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

Qibin Qi, Audrey Y. Chu, Jae H. Kang, Jinyan Huang, Lynda M. Rose, Majken K. Jensen, Liming Liang, Gary C. Curhan, Louis R. Pasquale, Janey L. Wiggs, Immaculata De Vivo, Andrew T. Chan, Hyon K. Choi, Rulla M. Tamimi, Paul M. Ridker, David J. Hunter, Walter C. Willett, Eric B. Rimm, Daniel I. Chasman, Frank B. HuLu Qi

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish (US)
Article numberg1610
JournalBMJ (Online)
Volume348
DOIs
StatePublished - Mar 19 2014

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Body Mass Index
Cohort Studies
Diet
Food
Genes
Obesity
Women's Health
Health
Alleles
Nurses
Genome
Men's Health
Adiposity
Genetic Predisposition to Disease
Central Nervous System
Fats
Odds Ratio
Outcome Assessment (Health Care)
Prospective Studies
Confidence Intervals

ASJC Scopus subject areas

  • Medicine(all)

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Fried food consumption, genetic risk, and body mass index : Gene-diet interaction analysis in three US cohort studies. / Qi, Qibin; Chu, Audrey Y.; Kang, Jae H.; Huang, Jinyan; Rose, Lynda M.; Jensen, Majken K.; Liang, Liming; Curhan, Gary C.; Pasquale, Louis R.; Wiggs, Janey L.; De Vivo, Immaculata; Chan, Andrew T.; Choi, Hyon K.; Tamimi, Rulla M.; Ridker, Paul M.; Hunter, David J.; Willett, Walter C.; Rimm, Eric B.; Chasman, Daniel I.; Hu, Frank B.; Qi, Lu.

In: BMJ (Online), Vol. 348, g1610, 19.03.2014.

Research output: Contribution to journalArticle

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 2014, 'Fried food consumption, genetic risk, and body mass index: Gene-diet interaction analysis in three US cohort studies', BMJ (Online), vol. 348, g1610. https://doi.org/10.1136/bmj.g1610
Qi, Qibin ; Chu, Audrey Y. ; Kang, Jae H. ; Huang, Jinyan ; Rose, Lynda M. ; Jensen, Majken K. ; Liang, Liming ; Curhan, Gary C. ; Pasquale, Louis R. ; Wiggs, Janey L. ; De Vivo, Immaculata ; Chan, Andrew T. ; Choi, Hyon K. ; Tamimi, Rulla M. ; Ridker, Paul M. ; Hunter, David J. ; Willett, Walter C. ; Rimm, Eric B. ; Chasman, Daniel I. ; Hu, Frank B. ; Qi, Lu. / Fried food consumption, genetic risk, and body mass index : Gene-diet interaction analysis in three US cohort studies. In: BMJ (Online). 2014 ; Vol. 348.
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title = "Fried food consumption, genetic risk, and body mass index: Gene-diet interaction analysis in three US cohort studies",
abstract = "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.",
author = "Qibin Qi and Chu, {Audrey Y.} and Kang, {Jae H.} and Jinyan Huang and Rose, {Lynda M.} and Jensen, {Majken K.} and Liming Liang and Curhan, {Gary C.} and Pasquale, {Louis R.} and Wiggs, {Janey L.} and {De Vivo}, Immaculata and Chan, {Andrew T.} and Choi, {Hyon K.} and Tamimi, {Rulla M.} and Ridker, {Paul M.} and Hunter, {David J.} and Willett, {Walter C.} and Rimm, {Eric B.} and Chasman, {Daniel I.} and Hu, {Frank B.} and Lu Qi",
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T1 - Fried food consumption, genetic risk, and body mass index

T2 - Gene-diet interaction analysis in three US cohort studies

AU - Qi, Qibin

AU - Chu, Audrey Y.

AU - Kang, Jae H.

AU - Huang, Jinyan

AU - Rose, Lynda M.

AU - Jensen, Majken K.

AU - Liang, Liming

AU - Curhan, Gary C.

AU - Pasquale, Louis R.

AU - Wiggs, Janey L.

AU - De Vivo, Immaculata

AU - Chan, Andrew T.

AU - Choi, Hyon K.

AU - Tamimi, Rulla M.

AU - Ridker, Paul M.

AU - Hunter, David J.

AU - Willett, Walter C.

AU - Rimm, Eric B.

AU - Chasman, Daniel I.

AU - Hu, Frank B.

AU - Qi, Lu

PY - 2014/3/19

Y1 - 2014/3/19

N2 - 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.

AB - 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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