Attention Paid to Autophagy
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Autophagy is good for you. You should be doing more of it.

Autophagy is, put simply, the process by which cells recycle damaged components. Of course like all cellular processes the reality on the ground is anything but simple, and autophagy interacts with all sorts of other processes in ways that can produce counter-intuitive results. But the weight of evidence points to more and better autophagy as beneficial overall, most likely because it leads to fewer lingering damaged components inside a cell. Repeated throughout all your cells, this should result in better functioning tissue, fewer errant biological systems, and a longer life - remember that aging itself is nothing more than accumulated damage and the thrashing of systems trying to adapt to that damage.

Research into autophagy and its significance to longevity has been picking up breadth and pace in the past few years. This has no doubt been helped by the rising level of interest (and potential commerical profit) in the biochemistry of calorie restriction - autophagy appears to be very important to the benefits derived from calorie restriction. So we shouldn't be too surprised to see the mainstream science press start to cover autophagy research in much the same way as it covers research into the mechanisms of calorie restriction. Here's an example from today's New York Times:

Unfortunately, as we get older, our cells lose their cannibalistic prowess. The decline of autophagy may be an important factor in the rise of cancer, Alzheimer’s disease and other disorders that become common in old age. Unable to clear away the cellular garbage, our bodies start to fail.

If this hypothesis turns out to be right, then it may be possible to slow the aging process by raising autophagy. It has long been known, for example, that animals that are put on a strict low-calorie diet can live much longer than animals that eat all they can. Recent research has shown that caloric restriction raises autophagy in animals and keeps it high. The animals seem to be responding to their low-calorie diet by feeding on their own cells, as they do during famines. In the process, their cells may also be clearing away more defective molecules, so that the animals age more slowly.

Some scientists are investigating how to manipulate autophagy directly. Dr. Cuervo and her colleagues, for example, have observed that in the livers of old mice, lysosomes produce fewer portals on their surface for taking in defective proteins. So they engineered mice to produce lysosomes with more portals. They found that the altered lysosomes of the old experimental mice could clear away more defective proteins. This change allowed the livers to work better.

"These mice were like 80-year-old people, but their livers were functioning as if they were 20," Dr. Cuervo said. "We were very happy about that."

Methods of enhancing human levels of autophagy will almost certainly emerge from the broader field of metabolic research, and likely on much the same timescale as such line items as calorie restriction mimetic drugs that can capture most of the benefits of actual calorie restriction, mitochondrially targeted antioxidants, and other similar manipulations.

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