Obesity: Encyclopedia II - Obesity - Causes

Obesity - Causes

Obesity - Causative factors

When 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 lbs 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 lbs 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:

• Sedentary lifestyle
• Genetic factors
• 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)
• Genetic disorders (e.g. Prader-Willi syndrome)
• Eating disorders (such as binge eating disorder)
• Stressful mentality
• Insufficient sleep
• Psychotropic medications
• Smoking cessation

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 satisfaction, 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.

Obesity - 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.

Obesity - Neurobiological mechanisms

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.

Obesity - 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 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^[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 [1]. 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 [2].

• 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.

Obesity - 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.

Adapted from the Wikipedia article "Causes", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki