# Obesity

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Obesity-waist circumference.PNG|
 ICD-10 ICD-9 E66 278 {{{OMIM}}} 9099 003101 med/1653 MeSH C23.888.144.699.500

Obesity is a condition in which excess body fat has accumulated to such an extent that health may be negatively affected.[1] It is commonly defined as a body mass index of 30 kg/m2 or higher.[1] This distinguishes it from being overweight as defined by a BMI of 25 kg/m2 or higher.[1]

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][3] As a result, obesity has been found to reduce life expectancy.[3] The primary treatment for obesity is dieting and physical exercise. If this fails, anti-obesity drugs and (in severe cases) bariatric surgery can be tried.[2][4] A combination of excessive caloric intake, lack of physical activity, and genetic susceptibility is thought to explain most cases of obesity, with a limited number of cases due solely to genetics, medical reasons, or psychiatric illness.

With rates of adult and childhood obesity increasing, authorities view it as a serious public health problem.[4] Between 1980-2000, obesity among adults has more than doubled; obesity among adolescents has tripled.[5] In the US, obesity is the second-leading cause of preventable death after smoking.[5]

Obesity is often stigmatized in the modern Western world. It has, however been perceived as a symbol of wealth and fertility at other times in history and still is in many parts of Africa.[3][6]

## Classification

Obesity, in absolute terms, is an increase of body adipose tissue (fat tissue) mass. In a practical setting it is difficult to determine this directly. Therefore, obesity is typically assessed by BMI (body mass index) and in terms of its distribution via the waist circumference.[7] In addition, the presence of obesity needs to be evaluated in the context of other risk factors such as medical conditions that could influence the risk of complications.[2]

### BMI

Body mass index or BMI is a simple and widely used method for estimating body fat mass.[8] BMI was developed in the 19th century by the Belgian statistician and anthropometrist Adolphe Quetelet.[9] BMI is an accurate reflection of body fat percentage in the majority of the adult population. It is less accurate in people such as body builders and pregnant women in whom body composition is affected.[2]

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 = mass/height (kilograms and metres)
US/Customary and imperial: $BMI=lb*703/in^2$

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

BMI Classification
Less than 18.5 underweight
18.5–24.9 normal weight
25.0–29.9 is overweight
30.0–34.9 is class I obesity
35.0–39.9 class II obesity
Over 40.0   class III obesity

The most commonly used definitions, established by the WHO in 1997 and published in 2000, provide the values listed in the table at right.[1]

Some modifications to the WHO definitions have been made by particular bodies:[10][11]

• A BMI of 35.0 or higher in the presence of at least one other significant comorbidity is also classified by some bodies as class III obesity.
• For Asians, overweight is a BMI between 23 and 29.9 kg/m2 and obesity a BMI >30 kg/m2.

The surgical literature breaks down "class III" obesity into further categories. [12]

• Any BMI > 40 is severe obesity
• A BMI of 40.0–49.9 is morbid obesity
• A BMI of >50 is super obese

### Waist circumference and waist–hip ratio

Main article: Central obesity

In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.[13] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.[14] In a study of 15,000 subjects, waist circumference also correlated better with metabolic syndrome than BMI.[15] Women who have abdominal obesity have a cardiovascular risk similar to that of men.[16] In people with a BMI over 35, measurement of waist circumference however adds little to the predictive power of BMI as most individuals with this BMI have an abnormal waist circumferences.[2]

The absolute waist circumference (>102 cm in men and >88 cm in women) or waist–hip ratio (>0.9 for men and >0.85 for women) are both used as measures of central obesity.[14]

### Body fat percentage

Body fat percentage is total body fat expressed as a percentage of total body weight. It is generally agreed that men with more than 25% body fat and women with more than 33% body fat are obese.[17] Body fat percentage can be estimated from a person's BMI by the following formula:

$Body fat % = 1.2*BMI+0.23*age-5.4-10.8*gender$
where gender is 0 if female and 1 if male

This formula takes into account the fact that body fat percentage is 10% greater in women than in men for a given BMI. It recognizes that a person's percentage body fat increases as they age even if their weight remains constant. The results have an accuracy of 4%.[18]

Direct attempts to determine body fat percent are difficult and often expensive. One of the most accurate methods is to weigh a person underwater which is known as hydrostatic weighing. Two other simpler and less accurate methods for measuring body fat therefore have historically been used. The first is the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer. It has not, however, been adequately evaluated in obese subjects.[18] The other is bioelectrical impedance analysis which uses electrical resistance. Bioelectrical impedance however has not been shown to provide an advantage over BMI. Therefore the routine use of these tests are discouraged.[4]

Body fat percentage measurement techniques used mainly for research include computed tomography (CT scan), magnetic resonance imaging (MRI), and dual energy X-ray absorptiometry (DEXA).[13] These techniques provide very accurate measurements, but it may be difficult to scan the severely obese due to weight limits of the equipment and insufficient diameter of the CT or MRI scanner.[18]

### Risk factors and comorbidities

The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. Coronary heart disease, type 2 diabetes, and sleep apnea are possible complications that would indicate a need to commence or intensify treatment for obesity.[2] Smoking, high blood pressure, age and family history are other risk factors that, in combination with obesity, may indicate an additional reason for treatment.[2]

### Childhood obesity

Main article: Childhood obesity

Obesity in children and adolescents is defined as a BMI greater then the 95th percentile.[19] Rates of obesity among this group have increased by 3 to 5 % from 1990 to the year 2000.[20] Rates have also increased in most other developed countries worldwide.[21]

