# Obesity

Obesity is a medical condition in which excess body fat has accumulated to an extent that it may have a negative effect on health.[1] People are generally considered obese when their body mass index (BMI), a measurement obtained by dividing a person's weight by the square of the person's height, is over 30 kg/m2; the range 25–30 kg/m2 is defined as overweight.[1] Some East Asian countries use lower values.[8] Obesity increases the likelihood of various diseases and conditions, particularly cardiovascular diseases, type 2 diabetes, obstructive sleep apnea, certain types of cancer, osteoarthritis, and depression.[2][3]

Obesity is most commonly caused by a combination of excessive food intake, lack of physical activity, and genetic susceptibility.[1][4] A few cases are caused primarily by genes, endocrine disorders, medications, or mental disorder.[9] The view that obese people eat little yet gain weight due to a slow metabolism is not medically supported.[10] On average, obese people have a greater energy expenditure than their normal counterparts due to the energy required to maintain an increased body mass.[10][11]

Obesity is mostly preventable through a combination of social changes and personal choices.[1] Changes to diet and exercising are the main treatments.[2] Diet quality can be improved by reducing the consumption of energy-dense foods, such as those high in fat or sugars, and by increasing the intake of dietary fiber.[1] Medications can be used, along with a suitable diet, to reduce appetite or decrease fat absorption.[5] If diet, exercise, and medication are not effective, a gastric balloon or surgery may be performed to reduce stomach volume or length of the intestines, leading to feeling full earlier or a reduced ability to absorb nutrients from food.[6][12]

Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children.[1][13] In 2015, 600 million adults (12%) and 100 million children were obese in 195 countries.[7] Obesity is more common in women than men.[1] Authorities view it as one of the most serious public health problems of the 21st century.[14] Obesity is stigmatized in much of the modern world (particularly in the Western world), though it was seen as a symbol of wealth and fertility at other times in history and still is in some parts of the world.[2][15] In 2013, the American Medical Association classified obesity as a disease.[16][17]

Obesity
Silhouettes and waist circumferences representing optimal, overweight, and obese
SpecialtyEndocrinology
SymptomsIncreased fat[1]
ComplicationsCardiovascular diseases, type 2 diabetes, obstructive sleep apnea, certain types of cancer, osteoarthritis, depression[2][3]
CausesExcessive food, lack of exercise, genetics[1][4]
Diagnostic methodBMI > 30 kg/m2[1]
PreventionSocietal changes, personal choices[1]
TreatmentDiet, exercise, medications, surgery[1][5][6]
PrognosisReduced life expectancy[2]
Frequency700 million / 12% (2015)[7]

## Classification

BMI (kg/m2) Classification[18]
from up to
18.5 underweight
18.5 25.0 normal weight
25.0 30.0 overweight
30.0 35.0 class I obesity
35.0 40.0 class II obesity
40.0 class III obesity
A "super obese" male with a BMI of 53 kg/m2: weight 182 kg (400 lb), height 185 cm (6 ft 1 in). He presents with stretch marks and enlarged breasts

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health.[19] 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.[20][21] BMI is closely related to both percentage body fat and total body fat.[22] 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.[23] The reference data on which these percentiles were based date from 1963 to 1994, and thus have not been affected by the recent increases in weight.[24] BMI is defined as the subject's weight divided by the square of their height and is calculated as follows.

${\displaystyle \mathrm {BMI} ={\frac {m}{h^{2}}}}$,
where m and h are the subject's weight and height respectively.

BMI is usually expressed in kilograms of weight per metre squared of height. To convert from pounds per inch squared multiply by 703 (kg/m2)/(lb/sq in).[25]

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.[26][27]

Some modifications to the WHO definitions have been made by particular organizations.[28] The surgical literature breaks down class II and III obesity into further categories whose exact values are still disputed.[29]

• Any BMI ≥ 35 or 40 kg/m2 is severe obesity.
• A BMI of ≥ 35 kg/m2 and experiencing obesity-related health conditions or ≥40–44.9 kg/m2 is morbid obesity.
• A BMI of ≥ 45 or 50 kg/m2 is super obesity.

As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; Japan has defined obesity as any BMI greater than 25 kg/m2[8] while China uses a BMI of greater than 28 kg/m2.[28]

## Effects on health

Excessive body weight is associated with various diseases and conditions, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, osteoarthritis,[2] and asthma.[2][30] As a result, obesity has been found to reduce life expectancy.[2]

### Mortality

Relative risk of death over 10 years for white men (left) and women (right) who have never smoked in the United States by BMI.[31]

Obesity is one of the leading preventable causes of death worldwide.[32][33][34] A number of reviews have found that mortality risk is lowest at a BMI of 20–25 kg/m2[35][36][37] in non-smokers and at 24–27 kg/m2 in current smokers, with risk increasing along with changes in either direction.[38][39] This appears to apply in at least four continents.[37] In contrast, a 2013 review found that grade 1 obesity (BMI 30–35) was not associated with higher mortality than normal weight, and that overweight (BMI 25–30) was associated with "lower" mortality than was normal weight (BMI 18.5–25).[40] Other evidence suggests that the association of BMI and waist circumference with mortality is U- or J-shaped, while the association between waist-to-hip ratio and waist-to-height ratio with mortality is more positive.[41] In Asians the risk of negative health effects begins to increase between 22–25 kg/m2.[42] A BMI above 32 kg/m2 has been associated with a doubled mortality rate among women over a 16-year period.[43] In the United States, obesity is estimated to cause 111,909 to 365,000 deaths per year,[2][34] while 1 million (7.7%) of deaths in Europe are attributed to excess weight.[44][45] On average, obesity reduces life expectancy by six to seven years,[2][46] a BMI of 30–35 kg/m2 reduces life expectancy by two to four years,[36] while severe obesity (BMI > 40 kg/m2) reduces life expectancy by ten years.[36]

### 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.[47]

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.[48]

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][49] Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state,[50][51] and a prothrombotic state.[49][52]

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.[74] The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,[74] and has subsequently been found in those with heart failure and peripheral artery disease (PAD).[75]

In people with heart failure, those with a BMI between 30.0 and 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.[76] 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, the risk of further cardiovascular events is increased.[77][78] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.[79] One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.[80] Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD, the benefit of obesity no longer exists.[75]

## Causes

At an individual level, a combination of excessive food energy intake and a lack of physical activity is thought to explain most cases of obesity.[81] A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness.[9] In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet,[82] increased reliance on cars, and mechanized manufacturing.[83][84]

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 increase the number of obese people by increasing population variance in weight).[85] While there is 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

1961
2001–03
Map of dietary energy availability per person per day in 1961 (left) and 2001–2003 (right)[86] Calories per person per day (kilojoules per person per day)
Average per capita energy consumption of the world from 1961 to 2002[86]

A 2016 review supported excess food as the primary factor.[87] Dietary energy supply per capita varies markedly between different regions and countries. It has also changed significantly over time.[86] From the early 1970s to the late 1990s the average food energy available per person per day (the amount of food bought) increased in all parts of the world except Eastern Europe. The United States had the highest availability with 3,654 calories (15,290 kJ) per person in 1996.[86] This increased further in 2003 to 3,754 calories (15,710 kJ).[86] During the late 1990s Europeans had 3,394 calories (14,200 kJ) per person, in the developing areas of Asia there were 2,648 calories (11,080 kJ) per person, and in sub-Saharan Africa people had 2,176 calories (9,100 kJ) per person.[86][88] Total food energy consumption has been found to be related to obesity.[89]

The widespread availability of nutritional guidelines[90] has done little to address the problems of overeating and poor dietary choice.[91] From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.[92] During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was 335 calories (1,400 kJ) per day (1,542 calories (6,450 kJ) in 1971 and 1,877 calories (7,850 kJ) in 2004), while for men the average increase was 168 calories (700 kJ) per day (2,450 calories (10,300 kJ) in 1971 and 2,618 calories (10,950 kJ) in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption.[93] The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America,[94] and potato chips.[95] Consumption of sweetened drinks such as soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks is believed to be contributing to the rising rates of obesity[96][97] and to an increased risk of metabolic syndrome and type 2 diabetes.[98] Vitamin D deficiency is related to diseases associated with obesity.[99]

As societies become increasingly reliant on energy-dense, big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning.[100] In the United States consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.[101]

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.[102] Calorie count laws and nutrition facts labels attempt to steer people toward making healthier food choices, including awareness of how much food energy is being consumed.

Obese people consistently under-report their food consumption as compared to people of normal weight.[103] This is supported both by tests of people carried out in a calorimeter room[104] and by direct observation.

### Sedentary lifestyle

A sedentary lifestyle plays a significant role in obesity.[105] Worldwide there has been a large shift towards less physically demanding work,[106][107][108] and currently at least 30% of the world's population gets insufficient exercise.[107] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.[106][107][108] In children, there appear to be declines in levels of physical activity due to less walking and physical education.[109] World trends in active leisure time physical activity are less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland[110] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.[111] A 2011 review of physical activity in children found that it may not be a significant contributor.[112]

In both children and adults, there is an association between television viewing time and the risk of obesity.[113][114][115] A review found 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.[116]

### Genetics

A 1680 painting by Juan Carreno de Miranda of a girl presumed to have Prader–Willi syndrome[117]

Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors.[118] Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient food energy is present. As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present.[119] People with two copies of the FTO gene (fat mass and obesity associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele.[120] The differences in BMI between people that are due to genetics varies depending on the population examined from 6% to 85%.[121]

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.)[122] 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.[123]

Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.[124] Different people exposed to the same environment have different risks of obesity due to their underlying genetics.[125]

The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone to obesity. 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 to survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies.[126] This theory has received various criticisms, and other evolutionarily-based theories such as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.[127][128]

### Other illnesses

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,[129] and some eating disorders such as 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.[130] The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.[131]

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

The disease scroll (Yamai no soshi, late 12th century) depicts a woman moneylender with obesity, considered a disease of the rich.
Obesity in developed countries is correlated with economic inequality

While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.[132] Though it is accepted that energy consumption in excess of energy 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.[133] 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.[134] 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 among US states: more adults, even in higher social classes, are obese in more unequal states.[135]

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.[134] Attitudes toward body weight held by people in one's life may also play a role in obesity. A correlation in BMI changes over time has been found among friends, siblings, and spouses.[136] Stress and perceived low social status appear to increase risk of obesity.[135][137][138]

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.[139] However, changing rates of smoking have had little effect on the overall rates of obesity.[140]

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.[141] This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.[142]

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%.[143]

Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.[144] Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.[144]

Consistent with cognitive epidemiological data, numerous studies confirm that obesity is associated with cognitive deficits.[145] Whether obesity causes cognitive deficits, or vice versa is unclear at present.

### Gut bacteria

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 people. There is an indication that gut flora can affect the metabolic potential. This apparent alteration 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.[146] The use of antibiotics among children has also been associated with obesity later in life.[147][148]

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.[149]

### Other factors

A number of reviews have found an association between short duration of sleep and obesity.[150][151] Whether one causes the other is unclear.[150] Even if shorts sleep does increase weight gain it is unclear if this is to a meaningful degree or increasing sleep would be of benefit.[152]

Certain aspects of personality are associated with being obese.[153] Neuroticism, impulsivity, and sensitivity to reward are more common in people who are obese while conscientiousness and self-control are less common in people who are obese.[153][154]

## Pathophysiology

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

There are many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[155] This field of research had been almost unapproached until the leptin gene was discovered in 1994 by J. M. Friedman's laboratory.[156] 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.[155] 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.[157]

The arcuate nucleus contains two distinct groups of neurons.[155] 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.[155]

## 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.[158] Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[159] The United States Preventive Services Task Force recommends screening for all adults followed by behavioral interventions in those who are obese.[160] 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 food energy consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct junk food marketing to children,[161] and decreasing access to sugar-sweetened beverages in schools.[162] The World Health Organization recommends the taxing of sugary drinks.[163] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[164]

### Reports

Many organizations 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".[165] In 2006 the Canadian Obesity Network, now known as Obesity Canada 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.[81]

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.[166] 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.[167] 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.[168] A 2007 report produced by 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.[169]

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.[170]

## Management

The main treatment for obesity consists of dieting and physical exercise.[81] Diet programs may produce weight loss over the short term,[171] but maintaining this weight loss is frequently difficult and often requires making exercise and a lower food energy diet a permanent part of a person's lifestyle.[172][173] Intensive behavioral interventions are recommended by the United States Preventive Services Task Force.[174]

