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'''Obesity''' is a condition in which the natural energy reserve, stored in the [[adipose tissue|fatty tissue]] of [[human]]s and [[mammal]]s 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 relatively rare among animals in the wild, but it is common in [[domestic animal]]s (who may be [[overeating|overfed]] and [[exercise|underexercised]]), and increasingly in [[humans]].
 
 
Excessive body weight has been shown to correlate with various important [[diseases]], particularly [[cardiovascular disease]], [[diabetes mellitus type 2]], [[sleep apnea]] and [[osteoarthritis]]. It is also considered a risk factor for certain cancers. Interventions, such as [[dieting|diet]] and [[exercise]] as well as [[medication]] and [[bariatrics|weight-loss surgery]] (in severe cases) are frequently recommended to reduce the risk of developing disease.
 
 
[[Image:Italienischer Maler des 17. Jahrhunderts 001.jpg|thumb|An obese man. Painting by Alessandro del Borro, 17th century.]]
 
 
==Definition==
 
 
{{DiseaseDisorder infobox |
 
{{DiseaseDisorder infobox |
 
Name = Obesity |
 
Name = Obesity |
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ICD9 = 278 |
 
ICD9 = 278 |
 
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[[Image:Italienischer Maler des 17. Jahrhunderts 001.jpg|thumb|An obese man. Painting by Alessandro del Borro, 17th century.]]
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'''Obesity''' is a condition in which the natural energy reserve, stored in the [[adipose tissue|fatty tissue]] of [[human]]s and [[mammal]]s 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 relatively rare among animals in the wild, but it is common in [[domestic animal]]s (who may be [[overeating|overfed]] and [[exercise|underexercised]]), and increasingly in [[humans]].
  +
 
Excessive body weight has been shown to correlate with various important [[diseases]], particularly [[cardiovascular disease]], [[diabetes mellitus type 2]], [[sleep apnea]] and [[osteoarthritis]]. It is also considered a risk factor for certain cancers. Interventions, such as [[dieting|diet]] and [[exercise]] as well as [[medication]] and [[bariatrics|weight-loss surgery]] (in severe cases) are frequently recommended to reduce the risk of developing disease.
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==Definition==
   
 
''Obesity'' is a concept that is being continually redefined, largely because accurate estimations of body fat are difficult to obtain, and different forms of fat have different health implications. The most commonly used parameters are the ''body mass index'', the ''waist-hip ratio'' and more advanced determinations of body fat.
 
''Obesity'' is a concept that is being continually redefined, largely because accurate estimations of body fat are difficult to obtain, and different forms of fat have different health implications. The most commonly used parameters are the ''body mass index'', the ''waist-hip ratio'' and more advanced determinations of body fat.

Revision as of 23:19, 25 July 2006

Obesity
ICD-10 E66
ICD-9 278
OMIM {{{OMIM}}}
DiseasesDB {{{DiseasesDB}}}
MedlinePlus {{{MedlinePlus}}}
eMedicine {{{eMedicineSubj}}}/{{{eMedicineTopic}}}
MeSH {{{MeshNumber}}}
Italienischer Maler des 17

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 relatively rare among animals in the wild, but it is common in domestic animals (who may be overfed and underexercised), and increasingly in humans.

Excessive body weight has been shown to correlate with various important diseases, particularly cardiovascular disease, diabetes mellitus type 2, sleep apnea and osteoarthritis. It is also considered a risk factor for certain cancers. Interventions, such as diet and exercise as well as medication and weight-loss surgery (in severe cases) are frequently recommended to reduce the risk of developing disease.


Definition

Obesity is a concept that is being continually redefined, largely because accurate estimations of body fat are difficult to obtain, and different forms of fat have different health implications. The most commonly used parameters are the body mass index, the waist-hip ratio and more advanced determinations of body fat.

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BMI

Body mass index (BMI), also called the Quetelet number or Quetelet index, is currently the most widely accepted calculation of excess body fat for human beings, especially for screening purposes and to monitor effect of treatments.

