From Harvard School of Public Health
Why do we age? Surprising revelations from a worm
HSPH’s Will Mair hopes his work in worms will identify molecules that have an effect on aging-related diseases—and which could ultimately be tested as treatments for humans.
“How old you are is immutable—you can’t change how old an animal is,” says William Mair, assistant professor of genetics and complex diseases at HSPH. “But you can change how it ages.”
That observation points to a new way of thinking about aging: not as a preordained decline, but as a malleable function of the body. And viewed in this way, aging belongs at the center of public health research. Rather than just treating endpoints—such as cardiovascular disease, metabolic disorders, cancer, and neurodegeneration—could researchers improve population health by targeting the aging process itself?
Mair’s young lab, launched last November, is trying to answer that question. “It’s not enough to say it’s inevitable that we get more frail,” says Mair. “There’s something that happens that makes an old animal more susceptible to getting these disease states. For example, if you look at cancer, one of the most common age-related diseases, it’s clearly not one pathology. Similar tumors can result from very different mutations in different individuals. Trying to find those specific mutations is one way to do research. But if you could make the environment more resistant to developing tumors in the first place, you can try to reduce the chances of getting cancer with age.”
Mair first became intrigued with aging as an evolutionary question: If infirmity isn’t just a product of wear and tear, why do we age at all? His research began with an observation known since the 1930s: A diet severely restricted in calories (about 30 percent below normal, but above starvation levels) can increase lifespan, lower rates of cancer, and slow declines in memory and movement. This effect, first seen in laboratory rats, has been replicated in species as diverse as yeast, fruit flies, worms, and even rhesus monkeys. Further research has uncovered genetic mutations in animals that can mimic the effects of dietary restriction, and some of these same mutations are found in people who live into their 90s.
But laboratory-manipulated longevity also comes with a price. Restricted-diet animals grow more slowly, reproduce less, and have dampened immune systems. More than just cutting calories, dietary restriction seems to switch the body into a survival mode in which growth and energy consumption are suppressed.
Read more from Harvard School of Public Health >>
Why do we age? Surprising revelations from a worm
HSPH’s Will Mair hopes his work in worms will identify molecules that have an effect on aging-related diseases—and which could ultimately be tested as treatments for humans.
“How old you are is immutable—you can’t change how old an animal is,” says William Mair, assistant professor of genetics and complex diseases at HSPH. “But you can change how it ages.”
That observation points to a new way of thinking about aging: not as a preordained decline, but as a malleable function of the body. And viewed in this way, aging belongs at the center of public health research. Rather than just treating endpoints—such as cardiovascular disease, metabolic disorders, cancer, and neurodegeneration—could researchers improve population health by targeting the aging process itself?
Mair’s young lab, launched last November, is trying to answer that question. “It’s not enough to say it’s inevitable that we get more frail,” says Mair. “There’s something that happens that makes an old animal more susceptible to getting these disease states. For example, if you look at cancer, one of the most common age-related diseases, it’s clearly not one pathology. Similar tumors can result from very different mutations in different individuals. Trying to find those specific mutations is one way to do research. But if you could make the environment more resistant to developing tumors in the first place, you can try to reduce the chances of getting cancer with age.”
Mair first became intrigued with aging as an evolutionary question: If infirmity isn’t just a product of wear and tear, why do we age at all? His research began with an observation known since the 1930s: A diet severely restricted in calories (about 30 percent below normal, but above starvation levels) can increase lifespan, lower rates of cancer, and slow declines in memory and movement. This effect, first seen in laboratory rats, has been replicated in species as diverse as yeast, fruit flies, worms, and even rhesus monkeys. Further research has uncovered genetic mutations in animals that can mimic the effects of dietary restriction, and some of these same mutations are found in people who live into their 90s.
But laboratory-manipulated longevity also comes with a price. Restricted-diet animals grow more slowly, reproduce less, and have dampened immune systems. More than just cutting calories, dietary restriction seems to switch the body into a survival mode in which growth and energy consumption are suppressed.
Read more from Harvard School of Public Health >>
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