In the short-term low carbohydrate diets appear better than low fat diets for weight loss.[175] In the long term; however, all types of low-carbohydrate and low-fat diets appear equally beneficial.[175][176] A 2014 review found that the heart disease and diabetes risks associated with different diets appear to be similar.[177] Promotion of the Mediterranean diets among the obese may lower the risk of heart disease.[175] Decreased intake of sweet drinks is also related to weight-loss.[175] Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2–20%.[178] Dietary and lifestyle changes are effective in limiting excessive weight gain in pregnancy and improve outcomes for both the mother and the child.[179] Intensive behavioral counseling is recommended in those who are both obese and have other risk factors for heart disease.[180]

Five medications have evidence for long-term use orlistat, lorcaserin, liraglutide, phentermine–topiramate, and naltrexone–bupropion.[181] They result in weight loss after one year ranged from 3.0 to 6.7 kg (6.6-14.8 lbs) over placebo.[181] Orlistat, liraglutide, and naltrexone–bupropion are available in both the United States and Europe, whereas lorcaserin and phentermine–topiramate are available only in the United States.[182] European regulatory authorities rejected the latter two drugs in part because of associations of heart valve problems with lorcaserin and more general heart and blood vessel problems with phentermine–topiramate.[182] Orlistat use is associated with high rates of gastrointestinal side effects[183] and concerns have been raised about negative effects on the kidneys.[184] There is no information on how these drugs affect longer-term complications of obesity such as cardiovascular disease or death.[5]

The most effective treatment for obesity is bariatric surgery.[6] The types of procedures include laparoscopic adjustable gastric banding, Roux-en-Y gastric bypass, vertical-sleeve gastrectomy, and biliopancreatic diversion.[181] Surgery for severe obesity is associated with long-term weight loss, improvement in obesity-related conditions,[185] 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.[186] Complications occur in about 17% of cases and reoperation is needed in 7% of cases.[185] Due to its cost and risks, researchers are searching for other effective yet less invasive treatments including devices that occupy space in the stomach.[187]

## Epidemiology

World obesity prevalence among males (left) and females (right) in 2008.[188]

See or edit source data.
Percentage of the population either overweight or obese by year.[189]

In earlier historical periods obesity was rare, and achievable only by a small elite, although already recognised as a problem for health. But as prosperity increased in the Early Modern period, it affected increasingly larger groups of the population.[190]

In 1997 the WHO formally recognized obesity as a global epidemic.[94] As of 2008 the WHO estimates that at least 500 million adults (greater than 10%) are obese, with higher rates among women than men.[191] The percentage of adults affected in the United States as of 2015–2016 is about 39.6% overall (37.9% of males and 41.1% of females).[192]

The rate of obesity also increases with age at least up to 50 or 60 years old[193] and severe obesity in the United States, Australia, and Canada is increasing faster than the overall rate of obesity.[29][194][195] The OECD has projected an increase in obesity rates until at least 2030, especially in the United States, Mexico and England with rates reaching 47%, 39% and 35% respectively.[196]

Once considered a problem only of high-income countries, obesity rates are rising worldwide and affecting both the developed and developing world.[44] These increases have been felt most dramatically in urban settings.[191] The only remaining region of the world where obesity is not common is sub-Saharan Africa.[2]

## History

### 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.[197] The Oxford English Dictionary documents its first usage in 1611 by Randle Cotgrave.[198]

### Historical attitudes

During the Middle Ages and the Renaissance obesity was often seen as a sign of wealth, and was relatively common among the elite: The Tuscan General Alessandro del Borro, attributed to Charles Mellin, 1645[199]
Venus of Willendorf created 24,000–22,000 BC

Ancient Greek medicine recognizes obesity as a medical disorder, and records that the Ancient Egyptians saw it in the same way.[190] Hippocrates wrote that "Corpulence is not only a disease itself, but the harbinger of others".[2] The Indian surgeon Sushruta (6th century BCE) related obesity to diabetes and heart disorders.[200] He recommended physical work to help cure it and its side effects.[200] For most of human history mankind struggled with food scarcity.[201] 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[199] as well as in Ancient East Asian civilizations.[202] In the 17th century, English medical author Tobias Venner is credited with being one of the first to refer to the term as a societal disease in a published English language book.[190][203]

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.[94] 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.[94] 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.[94] In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.[94][204] During this time period, insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.[2]

Many cultures throughout history have viewed obesity as the result of a character flaw. The obesus or fat character in Ancient Greek comedy was a glutton and figure of mockery. During Christian times the food was viewed as a gateway to the sins of sloth and lust.[15] 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.[205]

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%.[206] 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.[207] These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal.[207]

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.[15] 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.[15]

During the Renaissance some of the upper class began flaunting their large size, as can be seen in portraits of Henry VIII of England and Alessandro dal Borro.[15] 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.[208] 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.[15]

## Society and culture

### Economic impact

In addition to its health impacts, obesity leads to many problems including disadvantages in employment[209][210] and increased business costs. These effects are felt by all levels of society from individuals, to corporations, to governments.

In 2005, the medical costs attributable to obesity in the US were an estimated $190.2 billion or 20.6% of all medical expenditures,[211][212][213] while the cost of obesity in Canada was estimated at CA$2 billion in 1997 (2.4% of total health costs).[81] The total annual direct cost of overweight and obesity in Australia in 2005 was A$21 billion. Overweight and obese Australians also received A$35.6 billion in government subsidies.[214] The estimate range for annual expenditures on diet products is $40 billion to$100 billion in the US alone.[215]

The Lancet Commission on Obesity in 2019 called for a global treaty — modelled on the WHO Framework Convention on Tobacco Control — committing countries to address obesity and undernutrition, explicitly excluding the food industry from policy development. They estimate the global cost of obesity $2 trillion a year, about or 2.8% of world GDP.[216] 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.[217] Services accommodate obese people with specialized equipment such as much wider chairs.[218] Obesity can lead to social stigmatization and disadvantages in employment.[209] When compared to their normal weight counterparts, obese workers on average have higher rates of absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.[219] A study examining Duke University employees found that people with a BMI over 40 kg/m2 filed twice as many workers' compensation claims as those whose BMI was 18.5–24.9 kg/m2. 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.[220] The Alabama State Employees' Insurance Board approved a controversial plan to charge obese workers$25 a month for health insurance that would otherwise be free unless they take steps to lose weight and improve their health. These measures started in January 2010 and apply to those state workers whose BMI exceeds 35 kg/m2 and who fail to make improvements in their health after one year.[221]

Some research shows that obese people are less likely to be hired for a job and are less likely to be promoted.[205] 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.[222]

