been linked to the development of obesity when a favorable environment is present.^[91] The percentage of obesity that can be attributed to genetics varies, depending on the population examined, from 6% to 85%.^[92]

Obesity is a major feature in several syndromes, such as Prader-Willi syndrome, Bardet-Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term "non-syndromic obesity" is sometimes used to exclude these conditions.)^[93] In people with early-onset severe obesity (defined by an onset before 10 years of age and body mass index over three standard deviations above normal), 7% harbor a single point DNA mutation.^[94]

Studies that have focused upon inheritance patterns rather than upon specific genes have found that 80% of the offspring of two obese parents were obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.^[95]

The thrifty gene hypothesis postulates that certain ethnic groups may be more prone to obesity in an equivalent environment. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies.^[96] This is the presumed reason that Pima Indians, who evolved in a desert ecosystem, developed some of the highest rates of obesity when exposed to a Western lifestyle.^[97]

Medical and psychiatric illness

Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormone deficiency,^[98] and the eating disorders: binge eating disorder and night eating syndrome.^[2] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.^[99]

Certain medications may cause weight gain or changes in body composition; these include insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, certain anticonvulsants (phenytoin and valproate), pizotifen, and some forms of hormonal contraception.^[2]

Social determinants

Main article: Social determinants of obesity

While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.^[100] Though it is accepted that calorie consumption in excess of calorie expenditure leads to obesity on an individual basis, the cause of the shifts in these two factors on the societal scale is much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.

The correlation between social class and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant differences were seen among men of different social classes. In the developing world, women, men, and children from high social classes had greater rates of obesity.^[101] An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.^[102] Among developed countries, levels of adult obesity, and percentage of teenage children who are overweight, are correlated with income inequality. A similar relationship is seen between US states: more adults, even in higher social classes, are obese in more unequal states.^[103]

Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In undeveloped countries the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.^[102] Attitudes toward body mass held by people in one's life may also play a role in obesity. A correlation in BMI changes over time has been found between friends, siblings, and spouses.^[104] Stress and perceived low social status appear to increase risk of obesity.^{[103][105][106]}

Smoking has a significant effect on an individual's weight. Those who quit smoking gain an average of 4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years.^[107] However, changing rates of smoking have had little effect on the overall rates of obesity.^[108]

In the United States the number of children a person has is related to their risk of obesity. A woman's risk increases by 7% per child, while a man's risk increases by 4% per child.^[109] This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.^[110]

In the developing world urbanization is playing a role in increasing rate of obesity. In China overall rates of obesity are below 5%; however, in some cities rates of obesity are greater than 20%.^[111]

Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.^[112] Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more calories become available.^[112]

Infectious agents

See also: Infectobesity

The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.^[113]

An association between viruses and obesity has been found in humans and several different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.^[114]

Pathophysiology

A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right)

Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.^[115] This field of research had been almost unapproached until leptin was discovered in 1994. Since this discovery, many other hormonal mechanisms have been elucidated that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, and development of insulin resistance. Since leptin's discovery, ghrelin, insulin, orexin, PYY 3-36, cholecystokinin, adiponectin, as well as many other mediators have been studied. The adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases.

Leptin and ghrelin are considered to be complementary in their influence on appetite, with ghrelin produced by the stomach modulating short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is stretched). Leptin is produced by adipose tissue to signal fat storage reserves in the body, and mediates long-term appetitive controls (i.e. to eat more when fat storages are low and less when fat storages are high). Although administration of leptin may be effective in a small subset of obese individuals who are leptin deficient, most obese individuals are thought to be leptin resistant and have been found to have high levels of leptin.^[116] This resistance is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese people.^[115]

A graphic depiction of a leptin molecule

While leptin and ghrelin are produced peripherally, they control appetite through their actions on the central nervous system. In particular, they and other appetite-related hormones act on the hypothalamus, a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the melanocortin pathway being the most well understood.^[115] The circuit begins with an area of the hypothalamus, the arcuate nucleus, that has outputs to the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH), the brain's feeding and satiety centers, respectively.^[117]

The arcuate nucleus contains two distinct groups of neurons.^[115] The first group coexpresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH. The second group coexpresses pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating the POMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.^[115]

Management

The main treatment for obesity consists of dieting and physical exercise.^[58] Diet programs may produce weight loss over the short term,^[118] but keeping this weight off can be a problem and often requires making exercise and a lower calorie diet a permanent part of a person's lifestyle.^[119][120] Success rates of long-term weight loss maintenance are low and range from 2–20%.^[121] In a more structured setting, however, 67% of people who lost greater than 10% of their body mass maintained or continued to lose weight one year later.^[122] An average maintained weight loss of more than 3 kg (6.6 lb) or 3% of total body mass could be sustained for five years.^[123] Some studies have found significant benefits in mortality in certain populations with weight loss. In a prospective study of obese women with weight related diseases, intentional weight loss of any amount was associated with a 20% reduction in mortality. In obese women without obesity related illnesses a weight loss of greater than 9 kg (20 lb) was associated with a 25% reduction in mortality.^[124] A recent review concluded that certain subgroups such as those with type 2 diabetes and women show long term benefits in all cause mortality, while outcomes for men do not seem to be improved with weight loss.^[125] A subsequent study has found benefits in mortality from intentional weight loss in those who have severe obesity.^[126]

The most effective treatment for obesity is bariatric surgery; however, due to its cost and the risk of complications, researchers are searching for other effective yet less invasive treatments.

Dieting

Main article: Dieting

Diets to promote weight loss are generally divided into four categories: low-fat, low-carbohydrate, low-calorie, and very low calorie.^[118] A meta-analysis of six randomized controlled trials found no difference between three of the main diet types (low calorie, low carbohydrate, and low fat), with a 2–4 kilogram (4.4–8.8 lb) weight loss in all studies.^[118] At two years these three methods resulted in similar weight loss irrespective of the macronutrients emphasized.^[127]

Very low calorie diets provide 200–800 kcal/day, maintaining protein intake but limiting calories from both fat and carbohydrates. They subject the body to starvation and produce an average weekly weight loss of 1.5–2.5 kilograms (3.3–5.5 lb). These diets are not recommended for general use as they are associated with adverse side effects such as loss of lean muscle mass, increased risks of gout, and electrolyte imbalances. People attempting these diets must be monitored closely by a physician to prevent complications.^[118]

Exercise

See also: Physical exercise

With use, muscles consume energy derived from both fat and glycogen. Due to the large size of leg muscles, walking, running, and cycling are the most effective means of exercise to reduce body fat.^[128] Exercise affects macronutrient balance. During moderate exercise, equivalent to a brisk walk, there is a shift to greater use of fat as a fuel.^[129][130] To maintain health the American Heart Association recommends a minimum of 30 minutes of moderate exercise at least 5 days a week.^[130]

A meta-analysis of 43 randomized controlled trials by the Cochrane Collaboration found that exercising alone led to limited weight loss. In combination with diet, however, it resulted in a 1 kilogram weight loss over dieting alone. A 1.5 kilogram (3.3 lb) loss was observed with a greater degree of exercise.^[131] Even though exercise as carried out in the general population has only modest effects, a dose response curve is found, and very intense exercise can lead to substantial weight loss. During 20 weeks of basic military training with no dietary restriction, obese military recruits lost 12.5 kg (27.6 lb).^[132] High levels of physical activity seem to be necessary to maintain weight loss.^[133] A pedometer appears useful for motivation. Over an average of 18-weeks of use physical activity increased by 27% resulting in a 0.38 decreased in BMI.^[134]

Signs that encourage the use of stairs as well as community campaigns have been shown to be effective in increasing exercise in a population.^[135] The city of Bogota, Colombia for example blocks off 113 kilometers (70 miles) of roads every Sunday and on holidays to make it easier for its citizens to get exercise. These pedestrian zones are part of an effort to combat chronic diseases, including obesity.^[136]

Weight loss programs

Weight loss programs often promote lifestyle changes and diet modification. This may involve eating smaller meals, cutting down on certain types of food, and making a conscious effort to exercise more. These programs also enable people to connect with a group of others who are attempting to lose weight, in the hopes that participants will form mutually motivating and encouraging relationships.^[137]

A number of popular programs exist, including Weight Watchers, Overeaters Anonymous, and Jenny Craig. These appear to provide modest weight loss (2.9 kg, 6.4 lb) over dieting on one's own (0.2 kg, 0.4 lb) over a two year period.^[138] Internet-based programs appear to be ineffective.^[139] The Chinese government has introduced a number of "fat farms" where obese children go for reinforced exercise, and has passed a law which requires students to exercise or play sports for an hour a day at school (see Obesity in China).^[140][141]

Medication

Main article: Anti-obesity medication

The two most commonly used medications to treat obesity: orlistat (Xenical) and sibutramine (Meridia)

Only two anti-obesity medications are currently approved by the FDA for long term use.^[142] One is orlistat (Xenical), which reduces intestinal fat absorption by inhibiting pancreatic lipase; the other is sibutramine (Meridia), which acts in the brain to inhibit deactivation of the neurotransmitters norepinephrine, serotonin, and dopamine (very similar to some anti-depressants), therefore decreasing appetite. Rimonabant (Acomplia), a third drug, works via a specific blockade of the endocannabinoid system. It has been developed from the knowledge that cannabis smokers often experience hunger, which is often referred to as "the munchies". It has been approved in Europe for the treatment of obesity but has not yet received approval in the United States or Canada due to safety concerns.^[143][144]

Weight loss with these drugs is modest. Over the longer term, average weight loss on orlistat is 2.9 kg (6.4 lb), sibutramine is 4.2 kg (9.3 lb) and rimonabant is 4.7 kg (10.4 lb). Orlistat and rimonabant lead to a reduced incidence of diabetes, and all three drugs have some effect on cholesterol. However, there is little information on how these drugs affect the longer-term complications or outcomes of obesity.^[145]

There are a number of less commonly used medications. Some are only approved for short term use, others are used off-label, and still others are used illegally. Most are appetite suppressants that act on one or more neurotransmitters.^[146] Phendimetrazine (Bontril), diethylpropion (Tenuate), and phentermine (Adipex-P) are approved by the FDA for short term use, while bupropion (Wellbutrin), topiramate (Topamax), and zonisamide (Zonegran) are sometimes used off-label.^[142]

The usefulness of certain drugs depends upon the comorbities present. Metformin (Glucophage) is preferred in overweight diabetics, as it may lead to mild weight loss in comparison to sulfonylureas or insulin.^[147] The thiazolidinediones, on the other hand, may cause weight gain, but decrease central obesity.^[148] Diabetics also achieve modest weight loss with fluoxetine (Prozac), orlistat and sibutramine over 12–57 weeks. The long-term health benefits of these treatments, however, remain unclear.^[149]

