ORCID Profile
0000-0002-3088-4375
Current Organisations
Boston Children's Hospital
,
IT University of Copenhagen
,
Harvard Medical School
,
Region Zealand
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Publisher: Oxford University Press (OUP)
Date: 06-2019
DOI: 10.1373/CLINCHEM.2018.300335
Abstract: Associations between dairy intake and body composition and cardiometabolic traits have been inconsistently observed in epidemiological studies, and the causal relationship remains ill-defined. 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. 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. 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.
Publisher: Oxford University Press (OUP)
Date: 2018
DOI: 10.1373/CLINCHEM.2017.280701
Abstract: Associations between dairy intake and body mass index (BMI) have been inconsistently observed in epidemiological studies, and the causal relationship remains ill defined. 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. 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 × 10−12) and 0.12 (95% CI, 0.06–0.17) kg/m2 higher BMI (P = 2.11 × 10−5). 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 × 10−4). The present study provides strong evidence to support a causal effect of higher dairy intake on increased BMI among adults.
Publisher: Elsevier BV
Date: 11-2018
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2008
DOI: 10.1161/CIRCGENETICS.108.773176
Abstract: Background— Whether mutations in the hemochromatosis (HFE) gene increase cardiovascular disease risk is still undetermined. The main reason is the low frequency of the mutations, in particular of the compound C282Y/H63D genotype. We combined the data of 11 observational studies for an in idual patient data meta-analysis. Methods and Results— In idual patient data were obtained from published as well as unpublished studies that had information available on the C282Y mutation as well as the H63D mutation in relation to coronary heart disease risk. In idual records were provided on each of the 53 880 participants in 11 studies. In total, 10 541 patients with coronary events were documented, of whom 5724 had an acute myocardial infarction. The crude and adjusted association between HFE genotypes and coronary events was examined by logistic regression analysis. We explored potential effect modification of the association between traditional cardiovascular risk factors and coronary events by HFE genotypes. After full adjustment, the odds ratio for coronary heart disease was 1.12 (95% CI, 0.92 to 1.37) for subjects with the compound heterozygous (C282Y/H63D) genotype relative to those with the wild-type/wild-type genotype. The odds ratios for C282Y/C282Y, C282Y/wild-type, H63D/H63D, and H63D/wild-type were 0.78 (95% CI, 0.49 to 1.26), 0.98 (95% CI, 0.90 to 1.07), 1.16 (95% CI, 0.97 to 1.38), and 1.07 (95% CI, 1.00 to 1.14), respectively. There was no evidence for effect modification. Conclusions— The results of this large in idual patient data meta-analysis do not support the view that HFE gene mutations are associated with an increased risk of coronary heart disease or acute myocardial infarction.
Publisher: BMJ
Date: 16-03-2017
DOI: 10.1136/BMJ.J1000
Publisher: American Medical Association (AMA)
Date: 20-09-2019
Publisher: Springer Science and Business Media LLC
Date: 07-05-2020
No related grants have been discovered for Christina Ellervik.