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An obese man. Painting by Alessandro del Borro, 17th century.

Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and mammals is increased to a point where it is thought to be a significant risk factor in certain health conditions, leading to increased mortality. Obesity is a condition that develops from the interaction of individual biology and the environment. Excessive body weight has been shown to correlate with various important diseases, particularly cardiovascular disease, diabetes mellitus type 2, sleep apnea, stroke, and osteoarthritis[1]. Obesity is both an individual clinical condition and, recently, a serious public health problem.

Definition

Obesity
SpecialtyEndocrinology Edit this on Wikidata

Obesity as a clinical condition is usually assessed by BMI (Body Mass Index), waist circumference, and the presence of risk factors and comorbidities[1]. In epidemiological studies BMI alone is used to define obesity.

BMI

Graphic chart comparing obesity percentages of the total population in OECD member countries.

Body mass index (BMI) is currently the most widely accepted calculation of excess body fat for human beings, especially for screening purposes and to monitor effect of treatments. It also the calculation used in epidemiological or population-wide measurements of obesity.

BMI was developed by the Belgian statistician and anthropometrist Adolphe Quetelet[2]. It is calculated by dividing the subject's weight in kilograms by the square of his/her height in meters ().

The current definitions commonly in use establish the following values, agreed in 1997 and published in 2000[3]:

  • A BMI less than 18.5 is underweight
  • A BMI of 18.5 - 24.9 is normal weight
  • A BMI of 25.0 - 29.9 is overweight
  • A BMI of 30.0 - 39.9 is obese
  • A BMI of 40.0 or higher is severely (or morbidly) obese

BMI is a simple and accepted method for calculating body fat [4]. BMI as an indicator of a clinical condition is used in conjunction with other clinical assessments. In a clinical setting, physicians take into account race, ethnicity, athleticism (muscularity), age, sex, and other factors which can affect the interpretation of BMI.[1] BMI is used alone as an indicator of prevalence and incidence in epidemiological analysis.

Waist circumference

BMI does not take into account differing ratios of adipose to lean tissue; nor does it distinguish between differing forms of adiposity, some of which may correlate more closely with cardiovascular risk. Increasing understanding of the biology of different forms of adipose tissue has shown that visceral or central obesity (male-type or apple-type obesity) has a much stronger correlation, particularly with cardiovascular disease, than the BMI alone[5].

The absolute waist circumference (>102 cm in men and >88 cm in women) or waist-hip ratio (>0.9 for men and >0.85 for women)[5] are both used as measures of central obesity.

Body fat measurement

An alternative way to determine obesity is to assess percent body fat. Doctors and scientists generally agree that men with more than 25% body fat and women with more than 30% body fat are obese. However, it is difficult to measure body fat precisely. The most accepted method has been to weigh a person underwater, but underwater weighing is a procedure limited to laboratories with special equipment. Two simpler methods for measuring body fat are the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer; or bioelectrical impedance analysis, usually only carried out at specialist clinics.

Gestalt

In practice, in most examples of overweight that may designate risk, both doctor and patient can see "by eye" whether excess fat is a concern [2]. In these cases, BMI thresholds provide simple targets all patients can understand.

Risk factors and comorbidities

The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. Coronary heart disease, Type II diabetes, and sleep apnea are possible life-threatening risk factors that would indicate clinical treatment of obesity[1]. Smoking, hypertension, age and family history are other risk factors that may indicate treatment[1] Diabetes and heart disease are risk factors used in epidemiological studies of obesity.

Causes

Causative factors

When food energy intake exceeds energy expenditure, fat cells (and to a lesser extent muscle and liver cells) throughout the body take in the energy and store it as fat. In its simplest conception, therefore, obesity is only made possible when the lifetime energy intake exceeds lifetime energy expenditure by more than it does for individuals of "normal weight".

In all individuals, the excess energy utilized to generate fat reserves is minute relative to the total number of calories consumed. This means that very fine perturbations in the energy balance can lead to large fluctuations in weight over time. To illustrate, an obese 40 year old who carries 100 lb of adipose tissue has only consumed about 25 more calories per day than he has burned on average - or the equivalent of an apple every three days. In comparison a very lean 40-year-old who carries only 15 lb of body fat will have exceeded his daily energy expenditure by about four calories a day - the equivalent of an apple every 18 days.

