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Media Attention for the Dog Aging Project and Other Trials of Drugs to Modestly Slow the Progression of Aging

The Dog Aging Project launched last year, and is lavished with attention in this long press article. The initiative is a combined advocacy and research program intended to trial in pet dogs the small range of drug candidates - such as rapamycin - that have good data in mice to support both safety and the ability to modestly slow aging. In addition to the scientific side of things, this is a way to pull in more interest for the development of treatments for aging, and to gather greater support for moving to human studies. In that the goals of the Dog Aging Project are much the same as the human trial of metformin as a treatment to slow aging that is presently in the works. The bottom line is that we - the research and advocacy community - still have a long way to go when it comes to persuading the public, large funding institutions, and regulators that living longer through medical science is possible, plausible, and desirable.

Given the subject, the article here is narrowly focused on one particular view of aging and how to treat it. The scope is (a) traditional drug discovery and development, (b) slightly slowing the progression of aging by altering the operation of cellular metabolism, and (c) the prospect of a long, expensive slog to very marginal gains at some point in the decades ahead. This is a vision of the future in which humans gain a couple of years of additional healthy life sometime around 2030 because they can take a drug derived from or of a similar class to rapamycin. So on the one hand I think it is great that we now see more lengthy articles from the journalistic community that sensibly discuss both the treatment of aging and specific initiatives in aging research. It is also great that researchers are creating these innovative ways to both accomplish the science and attract more attention to the field. But at the same time, this particular approach of drug development and metabolic tinkering is an expensive and slow road to nowhere special. If it were the only path ahead, then fine, but it isn't. There is an entirely separate approach to treating aging based on targeted repair of cellular and molecular damage that could, if funded well, produce far greater gains in healthy life span for the same investment in money and time, as well achieving rejuvenation in the old.

You don't have to look far to see striking comparisons. Billions have been spent on trying to make drugs to slow aging out of sirtuins for example, and that collection of initiatives is an exemplar of the metabolic tinkering approach, hyped in its day. Yet the only concrete result has been to gain knowledge of a small slice of metabolism and its response to calorie restriction - no gain in health life or method to achieve that end has emerged. Meanwhile, for a tiny fraction of that sum, and in half the span of years, researchers taking the damage repair approach of clearing senescent cells in old tissues have already demonstrated robust benefits to health and life span in rodent studies. The pace of progress, the cost of progress, and the potential gains are night and day when comparing these two strategies. The type of longevity research that is carried out over the next few years matters greatly - our lives depend on the outcome.

Dogs Test Drug Aimed at Humans' Biggest Killer: Age

Ever since last summer, when Lynn Gemmell's dog, Bela, was inducted into the trial of a drug that has been shown to significantly lengthen the lives of laboratory mice, she has been the object of intense scrutiny among dog park regulars. The trial represents a new frontier in testing a proposition for improving human health: Rather than only seeking treatments for the individual maladies that come with age, we might do better to target the biology that underlies aging itself. While the diseases that now kill most people in developed nations - heart disease, stroke, Alzheimer's, diabetes, cancer - have different immediate causes, age is the major risk factor for all of them. That means that even treatment breakthroughs in these areas, no matter how vital to individuals, would yield on average four or five more years of life, epidemiologists say, and some of them likely shadowed by illness. A drug that slows aging, the logic goes, might instead serve to delay the onset of several major diseases at once.

But scientists who champion the study of aging's basic biology - they call it "geroscience" - say their field has received short shrift from the biomedical establishment. And it was not lost on researchers that exposing dog lovers to the idea that aging could be delayed might generate popular support in addition to new data. "Many of us in the biology of aging field feel like it is underfunded relative to the potential impact on human health this could have," said Dr. Matt Kaeberlein, who helped pay for the study with funds he received from the university for turning down a competing job offer. "If the average pet owner sees there's a way to significantly delay aging in their pet, maybe it will begin to impact policy decisions."

"I would resist the idea that we should shift funds away from cancer and diabetes and Alzheimer's, where there are clear drug targets, and say, 'We're going to work on this hypothesis,' " NIH Director Dr. Francis Collins said. "If you had a lot of money for geroscience right now, it's not clear what you would do with it that would be scientifically credible." Researchers in the field, in turn, say they might have more to show for themselves if they could better explain to Congress and the public why basic research on aging could be useful. "People understand 'my relative died of a heart attack, so I'm going to give money to that,' " said Dr. James L. Kirkland, a Mayo Clinic researcher. "It's harder to grasp 'my relative was older, that predisposes them to have a heart attack, so I should give money to research on aging.'"

Some companies have embraced the quest for drugs that delay aging. Google created Calico (for California Life Company) in 2013 with the goal of defeating aging. A start-up called UNITY has said it will develop drugs based on new research on aging mice suggesting that purging certain cells can extend a healthy life span. And a group of academic researchers is trying to persuade the FDA to recognize aging as a disease for which a drug can be marketed, which they hope will draw more interest from pharmaceutical firms. The agency recently greenlighted its proposed trial of a widely used diabetes drug, metformin, to see if it can delay the onset of other age-related diseases in older adults who have received a diagnosis of at least one, as one study suggests it might. But the group has yet to secure funding. One reason, the researchers say, is that the notion that aging is immutable is so deeply entrenched. "When I go out and try to raise money for this, the first thing people will say to me is, 'Eh, we're all getting older,' " said Steven Austad, a researcher at the University of Alabama.

Comments

This is why I think people favouring the damage repair/SENSRF approach to aging should set up a rival cat aging project ;-)

Or probably better, a chinese hamster aging project, as it would only take 3 years for people to see that hamsters that were supposed to be dead are still kicking.

Posted by: Jim at May 20th, 2016 10:20 PM

Having read that article in its entirety now, it sucks that they didn't mention (or seem to know about) the SENS Foundation damage repair approach. I think there will be a growing battle for airtime between the damage repair, slowing aging, and programmed aging camps. I saw that PBS documentary on treating aging that was linked to on here a while back, and the slowing aging metformin group around Nir Barzilai only mentioned Aubrey de Grey to slag off his 1000 year old LEV claim and portray him as an unhelpful weirdo.

Posted by: Jim at May 21st, 2016 4:03 AM

Ah, the comments section on that article is the place to go if you need a reminder of how against longevity the general public is against longevity. Tons of the usual comments about the normal things like having to work longer, population, environment, etc. I can't help but think that the overwhelming predominance of these attitudes (partly because of misconceptions) is really holding back funding, and will cause a real uproar when the first treatment for aging becomes available. Maybe I'm wrong. We'll see I guess.

Posted by: Ham at May 21st, 2016 8:46 AM

@Ham: Actually, I thought that comment section was distinguished by an unusually large number of people telling the naysayers that they were talking nonsense. But yes, the majority seems to feel the need to proclaim in public their desire to age to death, even as they take full advantage of all the newest medical technology of the day.

Posted by: Reason at May 21st, 2016 9:26 AM

Reason,

I definitely noticed that as well, but I think it was still disproportionate. Not to mention most of the NYTimes selected comments were for comments where people were expressing how bad it would be if people lived longer. My main problem with the need to proclaim their desire to age and die, is that it's always of the mindset of "I don't want it, so no one should have it". It almost always comes down to the same "only for the rich", "population level", "resources", "I don't want to live longer, because I have to work longer" or "I'll be sick longer" arguments against. Proponents of longevity never seem to demand that everyone be forced to live longer(which then becomes an only for the rich argument, anyways.) If someone wants to die at 20, 40, 60, 80 etc, who am I to tell them they have to live longer? No one should be telling anyone how long it's ok to live in either direction... Sorry. Not to mention that most of the commenters there clearly don't have reading comprehension as to what the goal of the dog study actually is, but that's a whole other can of worms to get into another day.

Part of the problem I think though, is something that you've also said... If they were born into a world where 120 was normal, it wouldn't be a problem... Talk of living longer and healthier like this is a breakaway from what people consider normal. I used to think that once a breakthrough was shown in mice, that more people would become excited about the potential in humans eventually, but I'm not so sure.