Specific industries, such as the airline, healthcare and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width.[223] In 2000, the extra weight of obese passengers cost airlines US$275 million.[224] The healthcare industry has had to invest in special facilities for handling severely obese patients, including special lifting equipment and bariatric ambulances.[225] Costs for restaurants are increased by litigation accusing them of causing obesity.[226] In 2005 the US Congress discussed legislation to prevent civil lawsuits against the food industry in relation to obesity; however, it did not become law.[226] With the American Medical Association's 2013 classification of obesity as a chronic disease,[16] it is thought that health insurance companies will more likely pay for obesity treatment, counseling and surgery, and the cost of research and development of fat treatment pills or gene therapy treatments should be more affordable if insurers help to subsidize their cost.[227] The AMA classification is not legally binding, however, so health insurers still have the right to reject coverage for a treatment or procedure.[227] In 2014, The European Court of Justice ruled that morbid obesity is a disability. The Court said that if an employee's obesity prevents him from "full and effective participation of that person in professional life on an equal basis with other workers", then it shall be considered a disability and that firing someone on such grounds is discriminatory.[228] ### Size acceptance United States President William Howard Taft was often ridiculed for being overweight The principal goal of the fat acceptance movement is to decrease discrimination against people who are overweight and obese.[229][230] However, some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes.[231] A number of organizations exist that promote the acceptance of obesity. They have increased in prominence in the latter half of the 20th century.[232] 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.[233] 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.[234] 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.[231] ### Industry influence on research In 2015 the New York Times published an article on the Global Energy Balance Network, a nonprofit founded in 2014 that advocated for people to focus on increasing exercise rather than reducing calorie intake to avoid obesity and to be healthy. The organization was founded with at least$1.5M in funding from the Coca-Cola Company, and the company has provided $4M in research funding to the two founding scientists Gregory A. Hand and Steven N. Blair since 2008.[235][236] ## Childhood obesity 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.[23] 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.[24] Childhood obesity has reached epidemic proportions in the 21st century, with rising rates in both the developed and the developing world. Rates of obesity in Canadian boys have increased from 11% in the 1980s to over 30% in the 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.[237] As with obesity in adults, many factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important causes for the recent increase in the incidence of child obesity.[238] Antibiotics in the first 6 months of life have been associated with excess weight at age seven to twelve years of age.[148] 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 disease.[81] Treatments used in children are primarily lifestyle interventions and behavioral techniques, although efforts to increase activity in children have had little success.[239] In the United States, medications are not FDA approved for use in this age group.[237] Multi-component behaviour change interventions that include changes to dietary and physical activity may reduce BMI in the short term in children aged 6 to 11 years, although the benefits are small and quality of evidence is low.[240] ## Other animals Obesity in pets is common in many countries. In the United States, 23–41% of dogs are overweight, and about 5.1% are obese.[241] The rate of obesity in cats was slightly higher at 6.4%.[241] In Australia the rate of obesity among dogs in a veterinary setting has been found to be 7.6%.[242] The risk of obesity in dogs is related to whether or not their owners are obese; however, there is no similar correlation between cats and their owners.[243] ## References 1. "Obesity and overweight Fact sheet N°311". WHO. January 2015. Retrieved 2 February 2016. 2. Haslam DW, James WP (October 2005). "Obesity". Lancet (Review). 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-1. PMID 16198769. 3. ^ a b Luppino FS, de Wit LM, Bouvy PF, Stijnen T, Cuijpers P, Penninx BW, Zitman FG (March 2010). "Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies". Archives of General Psychiatry. 67 (3): 220–9. doi:10.1001/archgenpsychiatry.2010.2. PMID 20194822. 4. ^ a b Yazdi FT, Clee SM, Meyre D (2015). "Obesity genetics in mouse and human: back and forth, and back again". PeerJ. 3: e856. doi:10.7717/peerj.856. PMC 4375971. PMID 25825681. 5. ^ a b c Yanovski SZ, Yanovski JA (January 2014). "Long-term drug treatment for obesity: a systematic and clinical review". JAMA (Review). 311 (1): 74–86. doi:10.1001/jama.2013.281361. PMC 3928674. PMID 24231879. 6. ^ a b c Colquitt JL, Pickett K, Loveman E, Frampton GK (August 2014). "Surgery for weight loss in adults". The Cochrane Database of Systematic Reviews (Meta-analysis, Review). 8 (8): CD003641. doi:10.1002/14651858.CD003641.pub4. PMID 25105982. 7. ^ a b Afshin A, Forouzanfar MH, Reitsma MB, Sur P, Estep K, Lee A, Marczak L, Mokdad AH, Moradi-Lakeh M, Naghavi M, Salama JS, Vos T, Abate KH, Abbafati C, Ahmed MB, Al-Aly Z, Alkerwi A, Al-Raddadi R, Amare AT, Amberbir A, Amegah AK, Amini E, Amrock SM, Anjana RM, Ärnlöv J, Asayesh H, Banerjee A, Barac A, Baye E, Bennett DA, Beyene AS, Biadgilign S, Biryukov S, Bjertness E, Boneya DJ, Campos-Nonato I, Carrero JJ, Cecilio P, Cercy K, Ciobanu LG, Cornaby L, Damtew SA, Dandona L, Dandona R, Dharmaratne SD, Duncan BB, Eshrati B, Esteghamati A, Feigin VL, Fernandes JC, Fürst T, Gebrehiwot TT, Gold A, Gona PN, Goto A, Habtewold TD, Hadush KT, Hafezi-Nejad N, Hay SI, Horino M, Islami F, Kamal R, Kasaeian A, Katikireddi SV, Kengne AP, Kesavachandran CN, Khader YS, Khang YH, Khubchandani J, Kim D, Kim YJ, Kinfu Y, Kosen S, Ku T, Defo BK, Kumar GA, Larson HJ, Leinsalu M, Liang X, Lim SS, Liu P, Lopez AD, Lozano R, Majeed A, Malekzadeh R, Malta DC, Mazidi M, McAlinden C, McGarvey ST, Mengistu DT, Mensah GA, Mensink GB, Mezgebe HB, Mirrakhimov EM, Mueller UO, Noubiap JJ, Obermeyer CM, Ogbo FA, Owolabi MO, Patton GC, Pourmalek F, Qorbani M, Rafay A, Rai RK, Ranabhat CL, Reinig N, Safiri S, Salomon JA, Sanabria JR, Santos IS, Sartorius B, Sawhney M, Schmidhuber J, Schutte AE, Schmidt MI, Sepanlou SG, Shamsizadeh M, Sheikhbahaei S, Shin MJ, Shiri R, Shiue I, Roba HS, Silva DA, Silverberg JI, Singh JA, Stranges S, Swaminathan S, Tabarés-Seisdedos R, Tadese F, Tedla BA, Tegegne BS, Terkawi AS, Thakur JS, Tonelli M, Topor-Madry R, Tyrovolas S, Ukwaja KN, Uthman OA, Vaezghasemi M, Vasankari T, Vlassov VV, Vollset SE, Weiderpass E, Werdecker A, Wesana J, Westerman R, Yano Y, Yonemoto N, Yonga G, Zaidi Z, Zenebe ZM, Zipkin B, Murray CJ (July 2017). "Health Effects of Overweight and Obesity in 195 Countries over 25 Years". The New England Journal of Medicine. 377 (1): 13–27. doi:10.1056/NEJMoa1614362. PMC 5477817. PMID 28604169. 8. ^ a b Kanazawa M, Yoshiike N, Osaka T, Numba Y, Zimmet P, Inoue S (2005). "Criteria and Classification of Obesity in Japan and Asia-Oceania". Nutrition and Fitness: Obesity, the Metabolic Syndrome, Cardiovascular Disease, and Cancer. World Review of Nutrition and Dietetics. 94. pp. 1–12. doi:10.1159/000088200. ISBN 978-3-8055-7944-5. PMID 16145245. 9. ^ a b Bleich S, Cutler D, Murray C, Adams A (2008). "Why is the developed world obese?". Annual Review of Public Health (Research Support). 29: 273–95. doi:10.1146/annurev.publhealth.29.020907.090954. PMID 18173389. 10. ^ a b Oxford Handbook of Medical Sciences (2nd ed.). Oxford: OUP Oxford. 2011. p. 180. ISBN 9780191652295. 11. ^ Kushner R (2007). Treatment of the Obese Patient (Contemporary Endocrinology). Totowa, NJ: Humana Press. p. 158. ISBN 978-1-59745-400-1. Retrieved 5 April 2009. 12. ^ 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". Obesity Surgery. 18 (7): 841–6. doi:10.1007/s11695-007-9331-8. PMID 18459025. 13. ^ Encyclopedia of Mental Health (2 ed.). Academic Press. 2015. p. 158. ISBN 9780123977533. 14. Dibaise JK, Foxx-Orenstein AE (July 2013). "Role of the gastroenterologist in managing obesity". Expert Review of Gastroenterology & Hepatology (Review). 7 (5): 439–51. doi:10.1586/17474124.2013.811061. PMID 23899283. 15. Woodhouse R (2008). "Obesity in Art – A Brief Overview". Obesity in art: a brief overview. Frontiers of Hormone Research. 36. pp. 271–86. doi:10.1159/000115370. ISBN 978-3-8055-8429-6. PMID 18230908. 16. ^ a b Pollack A (18 June 2013). "A.M.A. Recognizes Obesity as a Disease". New York Times. Archived from the original on 23 June 2013. 17. ^ Weinstock, Matthew (21 June 2013). "The Facts About Obesity". H&HN. American Hospital Association. Retrieved 24 June 2013. 18. ^ "BMI classification". World Health Organization. Retrieved 15 February 2014. 19. ^ WHO 2000 p.6 20. ^ Sweeting HN (October 2007). "Measurement and definitions of obesity in childhood and adolescence: a field guide for the uninitiated". Nutrition Journal. 6 (1): 32. doi:10.1186/1475-2891-6-32. PMC 2164947. PMID 17963490. 21. ^ NHLBI p.xiv 22. ^ Gray DS, Fujioka K (1991). "Use of relative weight and Body Mass Index for the determination of adiposity". Journal of Clinical Epidemiology. 44 (6): 545–50. doi:10.1016/0895-4356(91)90218-X. PMID 2037859. 23. ^ a b 24. ^ 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". The American Journal of Clinical Nutrition. 73 (6): 1086–93. doi:10.1093/ajcn/73.6.1086. PMID 11382664. 25. ^ 1 (lb/sq in) is more precisely 703.06957964 (kg/m2). 26. ^ WHO 2000 p.9 27. ^ Nikcevic AV, Kuczmierczyk AR, Bruch M (2009). Formulation and Treatment in Clinical Health Psychology. Routledge. ISBN 9781135452087. 28. ^ a b 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.; Originally printed as Zhou BF (March 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". Biomedical and Environmental Sciences. 15 (1): 83–96. PMID 12046553. 29. ^ 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. PMC 2864630. PMID 17399752. 30. ^ a b c d Poulain M, Doucet M, Major GC, Drapeau V, Sériès F, Boulet LP, Tremblay A, Maltais F (April 2006). "The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies". CMAJ. 174 (9): 1293–9. doi:10.1503/cmaj.051299. PMC 1435949. PMID 16636330. 31. ^ Berrington de Gonzalez A, Hartge P, Cerhan JR, Flint AJ, Hannan L, MacInnis RJ, Moore SC, Tobias GS, Anton-Culver H, Freeman LB, Beeson WL, Clipp SL, English DR, Folsom AR, Freedman DM, Giles G, Hakansson N, Henderson KD, Hoffman-Bolton J, Hoppin JA, Koenig KL, Lee IM, Linet MS, Park Y, Pocobelli G, Schatzkin A, Sesso HD, Weiderpass E, Willcox BJ, Wolk A, Zeleniuch-Jacquotte A, Willett WC, Thun MJ (December 2010). "Body-mass index and mortality among 1.46 million white adults". The New England Journal of Medicine. 363 (23): 2211–9. doi:10.1056/NEJMoa1000367. PMC 3066051. PMID 21121834. 32. ^ Barness LA, Opitz JM, Gilbert-Barness E (December 2007). "Obesity: genetic, molecular, and environmental aspects". American Journal of Medical Genetics. Part A. 143A (24): 3016–34. doi:10.1002/ajmg.a.32035. PMID 18000969. 33. ^ Mokdad AH, Marks JS, Stroup DF, Gerberding JL (March 2004). "Actual causes of death in the United States, 2000". JAMA. 291 (10): 1238–45. doi:10.1001/jama.291.10.1238. PMID 15010446. 34. ^ 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. 35. ^ Aune D, Sen A, Prasad M, Norat T, Janszky I, Tonstad S, Romundstad P, Vatten LJ (May 2016). "BMI and all cause mortality: systematic review and non-linear dose-response meta-analysis of 230 cohort studies with 3.74 million deaths among 30.3 million participants". BMJ. 353: i2156. doi:10.1136/bmj.i2156. PMC 4856854. PMID 27146380. 36. ^ a b c Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, Halsey J, Qizilbash N, Collins R, Peto R (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. PMC 2662372. PMID 19299006. 37. ^ a b Di Angelantonio E, Bhupathiraju S, Wormser D, Gao P, Kaptoge S, Berrington de Gonzalez A, et al. (The Global BMI Mortality Collaboration) (August 2016). "Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents". Lancet. 388 (10046): 776–86. doi:10.1016/S0140-6736(16)30175-1. PMC 4995441. PMID 27423262. 38. ^ 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". The New England Journal of Medicine. 341 (15): 1097–105. doi:10.1056/NEJM199910073411501. PMID 10511607. 39. ^ Pischon T, Boeing H, Hoffmann K, Bergmann M, Schulze MB, Overvad K, van der Schouw YT, Spencer E, Moons KG, Tjønneland A, Halkjaer J, Jensen MK, Stegger J, Clavel-Chapelon F, Boutron-Ruault MC, Chajes V, Linseisen J, Kaaks R, Trichopoulou A, Trichopoulos D, Bamia C, Sieri S, Palli D, Tumino R, Vineis P, Panico S, Peeters PH, May AM, Bueno-de-Mesquita HB, van Duijnhoven FJ, Hallmans G, Weinehall L, Manjer J, Hedblad B, Lund E, Agudo A, Arriola L, Barricarte A, Navarro C, Martinez C, Quirós JR, Key T, Bingham S, Khaw KT, Boffetta P, Jenab M, Ferrari P, Riboli E (November 2008). "General and abdominal adiposity and risk of death in Europe". The New England Journal of Medicine. 359 (20): 2105–20. doi:10.1056/NEJMoa0801891. PMID 19005195. 40. ^ Flegal KM, Kit BK, Orpana H, Graubard BI (January 2013). "Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis". JAMA. 309 (1): 71–82. doi:10.1001/jama.2012.113905. PMC 4855514. PMID 23280227. 41. ^ Carmienke S, Freitag MH, Pischon T, Schlattmann P, Fankhaenel T, Goebel H, Gensichen J (June 2013). "General and abdominal obesity parameters and their combination in relation to mortality: a systematic review and meta-regression analysis". European Journal of Clinical Nutrition. 67 (6): 573–85. doi:10.1038/ejcn.2013.61. PMID 23511854. 42. ^ WHO Expert Consultation (January 2004). "Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies". Lancet. 363 (9403): 157–63. doi:10.1016/s0140-6736(03)15268-3. PMID 14726171. 43. ^ Manson JE, Willett WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson SE, Hennekens CH, Speizer FE (September 1995). "Body weight and mortality among women". The New England Journal of Medicine. 333 (11): 677–85. doi:10.1056/NEJM199509143331101. PMID 7637744. 44. ^ a b Tsigos C, Hainer V, Basdevant A, Finer N, Fried M, Mathus-Vliegen E, Micic D, Maislos M, Roman G, Schutz Y, Toplak H, Zahorska-Markiewicz B (April 2008). "Management of obesity in adults: European clinical practice guidelines" (PDF). Obesity Facts. 1 (2): 106–16. doi:10.1159/000126822. PMID 20054170. Archived from the original (PDF) on 26 April 2012. 45. ^ Fried M, Hainer V, Basdevant A, Buchwald H, Deitel M, Finer N, Greve JW, Horber F, Mathus-Vliegen E, Scopinaro N, Steffen R, Tsigos C, Weiner R, Widhalm K (April 2007). "Inter-disciplinary European guidelines on surgery of severe obesity". International Journal of Obesity. 31 (4): 569–77. doi:10.1038/sj.ijo.0803560. PMID 17325689. 46. ^ 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". Annals of Internal Medicine. 138 (1): 24–32. doi:10.7326/0003-4819-138-1-200301070-00008. hdl:1765/10043. PMID 12513041. 47. ^ Grundy SM (June 2004). "Obesity, metabolic syndrome, and cardiovascular disease". The Journal of Clinical Endocrinology and Metabolism. 89 (6): 2595–600. doi:10.1210/jc.2004-0372. PMID 15181029. 48. ^ Seidell 2005 p.9 49. ^ a b Bray GA (June 2004). "Medical consequences of obesity". The Journal of Clinical Endocrinology and Metabolism. 89 (6): 2583–9. doi:10.1210/jc.2004-0535. PMID 15181027. 50. ^ Shoelson SE, Herrero L, Naaz A (May 2007). "Obesity, inflammation, and insulin resistance". Gastroenterology. 132 (6): 2169–80. doi:10.1053/j.gastro.2007.03.059. PMID 17498510. 51. ^ Shoelson SE, Lee J, Goldfine AB (July 2006). "Inflammation and insulin resistance". The Journal of Clinical Investigation. 116 (7): 1793–801. doi:10.1172/JCI29069. PMC 1483173. PMID 16823477. 52. ^ Dentali F, Squizzato A, Ageno W (July 2009). "The metabolic syndrome as a risk factor for venous and arterial thrombosis". Seminars in Thrombosis and Hemostasis. 35 (5): 451–7. doi:10.1055/s-0029-1234140. PMID 19739035. 53. ^ Lu Y, Hajifathalian K, Ezzati M, Woodward M, Rimm EB, Danaei G (March 2014). "Metabolic mediators of the effects of body-mass index, overweight, and obesity on coronary heart disease and stroke: a pooled analysis of 97 prospective cohorts with 1·8 million participants". Lancet. 383 (9921): 970–83. doi:10.1016/S0140-6736(13)61836-X. PMC 3959199. PMID 24269108. 54. ^ Aune D, Sen A, Norat T, Janszky I, Romundstad P, Tonstad S, Vatten LJ (February 2016). "Body Mass Index, Abdominal Fatness, and Heart Failure Incidence and Mortality: A Systematic Review and Dose-Response Meta-Analysis of Prospective Studies". Circulation. 133 (7): 639–49. doi:10.1161/CIRCULATIONAHA.115.016801. PMID 26746176. 55. ^ Darvall KA, Sam RC, Silverman SH, Bradbury AW, Adam DJ (February 2007). "Obesity and thrombosis". European Journal of Vascular and Endovascular Surgery. 33 (2): 223–33. doi:10.1016/j.ejvs.2006.10.006. PMID 17185009. 56. Yosipovitch G, DeVore A, Dawn A (June 2007). "Obesity and the skin: skin physiology and skin manifestations of obesity". Journal of the American Academy of Dermatology. 56 (6): 901–16, quiz 917–20. doi:10.1016/j.jaad.2006.12.004. PMID 17504714. 57. ^ Hahler B (June 2006). "An overview of dermatological conditions commonly associated with the obese patient". Ostomy/Wound Management. 52 (6): 34–6, 38, 40 passim. PMID 16799182. 58. ^ a b c Arendas K, Qiu Q, Gruslin A (June 2008). "Obesity in pregnancy: pre-conceptional to postpartum consequences". Journal of Obstetrics and Gynaecology Canada. 30 (6): 477–488. doi:10.1016/s1701-2163(16)32863-8. PMID 18611299. 59. ^ Harney D, Patijn J (2007). "Meralgia paresthetica: diagnosis and management strategies". Pain Medicine (Review). 