Early-life tobacco smoke, biological age acceleration and dementia in UK Biobank
In a UK Biobank cohort, prenatal tobacco smoke exposure and childhood/adolescence smoking were associated with modestly higher dementia hazards; biological-age acceleration explained only a small estimated part for childhood/adolescence smoking. [1]
Automatic summary · not editorially reviewed
The key findings
The prospective UK Biobank cohort included 285,009 participants who were dementia-free at the start. [1]
Over a mean follow-up of 13.67 years, 4,621 incident dementia cases were documented. [1]
For childhood/adolescence smoking, the estimated mediated proportion through biological-age acceleration was 3.63%. [1]
The source at a glance
- Study type / format
- Prospective cohort study with exploratory mediation analysis (abstract).
- Population / context
- 285,009 dementia-free UK Biobank participants.
- Summary based on
- Study abstract
- Original publication
- September 29, 2026
UK Biobank cohort of 285,009 dementia-free adults
This prospective cohort study followed 285,009 participants from the UK Biobank who were free of dementia at the start. It asked whether tobacco smoke exposure before birth and smoking during childhood or adolescence were associated with later dementia, and whether biological-age acceleration might be an intermediate component. Biological aging was measured with two methods: Klemera-Doubal method biological age acceleration and phenotypic age acceleration. The abstract does not report participants' ages or how exposure was recorded.
Supporting source [1]
Modestly higher dementia hazards over 13.67 years
During a mean follow-up of 13.67 years, 4,621 incident dementia cases were documented. Prenatal tobacco smoke exposure was associated with higher dementia hazards (hazard ratio 1.094, 95% confidence interval 1.025–1.168), as was childhood/adolescence smoking (hazard ratio 1.187, 95% confidence interval 1.106–1.275). The standardized 10-year absolute risk differences were 0.063 and 0.124 percentage points. These are associations, not proof that smoke exposure caused dementia.
Supporting source [1]
Small estimated mediation only for childhood/adolescence smoking
Exploratory mediation analyses estimated an indirect component through both biological-age measures combined. For childhood/adolescence smoking this indirect effect was small (hazard ratio 1.0062, 95% confidence interval 1.0002–1.0125), with an estimated mediated proportion of 3.63% (95% confidence interval 0.11%–8.77%). The abstract reports no such indirect estimate for prenatal exposure. Because the mediation analysis is exploratory and model-based, the indirect component is an estimate, not a confirmed mechanism. This abstract-only summary means the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The mediation analysis is described as exploratory and model-based, so the indirect component is an estimate, not a confirmed mechanism. Associations do not establish causation.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Yu L, Deng H, Yang M, Jiang DS, Liao C, Sun D, Song J, Luo H, Liu W, Wang X. · europepmc.org · September 29, 2026