James Peyer at TEDxStuttgart: Can We Defeat the Diseases of Aging?
My attention was drawn today to a recently published presentation by James Peyer. He heads up Apollo Ventures, one of the new crop of investment concerns focused on funding companies that are developing means to treat aging. These include the Longevity Fund, first out of the gate some years ago, as well as Juvenescence and the Methuselah Fund, created this year, and a repurposing of existing funds, such as Michael Greve's Kizoo ventures. Apollo Ventures is the source of the Geroscience online magazine that helps to advance and explain the position taken on aging by this group; this is something that more investors should do. It is a cost-effective means of talking up one's industry and positions, of reaching out to the community that includes founders and potential founders of companies to invest in, and so forth. In the best of worlds it does all of that and also provides a service that is useful.
So, my grandfather was kind of my hero, growing up. He was kind, smart, super-passionate about every little thing he was doing. And really argumentative about it too. He was happy, successful, loved his family, and if you asked me what living a good life meant when I was a kid, I would have told you it was to be like my granddad. So when he was diagnosed with cancer when I was 14 it shattered my world. We were going to go on vacation that summer, but his doctors found two tumors at the same time, one in his throat and another in his brain. So instead, I spent that summer watching week by week, month by month, as he got sicker and frailer, and also, heartbreakingly, forgetful and paranoid. He was given medicine that kept him alive a little bit longer, but he never really was himself again. And in my last conversations with him, he talked with me about how terrifying it was, knowing that, day by day, he was slipping away. Knowing that he wasn't getting better.
When he died I fell into a depression. I couldn't stop thinking about the fact that no matter how good of a life we live, every one of us has the same thing waiting for us that my granddad did. Months or years of suffering of some terrible disease, like cancer, or dementia, or a stroke. What was the point of getting 'A's in school or scoring the winning goal in the big game if that's all we have to look forward to? I spent months feeling this way, and it wasn't until I stumbled across an idea that I was finally able to crawl out of that depression. I latched on to something that gave me a purpose. What if I spent my life fighting against those diseases, so that other people didn't have to suffer from them the way that my granddad did? That purpose has been keeping me going until this very day.
So there I was, I had my epiphany, the big idea, but I had no idea how to go about doing it. How could I fight against the diseases that had killed every single person I knew who had died? I started casting around and learning as much as I could, and it didn't take me long to find something interesting. While cancer and heart attacks are today's biggest killers, they haven't always been. As recently as 1900, most people died of infectious diseases. The leading causes of death were pneumonia, tuberculosis, and influenza, and the average life expectancy was 45 years old.
Doctors and scientists spent the last century struggling heroically against these diseases - and we invented antibiotics and vaccines in order to fight them. Those were the biggest challenges of the 20th century. We've been so successful fighting them that now we live in a world where the average life expectancy is 80. In developed countries all ten of the leading causes of death are caused by simply living long enough to not die of anything else. The 21st century will be defined by our struggle against these diseases of aging, and it is not going to be an easy one. For 75 years, these have been the leading causes of death for humanity, and everything we've done to fight them has barely made a dent in the number of people dying of any one of them. In fact, they are rising as a fraction of total deaths in the world, as we continue to make strides against infectious disease, malnutrition, and violence around the world.
You see, as a society we look to medicines to make us well when we're sick, and so far almost everything that we've designed to treat the diseases of aging has fit in that paradigm. We wait for someone to get cancer, to have a stroke, or start losing their memories, and then we try to do something about it. But this approach hasn't really been working. Since 2000, we've done 200 clinical trials in humans just for Alzheimer's disease, and 99% of those have failed. The two that succeeded haven't even given us a drug that does much to treat Alzheimer's disease. We spend over $20 billion a year on cancer research and trials, but most of the gains we've made against cancer since 1970 have come from better diagnosis of cancer, not from curing the disease.
This should tell us that we're doing something wrong in our approach to the diseases of aging, because, unlike infections, the diseases of aging are caused by the slow, gradual build up of damage to our bodies over a lifetime, before they ever cause enough of a problem for us to go see a doctor. And by the time that we go to see that doctor, so much has happened inside of our bodies, that there is not much that they can do to help us. So this is how I started my academic career. I was one of a small group of scientists, and we were all thinking the same thing: if we ever wanted to eliminate Alzheimer's and cancer, the way that we eliminated smallpox, we would have to take a different approach to healthcare. We would have to treat the diseases of aging by anticipating them, building medicines that could remove damage caused by getting old before it ever accumulated enough to make us sick.