BMI was developed by the Belgian statistician and anthropometrist Adolphe Quetelet[1]. It is calculated by dividing the subject's weight in kilograms by the square of his/her height in meters (). For example, a person who weighs 75 kilograms and stands 1.8 meters tall would have a BMI of 75/(1.82)=23.148. The number 23.148 is then compared to a table of definitions.

The current definitions commonly in use establish the following values, agreed in 1997 and published in 2000[2]:

  • A BMI below 18.5 is characterized as underweight
  • A BMI of 18.5 - 24.999 is characterized as normal weight
  • A BMI of 25.0 - 29.999 is characterized as overweight or pre-obese
  • A BMI of 30.0 - 34.999 is characterized as obese
  • A BMI of 35.0 or higher is characterized as severely (or morbidly) obese

BMI is most accurate for people who live a sedentary lifestyle. It thus cannot distinguish between weight from body fat, muscle mass, or bone mass, so the table above is inaccurate for example in athletes, children or the elderly. Because muscle is more dense than fat, most amateur athletes would be classified as "overweight" and most professional athletes have enough muscle mass to be classified as "obese" or even "severely obese", when in fact their body fat percentage is very low and they are in no danger of developing any health problems correlative to carriage of excess fat. Children, meanwhile, have higher bone density in the years before puberty because of their smaller size, and that also results in skewed BMI values. In the case of elderly people, muscular atrophy and/or osteoporosis can also decrease the value of a BMI calculation.

There is the additional problem of sex differences between men and women. White and East Asian women tend to have less muscle mass and bone density than men of the same height. The same is not true of black and Polynesian women, however. In the future, a healthy BMI for a given individual may be defined to some extent by their ethnic group, racial origin, or sex, but that is not the case now.

Bmi30chart

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

The defining ranges of the categories are occasionally adjusted, and can differ from country to country - which underscores the arbitrary nature of the correlation. In June 1998 the National Institutes of Health brought official U.S. category definitions into line with those used by the WHO, moving the American "overweight" threshold from BMI 27 to BMI 25. Thresholds are in principle designed to be "best estimates" concerning health risk at the time they are established and are also designed to ensure cohort uniformity in epidemiological studies. About 30,000,000 Americans moved from "ideal" weight to being "overweight".

In 2000, the WHO was advised to consider lowering the BMI threshold for overweight in East Asians from BMI 25 to BMI 23, and for obesity in East Asians from BMI 30 to BMI 25, due to epidemiological studies indicating that East Asians suffer a greater number of obesity-related health conditions at lower BMI values[citation needed]. To date, the WHO has not made any changes pursuant to those recommendations.

Additionally, some clinicians suggest raising the BMI thresholds for people with sub-Saharan African and Polynesian ancestry, because members of these groups have a greater ratio of lean body mass to fat at all body weights. The proposed thresholds for these groups are BMI 26 for overweight, and BMI 32 for obesity. Again, to date, no major professional or medical organization has officially adopted this suggestion.

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 correllation, particularly with cardiovascular disease, than the BMI alone[3].

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)[3] 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 [1]. In these cases, BMI thresholds provide simple targets all patients can understand.

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 [4].

Cultural and social significance

Culture and obesity

VenusWillendorf

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 abilty 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 (15771640), 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." [5]

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.

Popular culture

PigsisPigs1

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, presumedly in compensation for social exclusion, 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).

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

Fatmouse

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.

Societal causes

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. [7]
  • 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 the Reagan administration lifted most regulations pertaining to 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.
  • The changing workforce as each year a greater percent of the population spends their entire workday behind a desk or computer, seeing virtually no exercise. In the kitchen the microwave oven has seen sales of calorie-dense frozen convenience foods skyrocket and has encouraged more elaborate snacking.
  • 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. [8]
  • 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 [2]. 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 [3].
  • 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.

Poverty link

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[9] 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-predomimant 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:

[10]

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 [4]. 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 [11]

In a clinical practice guideline by the American College of Physicians[12], 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.

Controversies

There is continuous debate over obesity, at several levels. While scientific evidence for particular risks and treatments is fairly firm, the evidence informing debates on exact causation, social impact and necessary policy responses is much less clear-cut. In the area of policy and public debate, statistics demonstrating correlations are typically misinterpreted as demonstrating causation, a fallacy known as the spurious relationship. As much of the data is open to interpretation, there have been many "experts" taking positions, as well as policy pressure groups, influencing the debate from various angles.

