BACKGROUND: Associations between dairy intake and body mass index (BMI) have been inconsistently observed in epidemiological studies, and the causal relationship remains ill defined. METHODS: We performed Mendelian randomization (MR) analysis using an established dairy intake-associated genetic polymorphism located upstream of the lactase gene (LCT- 13910 C/T, rs4988235) as an instrumental variable (IV). Linear regression models were fitted to analyze associations between (a) dairy intake and BMI, (b) rs4988235 and dairy intake, and (c) rs4988235 and BMI in each study. The causal effect of dairy intake on BMI was quantified by IV estimators among 184802 participants from 25 studies. RESULTS: Higher dairy intake was associated with higher BMI (β = 0.03 kg/m2 per serving/day; 95% CI, 0.00- 0.06; P=0.04), whereas the LCT genotype with 1 or 2 T allele was significantly associated with 0.20 (95% CI, 0.14-0.25) serving/day higher dairy intake (P=3.15 x 1012) and 0.12 (95% CI, 0.06-0.17) kg/m2 higher BMI (P = 2.11 x 105,). MR analysis showed that the genetically determined higher dairy intake was significantly associated with higher BMI (β = 0.60 kg/m2 per serving/day; 95% CI, 0.27- 0.92; P = 3.0 x 104). CONCLUSIONS: The present study provides strong evidence to support a causal effect of higher dairy intake on increased BMI among adults.
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Acknowledgments: The authors thank the staff and participants of the ARIC study for their important contributions. The authors thank the study participants, the staff from the Rotterdam Study and the participating general practitioners and pharmacists. The authors also acknowledge the funding agencies supporting the Northern Sweden Diet Database and the Västerbotten Intervention Project, including the Swedish Research Council. The authors thank Ville Aalto, Irina Lisi-nen, and Mika Helminen for their expert technical assistance in the statistical analyses. The PREDIMED-Valencia study also acknowledges the collaborative support provided by the Real Colegio Complutense at Harvard University. The authors thank the Raine Study participants and their families, as well as the Raine Study research staff for cohort coordination and data collection. The authors thank the NH&MRC for their long-term funding to the study during the past 25 years and also the following institutes for providing funding for Core Management of the Raine Study: The University of Western Australia (UWA), Curtin University, the Raine Medical Research Foundation, the UWA Faculty of Medicine, Dentistry and Health Sciences, the Telethon Kids Institute, the Women’s and Infants’ Research Foundation (King Edward Memorial Hospital), and Edith Cowan University. The authors thank the Western Australian DNA Bank (National Health and Medical Research Council of Australia National Enabling Facility)
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