Posted by: Ham at May 21st, 2016 10:34 AM

To add about those comments there, and in general: Opponents always tend to portray supporters as extremely selfish. Yes, how dare people want to live their life (the only one they get) in better health, and for longer. No, no, instead they should just accept the hand they are dealt, and refrain from partaking in any of these evil treatments. Ugh. Also, look at the way these articles are always framed. It says "chasing immortality" right above the actual headline. Every article like this goes right to people talking about "immortality". Gotta get those clicks though, I guess. Sorry for the rant. I'm done now

Posted by: Ham at May 21st, 2016 11:34 AM

I think that, when the first treatments are available (senolytics, for example), people somewhere will use them. Maybe it will be in Russia, where people are more supportive of life extension, or maybe in other place. The world is bigger and more diverse than most people think. Not all countries are equal.

Posted by: Antonio at May 21st, 2016 5:01 PM

I think the high belief in religion in the US plays a pretty big role in this too. While there's nothing fundamentally contradictory between life extension and most religions, most people still are under the impression that this life of theirs is only a brief prelude and they'll probably get another one when they die. Even nonreligious "spiritual" people hold this belief. Kinda takes the air out of the tires of the necessity for life extension if you think you're already immortal. If only they knew they were walking the tightrope without a net.

Regardless, in the end I think what will really move people's opinions is results. That's why funding research that demonstrates real robust results is so important.

Posted by: KC at May 21st, 2016 7:19 PM

The author's negative comments appear directed at the faulty theory advanced for rapamycin's success. There is another theory for which rapamycin observations fit VERY well, which goes like this:

From birth to death we walk a narrow path, with lupus on one side (from autoimmunity that becomes more problematical as cells collect mutations), and cancer on the other side (as some mutations develop into cancers). When we are young this path is wide, but it becomes extremely narrow with age. As we drift a little off the center of this path, we either die of an autoimmune illness, or die of cancer.

However, there ARE drugs that can adjust this path and push back its edges. Rapamycin is a tissue-rejection drug that reduces the effects of autoimmunity while increasing the likelihood of cancer - effectively steering the path away from the autoimmune side and toward the cancer side. Other drugs like dichloroacetate (DCA) push back the edge on the cancer side, thereby widening the path for rapamycin to work.

Correcting commonly-low body temperature appears to facilitate "steering" down the center of this path, with the result that people with a 37C=98.6F daytime body temperature live ~20 years longer than those with lower temperatures.

Nearly everyone dies of a failure to navigate this path, rather than reaching its end. John Rose's work on fruit flies suggests we would live several times longer if we weren't bred for short lifespans - mating with like-age people and bearing children only while young, passing our wealth on only when we die, etc. I strongly suspect the thing that has been broken by our dysfunctional mating and inheritance practices is our ability to dynamically navigate this path, which drugs might facilitate.

So, when something works but the theory for its operation stinks, let's work on the theory, and NOT object to what seems to work.

Steve

Posted by: Steve Richfield at May 22nd, 2016 4:10 PM

@Steve: "Correcting commonly-low body temperature appears to facilitate "steering" down the center of this path, with the result that people with a 37C=98.6F daytime body temperature live ~20 years longer than those with lower temperatures."

If you have some kind of legitimate human studies that demonstrate this please post them. All that I've heard on the temperature front is actually the opposite, like transgenic mice who are engineered to be colder than normal living 15-20% longer than controls (Which of course may not apply to humans).

Posted by: KC at May 22nd, 2016 8:50 PM

@KC: There are a fair number of posts on body temperature in the archives.

https://encrypted.google.com/search?q=site%3Afightaging.org+body%20temperature

Body temperature is lowered in calorie restricted animals, tends to fall with advancing age in humans, and lower body temperature might be associated with Alzheimer's progression. I don't think there's much overall unity in views of what is going on, and the various pieces of data I know of make it sound like there is a far from straightforward set of relationships at work here.

Posted by: Reason at May 22nd, 2016 9:07 PM

@Reason: Thanks for the reply. Indeed, I agree that temperature's relationship with aging is complicated. I'd still be interested to know where Steve got the idea that "correcting" body temperature to a warmer state makes people live decades longer. Sounds very fishy to me.

Posted by: KC at May 27th, 2016 5:57 PM

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