8 (8): 669–77. doi:10.1111/j.1526-4637.2006.00227.x. PMID 18028045. 60. ^ Bigal ME, Lipton RB (January 2008). "Obesity and chronic daily headache". Current Pain and Headache Reports (Review). 12 (1): 56–61. doi:10.1007/s11916-008-0011-8. PMID 18417025. 61. ^ Sharifi-Mollayousefi A, Yazdchi-Marandi M, Ayramlou H, Heidari P, Salavati A, Zarrintan S, Sharifi-Mollayousefi A (February 2008). "Assessment of body mass index and hand anthropometric measurements as independent risk factors for carpal tunnel syndrome". Folia Morphologica. 67 (1): 36–42. PMID 18335412. 62. ^ 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". Obesity Reviews (Meta-analysis). 9 (3): 204–18. doi:10.1111/j.1467-789X.2008.00473.x. PMC 4887143. PMID 18331422. 63. ^ Wall M (March 2008). "Idiopathic intracranial hypertension (pseudotumor cerebri)". Current Neurology and Neuroscience Reports (Review). 8 (2): 87–93. doi:10.1007/s11910-008-0015-0. PMID 18460275. 64. ^ Munger KL, Chitnis T, Ascherio A (November 2009). "Body size and risk of MS in two cohorts of US women". Neurology (Comparative Study). 73 (19): 1543–50. doi:10.1212/WNL.0b013e3181c0d6e0. PMC 2777074. PMID 19901245. 65. ^ Basen-Engquist K, Chang M (February 2011). "Obesity and cancer risk: recent review and evidence". Current Oncology Reports. 13 (1): 71–6. doi:10.1007/s11912-010-0139-7. PMC 3786180. PMID 21080117. 66. ^ Aune D, Norat T, Vatten LJ (December 2014). "Body mass index and the risk of gout: a systematic review and dose-response meta-analysis of prospective studies". European Journal of Nutrition. 53 (8): 1591–601. doi:10.1007/s00394-014-0766-0. PMID 25209031. 67. ^ Tukker A, Visscher TL, Picavet HS (March 2009). "Overweight and health problems of the lower extremities: osteoarthritis, pain and disability". Public Health Nutrition (Research Support). 12 (3): 359–68. doi:10.1017/S1368980008002103. PMID 18426630. 68. ^ Molenaar EA, Numans ME, van Ameijden EJ, Grobbee DE (November 2008). "[Considerable comorbidity in overweight adults: results from the Utrecht Health Project]". Nederlands Tijdschrift voor Geneeskunde (English abstract) (in Dutch). 152 (45): 2457–63. PMID 19051798. 69. ^ Corona G, Rastrelli G, Filippi S, Vignozzi L, Mannucci E, Maggi M (2014). "Erectile dysfunction and central obesity: an Italian perspective". Asian Journal of Andrology. 16 (4): 581–91. doi:10.4103/1008-682X.126386. PMC 4104087. PMID 24713832. 70. ^ Hunskaar S (2008). "A systematic review of overweight and obesity as risk factors and targets for clinical intervention for urinary incontinence in women". Neurourology and Urodynamics (Review). 27 (8): 749–57. doi:10.1002/nau.20635. PMID 18951445. 71. ^ Ejerblad E, Fored CM, Lindblad P, Fryzek J, McLaughlin JK, Nyrén O (June 2006). "Obesity and risk for chronic renal failure". Journal of the American Society of Nephrology (Research Support). 17 (6): 1695–702. doi:10.1681/ASN.2005060638. PMID 16641153. 72. ^ Makhsida N, Shah J, Yan G, Fisch H, Shabsigh R (September 2005). "Hypogonadism and metabolic syndrome: implications for testosterone therapy". The Journal of Urology (Review). 174 (3): 827–34. CiteSeerX 10.1.1.612.1060. doi:10.1097/01.ju.0000169490.78443.59. PMID 16093964. 73. ^ Pestana IA, Greenfield JM, Walsh M, Donatucci CF, Erdmann D (October 2009). "Management of "buried" penis in adulthood: an overview". Plastic and Reconstructive Surgery (Review). 124 (4): 1186–95. doi:10.1097/PRS.0b013e3181b5a37f. PMID 19935302. 74. ^ a b Schmidt DS, Salahudeen AK (2007). "Obesity-survival paradox-still a controversy?". Seminars in Dialysis (Review). 20 (6): 486–92. doi:10.1111/j.1525-139X.2007.00349.x. PMID 17991192. 75. ^ a b U.S. Preventive Services Task Force (June 2003). "Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale". American Family Physician (Review). 67 (12): 2573–6. PMID 12825847. 76. ^ Habbu A, Lakkis NM, Dokainish H (October 2006). "The obesity paradox: fact or fiction?". The American Journal of Cardiology (Review). 98 (7): 944–8. doi:10.1016/j.amjcard.2006.04.039. PMID 16996880. 77. ^ Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ, Allison TG, Mookadam F, Lopez-Jimenez F (August 2006). "Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies". Lancet (Review). 368 (9536): 666–78. doi:10.1016/S0140-6736(06)69251-9. PMID 16920472. 78. ^ 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". American Heart Journal (Meta-analysis, Review). 156 (1): 13–22. doi:10.1016/j.ahj.2008.02.014. PMID 18585492. 79. ^ 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 (Meta-analysis). 16 (2): 442–50. doi:10.1038/oby.2007.36. PMID 18239657. 80. ^ Diercks DB, Roe MT, Mulgund J, Pollack CV, Kirk JD, Gibler WB, Ohman EM, Smith SC, Boden WE, Peterson ED (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". American Heart Journal (Research Support). 152 (1): 140–8. doi:10.1016/j.ahj.2005.09.024. PMID 16824844. 81. 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 (Practice Guideline, Review). 176 (8): S1–13. doi:10.1503/cmaj.061409. PMC 1839777. PMID 17420481. 82. ^ Drewnowski A, Specter SE (January 2004). "Poverty and obesity: the role of energy density and energy costs". The American Journal of Clinical Nutrition (Review). 79 (1): 6–16. doi:10.1093/ajcn/79.1.6. PMID 14684391. 83. ^ Nestle M, Jacobson MF (2000). "Halting the obesity epidemic: a public health policy approach". Public Health Reports (Research Support). 115 (1): 12–24. doi:10.1093/phr/115.1.12. PMC 1308552. PMID 10968581. 84. ^ James WP (March 2008). "The fundamental drivers of the obesity epidemic". Obesity Reviews (Review). 9 Suppl 1 (Suppl 1): 6–13. doi:10.1111/j.1467-789X.2007.00432.x. PMID 18307693. 85. ^ Keith SW, Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC, Benca RM, Ruden D, Pietrobelli A, Barger JL, Fontaine KR, Wang C, Aronne LJ, Wright SM, Baskin M, Dhurandhar NV, Lijoi MC, Grilo CM, DeLuca M, Westfall AO, Allison DB (November 2006). "Putative contributors to the secular increase in obesity: exploring the roads less traveled". International Journal of Obesity (Review). 30 (11): 1585–94. doi:10.1038/sj.ijo.0803326. PMID 16801930. 86. "EarthTrends: Nutrition: Calorie supply per capita". World Resources Institute. Archived from the original on 11 June 2011. Retrieved 18 October 2009. 87. ^ Bojanowska E, Ciosek J (15 February 2016). "Can We Selectively Reduce Appetite for Energy-Dense Foods? An Overview of Pharmacological Strategies for Modification of Food Preference Behavior". Current Neuropharmacology. 14 (2): 118–42. doi:10.2174/1570159X14666151109103147. PMC 4825944. PMID 26549651. 88. ^ "USDA: frsept99b". United States Department of Agriculture. Archived from the original on 3 June 2010. Retrieved 10 January 2009. 89. ^ "Diet composition and obesity among Canadian adults". Statistics Canada. 90. ^ National Control for Health Statistics. "Nutrition For Everyone". Centers for Disease Control and Prevention. Retrieved 9 July 2008. 91. ^ Marantz PR, Bird ED, Alderman MH (March 2008). "A call for higher standards of evidence for dietary guidelines". American Journal of Preventive Medicine. 34 (3): 234–40. doi:10.1016/j.amepre.2007.11.017. PMID 18312812. 92. ^ Flegal KM, Carroll MD, Ogden CL, Johnson CL (October 2002). "Prevalence and trends in obesity among US adults, 1999–2000". JAMA. 288 (14): 1723–7. doi:10.1001/jama.288.14.1723. PMID 12365955. 93. ^ Centers for Disease Control Prevention (CDC) (February 2004). "Trends in intake of energy and macronutrients—United States, 1971–2000". MMWR. Morbidity and Mortality Weekly Report. 53 (4): 80–2. PMID 14762332. 94. Caballero B (2007). "The global epidemic of obesity: an overview". Epidemiologic Reviews. 29: 1–5. doi:10.1093/epirev/mxm012. PMID 17569676. 95. ^ Mozaffarian D, Hao T, Rimm EB, Willett WC, Hu FB (June 2011). "Changes in diet and lifestyle and long-term weight gain in women and men". The New England Journal of Medicine (Meta-analysis). 364 (25): 2392–404. doi:10.1056/NEJMoa1014296. PMC 3151731. PMID 21696306. 96. ^ Malik VS, Schulze MB, Hu FB (August 2006). "Intake of sugar-sweetened beverages and weight gain: a systematic review". The American Journal of Clinical Nutrition (Review). 84 (2): 274–88. doi:10.1093/ajcn/84.1.274. PMC 3210834. PMID 16895873. 97. ^ Olsen NJ, Heitmann BL (January 2009). "Intake of calorically sweetened beverages and obesity". Obesity Reviews (Review). 10 (1): 68–75. doi:10.1111/j.1467-789X.2008.00523.x. PMID 18764885. 98. ^ Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB (November 2010). "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis". Diabetes Care (Meta-analysis, Review). 33 (11): 2477–83. doi:10.2337/dc10-1079. PMC 2963518. PMID 20693348. 99. ^ Wamberg L, Pedersen SB, Rejnmark L, Richelsen B (December 2015). "Causes of Vitamin D Deficiency and Effect of Vitamin D Supplementation on Metabolic Complications in Obesity: a Review". Current Obesity Reports. 4 (4): 429–40. doi:10.1007/s13679-015-0176-5. PMID 26353882. 100. ^ Rosenheck R (November 2008). "Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk". Obesity Reviews (Review). 9 (6): 535–47. doi:10.1111/j.1467-789X.2008.00477.x. PMID 18346099. 101. ^ Lin BH, Guthrie J, Frazao E (1999). "Nutrient contribution of food away from home". In Frazão E (ed.). Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences. Washington, DC: US Department of Agriculture, Economic Research Service. pp. 213–39. Archived from the original on 8 July 2012. 102. ^ Pollan, Michael (22 April 2007). "You Are What You Grow". New York Times. Retrieved 30 July 2007. 103. ^ Kopelman and Caterson 2005:324. 104. ^ Metabolism alone doesn't explain how thin people stay thin. John Schieszer. The Medical Post. 105. ^ Seidell 2005 p. 10 106. ^ a b "Obesity and overweight". World Health Organization. Archived from the original on 18 December 2008. Retrieved 10 January 2009. 107. ^ a b c "WHO | Physical Inactivity: A Global Public Health Problem". World Health Organization. Retrieved 22 February 2009. 108. ^ a b Ness-Abramof R, Apovian CM (February 2006). "Diet modification for treatment and prevention of obesity". Endocrine (Review). 29 (1): 5–9. doi:10.1385/ENDO:29:1:135. PMID 16622287. 109. ^ Salmon J, Timperio A (2007). "Prevalence, Trends and Environmental Influences on Child and Youth Physical Activity". Pediatric Fitness (Review). Medicine and Sport Science. 50. pp. 183–99. doi:10.1159/000101391. ISBN 978-3-318-01396-2. PMID 17387258. 110. ^ 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". European Journal of Public Health (Research Support). 18 (3): 339–44. doi:10.1093/eurpub/ckm092. PMID 17875578. 111. ^ Brownson RC, Boehmer TK, Luke DA (2005). "Declining rates of physical activity in the United States: what are the contributors?". Annual Review of Public Health (Review). 26: 421–43. doi:10.1146/annurev.publhealth.26.021304.144437. PMID 15760296. 112. ^ Wilks DC, Sharp SJ, Ekelund U, Thompson SG, Mander AP, Turner RM, Jebb SA, Lindroos AK (February 2011). "Objectively measured physical activity and fat mass in children: a bias-adjusted meta-analysis of prospective studies". PLOS One. 6 (2): e17205. Bibcode:2011PLoSO...617205W. doi:10.1371/journal.pone.0017205. PMC 3044163. PMID 21383837. 113. ^ 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". Archives of Pediatrics & Adolescent Medicine (Review). 150 (4): 356–62. doi:10.1001/archpedi.1996.02170290022003. PMID 8634729. 114. ^ Vioque J, Torres A, Quiles J (December 2000). "Time spent watching television, sleep duration and obesity in adults living in Valencia, Spain". International Journal of Obesity and Related Metabolic Disorders (Research Support). 24 (12): 1683–8. doi:10.1038/sj.ijo.0801434. PMID 11126224. 115. ^ Tucker LA, Bagwell M (July 1991). "Television viewing and obesity in adult females". American Journal of Public Health. 81 (7): 908–11. doi:10.2105/AJPH.81.7.908. PMC 1405200. PMID 2053671. 116. ^ Emanuel EJ (2008). "Media + Child and Adolescent Health: A Systematic Review" (PDF). Common Sense Media. Retrieved 6 April 2009. 117. ^ 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. Archived from the original on 13 April 2009. Retrieved 6 April 2009. 118. ^ Albuquerque D, Nóbrega C, Manco L, Padez C (September 2017). "The contribution of genetics and environment to obesity". British Medical Bulletin. 123 (1): 159–173. doi:10.1093/bmb/ldx022. PMID 28910990. 119. ^ Poirier P, Giles TD, Bray GA, Hong Y, Stern JS, Pi-Sunyer FX, Eckel RH (May 2006). "Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss". Arteriosclerosis, Thrombosis, and Vascular Biology (Review). 26 (5): 968–76. CiteSeerX 10.1.1.508.7066. doi:10.1161/01.ATV.0000216787.85457.f3. PMID 16627822. 120. ^ Loos RJ, Bouchard C (May 2008). "FTO: the first gene contributing to common forms of human obesity". Obesity Reviews (Review). 9 (3): 246–50. doi:10.1111/j.1467-789X.2008.00481.x. PMID 18373508. 121. ^ Yang W, Kelly T, He J (2007). "Genetic epidemiology of obesity". Epidemiologic Reviews (Review). 29: 49–61. doi:10.1093/epirev/mxm004. PMID 17566051. 122. ^ Walley AJ, Asher JE, Froguel P (July 2009). "The genetic contribution to non-syndromic human obesity". Nature Reviews. Genetics (Review). 10 (7): 431–42. doi:10.1038/nrg2594. PMID 19506576. 123. ^ Farooqi S, O'Rahilly S (December 2006). "Genetics of obesity in humans". Endocrine Reviews (Review). 27 (7): 710–18. doi:10.1210/er.2006-0040. PMID 17122358. 124. ^ Kolata, Gina (2007). Rethinking thin: The new science of weight loss – and the myths and realities of dieting. Picador. p. 122. ISBN 978-0-312-42785-6. 125. ^ Walley AJ, Asher JE, Froguel P (July 2009). "The genetic contribution to non-syndromic human obesity". Nature Reviews. Genetics (Review). 10 (7): 431–42. doi:10.1038/nrg2594. PMID 19506576. However, it is also clear that genetics greatly influences this situation, giving individuals in the same 'obesogenic' environment significantly different risks of becoming obese. 126. ^ Chakravarthy MV, Booth FW (January 2004). "Eating, exercise, and "thrifty" genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases". Journal of Applied Physiology (Review). 96 (1): 3–10. doi:10.1152/japplphysiol.00757.2003. PMID 14660491. 127. ^ Wells JC (December 2009). "Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms". International Journal of Obesity (Review). 33 (12): 1331–8. doi:10.1038/ijo.2009.175. PMID 19752875. 128. ^ Wells JC (2011). "The thrifty phenotype: An adaptation in growth or metabolism?". American Journal of Human Biology (Review). 23 (1): 65–75. doi:10.1002/ajhb.21100. PMID 21082685. 129. ^ Rosén T, Bosaeus I, Tölli J, Lindstedt G, Bengtsson BA (January 1993). "Increased body fat mass and decreased extracellular fluid volume in adults with growth hormone deficiency". Clinical Endocrinology. 38 (1): 63–71. doi:10.1111/j.1365-2265.1993.tb00974.x. PMID 8435887. 130. ^ Zametkin AJ, Zoon CK, Klein HW, Munson S (February 2004). "Psychiatric aspects of child and adolescent obesity: a review of the past 10 years". Journal of the American Academy of Child and Adolescent Psychiatry (Review). 43 (2): 134–50. doi:10.1097/00004583-200402000-00008. PMID 14726719. 131. ^ Chiles C, van Wattum PJ (2010). "Psychiatric aspects of the obesity crisis". Psychiatr Times. 27 (4): 47–51. 132. ^ Yach D, Stuckler D, Brownell KD (January 2006). "Epidemiologic and economic consequences of the global epidemics of obesity and diabetes". Nature Medicine. 12 (1): 62–6. doi:10.1038/nm0106-62. PMID 16397571. 133. ^ Sobal J, Stunkard AJ (March 1989). "Socioeconomic status and obesity: a review of the literature". Psychological Bulletin (Review). 105 (2): 260–75. doi:10.1037/0033-2909.105.2.260. PMID 2648443. 134. ^ a b McLaren L (2007). "Socioeconomic status and obesity". Epidemiologic Reviews (Review). 29: 29–48. doi:10.1093/epirev/mxm001. PMID 17478442. 135. ^ a b Wilkinson R, Pickett K (2009). The Spirit Level: Why More Equal Societies Almost Always Do Better. London: Allen Lane. pp. 91–101. ISBN 978-1-84614-039-6. 136. ^ Christakis NA, Fowler JH (July 2007). "The spread of obesity in a large social network over 32 years". The New England Journal of Medicine (Research Support). 357 (4): 370–9. CiteSeerX 10.1.1.581.4893. doi:10.1056/NEJMsa066082. PMID 17652652. 137. ^ Björntorp P (May 2001). "Do stress reactions cause abdominal obesity and comorbidities?". Obesity Reviews. 2 (2): 73–86. doi:10.1046/j.1467-789x.2001.00027.x. PMID 12119665. 138. ^ Goodman E, Adler NE, Daniels SR, Morrison JA, Slap GB, Dolan LM (August 2003). "Impact of objective and subjective social status on obesity in a biracial cohort of adolescents". Obesity Research (Research Support). 11 (8): 1018–26. doi:10.1038/oby.2003.140. PMID 12917508. 139. ^ 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". The New England Journal of Medicine. 333 (18): 1165–70. doi:10.1056/NEJM199511023331801. PMID 7565970. 140. ^ Chiolero A, Faeh D, Paccaud F, Cornuz J (April 2008). "Consequences of smoking for body weight, body fat distribution, and insulin resistance". The American Journal of Clinical Nutrition (Review). 87 (4): 801–9. doi:10.1093/ajcn/87.4.801. PMID 18400700. 141. ^ 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". Journal of Women's Health (Comparative Study). 13 (1): 85–91. doi:10.1089/154099904322836492. PMID 15006281. 142. ^ Bellows-Riecken KH, Rhodes RE (February 2008). "A birth of inactivity? A review of physical activity and parenthood". Preventive Medicine (Review). 46 (2): 99–110. doi:10.1016/j.ypmed.2007.08.003. PMID 17919713. 143. ^ "Obesity and Overweight" (PDF). World Health Organization. Retrieved 22 February 2009. 144. ^ a b Caballero B (March 2001). "Introduction. Symposium: Obesity in developing countries: biological and ecological factors". The Journal of Nutrition (Review). 131 (3): 866S–870S. doi:10.1093/jn/131.3.866s. PMID 11238776. 145. ^ Smith E, Hay P, Campbell L, Trollor JN (September 2011). "A review of the association between obesity and cognitive function across the lifespan: implications for novel approaches to prevention and treatment". Obesity Reviews (Review). 12 (9): 740–55. doi:10.1111/j.1467-789X.2011.00920.x. PMID 21991597. 146. ^ 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 (Review). 