And this kind of makes sense, right? Because we all feel the effects of getting old right now, even when we're not sick. I mean, who here can run as fast as they could when they were 18 years old? Or maybe bounce back up after falling out of a tree like they could when they were 12. I am by no means old, and even though my risk of osteoporosis or cancer is diminishingly small, I am getting older, just like all of you are. My blood vessels are hardening. My neurons are starting to get tired. My DNA is mutating. I'm losing the battle to keep my cells and tissues in good condition. Right now we only think of this progressive accumulation of damage as a problem when everything goes to hell, and it erupts as some kind of disease. If we want to stop this gradual build up of damage in our bodies, we're told that the old things we can do are eat better, exercise, avoid smoking, hope that we've gotten lucky with our genes. It's not exactly a hopeful message. We're not leveraging the power of modern medicine to prevent us from getting sick from the things that are killing us the most.
But that is all changing. Because for the first time in history, we understand what makes us get older. We've traced to the biochemical level the diseases of aging and what causes them, and we've been able to categorize the damage of aging into nine buckets. Things like the random mutations of DNA, or the exhaustion of our stem cells. Our understanding is now at the cellular and molecular level, which means that we can actually design medicines to target and treat these things. And those medicines actually exist. We have a repository of over 50 interventions, whether a small molecule drug or a genetic change, that can extend healthy life by as much as 50%. Think about that: 50% longer without getting Alzheimer's disease, or cancer, or having a stroke, or having our bones and muscles wear down. 50%! In mice. And so the mice are super-excited about this. But what does it mean for us humans?
Well, luckily this is how new medicines are usually born. We take a piece of research and test it in mice to see if it works, and if it does then we advance that to human trials. And the good news is that we have 50 things that are ready to test. But making the jump from mice to humans for these sorts of diseases won't exactly be straightforward. You see, a trial to prevent a disease instead of to treat it has some additional challenges. It is more time-consuming and more expensive, which means the companies that would have to pay the tens of millions of dollars for these trials are often hesitant to do so, when they are used to doing the more traditional reactive trials. However, we have a glimmer of hope here too, that may be able to fast-track some of these preventative medicines into the clinic. You see, if you build a medicine that does a good job preventing damage that could eventually cause disease, it turns out that the same medicine can stop a disease from getting any worse by halting that same damage. And sometimes we can even repair the damage, reversing the effects of a disease.
Now, if you caught yourself thinking "but wait, that sounds completely obvious!" I might forgive you for that. It does seem reasonable that if something is going wrong with my cells, and I fix that thing, then it would help whether or not I've labelled my cells as diseased. But until very recently we just didn't know that, because it hadn't really been tested. The people who are working on studying what goes wrong in an old mouse and the people who are giving treatments to Alzheimer's patients weren't really talking to each other. But now they are, and armed with this new knowledge of what makes us age, and what we can do about it, we're able to pursue two ambitious goals at the same time. First, we have the ability to create new medicines to treat patients suffering from diseases of aging. This is what motivates me and the people that I work with, every single day, using this new research to come up with a medicine that can impact millions of people who are sick right now.
But there's also a second thing we can be doing. As we create new medicines for these diseases, and test them in the traditional way, we have to remember that what we really want is a medicine that can prevent disease instead of just treating it. And to get there, we're going to need to have proven, safe, effective medicines targeted at treating the damage of aging, and there has been progress on this front as well. One of the 50 interventions I told you guys about before happens to be an approved drug that's already been used in humans for decades. So after results in mice came out showing that we could extend their healthspan, a group of researchers started combing through hundreds of thousands of patient records who had been taking this drug, and they found something incredible. This drug - that people didn't take to prevent the diseases of aging, they took to prevent their blood glucose from going up, because they had diabetes - but when then were on this drug, they had a lower incidence of both cancer and Alzheimer's disease. Even compared to healthy people that didn't have diabetes.
So this thing may actually be working. This drug, which is called metformin, can extend mouse life span on average by 5-10%, which, if it works the same in humans, would mean 4 to 8 extra healthy years. And that's a lot, because if we invented a pill that miraculously cured all cancer in all of humanity right now, we would expect an average life span gain of about three and a half years, because we would succumb to another disease as we got older. So based on this research, a new clinical trial has started to test whether people who are healthy can take metformin and avoid cancer and Alzheimer's disease. So you might want to wait for the results of that trial before you go and beg your doctor for diabetes meds.