Many different factors contribute to the rising rates of childhood obesity. As more parents work children end up eating alone in front of the TVs. Parents also compensate for their absence by giving children fast food, sweets and chocolate. There has been an increase in snacking and soft drink consumption in children over the past years which might also play a major role. Over 50% of the commercials children view are based on food. The food depicted are generally sweetened and proceed and the advertisements encourage children to purchase and consume more.[5]

## Effects on health

### Mortality

Obesity is one of the leading preventable causes of death.[22][23][24] Large scale American and European studies have found that mortality risk varies with BMI; the lowest risk is found at a BMI of 21–24 kg/m2 in non smokers and at a BMI of 24-27 kg/m2 in current smokers and increases with changes in either direction.[25][26] Obesity increases the risk of death in current and former smokers as well as in those who have never smoked.[26] A BMI of over 32 is associated with a doubling of risk of death[27] and obesity is estimated to cause an excess 111,909 to 365,000 death per year in the United States.[28][3] Obesity on average reduces life expectancy by 6–7 years.[29][3] Severe obesity (BMIs >40) reduces life expectancy by 20 years for men and 5 years for women.[17]

### Morbidity

A large number of physical and mental conditions have been associated with obesity.

Health consequences can be categorized by the effects of increased fat mass (osteoarthritis, obstructive sleep apnea, social stigmatization) or by the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[3][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]

Central obesity, characterized by its high waist to hip ratio, is an important risk for metabolic syndrome. Metabolic syndrome is a combination of medical disorders which often includes diabetes mellitus type 2, high blood pressure, high blood cholesterol, and triglyceride levels.[31]

Obesity is related to a variety of other complications. Some of these are directly caused by obesity and others are indirectly related through mechanisms sharing a common cause such as 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 weight is behind 64% of cases of diabetes in men and 77% in women.[18]

Medical field Condition Medical field Condition
Cardiovascular Gastrointestinal
Endocrine and reproductive Respiratory
Musculoskeletal Psychological
Neurologic Skin
Cancer[37] Genitourinary

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.[41] The paradox was first described in 1999 in overweight and obese patients undergoing hemodialysis. Since then it has been found in a few other subgroups and explanations for its occurrence have been put forward.[41]

In people with heart failure, those with a BMI between 30.0–34.9 had lower mortality then those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.[42] 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.[43][44] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.[45] One study found that the increased survival could be explained by the more aggressive treatment obese people receive after a cardiac event.[46]

## Causes

Most researchers agree that a combination of excessive calorie consumption and a sedentary lifestyle are the primary causes of obesity.[47] In a minority of cases, increased food consumption can be attributed to genetic, medical, or psychiatric illness. Generally however the rising prevalence of obesity is attributed to the availability of an easily accessible and palatable diet,[48] car culture and mechanized manufacturing.[49][50] A 2006 review identifies ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors—food substances that interfere with lipid metabolism, (3) decreased variability in ambient temperature, (4) decreased rates of smoking as smoking suppresses appetite, (5) increased use of medication that leads to weight gain, (6) increased distribution of ethnic and age groups that tend to be heavier, (7) pregnancy at a later age, (8) intrauterine and intergenerational effects, (9) positive natural selection of people with a higher BMI, (10) assortative mating, heavier people tending to form relationships with each other.[51]

### Diet

Despite the widespread availability of nutritional information in schools, doctors' offices, on the internet and on product packaging,[52] it is evident that overeating remains a substantial problem. In the period of 1971–2000, obesity rates in the United States increased from 14.5% to 30.9%.[53] During the same time period, an increase occurred in the average amount of calories consumed. For women, the average increase was 335 calories per day (1542 calories in 1971 and 1877 calories in 2004), while for men the average increase was 168 calories per day (2450 calories in 1971 and 2618 calories in 2004). Most of these extra calories came from an increase in carbohydrate consumption rather than an increase in fat consumption.[54] The primary sources of these extra carbohydrates are sweetened beverages, which now accounts for almost 25 percent of daily calories in young adults.[55] Dietary trends have changed with reliance on energy-dense fast-food meals tripling between 1977 and 1995, and calorie intake from fast food quadrupling over the same period.[56] In the early 1980s, the administration of Ronald Reagan lifted regulations limiting the advertising of sweets and fast food to children, and advertisement of these products directed towards children has increased.[57] 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 relatively cheap compared to fruits and vegetables.[58]

There is little evidence to support the commonly expressed view that some obese people eat little yet gain weight due to a slow metabolism. What has been found, however, is that some obese people underreport how much food they consume compared to those of normal weight.[18]

### Sedentary lifestyle

A sedentary lifestyle plays a significant role in obesity.[18] Obese people are less active than those of normal weight. For example in Canada, 27.0% of sedentary men are obese as opposed to 19.6% of active men.[59] Normal weight people are more fidgety then their obese counterparts; this relationship is maintained even if normal weight people eat more or the obese person loses weight.[60]

In 2000 the CDC estimated that more than 40% of the US population was sedentary, another 30% was active but not sufficiently and less than 30% had an adequate level of physical activity.[55] There has been a trend toward decreased physical activity in part due to increasingly mechanized forms of work, changing modes of transportation, and increasing urbanization. A study from China found urbanization reduces daily energy expenditure by about 300–400 kcal and going to work by car or bus reduced it by a further 200 kcal.[50] Obesity rates have increased in relation to expanding suburbs. This has been attributed to increased time spent commuting, leading to less exercise and less meal preparation at home.[61] Driving one's children to school has become increasingly popular. In the USA the proportion of children who walk or bike to school declined between 1969 (42%) and 2001 (16%) resulting in less exercise.[55] Studies in children and adults have found an association between the number of hours of television watched and the prevalence of obesity.[62][63][64] 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.[65]

