Publication

The heritable basis of gene-environment interactions in cardiometabolic traits

Journal Paper/Review - Dec 21, 2016

Units
PubMed
Doi

Citation
Poveda A, Chen Y, Brändström A, Engberg E, Hallmans G, Johansson I, Renström F, Kurbasic A, Franks P. The heritable basis of gene-environment interactions in cardiometabolic traits. Diabetologia 2016; 60:442-452.
Type
Journal Paper/Review (English)
Journal
Diabetologia 2016; 60
Publication Date
Dec 21, 2016
Issn Electronic
1432-0428
Pages
442-452
Brief description/objective

AIMS/HYPOTHESIS
Little is known about the heritable basis of gene-environment interactions in humans. We therefore screened multiple cardiometabolic traits to assess the probability that they are influenced by genotype-environment interactions.

METHODS
Fourteen established environmental risk exposures and 11 cardiometabolic traits were analysed in the VIKING study, a cohort of 16,430 Swedish adults from 1682 extended pedigrees with available detailed genealogical, phenotypic and demographic information, using a maximum likelihood variance decomposition method in Sequential Oligogenic Linkage Analysis Routines software.

RESULTS
All cardiometabolic traits had statistically significant heritability estimates, with narrow-sense heritabilities (h 2) ranging from 24% to 47%. Genotype-environment interactions were detected for age and sex (for the majority of traits), physical activity (for triacylglycerols, 2 h glucose and diastolic BP), smoking (for weight), alcohol intake (for weight, BMI and 2 h glucose) and diet pattern (for weight, BMI, glycaemic traits and systolic BP). Genotype-age interactions for weight and systolic BP, genotype-sex interactions for BMI and triacylglycerols and genotype-alcohol intake interactions for weight remained significant after multiple test correction.

CONCLUSIONS/INTERPRETATION
Age, sex and alcohol intake are likely to be major modifiers of genetic effects for a range of cardiometabolic traits. This information may prove valuable for studies that seek to identify specific loci that modify the effects of lifestyle in cardiometabolic disease.