A study published in Aging that studied the Northern Finland Birth Cohort of 1966 has found some interesting and counterintuitive results regarding work stress and accelerated epigenetic aging.
Work stress is widely associated with premature death
It is common folk wisdom that too much stress leads to a shorter lifespan, and this belief has been supported by peer-reviewed scientific studies.
An open-access meta-study focused on the effort-reward imbalance model, which focuses on the gap between perceived rewards from work and the difficulty of that work, has found that blood pressure, heart rate variability, metabolic issues, and blood biomarkers of poor health are all associated with heavy effort and low rewards [1].
One study found that job strain was linked to the methylation of a gene associated with behavioral health, leading to depression [2]. Another study found that increased methylation across the genome was associated with reporting high job stress [3].
While not all studies agree as to the magnitude or importance of work-related stress, it has clearly been shown to be interesting enough to be examined by a study involving modern aging clocks.
Clocks don’t always agree with each other
Being based on a single-year birth cohort, this study examined 604 people of the same approximate age. Before the researchers went into studying job stress, they first looked at more well-known factors that are associated with lifespan, including obesity, smoking, education status, physical activity, and alcoholism. They studied the effects of these factors on the older Horvath and Hannum clocks, the newer PhenoAge and highly accurate GrimAge clocks, and a new clock called DunedinPoAM.
Some of the findings were contradictory between clocks. For example, men are likely to be considered epigenetically older according to the Horvath, Hannum, and GrimAge clocks, while the opposite is true for PhenoAge and the DunedinPoAM clock. Tertiary education was significantly associated with slowed aging according to GrimAge, while Horvath, Hannum, and PhenoAge non-significantly associated it with accelerated aging.
Smoking was, of course, associated with accelerated aging on all the clocks, some with more confidence than others, but GrimAge associated past smoking and aging very strongly and current smoking with aging extremely strongly. Obesity was associated with aging, significantly so with PhenoAge, GrimAge, and DunedinPoAM. Physical activity, as expected, was inversely associated with aging, significantly so as shown on GrimAge and DunedinPoAM.
Interestingly, neither being merely overweight nor alcohol use, even heavy alcohol use, was significantly associated with age acceleration on any of the clocks studied.
What did the clocks say about job stress?
A great many of the findings were inconclusive. In line with its result on tertiary education, the GrimAge clock associated white-collar work, government-funded work, and continuous employment with decreased epigenetic aging, and a corresponding increase with unemployment; however, the others did not. After adjusting for the other factors, only white-collar work was shown to be statistically significant in the GrimAge results.
The only significant association found between reported job strain and aging was discovered in the PhenoAge clock, which reported that intermediate strain and active work actually decreased aging. GrimAge found almost no association whatsoever with accelerated aging, although it did report that people who spent more effort at their jobs, including people with significant effort/reward imbalance, were more likely to be epigenetically older, as were people who engaged in intermediate physical activity.
However, the researchers found that physical activity at work was beneficial for men according to the Horvath and Hannum clocks, which also reported that everyone’s epigenetic aging suffered when working more than 40 hours a week.
Conclusion
While stress has been reported to have negative physical effects, its effects on epigenetic aging are far from proven. While the researchers reported some tentative links, most of the evidence presented in this study suggests a lack of direct association between stress and epigenetic aging; most of the correlations that popular wisdom would expect from a study like this were simply not there.
Such a negative result, however, is beneficial to the field as a whole. Knowing that job stress generally lacks any significant association with accelerated aging, at least among the cohort studied, allows researchers to narrow down their efforts towards possibly more fruitful lines of inquiry.
Literature
[1] Siegrist, J., & Li, J. (2017). Work stress and altered biomarkers: a synthesis of findings based on the effort–reward imbalance model. International journal of environmental research and public health, 14(11), 1373.
[2] Miyaki, K., Song, Y., Suzuki, T., Eguchi, H., & Kawakami, N. (2015). DNA Methylation Status of the Methylenetetrahydrofolate Reductase Gene is associated with Depressive Symptoms in Japanese Workers: A Cross-Sectional Study. J Neurol Neurol Disord, 2(3), 304.
[3] Duman, E. A., & Canli, T. (2015). Influence of life stress, 5-HTTLPR genotype, and SLC6A4 methylation on gene expression and stress response in healthy Caucasian males. Biology of mood & anxiety disorders, 5(1), 1-14.
