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Like many other medical conditions, obesity is the result of an interplay between environmental and genetic factors. [2] [3] Studies have identified variants in several genes that may contribute to weight gain and body fat distribution; although, only in a few cases are genes the primary cause of obesity.
Scientists from the University of Exeter Medical School have found that people missing a specific blood group due to a genetic variant may be genetically predisposed to having obesity or overweight.
This particular genetic finding doesn’t apply to a large population of people with obesity — only about 1 in 5,000 people have this genetic makeup, Frontini said.
“Obesity is a worldwide epidemic that is an increasing issue and burden to society, ... “Having a genetic predisposition to either skinny or overweight does not mean that this cannot be ...
Fat mass and obesity-associated protein also known as alpha-ketoglutarate-dependent dioxygenase FTO is an enzyme that in humans is encoded by the FTO gene located on chromosome 16. As one homolog in the AlkB family proteins, it is the first messenger RNA (mRNA) demethylase that has been identified. [ 5 ]
The main problem with this idea is the timing at which the transition is presumed to have happened, and how this would then translate into the genetic predisposition to type 2 diabetes and obesity [citation needed]. For example, the decline in reproductive investment in human societies (the so-called r to K shift) has occurred far too recently ...
Some people’s genetics predispose them to obesity. But nature is not destiny. Here are five tips for losing weight.
Set point theory does not on its own explain why body mass index for humans, measured as a proxy for fat, tends to change with increasing age or why obesity levels in a population vary depending on socioeconomic or environmental factors (or why weight tends to change for an individual when socioeconomic status and environment change).
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