A 1680 painting by Juan Carreño de Miranda of a girl presumed to have Prader-Willi syndrome[1]
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]
Polymorphisms in various genes controlling appetite and metabolism predispose to obesity under certain dietary conditions. The percentage of obesity that can be attributed to genetics varies widely, depending on the population examined, from 6% to 85%,[6] with the typical estimate at 50%. It is likely that in each person a number of genes contribute to the likelihood of developing obesity in small part, with each gene increasing or decreasing the odds marginally, and together determining how an individual responds to the environmental factors.[7] As of 2006, more than 41 sites on the human genome have been linked to the development of obesity when a favorable environment is present.[8] Some of these obesogenic (weight gain) or leptogenic (weight loss) genes may influence the obese individual's response to weight loss or weight management.[9]
^Mary Jones. "Case Study: Cataplexy and SOREMPs Without Excessive Daytime Sleepiness in Prader Willi Syndrome. Is This the Beginning of Narcolepsy in a Five Year Old?". European Society of Sleep Technologists. Retrieved April 6, 2009.
^Albuquerque D, Stice E, et al. (Mar 2015). "Current review of genetics of human obesity: from molecular mechanisms to an evolutionary perspective". Mol. Genet. Genomics. 290 (4): 1191–221. doi:10.1007/s00438-015-1015-9. hdl:10316/45814. PMID 25749980. S2CID 3238210.
^Albuquerque, David; Nóbrega, Clévio; Manco, Licínio; Padez, Cristina (7 July 2017). "The contribution of genetics and environment to obesity". British Medical Bulletin. Advance articles (1): 159–173. doi:10.1093/bmb/ldx022. PMID 28910990.
^Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrinology). Totowa, NJ: Humana Press. p. 158. ISBN 978-1-59745-400-1. Retrieved April 5, 2009.
^Yang W, Kelly T, He J (2007). "Genetic epidemiology of obesity". Epidemiol Rev. 29: 49–61. doi:10.1093/epirev/mxm004. PMID 17566051.
^Lyon, Helen N; Hirschhorn, Joel N (2005-07-01). "Genetics of common forms of obesity: a brief overview". The American Journal of Clinical Nutrition. 82 (1): 215S–217S. doi:10.1093/ajcn/82.1.215S. ISSN 0002-9165.
^Poirier P, Giles TD, Bray GA, et al. (May 2006). "Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss". Arterioscler. Thromb. Vasc. Biol. 26 (5): 968–76. CiteSeerX 10.1.1.508.7066. doi:10.1161/01.ATV.0000216787.85457.f3. PMID 16627822. S2CID 6052584.
^Hainer, Vojtĕch; Hermann Toplak; Asimina Mitrakou (February 2008). "Treatment Modalities of Obesity: What fits whom?". Diabetes Care. 31: 269–277. doi:10.2337/dc08-s265. PMID 18227496.
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