Medicalization of obesity

Controversy exists as to whether the concept of "obesity" is a valid one. Critics assert that physically active people are healthier than the sedentary regardless of their body weight. The focus on weight and body mass is fed, in their view, by a diet promotion industry, drug companies, and segments of the medical profession for profit purposes, by promoting a vision that equates health with slenderness, and makes extreme slenderness of a sort that is quite difficult for most people to achieve an ideal. In The Obesity Myth, Paul Campos writes that:

... (F)rom the perspective of a profit-maximising medical and pharmaceutical industry, the ideal disease would be one that never killed those who suffered from it, that could not be treated effectively, and that doctors and their patients would nevertheless insist on treating anyway. Luckily for it, the American health care industry has discovered (or rather invented) just such a disease. It is called "obesity". Basically, obesity research in America is funded by the diet and drug industry — that is, the economic actors who have the most to gain from the conclusion that being fat is a disease that requires aggressive treatment. Many researchers have direct financial relationships with the companies whose products they are evaluating. [13]

Health effects of obesity

Opposing Campos are voices such as Greg Critser, who writes in Fat Land that the statistics such campaigners use are based on a selective sample of research data — a selection designed to emphasise obesity co-factors such as poor fitness, rather than obesity itself. Critser notes that advocates of the Obesity Myth position typically rely heavily on a study by Dr. Steven Blair at the Cooper Institute, Texas, which showed that fit, fat subjects were healthier than unfit, skinny subjects:

... Taking out the fitness variable and looking at body weight only, Blair admitted: "Men with a BMI of >30 were generally less physically fit and had more unfavorable risk factors than men in the lower BMI groups". Lower weight men had higher good cholesterol, lower bad cholesterol, and higher treadmill times than fatter men. "The highest death rate," he added, "was observed among those men in the highest BMI category and correspondingly lower death rates were observed in each subsequently lower BMI category." And when one looks at the difference between low fit men in all categories — which one might think would be most useful since most obese people are not fit — Blair's upbeat message fades: Normal weight nonfit men had an age-adjusted death rate (the number of excess deaths in the studied group) of 52.1; unfit fat men had the higher rate of 62.1. More: Unfit lean men were half as likely to have a history of hypertension than unfit fat men. In the real world, even according to Blairism, the fat are more likely to die early — and to live precariously — than the lean.[14]

Medical responses to obesity

Conventional wisdom recommends that the obese adopt strategies to lose weight in order to mitigate the health risks associated with obesity. There is controversy both over what those strategies realistically include, and also whether such a goal does actually result in better health outcomes.

Weight reduction strategies include dietary changes, exercise regimes, weight loss drugs, and surgical interventions (see Therapy, above, for complete list). Of these, "miracle diets" are most contested, with several studies suggesting that short-term weight loss typically results in metabolic adjustments leading to weight gain in the longer term.

Conventional wisdom holds that obesity is caused by over-indulgence in fatty or sugary foods, portrayed as either a failure of will power or a species of addiction. Various specialists strongly oppose this view. For example, Professor Thomas Sanders of King's College London emphasises the need for balance between activity and consumption:

In trials, there is no evidence suggesting that reducing fat intake has an effect on obesity. As long as your expenditure equals what you eat, you won't put on weight, regardless of how high the fat content is in your diet (The Times, London, 10 March 2004).

Prevalence and public interest

What qualifies a medical condition as a matter of public interest, rather than a private health issue between doctor and patient, are its social costs. The estimation or measurement of the social cost of obesity is an extraordinarily hazardous statistical task, for two separate reasons.

Firstly, the collation of evidence concerning the prevalence of obesity, or especially changing rates of prevalence, is open to several types of distortion. In the case of the UK, for one example, uninterpreted public health statistics may contradict the common belief that obesity is reaching epidemic proportions [5]. More generally, average weight increases with age — so a population with an increasing proportion of older people will have a higher average weight, regardless of changes to diet or activity.