Factors that have been suggested to contribute to the development of obesity include:

As with many medical conditions, the caloric imbalance that results in obesity often develops from a combination of genetic and environmental factors. Polymorphisms in various genes controlling appetite, metabolism, and adipokine release predispose to obesity, but the condition requires availability of sufficient calories, and possibly other factors, to develop fully. Various genetic abnormalities that predispose to obesity have been identified (such as Prader-Willi syndrome and leptin receptor mutations), but known single-locus mutations have been found in only about 5% of obese individuals. While it is thought that a large proportion of the causative genes are still to be identified, much obesity is likely the result of interactions between multiple genes, and non-genetic factors are likely also important.

Some eating disorders are associated with obesity, especially binge eating disorder (BED). As the name indicates, patients with this disorder are prone to overeat, often in binges. A proposed mechanism is that the eating serves to reduce anxiety, and some parallels with substance abuse can be drawn. An important additional factor is that BED patients often lack the ability to recognize hunger and satiety, something that is normally learned in childhood. Learning theory suggests that early childhood conceptions may lead to an association between food and a calm mental state.

Evolutionary aspects

Although there is no definitive explanation for the recent increase of obesity, the thrifty gene hypothesis provides some understanding of this phenomenon. In times when food was scarce, the ability to take advantage of rare periods of abundance and use such abundance by storing energy efficiently was undoubtedly an evolutionary advantage. Individuals with greater adipose reserves were more likely to survive famine. This tendency to store fat is likely maladaptive in a society with adequate and stable food supplies. Although many people likely have a genetic propensity towards obesity, in most cases this propensity requires the modern environment with increased caloric availability and decreased requirements for physical labor in order to be expressed fully.

Neurobiological mechanisms

Scientists investigating the mechanisms and treatment of obesity may use animal models such as mice to conduct experiments.

Flier[6] summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until leptin was discovered in 1994. Since this discovery, many other hormonal mechanisms have been elucidated that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, development of insulin resistance. Since leptin's discovery, ghrelin, orexin, PYY 3-36, cholecystokinin, adiponectin, and numerous other mediators have been studied. The adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases.

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

Neuroscientific approaches hinge on the action of the aforementioned hormones and mediators on the hypothalamus, the part of the brain that is thought to produce hunger signals for higher centers and induce food intake behavior. Lesion studies in the 1940s and 1950s identified two regions of the hypothalamus — the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH) — as the brain's hunger and satiety centers, respectively. Specific lesions to a mouse's LH suppressed its appetite while damaging the VMH caused overeating.

Studies of the distribution of the leptin receptor in the mid-1990s cast doubt upon this dual center theory of hunger and satiety. Leptin's effect on the arcuate nucleus melanocortin system is now considered central to the regulation of feeding and metabolism.

Some obesity co-factors are resistant to the theory that the "epidemic" is a new phenomenon. In particular, a class co-factor consistently appears across many studies. Comparing net worth with BMI scores, a 2004 study[7] found obese American subjects approximately half as wealthy as thin ones. When income differentials were factored out, the inequity persisted — thin subjects were inheriting more wealth than fat ones. Another study finds women who married into higher status predictably thinner than women who married into lower status.

Complications

Obesity, especially central obesity (male-type or waist-predominant obesity), is an important risk factor for the "metabolic syndrome" ("syndrome X"), the clustering of a number of diseases and risk factors that heavily predispose for cardiovascular disease. These are diabetes mellitus type 2, high blood pressure, high blood cholesterol, and triglyceride levels (combined hyperlipidemia). An inflammatory state is present, which — together with the above — has been implicated in the high prevalence of atherosclerosis (fatty lumps in the arterial wall), and a prothrombotic state may further worsen cardiovascular risk.