So now you may be asking yourself, whether it's this trial or another medicine that gets approved, who is going to pay for these preventative medicines? And it's worth pausing here for a moment to reflect that insurance companies are actually already paying for something very similar. Many of us in this room may be taking medicines that lower our cholesterol, which reduce the chances of getting stroke. When we invent new medicines that can not just reduce your chances of getting a stroke, but also Alzheimer's disease and cancer, which are way more expensive for those insurance companies to treat, you can bet that they'll be lining up to pay for those drugs too. With insurance companies in the game, this means that pharma companies are going to pay top dollar for the rights to test and sell these medicines. And that means that scientists working at universities or at biotech companies are going to be competing with each other to create the next greatest preventative medicine. It's a positive feedback loop, and the cycle can be kicked off with just one victory. Even a drug that extends healthy life span by a year or two can start a cycle of investment and research and testing that can change the way we do healthcare forever.
And I have good news, because there are 50 interventions that we already have ready to go. We just need to get to work. As I close up here, I think it's worth addressing one little thing, which is that I get asked all the time if we even should be trying to treat aging or extend life. I think that this is absolutely the wrong question. I think that the question we should be asking ourselves is "when do you want to get Alzheimer's disease?" When do you want to have a stroke? When do you want your muscles to break down? For most of these, I think everyone that I know would say "never". It's like asking someone in 1900 at what age they'd like to get tuberculosis. Or polio. "No thank you!" The evidence we have suggests that we can make new medicines based on our understanding of aging that can help people who are suffering from today's biggest killers. Yes, this will change healthcare. It will redefine medicine in the 21st century in the same way that vaccines and antibiotics redefined medicine in the 20th. But that's good! That's progress. Because I want to be able to enter the 22nd century and face our newest medical challenges, whatever those may be.
We have the opportunity in our lifetimes to flip healthcare on its head, by wedding the power of modern medicine with our understanding of what makes us age. We're going to invent new medicines that can treat the damage caused by getting old before we ever get sick. And that? That's a future that I can look forward to.
Peyer's position on aging incorporates the views of the Hallmarks of Aging authors and the Longevity Dividend scientists, in that while he views aging as damage accumulation, and our responsibility as being to build the means to repair and prevent that damage, he has enthusiasm for moving ahead with approaches to slow aging that I consider to be largely a waste of time and effort. Take metformin, for example. To my eyes the animal data is shabby and unreliable, with studies showing all sorts of outcomes, and the effects in humans are too small to spend any time on in a world that includes the SENS rejuvenation research programs and the senolytic therapies to clear senescent cells currently under development.
For Peyer, the present TAME metformin trial is a useful step on the road towards obtaining more funding and attention in order to build better therapies: it is a wake up call. I'm dubious, however, that all it will take to start the avalanche is just a little success in the matter of life span, health, and mortality. We have plenty of examples from past years of what I would call a little success: the effects of statins on cardiovascular mortality, the bisphosphonate studies showing significant reductions in mortality, and so forth. The revolution hasn't happened in response to any of this; 99% of medical research and development is still business as usual, creating expensive and marginal patches that fail to address aging in any meaningful way. So why would it happen over a modest reduction in rates of age-related disease for people taking metformin?
I think we need bigger and better successes. Marginal improvement won't cut it. We need outright, obvious, sizable rejuvenation. Will senolytics wake the world if they produce a reliable five year gain in healthy life expectancy, as well as reversing numerous diseases and conditions of aging? I don't know. It may be that even that will just be absorbed into the current state of things, and 95% rather than 99% of medical research and development will continue to be business as usual. Inertia is an impressive thing in these large institutional scientific and regulatory communities. Nonetheless, we need to keep aiming high. If we aim low, then all we'll get in the end is poor results on the only metric that matters, the degree to which health is restored and extended.
What you say at the end is what worries me about the Hallmarks. If they become the favourite challenger to the mainstream instead of SENS, as it seems very likely, then, since the Hallmarks aren't comprehensive, there is a real possibility that they don't produce a big enough increase in lifespan or health metrics to replace the mainstream and the stablishment will return to the one-disease-at-a-time approach.
Hi,
it's sad that the CR messaage lingers and we are destined to more 'let's make metforming/CR' our cure for diseases...and aging (because CR/metformin WILL cure aging, of course (sarc.))
