Doing a better job of explaining obesity in terms of genes and environment factors could help encourage people who are trying to reach and maintain a healthy weight. Health care practitioners routinely collect family health history to help identify people at high risk of obesity-related diseases such as diabetes, cardiovascular diseases, and some forms of cancer.
Family health history reflects the effects of shared genetics and environment among close relatives. Those changes can improve the health of family members—and improve the family health history of the next generation. Skip directly to site content Skip directly to page options Skip directly to A-Z link. Section Navigation. Facebook Twitter LinkedIn Syndicate. Behavior, environment, and genetic factors all have a role in causing people to be overweight and obese.
Minus Related Pages. Links with this icon indicate that you are leaving the CDC website. Regulation of body composition It is important to understand that it is regulation of body composition itself that appears to be under genetic control. Syndromic obesity Obesity is sometimes part of a rare but recognised syndrome characterised by cognitive delay, dysmorphic features and organ-specific abnormalities. These can be identified in children: Prader—Willi syndrome , an imprinting disorder, is the most common, occurring at a rate of one in 15, Over the first two years, the infant slowly develops a ravenous appetite, and has cognitive delay and behavioural issues.
It is an imprinting defect, in the region of chromosome 15q11— A variant of the Fragile X syndrome has also been described that has features of Prader—Willi syndrome, with severe obesity developing early. It has so far been mapped to 19 different genes. The GNAS gene mutation results in resistance to hormones such as parathormone, thyroid hormone and gonadotrophins. WAGR syndrome 11p14 deletions leading to brain-derived neurotrophic factor haploinsufficiency is characterised by aniridia, obesity, growth retardation, cognitive delay and genitourinary deformities.
So far, this is in the research stage, but some progress has been made: Successful testing of an MC4R partial agonist for appetite normalisation and inhibition of compulsive eating has been reported in two patients with the genetic defect. However, there is a recent report of a mutation in a gene called KSR2 , which codes for a scaffolding protein that appears to be associated with a lower metabolic rate. A promising early report suggests that metformin may be beneficial in reversing the defect in KSR2 carriers, but more studies are needed.
Early lifestyle advice including regular activity may prevent or delay the onset of lifetime weight problems. Physicians should not add more blame or guilt.
Early-onset hyperphagia and obesity in children should be regarded as a flag to consider specialist referral, especially for those with a positive family history or syndromic features, such as cognitive problems, growth disorders or developmental delay.
Early treatment can prevent severe obesity and help with family counselling. Patients are interested in knowing about any predisposing genetic findings. Provenance and peer review: Commissioned, externally peer reviewed. Obes Res Clin Pract ;9 6 — Public Health Nutr ;18 17 — The hunger genes: Pathways to obesity: Review. Cell ;— Genetic influences on central abdominal fat: A twin study. Overweightness, obesity and arterial stiffness in healthy subjects: A systematic review and meta-analysis of literature studies.
Postgrad Med ; 2 — Probability of an obese person attaining normal body weight: Cohort study using electronic health records.
Am J Public Health ;e54— Heritability of body size and muscle strength in young adulthood: A study of one million Swedish men. Genet Epidemiol ;32 4 — Future management of human obesity: Understanding the meaning of genetic susceptibility. Advances in Genomics and Genetics ;— A twin study of human obesity.
JAMA ; 1 — Genetic effects in human energy expenditure components. Int J Obes ;14 Suppl 1 —55; discussion 55— Genetic, molecular and physiological mechanisms involved in human obesity: Society for Endocrinology Medal Lecture Clin Endocrinol Oxf ;82 1 — Recent progress in genetics, epigenetics and metagenomics unveils the pathophysiology of human obesity.
Clinical Science ;— Segregation of a latent high adiposity phenotype in families with a history of type 2 diabetes mellitus implicates rare obesity-susceptibility genetic variants with large effects in diabetes-related obesity. In the presence of readily accessible food, those with the fat mass and obesity-associated gene may have challenges limiting their caloric intake.
The presence of this gene and other genes can cause:. While testing for genetic defects in children for early childhood obesity may be considered, testing for genetic forms of obesity in adults is of limited value. Testing for the FTO gene and other genes can be performed practically, but it is not very helpful because the treatment interventions are the same for individuals with and without the FTO gene.
Knowing your family history can help you understand your risk for obesity and obesity-related conditions like diabetes and heart disease.
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