### Genetics

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 may predispose to obesity when sufficient calories are present. Obesity is a major feature in a number of rare genetic conditions: Prader-Willi syndrome, Bardet-Biedl syndrome, MOMO syndrome, leptin receptor mutations, congenital leptin deficiency, and melanocortin receptor mutations. In a people with early-onset severe obesity (defined by an onset before ten years of age and body mass index over three standard deviations above normal), 7% harbor a single locus mutation.[66] Apart from the above syndromes, an association has been found between an FTO gene polymorphism and weight. The adults in the study who were homozygous for this allele weighed about 3 kilograms more and had a 1.6-fold greater rate of obesity than those who had not inherited this trait.[67] The association disappeared, though, when those with FTO polymorphisms participated in moderately intensive physical activity equivalent to 3 to 4 hours of brisk walking.[68] One study 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.[35][18]

The percentage of obesity that can be attributed to genetics varies from 6% to 85% depending on the population examined.[69] 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.[70] 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.[48]

### 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,[71] and the eating disorders: binge eating disorder and night eating syndrome.[3] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[35]

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.[3]

### Socioeconomic

While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.[48] 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.[72] 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.[73]

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.[73] 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.[74]

Smoking has a significant effect on a individual's weight. Those who quit smoking gain an average of 4.4 kilograms for men and 5.0 kg for women over ten years.[75] Changing rates of smoking however have had little effect on the overall rates of obesity.[76]

### Gut Flora

Main article: Gut flora

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.[77]

## Neurobiological mechanisms

Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[78] 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, 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.[79] 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 subjects.[78]

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.[78] 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.[80]

The arcuate nucleus contains two distinct groups of neurons.[78] 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.[78]

## Management

Main article: Weight loss#Intentional weight loss

The main treatment for obesity consists of dieting and physical exercise. Diet programs may produce weight loss over the short term,[81] but keeping this weight off can be a problem. It often requires making exercise and a lower calorie diet a permanent part of a person's lifestyle.[82][83] In the general population only 20% are successful at long-term weight loss maintenance.[84] In a more structured setting, however, 67% of people who lost greater then 10% of their body mass maintained or continued to lose weight one year later.[85] An average maintained weight loss of more than 3 kg or 3% of total body mass could be sustained for five years.[86] There are significant benefits to weight loss. In a prospective study, intentional weight loss of any amount was associated with a 20% reduction in all-cause mortality.[87]

The most effective, but also most risky treatment for obesity is bariatric surgery. Due to its cost and risk of complications, researchers are fervently searching for new obesity treatments. One particularly promising domain is that of the use of gut hormones (i.e. ghrelin) in appetite control. Gut hormones, molecules designed by evolution to be peripherally administered to target appetite circuits in the central nervous system (CNS), may be able to influence food intake in humans, even if such hormones do not significantly regulate hunger on a day-to-day basis[88]. Before such treatments could be implemented however, further research into the physiological and pathophysiological roles of gut hormones must occur.

### Behavioral therapy

This involves changing diets (by eating smaller meals), habits (by cutting down on certain types of food) and physical activities (by making a conscious effort to exercise for a longer period) to new behaviors that encourage weight loss. This program enables people to connect with a group of others that are attempting to lose weight so as to encourage and help each other out. This form of therapy helps provide realistic goals, partnership and frequent contact with health care provider, encourage self monitoring of diet and exercise to increase one's awareness of the activities and much more. Long term results are modest and can be done on the internet or in person by counseling.[5]

### 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.[81] A meta-analysis of six randomized controlled trials found no difference between the main diet types (low calorie, low carbohydrate, and low fat), with a 2–4 kilogram weight loss in all studies.[81]

Low-fat diets

Low-fat diets involve the reduction of the percentage of fat in one's diet. Calorie consumption is reduced but not purposely so. Diets of this type include NCEP Step I and II. A meta-analysis of 16 trials of 2–12 months' duration found that low-fat diets resulted in weight loss of 3.2 kg over eating as normal.[81]

Low-carbohydrate diets

Low carbohydrate diets such as Atkins and Protein Power are relatively high in fat and protein. They are very popular in the press but are not recommended by the American Heart Association. A review of 94 trials found that weight loss was associated with increased satiety and thus decreased calorie consumption. No adverse affect from low carbohydrate diets were detected.[89]

Low-calorie diets

Low-calorie diets usually produce an energy deficit of 500–1000 calories per day, which can result in a 0.5 kilogram weight loss per week. They include the DASH diet and Weight Watchers among others. The National Institutes of Health reviewed 34 randomized controlled trials to determine the effectiveness of low-calorie diets. They found that these diet lowered total body mass by 8% over 3–12 months.[81]

Very low-calorie diets

Very low calorie diets provide 200–800 kcal/day while maintaining protein intake and 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. 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.[81]

### Exercise

Main article: 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.[90][91] Exercise affects macronutrient balance. During exercise, there is a shift to greater use of fat as a fuel. [5]

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 loss was observed with a greater degree of exercise.[92] 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.[93]

A systematic review found that people who use pedometers, during on average an 18 week period, increased their physical activity by 27% and subsequently decreased their BMI by 0.38.[94]

