Most of the popular literature on slowing senescence tends to extravagant predictions. By comparison, this brief 5/6/07 NYT article is quite modest. If everything works today's 30 year olds might get another 10 years, and today's 10 year olds might get more.
I also like the description of the aging brain, though I think they're being optimistic about the relationship between disability in your 70s and forgetting your keys in your 40s. Emphases mine.
May 6, 2007
Participants: Lenny GUARENTE, PH.D.: Novartis professor of biology at M.I.T. and author of “Ageless Quest: One Scientist’s Search for Genes That Prolong Youth.”; Robert N. BUTLER, M.D.: Founding director of the National Institute on Aging, a founder of the Alzheimer’s Disease Association and winner of a Pulitzer Prize in 1976 for “Why Survive? Being Old in America.” He heads the International Longevity Center.; SARA DAVIDSON: Author, most recently, of “Leap! What Will We Do With the Rest of Our Lives?”
... LENNY GUARENTE: The research that I’m involved in is not about extending life after people are infirm. I don’t think of life span as the gold standard. The gold standard is health span. All the indicators from the laboratory are that the genes we’re studying and the kinds of drugs we would be developing would extend health span. If you can extend health span, and you also happen to extend life span, so be it. That’s a side benefit...
... The genes we study counteract aging. First we studied yeast cells, and it took us eight years to identify a gene called SIR2, which protects the cells from damage during the aging process. Then we did a similar experiment in a more complex critter, the roundworm, and what was remarkable is, we identified the same gene. That told us that this type of gene is performing an antiaging function broadly in nature.
Do humans have this gene?
GUARENTE: There’s one gene in our genome, SIRT1, that would be a dead ringer for this one — the technical term is ortholog — but we also have six other genes that have a related sequence to this. They’re called sirtuins, and they’re all going to play a role, but I think the dead ringer is undoubtedly the most important based on experiments that have been done.
... We think the sirtuin genes are there to recognize lack of food or other stressful situations and to spring into action to create a physiology that will promote longevity. The evolutionary value is that in times of stress — food scarcity, for example — this gene would slow down the aging process and keep you alive longer, so that when times are better, you could reproduce. ..
... In our lifetimes, could this happen?
GUARENTE: I think one can expect perhaps another decade of robust health...
... How close are we to such a drug being available?
GUARENTE: Ten, maybe 15 years. I think the drugs that aim at sirtuins, for example, will be tested initially for a particular disease, say, diabetes. And it will turn out that the drugs have broader benefits than one initially imagined.
What about resveratrol? There has been a lot of publicity about this substance that’s found in red wine. Does it do the same thing as calorie restriction?
GUARENTE: It’s a natural product, made by plants, and recently one of my former postdoctoral students, David Sinclair, found that resveratrol can regulate the activity of SIRT1.
Do you take resveratrol?
GUARENTE: No, partly because neutraceuticals are not regulated by the F.D.A. If I was sure of the quality control, I would consider it, but I’m still not certain I would do it, because you may have to take a lot — one or two grams a day.
What intrigues me is that I read that if fruit flies are fed resveratrol, they live longer and can eat all they want...
... BUTLER: .. we don’t even have the means to evaluate or measure whether a substance prolongs life. We have yet to create biomarkers that would measure, short of death, actual changes in the body that reflect aging...
... BUTLER: There are many types of dementia, which result from different causes. The most common is Alzheimer’s, which is characterized by neurofibrillary tangles — misshaped proteins — and plaques. The second most common is multi-infarct dementia, which is the result of small, repeated strokes. Scientists who are studying Alzheimer’s have differentiated three categories for research purposes. The first is what’s called age-associated memory impairment. These are the kinds of things ordinary people are going through: forgetfulness, not remembering why you’ve walked into a room or where you put the paper you were just holding in your hand. If you’re in this category, we have no data that suggest you’re necessarily on your way to Alzheimer’s.
The second category is mild cognitive impairment — getting confused on the street, not remembering you’re supposed to have coins when you get on a bus. At that point, the conversion rate to the third — full-blown Alzheimer’s — sadly, is very high. After three years, about half the people will not be able to take care of themselves, but the conversion is not total. Some people plateau and seem to go on for a long time.
How do you know when to be concerned?
BUTLER: One of the rules we use as clinicians is: if you forget your keys, that’s not so terrible, but if you forget what a key is for, that becomes serious...
... BUTLER: I’m afraid there’s a lot of romance in the literature suggesting that we can stop Alzheimer’s disease by cognitive exercises...
... There’s a distinction between advancing life expectancy and breaking the genetic barrier. Every species has a predetermined genetic life span. Certain fish live about a year. Some turtles live 200 years. Humans have about 110, 120 years at the outside of their genetic life span. We’re talking about increasing healthy years within that life span.
But wait you say -- what about us boomers feeling the steel jaws closing? Ask not for whom the bell tolls ... I do think there's hope that we'll delay our cognitive disability by a few years.
BTW, bravo to Butler for breaking the happy illusion that crossword puzzles are going to slow dementia development. It's such a sweet idea, but it's silly.