Fenfluramine and dexfenfluramine were withdrawn from the market in 1997,^[142] while ephedrine (found in the traditional Chinese herbal medicine má huáng made from the Ephedra sinica) was removed from the market in 2004.^[150] Dexamphetamines are not approved by the FDA for the treatment of obesity^[151] due to concerns regarding addiction.^[142] The use of these drugs is not recommended due to potential side effects.^[152] However, people do occasionally use these drugs illegally.^[153]

Surgery

Main article: Bariatric surgery

Bariatric surgery ("weight loss surgery") is the use of surgical intervention in the treatment of obesity. As every operation may have complications, surgery is only recommended for severely obese people (BMI > 40) who have failed to lose weight following dietary modification and pharmacological treatment. Weight loss surgery relies on various principles: the two most common approaches are reducing the volume of the stomach (e.g. by adjustable gastric banding and vertical banded gastroplasty), which produces an earlier sense of satiation, and reducing the length of bowel that comes into contact with food (gastric bypass surgery), which directly reduces absorption. Band surgery is reversible, while bowel shortening operations are not. Some procedures can be performed laparoscopically. Complications from weight loss surgery are frequent.^[154]

Surgery for severe obesity is associated with long-term weight loss and decreased overall mortality. One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10 years, and a 29% reduction in all cause mortality when compared to standard weight loss measures.^[155] A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer has also been found after bariatric surgery.^[156][157] Marked weight loss occurs during the first few months after surgery, and the loss is sustained in the long term. In one study there was an unexplained increase in deaths from accidents and suicide, but this did not outweigh the benefit in terms of disease prevention.^[157] When the two main techniques are compared, gastric bypass procedures are found to lead to 30% more weight loss than banding procedures one year after surgery.^[158]

The effects of liposuction on obesity are less well determined. Some small studies show benefits^[159] while others show none.^[160] A treatment involving the placement of an intragastric balloon via gastroscopy has shown promise. One type of balloon lead to a weight loss of 5.7 BMI units over 6 months or 14.7 kg (32.4 lb). Regaining lost weight is common after removal, however, and 4.2% of people were intolerant of the device.^[7]

Clinical protocols

Much of the Western world has created clinical practice guidelines in an attempt to address rising rates of obesity. Australia,^[161] Canada,^[58] the European Union,^[25] and the United States^[162] have all published statements since 2004.

In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:^[162]

1. People with a BMI of over 30 should be counseled on diet, exercise and other relevant behavioral interventions, and set a realistic goal for weight loss.
2. If these goals are not achieved, pharmacotherapy can be offered. The person needs to be informed of the possibility of side-effects and the unavailability of long-term safety and efficacy data.
3. Drug therapy may consist of sibutramine, orlistat, phentermine, diethylpropion, fluoxetine, and bupropion. For more severe cases of obesity, stronger drugs such as amphetamine and methamphetamine may be used on a selective basis. Evidence is not sufficient to recommend sertraline, topiramate, or zonisamide.
4. In people with a BMI over 40 who fail to achieve their weight loss goals (with or without medication) and who develop obesity-related complications, referral for bariatric surgery may be indicated. The person needs to be aware of the potential complications.
5. Those requiring bariatric surgery should be referred to high-volume referral centers, as the evidence suggests that surgeons who frequently perform these procedures have fewer complications.

A clinical practice guideline by the US Preventive Services Task Force (USPSTF) concluded that the evidence is insufficient to recommend for or against routine behavioral counseling to promote a healthy diet in unselected people in primary care settings, but that intensive behavioral dietary counseling is recommended in those with hyperlipidemia and other known risk factors for cardiovascular and diet-related chronic disease. Intensive counseling can be delivered by primary care clinicians or by referral to other specialists, such as nutritionists or dietitians.^[52][163]

Canada developed and published evidence-based practice guidelines in 2006. The guidelines attempt to address the prevention and management of obesity at both the individual and population levels in both children and adults.^[58] The European Union published clinical practice guidelines in 2008 in an effort to address the rising rates of obesity in Europe.^[25] Australia came out with practice guidelines in 2004.^[161]

Epidemiology

Main article: Epidemiology of obesity

World obesity prevalence among males[164]      <5%      5–10%      10–15%      15–20%      20–25%      25–30%      30–35%      35–40%      40–45%      45–50%      50–55%      >55%

World obesity prevalence among females[164]      <5%      5–10%      10–15%      15–20%      20–25%      25–30%      30–35%      35–40%      40–45%      45–50%      50–55%      >55%

Before the 20th century, obesity was rare;^[165] in 1997 the WHO formally recognized obesity as a global epidemic.^[71] As of 2005 the WHO estimates that at least 400 million adults (9.8%) are obese, with higher rates among women than men.^[166] The rate of obesity also increases with age at least up to 50 or 60 years old^[167] and severe obesity in the United States, Australia, and Canada is increasing faster than the overall rate of obesity.^{[15][168][169]} Once considered a problem only of high-income countries, obesity rates are rising worldwide and affecting both the developed and developing world.^[25] These increases have been felt most dramatically in urban settings.^[166] The only remaining region of the world where obesity is not common is sub-Saharan Africa.^[2]

Public health

The World Health Organization (WHO) predicts that overweight and obesity may soon replace more traditional public health concerns such as undernutrition and infectious diseases as the most significant cause of poor health.^[170] Obesity is a public health and policy problem because of its prevalence, costs, and health effects.^[171] Public health efforts seek to understand and correct the environmental factors responsible for the increasing prevalence of obesity in the population. Solutions look at changing the factors that cause excess calorie consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct junk food marketing to children,^[172] and decreasing access to sweetened beverages in schools.^[173] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.^[174]

Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".^[175] In 2006 the Canadian Obesity Network published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideline to address the management and prevention of overweight and obesity in adults and children.^[176] In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growing problem of obesity in the UK.^[177] The same year, the House of Commons Health Select Committee published its "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.^[178] In 2006, the National Institute for Health and Clinical Excellence (NICE) issued a guideline on the diagnosis and management of obesity, as well as policy implications for non-healthcare organizations such as local councils.^[179] A 2007 report produced by Sir Derek Wanless for the King's Fund warned that unless further action was taken, obesity had the capacity to cripple the National Health Service financially.^[180]

Comprehensive approaches are being looked at to address the rising rates of obesity. The Obesity Policy Action (OPA) framework divides measure into 'upstream' policies, 'midstream' policies, 'downstream' policies. 'Upstream' policies look at changing society, 'midstream' policies try to alter individuals' behavior to prevent obesity, and 'downstream' policies try to treat currently afflicted people.^[181]

Economic impact

Services must accommodate obese people with specialist equipment such as much wider chairs.^[182]

In addition to its health impacts, obesity leads to many problems including disadvantages in employment^[183] and increased business costs. These effects are felt by all levels of society from individuals, to corporations, to governments.

The estimate range for annual expenditures on diet products is $40 billion to $100 billion in the US alone.^[184] In 1998, the medical costs attributable to obesity in the US were $78.5 billion USD or 9.1% of all medical expenditures,^[185][186] while the cost of obesity in Canada was estimated at $2 billion CAD in 1997 (2.4% of total health costs).^[58]

Obesity prevention programs have been found to reduce the cost of treating obesity-related disease. However, the longer people live, the more medical costs they incur. Researchers therefore conclude that reducing obesity may improve the public's health, but it is unlikely to reduce overall health spending.^[187]

Obesity can lead to social stigmatization and disadvantages in employment.^[183] When compared to their normal weight counterparts, obese workers on average have higher rates absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.^[188] A study examining Duke University employees found that people with a BMI over 40 filed twice as many workers' compensation claims as those whose BMI was 18.5–24.9. They also had more than 12 times as many lost work days. The most common injuries in this group were due to falls and lifting, thus affecting the lower extremities, wrists or hands, and backs.^[189] The US state of Alabama Employees' Insurance Board approved a controversial plan to charge obese workers $25 per month if they do not take measures to reduce their weight and improve their health. These measures are set to start January 2010 and apply to those with a BMI of greater than 35 kg/m² who fail to make improvements in their health after one year.^[190]

Some research shows that obese people are less likely to be hired for a job and are less likely to be promoted.^[191] Obese people are also paid less than their non-obese counterparts for an equivalent job. Obese women on average make 6% less and obese men make 3% less.^[192]

Specific industries, such as the airline and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width.^[193] In 2000, the extra weight of obese passengers cost airlines US$275 million.^[194] Costs for restaurants are increased by litigation accusing them of causing obesity.^[195] In 2005 the US Congress discussed legislation to prevent civil law suits against the food industry in relation to obesity; however, it did not become law.^[195]

History and culture

Venus of Willendorf created 24,000–22,000 BC

Etymology

Obesity is from the Latin obesitas, which means "stout, fat, or plump." Ēsus is the past participle of edere (to eat), with ob (over) added to it.^[196] The Oxford English Dictionary documents its first usage in 1611 by Randle Cotgrave in A Dictionarie of the French and English Tongues.^[197]

Historical trends

During the Middle Ages and the Renaissance obesity was often seen as a sign of wealth and was relatively common among officials: The Tuscan General Alessandro del Borro, attributed to Charles Mellin, 1645^[198]

The Greeks were the first to recognize obesity as a medical disorder.^[165] Hippocrates states that "Corpulence is not only a disease itself, but the harbinger of others".^[2] It was known to the Indian surgeon Sushruta (6th century BCE), who related obesity to diabetes and heart disorder.^[199] He recommended physical work to help cure it and its side effects.^[199] For most of human history mankind struggled with food scarcity.^[200] Obesity has thus historically been viewed as a sign of wealth and prosperity. It was common among high officials in Europe in the Middle Ages and the Renaissance^[198] as well as in Ancient East Asian civilizations.^[201] With the onset of the industrial revolution it was realized that the military and economic might of nations were dependent on both the body size and strength of their soldiers and workers. Increasing the average body mass index from what is now considered underweight to what is now the normal range played a significant role in the development of industrialized societies. Height and weight thus both increased through the 19th century in the developed world. During the 20th century, as populations reached their genetic potential for height, weight began increasing much more than height, resulting in obesity.^[71] In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.^[71][202] During this time period insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.^[2]

Overweight people, such as President William Howard Taft, have been ridiculed at various times in the past.

