Wednesday, September 15, 2010

Russian Scientist Claims to Have Found Cure for Aging

Could there really be one pill that keeps you young indefinitely?

This news recently hit the media (link), and the headlines so far have been pretty wild. Catchphrases like "forever young" and "secret to eternal life" will surely spark interest even among the non-immortalist crowd, but how much of it is just hype?

So what is this news all about? The drug in question is the work of professor Vladimir Skulachev, who has dedicated his life to study (and solve) aging. Now he's finally found an antioxidant with anti-aging properties and plans to start selling it in just a few years.

Despite what supplement salesmen will tell you, antioxidants by themselves are not worth much in terms of extending lifespan. In fact, the whole "free radical theory of aging" was put to rest a long time ago. Yes,  antioxidants extend the lifespan of simple organisms, but they've repeatedly failed in mice and rats, and there's no evidence that antioxidants would make humans live longer.

There's a pretty simple reason for that, too: normal antioxidants don't reach the mitochondria where most of the free radical damage occurs. No matter how much vitamin C pills you pop or how many acai berry shots you down, you won't be making any difference in the rate of mitochondrial damage.

It appears that Skulachev has synthesized a mitochondrially targeted antioxidant. There's no detailed information in the article, but based on the papers Skulachev's group has published in the past, it looks like the compound in question is SkQ1, an antioxidant attached to a positively charged ion. Experiments have shown that SkQ1 prolongs the lifespan of a variety of species, including mice (link, link).

Clinical trials on humans are underway, and if everything goes smoothly, the drug will be out in a few years. After successful results from animal studies using eye drops, Skulachev tried it on his own cataract. After six months, his cataract was gone.

So what's the catch here? Well, looking at the lifespan data from mice, they're not talking about an increase in maximum lifespan but in median lifespan. The oldest mice receiving the drug did not live longer than the oldest mice in the control group, they just had a squared mortality curve. In other words, the mice that got SkQ1 made it to old age more often than the control mice.

In humans, this would translate to something like being relatively healthy at 90 years old but still dying around 100 years of age. There's no evidence that you could live to be 150 by taking SkQ1. Thus, claiming that "the cure for aging" has been found or that the "fountain of youth" is finally here is just plain wrong.

Aside from the reality check, this is still very good news. Even squaring the curve would be a fantastic thing in humans – if it works in humans. That would mean that a lot of the diseases associated with aging would be postponed significantly and old people would enjoy a better quality of life.

And, for those of us trying to stay as healthy as possible while waiting on true rejuvenation therapies, drugs like this would be warmly welcome.

For more information on aging and longevity, see these posts:

Selegiline and Lifespan Extension
Does Intermittent Fasting Increase Lifespan?
The Curious Case of Human Hibernation
How Do People Feel about Life Extension?

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10 kommenttia:

Anonymous September 16, 2010 at 12:36 AM  

Ray Kurzweil will be ecstatic.

Eric Drexler September 16, 2010 at 9:02 PM  

Antioxidants have a history of great promise and great disappointment for life extension, and I doubt that this will be an exception. A basic problem is that the presence of reactive oxide species not only causes damage, but also stimulates mechanisms for protection and repair. Reducing ROS does not necessarily shift the balance much, or even in the right direction.

Calorie restriction, by contrast, stimulates repair by stimulating autophagy (as you've discussed on this blog). There's increasing recognition of the central importance of autophagy, and that autophagy can be stimulated by many different means, including resveratrol and trehalose.

I've recently posted some discussion and abstracts on this:

“Autophagy: Why you should eat yourself”, and

“Trehalose, autophagy, and brain repair: Sweet”.

JLL September 16, 2010 at 10:54 PM  

@Eric Drexler,

At least this is an improvement over previous antioxidants. IIRC, melatonin can also reduce mitochondrial ROS and extend lifespan in mice -- unlike ascorbic acid, for example. So I think mitochondrial antioxidants hold at least some promise.

I agree on the hormetic aspect (some pro-oxidants may actually be good), but if this antioxidant really did increase median lifespan then I guess it was a net positive.

As for autophagy, yes it seems to be an important part of CR, but if autophagy alone extends lifespan, why doesn't intermittent fasting extend lifespan? I don't see why it wouldn't increase autophagy. Resveratrol doesn't increase maximum lifespan either.

Trehalose looks interesting, I'm going to check out your posts in more detail now. I remember trying to order some trehalose in the past but I guess the shipping costs were too high.


Eric Drexler September 18, 2010 at 10:47 PM  

@ JLL —

Your point regarding autophagy, CR, and maximum lifespan is important and correct: While strong autophagy appears to be necessary for long life and health, it appears to be insufficient for extending maximum lifespan.

Also, thanks for prompting me to examine the second paper and learn more about the research. The results that the authors describe are impressive and surprising, and as they say, unlike the effect of other antioxidants:

“ROS-induced injuries are known to be accumulated in especially large quantities at late ages. Therefore, one might expect that SkQ1 would be more effective near the end of life. In our experiments, we observed, in fact, quite opposite relationships. SkQ1 prevented age-dependent death at early and middle stages of aging, being efficient only slightly in increasing the maximal lifespan.”

The authors attribute this to an indirect, signaling effect operating through an “aging program”. The evolutionary reason they offer for the existence of such a mechanism doesn’t make evolutionary sense — gene-level selection overwhelms the kind of species-level selection that they postulate. Nonetheless, a mechanism might exist that has similar effects, but a different origin.

If these results can be confirmed, then they are of course important regardless of the mechanism.

Regarding antioxidants in general, if antioxidants have positive effects offset by an anti-hormetic effect on autophagy, I would be interested in seeing the results of combining well-chosen antioxidants with well-chosen means of autophagy induction (other than CR).

Jan September 22, 2010 at 1:47 PM  

This reminds me of Juvenon, which was also aimed at the mitochondria and had the advantage of having a great name (Ames) behind it.

Juvenon looked very interesting, but as the results of research into its effects doesn't seem to be published, even on the company's own website, I suppose it didn't work as good as they hoped it would.

Anonymous October 1, 2010 at 9:21 PM  

Hey JLL, just came across the blog, love it. I want to post a couple of your articles on my website. Do you have an email I can contact you at, couldn't find one here. I want to make sure you approve of the posting and find out exactly how you want to be credited as the author.


Anonymous March 7, 2013 at 4:07 PM  

I am very interested in this. When will it be available for human use? Please e-mail at:

Anonymous January 28, 2014 at 11:12 PM  

This is in addition to my previous post. I was curious as to how long it will be before I can get a response to my inquiry. Please let me know and e-mail me at: peggyfrz@aol. Thank you and have a good day.

JLL January 31, 2014 at 11:48 AM  


I have no idea.


maxhealth March 26, 2014 at 12:42 PM  

One would need to search hard for a blog in which more inaccurate, pseudo science and laughably simplistic statements reside. Doesn't the word "evidence" mean anything to any of you?

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