Obesity, genetic risk, and environmentBMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g1900 (Published 19 March 2014) Cite this as: BMJ 2014;348:g1900
- Alexandra I F Blakemore, professor of human molecular genetics,
- Jessica L Buxton, research associate
- 1Section of Investigative Medicine, Division of Diabetes, Endocrinology, and Metabolism, Faculty of Medicine, Imperial College, London W12 0NN, UK
- Correspondence to:
The alarming global rise in prevalence of obesity is caused by unhealthy obesogenic environments. In westernised societies we are all exposed to calorie dense food, sedentary lives, stress, and sleep deficit. Some people seem relatively insensitive to these environmental pressures, while others are severely affected and become obese.
In a linked paper, Qi and colleagues (doi:10.1136/bmj.g1610) examined the interaction between common genetic variants associated with body mass index (BMI) and frequency of fried food consumption in over 37 000 people.1 The large study size was necessary to obtain adequate statistical power because the individual effects of these variants (single nucleotide polymorphisms, SNPs) on BMI are relatively subtle.2 The authors combined the weighted individual effects of 32 SNPs into a single “genetic risk score” for each participant.
As expected, participants who ate fried food more often tended to have higher BMI, and, independently, those with the highest genetic risk score also had higher BMI. The novel finding in this study is the observed interaction between genetic risk and fried food consumption: people in the highest risk groups for both had the …
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