Many cultures throughout history have viewed obesity as the result of a character flaw. The obesus or fat character in Greek comedy was a glutton and figure of mockery. During Christian times food was viewed as a gateway to the sins of sloth and lust.^[9] In modern Western culture, excess weight is often regarded as unattractive, and obesity is commonly associated with various negative stereotypes. People of all ages can face social stigmatization, and may be targeted by bullies or shunned by their peers. Obesity is once again a reason for discrimination.^[191]

Public perceptions in Western society regarding healthy body weight differ from those regarding the weight that is considered ideal  – and both have changed since the beginning of the 20th century. The weight that is viewed as an ideal has become lower since the 1920s. This is illustrated by the fact that the average height of Miss America pageant winners increased by 2% from 1922 to 1999, while their average weight decreased by 12%.^[203] On the other hand, people's views concerning healthy weight have changed in the opposite direction. In Britain the weight at which people considered themselves to be overweight was significantly higher in 2007 than in 1999.^[204] These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal.^[204]

Obesity is still seen as a sign of wealth and well-being in many parts of Africa. This has become particularly common since the HIV epidemic began.^[2]

The arts

The first sculptural representations of the human body 20,000–35,000 years ago depict obese females. Some attribute the Venus figurines to the tendency to emphasize fertility while others feel they represent "fatness" in the people of the time.^[9] Corpulence is, however, absent in both Greek and Roman art, probably in keeping with their ideals regarding moderation. This continued through much of Christian European history, with only those of low socioeconomic status being depicted as obese. During the Renaissance some of the upper class began flaunting their large size, as can be seen in portraits of Henry the VIII and Alessandro del Borro.^[9] Rubens (1577–1640) regularly depicted full-bodied women in his pictures, from which derives the term Rubenesque. These women, however, still maintained the "hourglass" shape with its relationship to fertility.^[205] During the 19th century, views on obesity changed in the Western world. After centuries of obesity being synonymous with wealth and social status, slimness began to be seen as the desirable standard.^[9]

Size acceptance and the obesity controversy

See also: Fat acceptance movement

The principal goal of the fat acceptance movement is to decrease discrimination against people who are overweight and obese.^[206][207] However, some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes.^[208]

A number of organizations exist that promote the acceptance of obesity. They have increased in prominence in the latter half of the 20th century.^[209] The US-based National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.^[210] The International Size Acceptance Association (ISAA) is a non-governmental organization (NGO) which was founded in 1997. It has more of a global orientation and describes its mission as promoting size acceptance and helping to end weight-based discrimination.^[211] These groups often argue for the recognition of obesity as a disability under the US Americans With Disabilities Act (ADA). The American legal system, however, has decided that the potential public health costs exceed the benefits of extending this anti-discrimination law to cover obesity.^[208]

Multiple books such as The Diet Myth by Paul Campos argue that the health risks of obesity are mostly unproven and the real problem is the social stigma facing the obese.^[212] Similarly, The Obesity Epidemic by Michael Gard argues that obesity is a moral and ideological construct, rather than a health problem.^[213] Other groups are also trying to challenge obesity's connection to poor health. The Center for Consumer Freedom, an organization partly supported by the restaurant and food industry, has run ads saying that obesity is not an epidemic but "hype".^[214]

People are known to select potential partners based on a similar body mass.^[215] The rising rates of obesity have therefore provided greater opportunities for overweight people to find partners. Certain subcultures also label themselves as particularly attracted to the obese. Chubby culture^[216] and fat admirers^[217] are examples.

Childhood obesity

Main article: Childhood obesity

An overweight child

The healthy BMI range varies with the age and sex of the child. Obesity in children and adolescents is defined as a BMI greater than the 95th percentile.^[13] The reference data that these percentiles are based on is from 1963 to 1994 and thus has not been affected by the recent increases in rates of obesity.^[14]

Childhood obesity has reached epidemic proportions in 21st century, with rising rates in both the developed and developing world. Rates of obesity in Canadian boys have increased from 11% in 1980s to over 30% in 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.^[218]

As with obesity in adults, many different factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important in causing the recent increase in the rates.^[219]

Because childhood obesity often persists into adulthood and is associated with numerous chronic illnesses, children who are obese are often tested for hypertension, diabetes, hyperlipidemia, and fatty liver.^[58]

Treatments used in children are primarily lifestyle interventions and behavioral techniques. Medications are not FDA approved for use in this age group.^[218]

In other animals

Main article: Obesity in pets

Obesity in pets is common in many countries. Rates of overweight and obesity in dogs in the United States range from 23% to 41% with about 5.1% obese.^[220] Rates of obesity in cats was slightly higher at 6.4%.^[220] In Australia the rate of obesity among dogs in a veterinary setting has been found to be 7.6%.^[221] The risk of obesity in dogs but not cats is related to whether or not their owners are obese.^[222]

