Skepticism on the Near Future of Rejuvenation Biotechnology

Many in the mainstream research community still believe that the only viable way forward to extend life is to slow aging by manipulating metabolism - such as by trying to replicate the effects of calorie restriction through drugs. In their view, this is a long, hard, slow project that is unlikely to produce meaningful results within our lifetimes, and when it does produce results they will only induce a modest extension of healthy life.

These researchers do not yet acknowledge the potential of repair-based strategies that aim to reverse the forms of age-related cellular damage that most likely cause aging - the known fundamental differences between old tissue and young tissue - and thus produce rejuvenation. This should be less expensive and faster in addition to producing a better end result, such as indefinite extension of healthy life.

Extending life by slowing aging has been accomplished in many different species and in many different ways, but rejuvenation research is a younger, underfunded field that has yet to advance to the point at which it can boast the same panoply of demonstrations. All we have so far are examples of rejuvenation achieved in some aspects or mechanisms of some tissues, and not so many of those either. Even in the scientific community, people tend to believe in what they can see rather than what is plausible but not yet in evidence:

In an age of breakneck technological and scientific progress, it can seem at times like anything's possible. [For] all the exponential advances, though, some technologies remain firmly in the realm of science fiction. We can't engineer genius babies. We're never getting our hoverboards. And, perhaps most dispiritingly of all, we haven't figured out a way to cheat death.

It isn't for lack of trying. Research centers around the world have teams devoted to the study of human longevity, and scientists have been working furiously for years to uncover the secrets of long life in everything from mice to yeast to hydra. In fact, they're making a lot of progress, and there's good reason to be optimistic that they'll someday hit on a breakthrough that will allow people to live significantly longer than they do today. But if you're sitting around waiting for the singularity, you might want to stand up and go for a jog instead.

One problem is that humans are a lot harder to study than mice. A [study] found that mice injected with a substance that inhibited a molecule known as NF-KB lived longer than normal. Mice injected with NF-KB itself died young. That seems like compelling evidence that the molecule, which is involved in the body's response to stress, plays a role in how mice age. But what works in mice doesn't necessarily work in humans. And who's going to approve the study that injects people with an NF-KB inhibitor and to see how soon they die?

No one - especially since the FDA doesn't recognize aging as a disease. That makes regulations and approvals trickier for potential anti-aging treatments. And some researchers in the field complain that it makes it harder to get funding for big studies. The bigger-picture problem is that human longevity is a confluence of so many factors - genes, nutrition, lifestyle, luck - interacting in so many complex ways that there is unlikely ever to be a surefire way to live to 120.



Shouldn't any effective anti-aging therapy also be an effective therapy for one or more specific diseases of aging, and thus eligible for FDA approval on those grounds? That is, if it can reduce deaths from heart attacks, improve cognitive function in Alzheimer's patients, improve bone density in osteoporosis patients, cure cancer, prevent age-related macular degeneration, or treat any of the countless maladies of aging, then the FDA will consider it on those grounds. If not, how good of an anti-aging therapy can it really be?

Posted by: Brandon Berg at June 3rd, 2013 9:11 PM


That's part of why I started contributing to SENS: the A2E and 7KC projects, which are pretty far along, have this sort of direct affect. If either of them can be made to work, they have specific enough targets that it can be expected that they will get approval. They will also be strong 'proof of concepts' therapies for one of DeGray's seven categories of aging damage.

Posted by: Dennis Towne at June 4th, 2013 1:59 PM

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