The Key to Aging and Illness?
Today, the New England Journal of Medicine published a lecture given by a scientist at MIT that goes a
long way towards establishing a new approach to thinking about why and how we age, and how that process
is at the heart of most of the terrible afflictions that face us as we get older, namely:
dementia, heart disease, auto-immune disorders (such as arthritis), and cancer.
For most of us aging just seems to be the fault of time. As time goes on, things wear out. Why would our
bodies be any different? But the problem with that concept of aging is that bodies don't actually wear out.
The materials that make up our body are renewed constantly by the food we eat and the air we breathe.
For example, we have a new layer of skin created every three weeks.
Further, each species ages at a different rate. If aging was just a matter of wear and tear, the bones of a dog and bear and human ought to wear out at the same rate, but they do not.
And finally, there is the observation that all animals age in the same way. All animals see their skin get wrinkly, their hair lose its pigment and shine, their joints get sore and inflamed, their hearts begin to fail, and cancers to appear.
A lot of research is now proving that aging is a program. Our DNA and biology contains a program, like a piece of software, that dictates the decline in function that we call aging and its characteristic diseases.
Abundant examples now exist in animals and even humans that demonstrate if you change that program, you change the rate of aging. And the center of control of the program we call aging is the part of the cell that creates all the cell's energy, a structures called the mitochondria.
It is now becoming clear that mitochondria set the pace and the program of aging, and changes to that program can change a person's experience of aging. There are human populations whose mitochondria have a different approach to aging, and these populations live far longer with far less dementia, heart disease, cancer, and auto-immune disease.
Today's publication in the New England Journal reviews much of the science known about one set of genes that control this program we call aging. The group of genes is called the sirtuins. Dr. Gurante of MIT does a masterful job of reviewing what we know about the sirtuin genes and how they control aging.
The lecture is highly technical, so I apologize to those not so interested in such a technical paper, but even so, take a look at the section headings and marvel at the breadth of control the aging process commands: with the right sirtuin genes animals, and likely humans, have less diabetes from obesity, less heart disease, less dementia, less cancer, and slower aging.
I share all this with you today, because I am convinced that the priorities of medical research need to shift. Our usual approach to managing the illnesses of old age has been to have major research institutes devoted to researching each of these diseases. These efforts should continue. But with the emergence of knowledge about a very central control point on all these problems, the time has come for our science grants to push for a major effort to learn how to manage our aging software, and perhaps unlock a future where cancer, dementia, heart disease, arthritis are all held at bay as we enjoy a much longer and healthier life.
No research project aimed at a single disease can deliver this amazing goal, but it is increasingly likely that research aimed at our software for aging could.
To a good life,
Dr. Arthur Lavin
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