References

1. ^ ^{a b} WHO 2000 p.6
2. ^ ^{a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai} Haslam DW, James WP (2005). "Obesity". Lancet 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769. 
3. ^ ^{a b} WHO 2000 p.9
4. ^ Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrinology). Totowa, NJ: Humana Press. pp. 158. ISBN 1-59745-400-1. http://books.google.ca/books?id=vWjK5etS7PMC&pg=PA121&lpg=PA121&dq=measurement+of+metabolism+in+obese+Bessesen&source=bl&ots=smPOi1tty9&sig=NvEWR4qspDeN3bq6g8pdvIdXwYA&hl=en&ei=5xTZSa61FY7CMfmqqPEO&sa=X&oi=book_result&ct=result&resnum=1#PPA158,M1. Retrieved April 5, 2009. 
5. ^ ^{a b} Adams JP, Murphy PG (July 2000). "Obesity in anaesthesia and intensive care". Br J Anaesth 85 (1): 91–108. doi:10.1093/bja/85.1.91. PMID 10927998. http://bja.oxfordjournals.org/cgi/content/full/85/1/91. 
6. ^ NICE 2006 p.10–11
7. ^ ^{a b} Imaz I, Martínez-Cervell C, García-Alvarez EE, Sendra-Gutiérrez JM, González-Enríquez J (July 2008). "Safety and effectiveness of the intragastric balloon for obesity. A meta-analysis". Obes Surg 18 (7): 841–6. doi:10.1007/s11695-007-9331-8. PMID 18459025. 
8. ^ ^{a b} Barness LA, Opitz JM, Gilbert-Barness E (December 2007). "Obesity: genetic, molecular, and environmental aspects". Am. J. Med. Genet. A 143A (24): 3016–34. doi:10.1002/ajmg.a.32035. PMID 18000969. 
9. ^ ^{a b c d e} Woodhouse R (2008). "Obesity in art: A brief overview". Front Horm Res 36: 271–86. doi:10.1159/000115370. PMID 18230908. http://books.google.ca/books?id=nXRU4Ea1aMkC&pg=PA271&lpg=PA271&dq=Obesity+in+art:+a+brief+overview&source=web&ots=G2ofZTj__r&sig=7HbW8aAnoQ-RIwt09ocD3xOHJZU&hl=en&sa=X&oi=book_result&resnum=5&ct=result#PPA271,M1. 
10. ^ Sweeting HN (2007). "Measurement and definitions of obesity in childhood and adolescence: A field guide for the uninitiated". Nutr J 6: 32. doi:10.1186/1475-2891-6-32. PMID 17963490. PMC 2164947. http://www.nutritionj.com/content/6/1/32. 
11. ^ NHLBI p.xiv
12. ^ Gray DS, Fujioka K (1991). "Use of relative weight and Body Mass Index for the determination of adiposity". J Clin Epidemiol 44 (6): 545–50. doi:10.1016/0895-4356(91)90218-X. PMID 2037859. 
13. ^ ^{a b} "Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Teens". Center for disease control and prevention. http://www.cdc.gov/nccdphp/dnpa/healthyweight/assessing/bmi/childrens_BMI/about_childrens_BMI.htm. Retrieved April 6, 2009. 
14. ^ ^{a b} Flegal KM, Ogden CL, Wei R, Kuczmarski RL, Johnson CL (June 2001). "Prevalence of overweight in US children: comparison of US growth charts from the Centers for Disease Control and Prevention with other reference values for body mass index". Am. J. Clin. Nutr. 73 (6): 1086–93. PMID 11382664. http://www.ajcn.org/cgi/content/full/73/6/1086. 
15. ^ ^{a b} Sturm R (July 2007). "Increases in morbid obesity in the USA: 2000–2005". Public Health 121 (7): 492–6. doi:10.1016/j.puhe.2007.01.006. PMID 17399752. 
16. ^ Kanazawa M, Yoshiike N, Osaka T, Numba Y, Zimmet P, Inoue S (December 2002). "Criteria and classification of obesity in Japan and Asia-Oceania". Asia Pac J Clin Nutr 11 Suppl 8: S732–S737. doi:10.1046/j.1440-6047.11.s8.19.x. PMID 12534701. 
17. ^ Bei-Fan Z (December 2002). "Predictive values of body mass index and waist circumference for risk factors of certain related diseases in Chinese adults: study on optimal cut-off points of body mass index and waist circumference in Chinese adults". Asia Pac J Clin Nutr 11 Suppl 8: S685–93. doi:10.1046/j.1440-6047.11.s8.9.x. PMID 12534691. 
18. ^ ^{a b} Freedman DM, Ron E, Ballard-Barbash R, Doody MM, Linet MS (May 2006). "Body mass index and all-cause mortality in a nationwide US cohort". Int J Obes (Lond) 30 (5): 822–9. doi:10.1038/sj.ijo.0803193. PMID 16404410. 
19. ^ Mokdad AH, Marks JS, Stroup DF, Gerberding JL (March 2004). "Actual causes of death in the United States, 2000" (PDF). JAMA 291 (10): 1238–45. doi:10.1001/jama.291.10.1238. PMID 15010446. http://www.csdp.org/research/1238.pdf. 
20. ^ ^{a b} Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB (October 1999). "Annual deaths attributable to obesity in the United States". JAMA 282 (16): 1530–8. doi:10.1001/jama.282.16.1530. PMID 10546692. http://jama.ama-assn.org/cgi/content/full/282/16/1530. 
21. ^ ^{a b c} Whitlock G, Lewington S, Sherliker P, et al. (March 2009). "Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies". Lancet 373 (9669): 1083–96. doi:10.1016/S0140-6736(09)60318-4. PMID 19299006. 
22. ^ Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW (October 1999). "Body-mass index and mortality in a prospective cohort of U.S. adults". N. Engl. J. Med. 341 (15): 1097–105. doi:10.1056/NEJM199910073411501. PMID 10511607. http://content.nejm.org/cgi/content/full/341/15/1097. 
23. ^ Pischon T, Boeing H, Hoffmann K, et al. (November 2008). "General and abdominal adiposity and risk of death in Europe". N. Engl. J. Med. 359 (20): 2105–20. doi:10.1056/NEJMoa0801891. PMID 19005195. 
24. ^ Manson JE, Willett WC, Stampfer MJ, et al. (1995). "Body weight and mortality among women". N. Engl. J. Med. 333 (11): 677–85. doi:10.1056/NEJM199509143331101. PMID 7637744. 
25. ^ ^{a b c d} Tsigosa Constantine (April 2008). "Management of Obesity in Adults: European Clinical Practice Guidelines". The European Journal of Obesity 1: 106. doi:10.1159/000126822. 
26. ^ Fried M, Hainer V, Basdevant A, et al. (April 2007). "Inter-disciplinary European guidelines on surgery of severe obesity". Int J Obes (Lond) 31 (4): 569–77. doi:10.1038/sj.ijo.0803560. PMID 17325689. 
27. ^ Peeters A, Barendregt JJ, Willekens F, Mackenbach JP, Al Mamun A, Bonneux L (January 2003). "Obesity in adulthood and its consequences for life expectancy: A life-table analysis" (PDF). Ann. Intern. Med. 138 (1): 24–32. PMID 12513041. http://www.annals.org/cgi/reprint/138/1/24. 
28. ^ Grundy SM (2004). "Obesity, metabolic syndrome, and cardiovascular disease". J. Clin. Endocrinol. Metab. 89 (6): 2595–600. doi:10.1210/jc.2004-0372. PMID 15181029. 
29. ^ Seidell 2005 p.9
30. ^ ^{a b} Bray GA (2004). "Medical consequences of obesity". J. Clin. Endocrinol. Metab. 89 (6): 2583–9. doi:10.1210/jc.2004-0535. PMID 15181027. 
31. ^ Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study". Lancet 364 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185. 
32. ^ Darvall KA, Sam RC, Silverman SH, Bradbury AW, Adam DJ (February 2007). "Obesity and thrombosis". Eur J Vasc Endovasc Surg 33 (2): 223–33. doi:10.1016/j.ejvs.2006.10.006. PMID 17185009. 
33. ^ ^{a b c d e} Yosipovitch G, DeVore A, Dawn A (June 2007). "Obesity and the skin: skin physiology and skin manifestations of obesity". J. Am. Acad. Dermatol. 56 (6): 901–16; quiz 917–20. doi:10.1016/j.jaad.2006.12.004. PMID 17504714. 
34. ^ Hahler B (June 2006). "An overview of dermatological conditions commonly associated with the obese patient". Ostomy Wound Manage 52 (6): 34–6, 38, 40 passim. PMID 16799182. 
35. ^ ^{a b c} Arendas K, Qiu Q, Gruslin A (June 2008). "Obesity in pregnancy: pre-conceptional to postpartum consequences". J Obstet Gynaecol Can 30 (6): 477–88. PMID 18611299. 
36. ^ Anand G, Katz PO (2008). "Gastroesophageal reflux disease and obesity". Rev Gastroenterol Disord 8 (4): 233–9. PMID 19107097. http://www.medreviews.com/pubmed.cfm?j=3&v=8&i=4&p=233. 
37. ^ Harney D, Patijn J (2007). "Meralgia paresthetica: diagnosis and management strategies". Pain Med 8 (8): 669–77. doi:10.1111/j.1526-4637.2006.00227.x. PMID 18028045. 
38. ^ Bigal ME, Lipton RB (January 2008). "Obesity and chronic daily headache". Curr Pain Headache Rep 12 (1): 56–61. doi:10.1007/s11916-008-0011-8. PMID 18417025. 
39. ^ Sharifi-Mollayousefi A, Yazdchi-Marandi M, Ayramlou H, et al. (February 2008). "Assessment of body mass index and hand anthropometric measurements as independent risk factors for carpal tunnel syndrome". Folia Morphol. (Warsz) 67 (1): 36–42. PMID 18335412. 
40. ^ Beydoun MA, Beydoun HA, Wang Y (May 2008). "Obesity and central obesity as risk factors for incident dementia and its subtypes: A systematic review and meta-analysis". Obes Rev 9 (3): 204–18. doi:10.1111/j.1467-789X.2008.00473.x. PMID 18331422. 
41. ^ Wall M (March 2008). "Idiopathic intracranial hypertension (pseudotumor cerebri)". Curr Neurol Neurosci Rep 8 (2): 87–93. doi:10.1007/s11910-008-0015-0. PMID 18460275. 
42. ^ Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ (April 2003). "Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults". N. Engl. J. Med. 348 (17): 1625–38. doi:10.1056/NEJMoa021423. PMID 12711737. 
43. ^ ^{a b c} Poulain M, Doucet M, Major GC, et al. (April 2006). "The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies". CMAJ 174 (9): 1293–9. doi:10.1503/cmaj.051299. PMID 16636330. PMC 1435949. http://www.cmaj.ca/cgi/content/full/174/9/1293. 
44. ^ Choi HK, Atkinson K, Karlson EW, Curhan G (April 2005). "Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study". Arch. Intern. Med. 165 (7): 742–8. doi:10.1001/archinte.165.7.742 (inactive 2009-10-31). PMID 15824292. 
45. ^ Tukker A, Visscher T, Picavet H (April 2008). "Overweight and health problems of the lower extremities: osteoarthritis, pain and disability". Public Health Nutr 12 (3): 1–10. doi:10.1017/S1368980008002103. PMID 18426630. 
46. ^ Molenaar EA, Numans ME, van Ameijden EJ, Grobbee DE (November 2008). "[Considerable comorbidity in overweight adults: results from the Utrecht Health Project]" (in Dutch; Flemish). Ned Tijdschr Geneeskd 152 (45): 2457–63. PMID 19051798. 
47. ^ Esposito K, Giugliano F, Di Palo C, Giugliano G, Marfella R, D'Andrea F, D'Armiento M, Giugliano D (2004). "Effect of lifestyle changes on erectile dysfunction in obese men: A randomized controlled trial". JAMA 291 (24): 2978–84. doi:10.1001/jama.291.24.2978. PMID 15213209. 
48. ^ Hunskaar S (2008). "A systematic review of overweight and obesity as risk factors and targets for clinical intervention for urinary incontinence in women". Neurourol. Urodyn. 27 (8): 749–57. doi:10.1002/nau.20635. PMID 18951445. 
49. ^ Ejerblad E, Fored CM, Lindblad P, Fryzek J, McLaughlin JK, Nyrén O (2006). "Obesity and risk for chronic renal failure". J. Am. Soc. Nephrol. 17 (6): 1695–702. doi:10.1681/ASN.2005060638. PMID 16641153. 
50. ^ Makhsida N, Shah J, Yan G, Fisch H, Shabsigh R (September 2005). "Hypogonadism and metabolic syndrome: Implications for testosterone therapy". J. Urol. 174 (3): 827–34. doi:10.1097/01.ju.0000169490.78443.59. PMID 16093964. 
51. ^ ^{a b} Schmidt DS, Salahudeen AK (2007). "Obesity-survival paradox-still a controversy?". Semin Dial 20 (6): 486–92. doi:10.1111/j.1525-139X.2007.00349.x. PMID 17991192. 
52. ^ ^{a b c} U.S. Preventive Services Task Force (June 2003). "Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale". Am Fam Physician 67 (12): 2573–6. PMID 12825847. http://www.aafp.org/afp/20030615/us.html. 
53. ^ Habbu A, Lakkis NM, Dokainish H (October 2006). "The obesity paradox: Fact or fiction?". Am. J. Cardiol. 98 (7): 944–8. doi:10.1016/j.amjcard.2006.04.039. PMID 16996880. 
54. ^ Romero-Corral A, Montori VM, Somers VK, et al. (2006). "Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: A systematic review of cohort studies". Lancet 368 (9536): 666–78. doi:10.1016/S0140-6736(06)69251-9. PMID 16920472. 
55. ^ Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA (July 2008). "Body mass index and mortality in heart failure: A meta-analysis". Am. Heart J. 156 (1): 13–22. doi:10.1016/j.ahj.2008.02.014. PMID 18585492. 
