Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies.
Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies.
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DOI:
10.1136/bmj.g1610
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发表时间:
2014-03-19
期刊:
影响因子:
--
通讯作者:
Qi L
中科院分区:
文献类型:
--
作者:
Qi Q;Chu AY;Kang JH;Huang J;Rose LM;Jensen MK;Liang L;Curhan GC;Pasquale LR;Wiggs JL;De Vivo I;Chan AT;Choi HK;Tamimi RM;Ridker PM;Hunter DJ;Willett WC;Rimm EB;Chasman DI;Hu FB;Qi L
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.
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影响因子:
8
作者:
Bowman, SA;Gortmaker, SL;Ludwig, DS
通讯作者:
Ludwig, DS
影响因子:
5.8
作者:
Greenfield, JR;Samaras, K;Campbell, LV
通讯作者:
Campbell, LV
影响因子:
37.8
作者:
Lutsey, Pamela L.;Steffen, Lyn M.;Stevens, June
通讯作者:
Stevens, June
DOI:
10.1056/nejmoa1014296
发表时间:
2011-06-23
期刊:
The New England journal of medicine
影响因子:
--
作者:
Mozaffarian D;Hao T;Rimm EB;Willett WC;Hu FB
通讯作者:
Hu FB
影响因子:
16.2
作者:
Ahmad T;Lee IM;Paré G;Chasman DI;Rose L;Ridker PM;Mora S
通讯作者:
Mora S