Key molecular programs known to promote longevity do not last beyond midlife. An interesting study provides a possible new reason why the human disease burden increases so sharply from the sixth decade of life onward as health-protective mechanisms disappear.
Just as a computer requires code to work, our bodies are regulated by molecular “programs” that are written early in life and then have to do their job properly for a lifetime. But do they? It’s a question that has intrigued researchers for years.
Lifestyle changes after 60 “too late”?
If one wishes to boost these established “anti-ageing” programs with drugs, nutrients, or lifestyle choices, is it too late to start by the time you reach your 60s? Possibly, said Dr. Wahlestedt — at least if you hope to benefit fully from such interventions.
Claes Wahlestedt, M.D., Ph.D., professor of psychiatry and behavioural sciences and associate dean for therapeutic innovation at the University of Miami Miller School of Medicine, is the senior author of a study on longevity-related molecular pathways in humans.
Humans stop using “longevity pathways” as they hit 50
“For over a decade, it has been clear that key biochemical events regulate the longevity of small short-lived animals such as worms, flies, and mice, but these mechanisms had not been observed to be active in humans,” Dr Wahlestedt said.
“In this international clinical and genomic study, we report for the first time that humans use these same biochemical pathways during aging. Surprisingly, however, humans appear to stop using these pathways from about 50 years of age onward. Therefore, how long and how ‘hard’ each person regulates these pathways may influence human lifespan.”
No guarantees after 50
Dr Wahlestedt said the new study was the result of two decades of persistent efforts initiated while he and first author Jamie Timmons PhD, King’s College London, worked at the Karolinska Institutet in Stockholm, Sweden. They made their discovery when using a new method for quantifying comprehensive gene expression patterns, applied to carefully-curated sets of tissue samples from humans at various ages.
“Our study revealed that the complexity of regulation of ageing programs may be much greater in humans as compared to other species,” Dr Wahlestedt said.
“This is related to our more complex genome, which may have evolved to allow for longer and healthier lifespan. But perhaps humans were not really meant to last beyond their 50’s.”
This article is based on materials provided by the University of Miami Miller School of Medicine. Content may have been edited for style and length.
Original study: Timmons, J. A., Volmar, C., Crossland, H., Phillips, B. E., Sood, S., Janczura, K. J., … Wahlestedt, C. (2019). Longevity‐related molecular pathways are subject to midlife “switch” in humans. Aging Cell, 18(4). https://doi.org/10.1111/acel.12970