56. ^ Oreopoulos A, Padwal R, Norris CM, Mullen JC, Pretorius V, Kalantar-Zadeh K (February 2008). "Effect of obesity on short- and long-term mortality postcoronary revascularization: A meta-analysis". Obesity (Silver Spring) 16 (2): 442–50. doi:10.1038/oby.2007.36. PMID 18239657. 
57. ^ Diercks DB, Roe MT, Mulgund J et al. (July 2006). "The obesity paradox in non-ST-segment elevation acute coronary syndromes: Results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association Guidelines Quality Improvement Initiative". Am Heart J 152 (1): 140–8. doi:10.1016/j.ahj.2005.09.024. PMID 16824844. 
58. ^ ^{a b c d e f} Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E (April 2007). "2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children [summary]". CMAJ 176 (8): S1–13. doi:10.1503/cmaj.061409. PMID 17420481. 
59. ^ Bleich S, Cutler D, Murray C, Adams A (2008). "Why is the developed world obese?". Annu Rev Public Health 29: 273–95. doi:10.1146/annurev.publhealth.29.020907.090954. PMID 18173389. 
60. ^ Drewnowski A, Specter SE (January 2004). "Poverty and obesity: the role of energy density and energy costs". Am. J. Clin. Nutr. 79 (1): 6–16. PMID 14684391. http://www.ajcn.org/cgi/content/full/79/1/6. 
61. ^ Nestle M, Jacobson MF (2000). "Halting the obesity epidemic: A public health policy approach". Public Health Rep 115 (1): 12–24. doi:10.1093/phr/115.1.12. PMID 10968581. 
62. ^ James WP (March 2008). "The fundamental drivers of the obesity epidemic". Obes Rev 9 Suppl 1: 6–13. doi:10.1111/j.1467-789X.2007.00432.x. PMID 18307693. 
63. ^ Keith SW, Redden DT, Katzmarzyk PT, et al. (2006). "Putative contributors to the secular increase in obesity: Exploring the roads less traveled". Int J Obes (Lond) 30 (11): 1585–94. doi:10.1038/sj.ijo.0803326. PMID 16801930. http://www.nature.com/ijo/journal/v30/n11/full/0803326a.html. 
64. ^ ^{a b c d e f} "EarthTrends: Nutrition: Calorie supply per capita". World Resources Institute. http://earthtrends.wri.org/searchable_db/index.php?theme=8&variable_ID=212&action=select_countries. Retrieved Oct. 18, 2009. 
65. ^ "FAO: Food Security Statistics". Food and Agriculture Organization of the United Nations. http://www.fao.org/economic/ess/food-security-statistics/en/. Retrieved Oct. 18, 2009. 
66. ^ "USDA: frsept99b". United States Department of Agriculture. http://www.scribd.com/doc/1470965/USDA-frsept99b. Retrieved January 10, 2009. 
67. ^ National Control for Health Statistics. "Nutrition For Everyone". Centers for Disease Control and Prevention. http://www.cdc.gov/nccdphp/dnpa/nutrition/nutrition_for_everyone. Retrieved 2008-07-09. 
68. ^ Marantz PR, Bird ED, Alderman MH (March 2008). "A call for higher standards of evidence for dietary guidelines". Am J Prev Med 34 (3): 234–40. doi:10.1016/j.amepre.2007.11.017. PMID 18312812. 
69. ^ Flegal KM, Carroll MD, Ogden CL, Johnson CL (October 2002). "Prevalence and trends in obesity among US adults, 1999–2000". JAMA 288 (14): 1723–1727. doi:10.1001/jama.288.14.1723. PMID 12365955. http://jama.ama-assn.org/cgi/content/full/288/14/1723. 
70. ^ Wright JD, Kennedy-Stephenson J, Wang CY, McDowell MA, Johnson CL (February 2004). "Trends in intake of energy and macronutrients—United States, 1971–2000". MMWR Morb Mortal Wkly Rep 53 (4): 80–2. PMID 14762332. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm. 
71. ^ ^{a b c d} Caballero B (2007). "The global epidemic of obesity: An overview". Epidemiol Rev 29: 1–5. doi:10.1093/epirev/mxm012. PMID 17569676. 
72. ^ Malik VS, Schulze MB, Hu FB (August 2006). "Intake of sugar-sweetened beverages and weight gain: a systematic review". Am. J. Clin. Nutr. 84 (2): 274–88. PMID 16895873. http://www.ajcn.org/cgi/content/full/84/2/274. 
73. ^ Olsen NJ, Heitmann BL (January 2009). "Intake of calorically sweetened beverages and obesity". Obes Rev 10 (1): 68–75. doi:10.1111/j.1467-789X.2008.00523.x. PMID 18764885. 
74. ^ Rosenheck R (November 2008). "Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk". Obes Rev 9 (6): 535–47. doi:10.1111/j.1467-789X.2008.00477.x. PMID 18346099. 
75. ^ Lin BH, Guthrie J and Frazao E (1999). "Nutrient contribution of food away from home". in Frazão E. Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences. Washington, DC: US Department of Agriculture, Economic Research Service. pp. 213–239. http://www.ers.usda.gov/publications/aib750/. 
76. ^ Pollan, Michael (22 April 2007). "You Are What You Grow". New York Times. http://www.nytimes.com/2007/04/22/magazine/22wwlnlede.t.html?ex=1186027200&en=bbe0f6a2c10e3b3c&ei=5070. Retrieved 2007-07-30. 
77. ^ Kopelman and Caterson 2005:324.
78. ^ "Metabolism alone doesn't explain how thin people stay thin" (registration required). John Schieszer. The Medical Post. http://www.medicalpost.com/therapeutics/nutrition/article.jsp?content=20080818_121920_25640. Retrieved December 31, 2008. 
79. ^ Seidell 2005 p.10
80. ^ ^{a b} "WHO: Obesity and overweight". World Health Organization. http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/. Retrieved January 10, 2009. 
81. ^ ^{a b c} "WHO | Physical Inactivity: A Global Public Health Problem". World Health Organization. http://www.who.int/dietphysicalactivity/factsheet_inactivity/en/index.html. Retrieved February 22, 2009. 
82. ^ ^{a b} Ness-Abramof R, Apovian CM (February 2006). "Diet modification for treatment and prevention of obesity". Endocrine 29 (1): 5–9. doi:10.1385/ENDO:29:1:135. PMID 16622287. 
83. ^ Salmon J, Timperio A (2007). "Prevalence, trends and environmental influences on child and youth physical activity". Med Sport Sci 50: 183–99. doi:10.1159/0000101391 (inactive 2009-10-31). PMID 17387258. 
84. ^ Borodulin K, Laatikainen T, Juolevi A, Jousilahti P (June 2008). "Thirty-year trends of physical activity in relation to age, calendar time and birth cohort in Finnish adults". Eur J Public Health 18 (3): 339–44. doi:10.1093/eurpub/ckm092. PMID 17875578. 
85. ^ Brownson RC, Boehmer TK, Luke DA (2005). "Declining rates of physical activity in the United States: what are the contributors?". Annu Rev Public Health 26: 421–43. doi:10.1146/annurev.publhealth.26.021304.144437. PMID 15760296. 
86. ^ Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH (April 1996). "Television viewing as a cause of increasing obesity among children in the United States, 1986–1990". Arch Pediatr Adolesc Med 150 (4): 356–62. PMID 8634729. 
87. ^ Vioque J, Torres A, Quiles J (December 2000). "Time spent watching television, sleep duration and obesity in adults living in Valencia, Spain". Int. J. Obes. Relat. Metab. Disord. 24 (12): 1683–8. doi:10.1038/sj.ijo.0801434. PMID 11126224. 
88. ^ Tucker LA, Bagwell M (July 1991). "Television viewing and obesity in adult females" (PDF). Am J Public Health 81 (7): 908–11. doi:10.2105/AJPH.81.7.908. PMID 2053671. PMC 1405200. http://www.ajph.org/cgi/reprint/81/7/908. 
89. ^ "Media + Child and Adolescent Health: A Systematic Review" (pdf). Ezekiel J. Emanuel. Common Sense Media. 2008. http://www.commonsensemedia.org/sites/default/files/CSM_media+health_v2c%20110708.pdf. Retrieved April 6, 2009. 
90. ^ Mary Jones. "Case Study: Cataplexy and SOREMPs Without Excessive Daytime Sleepiness in Prader Willi Syndrome. Is This the Beginning of Narcolepsy in a Five Year Old?". European Society of Sleep Technologists. http://www.esst.org/newsletter2000.htm. Retrieved April 6, 2009. 
91. ^ Poirier P, Giles TD, Bray GA, et al. (May 2006). "Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss". Arterioscler. Thromb. Vasc. Biol. 26 (5): 968–76. doi:10.1161/01.ATV.0000216787.85457.f3. PMID 16627822. 
92. ^ Yang W, Kelly T, He J (2007). "Genetic epidemiology of obesity". Epidemiol Rev 29: 49–61. doi:10.1093/epirev/mxm004. PMID 17566051. 
93. ^ Walley AJ, Asher JE, Froguel P (June 2009). "The genetic contribution to non-syndromic human obesity". Nat. Rev. Genet. 10 (7): 431–42. doi:10.1038/nrg2594. PMID 19506576. 
94. ^ Farooqi S, O'Rahilly S (December 2006). "Genetics of obesity in humans". Endocr. Rev. 27 (7): 710–18. doi:10.1210/er.2006-0040. PMID 17122358. http://edrv.endojournals.org/cgi/content/full/27/7/710. 
95. ^ Kolata,Gina (2007). Rethinking thin: The new science of weight loss – and the myths and realities of dieting. Picador. pp. 122. ISBN 0-312-42785-9. 
96. ^ Chakravarthy MV, Booth FW (2004). "Eating, exercise, and "thrifty" genotypes: Connecting the dots toward an evolutionary understanding of modern chronic diseases". J. Appl. Physiol. 96 (1): 3–10. doi:10.1152/japplphysiol.00757.2003. PMID 14660491. 
97. ^ Wells JC (February 2009). "Ethnic variability in adiposity and cardiovascular risk: the variable disease selection hypothesis". Int J Epidemiol 38 (1): 63–71. doi:10.1093/ije/dyn183. PMID 18820320. 
98. ^ Rosén T, Bosaeus I, Tölli J, Lindstedt G, Bengtsson BA (1993). "Increased body fat mass and decreased extracellular fluid volume in adults with growth hormone deficiency". Clin. Endocrinol. (Oxf) 38 (1): 63–71. doi:10.1111/j.1365-2265.1993.tb00974.x. PMID 8435887. 
99. ^ Zametkin AJ, Zoon CK, Klein HW, Munson S (February 2004). "Psychiatric aspects of child and adolescent obesity: a review of the past 10 years". J Am Acad Child Adolesc Psychiatry 43 (2): 134–50. doi:10.1097/01.chi.0000100427.25002.06 (inactive 2009-04-10). PMID 14726719. 
100. ^ Yach D, Stuckler D, Brownell KD (January 2006). "Epidemiologic and economic consequences of the global epidemics of obesity and diabetes". Nat. Med. 12 (1): 62–6. doi:10.1038/nm0106-62. PMID 16397571. 
101. ^ Sobal J, Stunkard AJ (March 1989). "Socioeconomic status and obesity: A review of the literature". Psychol Bull 105 (2): 260–75. doi:10.1037/0033-2909.105.2.260. PMID 2648443. 
102. ^ ^{a b} McLaren L (2007). "Socioeconomic status and obesity". Epidemiol Rev 29: 29–48. doi:10.1093/epirev/mxm001. PMID 17478442. 
103. ^ ^{a b} Wilkinson, Richard; Pickett, Kate (2009). The Spirit Level: Why More Equal Societies Almost Always Do Better. London: Allen Lane. pp. 91–101. ISBN 978-1-846-14039-6. http://www.equalitytrust.org.uk/why/evidence/obesity. 
104. ^ Christakis NA, Fowler JH (2007). "The Spread of Obesity in a Large Social Network over 32 Years". New England Journal of Medicine 357 (4): 370–379. doi:10.1056/NEJMsa066082. PMID 17652652. 
105. ^ Bjornstop P (2001). "Do stress reactions cause abdominal obesity and comorbidities?". Obesity Reviews 2 (2): 73–86. 
106. ^ Goodman E, Adler NE, Daniels SR, Morrison JA, Slap GB, Dolan LM (2003). "Impact of objective and subjective social status on obesity in a biracial cohort of adolescents". Obesity Reviews 11 (8): 1018–26. 
107. ^ Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ, Campbell SM (November 1995). "The influence of smoking cessation on the prevalence of overweight in the United States". N. Engl. J. Med. 333 (18): 1165–70. doi:10.1056/NEJM199511023331801. PMID 7565970. http://content.nejm.org/cgi/content/full/333/18/1165. 
108. ^ Chiolero A, Faeh D, Paccaud F, Cornuz J (01 April 2008). "Consequences of smoking for body weight, body fat distribution, and insulin resistance". Am. J. Clin. Nutr. 87 (4): 801–9. PMID 18400700. http://www.ajcn.org/cgi/content/full/87/4/801. 
109. ^ Weng HH, Bastian LA, Taylor DH, Moser BK, Ostbye T (2004). "Number of children associated with obesity in middle-aged women and men: results from the health and retirement study". J Womens Health (Larchmt) 13 (1): 85–91. doi:10.1089/154099904322836492. PMID 15006281. 
110. ^ Bellows-Riecken KH, Rhodes RE (February 2008). "A birth of inactivity? A review of physical activity and parenthood". Prev Med 46 (2): 99–110. doi:10.1016/j.ypmed.2007.08.003. PMID 17919713. 
