Dataset Information

Parental age and offspring leukocyte telomere length and attrition in midlife: Evidence from the 1946 British birth cohort.

ABSTRACT:

Background

There is evidence that paternal age may influence offspring telomere length, but the joint effects of father's and mother's age are unclear. We evaluated whether parental ages, individually and jointly, were associated with offspring telomere length and shortening.

Methods

We included 2305 British birth cohort participants with measured leukocyte telomere length (LTL) at age 53, among whom 941 had a second measurement at age 60-64. Linear regressions were performed to assess the associations of father's and mother's age at birth and the parental age gap, i.e. the difference between maternal and paternal age with LTL and LTL change.

Results

A one year increase in father's age corresponded to a 0.26% (95% CI: 0.04-0.47%) increase in offspring LTL at age 53 in the sex-adjusted model. No association was observed for mother's age. Associations of father's or mother's age with offspring LTL at age 53 went to opposite directions when both parental ages were included together. For the difference in parental age, every year that fathers were older than mothers corresponded to a 0.94% (95% CI, 0.38-1.50%) increase in LTL at age 53 after adjustment for potential confounders. Neither parental ages nor the difference in parental ages were correlated with LTL change.

Conclusion

There was a joint effect of parental ages on offspring telomere length, further denoting a complex role of reproductive age in offspring health and ageing.

SUBMITTER: Wulaningsih W

PROVIDER: S-EPMC6189452 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Publications

Parental age and offspring leukocyte telomere length and attrition in midlife: Evidence from the 1946 British birth cohort.

Wulaningsih Wahyu W Hardy Rebecca R Wong Andrew A Kuh Diana D

Experimental gerontology 20180915

<h4>Background</h4>There is evidence that paternal age may influence offspring telomere length, but the joint effects of father's and mother's age are unclear. We evaluated whether parental ages, individually and jointly, were associated with offspring telomere length and shortening.<h4>Methods</h4>We included 2305 British birth cohort participants with measured leukocyte telomere length (LTL) at age 53, among whom 941 had a second measurement at age 60-64. Linear regressions were performed to a ...[more]

PMID: 30223048

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Project description:Investigating associations between metabolites and late midlife cognitive function could reveal potential markers and mechanisms relevant to early dementia. Here, we systematically explored the metabolic correlates of cognitive outcomes measured across the seventh decade of life, while untangling influencing life course factors. Using levels of 1019 metabolites profiled by liquid chromatography-mass spectrometry (age 60-64), we evaluated relationships between metabolites and cognitive outcomes in the British 1946 Birth Cohort (N = 1740). We additionally conducted pathway and network analyses to allow for greater insight into potential mechanisms, and sequentially adjusted for life course factors across four models, including sex and blood collection (Model 1), Model 1 + body mass index and lipid medication (Model 2), Model 2 + social factors and childhood cognition (Model 3) and Model 3 + lifestyle influences (Model 4). After adjusting for multiple tests, 155 metabolites, 10 pathways and 5 network modules were associated with cognitive outcomes. Of the 155, 35 metabolites were highly connected in their network module (termed 'hub' metabolites), presenting as promising marker candidates. Notably, we report relationships between a module comprised of acylcarnitines and processing speed which remained robust to life course adjustment, revealing palmitoylcarnitine (C16) as a hub (Model 4: β = -0.10, 95% confidence interval = -0.15 to -0.052, P = 5.99 × 10-5). Most associations were sensitive to adjustment for social factors and childhood cognition; in the final model, four metabolites remained after multiple testing correction, and 80 at P < 0.05. Two modules demonstrated associations that were partly or largely attenuated by life course factors: one enriched in modified nucleosides and amino acids (overall attenuation = 39.2-55.5%), and another in vitamin A and C metabolites (overall attenuation = 68.6-92.6%). Our other findings, including a module enriched in sphingolipid pathways, were entirely explained by life course factors, particularly childhood cognition and education. Using a large birth cohort study with information across the life course, we highlighted potential metabolic mechanisms associated with cognitive function in late midlife, suggesting marker candidates and life course relationships for further study.

Dataset Information

Parental age and offspring leukocyte telomere length and attrition in midlife: Evidence from the 1946 British birth cohort.

Background

Methods

Results

Conclusion

Publications

Parental age and offspring leukocyte telomere length and attrition in midlife: Evidence from the 1946 British birth cohort.

Similar Datasets

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