### Medication

Main article: Anti-obesity drug

Most drugs are anorexiants; appetite suppressants that act on either one or more neurotransmitters. They act by increasing secretion of the neurotransmitter(s) such as dopamine, norepinephrine, serotonin, or by inhibiting the reuptake, or by a combination of these mechanisms.[5] There are two commonly prescribed medications for obesity. One is orlistat, which reduces intestinal fat absorption by inhibiting pancreatic lipase; the other is sibutramine, 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, a third drug, works via a specific blockade of the endocannabinoid system. It has been developed from the knowledge that cannabis smokers often experience extreme hunger pangs, which cannabis smokers refer 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.[95][96] Weight loss with these drugs is modest; over the longer term, average weight loss on orlistat is 2.9 kg, sibutramine is 4.2 kg and rimonabant is 4.7 kg. Orlistat and rimonabant lead to a reduced incidence of diabetes, and all drugs have some effect on cholesterol. There is little data on how these drugs affect the longer-term complications of obesity.[97] It is common for weight loss drugs to be tried and if there is little or no benefit from them to discontinue treatment.[4] A meta-analysis of randomized controlled trials by the Cochrane Collaboration concluded that in diabetic patients fluoxetine (Prozac), orlistat and sibutramine could achieve modest but significant weight loss over 12–57 weeks. The long-term health benefits remained unclear.[98]

Obesity may also influence the choice of drugs used to treat diabetes. Metformin may lead to mild weight loss in comparison to sulfonylureas and insulin. It has been show to reduce the risk of cardiovascular disease in obese type 2 diabetics.[99] The thiazolidinediones, on the other hand, may cause weight gain, but decrease central obesity and therefore can be used in obese diabetics.[100]

Ephedrine (Ma Huang) is a stimulant effective for weight loss; however it is not recommended due to potential side effects.[101]

### Surgery

Main article: bariatric surgery

Bariatric surgery ("weight loss surgery") is the use of surgical interventions 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 with dietary modification and pharmacological treatment. Weight loss surgery relies on various principles; the most common approaches are reducing the volume of the stomach, producing an earlier sense of satiation (e.g. by adjustable gastric banding and vertical banded gastroplasty) and reduce the length of bowel that food will be in contact with, directly reducing absorption (gastric bypass surgery). Band surgery is reversible, while bowel shortening operations are not. Some procedures can be performed laparoscopically. Complications from weight loss surgery are frequent.[102]

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% at 10 years depending on the type of procedure performed and a 29% reduction in all cause mortality when compared to standard weight loss measures.[103] A marked decrease in the risk of diabetes mellitus, cardiovascular disease and cancer has also been found after bariatric surgery.[104][105] Weight loss is marked in the first few months after surgery and 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.[105] When the two main techniques are compared gastric bypass procedures are found to lead to 30% more weight lose than banding procedures one year after surgery.[106]

The effects of liposuction however are less well determined, with some small studies showing benefits[107] and others showing none.[108]

### Clinical protocols

In a clinical practice guideline by the American College of Physicians, the following five recommendations are made:[109]

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 patient 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 patients with 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 patient 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 patients 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.[110][111]

## Epidemiology

The World Health Organization formally recognized the global nature of the obesity epidemic in 1997.[55] As of 2005 the WHO estimates that at least 400 million adults (9.8%) are obese, with higher rates among women than men.[1] The rate of obesity also increases with age at least up to 50 or 60 years old.[18] Once considered a problem only of high-income countries, obesity rates are rising worldwide. These increases have been felt most dramatically in urban settings.[1] The only remaining region of the world where obesity is not common is sub-Saharan Africa.[3]

South Pacific

Many of the island nations of the South Pacific have very high rates of obesity. Nauru has the highest rates of obesity in the world (80%) followed by Tonga, the Federated States of Micronesia, and the Cook Islands. Being big has traditionally been associated with health, beauty, and status and many of these beliefs remain prevalent today.[113]

Australia

Studies conducted in 2006 found that close to 52% of Australian women and up to 67% of Australian men aged 25 or over are overweight or obese.[114]

China

Because the booming economy has increased average incomes, the population of China has since the 1980s taken up a more sedentary lifestyle and begun consuming more calorie-rich foods.

```From 1991 to 2004 the percentage of overweight or obese adults increased from 12.9% to 27.3%.[115]
```
India
Main article: Obesity in India

In India urbanization and modernization has been associated with obesity. As of 1999 in northern India 11% of urban women were found to be obese in contrast to 3.7% of rural women. Well women of high socioeconomic class had a rate of obesity of 10.4% as opposed to 0.9% in women of low socioeconomic class.[116] With people moving into urban centers and wealth increasing, concerns about an obesity epidemic in India are growing.

European Union

Between the 1970s and the 2000s, rates of obesity in most European countries have increased. During the 1990s and 2000s the 27 countries making up the EU reported rates of obesity from 10–27% in men and from 10–38% in women.[117]

United Kingdom

In the UK the rate of obesity has increased about fourfold over the last 25 years, reaching current levels of 22%.[18]

Mexico
Main article: Obesity in Mexico

Mexico has the second-highest rate of obesity in the developed world, at 24.2% of the population.[112]

United States
Main article: Obesity in the United States

The United States has the highest rates of obesity in the developed world.[112] From 1980 to 2002, obesity rates have doubled, reaching the current rate of 32% of the adult population.[118] Rates of obesity vary by ethnicity and gender. In the US, 28% of men and 34% of women are obese, with rates rising to as high as 50% among African American women. [119] The prevalence of class III obesity (BMI ≥40) has increased the most dramatically from 0.78 percent in 1990 to 2.2 percent in 2000.[120]