111. ^ "Obesity and Overweight" (PDF). World Health Organization. http://www.who.int/dietphysicalactivity/media/en/gsfs_obesity.pdf. Retrieved February 22, 2009. 
112. ^ ^{a b} Caballero B (March 2001). "Introduction. Symposium: Obesity in developing countries: biological and ecological factors". J. Nutr. 131 (3): 866S–870S. PMID 11238776. http://jn.nutrition.org/cgi/content/full/131/3/866S. 
113. ^ DiBaise JK, Zhang H, Crowell MD, Krajmalnik-Brown R, Decker GA, Rittmann BE (April 2008). "Gut microbiota and its possible relationship with obesity". Mayo Clinic proceedings. Mayo Clinic 83 (4): 460–9. doi:10.4065/83.4.460. PMID 18380992. 
114. ^ Falagas ME, Kompoti M (July 2006). "Obesity and infection". Lancet Infect Dis 6 (7): 438–46. doi:10.1016/S1473-3099(06)70523-0. PMID 16790384. 
115. ^ ^{a b c d e} Flier JS (2004). "Obesity wars: Molecular progress confronts an expanding epidemic". Cell 116 (2): 337–50. doi:10.1016/S0092-8674(03)01081-X. PMID 14744442. 
116. ^ Hamann A, Matthaei S (1996). "Regulation of energy balance by leptin". Exp. Clin. Endocrinol. Diabetes 104 (4): 293–300. doi:10.1055/s-0029-1211457. PMID 8886745. 
117. ^ Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiologya: A cellular and molecular approach. Philadelphia: Saunders. pp. 1227. ISBN 0-7216-3256-4. 
118. ^ ^{a b c d} Strychar I (January 2006). "Diet in the management of weight loss". CMAJ 174 (1): 56–63. doi:10.1503/cmaj.045037. PMID 16389240. PMC 1319349. http://www.cmaj.ca/cgi/content/full/174/1/56. 
119. ^ Shick SM, Wing RR, Klem ML, McGuire MT, Hill JO, Seagle H (April 1998). "Persons successful at long-term weight loss and maintenance continue to consume a low-energy, low-fat diet". J Am Diet Assoc 98 (4): 408–13. doi:10.1016/S0002-8223(98)00093-5. PMID 9550162. 
120. ^ Tate DF, Jeffery RW, Sherwood NE, Wing RR (01 April 2007). "Long-term weight losses associated with prescription of higher physical activity goals. Are higher levels of physical activity protective against weight regain?". Am. J. Clin. Nutr. 85 (4): 954–9. PMID 17413092. http://www.ajcn.org/cgi/content/full/85/4/954. 
121. ^ Wing, Rena R; Phelan, Suzanne (01 July 2005). "Science-Based Solutions to Obesity: What are the Roles of Academia, Government, Industry, and Health Care? Proceedings of a symposium, Boston, Massachusetts, USA, 10–11 March 2004 and Anaheim, California, USA, 2 October 2004". Am. J. Clin. Nutr. 82 (1 Suppl): 207S–273S. PMID 16002825. http://www.ajcn.org/cgi/content/full/82/1/222S. 
122. ^ Weiss EC, Galuska DA, Kettel Khan L, Gillespie C, Serdula MK (July 2007). "Weight regain in U.S. adults who experienced substantial weight loss, 1999–2002". Am J Prev Med 33 (1): 34–40. doi:10.1016/j.amepre.2007.02.040. PMID 17572309. 
123. ^ Anderson JW, Konz EC, Frederich RC, Wood CL (01 November 2001). "Long-term weight-loss maintenance: A meta-analysis of US studies". Am. J. Clin. Nutr. 74 (5): 579–84. PMID 11684524. http://www.ajcn.org/cgi/content/full/74/5/579. 
124. ^ Williamson DF, Pamuk E, Thun M, Flanders D, Byers T, Heath C (June 1995). "Prospective study of intentional weight loss and mortality in never-smoking overweight US white women aged 40–64 years". Am. J. Epidemiol. 141 (12): 1128–41. PMID 7771451. 
125. ^ Poobalan AS, Aucott LS, Smith WC, Avenell A, Jung R, Broom J (November 2007). "Long-term weight loss effects on all cause mortality in overweight/obese populations". Obes Rev 8 (6): 503–13. doi:10.1111/j.1467-789X.2007.00393.x. PMID 17949355. 
126. ^ Peeters A, O'Brien PE, Laurie C, et al. (December 2007). "Substantial intentional weight loss and mortality in the severely obese". Ann. Surg. 246 (6): 1028–33. doi:10.1097/SLA.0b013e31814a6929. PMID 18043106. 
127. ^ Sacks FM, Bray GA, Carey VJ, et al. (February 2009). "Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates". N. Engl. J. Med. 360 (9): 859–73. doi:10.1056/NEJMoa0804748. PMID 19246357. 
128. ^ Gwinup G (1987). "Weight loss without dietary restriction: Efficacy of different forms of aerobic exercise". Am J Sports Med 15 (3): 275–9. doi:10.1177/036354658701500317. PMID 3618879. 
129. ^ Sahlin K, Sallstedt EK, Bishop D, Tonkonogi M (December 2008). "Turning down lipid oxidation during heavy exercise—what is the mechanism?". J. Physiol. Pharmacol. 59 Suppl 7: 19–30. PMID 19258655. http://www.jpp.krakow.pl/journal/archive/1208_s7/pdf/19_1208_s7_article.pdf. 
130. ^ ^{a b} Haskell WL, Lee IM, Pate RR, et al. (August 2007). "Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association". Circulation 116 (9): 1081–93. doi:10.1161/CIRCULATIONAHA.107.185649. PMID 17671237. 
131. ^ Shaw K, Gennat H, O'Rourke P, Del Mar C (2006). "Exercise for overweight or obesity". Cochrane database of systematic reviews (Online) (4): CD003817. doi:10.1002/14651858.CD003817.pub3. PMID 17054187. 
132. ^ Lee L, Kumar S, Leong LC (February 1994). "The impact of five-month basic military training on the body weight and body fat of 197 moderately to severely obese Singaporean males aged 17 to 19 years". Int. J. Obes. Relat. Metab. Disord. 18 (2): 105–9. PMID 8148923. 
133. ^ Bessesen DH (June 2008). "Update on obesity". J. Clin. Endocrinol. Metab. 93 (6): 2027–34. doi:10.1210/jc.2008-0520. PMID 18539769. 
134. ^ Bravata DM, Smith-Spangler C, Sundaram V, et al. (November 2007). "Using pedometers to increase physical activity and improve health: a systematic review". JAMA : the journal of the American Medical Association 298 (19): 2296–304. doi:10.1001/jama.298.19.2296. PMID 18029834. 
135. ^ Kahn EB, Ramsey LT, Brownson RC, et al. (May 2002). "The effectiveness of interventions to increase physical activity. A systematic review". Am J Prev Med 22 (4 Suppl): 73–107. doi:10.1016/S0749-3797(02)00434-8. PMID 11985936. 
136. ^ "www.paho.org". Pan American Health Organization. http://www.paho.org/English/DD/PIN/ePersp001_article01.htm. Retrieved January 10, 2009. 
137. ^ Baron M (November 2004). "Commercial weight-loss programs". Health Care Food Nutr Focus 21 (11): 8–9. PMID 15559885. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1090-2260&volume=21&issue=11&spage=8. 
138. ^ Heshka S, Anderson JW, Atkinson RL, et al. (April 2003). "Weight loss with self-help compared with a structured commercial program: a randomized trial". JAMA 289 (14): 1792–8. doi:10.1001/jama.289.14.1792 (inactive 2009-10-31). PMID 12684357. 
139. ^ Tsai AG, Wadden TA (January 2005). "Systematic review: an evaluation of major commercial weight loss programs in the United States". Ann. Intern. Med. 142 (1): 56–66. PMID 15630109. 
140. ^ Hewitt, Duncan (May 23, 2000). "China battles obesity". BBC. http://news.bbc.co.uk/2/hi/health/760787.stm. Retrieved August 8, 2009. 
141. ^ MacLeod, Calum (August 1, 2007). "Obesity of China's kids stuns officials". USA Today. http://www.usatoday.com/news/world/2007-01-08-chinese-obesity_x.htm. Retrieved August 8, 2009. 
142. ^ ^{a b c d} "WIN – Publication – Prescription Medications for the Treatment of Obesity". National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). National Institutes of Health. http://win.niddk.nih.gov/publications/prescription.htm#fdameds. Retrieved January 14, 2009. 
143. ^ "Anti-obesity drug no magic bullet". Canadian Broadcasting Corporation. January 2, 2007. http://www.cbc.ca/health/story/2007/01/02/rimonabant.html. Retrieved 2008-09-19. 
144. ^ "FDA Briefing Document NDA 21-888 Zimulti (rimonabant) Tablets, 20 mg Sanofi Aventis Advisory Committee" (PDF). Food and Drug Administration. June 13, 2007. http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4306b1-fda-backgrounder.pdf. Retrieved 2008-09-19. 
145. ^ Rucker D, Padwal R, Li SK, Curioni C, Lau DC (2007). "Long term pharmacotherapy for obesity and overweight: Updated meta-analysis". BMJ 335 (7631): 1194–99. doi:10.1136/bmj.39385.413113.25. PMID 18006966. PMC 2128668. http://www.bmj.com/cgi/content/full/335/7631/1194. 
146. ^ Li Z, Maglione M, Tu W, et al. (April 2005). "Meta-analysis: pharmacologic treatment of obesity". Ann. Intern. Med. 142 (7): 532–46. PMID 15809465. http://www.annals.org/cgi/content/full/142/7/532. 
147. ^ UK Prospective Diabetes Study (UKPDS) Group (1998). "Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34)". Lancet 352 (9131): 854–65. doi:10.1016/S0140-6736(98)07037-8. PMID 9742977. 
148. ^ Fonseca V (2003). "Effect of thiazolidinediones on body weight in patients with diabetes mellitus". Am. J. Med. 115 Suppl 8A: 42S–48S. doi:10.1016/j.amjmed.2003.09.005. PMID 14678865. 
149. ^ Norris SL, Zhang X, Avenell A, Gregg E, Schmid CH, Lau J (2005). "Pharmacotherapy for weight loss in adults with type 2 diabetes mellitus". Cochrane database of systematic reviews (Online) (1): CD004096. doi:10.1002/14651858.CD004096.pub2. PMID 15674929. 
150. ^ Rados C (2004). "Ephedra ban: no shortage of reasons". FDA Consum 38 (2): 6–7. PMID 15101356. 
151. ^ Boss, Olivier; Karl G. Hofbauer (2004). Pharmacotherapy of obesity: options and alternatives. Boca Raton: CRC Press. pp. 286. ISBN 0-415-30321-4. http://books.google.ca/books?id=v7o5e8aSXB0C&pg=PA286&lpg=PA286&dq=Amphetamines+are+not+FDA+approved+to+treat+obesity&source=web&ots=6pX54AHIK-&sig=eQOKZW0RA6xuZvsd3G5GG_aCc38&hl=en&sa=X&oi=book_result&resnum=5&ct=result#PPA286,M1. Retrieved January 14, 2009. 
152. ^ Flanagan CM, Kaesberg JL, Mitchell ES, Ferguson MA, Haigney MC (August 2008). "Coronary artery aneurysm and thrombosis following chronic ephedra use". Int. J. Cardiol.. doi:10.1016/j.ijcard.2008.06.081. PMID 18718687. 
153. ^ Cohen PA, McCormick D, Casey C, Dawson GF, Hacker KA (December 2007). "Imported Compounded Diet Pill Use Among Brazilian Women Immigrants in the United States". J Immigr Minor Health 11 (3): 229–36. doi:10.1007/s10903-007-9099-x. PMID 18066718. 
154. ^ Encinosa WE, Bernard DM, Chen CC, Steiner CA (2006). "Healthcare utilization and outcomes after bariatric surgery". Medical care 44 (8): 706–12. doi:10.1097/01.mlr.0000220833.89050.ed. PMID 16862031. 
155. ^ Sjöström L, Narbro K, Sjöström CD, et al. (August 2007). "Effects of bariatric surgery on mortality in Swedish obese subjects". N. Engl. J. Med. 357 (8): 741–52. doi:10.1056/NEJMoa066254. PMID 17715408. 
156. ^ Sjöström L, Narbro K, Sjöström CD, et al. (2007). "Effects of bariatric surgery on mortality in Swedish obese subjects". N. Engl. J. Med. 357 (8): 741–52. doi:10.1056/NEJMoa066254. PMID 17715408. 
157. ^ ^{a b} Adams TD, Gress RE, Smith SC, et al. (2007). "Long-term mortality after gastric bypass surgery". N. Engl. J. Med. 357 (8): 753–61. doi:10.1056/NEJMoa066603. PMID 17715409. 
158. ^ Tice JA, Karliner L, Walsh J, Petersen AJ, Feldman MD (October 2008). "Gastric banding or bypass? A systematic review comparing the two most popular bariatric procedures". Am. J. Med. 121 (10): 885–93. doi:10.1016/j.amjmed.2008.05.036. PMID 18823860. 
159. ^ Giugliano G, Nicoletti G, Grella E, et al. (April 2004). "Effect of liposuction on insulin resistance and vascular inflammatory markers in obese women". Br J Plast Surg 57 (3): 190–4. doi:10.1016/j.bjps.2003.12.010. PMID 15006519. 
160. ^ Klein S, Fontana L, Young VL, et al. (June 2004). "Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease". N. Engl. J. Med. 350 (25): 2549–57. doi:10.1056/NEJMoa033179. PMID 15201411. 
161. ^ ^{a b} "Obesity Guidelines Website". Australian Government Department of Health and Ageing. http://www.health.gov.au/internet/main/publishing.nsf/Content/obesityguidelines-index.htm. Retrieved Oct. 25, 2009. 
162. ^ ^{a b} Snow V, Barry P, Fitterman N, Qaseem A, Weiss K (2005). "Pharmacologic and surgical management of obesity in primary care: A clinical practice guideline from the American College of Physicians". Ann Intern Med 142 (7): 525–31. PMID 15809464.  Fulltext.
