Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies (original) (raw)

1. Research
2. Fried food consumption...
3. Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies

Research BMJ 2014;348 doi: https://doi.org/10.1136/bmj.g1610 (Published 19 March 2014) Cite this as: BMJ 2014;348:g1610

1. Qibin Qi, assistant professor12,
2. Audrey Y Chu, research fellow3,
3. Jae H Kang, assistant professor4,
4. Jinyan Huang, research fellow5,
5. Lynda M Rose, statistician3,
6. Majken K Jensen, assistant professor1,
7. Liming Liang, assistant professor5,
8. Gary C Curhan, professor45,
9. Louis R Pasquale, associate professor46,
10. Janey L Wiggs, associate professor6,
11. Immaculata De Vivo, associate professor45,
12. Andrew T Chan, associate professor47,
13. Hyon K Choi, professor48,
14. Rulla M Tamimi, associate professor45,
15. Paul M Ridker, professor3910,
16. David J Hunter, professor145,
17. Walter C Willett, professor145,
18. Eric B Rimm, associate professor145,
19. Daniel I Chasman, associate professor310,
20. Frank B Hu, professor145,
21. Lu Qi, assistant professor14
22. 1Department of Nutrition, Harvard School of Public Health, Boston, MA, USA
23. 2Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA
24. 3Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
25. 4Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
26. 5Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA
27. 6Department of Ophthalmology, Mass Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA
28. 7Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
29. 8Section of Rheumatology and Clinical Epidemiology Unit, Boston University School of Medicine, Boston, MA, USA
30. 9Division of Cardiovascular Disease, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
31. 10Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
32. Correspondence to: L Qi, Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 nhlqi{at}channing.harvard.edu

• Accepted 31 January 2014

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.

Footnotes

• Contributors: QQ and LQ designed the study and wrote the first draft. QQ and AYC analyzed the data. JHK, MKJ, GCC, LRP, JLW, IDV, ATC, HKC, RMT, PMR, DJH, WCW, EBR, DIC, FBH, and LQ were involved in data collection. JH, LMR, and LL provided statistical expertise. All authors contributed to the interpretation of the results and critical revision of the manuscript for important intellectual content and approved the final version of the manuscript. QQ and LQ are guarantors.
• Funding: This study was supported by grants DK091718, HL071981, HL073168, CA87969, CA49449, CA055075, HL34594, HL088521, U01HG004399, DK080140, P30DK46200, U01CA137088, U54CA155626, DK58845, DK098311, U01HG004728, EY015473, CA134958, DK70756 and DK46200 from the National Institutes of Health, with additional support for genotyping from Merck Research Laboratories, North Wales, PA. The Women’s Genome Health Study is supported by HL043851, HL080467 and CA047988 from the National Institutes of Health, with collaborative scientific support and funding for genotyping provided by Amgen. LQ is a recipient of the American Heart Association Scientist Development Award (0730094N). LRP is supported by the Arthur Ashley Williams Foundation and a Harvard Ophthalmology Scholar Award (Harvard Medical School) from the Harvard Glaucoma Center of Excellence. ATC is a Damon Runyon Cancer Foundation Clinical Investigator. The funding sources had no role in the design or conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript.
• Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organization for the submitted work; no financial relationships with any organizations that might have an interest in the submitted work in the previous three years, no other relationships or activities that could appear to have influenced the submitted work.
• Ethical approval: The study protocol was approved by the institutional review boards of the Brigham and Women’s Hospital, and the Harvard School of Public Health. The completion of the self administered questionnaire was considered to imply informed consent.
• Data sharing: No additional data available.
• Transparency: The lead authors (the manuscript’s guarantors) affirm that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

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