The number of Canadians who are obese has risen dramatically in recent years. In 2004, direct measurements of height and weight found 23.1% of Canadians older than 18 had a BMI greater than 30. When broken down into degrees of obesity, 15.2% were class I (BMI 30–34.9), 5.1% were class II (BMI 35–39.9), and 2.7%, class III (BMI > 40). This is in contrast to self-reported data the previous year of 15.2% and in 1978/1979 of 13.8%. The greatest increases occurred among the more severe degrees of obesity; class III obesity increased from 0.9% to 2.7% from 1978/1979 to 2004. Obesity in Canada varies by ethnicity; people of Aboriginal origin have a significantly higher rate of obesity (37.6%) than the national average.[59]

## 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.[121]Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[122] 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,[123] and decreasing access to sweetened beverages in schools.[124] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[125]

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".[2] 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.[126] 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.[127] 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.[128] 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.[4] 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.[129]

## History and culture

### Etymology

Obesity is the nominal form of obese which comes from the Latin obēsus, which means "stout, fat, or plump." Ēsus is the past participle of edere (to eat), with ob added to it. In Classical Latin, this verb is seen only in past participial form. Its first attested usage in English was in 1651, in Noah Biggs's Matæotechnia Medicinæ Praxeos.[130]

### Historical trends

Obesity has been recognized as a medical disorder at least since the time of Hippocrates when he stated that "Corpulence is not only a disease itself, but the harbinger of others".[3] It was known to the Indian surgeon Sushruta (6th century BCE), who related obesity to diabetes and heart disorder.[132] He recommended physical work to help cure it and its side effects.[132] For most of human history mankind struggled with food scarcity. 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 underweight to 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.[55] In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.[55][133] During this time period insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.[3]

Many cultures throughout history have viewed obesity as a 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.[6] In modern Western culture, excess weight is often regarded as unattractive, and obesity is commonly associated with various negative stereotypes. All ages can face social stigmatization and may be targeted by bullies or shunned by their peers. In Western culture obesity is once again seen as a sign of a low socio-economic status.[134] Obese people are less likely to be hired for a job and are less likely to be promoted.[35] 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.[18] The weight that is generally viewed as an ideal has become lower since the 1920s. The average height of Miss America pageant winners increased by 2% from 1922 to 1999, while their average weight decreased by 12%.[35]

In many part of Africa obesity is still seen as a sign of wealth and well being. This has become particularly common since the HIV epidemic began.[3]

### Weight loss drugs

The first described attempts at producing weight loss are those of Soranus of Ephesus, a Greek physician, in the second century AD. He prescribed elixirs of laxatives and purgatives, as well as heat, massage, and exercise. This remained the mainstay of treatment for well over a thousand years. It was not until the 1920s and 1930s that new treatments began to appear. Based on its effectiveness for hypothyroidism, thyroid hormone became a popular treatment for obesity in otherwise healthy people. It had a modest effect but produced the symptoms of hyperthyroidism as a side effect, such as palpitations and difficulty sleeping. Dinitrophenol (DNP) was introduced in 1933; this worked by uncoupling the biological process of oxidative phosphorylation in mitochondria, causing them to produce heat instead of ATP. The most significant side effect was a dramatic rise in body temperature, frequently causing death. By the end of the 1930s DNP had fallen out of use.[48]

Amphetamines (marketed as Benzedrine) became popular for weight loss during the late 1930s. They worked primarily by suppressing appetite, and had other beneficial effects such as increased alertness. Use of amphetamines increased over the subsequent decades, culminating in the "rainbow pill" regime. This was a combination of multiple pills, all thought to help with weight loss, taken throughout the day. Typical regimens included stimulants, such as amphetamines and thyroid hormone, diuretics, digitalis, laxatives, and often a barbiturate to suppress the side effects of the stimulants. In 1967/1968 a number of deaths attributed to diet pills triggered a Senate investigation and the gradual implementation of greater restrictions on the market. This culminating in 1979 with the FDA banning the use of amphetamines, then the most effective of the diet drugs, in diet pills.[48]

Meanwhile, phentermine had been FDA approved in 1959 and fenfluramine in 1973. The two were no more popular then other drugs until in 1992 a researcher reported that the two caused a 10% weight loss which was maintained for over two years.[135] Fen-phen was born and rapidly became the most commonly prescribed diet medication. Dexfenfluramine (Redux) was developed in the mid-1990s as an alternative to fenfluramine with less side-effects, and received regulatory approval in 1996. However, this coincided with mounting evidence that the combination could cause valvular heart disease in up to 30% of those who had taken it, leading to withdrawal of Fen-phen and dexfenfluramine from the market in September 1997.[48]

Ephedra was removed from the US market in 2004 over concerns that it raises blood pressure and could lead to strokes and death.[35]

### Non-medical effects

In addition to its health impacts, obesity leads to many problems including social stigmatization, disadvantages in employment, and increased business costs.[18] These effects are felt by all levels of society from individuals, to corporations, to governments.

Obesity and its health effects create sizable economic costs. In 1998 in the US, the medical costs attributable to obesity were \$78.5 billion USD, or 9.1% of all medical expenditures.[136][137] Obesity prevention programs have been found to reduce the cost of treating obesity-related disease. Those reductions, however, are offset by medical costs incurred during the additional years of life gained. The authors therefore conclude that reducing obesity may improve the public's health, but it is unlikely to reduce overall health spending.[138]

Obese workers have higher rates absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.[139] 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.[140] 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 Jan. 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.[141]

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.[142] In 2000, the extra weight of obese passengers cost airlines US\$275 million.[143] Costs for restaurants are increased by litigation accusing them of causing obesity.[144] 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.[144]

### 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 characteristics that portray fertility while others feel these could be actual representations of the people at the time.[6] Corpulence is, however, absent in both Greek and Roman art, probably fitting with their ideals of 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. This can be seen in portraits of Henry the VIII and Alessandro del Borro.[6] 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.[91] 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.[6]

