TY - JOUR
T1 - Dairy intake and body composition and cardiometabolic traits among adults
T2 - Mendelian randomization analysis of 182041 individuals from 18 studies
AU - Mendelian Randomization of Dairy Consumption Working Group
AU - Huang, Tao
AU - Sun, Dianjianyi
AU - Heianza, Yoriko
AU - Bergholdt, Helle K.M.
AU - Gao, Meng
AU - Fang, Zhe
AU - Ding, Ming
AU - Frazier-Wood, Alexis C.
AU - North, Kari E.
AU - Marouli, Eirini
AU - Graff, Mariaelisa
AU - Smith, Caren E.
AU - Varbo, Anette
AU - Lemaitre, Rozenn N.
AU - Corella, Dolores
AU - Wang, Carol A.
AU - Tjønneland, Anne
AU - Overvad, Kim
AU - Sørensen, Thorkild I.A.
AU - Feitosa, Mary F.
AU - Wojczynski, Mary K.
AU - Kähönen, Mika
AU - Mikkilä, Vera
AU - Bartz, Traci M.
AU - Psaty, Bruce M.
AU - Siscovick, David S.
AU - Danning, Rebecca D.
AU - Dedoussis, George
AU - Pedersen, Oluf
AU - Hansen, Torben
AU - Havulinna, Aki S.
AU - Männistö, Satu
AU - Rotter, Jerome I.
AU - Sares-Jäske, Laura
AU - Allison, Mathew A.
AU - Rich, Stephen S.
AU - Sorlí, Jose V.
AU - Coltell, Oscar
AU - Pennell, Craig E.
AU - Eastwood, Peter
AU - Ridker, Paul M.
AU - Viikari, Jorma
AU - Raitakari, Olli
AU - Lehtimäki, Terho
AU - Helminen, Mika
AU - Wang, Yujie
AU - Deloukas, Panagiotis
AU - Knekt, Paul
AU - Kanerva, Noora
AU - Kilpeläinen, Tuomas O.
AU - Province, Michael A.
AU - the CHARGE consortium
AU - Mozaffarian, Dariush
AU - Chasman, Daniel I.
AU - Nordestgaard, Børge G.
AU - Ellervik, Christina
AU - Qi, Lu
PY - 2019/6/1
Y1 - 2019/6/1
N2 - BACKGROUND: Associations between dairy intake and body composition and cardiometabolic traits have been inconsistently observed in epidemiological studies, and the causal relationship remains ill-defined. METHODS: We performed Mendelian randomization analysis using an established genetic variant located upstream of the lactase gene (LCT-13910 C/T, rs4988235) associated with dairy intake as an instrumental variable (IV). The causal effects of dairy intake on body composition and cardiometabolic traits (lipids, glycemic traits, and inflammatory factors) were quantified by IV estimators among 182041 participants from 18 studies. RESULTS: Each 1 serving/day higher dairy intake was associated with higher lean mass [β (SE) = 0.117 kg (0.035); P = 0.001], higher hemoglobin A1c [0.009% (0.002); P < 0.001], lower LDL [-0.014 mmol/L (0.006); P = 0.013], total cholesterol (TC) [-0.012 mmol/L (0.005); P = 0.023], and non-HDL [-0.012 mmol/L (0.005); P = 0.028]. The LCT-13910 C/T CT + TT genotype was associated with 0.214 more dairy servings/day (SE = 0.047; P < 0.001), 0.284 cm higher waist circumference (SE = 0.118; P = 0.017), 0.112 kg higher lean mass (SE = 0.027; P = 3.8 × 10-5), 0.032 mmol/L lower LDL (SE = 0.009; P = 0.001), and 0.032 mmol/L lower TC (SE = 0.010; P = 0.001). Genetically higher dairy intake was associated with increased lean mass [0.523 kg per serving/day (0.170); P = 0.002] after correction for multiple testing (0.05/18). However, we find that genetically higher dairy intake was not associated with lipids and glycemic traits. CONCLUSIONS: The present study provides evidence to support a potential causal effect of higher dairy intake on increased lean mass among adults. Our findings suggest that the observational associations of dairy intake with lipids and glycemic traits may be the result of confounding.
AB - BACKGROUND: Associations between dairy intake and body composition and cardiometabolic traits have been inconsistently observed in epidemiological studies, and the causal relationship remains ill-defined. METHODS: We performed Mendelian randomization analysis using an established genetic variant located upstream of the lactase gene (LCT-13910 C/T, rs4988235) associated with dairy intake as an instrumental variable (IV). The causal effects of dairy intake on body composition and cardiometabolic traits (lipids, glycemic traits, and inflammatory factors) were quantified by IV estimators among 182041 participants from 18 studies. RESULTS: Each 1 serving/day higher dairy intake was associated with higher lean mass [β (SE) = 0.117 kg (0.035); P = 0.001], higher hemoglobin A1c [0.009% (0.002); P < 0.001], lower LDL [-0.014 mmol/L (0.006); P = 0.013], total cholesterol (TC) [-0.012 mmol/L (0.005); P = 0.023], and non-HDL [-0.012 mmol/L (0.005); P = 0.028]. The LCT-13910 C/T CT + TT genotype was associated with 0.214 more dairy servings/day (SE = 0.047; P < 0.001), 0.284 cm higher waist circumference (SE = 0.118; P = 0.017), 0.112 kg higher lean mass (SE = 0.027; P = 3.8 × 10-5), 0.032 mmol/L lower LDL (SE = 0.009; P = 0.001), and 0.032 mmol/L lower TC (SE = 0.010; P = 0.001). Genetically higher dairy intake was associated with increased lean mass [0.523 kg per serving/day (0.170); P = 0.002] after correction for multiple testing (0.05/18). However, we find that genetically higher dairy intake was not associated with lipids and glycemic traits. CONCLUSIONS: The present study provides evidence to support a potential causal effect of higher dairy intake on increased lean mass among adults. Our findings suggest that the observational associations of dairy intake with lipids and glycemic traits may be the result of confounding.
KW - dairy intake
KW - Dairy Consumption
KW - body composition
KW - cardiometabolic traits
KW - Mendelian randomization analysis
KW - lactase gene
UR - http://www.scopus.com/inward/record.url?scp=85066443315&partnerID=8YFLogxK
U2 - 10.1373/clinchem.2018.300335
DO - 10.1373/clinchem.2018.300335
M3 - Article
C2 - 31138550
AN - SCOPUS:85066443315
VL - 65
SP - 751
EP - 760
JO - Clinical Chemistry
JF - Clinical Chemistry
SN - 0009-9147
IS - 6
ER -