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Researchers find cause for increased disease burden after midlife

Worms, flies and mice have biochemical events that regulate the longevity of their lives -- and it turns out that humans have a similar molecular program.

By Tauren Dyson
Researchers find cause for increased disease burden after midlife
When important molecular programs that encourage longevity begin to break down, disease burden in the body starts to increase. File Photo by Gualtiero Boffi/Shutterstock

June 6 (UPI) -- When important molecular programs that encourage longevity begin to breakdown, that's when the body crosses over into the stage of a midlife crisis, new research shows.

The study, published Thursday in Aging Cell, may shed light on why human disease burden rises so drastically after age 60.

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"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," Claes Wahlestedt, a researcher the University of Miami and study author, said in a news release.

"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," Wahlestedt said.

According to the researchers, this work is a culmination of two decades of research that led to their method. They quantified comprehensive gene expression patterns based on human tissue samples from various age groups.

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For the study, the researchers identified the large role of the mTOR protein complex, which operates several protector programs within cells and production of the mitochondrial reactive oxygen species. Combined, these cellular mechanisms are responsible for roughly two-thirds of human molecular aging.

"Our study revealed that the complexity of regulation of aging programs may be much greater in humans as compared to other species," 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 50s."

The researchers say past studies have delved into how these protein regulators affect longevity in animals that live relatively short lives. They think this "dark matter" within the human genome could also help repair molecules involved in aging.

This could mean that anti-aging products currently sold in stores that use nutrients or medications may not be effective by the time a person reaches midlife.

"We've demonstrated that the most valid of 'anti-aging' programs are naturally active in humans and for some reason stop when we reach our 50s," Wahlestedt said. "This not only provides a specific time window to now study human aging, it also indicates that these established anti-aging strategies may no longer be effective (if too active there can be side effects) and so new approaches will be needed in long-lived humans."

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