''As we create new medicines for these diseases, and test them in the traditional way, we have to remember that what we really want is a medicine that can prevent disease instead of just treating it. And to get there, we're going to need to have proven, safe, effective medicines targeted at treating the damage of aging, and there has been progress on this front as well. One of the 50 interventions I told you guys about before happens to be an approved drug that's already been used in humans for decades. So after results in mice came out showing that we could extend their healthspan, a group of researchers started combing through hundreds of thousands of patient records who had been taking this drug, and they found something incredible. This drug - that people didn't take to prevent the diseases of aging, they took to prevent their blood glucose from going up, because they had diabetes - but when then were on this drug, they had a lower incidence of both cancer and Alzheimer's disease. Even compared to healthy people that didn't have diabetes.
So this thing may actually be working. This drug, which is called metformin, can extend mouse life span on average by 5-10%, which, if it works the same in humans, would mean 4 to 8 extra healthy years.''
I really don'T undertand, people still cling to this bs. To have faith in CR mimetics because that's all there is available right now is understandable and what we can say to the large public. Why not talk about SENS instead or like something that acutally has a concrete Plan..instead of resassing of old stuff. At least they are saying we must repair the damages, but they still think about CR-like methods as 'their plan'. It's doomed.
'' I think that the question we should be asking ourselves is "when do you want to get Alzheimer's disease?" When do you want to have a stroke? When do you want your muscles to break down? For most of these, I think everyone that I know would say "never"''
Exactly, never, which means you have to act 'at the source' not continue thumping 'let's prevent diseases' by 'preventing them', you are just putting a band-aid on the diseases and you might not have Any disease - but you will Still die anyway. They are taking the softer road - patch the diseases and you wil liver a long life to maybe 122 that's it.
Never means never. Which means for it be never, you will have to cure the cause of these diseases : aging. But that has not gotten 'through' yet in the large sphere. Because they think there is notthing we can do about 'aging' but only 'diseases/health'. At least, they talk about 'Repairing damages' that's a good thing, but then the whole endeavor ends 'at preventing diseases'...why do they not talk about LIFESPAN extension - you know like going over a century..oh not that,s too far fetched boguss....that's why there 50 interventions will fail : they all aim at 'slowing diseases (à la CR) and 'metformin''. It is not going to work if we wish to Defeat/Cure Death, end aging. That video we saw a few weeks ago is Far better in its message, because it talks about ENDING aging. As far far fetched it sounds, we need to talk about it and use SENS, and other Proven studies that show the repairing damages is not about keeping 'healthy' and that's it you die later in few decades. Because THAT is what they are saying. We are talking about Rejuvenation, but they never talk about that in with Truth and TALK about it so people stop saying I wish to be healthy and die at 101. because that is what stops us from getting funds towards SENS and other rejuvenations endeavors that just dont' stop diseases and make you healthy - they CURE aging BECAUSE aging is THE CAUSE; yet they say 'we have to reapair damages' because it is the case - oblivious or hypocritic at the same time; it is so difficult to understand. But people will bring so many 'Excuses' No no we can't live for an eternity - overpopulation, no ethics moral, immrtal are bad self people, How Could You WANT to live about 120, Unfathomable...blablabla more bs
But it's not all a loss, at least there are developments, sadly this huge money is going For tHem, and SENS and other REAL stuff that will REVOLUTIONIZE our future and HUMANITY
gets chump change. But that'S because there are many dissidents and counter people who Hate this whole rejuvenation (including biogerotonlogists) and think SENS and other rejuvenation are full of sh...as such wehat do we end up ni the news with, more CR/metformin funding research bs
''What was the point of getting 'A's in school or scoring the winning goal in the big game if that's all we have to look forward to? I spent months feeling this way, and it wasn't until I stumbled across an idea that I was finally able to crawl out of that depression. I latched on to something that gave me a purpose. What if I spent my life fighting against those diseases, so that other people didn't have to suffer from them the way that my granddad did? That purpose has been keeping me going until this very day. ''
No sh... How about MORE...'I spent my life fighting against DEATH/AGING'...not just diseases...let me repharse it for you
''What was the point of getting 'A's in school or scoring the winning goal in the big game if that's all we have to look forward to? I spent months feeling this way, and it wasn't until I stumbled across an idea that I was finally able to crawl out of that depression....when I foudn out I had atherosclerosis and I wans on my death bed...and I would be dead in a few decades...I had a n epiphany, I NEEDED to stop aging CURE death, yes very much said like that, not just put band aids on and keep on saying 'let's fight diseases. period. I realized I had no choice but to reverse aging and thus, post-pone time of death (in my case atherosclerosis death). Sure it's a disease like any other...but I still age, and with that one, even faster...so you see what I mean...AGAIN, the problem is AGING/DEATH, that's the problem, not the diseases; they are SECONDARY to aging/death and should be seen as so; they dependent/interIndependent (Entwined) but you still age; that's the CRUX of it, you can keep Avoiding talking about the MOMENT you die (whether at 70 or 120) death will still will come''
''''What was the point of getting 'A's in school or scoring the winning goal in the big game if that's all we have to look forward to? ''
Just a 2 cent.