83 (4): 460–9. doi:10.4065/83.4.460. PMID 18380992. 147. ^ "Antibiotics: repeated treatments before the age of two could be a factor in obesity". Prescrire International. 2018. Retrieved 2 July 2018. 148. ^ a b Cox LM, Blaser MJ (March 2015). "Antibiotics in early life and obesity". Nature Reviews. Endocrinology. 11 (3): 182–90. doi:10.1038/nrendo.2014.210. PMC 4487629. PMID 25488483. 149. ^ Falagas ME, Kompoti M (July 2006). "Obesity and infection". The Lancet. Infectious Diseases (Review). 6 (7): 438–46. doi:10.1016/S1473-3099(06)70523-0. PMID 16790384. 150. ^ a b Cappuccio FP, Taggart FM, Kandala NB, Currie A, Peile E, Stranges S, Miller MA (May 2008). "Meta-analysis of short sleep duration and obesity in children and adults". Sleep. 31 (5): 619–26. doi:10.1093/sleep/31.5.619. PMC 2398753. PMID 18517032. 151. ^ Miller MA, Kruisbrink M, Wallace J, Ji C, Cappuccio FP (April 2018). "Sleep duration and incidence of obesity in infants, children, and adolescents: a systematic review and meta-analysis of prospective studies". Sleep. 41 (4). doi:10.1093/sleep/zsy018. PMID 29401314. 152. ^ Horne, J (May 2011). "Obesity and short sleep: unlikely bedfellows?". Obesity Reviews. 12 (5): e84–94. doi:10.1111/j.1467-789X.2010.00847.x. PMID 21366837. 153. ^ a b Gerlach G, Herpertz S, Loeber S (January 2015). "Personality traits and obesity: a systematic review". Obesity Reviews. 16 (1): 32–63. doi:10.1111/obr.12235. PMID 25470329. 154. ^ Jokela M, Hintsanen M, Hakulinen C, Batty GD, Nabi H, Singh-Manoux A, Kivimäki M (April 2013). "Association of personality with the development and persistence of obesity: a meta-analysis based on individual-participant data". Obesity Reviews. 14 (4): 315–23. doi:10.1111/obr.12007. PMC 3717171. PMID 23176713. 155. ^ a b c d Flier JS (January 2004). "Obesity wars: molecular progress confronts an expanding epidemic". Cell (Review). 116 (2): 337–50. doi:10.1016/S0092-8674(03)01081-X. PMID 14744442. 156. ^ Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (December 1994). "Positional cloning of the mouse obese gene and its human homologue". Nature (Research Support). 372 (6505): 425–32. Bibcode:1994Natur.372..425Z. doi:10.1038/372425a0. PMID 7984236. 157. ^ Boulpaep, Emile L.; Boron, Walter F. (2003). Medical physiology: A cellular and molecular approach. Philadelphia: Saunders. p. 1227. ISBN 978-0-7216-3256-8. 158. ^ World Health Organization (2000). Obesity: preventing and managing the global epidemic (Report). World Health Organization. pp. 1–2. Retrieved 1 February 2014. 159. ^ Satcher D (2001). The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. Publications and Reports of the Surgeon General. U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General. ISBN 978-0-16-051005-2. 160. ^ Moyer VA (September 2012). "Screening for and management of obesity in adults: U.S. Preventive Services Task Force recommendation statement". Annals of Internal Medicine (Practice Guideline). 157 (5): 373–8. doi:10.7326/0003-4819-157-5-201209040-00475. PMID 22733087. 161. ^ Brook Barnes (18 July 2007). "Limiting Ads of Junk Food to Children". New York Times. Retrieved 24 July 2008. 162. ^ "Fewer Sugary Drinks Key to Weight Loss". U.S. Department of Health and Human Services. Retrieved 18 October 2009. 163. ^ "WHO urges global action to curtail consumption and health impacts of sugary drinks". WHO. Retrieved 13 October 2016. 164. ^ Brennan Ramirez LK, Hoehner CM, Brownson RC, Cook R, Orleans CT, Hollander M, Barker DC, Bors P, Ewing R, Killingsworth R, Petersmarck K, Schmid T, Wilkinson W (December 2006). "Indicators of activity-friendly communities: an evidence-based consensus process". American Journal of Preventive Medicine (Research Support). 31 (6): 515–24. doi:10.1016/j.amepre.2006.07.026. PMID 17169714. 165. ^ National Heart, Lung, and Blood Institute (1998). Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (PDF). International Medical Publishing, Inc. ISBN 978-1-58808-002-8. 166. ^ Storing up problems; the medical case for a slimmer nation. London: Royal College of Physicians. 11 February 2004. ISBN 978-1-86016-200-8. 167. ^ 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: TSO (The Stationery Office). ISBN 978-0-215-01737-6. Retrieved 17 December 2007. 168. ^ "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. Retrieved 8 April 2009. 169. ^ Wanless D, Appleby J, Harrison A, Patel D (2007). Our Future Health Secured? A review of NHS funding and performance. London: The King's Fund. ISBN 978-1-85717-562-2. 170. ^ Sacks G, Swinburn B, Lawrence M (January 2009). "Obesity Policy Action framework and analysis grids for a comprehensive policy approach to reducing obesity". Obesity Reviews. 10 (1): 76–86. doi:10.1111/j.1467-789X.2008.00524.X. PMID 18761640. 171. ^ Strychar I (January 2006). "Diet in the management of weight loss". CMAJ (Review). 174 (1): 56–63. doi:10.1503/cmaj.045037. PMC 1319349. PMID 16389240. 172. ^ 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". Journal of the American Dietetic Association. 98 (4): 408–13. doi:10.1016/S0002-8223(98)00093-5. PMID 9550162. 173. ^ 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?". The American Journal of Clinical Nutrition (Randomized Controlled Trial). 85 (4): 954–9. doi:10.1093/ajcn/85.4.954. PMID 17413092. 174. ^ US Preventive Services Task Force (2018). "Behavioral Weight Loss Interventions to Prevent Obesity-Related Morbidity and Mortality in Adults US Preventive Services Task Force Recommendation Statement". JAMA. 320 (11): 1163–1171. doi:10.1001/jama.2018.13022. PMID 30326502. 175. ^ a b c d Services, Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU) (1987). "Dietary treatment of obesity". Annals of the New York Academy of Sciences. 499 (1): 250–263. Bibcode:1987NYASA.499..250B. doi:10.1111/j.1749-6632.1987.tb36216.x. Retrieved 17 June 2016. 176. ^ Johnston BC, Kanters S, Bandayrel K, Wu P, Naji F, Siemieniuk RA, Ball GD, Busse JW, Thorlund K, Guyatt G, Jansen JP, Mills EJ (September 2014). "Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis". JAMA. 312 (9): 923–33. doi:10.1001/jama.2014.10397. PMID 25182101. 177. ^ Naude CE, Schoonees A, Senekal M, Young T, Garner P, Volmink J (2014). "Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis". PLOS One (Research Support). 9 (7): e100652. Bibcode:2014PLoSO...9j0652N. doi:10.1371/journal.pone.0100652. PMC 4090010. PMID 25007189. 178. ^ Wing RR, Phelan S (July 2005). "Long-term weight loss maintenance". The American Journal of Clinical Nutrition (Review). 82 (1 Suppl): 222S–225S. doi:10.1093/ajcn/82.1.222S. PMID 16002825. 179. ^ Thangaratinam S, Rogozinska E, Jolly K, Glinkowski S, Roseboom T, Tomlinson JW, Kunz R, Mol BW, Coomarasamy A, Khan KS (May 2012). "Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence". BMJ (Meta-analysis). 344: e2088. doi:10.1136/bmj.e2088. PMC 3355191. PMID 22596383. 180. ^ LeFevre ML (October 2014). "Behavioral counseling to promote a healthful diet and physical activity for cardiovascular disease prevention in adults with cardiovascular risk factors: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine. 161 (8): 587–93. doi:10.7326/M14-1796. PMID 25155419. 181. ^ a b c Heymsfield SB, Wadden TA (January 2017). "Mechanisms, Pathophysiology, and Management of Obesity". The New England Journal of Medicine. 376 (3): 254–266. doi:10.1056/NEJMra1514009. PMID 28099824. 182. ^ a b Wolfe SM (August 2013). "When EMA and FDA decisions conflict: differences in patients or in regulation?". BMJ. 347: f5140. doi:10.1136/bmj.f5140. PMID 23970394. 183. ^ Rucker D, Padwal R, Li SK, Curioni C, Lau DC (December 2007). "Long term pharmacotherapy for obesity and overweight: updated meta-analysis". BMJ (Meta-analysis). 335 (7631): 1194–9. doi:10.1136/bmj.39385.413113.25. PMC 2128668. PMID 18006966. 184. ^ Wood, Shelley. "Diet Drug Orlistat Linked to Kidney, Pancreas Injuries". Medscape. Medscape News. Retrieved 26 April 2011. 185. ^ a b Chang SH, Stoll CR, Song J, Varela JE, Eagon CJ, Colditz GA (March 2014). "The effectiveness and risks of bariatric surgery: an updated systematic review and meta-analysis, 2003–2012". JAMA Surgery (Meta-analysis, Review). 149 (3): 275–87. doi:10.1001/jamasurg.2013.3654. PMC 3962512. PMID 24352617. 186. ^ Sjöström L, Narbro K, Sjöström CD, Karason K, Larsson B, Wedel H, Lystig T, Sullivan M, Bouchard C, Carlsson B, Bengtsson C, Dahlgren S, Gummesson A, Jacobson P, Karlsson J, Lindroos AK, Lönroth H, Näslund I, Olbers T, Stenlöf K, Torgerson J, Agren G, Carlsson LM (August 2007). "Effects of bariatric surgery on mortality in Swedish obese subjects". The New England Journal of Medicine (Research Support). 357 (8): 741–52. doi:10.1056/NEJMoa066254. PMID 17715408. 187. ^ Weintraub, Karen. "New allies in war on weight". The Boston Globe. The Boston Globe. Retrieved 30 June 2014. 188. ^ "Global Prevalence of Adult Obesity" (PDF). International Obesity Taskforce. Archived from the original (PDF) on 11 December 2009. Retrieved 29 January 2008. 189. ^ "Obesity". Our World in Data. Retrieved 31 December 2017. 190. ^ a b c Haslam D (March 2007). "Obesity: a medical history". Obesity Reviews (Review). 8 Suppl 1: 31–6. doi:10.1111/j.1467-789X.2007.00314.x. PMID 17316298. 191. ^ a b "Obesity and overweight". World Health Organization. Retrieved 8 April 2009. 192. ^ Hales CM, Carroll MD, Fryar CD, Ogden CL (October 2017). "Prevalence of Obesity Among Adults and Youth: United States, 2015–2016". NCHS Data Brief (288): 1–8. PMID 29155689. 193. ^ Seidell 2005 p.5 194. ^ Howard NJ, Taylor AW, Gill TK, Chittleborough CR (March 2008). "Severe obesity: Investigating the socio-demographics within the extremes of body mass index". Obesity Research & Clinical Practice. 2 (1): I–II. doi:10.1016/j.orcp.2008.01.001. PMID 24351678. 195. ^ Tjepkema M (6 July 2005). "Measured Obesity–Adult obesity in Canada: Measured height and weight". Nutrition: Findings from the Canadian Community Health Survey. Ottawa, Ontario: Statistics Canada. 196. ^ "Obesity Update 2017" (PDF). Organisation for Economic Co-operation and Development. Retrieved 6 October 2018. 197. ^ "Online Etymology Dictionary: Obesity". Douglas Harper. Retrieved 31 December 2008. 198. ^ "Obesity, n". Oxford English Dictionary 2008. Archived from the original on 11 January 2008. Retrieved 21 March 2009. 199. ^ a b Bloomgarden ZT (November 2003). "Prevention of obesity and diabetes". Diabetes Care (Review). 26 (11): 3172–8. doi:10.2337/diacare.26.11.3172. PMID 14578257. 200. ^ a b "History of Medicine: Sushruta – the Clinician – Teacher par Excellence" (PDF). Dwivedi, Girish & Dwivedi, Shridhar. 2007. Archived from the original (PDF) on 10 October 2008. Retrieved 19 September 2008. 201. ^ Theodore Mazzone; Giamila Fantuzzi (2006). Adipose Tissue And Adipokines in Health And Disease (Nutrition and Health). Totowa, NJ: Humana Press. p. 222. ISBN 978-1-58829-721-1. 202. ^ Keller p. 49 203. ^ Gilman, Sander L (2004). Fat Boys: A Slim Book. University of Nebraska Press. p. 18. ISBN 978-0803221833. 204. ^ Breslow L (September 1952). "Public health aspects of weight control". American Journal of Public Health and the Nation's Health. 42 (9): 1116–20. doi:10.2105/AJPH.42.9.1116. PMC 1526346. PMID 12976585. 205. ^ a b Puhl R, Brownell KD (December 2001). "Bias, discrimination, and obesity". Obesity Research (Review). 9 (12): 788–805. doi:10.1038/oby.2001.108. PMID 11743063. 206. ^ Rubinstein S, Caballero B (2000). "Is Miss America an undernourished role model?". JAMA (Letter). 283 (12): 1569. doi:10.1001/jama.283.12.1569. PMID 10735392. 207. ^ a b Johnson F, Cooke L, Croker H, Wardle J (July 2008). "Changing perceptions of weight in Great Britain: comparison of two population surveys". BMJ. 337: a494. doi:10.1136/bmj.a494. PMC 2500200. PMID 18617488. 208. ^ Fumento, Michael (1997). The Fat of the Land: Our Health Crisis and How Overweight Americans Can Help Themselves. Penguin (Non-Classics). p. 126. ISBN 978-0-14-026144-8. 209. ^ a b Puhl R., Henderson K., and Brownell K. 2005 p.29 210. ^ Johansson E, Böckerman P, Kiiskinen U, Heliövaara M (March 2009). "Obesity and labour market success in Finland: the difference between having a high BMI and being fat". Economics and Human Biology. 7 (1): 36–45. doi:10.1016/j.ehb.2009.01.008. PMID 19249259. 211. ^ Cawley J, Meyerhoefer C (January 2012). "The medical care costs of obesity: an instrumental variables approach". Journal of Health Economics. 31 (1): 219–30. doi:10.1016/j.jhealeco.2011.10.003. PMID 22094013. 212. ^ Finkelstein EA, Fiebelkorn IA, Wang G (1 January 2003). "National medical spending attributable to overweight and obesity: How much, and who's paying". Health Affairs. Online (May): W3–219–W3–226. doi:10.1377/hlthaff.w3.219. 213. ^ "Obesity and overweight: Economic consequences". Centers for Disease Control and Prevention. 22 May 2007. Retrieved 5 September 2007. 214. ^ Colagiuri S, Lee CM, Colagiuri R, Magliano D, Shaw JE, Zimmet PZ, Caterson ID (March 2010). "The cost of overweight and obesity in Australia". The Medical Journal of Australia (Comparative Study). 192 (5): 260–4. PMID 20201759. 215. ^ Cummings, Laura (5 February 2003). "The diet business: Banking on failure". BBC News. Retrieved 25 February 2009. 216. ^ "Public health experts call for global food treaty". Financial Times. 27 January 2019. Retrieved 7 March 2019. 217. ^ van Baal PH, Polder JJ, de Wit GA, Hoogenveen RT, Feenstra TL, Boshuizen HC, Engelfriet PM, Brouwer WB (February 2008). "Lifetime medical costs of obesity: prevention no cure for increasing health expenditure". PLoS Medicine (Comparative Study). 5 (2): e29. doi:10.1371/journal.pmed.0050029. PMC 2225430. PMID 18254654. 218. ^ Bakewell J (2007). "Bariatric furniture: Considerations for use". Int J Ther Rehabil. 14 (7): 329–33. doi:10.12968/ijtr.2007.14.7.23858. Archived from the original on 8 October 2011. 219. ^ Neovius K, Johansson K, Kark M, Neovius M (January 2009). "Obesity status and sick leave: a systematic review". Obesity Reviews (Review). 10 (1): 17–27. doi:10.1111/j.1467-789X.2008.00521.x. PMID 18778315. 220. ^ Ostbye T, Dement JM, Krause KM (April 2007). "Obesity and workers' compensation: results from the Duke Health and Safety Surveillance System". Archives of Internal Medicine (Research Support). 167 (8): 766–73. doi:10.1001/archinte.167.8.766. PMID 17452538. 221. ^ "Alabama "Obesity Penalty" Stirs Debate". Don Fernandez. Retrieved 5 April 2009. 222. ^ Puhl R., Henderson K., and Brownell K. 2005 p.30 223. ^ Lisa DiCarlo (24 October 2002). "Why Airlines Can't Cut The Fat". Forbes.com. Retrieved 23 July 2008. 224. ^ Dannenberg AL, Burton DC, Jackson RJ (October 2004). "Economic and environmental costs of obesity: the impact on airlines". American Journal of Preventive Medicine (Letter). 27 (3): 264. doi:10.1016/j.amepre.2004.06.004. PMID 15450642. 225. ^ Lauren Cox (2 July 2009). "Who Should Pay for Obese Health Care?". ABC News. Retrieved 6 August 2012. 226. ^ 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. Retrieved 24 July 2008. 227. ^ a b Basulto, Dominic (20 June 2013). "A changing battlefield in the fight against fat". The Washington Post. Archived from the original on 21 June 2013. Retrieved 20 June 2013. 228. ^ "Obesity can be deemed a disability at work – EU court". Reuters. 18 December 2014. Retrieved 18 December 2014. 229. ^ "What is NAAFA". National Association to Advance Fat Acceptance. Archived from the original on 12 March 2009. Retrieved 17 February 2009. 230. ^ "ISAA Mission Statement". International Size Acceptance Association. Retrieved 17 February 2009. 231. ^ a b Pulver, Adam (2007). An Imperfect Fit: Obesity, Public Health, and Disability Anti-Discrimination Law. Social Science Electronic Publishing. SSRN 1316106. 232. ^ Neumark-Sztainer D (March 1999). "The weight dilemma: a range of philosophical perspectives". International Journal of Obesity and Related Metabolic Disorders (Review). 23 Suppl 2: S31–7. doi:10.1038/sj.ijo.0800857. PMID 10340803. 233. ^ National Association to Advance Fat Acceptance (2008). "We come in all sizes". NAAFA. Retrieved 29 July 2008. 234. ^ "International Size Acceptance Association – ISAA". International Size Acceptance Association. Retrieved 13 January 2009. 235. ^ O’Connor, Anahad (9 August 2015). "Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets". New York Times. 236. ^ Nestle M (November 2016). "Food Industry Funding of Nutrition Research: The Relevance of History for Current Debates". JAMA Internal Medicine. 176 (11): 1685–1686. doi:10.1001/jamainternmed.2016.5400. PMID 27618496. 237. ^ a b Flynn MA, McNeil DA, Maloff B, Mutasingwa D, Wu M, Ford C, Tough SC (February 2006). "Reducing obesity and related chronic disease risk in children and youth: a synthesis of evidence with 'best practice' recommendations". Obesity Reviews (Review). 7 Suppl 1: 7–66. doi:10.1111/j.1467-789X.2006.00242.x. PMID 16371076. 238. ^ Dollman J, Norton K, Norton L (December 2005). "Evidence for secular trends in children's physical activity behaviour". British Journal of Sports Medicine (Review). 39 (12): 892–7, discussion 897. doi:10.1136/bjsm.2004.016675. PMC 1725088. PMID 16306494. 239. ^ Metcalf B, Henley W, Wilkin T (September 2012). "Effectiveness of intervention on physical activity of children: systematic review and meta-analysis of controlled trials with objectively measured outcomes (EarlyBird 54)". BMJ (Review, Meta-analysis). 345: e5888. doi:10.1136/bmj.e5888. PMID 23044984. 240. ^ Mead E, Brown T, Rees K, Azevedo LB, Whittaker V, Jones D, Olajide J, Mainardi GM, Corpeleijn E, O'Malley C, Beardsmore E, Al-Khudairy L, Baur L, Metzendorf MI, Demaio A, Ells LJ (June 2017). "Diet, physical activity and behavioural interventions for the treatment of overweight or obese children from the age of 6 to 11 years" (PDF). The Cochrane Database of Systematic Reviews. 6: CD012651. doi:10.1002/14651858.CD012651. PMID 28639319. 241. ^ a b Lund EM (2006). "Prevalence and Risk Factors for Obesity in Adult Dogs from Private US Veterinary Practices" (PDF). Intern J Appl Res Vet Med. 4 (2): 177–86. 242. ^ 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". The Veterinary Record. 