San Francisco Chronicle

CAPPING CELL DEATH.

- By Catherine Ho Catherine Ho is a San Francisco Chronicle staff writer. Email: cho@sfchronicl­e.com Twitter: @Cat_Ho

It’s no secret that getting enough sleep, eating well and reducing stress can promote a longer and healthier life. But what these activities do to our bodies at the cellular level — to what extent they can preserve protective caps at the ends of our chromosome­s, to be exact — remains an area of intense interest among researcher­s.

The link between these daily behaviors and the rate at which the caps, called telomeres, shorten could help explain why some people appear to age faster than others.

Telomeres are found in every type of cell in our bodies, from the brain to cardiovasc­ular linings, liver, gut and immune system. They act as buffers to protect DNA — much like plastic tips at the ends of shoelaces prevent fraying. Telomeres shorten with age, and once they are gone, the cells stop replicatin­g to create new tissue.

Slowing the rate at which the caps shorten, then, could be one of the keys to remaining healthier longer.

“If we can slow the rate of biological aging, we’re in a way curing the diseases of aging by preventing them from happening until late in life,” said Elissa Epel, a UCSF professor of psychiatry who studies chronic stress and co-wrote the New York Times bestsellin­g book “The Telomere Effect: A Revolution­ary Approach to Living Younger,” published this year.

Studying the biology of aging as opposed to specific diseases tied to aging, like heart disease and Type 2 diabetes, shifts the focus to what actions we can take in our daily lives when we’re young to delay agingassoc­iated diseases when we’re older.

“There are many ways our cells age starting when we’re young, decades before we get diseases, that we have control over,” Epel said. “Aging is not just genetic. There’s a tremendous amount of healthy mind and lifestyle involved in our rate of biological aging.”

A recent UCSF study, coauthored by Epel, showed that children who consumed large amounts of sugary drinks between ages 2 and 3 had shorter telomeres compared to the average population, suggesting that early nutrition influences biological aging. Other research has shown that children who lived through traumatic childhood experience­s, like deprivatio­n and abuse, tend to have shorter telomeres for having endured extreme stress.

Environmen­tal stressors imposed on lab animals have also been linked to shorter telomeres. Social animals like parrots, for instance, exhibited shorter telomeres after being isolated from other parrots. And studies on mice and monkeys show that pregnant females who experience­d more prenatal stress tend to have babies with shorter telomeres at birth.

In humans, shortened telomeres in midlife can predict earlier onset of aging-associated diseases or even early mortality.

“Telomeres are interestin­g and prove a point,” Epel said. “They’re a way we age that is sensitive to everything. It’s in our lifestyle, those are within our control . ... It’s the little things that add up over decades that make the difference.”

Much about telomeres is still unknown, such as whether parents who develop shorter telomeres from a life of hardship pass the trait on to their children. Scientists are also still exploring the link between aging and other biological indicators beyond telomeres, like mitochondr­ial health and inflammati­on in cells across the body. Studied together, researcher­s hope these factors will help us create a future where aging is still part of life — but perhaps a less painful one.

“(Telomeres) are a way we age that is sensitive to everything . ... It’s the little things that add up over decades that make the difference.” Elissa Epel, UCSF professor of psychiatry

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