Corley · Translational psychiatry 2019 · cohort study · n=895

Epigenetic signatures of smoking associate with cognitive function, brain structure, and mental and physical health outcomes in the Lothian Birth Cohort 1936.

Cited 63 times in the scientific literature.

Level 3 - non-randomized controlled study

Cohort study evaluating cross-sectional health associations at age 70 and MRI follow-up at age 73.

PubMed 31591380 · doi:10.1038/s41398-019-0576-5 · record verified 2026-08-29

What was done

Blood DNA methylation was profiled using the Illumina 450K assay in 895 adults aged 70 years from the Lothian Birth Cohort 1936 (LBC1936). A 230-CpG DNA methylation score was computed as an epigenetic proxy for smoking exposure. General linear models (ANCOVA) and logistic regression were used to examine associations of self-reported smoking and the methylation score with cognitive, physical, and psychosocial outcomes at age 70, as well as brain MRI volumetric measures at age 73 in a subset (n = 532).

What was found

The smoking DNA methylation score correlated with self-reported smoking status (P < 0.001, η² = 0.63) and pack years (r = 0.69, P < 0.001). Compared to self-reported smoking, the methylation marker showed stronger associations across outcomes, including visuospatial ability (P < 0.001, ηp² = 0.022), processing speed (P < 0.001, ηp² = 0.030), inflammatory markers (all P < 0.001, ηp² = 0.021 to 0.030), healthy diet (P < 0.001, ηp² = 0.052), traditional diet (P < 0.001, ηp² = 0.032), stroke (P = 0.006, OR 1.48, 95% CI 1.12, 1.96), mortality (P < 0.001, OR 1.59, 95% CI 1.42, 1.79), and age 73 MRI volumetric measures (all P < 0.001, ηp² = 0.030 to 0.052).

Why it matters

Epigenetic markers of smoking capture biologically relevant exposure beyond self-report and account for additional variance in late-life brain structure, cognitive performance, and mortality risk.

Limits

The sample is restricted to a racially and geographically homogeneous Scottish birth cohort at age 70–73, which may not generalize to younger or more diverse populations. MRI analysis was limited to an attrition-selected subset (n = 532), and the observational design cannot establish whether methylation changes causally mediate these health outcomes.

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