Genetics of Obesity in Humans | Endocrine Reviews | Oxford Academic

Considerable attention has focused on deciphering the hypothalamic pathways that mediate the behavioral and metabolic effects of leptin. We and others have iden

Source: https://academic.oup.com/edrv/article/27/7/710/2355201

On the Futility of Screening for Genes That Make You Fat

This article has been cited by other articles in PMC.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3206018/

Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies | The BMJ

Objective To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity. Design Prospective cohort study. Setting Health professionals in the United States. Participants 9623 women from the Nurses’ Health Study, 6379 men from the Health Professionals Follow-up Study, and a replication cohort of 21 421 women from the Women’s Genome Health Study. Main outcome measure Repeated measurement of BMI over follow-up. Results There was an interaction between fried food consumption and a genetic risk score based on 32 BMI-associated variants on BMI in both the Nurses’ Health Study and Health Professionals Follow-up Study (P≤0.001 for interaction). Among participants in the highest third of the genetic risk score, the differences in BMI between individuals who consumed fried foods four or more times a week and those who consumed fried foods less than once a week amounted to 1.0 (SE 0.2) in women and 0.7 (SE 0.2) in men, whereas the corresponding differences were 0.5 (SE 0.2) and 0.4 (SE 0.2) in the lowest third of the genetic risk score. The gene-diet interaction was replicated in the Women’s Genome Health Study (P<0.001 for interaction). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.1 (SE 0.2), 1.6 (SE 0.3), and 2.2 (SE 0.6) for fried food consumption less than once, one to three times, and four or more times a week (P<0.001 for interaction); and the odds ratios (95% confidence intervals) for obesity per 10 risk alleles were 1.61 (1.40 to 1.87), 2.12 (1.73 to 2.59), and 2.72 (2.12 to 3.48) across the three categories of consumption (P=0.002 for interaction). In addition, the variants in or near genes highly expressed or known to act in the central nervous system showed significant interactions with fried food consumption, with the FTO (fat mass and obesity associated) variant showing the strongest result (P<0.001 for interaction). Conclusion Our findings suggest that consumption of fried food could interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity.

Source: https://www.bmj.com/content/348/bmj.g1610

Genes Are Not Destiny | Obesity Prevention Source | Harvard T.H. Chan School of Public Health

Obesity-Promoting Genes in an Obesity-Promoting World Genes influence every aspect of human physiology, development, and adaptation. Obesity is no exception. Yet relatively little is known regardin…

Source: https://www.hsph.harvard.edu/obesity-prevention-source/obesity-causes/genes-and-obesity/

Genetics of Obesity: What have we Learned?

Candidate gene and genome-wide association studies have led to the discovery of nine loci involved in Mendelian forms of obesity and 58 loci contributing to polygenic obesity. These loci explain a small fraction of the heritability for obesity and many ...

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137002/

The Genetics of Obesity

Obesity is a result of excess body fat accumulation. This excess is associated with adverse health effects such as CVD, type 2 diabetes, and cancer. The development of obesity has an evident environmental contribution, but as shown by heritability estimates ...

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955913/