Apart from the metabolic syndrome, obesity is also correlated (in population studies) with a variety of other complications. For many of these complaints, it has not been clearly established to what extent they are caused directly by obesity itself, or have some other cause (such as limited exercise) that causes obesity as well. Most confidence in a direct cause is given to the mechanical complications in the following list, compiled by the American Medical Association for general physicians:

While being severely obese has many health ramifications, those who are somewhat overweight face little increased mortality or morbidity. Some studies suggest that the somewhat "overweight" tend to live longer than those at their "ideal" weight [3]. This may in part be attributable to lower mortality rates in diseases where death is either caused or contributed to by significant weight loss due to the greater risk of being underweight experienced by those in the ideal category. Another factor which may confound mortality data is smoking, since obese individuals are less likely to smoke. Osteoporosis is known to occur less in slightly overweight people.

Therapy

The mainstay of treatment for obesity is an energy-limited diet and increased exercise. In studies, diet and exercise programs have consistently produced an average weight loss of approximately 8% of total body mass on average (excluding study drop-outs). While not all dieters will be satisfied with this outcome, studies have shown that a loss of as little as 5% of body mass can create enormous health benefits.

A more intractable therapeutic problem appears to be weight loss maintenance. Of dieters who manage to lose 10% or more of their body mass in studies, 80-95% will regain that weight within two to five years. It appears that the homeostatic mechanisms regulating body weight are very robust (see leptin, for example), and vigorously defend against weight loss. Much important research is now being devoted to determining what factors can improve the currently dismal weight loss maintenance rates.

Recent scientific research has cast some doubt over whether or not dieting actually improves health, with some studies indicating that dieting may in fact be more detrimental than remaining overweight [9]

In a clinical practice guideline by the American College of Physicians[10], the following five recommendations are made:

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

Much research focuses on new drugs to combat obesity, which is seen as the biggest health problem facing developed countries. Nutritionists and many doctors feel that these research funds would be better devoted to advice on good nutrition, healthy eating, and promoting a more active lifestyle.

Medication most commonly prescribed for diet/exercise-resistant obesity is orlistat (Xenical®, which reduces intestinal fat absorption by inhibiting pancreatic lipase) and sibutramine (Reductil®, Meridia®, an anorectic). In the presence of diabetes mellitus, there is evidence that the anti-diabetic drug metformin (Glucophage®) can assist in weight loss — rather than sulfonylurea derivatives and insulin, which often lead to further weight gain. The thiazolidinediones (rosiglitazone or pioglitazone) can cause slight weight gain, but decrease the "pathologic" form of abdominal fat, and are therefore often used in obese diabetics.

Increasingly, bariatric surgery is being used to combat obesity. The most common weight loss surgery in Europe and Australia is the adjustable gastric band where a silicone ring is placed around the top of the stomach to help restrict the amount of food eaten in a sitting. This surgery has been FDA approved in the United States since 2001 but has been being used in other parts of the world since the early 1990s. It is considered the safest and least invasive of the available weight loss surgeries such as Roux-en-Y gastric bypass surgery (RNY), biliopancreatic diversion, and stomach stapling (also known as "vertical banded gastroplasty", VBG). Unlike those more invasive techniques the band surgery does not cut into or reroute any of the digestive tract and is completely reversible. Removing the implant returns the stomach to its pre-surgical norm. All of these surgeries can be done laparoscopically. The more invasive of the surgeries usually bypass or remove some portion of the patient's intestines which causes malabsorption and dumping. All of these surgeries come with risk to the patient, from the LAP-BAND which has a mortality rate of 1 in 2000 to the RNY Bypass which has a mortality rate of 1 in 200. RNY surgery appears to be popular because the weight tends to come off faster than with the band but studies have shown that at 3-6 years out the amount of weight lost and the amount of loss maintained is nearly identical. Therefore the patient needs to consider the long term ramifications of their choice.

None of these weight loss surgeries should be considered lightly and all risks must be examined and weighed against the risks of remaining obese. Bariatric surgery is not the easy way out, it requires the patient to make lifelong changes to their diet if they are to keep the lost weight off in the long term. Restrictive surgeries such as the adjustable gastric band offer the patient a built-in tool but it should be considered a tool not a magic solution. They can help a person to eat less but they cannot choose what the patient puts in their mouth, thus the need for long term commitments to eat properly.

