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Heritability of metabolic syndrome traits in a large population-based sample.

ABSTRACT: Heritability estimates of metabolic syndrome traits vary widely across studies. Some studies have suggested that the contribution of genes may vary with age or sex. We estimated the heritability of 11 metabolic syndrome-related traits and height as a function of age and sex in a large population-based sample of twin families (N = 2,792-27,021, for different traits). A moderate-to-high heritability was found for all traits [from H(2) = 0.47 (insulin) to H(2) = 0.78 (BMI)]. The broad-sense heritability (H(2)) showed little variation between age groups in women; it differed somewhat more in men (e.g., for glucose, H(2) = 0.61 in young females, H(2) = 0.56 in older females, H(2) = 0.64 in young males, and H(2)= 0.27 in older males). While nonadditive genetic effects explained little variation in the younger subjects, nonadditive genetic effects became more important at a greater age. Our findings show that in an unselected sample (age range, ~18-98 years), the genetic contribution to individual differences in metabolic syndrome traits is moderate to large in both sexes and across age. Although the prevalence of the metabolic syndrome has greatly increased in the past decades due to lifestyle changes, our study indicates that most of the variation in metabolic syndrome traits between individuals is due to genetic differences.

SUBMITTER: van Dongen J

PROVIDER: S-EPMC3770104 | biostudies-literature | 2013 Oct

REPOSITORIES: biostudies-literature

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Heritability of metabolic syndrome traits in a large population-based sample.

van Dongen Jenny J Willemsen Gonneke G Chen Wei-Min WM de Geus Eco J C EJ Boomsma Dorret I DI

Journal of lipid research 20130805 10

Heritability estimates of metabolic syndrome traits vary widely across studies. Some studies have suggested that the contribution of genes may vary with age or sex. We estimated the heritability of 11 metabolic syndrome-related traits and height as a function of age and sex in a large population-based sample of twin families (N = 2,792-27,021, for different traits). A moderate-to-high heritability was found for all traits [from H(2) = 0.47 (insulin) to H(2) = 0.78 (BMI)]. The broad-sense heritab ...[more]

PMID: 23918046

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Project description:ImportanceMost evidence to date highlights the importance of genetic influences on the liability to autism and related traits. However, most of these findings are derived from clinically ascertained samples, possibly missing individuals with subtler manifestations, and obtained estimates may not be representative of the population.ObjectivesTo establish the relative contributions of genetic and environmental factors in liability to autism spectrum disorder (ASD) and a broader autism phenotype in a large population-based twin sample and to ascertain the genetic/environmental relationship between dimensional trait measures and categorical diagnostic constructs of ASD.Design, setting, and participantsWe used data from the population-based cohort Twins Early Development Study, which included all twin pairs born in England and Wales from January 1, 1994, through December 31, 1996. We performed joint continuous-ordinal liability threshold model fitting using the full information maximum likelihood method to estimate genetic and environmental parameters of covariance. Twin pairs underwent the following assessments: the Childhood Autism Spectrum Test (CAST) (6423 pairs; mean age, 7.9 years), the Development and Well-being Assessment (DAWBA) (359 pairs; mean age, 10.3 years), the Autism Diagnostic Observation Schedule (ADOS) (203 pairs; mean age, 13.2 years), the Autism Diagnostic Interview-Revised (ADI-R) (205 pairs; mean age, 13.2 years), and a best-estimate diagnosis (207 pairs).Main outcomes and measuresParticipants underwent screening using a population-based measure of autistic traits (CAST assessment), structured diagnostic assessments (DAWBA, ADI-R, and ADOS), and a best-estimate diagnosis.ResultsOn all ASD measures, correlations among monozygotic twins (range, 0.77-0.99) were significantly higher than those for dizygotic twins (range, 0.22-0.65), giving heritability estimates of 56% to 95%. The covariance of CAST and ASD diagnostic status (DAWBA, ADOS and best-estimate diagnosis) was largely explained by additive genetic factors (76%-95%). For the ADI-R only, shared environmental influences were significant (30% [95% CI, 8%-47%]) but smaller than genetic influences (56% [95% CI, 37%-82%]).Conclusions and relevanceThe liability to ASD and a more broadly defined high-level autism trait phenotype in this large population-based twin sample derives primarily from additive genetic and, to a lesser extent, nonshared environmental effects. The largely consistent results across different diagnostic tools suggest that the results are generalizable across multiple measures and assessment methods. Genetic factors underpinning individual differences in autismlike traits show considerable overlap with genetic influences on diagnosed ASD.

Dataset Information

Heritability of metabolic syndrome traits in a large population-based sample.

Publications

Heritability of metabolic syndrome traits in a large population-based sample.

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