Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies
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 t...
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| Published in | BMJ (Online) Vol. 348; no. mar19 1; p. g1610 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
British Medical Journal Publishing Group
19.03.2014
BMJ Publishing Group LTD BMJ Publishing Group Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0959-8138 1756-1833 1756-1833 |
| DOI | 10.1136/bmj.g1610 |
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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. |
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| AbstractList | To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity.
Prospective cohort study.
Health professionals in the United States.
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.
Repeated measurement of BMI over follow-up.
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).
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. 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. 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. To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity.OBJECTIVETo examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity.Prospective cohort study.DESIGNProspective cohort study.Health professionals in the United States.SETTINGHealth professionals in the United States.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.PARTICIPANTS9623 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.Repeated measurement of BMI over follow-up.MAIN OUTCOME MEASURERepeated measurement of BMI over follow-up.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).RESULTSThere 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).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.CONCLUSIONOur 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 | Pasquale, Louis R Hu, Frank B Qi, Lu Liang, Liming Rose, Lynda M Willett, Walter C Choi, Hyon K Curhan, Gary C Wiggs, Janey L Kang, Jae H Jensen, Majken K De Vivo, Immaculata Tamimi, Rulla M Qi, Qibin Ridker, Paul M Rimm, Eric B Chu, Audrey Y Chan, Andrew T Huang, Jinyan Hunter, David J Chasman, Daniel I |
| Author_xml | – sequence: 1 givenname: Qibin surname: Qi fullname: Qi, Qibin email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 2 givenname: Audrey Y surname: Chu fullname: Chu, Audrey Y email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 3 givenname: Jae H surname: Kang fullname: Kang, Jae H email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 4 givenname: Jinyan surname: Huang fullname: Huang, Jinyan email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 5 givenname: Lynda M surname: Rose fullname: Rose, Lynda M email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 6 givenname: Majken K surname: Jensen fullname: Jensen, Majken K email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 7 givenname: Liming surname: Liang fullname: Liang, Liming email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 8 givenname: Gary C surname: Curhan fullname: Curhan, Gary C email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 9 givenname: Louis R surname: Pasquale fullname: Pasquale, Louis R email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 10 givenname: Janey L surname: Wiggs fullname: Wiggs, Janey L email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 11 givenname: Immaculata surname: De Vivo fullname: De Vivo, Immaculata email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 12 givenname: Andrew T surname: Chan fullname: Chan, Andrew T email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 13 givenname: Hyon K surname: Choi fullname: Choi, Hyon K email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 14 givenname: Rulla M surname: Tamimi fullname: Tamimi, Rulla M email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 15 givenname: Paul M surname: Ridker fullname: Ridker, Paul M email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 16 givenname: David J surname: Hunter fullname: Hunter, David J email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 17 givenname: Walter C surname: Willett fullname: Willett, Walter C email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 18 givenname: Eric B surname: Rimm fullname: Rimm, Eric B email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 19 givenname: Daniel I surname: Chasman fullname: Chasman, Daniel I email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 20 givenname: Frank B surname: Hu fullname: Hu, Frank B email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA – sequence: 21 givenname: Lu surname: Qi fullname: Qi, Lu email: nhlqi@channing.harvard.edu organization: Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24646652$$D View this record in MEDLINE/PubMed |
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| Snippet | Objective To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity.Design... To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity. Prospective cohort... Objective To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity. Design... To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity.OBJECTIVETo examine... Objective To examine the interactions between genetic predisposition and consumption of fried food in relation to body mass index (BMI) and obesity. Design... |
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| SubjectTerms | Adipose tissue Adult Aged Alcohol Alleles Body fat Body mass Body Mass Index Cancer Central nervous system Chronic illnesses Cohort Studies Cooking Diabetes Diet Diet - adverse effects Diet - statistics & numerical data Family medical history Female Food Food consumption Gene-Environment Interaction Genetic Predisposition to Disease - etiology Genetic Predisposition to Disease - genetics Genomes Genotyping Techniques Health risk assessment Humans Lifestyles Male Medical personnel Mens health Middle Aged Nurses Nutrition research Obesity Obesity - etiology Obesity - genetics Prospective Studies Questionnaires Risk Factors Studies United States - epidemiology Validity Womens health |
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| Title | Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies |
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