### Fat acceptance and the obesity controversy

Main article: Fat acceptance movement

The main effort of the fat acceptance movement is to decrease discrimination against people who are overweight.[145] However some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes. The National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.[146] Multiple books such as The Diet Myth by Paul Campos argue that the health risks of obesity are a conspiracy and the real problem is the social stigma facing the obese.[147] Similarly, The Obesity Epidemic by Michael Gard argues that obesity is a moral and ideological construct.[148] Other groups are also trying to challenge obesity's connection to poor health. The Center for Consumer Freedom, a organization partly supported by the restaurant and food industry, has run ads saying that obesity is not an epidemic but "hype".[149]

Some people are particularly attracted to the obese. Chubby culture[150] and fat admirers[151] have become recognized subcultures.

## References

1. 1.0 1.1 1.2 1.3 1.4 1.5 World Health Organization (2000). Technical report series 894: Obesity: Preventing and managing the global epidemic. (PDF), Geneva: World Health Organization.
2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 National Heart, Lung, and Blood Institute. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (PDF), International Medical Publishing, Inc.
3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 3.25 3.26 3.27 3.28 Haslam DW, James WP (2005). Obesity. Lancet 366 (9492): 1197–209.
4. 4.0 4.1 4.2 4.3 4.4 Template:NICE
5. 5.0 5.1 5.2 5.3 5.4 5.5 Wexler Barbara, Gale Thomas. Weight in American: Obesity, Eating Disorders, and Other Health Risks. 2007
6. 6.0 6.1 6.2 6.3 6.4 Woodhouse R (2008). Obesity in art: A brief overview. Front Horm Res 36: 271–86.
7. Sweeting HN (2007). Measurement and definitions of obesity in childhood and adolescence: A field guide for the uninitiated. Nutr J 6: 32.
8. Mei Z, Grummer-Strawn LM, Pietrobelli A, Goulding A, Goran MI, Dietz WH (2002). Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents. Am J Clin Nutr 75: 978–85.
9. Quetelet LAJ (1871). Antropométrie ou Mesure des Différences Facultés de l'Homme, Brussels: Musquardt.
10. NICE issues guidance on surgery for morbid obesity. National Institute for Health and Clinical Excellence. URL accessed on 2007-03-08.
11. (2006). Bariatric Surgery. USC Center for Colorectal and Pelvic Floor Disorders. University of Southern California. URL accessed on 2007-03-08.
12. Gabriel I Uwaifo. Obesity. URL accessed on 2008-09-29.
13. 13.0 13.1 U.S. Preventive Services Task Force Evidence Syntheses (2000). HSTAT: Guide to Clinical Preventive Services, 3rd Edition: Recommendations and Systematic Evidence Reviews, Guide to Community Preventive Services.
14. 14.0 14.1 14.2 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: 937–52.
15. Janssen I, Katzmarzyk PT, Ross R (2004). Waist circumference and not body mass index explains obesity-related health risk. Am. J. Clin. Nutr. 79 (3): 379–84.
16. Larsson B, Bengtsson C, Björntorp P et al. (February 1992). Is abdominal body fat distribution a major explanation for the sex difference in the incidence of myocardial infarction? The study of men born in 1913 and the study of women, Göteborg, Sweden. Am J Epidemiol 135 (3): 266–73.
17. 17.0 17.1 Schwarz, Steven. Obesity. emedicine. URL accessed on 2008-09-30.
18. 18.00 18.01 18.02 18.03 18.04 18.05 18.06 18.07 18.08 18.09 18.10 Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children, 493, Blackwell Publishing.
19. Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Teens.
20. Ogden CL, Flegal KM, Carroll MD, Johnson CL (October 2002). Prevalence and trends in overweight among US children and adolescents, 1999-2000. JAMA : the journal of the American Medical Association 288 (14): 1728–32.
21. EU Platform on Diet, Physical Activity, and Health. (PDF) International Obesity Task Force.
22. Barness LA, Opitz JM, Gilbert-Barness E (December 2007). Obesity: genetic, molecular, and environmental aspects. Am. J. Med. Genet. A 143A (24): 3016–34.
23. Mokdad AH, Marks JS, Stroup DF, Gerberding JL (March 2004). Actual causes of death in the United States, 2000. JAMA 291 (10): 1238–45.
24. 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.
25. 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.
26. 26.0 26.1 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.
27. Manson JE, Willett WC, Stampfer MJ, et al. (1995). Body weight and mortality among women. N. Engl. J. Med. 333 (11): 677–85.
28. 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.
29. 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. Ann. Intern. Med. 138 (1): 24–32.
30. 30.0 30.1 Bray GA (2004). Medical consequences of obesity. J. Clin. Endocrinol. Metab. 89 (6): 2583–9.
31. Grundy SM (2004). Obesity, metabolic syndrome, and cardiovascular disease. J. Clin. Endocrinol. Metab. 89 (6): 2595–600.
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.
33. 33.0 33.1 33.2 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.
34. 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.
35. 35.0 35.1 35.2 35.3 35.4 35.5 Kolata,Gina (2007). Rethinking thin: The new science of weight loss - and the myths and realities of dieting, Picador.
36. 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.
37. 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.
38. 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.
39. 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.
40. 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.
41. 41.0 41.1 Schmidt DS, Salahudeen AK (2007). Obesity-survival paradox-still a controversy?. Semin Dial 20 (6): 486–92.
42. Habbu A, Lakkis NM, Dokainish H (October 2006). The obesity paradox: Fact or fiction?. Am. J. Cardiol. 98 (7): 944–8.