Cultural and social significance

Etymology

Obesity is the nominal form of obese which comes from the Latin obēsus, which means "stout, fat, or plump." Ēsus is the past participle of edere (to eat), with ob added to it. In Classical Latin, this verb is seen only in past participial form. Its first attested usage in English was in 1651, in Noah Biggs's Matæotechnia Medicinæ Praxeos [11].

Culture and obesity

Venus of Willendorf

In several human cultures, obesity is associated with physical attractiveness, strength, and fertility. Some of the earliest known cultural artifacts, known as Venus figurines, are pocket-sized statuettes representing an obese female figure. Although their cultural significance is unrecorded, their widespread use throughout pre-historic Mediterranean and European cultures suggests a central role for the obese female form in magical rituals, and suggests cultural approval of (and perhaps reverence for) this body form. This is most likely due to their ability to easily bear children and survive famine.

In contrast, in modern Western culture, a more slender body shape is more typically considered desirable. "Thinness" is often considered more important for women than men.

Obesity was occasionally considered a symbol of wealth and social status in cultures prone to food shortages or famine. Well into the early modern period in European cultures, it often served this role. But as food security was realised, it came to serve more as a visible signifier of "lust for life", appetite, and immersion in the realm of the erotic. This was especially the case in the visual arts, such as the paintings of Rubens (1577–1640), whose regular use of the full female figures gives us the description Rubenesque for plumpness. Obesity can also be seen as a symbol within a system of prestige. "The kind of food, the quantity, and the manner in which it is served are among the important criteria of social class. In most tribal societies, even those with a highly stratified social system, everyone - royalty and the commoners - ate the same kind of food, and if there was famine everyone was hungry. With the ever increasing diversity of foods, food has become not only a matter of social status, but also a mark of one's personality and taste." [12]

Not all contemporary cultures disapprove of obesity, although the Western preference for thinness is increasingly being exported worldwide as part of the process of globalization. Few cultures have escaped the "Westernization" of body shape preference, though cultures which are traditionally more approving (to varying degrees), include some African, Arabic, Indian, and Pacific Island cultures. Especially in the past decades, obesity has come to be seen more as a medical condition. There is also a small but vocal fat acceptance movement that seeks to challenge weight-based discrimination.

File:PigsisPigs1.jpg
In cartoons, obesity is often used for comic effect.

Various stereotypes of obese people have found their way into expressions of popular culture. A common stereotype is the obese character who has a warm and dependable personality, but equally common is the obese vicious bully. Gluttony and obesity are commonly depicted together in works of fiction. In cartoons, obesity is often used to comedic effect, with fat cartoon characters having to squeeze through narrow spaces, frequently getting stuck or even exploding.

It can be argued that depiction in popular culture adds to and maintains commonly perceived stereotypes, in turn harming self esteem of obese people. A charge of discrimination on the basis of appearance could be leveled against these depictions.

On the other hand, obesity is often associated with positive characteristics such as good humor (the stereotype of the jolly fat man like Santa Claus), and some people are more sexually attracted to obese people than to slender people (see chubby culture, fat admirer).

Public health and policy

The prevalence of overweight and obesity in the United States makes obesity a leading public health problem. From 1980 to 2002, obesity prevalence has doubled in adults and overweight prevalence has has tripled in children and adolescents [13]. From 2003-2004, "children and adolescents aged 2 to 19 years, 17.1% were overweight...and 32.2% of adults aged 20 years or older were obese."[13] The prevalence in the United States continues to rise.Cite error: A <ref> tag is missing the closing </ref> (see the help page).. The prevalence of obesity has been continually rising for two decades.[14] This sudden rise in obesity prevalence is attributed to environmental and population factors rather than individual behavior and biology because of the rapid and continual rise in the number of overweight and obese individuals.[15]. The current environment produces risk factors for decreased physical activity and for increased calorie consumption. These environmental factors operate on the population to decrease physical activity and increase calorie consumption.

Environmental causes of obesity

While it may often appear obvious why a certain individual gets fat, it is far more difficult to understand why the average weight of certain societies have recently been growing. While genetic causes are central to understanding obesity, they cannot fully explain why one culture grows fatter than another.

