Obesity

Obesity is a condition in which the natural energy reserve of humans or other mammals, which is stored in fat tissue, is expanded far beyond usual levels to the point where it impairs health. Obesity in wild animals is relatively rare, but it is common in domestic animals like pigs and household pets who may be overfed and underexercised. In humans it is considered a major challenge to health.

Causes

Causative factors

Obesity is generally a result of a combination of factors:

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• Genetic predisposition
• Limited exercise and sedentary lifestyle
• A high glycemic diet (i.e. a diet that consists of meals that give high postprandial blood sugar)
• Weight cycling, caused by repeated attempts to lose weight by dieting
• Underlying illness (e.g. hypothyroidism)
• An eating disorder (such as binge eating disorder)
• Stressful mentality (debated)
• Insufficient sleeping (debated)

As with many medical conditions, obesity develops due to a combination between genetic and environmental factors. Polymorphisms in various genes controlling appetite, rate of metabolism, and adipokine release predispose to obesity, but the condition, to some extent, requires availability of sufficient calories and/or limited exercise, 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 these are absent in most people with obesity. It is presumed that a large proportion of the causative genes are still to be identified.

Related Topics:
Polymorphism - Gene - Appetite - Metabolism - Adipokine - Prader-Willi syndrome - Leptin

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Some eating disorders can lead to 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 satisfaction, something that is normally learnt in childhood. Learning theory suggests that early childhood conceptions may lead to an association between food and a calm mental state.

Related Topics:
Binge eating disorder - Substance abuse - Learning theory

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Some recent research has suggested that some human obesity may be caused by a viral infection. The adenovirus vectors AD-36 and AD-37 have been identified as a cause of obesity in animals and as potential stimulants on human preadipocytes{{mn|Vangipuram|3}}. While these viruses occur in humans, there is no clear evidence that their presence leads to in increased risk of obesity.

Related Topics:
Viral - Infection - Adenovirus - AD-36 - Preadipocytes

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Evolutionary aspects

Although there is no definitive explanation for the recent increase of obesity, the evolutionary hypothesis comes closest to providing 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. This is precisely the opposite of what is required in a sedentary society, where high-energy food is available in abundant quantities in the context of decreased exercise. Although many people may have a genetic propensity towards obesity, it is only with the reduction in physical activity and a move towards high-calorie diets of modern society that it has become widespread.

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Neurobiological mechanisms

Flier{{mn|ref|4}} 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 proposed that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, development of insulin resistance, and possible ways of interfering with these mechanisms. 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.

Related Topics:
Pathophysiological - Leptin - 1994 - Appetite - Adipose tissue - Insulin resistance - Ghrelin - Orexin - PYY 3-36 - Cholecystokinin - Adiponectin - Adipokine

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Leptin and ghrelin are considered to be complementary in their influence on appetite, with the stomach producing ghrelin when relatively empty and leptin being produced by adipose tissue when satiated with nutrients. Resistance to the leptin signal and causes for this resistance have been implicated in dysregulation of appetite, although administration of leptin has not proven to be a feasible way of suppressing appetite in humans.

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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.

Related Topics:
Neuroscientific - Hypothalamus - Lesion studies

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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.

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Societal causes

While it may often be 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 who is obese, they cannot explain why one culture grows fatter than another.

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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 1960 almost the entire population was well fed, but not overweight. 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.

Related Topics:
United States - Second World War - 1960 - 1980 - Public health

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

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• 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{{mn|Levine|5}}.
• 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 commercials seen by the average child increased greatly, and a large proportion of these were for fast food and candy.
• 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 unhealthy 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 where 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{{mn|Lopez|6}}.
• 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 likely 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 http://www.iotf.org/. 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 http://www.cdc.gov/brfss/.

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.

Related Topics:
Exercise - Diet

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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{{mn|Zagorsky|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.

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