PS: TL DR, the message is wrong.
Aubrey de Grey say that 'Hallmarks' is the same as SENS, yeah, they are less clear, messing things from different levels, but the idea is the same. I believe we should not blame Mr Peyer too much. The good news is that 5 years ago we hadn't got even that -- now we have some mix of that in 'Hallmarks' and in next 5 years we will get SENS finally accepted by business. We just can see the odds of transition period. Hovewer, not everyone can wait 5 years, people die every day -- that is the real problem.
Yes it is a shame that he is enthusiastic about metformin.
Still it is nice to see a speech other than Aubrey De Grey's standard stump speech for the bits on why aging is bad, and how trying to treat the diseases of aging is the wrong approach.
@Jim
Bro he is in his early longevity research , as everyone get excited when they hear of metformin,resveratrol, he will be soon realize that it can give 1-2 year that is all , dont worry he will find his way as long as he come to know these drug does not rejuvenate. I am sure because I was one of them some time ago
@Ariel
No, he didn't say they are the same but similar. There are hallmarks that aren't part of SENS (telomere attrition, epigenetic alterations, deregulated nutrient sensing, altered intercellular communication) and SENS categories that aren't hallmarks (crosslinks, overspecialized T-cells) and, even for the categories and hallmarks that are the same, the treatments differ (WILT and allotopic expression vs compounds that enhace natural DNA repair mechanisms).
The Hallmarks incorporate the SENS damages and visa versa and are essentially the same thing. Aubrey has said this many times so it is not a Hallmarks vs SENS situation, Hallmarks is a repair approach to aging and to make it SENS vs Hallmarks is a pointless and potentially damaging slapfight.
At Madrid conference, he talks about it once again. 23:10 "It's exactly the same idea as I have already put forward"
https://www.youtube.com/watch?v=ZXxt7V53Uvw&t=1271s
Regards the approaches to the damage, there is more than one way to skin a cat in biology and adherence to one and only one approach is dogma, not science. If something works then it works, simple as that.
At least things are moving in the right direction. If we can get the (to us) conservative message out there that we need to address aging to prevent Alzheimer's, cancer, heart disease, etc., then that's half the battle. The next stage is the argument that slowing aging with rapamycin, metformin, NAD precursors, etc., is only going to help healthspan and we should be looking to really turn the clock back rather than just slow it. In my view both SENS and the Hallmarks paper give us some ideas about how we can go about doing it.
While you do have a point that small molecule interventions are inherently limited, the radical approaches of SENS involving gene and cell therapy are mostly still far off. Apollo and similar funds aim to open the floodgates of interest in geroscience, starting with some proofs of principle.
Apollo has been involved in senolytics, BTW, just behind the scenes so far.
In defense of my friend James Peyer, who was involved with SENS years ago (as was I), how many millions of dollars have YOU personally brought into the geroscience ecosystem lately? Probably a few million less than James.
Let's not let the perfect be the enemy of the good. Political infighting will misdirect the energy of the geroscience community when we need to stick together.
@Sebastian A: What funds are spent on, the expectation value of the research and development, is of vital importance. Apollo can't possibly bring in more funding for geroscience than has already been allocated by the NIA, for example, and yet here we are having the discussion about needing to open the floodgates. We understand quite well that NIA geroscience funding is going to projects that in 99% of cases won't do much for life span, and therefore different projects are needed to advance towards practical therapies.
A billion dollars has been spent on sirtuin research over the past twenty years under exactly the same rationale as is presently applied to metformin and the like. What came of that in terms of practical outcomes for human therapies? Nothing. Geroscience as a philosophy of development is near entirely a matter of doubling down on the high level strategy that produced sirtuin research: tinker with metabolism to slow aging based on outgrowths of calorie restriction mimetic research. The only place it isn't this is where it adopts SENS approaches that can run through the established small molecule drug development infrastructure, such as senolytics.