43. 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.
44. 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.
45. 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.
46. 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.
47. Sara Bleich, David Cutler, Christopher Murray, Alyce Adams (March 2007). Working paper 12954: Why is the developed world obese?, National Bureau of Economic Research.
48. 48.0 48.1 48.2 48.3 48.4 48.5 Pool, Robert (2001). Fat: Fighting the Obesity Epidemic, Oxford, UK: Oxford University Press.
49. Nestle M, Jacobson MF (2000). Halting the obesity epidemic: A public health policy approach. Public Health Rep 115 (1): 12–24.
50. 50.0 50.1 James WP (March 2008). The fundamental drivers of the obesity epidemic. Obes Rev 9 Suppl 1: 6–13.
51. 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.
52. National Control for Health Statistics. Nutrition For Everyone. Centers for Disease Control and Prevention. URL accessed on 2008-07-09.
53. Flegal KM, Carroll MD, Ogden CL, Johnson CL (October 2002). Prevalence and trends in obesity among US adults, 1999–2000. JAMA 288: 1723–1727.
54. 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.
55. 55.0 55.1 55.2 55.3 55.4 55.5 Caballero B (2007). The global epidemic of obesity: An overview. Epidemiol Rev 29: 1–5.
56. Lin BH, Guthrie J and Frazao E (1999). "Nutrient contribution of food away from home" Frazão E Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences, 213–239, Washington, DC: US Department of Agriculture, Economic Research Service.
57. Brian Wansink and Mike Huckabee (2005), “De-Marketing Obesity,” California Management Review, 47:4 (Summer), 6–18.
58. includeonly>Pollan, Michael. "You Are What You Grow", New York Times, 22 April 2007. Retrieved on 2007-07-30.
59. 59.0 59.1 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.
60. Levine JA, Lanningham-Foster LM, McCrady SK, Krizan AC, Olson LR, Kane PH, Jensen MD, Clark MM (2005). Interindividual variation in posture allocation: Possible role in human obesity. Science 307 (5709): 584–6.
61. Lopez R (2004). Urban sprawl and risk for being overweight or obese. Am J Public Health 94 (9): 1574–9.
62. 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.
63. 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.
64. Tucker LA, Bagwell M (July 1991). Television viewing and obesity in adult females. Am J Public Health 81 (7): 908–11.
65. www.commonsensemedia.org. (pdf) Ezekiel J. Emanuel.
66. Farooqi S, O'Rahilly S (December 2006). Genetics of obesity in humans. Endocr. Rev. 27 (7): 710–18.
67. Frayling TM, Timpson NJ, Weedon MN, et al. (2007). A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science 316 (5826): 889–94.
68. Rampersaud E, Mitchell BD, Pollin TI et al. (2008). Physical activity and the association of common FTO gene variants with body mass index and obesity. Arch Intern Med 16: 1791–97.
69. Yang W, Kelly T, He J (2007). Genetic epidemiology of obesity. Epidemiol Rev 29: 49–61.
70. 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.
71. 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.
72. Sobal J, Stunkard AJ (March 1989). Socioeconomic status and obesity: A review of the literature. Psychol Bull 105 (2): 260–75.
73. 73.0 73.1 McLaren L (2007). Socioeconomic status and obesity. Epidemiol Rev 29: 29–48.
74. 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.
75. 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.
76. Chiolero A, Faeh D, Paccaud F, Cornuz J (April 2008). Consequences of smoking for body weight, body fat distribution, and insulin resistance. Am. J. Clin. Nutr. 87 (4): 801–9.
77. 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.
78. 78.0 78.1 78.2 78.3 78.4 Flier JS (2004). Obesity wars: Molecular progress confronts an expanding epidemic. Cell 116 (2): 337–50.
79. Hamann A, Matthaei S (1996). Regulation of energy balance by leptin. Exp. Clin. Endocrinol. Diabetes 104 (4): 293–300.
80. Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiologya: A cellular and molecular approach, Philadelphia: Saunders.
81. 81.0 81.1 81.2 81.3 81.4 81.5 Strychar I (January 2006). Diet in the management of weight loss. CMAJ 174 (1): 56–63.
82. 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.
83. Tate DF, Jeffery RW, Sherwood NE, Wing RR (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.
84. (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.
85. 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.
86. Anderson JW, Konz EC, Frederich RC, Wood CL (November 2001). Long-term weight-loss maintenance: A meta-analysis of US studies. Am. J. Clin. Nutr. 74 (5): 579–84.
87. 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.
88. Kevin G. Murphy, Stephen R. Bloom. Gut hormones and the regulation of energy homeostasis. Nature 444, (13 Dec 2006).
89. Bravata DM, Sanders L, Huang J, et al. (April 2003). Efficacy and safety of low-carbohydrate diets: A systematic review. JAMA 289 (14): 1837–50.
90. Gwinup G (1987). Weight loss without dietary restriction: Efficacy of different forms of aerobic exercise. Am J Sports Med 15 (3): 275–9.
91. 91.0 91.1 Fumento, Michael (1997). The Fat of the Land: Our Health Crisis and How Overweight Americans Can Help Themselves, 126, Penguin (Non-Classics).
92. Shaw K, Gennat H, O'Rourke P, Del Mar C (2006). Exercise for overweight or obesity. Cochrane database of systematic reviews (Online) (4): CD003817.
93. 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.
94. 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.
95. Anti-obesity drug no magic bullet. CBC. URL accessed on 2008-09-19.
96. FDA Briefing Document NDA 21-888 Zimulti (rimonabant) Tablets, 20 mg Sanofi Aventis Advisory Committee. (PDF) FDA. URL accessed on 2008-09-19.
