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Causes of obesity and its role in the evolution

In ancient times the individuals with greater adipose reserves had more chances to survive the periods of famine than those with lesser reserves. That is why the ability of organism to store excessive energy during the rare periods of abundance as an adipose tissue was cultivated by nature. Once a symbol of health and prosperity, today an excessive weight is associated with diseases and poverty.

Some obesity conditions are resistant to the theory that the epidemic of adiposity is a new tendency. For example, a class co-factor in mentioned time and again in many papers. Comparing net significance with BMI scores, a 2004 study found out that overweight American subjects are roughly half as prosperous as lean ones. When income differentials were calculated, the bias remained - slender subjects were inheriting more capital than stout ones. Another revise finds women who married into higher status are leaner than ladies who married into lower status.

Notwithstanding the fact that obesity usually causes cardio-vascular and other diseases, the amount of fat people rises. What are the possible reasons that cause obesity? Let's look at them closer.

When the energy that comes with food is not spent during the periods of physical activity, than fat, muscle and liver cells store it as fat. Obesity occurs when the amount of consumed energy exceeds the amount of the energy being spent.

The excess energy utilized by an individual to make fat reserves is closely connected to the total number of absorbed calories. This means that the slightest changes in the energy balance can result in instability in weight later on. For example, a stout 40 year old man with 100 lb of adipose tissue consumes about 25 more calories per day than he averagely spends - the equivalent of an apple eaten once per three days. Compare with a slender 40-year-old carrying only 15 lb of fat who will have exceeded his daily life energy expenditure by four calories per day - the equivalent of an apple eaten once every 18 days.

There are some factors that are generally considered to be causes of obesity including the following ones:

• Genetic disorders and factors of inheritance (like Prader-Willy syndrome)
• Latent illness (like Hypothyroidism)
• Some medications (like uncharacteristic antipsychotics)
• Motionless lifestyle
• Certain diet (dishes giving high postprandial blood sugar)
• Regular attempts to lose weight leading to weight cycling
• Chaotic ingestion of food (like binge eating disorder)
• Nervous instability
• Sleep deficit
• Giving up smoking

Like many other diseases, obesity often originates from a combination of environmental and genetic factors. Obesity is determined by metabolism, polymorphisms in various gånås controlling appetite and a release of adipokine. Nevertheless obesity requires a sufficient amount of calories to develop fully. Different genetic divergences that predispose to obesity have been defined (like leptin receptor mutations and Prader-Willi syndrome), but well-known single-locus genetic changes have been registered in only about 5% of obese patients. While it is considered that a great deal of the causative genes are still to be found, many cases of obesity can be the result of contact between multiple genes, though non-genetic factors are important as well.

Some eating derangements are closely connected with obesity, for example binge eating disorder (BED). As it can be derived from the term, patients suffering this disorder are disposed to overeat, especially in binges. Food calms some individuals and they abuse this calming effect. Interestingly enough, BED patients often fail to recognize satiety and hunger, an ability that is usually learned in childhood. An association between food and a state of satisfaction and mental calm can be a result of early childhood conceptions.

Mechanisms in detail

Animal models like mice are widely used by scientists investigating the mechanisms and treatment of obesity to conduct experiments.

Many pathophysiological processes taking part in the development and maintenance of adiposity are summarized by Flier. This branch of knowledge had been almost untouched until leptin was discovered in 1994. Since then, many other hormonal mechanisms involved in the regulation of appetite and food intake, development of insulin resistance and storage patterns of adipose tissue have been identified. Many mediators like cholecystokinin, orexin, adiponectin, PYY 3-36, ghrelin etc. have been studied. Adipose tissue produces the mediators called adipokines; they are believed to modify many obesity-related diseases.

Ghrelin and Leptin are thought to influence appetite complementary, with ghrelin secreted by the stomach performing short-term appetitive control (that is to eat when the stomach is void and to cease when the stomach is full). Leptin is worked out by adipose tissue to signalize fat storage reserves in the organism, and is responsible for long-term appetitive controls (this means to eat more when fat storages are exhausted and eat less when fat storages are sufficient). Although taking in leptin may be effective for a small part of obese individuals who are lacking leptin, many more obese individuals are believed to be leptin-resistant, and this resistance leads to obesity in some cases, is thought to explain in part why intake of leptin was not effective in suppressing appetite in most obese patients.

Neuroscientific means are influenced by the action of the abovementioned mediators on the hypothalamus, the part of the brain that is believed to process signals related to energy storage and metabolic state and to move the energy balance in either a positive or negative direction, first and foremost by affecting appetite and expenditure of energy. Scientific studies in the 1940s and 1950s marked off two areas of the hypothalamus - the ventromedial hypothalamus (VMH) and lateral hypothalamus (LH)- as the brain's centers of satiety and hunger, respectively. Specific lesions to a LH of a mouse suppressed its appetite while bringing damage to the VMH caused overeating.

Studies of the expansion of the receptor of leptin in the mid-1990s shook the theory of dual center of hunger and satiety. Leptin's influence on the arcuate nucleus melanocortin system is now considered the most important to the regulation of metabolism and feeding.