Research is revealing the cellular mechanisms that link mental well-being and longevity.
There might be a paradox in the biology of ageing. As humans grow older, their metabolisms tend to slow, they lose muscle mass and they burn many fewer calories. But certain cells in older people appear to do the exact opposite — they consume more energy than when they were young.
These potential energy hogs are senescent cells, older cells that have stopped dividing and no longer perform the essential functions that they used to. Because they seem idle, biologists had assumed that zombie-like senescent cells use less energy than their younger, actively replicating counterparts, says Martin Picard, a psychobiologist at Columbia University in New York City.
But in 2022, Gabriel Sturm, a former graduate student of Picard’s, painstakingly observed the life course of human skin cells cultured in a dish1 and, in findings that have not yet been published in full, found that cells that had stopped dividing had a metabolic rate about double that of younger cells.
For Picard and his colleagues, the energetic mismatch wasn’t a paradox at all: ageing cells accumulate energetically costly forms of damage, such as alterations in DNA, and they initiate pro-inflammatory signalling. How that corresponds with the relatively low energy expenditure for ageing organisms is still unclear, but the researchers hypothesize that this tension might be an important driver of many of the negative effects of growing old, and that the brain might be playing a key part as mediator2. As some cells get older and require more energy, the brain reacts by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass (see ‘Energy management and ageing’).
And there is that “Stress” as a factor in accelerated aging again… from the same above article…
Since then, teams have also found evidence of telomere shortening in people exposed to other stressors, such as adverse experiences in childhood and work-related exhaustion4. Although some of the results have been mixed when it comes to telomere length, researchers have also amassed evidence linking stress to other molecular markers of ageing.
For example, Anthony Zannas, a physician–scientist at the University of North Carolina at Chapel Hill, and his colleagues have shown, through studies of large cohorts of people, that high levels of stress throughout life were associated with signs of accelerated ageing in the epigenome, the patterns of chemical modifications to the genome, such as DNA methylation, that help to regulate what genes are expressed. These changes might be mediated by stress hormones such as cortisol. Zannas’s team found that, in women, higher levels of cortisol were linked to lower levels of DNA methylation, as well as an increase in the expression of the gene coding for tumour necrosis factor (TNF), a signalling molecule associated with inflammation5.