97. 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.
98. 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.
99. 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.
100. Fonseca V (2003). Effect of thiazolidinediones on body weight in patients with diabetes mellitus. Am. J. Med. 115 Suppl 8A: 42S–48S.
101. Flanagan CM, Kaesberg JL, Mitchell ES, Ferguson MA, Haigney MC (August 2008). Coronary artery aneurysm and thrombosis following chronic ephedra use. Int. J. Cardiol..
102. Encinosa WE, Bernard DM, Chen CC, Steiner CA (2006). Healthcare utilization and outcomes after bariatric surgery. Medical care 44 (8): 706–12.
103. 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.
104. 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.
105. 105.0 105.1 Adams TD, Gress RE, Smith SC, et al. (2007). Long-term mortality after gastric bypass surgery. N. Engl. J. Med. 357 (8): 753–61.
106. 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.
107. 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.
108. 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.
109. 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. Fulltext.
110. Behavioral counseling in primary care to promote a healthy diet: Recommendations and rationale.. URL accessed on 2007-05-22.
111. 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.
112. 112.0 112.1 112.2 Anon (2005). OECD Factbook: Economic, Environmental and Social Statistics, Organization for Economic Co-operation and Development.
113. (2002). Obesity in the Pacific Too Big To Ignore. (PDF) Secretariat of the Pacific Community. WHO. URL accessed on 2008-09-30.
114. Childhood Obesity. Government of New South Wales. URL accessed on 2008-06-22.
115. includeonly>Popkin, Barry. "The World Is Fat", Scientific American, September, 2007, pp. 94. ISSN 0036-8733. Retrieved on 2008-07-24.
116. Praween Kumar Agrawal. Emerging obesity in northern Indian states: A serious threat for health. (PDF) IUSSP Conference, Bankik, 10 June–12-2002. URL accessed on 2008-07-24.
117. Tim Lobstein, Neville Rigby, Rachel Leach (2005-03-15). EU platform on diet, physical activity and health: International Obesity Task Force EU Platform Briefing Paper (PDF), International Obesity Task Force. URL accessed 2008-07-23.
118. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM (2006). Prevalence of overweight and obesity in the United States, 1999–2004. JAMA 295 (13): 1549–55.
119. International Obesity Task Force. (PDF) URL accessed on 2008-09-19.
120. Freedman DS, Khan LK, Serdula MK, Galuska DA, Dietz WH (October 2002). Trends and correlates of class 3 obesity in the United States from 1990 through 2000. JAMA 288 (14): 1758–61.
121. 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.
122. 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.
123. includeonly>Brook Barnes. "Limiting Ads of Junk Food to Children", New York Times, 2007-07-18. Retrieved on 2008-07-24.
124. includeonly>Tara McClair. "Junk-food ban receives mixed reactions in schools", 2007-01-30. Retrieved on 2008-07-24.
125. 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.
126. 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.
127. (2004-02-11) Storing up problems; the medical case for a slimmer nation (PDF), London: Royal College of Physicians.
128. 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). URL accessed 2007-12-17.
129. 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. URL accessed 2007-12-17.
130. The Oxford English Dictionary (website)
131. Carol Gerten-Jackson. The Tuscan General Alessandro del Borro.
132. 132.0 132.1 (2007). History of Medicine: Sushruta – the Clinician – Teacher par Excellence. (PDF) Dwivedi, Girish & Dwivedi, Shridhar. URL accessed on 2008-09-19.
133. Breslow L (September 1952). Public health aspects of weight control. Am J Public Health Nations Health 42 (9): 1116–20.
134. Critser, Greg (2004). Fat Land, London, England: Penguin Books Ltd.
135. Weintraub M (May 1992). Long-term weight control: The National Heart, Lung, and Blood Institute funded multimodal intervention study. Clin. Pharmacol. Ther. 51 (5): 581–5.
136. Finkelstein EA, Fiebelkorn IA, Wang G (2003). National medical spending attributable to overweight and obesity: How much, and who’s paying. Health Affairs Online (May).
137. Obesity and overweight: Economic consequences. CDC. URL accessed on 2007-09-05.
138. 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.
139. Chenoweth & Associates Inc. (2005). The Economic Costs of Physical Inactivity, Obesity, and Overweight in California Adults. (PDF) Cancer Prevention and Nutrition Section, California Center for Physical Activity, California Department of Health Services, Sacramento, CA. URL accessed on 2008-07-23.
140. 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.
141. Extra pounds mean insurance fees for Ala. workers. Associated Press Writer. URL accessed on 2008-09-09.
142. Lisa DiCarlo. Why Airlines Can't Cut The Fat. Forbes.com. URL accessed on 2008-07-23.
143. 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.
144. 144.0 144.1 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. URL accessed on 2008-07-24.
145. WHAT IS NAAFA?. NAAFA. URL accessed on 2008-09-29.
146. National Association to Advance Fat Acceptance, We come in all sizes, NAAFA, [[{{{date}}}|{{{date}}}]].
147. Campos, Paul F. (2005). The Diet Myth, Gotham.
148. Gard, Michael (2005). The Obesity Epidemic: Science, Morality and Ideology, Routledge.
149. Obesity: Time bomb or dud?. USA Today. URL accessed on 2008-09-21.
150. includeonly>Douglas Martin. "About New York", New York Times, 1991-07-31. Retrieved on 2008-07-24.
151. Areton (January 2002). Factors in the sexual satisfaction of obese women in relationships. Electronic Journal of Human Sexuality 5.