163. ^ Pignone MP, Ammerman A, Fernandez L, et al. (2003). "Counseling to promote a healthy diet in adults: A summary of the evidence for the U.S. Preventive Services Task Force". American journal of preventive medicine 24 (1): 75–92. doi:10.1016/S0749-3797(02)00580-9. PMID 12554027. 
164. ^ ^{a b} "Global Prevalence of Adult Obesity" (PDF). International Obesity Taskforce. http://www.iotf.org/database/documents/GlobalPrevalenceofAdultObesity16thDecember08.pdf. Retrieved January 29, 2008. 
165. ^ ^{a b} Haslam D (March 2007). "Obesity: a medical history". Obes Rev 8 Suppl 1: 31–6. doi:10.1111/j.1467-789X.2007.00314.x. PMID 17316298. 
166. ^ ^{a b} "Obesity and overweight". World Health Organization. http://www.who.int/mediacentre/factsheets/fs311/en/index.html. Retrieved April 8th, 2009. 
167. ^ Seidell 2005 p.5
168. ^ Howard, Natasha J. (March 2008). "Severe obesity: Investigating the socio-demographics within the extremes of body mass index". Obesity Research &Clinical Practice 2 (1): 51–59. doi:10.1016/j.orcp.2008.01.001. 
169. ^ Tjepkema M (2005-07-06). "Measured Obesity–Adult obesity in Canada: Measured height and weight". Nutrition: Findings from the Canadian Community Health Survey. Ottawa, Ontario: Statistics Canada. http://www.statcan.gc.ca/pub/82-620-m/2005001/article/adults-adultes/8060-eng.htm. 
170. ^ Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-146633-9. 
171. ^ Satcher D (2001). The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General. ISBN 0-16051-005-8. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=hssurggen&part=A2. 
172. ^ Brook Barnes (2007-07-18). "Limiting Ads of Junk Food to Children". New York Times. http://www.nytimes.com/2007/07/18/business/18food.html. Retrieved 2008-07-24. 
173. ^ "Fewer Sugary Drinks Key to Weight Loss - healthfinder.gov". U.S. Department of Health and Human Services. http://www.healthfinder.gov/news/newsstory.aspx?docID=625759. Retrieved Oct 18,2009. 
174. ^ Brennan Ramirez LK, Hoehner CM, Brownson RC et al. (December 2006). "Indicators of activity-friendly communities: An evidence-based consensus process". Am J Prev Med 31 (6): 530–32. doi:10.1016/j.amepre.2006.07.026. PMID 17169714. 
175. ^ National Heart, Lung, and Blood Institute (1998) (PDF). Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. International Medical Publishing, Inc. ISBN 1-58808-002-1. http://www.nhlbi.nih.gov/guidelines/obesity/ob_gdlns.pdf. 
176. ^ Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E (April 2007). "2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children [summary]". CMAJ 176 (8): S1–13. doi:10.1503/cmaj.061409. PMID 17420481. PMC 1839777. http://www.cmaj.ca/cgi/content/full/176/8/S1. 
177. ^ (PDF) Storing up problems; the medical case for a slimmer nation. London: Royal College of Physicians. 2004-02-11. ISBN 1-86016-200-2. http://www.rcplondon.ac.uk/pubs/contents/ca4032bf-7b10-4e2f-8701-b24874f84514.pdf. 
178. ^ Great Britain Parliament House of Commons Health Committee (May 2004). Obesity – Volume 1 – HCP 23-I, Third Report of session 2003–04. Report, together with formal minutes. London, UK: TSO (The Stationery Office). ISBN 0-21501-737-4. http://www.publications.parliament.uk/pa/cm200304/cmselect/cmhealth/23/2302.htm. Retrieved 2007-12-17. 
179. ^ "Obesity: guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children" (pdf). National Institute for Health and Clinical Excellence(NICE). National Health Services (NHS). 2006. http://www.nice.org.uk/nicemedia/pdf/CG43NICEGuideline.pdf. Retrieved April 8th,2009. 
180. ^ Wanless, Sir Derek; John Appleby, Anthony Harrison, Darshan Patel (2007). Our Future Health Secured? A review of NHS funding and performance. London, UK: The King's Fund. ISBN 185717562X. http://www.kingsfund.org.uk/research/publications/our_future.html. Retrieved 2007-12-17. 
181. ^ Sacks G, Swinburn B, Lawrence M (January 2009). "Obesity Policy Action framework and analysis grids for a comprehensive policy approach to reducing obesity". Obes Rev 10 (1): 76–86. doi:10.1111/j.1467-789X.2008.00524.x. PMID 18761640. 
182. ^ Bakewell J (2007). "Bariatric furniture: Considerations for use.". Int J Ther Rehabil (7): 329–33. http://www.ijtr.co.uk/cgi-bin/go.pl/library/article.cgi?uid=23858;article=IJTR_14_7_329_333. 
183. ^ ^{a b} Puhl R., Henderson K., and Brownell K. 2005 p.29
184. ^ Cummings, Laura (5 February 2003). "The diet business: Banking on failure". BBC News. http://news.bbc.co.uk/2/hi/business/2725943.stm. Retrieved 25 February 2009. 
185. ^ Finkelstein EA, Fiebelkorn IA, Wang G (01 Jan 2003). "National medical spending attributable to overweight and obesity: How much, and who’s paying". Health Affairs Online (May). http://content.healthaffairs.org/cgi/content/full/hlthaff.w3.219v1/DC1. 
186. ^ "Obesity and overweight: Economic consequences". Centers for Disease Control and Prevention. http://www.cdc.gov/nccdphp/dnpa/obesity/economic_consequences.htm. Retrieved 2007-09-05. 
187. ^ van Baal PH, Polder JJ, de Wit GA, et al. (February 2008). "Lifetime medical costs of obesity: Prevention no cure for increasing health expenditure". PLoS Med. 5 (2): e29. doi:10.1371/journal.pmed.0050029. PMID 18254654. PMC 2225430. http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0050029. 
188. ^ Neovius K, Johansson K, Kark M, Neovius M (January 2009). "Obesity status and sick leave: a systematic review". Obes Rev 10 (1): 17–27. doi:10.1111/j.1467-789X.2008.00521.x. PMID 18778315. 
189. ^ Ostbye T, Dement JM, Krause KM (2007). "Obesity and workers' compensation: Results from the Duke Health and Safety Surveillance System". Arch. Intern. Med. 167 (8): 766–73. doi:10.1001/archinte.167.8.766. PMID 17452538. 
190. ^ "Alabama "Obesity Penalty" Stirs Debate". Don Fernandez. http://www.webmd.com/diet/news/20080825/alabama-obesity-penalty-stirs-debate. Retrieved April 5, 2009. 
191. ^ ^{a b} Puhl R, Brownell KD (December 2001). "Bias, discrimination, and obesity". Obes. Res. 9 (12): 788–805. doi:10.1038/oby.2001.108. PMID 11743063. 
192. ^ Puhl R., Henderson K., and Brownell K. 2005 p.30
193. ^ Lisa DiCarlo (2002-10-24). "Why Airlines Can't Cut The Fat". Forbes.com. http://www.forbes.com/2002/10/24/cx_ld_1024obese.html. Retrieved 2008-07-23. 
194. ^ Dannenberg AL, Burton DC, Jackson RJ (2004). "Economic and environmental costs of obesity: The impact on airlines". American journal of preventive medicine 27 (3): 264. doi:10.1016/j.amepre.2004.06.004. PMID 15450642. 
195. ^ ^{a b} "109th U.S. Congress (2005–2006) H.R. 554: 109th U.S. Congress (2005–2006) H.R. 554: Personal Responsibility in Food Consumption Act of 2005". GovTrack.us. http://www.govtrack.us/congress/bill.xpd?bill=h109-554. Retrieved 2008-07-24. 
196. ^ "Online Etymology Dictionary: Obesity". Douglas Harper. http://www.etymonline.com/index.php?term=obesity. Retrieved December 31, 2008. 
197. ^ "Obesity, n". Oxford English Dictionary 2008. http://www.oed.com/. Retrieved March 21, 2009. 
198. ^ ^{a b} Zachary Bloomgarden (2003). "Prevention of Obesity and Diabetes". Diabetes Care 26 (11): 3172–3178. doi:10.2337/diacare.26.11.3172. PMID 14578257. http://care.diabetesjournals.org/content/26/11/3172.full. 
199. ^ ^{a b} "History of Medicine: Sushruta – the Clinician – Teacher par Excellence" (PDF). Dwivedi, Girish & Dwivedi, Shridhar. 2007. http://medind.nic.in/iae/t07/i4/iaet07i4p243.pdf. Retrieved 2008-09-19. 
200. ^ Theodore Mazzone; Giamila Fantuzzi (2006). Adipose Tissue And Adipokines in Health And Disease (Nutrition and Health). Totowa, NJ: Humana Press. pp. 222. ISBN 1-58829-721-7. 
201. ^ Keller p. 49
202. ^ Breslow L (September 1952). "Public health aspects of weight control". Am J Public Health Nations Health 42 (9): 1116–20. PMID 12976585. 
203. ^ Rubinstein S, Caballero B (2000). "Is Miss America an undernourished role model?". JAMA 283 (12): 1569. doi:10.1001/jama.283.12.1569. PMID 10735392. 
204. ^ ^{a b} Johnson F, Cooke L, Croker H, Wardle J (2008). "Changing perceptions of weight in Great Britain: comparison of two population surveys". BMJ 337: a494. doi:10.1136/bmj.a494. PMID 18617488. PMC 2500200. http://www.bmj.com/cgi/content/full/337/jul10_1/a494. 
205. ^ Fumento, Michael (1997). The Fat of the Land: Our Health Crisis and How Overweight Americans Can Help Themselves. Penguin (Non-Classics). pp. 126. ISBN 0-14-026144-3. 
206. ^ "What is NAAFA". National Association to Advance Fat Acceptance. http://www.capitalnaafa.org/whatisnaafa.html. Retrieved February 17, 2009. 
207. ^ "ISAA Mission Statement". International Size Acceptance Association. http://www.size-acceptance.org/mission.html. Retrieved February 17, 2009. 
208. ^ ^{a b} Pulver, Adam (2007). An Imperfect Fit: Obesity, Public Health, and Disability Anti-Discrimination Law. Social Science Electronic Publishing. http://papers.ssrn.com/sol3/papers.cfm?abstract_id=1316106. Retrieved January 13, 2009. 
209. ^ Neumark-Sztainer D (March 1999). "The weight dilemma: a range of philosophical perspectives". Int. J. Obes. Relat. Metab. Disord. 23 Suppl 2: S31–7. doi:10.1038/sj.ijo.0800857. PMID 10340803. 
210. ^ National Association to Advance Fat Acceptance (2008), We come in all sizes, NAAFA, http://www.naafaonline.com/dev2/, retrieved 2008-07-29 
211. ^ "International Size Acceptance Association – ISAA". International Size Acceptance Association. http://www.size-acceptance.org/. Retrieved January 13, 2009. 
212. ^ Campos, Paul F. (2005). The Diet Myth. Gotham. pp. xiv,xvii. ISBN 1-59240-135-X. 
213. ^ Gard, Michael (2005). The Obesity Epidemic: Science, Morality and Ideology. Routledge. pp. 15 and 153. ISBN 0415318963. 
214. ^ "Obesity: Time bomb or dud?". USA Today. 2005-05-25. http://www.usatoday.com/news/health/2005-05-25-obesity_x.htm. Retrieved 2008-09-21. 
215. ^ Di Castelnuovo A, Quacquaruccio G, Donati MB, de Gaetano G, Iacoviello L (January 2009). "Spousal concordance for major coronary risk factors: a systematic review and meta-analysis". Am. J. Epidemiol. 169 (1): 1–8. doi:10.1093/aje/kwn234. PMID 18845552. 
216. ^ Douglas Martin (1991-07-31). "About New York". New York Times. http://www.nytimes.com/1991/07/31/nyregion/about-new-york.html. Retrieved 2008-07-24. 
217. ^ Areton (January 2002). "Factors in the sexual satisfaction of obese women in relationships". Electronic Journal of Human Sexuality 5. http://www.ejhs.org/volume5/Areton/06Partners.htm. 
218. ^ ^{a b} Flynn MA, McNeil DA, Maloff B, et al. (February 2006). "Reducing obesity and related chronic disease risk in children and youth: a synthesis of evidence with 'best practice' recommendations". Obes Rev 7 Suppl 1: 7–66. doi:10.1111/j.1467-789X.2006.00242.x. PMID 16371076. 
219. ^ Dollman J, Norton K, Norton L (December 2005). "Evidence for secular trends in children's physical activity behaviour". Br J Sports Med 39 (12): 892–7; discussion 897. doi:10.1136/bjsm.2004.016675. PMID 16306494. 
220. ^ ^{a b} Lund Elizabeth M. (2006). "Prevalence and Risk Factors for Obesity in Adult Dogs from Private US Veterinary Practices". Intern J Appl Res Vet Med 4 (2): 177–86. http://www.jarvm.com/articles/Vol4Iss2/Lund.pdf. 
221. ^ McGreevy PD, Thomson PC, Pride C, Fawcett A, Grassi T, Jones B (May 2005). "Prevalence of obesity in dogs examined by Australian veterinary practices and the risk factors involved". Vet. Rec. 156 (22): 695–702. PMID 15923551. 
222. ^ Nijland ML, Stam F, Seidell JC (June 2009). "Overweight in dogs, but not in cats, is related to overweight in their owners". Public Health Nutr: 1–5. doi:10.1017/S136898000999022X. PMID 19545467. 