156 (22): 695–702. doi:10.1136/vr.156.22.695. PMID 15923551. 243. ^ Nijland ML, Stam F, Seidell JC (January 2010). "Overweight in dogs, but not in cats, is related to overweight in their owners". Public Health Nutrition. 13 (1): 102–6. doi:10.1017/S136898000999022X. PMID 19545467. ### Cited sources ## Further reading Abdominal obesity Abdominal obesity, also known as central obesity, occurs when excessive abdominal fat around the stomach and abdomen has built up to the extent that it is likely to have a negative impact on health. Central obesity has been strongly linked to cardiovascular disease, Alzheimer's disease, and other metabolic and vascular diseases.Visceral and central abdominal fat and waist circumference show a strong association with type 2 diabetes.Visceral fat, also known as organ fat or intra-abdominal fat, is located inside the peritoneal cavity, packed in between internal organs and torso, as opposed to subcutaneous fat, which is found underneath the skin, and intramuscular fat, which is found interspersed in skeletal muscle. Visceral fat is composed of several adipose depots including mesenteric, epididymal white adipose tissue (EWAT) and perirenal fat. An excess of visceral fat is known as central obesity, the "pot belly" or "beer belly" effect, in which the abdomen protrudes excessively. This body type is also known as "apple shaped", as opposed to "pear shaped", in which fat is deposited on the hips and buttocks. Researchers first started to focus on abdominal obesity in the 1980s when they realized it had an important connection to cardiovascular disease, diabetes, and dyslipidemia. Abdominal obesity was more closely related with metabolic dysfunctions connected with cardiovascular disease than was general obesity. In the late 1980s and early 1990s insightful and powerful imaging techniques were discovered that would further help advance the understanding of the health risks associated with body fat accumulation. Techniques such as computed tomography and magnetic resonance imaging made it possible to categorize mass of adipose tissue located at the abdominal level into intra-abdominal fat and subcutaneous fat. Adipose tissue In biology, adipose tissue, body fat, or simply fat is a loose connective tissue composed mostly of adipocytes. In addition to adipocytes, adipose tissue contains the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages. Adipose tissue is derived from preadipocytes. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body. Far from being hormonally inert, adipose tissue has, in recent years, been recognized as a major endocrine organ, as it produces hormones such as leptin, estrogen, resistin, and the cytokine TNFα. The two types of adipose tissue are white adipose tissue (WAT), which stores energy, and brown adipose tissue (BAT), which generates body heat. The formation of adipose tissue appears to be controlled in part by the adipose gene. Adipose tissue – more specifically brown adipose tissue – was first identified by the Swiss naturalist Conrad Gessner in 1551. Anorectic An anorectic or anorexic is a drug which reduces appetite, resulting in lower food consumption, leading to weight loss. By contrast, an appetite stimulant is referred to as orexigenic. The term is (from the Greek ἀν- (an-) = "without" and ὄρεξις (órexis) = "appetite"), and such drugs are also known as anorexigenic, anorexiant, or appetite suppressant. Anti-obesity medication Anti-obesity medication or weight loss drugs are pharmacological agents that reduce or control weight. These drugs alter one of the fundamental processes of the human body, weight regulation, by altering either appetite, or absorption of calories. The main treatment modalities for overweight and obese individuals remain dieting and physical exercise. In the United States orlistat (Xenical) is currently approved by the FDA for long-term use. It reduces intestinal fat absorption by inhibiting pancreatic lipase. Rimonabant (Acomplia), a second 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 had been approved in Europe for the treatment of obesity but has not received approval in the United States or Canada due to safety concerns. The European Medicines Agency in October 2008 recommended the suspension of the sale of rimonabant as the risks seem to be greater than the benefits. Sibutramine (Meridia), which acts in the brain to inhibit deactivation of the neurotransmitters, thereby decreasing appetite was withdrawn from the United States and Canadian markets in October 2010 due to cardiovascular concerns.Because of potential side effects, and limited evidence of small benefits in weight reduction especially in obese children and adolescents, it is recommended that anti-obesity drugs only be prescribed for obesity where it is hoped that the benefits of the treatment outweigh its risks. Bariatric surgery Bariatric surgery (or weight loss surgery) includes a variety of procedures performed on people who have obesity. Weight loss is achieved by reducing the size of the stomach with a gastric band or through removal of a portion of the stomach (sleeve gastrectomy or biliopancreatic diversion with duodenal switch) or by resecting and re-routing the small intestine to a small stomach pouch (gastric bypass surgery). Long-term studies show the procedures cause significant long-term loss of weight, recovery from diabetes, improvement in cardiovascular risk factors, and a mortality reduction from 40% to 23%. The U.S. National Institutes of Health recommends bariatric surgery for obese people with a body mass index (BMI) of at least 40, and for people with BMI of at least 35 and serious coexisting medical conditions such as diabetes. However, research is emerging that suggests bariatric surgery could be appropriate for those with a BMI of 35 to 40 with no comorbidities or a BMI of 30 to 35 with significant comorbidities. The most recent American Society for Metabolic & Bariatric Surgery guidelines suggest the position statement on consensus for BMI as an indication for bariatric surgery. The recent guidelines suggest that any patient with a BMI of more than 30 with comorbidities is a candidate for bariatric surgery.A National Institute of Health symposium held in 2013 that summarized available evidence found a 29% mortality reduction, a 10-year remission rate of Type 2 Diabetes of 36%, fewer cardiovascular events, and a lower rate of diabetes-related complications in a long-term, non-randomized, matched intervention 15-20 year follow-up study, the Swedish Obese Subjects Study. The symposium also found similar results from a Utah study using more modern gastric bypass techniques, though the follow-up periods of the Utah studies are only up to 7 years. While randomized controlled trials of bariatric surgery exist, they are limited by short follow-up periods. Body mass index The body mass index (BMI) or Quetelet index is a value derived from the mass (weight) and height of an individual. The BMI is defined as the body mass divided by the square of the body height, and is universally expressed in units of kg/m2, resulting from mass in kilograms and height in metres. The BMI may also be determined using a table or chart which displays BMI as a function of mass and height using contour lines or colours for different BMI categories, and which may use other units of measurement (converted to metric units for the calculation).The BMI is an attempt to quantify the amount of tissue mass (muscle, fat, and bone) in an individual, and then categorize that person as underweight, normal weight, overweight, or obese based on that value. That categorization is the subject of some debate about where on the BMI scale the dividing lines between categories should be placed. Commonly accepted BMI ranges are underweight: under 18.5 kg/m2, normal weight: 18.5 to 25, overweight: 25 to 30, obese: over 30.BMIs under 20.0 and over 25.0 have been associated with higher all-cause mortality, increasing risk with distance from the 20.0-25.0 range. The prevalence of overweight and obesity is the highest in the Americas and lowest in South East Asia. The prevalence of overweight and obesity in high income and upper middle income countries is more than double that of low and lower middle income countries. Childhood obesity Childhood obesity is a condition where excess body fat negatively affects a child's health or well-being. As methods to determine body fat directly are difficult, the diagnosis of obesity is often based on BMI. Due to the rising prevalence of obesity in children and its many adverse health effects it is being recognized as a serious public health concern. The term overweight rather than obese is often used when discussing childhood obesity, especially in open discussion, as it is less stigmatizing. Health in Brazil According to the Brazilian Government, the most serious health problems are: Childhood mortality: about 1.51% of childhood mortality, reaching 2.77% in the northeast region. Motherhood mortality: about 42.1 deaths per 100,000 born children in 2016. Mortality by non-transmissible illness: 65.7 deaths per 100,000 inhabitants caused by heart and circulatory diseases, along with 26.7 deaths per 100,000 inhabitants caused by cancer. Mortality caused by external causes (transportation, violence and suicide): 55.7 deaths per 100,000 inhabitants (10.9% of all deaths in the country), reaching 62.3 deaths in the southeast region.In 2002, Brazil accounted for 40% of malaria cases in the Americas. Nearly 99% are concentrated in the Legal Amazon Region, which is home to not more than 12% of the population. Junk food Junk food is a pejorative term, dating back at least to the 1950s, describing food that is high in calories from sugar or fat, with little dietary fiber, protein, vitamins or minerals. It can also refer to high protein food like meat prepared with saturated fat. The term HFSS foods (high in fat, salt and sugar) is used synonymously. Fast food and fast food restaurants are often equated with junk food, although fast foods cannot be categorically described as junk food.Concerns about the negative health effects resulting from a junk food-heavy diet, especially obesity, have resulted in public health awareness campaigns, and restrictions on advertising and sale in several countries. Leptin Leptin (from Greek λεπτός leptos, "thin") is a hormone predominantly made by adipose cells that helps to regulate energy balance by inhibiting hunger. This hormone acts on receptors in the arcuate nucleus of the hypothalamus. In obesity, a decreased sensitivity to leptin occurs (similar to insulin resistance in type 2 diabetes), resulting in an inability to detect satiety despite high energy stores and high levels of leptin.Although regulation of fat stores is deemed to be the primary function of leptin, it also plays a role in other physiological processes , as evidenced by its many sites of synthesis other than fat cells, and the many cell types beside hypothalamic cells that have leptin receptors. Many of these additional functions are yet to be defined. Monosodium glutamate Monosodium glutamate (MSG, also known as sodium glutamate) is the sodium salt of glutamic acid, one of the most abundant naturally occurring non-essential amino acids. Glutamic acid is found naturally in tomatoes, grapes, cheese, mushrooms and other foods.MSG is used in the food industry as a flavor enhancer with an umami taste that intensifies the meaty, savory flavor of food, as naturally occurring glutamate does in foods such as stews and meat soups. It was first prepared in 1908 by Japanese biochemist Kikunae Ikeda, who was trying to isolate and duplicate the savory taste of kombu, an edible seaweed used as a base for many Japanese soups. MSG as a flavor enhancer balances, blends, and rounds the perception of other tastes.MSG has been used for over a hundred years and today is commonly found in stock cubes (Bouillon cube), soups, ramen, gravy, stews, condiments, savoury snacks etc. The U.S. Food and Drug Administration has given MSG its generally recognized as safe (GRAS) designation. A popular misconception is that MSG can cause headaches and other feelings of discomfort, known as "Chinese restaurant syndrome," but double-blind tests fail to find evidence of such a reaction. The European Union classifies it as a food additive permitted in certain foods and subject to quantitative limits. MSG has the HS code 29224220 and the E number E621. Obesity hypoventilation syndrome Obesity hypoventilation syndrome (also known as Pickwickian syndrome) is a condition in which severely overweight people fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels and high blood carbon dioxide (CO2) levels. Many people with this condition also frequently stop breathing altogether for short periods of time during sleep (obstructive sleep apnea), resulting in many partial awakenings during the night, which leads to continual sleepiness during the day. The disease puts strain on the heart, which eventually may lead to the symptoms such as heart failure, leg swelling and various other related symptoms. The most effective treatment is weight loss, but it is often possible to relieve the symptoms by nocturnal ventilation with positive airway pressure (CPAP) or related methods.Obesity hypoventilation syndrome is defined as the combination of obesity (body mass index above 30 kg/m2), hypoxemia (falling oxygen levels in blood) during sleep, and hypercapnia (increased blood carbon dioxide levels) during the day, resulting from hypoventilation (excessively slow or shallow breathing). The disease has been known since the 1950s, initially as "Pickwickian syndrome" in reference to a Dickensian character but currently under a more descriptive name. Obesity in Saudi Arabia Obesity in Saudi Arabia is a growing health concern, with health officials stating that it is one of the leading causes of preventable deaths in Saudi Arabia. According to Forbes, Saudi Arabia ranks 29 on a 2007 list of the fattest countries with a percentage of 68.3% of its citizens being overweight (BMI>25). Compounding the problem, according to a presentation at the 3rd International Obesity Conference in February 2014, is that obesity-related surgeries are not covered under Saudi healthcare.According to statistics, obesity in Saudi Arabia is found among females more than males. However, the case is the opposite in urban areas.[1] Obesity in the United States Obesity in the United States is a major health issue, resulting in numerous diseases, specifically increased risk of certain types of cancer, coronary artery disease, type 2 diabetes, stroke, as well as significant increase in early mortality and economic costs. While many industrialized countries have experienced similar increases, obesity rates in the United States are the highest in the world.An obese person in America incurs an average of$1,429 more in medical expenses annually. Approximately $147 billion is spent in added medical expenses per year within the United States. This number is suspected to increase approximately$1.24 billion per year until the year 2030.The United States had the highest rate of obesity within the OECD grouping of large trading economies. From 23% obesity in 1962, estimates have steadily increased. The following statistics comprise adults age 20 and over. The overweight percentages for the overall US population are higher reaching 39.4% in 1997, 44.5% in 2004, 56.6% in 2007, and 63.8% (adults) and 17% (children) in 2008. In 2010, the Centers for Disease Control and Prevention (CDC) reported higher numbers once more, counting 65.7% of American adults as overweight, and 17% of American children, and according to the CDC, 63% of teenage girls become overweight by age 11. In 2013 the Organisation for Economic Co-operation and Development (OECD) found that 57.6% of American citizens were overweight or obese. The organization estimates that 3/4 of the American population will likely be overweight or obese by 2020. 2014 figures from the CDC found that more than one-third (36.5%) of U.S. adults age 20 and older and 17% of children and adolescents aged 2–19 years were obese. A second study from the National Center for Health Statistics at the CDC showed that 39.6% of US adults age 20 and older were obese as of 2015-2016 (37.9% for men and 41.1% for women).Obesity has been cited as a contributing factor to approximately 100,000–400,000 deaths in the United States per year and has increased health care use and expenditures, costing society an estimated $117 billion in direct (preventive, diagnostic, and treatment services related to weight) and indirect (absenteeism, loss of future earnings due to premature death) costs. This exceeds health care costs associated with smoking and accounts for 6% to 12% of national health care expenditures in the United States. Phentermine Phentermine (phenyl-tertiary-butylamine), sold under the brand name Ionamin among others, is a medication used together with diet and exercise to treat obesity. It is taken by mouth for up to a few weeks. After a few weeks the beneficial effects no longer occur. It is also available as the combination phentermine/topiramate.Common side effects include a fast heart beat, high blood pressure, trouble sleeping, dizziness, and restlessness. Serious side effects may include pulmonary hypertension, valvular heart disease, and abuse. Use is not recommended during pregnancy or breastfeeding. Use is not recommended together with SSRIs or MAO inhibitors. It works as an appetite suppressant likely as a result of being a CNS stimulant. Chemically, phentermine is a substituted amphetamine.Phentermine was approved for medical use in the United States in 1959. It is available as a generic medication. The wholesale cost of a month supply in the United States is about US$2.55. In 2016 it was the 226th most prescribed medication in the United States with more than 2 million prescriptions. Phentermine was withdrawn from the market in the United Kingdom in 2000 while the combination medication fen-phen, of which it was a part, was withdrawn from the market in 1997 due to side effects.

