A recent study examining the effect of early-life tobacco smoking on aging-related disorders was published in the journal Science Advances. They discovered that exposure to smoke during pregnancy is linked to faster biological ageing.
According to their research, lowering tobacco exposure in early life is essential for promoting healthy aging because it has a substantial impact on biological aging and interacts with a number of variables, including age, sex, deprivation, and food.
The intricate process of biological ageing is marked by cellular alterations that build up over time and gradually compromise the integrity of tissues and organs. This puts a significant financial strain on healthcare systems and increases susceptibility to morbidity and mortality.
The significance of effectively predicting health outcomes by measuring biological age (BA) using many biomarkers has been emphasized in recent reviews. Early environmental exposures, especially tobacco use, have been shown to be important risk factors for unfavourable adult health outcomes. While earlier studies have connected tobacco use to early-life accelerated ageing, its effects on biological ageing in adults are still unknown, particularly when it comes to the timing of exposure and genetic vulnerability.
This work investigated the relationship between tobacco exposure during early life and biological ageing in adults by utilizing a variety of indicators, such as composite clinical-parameter algorithms and telomere length (TL).
It also looked into how tobacco use and genetic predisposition together accelerate biological aging in an effort to offer guidance for therapeutic and preventive measures that promote healthy aging.
The UK Biobank, a population-based cohort research with almost 500,000 participants enrolled between 2006 and 2010 with ages ranging from 37 to 73, provided data for the study. A total of 276,259 participants remained after exclusions.
Self-reported questionnaires were used to measure early-life tobacco exposure, including exposure during pregnancy and the age at which smoking beginning occurred. BA was calculated using methods for phenotypic age (PhenoAge) and Klemera-Doubal Biological Age (KDM-BA), which were verified using NHANES data.
A quantitative polymerase chain reaction was used to assess TL in leukocytes. TL and genetic variations connected to aging symptoms were used to create polygenic risk scores (PRS).
Lifestyle and demographic characteristics were included in the covariates. Biological aging indicators, PRS, and tobacco exposure were analyzed statistically using linear regression models that were covariate-adjusted.
To evaluate robustness, sensitivity analyses were carried out, which involved stratified analyses based on lifestyle and demographic characteristics and adjustments for extra confounders.
Initial participant comparisons indicated that individuals with in-utero exposure tended to be marginally younger, predominantly male, and more inclined towards alcohol consumption. Moreover, they exhibited elevated metrics such as body mass index (BMI) and Townsend deprivation index (TDI), along with a higher prevalence of major diseases.
Robust correlations between early-life tobacco exposure and accelerated biological ageing were found through additional statistical research.
Interestingly, participants exposed in utero showed notable increases in KDM-BA and PhenoAge acceleration along with a notable decrease in TL. In particular, an increase of 0.49 years in PhenoAge acceleration, a 0.26-year increase in KDM-BA acceleration, and a 5.34% decrease in TL were associated with in-utero exposure.
In addition, a distinct dose-response pattern was observed for the age at which smoking beginning occurs, with earlier initiations being associated with a more marked acceleration of biological aging markers.
For example, compared to never-smokers, childhood tobacco exposure was linked to an acceleration of KDM-BA of 0.88 years, an acceleration of PhenoAge of 2.51 years, and a decrease in TL of 10.53%.
Research on the combined effects of early-life tobacco exposure and genetic predisposition has shown significant implications on hastened ageing.
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