Can we stay forever young?

[Guest guest]

Can we stay forever young?Scientific

research can tell us why and how we age, but does this insight help us

stay younger, longer? Until very recently, most experts would have said

no. Many held that the aging of cells, and of multicellular organisms

like humans, was inevitable­and therefore, there was a limit to how long

each species could live. One theory held that the biological life span of

any species is roughly six times the stretch between birth and maturity.

Using this formula, the maximum lifespan for humans is 120 years. In

fact, one well-documented contender for the title of longest-lived person

is a French woman believed to be 122 years old when she died in 1997.

 

Today, some researchers are having second thoughts about a maximum life

span, and indeed about the inevitability of aging. While nothing may seem

more unavoidable than aging and death­not even taxes­some animals do not

seem to age. Many cold-water ocean fish, some amphibians, and the

American lobster never reach a fixed size. They continue to grow bigger,

reproduce, and live until something­an accident, a predator, or a

disease­kills them.

Clearly, though, this is not the case for humans. So why do some

scientists think we might be able to overcome the biological cap on

aging? Recent research indicates that while our genes may indeed

“program” us for a particular life span by affecting how rapidly our

cells age, we may be learning enough about how the “program” works to

change it.

Calorie restriction and aging

The first suggestion that the process of aging might not be

inevitable­or at least that it could be slowed­emerged about 70 years

ago. Scientists discovered that when animals are forced to live on 30% to

40% fewer calories than they would normally consume, something unusual

happens: they become resistant to most age-related diseases­cancer, heart

disease, diabetes, Alzheimer’s disease­and live 30% to 50%

longer.

Scientists set out to understand what genes are turned on by calorie

restriction because if they could figure that out, they might be able to

develop medications that turn those genes on just like calorie

restriction does (but without people having to drastically reduce food

intake). Over the past 15 years, scientists at MIT and Harvard Medical

School identified a family of genes called sirtuins that are responsible

for the health benefits of calorie restriction. Then they developed

compounds called sirtuin-activating compounds (STACs) that turn on the

sirtuin genes. The first STAC is called resveratrol, which is found in

red wine. Resveratrol can extend the life span of simple organism like

yeast, fruit flies, worms, and fish. In late 2006, resveratrol was shown

to extend the life span of mice fed a high-calorie, high-fat diet. Not

only did it extend life span in all these animals, but the animals were

protected against several diseases of aging and remained physically

active and vital until very late in their extended lives.

It’s easy to see why this research is potentially relevant to humans.

Like the mice in these studies, many of us are middle-aged mammals who

eat a high-calorie, high-fat diet. While research results in mice do not

always prove true in humans, they often do. Still, we are a long way from

knowing whether human life span can be extended, and the added years made

vital and active, by such knowledge of the biology of aging.

Antioxidants

If oxidants damage cells and contribute to cellular aging, it seems

logical that increasing levels of antioxidants might help. Several

vitamins are antioxidants­particularly vitamins E, C, and beta carotene

(a form of vitamin A). Foods rich in those vitamins seemed to be

associated with improved health. That led to the attractive theory that

supplements of vitamins E and C and beta carotene might as well.

But the evidence so far has been disappointing. At the same time, there

are other clues that finding other ways of harnessing the body’s

antioxidant systems might prove valuable. For example, there is a genetic

mutation in worms that triggers an overabundance of the antioxidant

enzymes superoxide dismutase (SOD) and catalase­the result being a

doubled lifespan for the worms. These enzymes work in concert to

neutralize oxidants and help prevent oxidative damage.

Other researchers found the gene that churned out SOD was more active in

a group of longer-lived fruit flies than in flies of average life span.

Likewise, fruit flies given extra copies of the SOD gene lived

longer.

The Daf genes

A series of genes dubbed Daf­decay accelerating factor­in worms has a

counterpart in humans that helps manage insulin levels and a growth

factor called IGF-1. When researchers deliberately immobilize certain Daf

genes in worms, they can live up to five times longer and continue to be

active and capable of reproducing until late in their greatly lengthened

lives.

The Indy gene

When researchers introduced any one of five mutations into a single

gene dubbed Indy­an acronym inspired by a Monty Python line, “I’m not

dead yet”­the flies’ life span nearly doubled. Moreover, the long-lived

flies stayed frisky and reproduced far longer. When the mutation was

reversed, fly life span returned to normal. This research not only

identified another gene of possible importance in aging, it demonstrated

that even when engaged in the serious business of discovering and naming

new genes, scientists can have a sense of humor.

 

Reprinted from Living Better, Living Longer: The secrets of healthy

aging, a Special Health Report from Harvard Medical School, Copyright

© 2008 by Harvard University. All rights reserved.