Prader–Willi syndrome (PWS) is a genetic disorder due to loss of function of specific genes. In newborns, symptoms include weak muscles, poor feeding, and slow development. Beginning in childhood, the person becomes constantly hungry, which often leads to obesity and type 2 diabetes. Also, mild to moderate intellectual impairment and behavioral problems are typical. Often, the forehead is narrow, hands and feet are small, height is short, skin is light in color, and most of the affected are unable to have children.About 74% of cases occur when part of the father's chromosome 15 is deleted. In another 25% of cases, the person has two copies of chromosome 15 from their mother and none from their father. As parts of the chromosome from the mother are turned off, they end up with no working copies of certain genes. PWS is not generally inherited, but instead the genetic changes happen during the formation of the egg, sperm, or in early development. No risk factors are known. Those who have one child with PWS have less than a 1% chance of the next child being affected. A similar mechanism occurs in Angelman syndrome, except the defective chromosome 15 is from the mother or two copies are from the father.Prader–Willi syndrome has no cure. Treatment, however, may improve outcomes, especially if carried out early. In newborns, feeding difficulties may be supported with feeding tubes. Strict food supervision is typically required starting around the age of three in combination with an exercise program. Growth hormone therapy also improves outcomes. Counseling and medications may help with some behavioral problems. Group homes are often necessary in adulthood.PWS affects between one in 10,000 and one in 30,000 people. Males and females are affected equally. The condition is named after Andrea Prader, Heinrich Willi, and Alexis Labhart, who described it in detail in 1956. An earlier description was made in 1887 by John Langdon Down.