This is most notable in the United States. In the years from just after the Second World War until 1960 the average person's weight increased, but few were obese. In the two and a half decades since 1980 the growth in the rate of obesity has accelerated markedly and is increasingly becoming a public health concern.

There are a number of theories as to the cause of this change since 1980. Most believe it is a combination of various factors.

  • Lack of activity: obese people appear to be less active in general than lean people, and not just because of their obesity. A controlled increase in calorie intake of lean people did not make them less active; correspondingly when obese people lost weight they did not become more active. Weight change does not affect activity levels, but the converse seems to be the case. [16]
  • One of the most important is the much lower relative cost of foodstuffs: massive changes in agricultural policy in the United States and Europe have led to food prices for consumers being lower than at any point in history. Sugar and corn syrup, two huge sources of food energy, are some of the most subsidized products by the United States government. This can raise costs for consumers in some areas but greatly lower it in others. Current debates into trade policy highlight disagreements on the effects of subsidies.
  • Increased marketing has also played a role. In the early 1980s in America the Reagan administration lifted most regulations pertaining to sweets and fast food advertising to children. As a result, the number of advertisements seen by the average child increased greatly, and a large proportion of these were for fast food and sweets.
  • Changes in the price of mineral oil and petrol are also believed to have had an effect, as unlike during the 1970s it is now affordable in the United States to drive everywhere — at a time when public transit goes underused. At the same time more areas have been built without sidewalks and parks.
  • A social cause that is believed by many to play a role is the increasing number of two income households in which one parent no longer remains home to look after the house. This increases the number of restaurant and take-out meals.
  • Urban sprawl may be a factor: obesity rates increase as urban sprawl increases, possibly due to less walking and less time for cooking. [17]
  • Since 1980 both sit-in and fast food restaurants have seen dramatic growth in terms of the number of outlets and customers served. Low food costs, and intense competition for market share, led to increased portion sizes — for example, McDonalds french fries portions rose from 200 Calories (840 kilojoules) in 1960 to over 600 Calories (2,500 kJ) today.
  • Increased food production is a probable factor. The U.S. produces three times more food than U.S. residents eat.
  • Increasing affluence itself (including many of the above factors as accompaniments of affluence) may be a cause, or contributing factor since obesity tends to flourish as a disease of affluence in countries which are developing and becoming westernised [4]. This is supported by a dip in American GDP after 1990, the year of the Gulf War, followed by an exponential increase. U.S. obesity statistics followed the same pattern, offset by two years [5].
  • An aging population may also be a major factor, as the likelihood of becoming obese increases with age. Beyond their twenties, the older a person becomes the slower their metabolism becomes, reducing the amount of calories required to sustain the body, thus if a person does not reduce their intake of food with age, they will become obese over time. As the average age of individuals within a society increases, the rate of obesity also increases. This situation is exacerbated by the baby boom generation, which represents a disproportionately large portion of the population in many countries and is currently nearing the latter end of the typical lifespan in affluent nations, and therefore is in the high-risk zone for obesity.

Interestingly an increase in the number of Americans who exercise and diet occurred before the increase in obesity, and some scholars have even argued that these trends actually encouraged obesity. Nearly all diets fail, with participants resuming their previous eating habits or even engaging in binge eating. Many then see an overall increase in their weight. If the diet is then repeated and abandoned again, a pattern of rising and falling weight is established, known as weight cycling. Similarly those who work out but then stop can end up being heavier than those who never exercised.

Public health and policy responses to obesity

On top of controversies about the causes of obesity, and about its precise health implications, come policy controversies about the correct policy approach to obesity. The main debate is between "personal responsibility" advocates, who resist regulatory attempts to intervene in citizen's private dietary habits, and "public interest" advocates, who promote regulations, on the same public health grounds as the restrictions applied to tobacco products. In the U.S., a recent bout in this controversy involves the so-called Cheeseburger Bill, an attempt to indemnify food industry businesses from frivolous law suits by obese clients.

