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Obesity is often considered to be the outcome of a unhealthy lifestyle with little exercise, too much binge eating, and a lack of self control. This may be true to an extent, but not completely. Obesity is not the result of poor lifestyle choices only. Its development may also be accelerated by a number of environmental as well as genetic factors.
Genetics And Obesity
Researchers studied genetic influences on body weight management for many decades, but still there are a lot of things we don’t know about or have to study further. These days, experts are sure that obesity has a polygenic cause, meaning there is more than one gene which influences the obesity in an individual.
Recent research related to obesity and consumption of certain foods brings more clarity into our understanding of the interaction between food, obesity, and genes. It is proven now beyond any reasonable doubts that genetic factors are not the only ones that contribute to the risk of obesity. Many individuals who carry the known "obesity genes" do not become overweight.
Fat Mass And Obesity-Associated Gene
The first obesity-related gene variant was found in 2007 and was named the "fat mass and obesity-associated" (FTO) gene. The gene is located on chromosome 16. This FTO gene produces a protein that is related to the control of appetite as well as the level of satiety. There are several alleles (forms) of this gene. Different alleles of the FTO gene were found to be positively correlated with weight gain in a person, individual insulin sensitivity, body fat distribution and energy intake and expenditure. But it may be possible to reduce the genetic obesity risks by changing eating patterns, and adopting healthy lifestyle habits like regular physical exercises, and being vigilant about food choices.
In a study conducted on 2000 individuals, the participants underwent genotyping and were asked to complete a questionnaire about their eating habits over a period of six months. The researchers focused on whether the genetic markers influenced an individual’s diet. The results showed that variations in FTO gene were related to number of meals or snacks per day and to the increased servings of fat, oil and sweet stuff in the diet.
Brain-Derived Neurotrophic Factor
A number of variations found in another gene, BDNF (brain derived neurotrophic factor), were related to an elevated consumption of dairy, eggs, meat and nuts in different individuals. The individuals with these genetic versions of BDNF gene also consumed approximately 100 more calories per day thus affecting their overall weight.
Mice and humans have similar obesity genetic signatures. This fact allows to extrapolate the findings from mice experiments to humans, at least to a certain degree. One such experiment reveals how much our weight can indeed be controlled by genes. The experiment involved placing large group of mice on a controlled identical diet over long period of time. The animals were on a normal diet for the first eight weeks of life and were subsequently switched to a high-fat and high-carbohydrate diet for the following eight weeks.
Most of the mice, however, increased their body fat to a certain varying degree during the first four weeks of unhealthy diet and then did not gain any additional weight. This clearly suggested a presence of specific point after which the body fat gain is resisted by the genetic mechanisms. The exact weight at which this point is reached is specific to every animal. We may assume that something similar might be at work in humans.