Secondly, since obesity is the correlate of a long list of factors which have significant health consequences in their own right, there may be no fact of the matter about which costs to attribute to obesity per se, and which are more properly costed to these co-factors. For one example, the proven relationship between obesity and low social status means that any group of obese persons' health outcomes will be significantly lowered by their average access to medical care, as a socioeconomic class, which will be, on average, lower than that of any non-obese control group.

Researchers from the U.S. Centers of Disease Control and Prevention in Atlanta[15] erroneously reported that approximately 400,000 US deaths annually were associated with poor diet and little exercise, and that if the trend continued, this would be 500,000 in 2005, overtaking smoking as the leading cause of death. These statistics are fiercely contested [6], and error was admitted by the CDC in November 2004 [7]. In particular, studies of this nature are normally unable to distinguish causes of death, so include many accidental deaths, murders etc., which ought not to be costed to obesity.

Canada and Europe are generally considered to be somewhat behind the United States in the trend towards overweight, with the rest of the world mixed. Some nations like Egypt, China and Mexico have also suffered from greatly increasing rates of obesity.

In March 2005 the International Obesity Task Force, a global coalition of obesity scientists and research centres advising the European Union, estimated that Finland, Germany, Greece, Cyprus, the Czech Republic, Slovakia, and Malta have exceeded the United States figure of 67% for overweight or obese males. The task force estimated in 2003 that about 200 m of the 350 m adults living in what is now the European Union may be overweight or obese [8].

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" [9]. 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 [10]. Not food regulation, but personal exercising, is moved as the solution.

The "public interest" advocate John Banzhaf has found a way to harness personal responsibility arguments to the public interest side of the debate in the U.S., via recent changes [11] to HMO regulations which enable health insurance providers to differentiate between obese and regular customers in their pricing. The "public interest" objective is that obese people will have to pay extra for their health maintenance, bringing "personal responsibility" to bear on their consumption choices. This new tactic is controversial itself — if a causal link pertains from low social status to obesity (see above), the net effect will be increased costs for low income members of HMOs, particularly ethnic minorities, and reduced costs for slim, middle class white members.

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.

Prevalence of obesity in American children

A recent study [16] has shown the prevalence of obesity in children in the United States in 1999 to 2000 to be as follows:

  • Ages 2 to 5 - Boys 9.9%, Girls 11%
  • Ages 6 to 11 - Boys 16%, Girls 14.5%
  • Ages 12 to 19 - Boys 15.5%, Girls 15.5%

A study conducted at the American Institute for Research of Dietary Habits found that by 2010, 21% of American children will be considered obese.

See also

References

  1. Quetelet LAJ (1871). Antropométrie ou Mesure des Différences Facultés de l'Homme. Brussels: Musquardt.
  2. World Health Orginization. Technical report series 894: "Obesity: preventing and managing the global epidemic.". Geneva: World Health Organization, 2000. PDF.
  3. 3.0 3.1 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.
  4. The Oxford English Dictionary (website)
  5. 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.
  6. Flier JS (2004). Obesity wars: molecular progress confronts an expanding epidemic. Cell 116 (2): 337-50. PMID 14744442.
  7. 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.
  8. Lopez R (2004). Urban sprawl and risk for being overweight or obese. Am J Public Health 94 (9): 1574-9. PMID 15333317.
  9. 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 �UNIQ7a61495550be8a28-HTMLCommentStrip12dc462fa1c106000000001
  10. 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.
  11. 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.
  12. 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.
  13. Campos, Paul (May 2004). The Obesity Myth, Gotham Books. ISBN 1592400663.
  14. Critser, Greg (January 2003). Fat Land: how Americans became the fattest people in the World, Houghton Miffin. ISBN 0618164723.
  15. Mokdad AH, Marks JS, Stroup DF, Gerberding JL (2004). Actual causes of death in the United States, 2000. JAMA 291 (10): 1238-45. PMID 15010446.
  16. Slyper AH (2004). The pediatric obesity epidemic: causes and controversies. J Clin Endocrinol Metab 89 (6): 2540-7. PMID 15181021.

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