Back in 2004 I predicted that we’d have life extension by 2014. I have on several occasions reaffirmed this prediction. Last year I added:
This idea – that progress in life extension science continues regardless of its description – is part of the reasoning behind my prediction that we will have some form of life extension by 2014. Perhaps I should modify this prediction to say that it will be an off-label treatment – something gerontologists know extends life, but won’t publicly admit extends life.
I was responding to the timidness of some gerontologists to admit that the they are engaged in life extension science. But there’s more than timidness at work here. Life extension will, I think, turn out that the best treatment for a host of diseases. What physical problem would not benefit from a younger biochemistry?
Phil said in our most recent FastForward Radio show that solutions for diseases will “come along for the ride” when we get life extension. It could also work the other way around. Especially with the earliest incarnations, life extension could come along for the ride while we are searching for treatments for specific diseases. Case in point:
Human clinical trials to test [SIRT1 activating] compounds in diabetes are slated to begin early next year, according to Sirtris Pharmaceuticals, based in Cambridge, MA, which developed the drugs. “As far as I’m aware, this is the first anti-aging molecule going into [testing in] man,” says David Sinclair, a biologist at Harvard Medical School, in Boston, and cofounder of Sirtris. “From that standpoint, this is a major milestone in medicine.”
If these trials prove this drug to be effective, it will be marketed as a drug for diabetics and people who are at risk of diabetes. But the truth is that it could be good for everybody because it will duplicate the chemistry of caloric restriction for those of us who would perfer not to live on starvation rations.
For several years, scientists have been on the hunt for a drug that could bring the benefits of caloric restriction without the strict diet. Last fall, Sinclair and his colleagues took a first step when they showed that mice given resveratrol, a molecule that activates SIRT1, stayed healthy when fed high-fat foods. But there was a catch: mice were dosed with the human equivalent of more than 1,000 wine bottles’ worth of the compound, an amount not possible for humans to imbibe or take in pill form.
Now a team at Sirtris, led by CEO Christoph Westphal, has identified a group of compounds that activate SIRT1 1,000 times more potently than resveratrol does. According to findings published today in the journal Nature, the compounds bind to the enzyme and dramatically increase its activity. Because the new compounds are more powerful, much lower doses are likely needed to achieve the same beneficial effects. “We believe doses needed in humans for the novel compounds are probably on the order of hundreds of milligrams, similar to many marketed drugs,” says Westphal.