My hope is that the advent of true rejuvenation will cause the low expectation value projects to wither away, but I'm not optimistic. The alternative is that everyone will point to senolytics to say that standard small molecule development can win against aging, ignore the radical differences in underlying science and philosophy of development entirely, and waste the majority of time and funding in more sirtuin-like projects that can't possibly produce sizable effects.
Expectation value for size of effect matters. It is the primary concern once people are persuaded to treat aging as a medical condition at all.
@Sebastian, I agree with you, and I would agree even more if we are talking on things like AI or Mars colony. But not everyone can wait 5 years when Mr Peyers switch his focus from metformin to glucosepane. Remember, we are talking on human lives. People die everyday in pain. Another very important thing I wish to say you is that you are saing *as though* he do something special for *them* or for *us*, hovewer, he do that for all, including him. Because rejuvenation biotechnology (I prefer to use right terms -- in fact our goal is not prolong life per se, using various compensatory approaches, but fix the damage and rejuvenate organism literally) is the rare example when philanthropist or investor not just donate or invest money, but personally benefit from it. His own life and health will depend on his present desisions in the (I hope not so distant) future.
If you take a close look at NIH funded work... well... You will find hundreds of publications about obesity, life style, air pollution and their impact on longevity. Also you can find many publications about calorie restriction and various genetic manipulations on worms and other model organisms that mimic it. Calorie restriction is everywhere! While we know for twenty years that CR does not work for humans. In 2015 $500,000 was given to projects like "A Large Randomized Trial of Vitamin D, Omega-3 Fatty Acids and Cognitive Decline". It's not a joke, it's a real research work! You can find more here https://report.nih.gov/categorical_spending_project_listing.aspx?FY=2015&ARRA=N&DCat=Aging . All that is useless because you cannot use it to produce working rejuvenation therapies.
At the same time really important research projects like work on glucosepane breaker therapy (which will end many ageing pathologies like arterial stiffness, chronic inflammation, hypertension, strokes, even skin wrinkles and will save many lives) in Spiegel Lab at Yale is permanently underfunded and would be closed last year without financial support from SENS Research Foundation and *German* entrepreneur Michael Greve. Doesn't US have enough millionaires?
@Reason, I prefer to be more optimistic. Small molecules pharmacology is dying, in fact it's already dead. Just compare Unity 's small molecule based solutions and Oisin 's universal synthetic biology system, which can be reprogrammed to target not only senescent but also cancerous or any cells. It is like compare cannon which fires stone balls and modern fully autonomous missile system.
@Reason: Thanks for the transcript. I suffer from a hearing disorder.
@Ariel - I don't know if glucosepane is going to exactly follow in the footsteps of senescent cells, and with a few million dollars of research funding make the jump to the clinic.
The removal of glucosepane is by no means a done deal. The Spiegel Lab at Yale is just creating antibodies to tag it in tissues. And even these probes may not turn out to be that successful as antibodies may be much to large to get at a lot of the glucosepane in the extra cellular matrix.
Luckily there are companies such as Bicycle Therpeutics and Elasmogen that are developing antibody like peptides that may be able to get into these small spaces better either as probes or conjurgated to therapeutics.
If there were signs in 2011 that bisphosphonates can extend life by 5 years and no one has done anything about it, why would senolytics "wake the world" with the exact same feat? Unless the rejuvenation is somewhat visible and the life extension in the double digits, the debate about the value of repair strategies versus that of tinkering ones will carry on.
The rejuvenation should be visible yes given the results in other animals. Mice for example had lush hair growth and a change in hair colour, people are vain this sort of change may well grab their attention. End of the day, we do not need to convince everyone anyway, just enough and that tide is definately turning I can assure you.
@Steve - I think you may be a little optimistic as rodents sprout hair via many interventions, which then fail to produce hair growth in bald humans.
But even a change in hair colour could be enough to gain worldwide attention.
I think Unity Biotechnology are testing out senescent cell removal via local injection into the knee, which might not change appearances much.
@Jim, as far as I know Spiegel Lab and SENS look for in various approaches -- small molecules, catabodies, peptides, enzymes in bacteria using "metagenomic" strategy . And this research highly needs financial support as ever. https://www.fightaging.org/archives/2016/02/an-interview-with-researcher-david-spiegel-on-the-development-of-glucosepane-cross-link-breakers
@Jim nah im really not. Cannot say more at this point.
A life extension of 5 years is still in the range of what you can get with a healthy lifestyle or potentially with metabolism modifiers like metformin and rapamycin. I really can't see how such a small improvement, which of course will take years to be proved reliable, is going to be a game changer.