Social stigma of obesity

The social stigma of obesity or anti-fat bias has resulted in additional difficulties and disadvantages for overweight and obese people. Weight stigma is similar and has been broadly defined as bias or discriminatory behaviors targeted at individuals, because of their weight. Such social stigmas can span one's entire life, as long as excess weight is present, starting from a young age and lasting into adulthood. Several studies from across the world (e.g., United States, University of Marburg, University of Leipzig) indicate overweight and obese individuals experience higher levels of stigma relative to their thinner counterparts. In addition, they marry less often, experience fewer educational and career opportunities, and on average earn a lesser income than normal weight individuals. Although public support regarding disability services, civil rights and anti-workplace discrimination laws for obese individuals have gained support across the years, overweight and obese individuals still experience discrimination, which may have implications to physiological and psychological health. These issues are compounded with the significant negative physiological effects associated with obesity.Anti-fat bias refers to the prejudicial assumption of personality characteristics based on an assessment of a person as being overweight or obese. It is also known as "fat shaming". Fat activists allege anti-fat bias can be found in many facets of society, and blame the media for the pervasiveness of this phenomenon.

Texas

Texas (, locally ; Spanish: Texas or Tejas Spanish pronunciation: [ˈtexas] (listen)) is the second largest state in the United States by both area and population. Geographically located in the South Central region of the country, Texas shares borders with the U.S. states of Louisiana to the east, Arkansas to the northeast, Oklahoma to the north, New Mexico to the west, and the Mexican states of Chihuahua, Coahuila, Nuevo León, and Tamaulipas to the southwest, while the Gulf of Mexico is to the southeast.

Houston is the most populous city in Texas and the fourth largest in the U.S., while San Antonio is the second-most populous in the state and seventh largest in the U.S. Dallas–Fort Worth and Greater Houston are the fourth and fifth largest metropolitan statistical areas in the country, respectively. Other major cities include Austin, the second-most populous state capital in the U.S., and El Paso. Texas is nicknamed "The Lone Star State" to signify its former status as an independent republic, and as a reminder of the state's struggle for independence from Mexico. The "Lone Star" can be found on the Texas state flag and on the Texan state seal. The origin of Texas's name is from the word taysha, which means "friends" in the Caddo language.Due to its size and geologic features such as the Balcones Fault, Texas contains diverse landscapes common to both the U.S. Southern and Southwestern regions. Although Texas is popularly associated with the U.S. southwestern deserts, less than 10% of Texas's land area is desert. Most of the population centers are in areas of former prairies, grasslands, forests, and the coastline. Traveling from east to west, one can observe terrain that ranges from coastal swamps and piney woods, to rolling plains and rugged hills, and finally the desert and mountains of the Big Bend.

The term "six flags over Texas" refers to several nations that have ruled over the territory. Spain was the first European country to claim the area of Texas. France held a short-lived colony. Mexico controlled the territory until 1836 when Texas won its independence, becoming an independent Republic. In 1845, Texas joined the union as the 28th state. The state's annexation set off a chain of events that led to the Mexican–American War in 1846. A slave state before the American Civil War, Texas declared its secession from the U.S. in early 1861, and officially joined the Confederate States of America on March 2nd of the same year. After the Civil War and the restoration of its representation in the federal government, Texas entered a long period of economic stagnation.

Historically four major industries shaped the Texas economy prior to World War II: cattle and bison, cotton, timber, and oil. Before and after the U.S. Civil War the cattle industry, which Texas came to dominate, was a major economic driver for the state, thus creating the traditional image of the Texas cowboy. In the later 19th century cotton and lumber grew to be major industries as the cattle industry became less lucrative. It was ultimately, though, the discovery of major petroleum deposits (Spindletop in particular) that initiated an economic boom which became the driving force behind the economy for much of the 20th century. With strong investments in universities, Texas developed a diversified economy and high tech industry in the mid-20th century. As of 2015, it is second on the list of the most Fortune 500 companies with 54. With a growing base of industry, the state leads in many industries, including agriculture, petrochemicals, energy, computers and electronics, aerospace, and biomedical sciences. Texas has led the U.S. in state export revenue since 2002, and has the second-highest gross state product. If Texas were a sovereign state, it would be the 10th largest economy in the world.

Weight loss

Weight loss, in the context of medicine, health, or physical fitness, refers to a reduction of the total body mass, due to a mean loss of fluid, body fat or adipose tissue or lean mass, namely bone mineral deposits, muscle, tendon, and other connective tissue. Weight loss can either occur unintentionally due to malnourishment or an underlying disease or arise from a conscious effort to improve an actual or perceived overweight or obese state. "Unexplained" weight loss that is not caused by reduction in calorific intake or exercise is called cachexia and may be a symptom of a serious medical condition. Intentional weight loss is commonly referred to as slimming.

Malnutrition or nutrition disorders (E40–E68, 260–269)
Malnutrition
Overnutrition

This page is based on a Wikipedia article written by authors (here).
Text is available under the CC BY-SA 3.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.