"Personal responsibility" advocates work on the basis that, as the microbiologist Rene Dubos once said, health ought not to be considered an end in itself, but "the condition best suited to reach goals that each individual formulates for himself" [6]. Any other definition permits authorities to curtail the autonomy of the self-determining individual, imposing quantity over quality of life onto them, undermining their civil liberties. As much as principled doctors, personal responsibility arguments have also been offered by food producer lobbies. In 1961, for example, as President John F Kennedy raised concerns about a lack of fitness in American society, a spokesman for the U.S. Dairy industry, Frank R. Neu, wrote advertorials warning We May Be Sitting Ourselves To Death [7]. Not food regulation, but personal exercising, is moved as the solution.

On July 16, 2004, the United States Department of Health and Human Services officially classified obesity as a disease. Speaking to a Senate committee, Tommy Thompson, the Secretary of Health and Human Services, stated that Medicare would cover obesity-related health problems. However, reimbursement would not be given if a treatment was not proven to be effective.

See Also

Notes

  1. ^ a b c d e U.S. Dept. of Health and Human Services, National Institutes of Health, 'The Practical Guide: Identification, Evaluation and Treatment of Overweight and Obesity in Adults 5 (2000) PDF
  2. ^ Quetelet LAJ (1871). Antropométrie ou Mesure des Différences Facultés de l'Homme. Brussels: Musquardt.
  3. ^ World Health Organization. Technical report series 894: "Obesity: preventing and managing the global epidemic.". Geneva: World Health Organization, 2000. PDF.
  4. ^ Z. Mei, L. Grummer-Strawn, A. Pietrobelli, A. Goulding, W. Dietz, "Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents", American Journal of Clinical Nutrition, 75:978-985 (2002).
  5. ^ a b Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study". Lancet. 364: 937–52. PMID 15364185.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Flier JS (2004). "Obesity wars: molecular progress confronts an expanding epidemic". Cell. 116 (2): 337–50. PMID 14744442.
  7. ^ Zagorsky JL. Is Obesity as Dangerous to Your Wealth as to Your Health? Res Aging 2004;26:130-152. PDF fulltext.doi:10.1177/0164027503258519.
  8. ^ Whitmer RA, Gunderson EP, Barrett-Connor E, Quesenberry CP Jr, Yaffe K (2005). "Obesity in middle age and future risk of dementia: a 27 year longitudinal population based study". BMJ. 330 (7504): 1360. PMID 15863436.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Sørensen TI, Rissanen A, Korkeila M, Kaprio J (2005). "Intention to lose weight, weight changes, and 18-y mortality in overweight individuals without co-morbidities". PLoS Med. 2 (6): e171. PMID 15971946.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Snow V, Barry P, Fitterman N, Qaseem A, Weiss K (2005). "Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians". Ann Intern Med. 142 (7): 525–31. PMID 15809464.{{cite journal}}: CS1 maint: multiple names: authors list (link) Fulltext.
  11. ^ The Oxford English Dictionary (website)
  12. ^ Powdermaker H. "An anthropological approach to the problem of obesity." Food and Culture: A Reader. Ed. Carole Counihan and Penny van Esterik. New York: Routledge, 1997. 206.
  13. ^ a b Ogden C, Carroll M, Curtin L, McDowell M, Tabak C, Flegal K. Prevalence of Overweight and Obesity in the Unites States, 1999 - 2004. JAMA 2006;295:1549-1555. PMID 16595758.
  14. ^ Centers for Disease Control and Prevention, U.S. Obesity Trends 1984 - 2002 [1].
  15. ^ Morrill A, Chinn C. The obesity epidemic in the United States. J Public Health Policy 2004;25:353-366. PMID 15683071.
  16. ^ Levine JA, Lanningham-Foster LM, McCrady SK, Krizan AC, Olson LR, Kane PH, Jensen MD, Clark MM (2005). "Interindividual variation in posture allocation: possible role in human obesity". Science. 307 (5709): 584–6. PMID 15681386 doi:10.1126/science.1106561.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Lopez R (2004). "Urban sprawl and risk for being overweight or obese". Am J Public Health. 94 (9): 1574–9. PMID 15333317.
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