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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. [4] [5]
16p11.2 deletion syndrome is a rare genetic condition caused by microdeletion on the short arm of chromosome 16. Most affected individuals experience global developmental delay and intellectual disability, as well as childhood-onset obesity. [1] 16p11.2 deletion is estimated to account for approximately 1% of autism spectrum disorder cases. [3] [4]
A genetic predisposition among East Asians is suggested. [9] The disease is more common in males, [25] with the male to female ratio at 1.4–2:1 (or about 5 men to 3 women). [4] The average onset of the disease is around age 40, and two-thirds of those affected are non-smokers, although smoking is not believed to be a cause. [7]
Monogenic obesity is excess weight caused by a mutation in a single gene, as opposed to syndromic obesity not tied to a single gene variation and most obesity, which is caused by multiple genetic and environmental risk factors. Monogenetic obesity mostly affects the hypothalamus and leptin–melanocortin system (see hypothalamic obesity ...
In medicine, genetic susceptibility to a disease refers to a genetic predisposition to a health problem, [1] which may eventually be triggered by particular environmental or lifestyle factors, such as tobacco smoking or diet. Genetic testing is able to identify individuals who are genetically predisposed to certain diseases.
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Absence of obesity (although overweight or obese people can get MODY) or other problems associated with type 2 diabetes or metabolic syndrome (e.g., hypertension, hyperlipidemia, polycystic ovary syndrome). [7] Insulin resistance very rarely happens. [8] Cystic kidney disease in patient or close relatives.
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 ...