Bibliography

• Jebb S. and Wells J. Measuring body composition in adults and children In:Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. pp. 12–28. ISBN 140-511672-2. 
• Kopelman P., Caterson I. An overview of obesity management In:Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. pp. 319–326. ISBN 140-511672-2. 
• National Heart, Lung, and Blood Institute (NHLBI) (1998) (PDF). Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. International Medical Publishing, Inc. ISBN 1-58808-002-1. http://www.nhlbi.nih.gov/guidelines/obesity/ob_gdlns.pdf. 
• "Obesity: guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children" (pdf). National Institute for Health and Clinical Excellence(NICE). National Health Services (NHS). 2006. http://www.nice.org.uk/nicemedia/pdf/CG43NICEGuideline.pdf. Retrieved April 8th,2009. 
• Puhl R., Henderson K., and Brownell K. Social consequences of obesity In:Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. pp. 29–45. ISBN 140-511672-2. 
• Seidell JC. Epidemiology — definition and classification of obesity In:Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. pp. 3–11. ISBN 140-511672-2. 
• World Health Organization (WHO) (2000) (PDF). Technical report series 894: Obesity: Preventing and managing the global epidemic.. Geneva: World Health Organization. ISBN 92-4-120894-5. http://whqlibdoc.who.int/trs/WHO_TRS_894_(part1).pdf. 

Further reading

• Fumento, Michael (1997). The Fat of the Land: Our Health Crises and How Overweight Americans can Help Themselves. New York: Penguin Books. ISBN 0-140261443. 
• Keller, Kathleen (2008). Encyclopedia of Obesity. Thousand Oaks, Calif: Sage Publications, Inc. ISBN 1-4129-5238-7. http://books.google.ca/books?id=aRp2rJrEqZsC&dq=IOTF+obesity+map&source=gbs_summary_s&cad=0. 
• Kolata, Gina (2007). Rethinking Thin: The new science of weight loss – and the myths and realities of dieting. Picador. ISBN 0-312-42785-9. 
• Kopelman, Peter G. (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. pp. 493. ISBN 140-511672-2. http://books.google.ca/books?id=u7RvldSr5M0C&pg=PA87&dq=80+percent+of+the+offspring+of+two+obese+parents+become+obese&source=gbs_selected_pages&cad=0_1&sig=ACfU3U2CHXfbaH8sZKLHC_nWOf03HG_LJw#PPA3,M1. 
• Levy-Navarro, Elena (2008). The Culture of Obesity in Early and Late Modernity. Palgrave Macmillan. ISBN 0230601235. 
• Pool, Robert (2001). Fat: Fighting the Obesity Epidemic. Oxford, UK: Oxford University Press. ISBN 0-19-511853-7. 

External links

Find more about Obesity on Wikipedia's sister projects:

Definitions from Wiktionary
Textbooks from Wikibooks
Quotations from Wikiquote
Source texts from Wikisource
Images and media from Commons
News stories from Wikinews
Learning resources from Wikiversity

• World Health Organization – Obesity pages
• Diet, Nutrition and the prevention of chronic diseases (including obesity) by a Joint WHO/FAO Expert consultation (2003).
• Obesity at Endotext.org
• International Task Force on Obesity
• Obesity at the Centers for Disease Control (USA)
• The Obesity Society (USA)
• National Obesity Forum (UK)
• Australasian Society for the Study of Obesity

v • d • e Nutrition disorders (E40-68, 260-269) Hypoalimentation/ malnutrition Protein-energy malnutrition Kwashiorkor · Marasmus · Catabolysis Avitaminosis B vitamins B1: Beriberi/Wernicke's encephalopathy(Thiamine deficiency) · B2: Ariboflavinosis · B3: Pellagra(Niacin deficiency) · B6: Pyridoxine deficiency · B7: Biotin deficiency · B9: Folate deficiency · B12: Vitamin B12 deficiency Other vitamins A: Vitamin A deficiency/Bitot's spots · C: Scurvy · D: Hypovitaminosis D/Rickets/Osteomalacia · E: Vitamin E deficiency · K: Vitamin K deficiency Mineral deficiency Zinc · Iron · Magnesium · Chromium · Selenium (Keshan disease) · Manganese · Molybdenum · Copper · Calcium · Potassium Hyperalimentation Overweight · Obesity Childhood obesity · Obesity hypoventilation syndrome · Abdominal obesity Vitamin poisoning Hypervitaminosis A · Hypervitaminosis D · Hypervitaminosis E Mineral overload see inborn errors of metal metabolism, toxicity nutrition navs: disorders, symptoms+signs/eponymous

This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)