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Longevity Panel – The Scientists working on Reversing Aging | Part 2

7 July 2021

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A couple of weeks ago Avi Roy, alongside Nathan Cheng & Laura Minquini, hosted the Longevity Panel discussion, which assembled some of the biggest scientists in the field currently working on reversing aging.

This discussion was intended to illuminate how they are approaching longevity and to know if we are any closer in achieving it.

The talk was split into two sections: the first being open discussion guided by questions from the hosts. In the second section, the talk was then opened up to the floor, allowing audience questions. Part 2 will provide the show notes from the Q&A section of the Longevity Panel discussion. Enjoy!

The hosts:

  1. Laura Minquini – the founder of MYKIGAI, a DTC longevity platform dedicated to the education, vetted curation and management tools for people to get on board with longevity as a lifestyle. Having spent most of her career in trend forecasting and branding design and fashion products she sees the potential of longevity becoming the next big consumer category empowering people to take their health in their own hands.
  2. Avi Roy – a biomedical scientist and entrepreneur based in Oxford. He advises and funds startups in the health and longevity space in North America, the EU, and India. He also work with governments to develop and refine policies that enable the longevity infrastructure.
  3. Nathan Cheng – the founder of the Longevity Marketcap Newsletter, a once a week roundup of the developments in the longevity biotech industry. He is also the founder of Longevity List — a website where you can find jobs, companies, and investors in the longevity biotech industry.

The panel:

  1. Alexandra Stolzing – the head of research at SENS research foundation and Professor at Loughborough University. Her research focuses around the amelioration of the hallmarks of aging.
  2. David Sinclair – a Professor of genetics and co-director of the Paul F. Glenn centre for the biology of aging at Harvard medical school. Devid is also the author of ‘Lifespan‘, and his research focuses on understanding and slowing the pace of aging through a variety of approaches.
  3. Liz Parrish – the founder and CEO of Bioviva sciences. Liz’s focus is the advancement of gene therapy for the purpose of extending healthy lifespan in humans.
  4. Aubrey de Grey – the chief scientist officer and co-founder of the SENS research foundation. Aubrey is a biomedical gerontologist, author of ‘Ending Aging‘ and one of the longest proponents to study the field of longevity.
  5. David Gobel – the co-founder and CEO of Methuselah foundation. David’s focus is establishing and supporting research, breakthrough technologies, and regenerative medicine.
  6. Joao Pedro de Magalhaes – a microbiologist and Professor at the University of Liverpool. The goal of Joao’s work is to understand the genetic cellular and molecular mechanisms of aging across all organisms.
  7. Jean Hebert – Associate Professor in the department of genetics at the Albert Einstein college of medicine, and author Replacing Aging. Jean spends his time devising methods of cell replacement for the adult neocortex, where its cells are lost due to damage or age-related to degeneration.
  8. Greg Fahy – the vice president and chief scientist officers of 21st century medicine and founder of Intervene Immune. Greg is also a cryobiologist, biogerontologist, and businessman based in California. His research focuses on organ cryopreservation by vitrification.

The questions:
(The timestamps relates to when the question in asked in the full video)

00:10 – What is the most overlooked/undervalues area, where 10x the resources can create the biggest leverage and impact on moving the space forward? Also, what is the craziest but exciting, recent idea, you’ve heard, that you think might just work.

08:03 – According to the Singapore-based company, Gero.AI, maximum lifespan, if you have perfect health, would be between 120 and 150 years. Is that something that you support? Yes or no?

10:07 – Are there any big issues that you see in the industry that might just need some out of the box thinking?

12:46 – Why do you think there is no further, no wider adoption of stem cell tissues, organoids, and more physiological irrelevant human tissues, in terms of preclinical studies.

21:09 – What do you see are the non-pharmacological lifestyle based key drivers of longevity, expanding life span and reversing aging?

23:38 – Do you think aging is programmed? And then to what extent do you think aging is programmed?

29:23 – One of the major problems with the widely criticised mouse models for replicating ageing is their artificially elongated telomeres. But given all the data that’s already been generated in mice, what do you think the best way is to interpret these studies?

33:10 – Is any correlation between posture and the design of the body and what the impact that it has at the cellular level?

Here’s what was said:

Laura Minquini: We’re going to go now to our Q&A part of the discussion and the first one up is Adam. Nice to see you. Welcome on stage, please go ahead and ask your question.

00:10 – Guest: Hi Laura. Thank you, and thanks to the panel and the moderators, this has been incredible.

I’m an entrepreneur and an angel investor, and I have had an interest in longevity for more than a decade, and now getting me involved on a functional basis.

I have two kinds of questions. One is: what is, in your opinion, the most overlooked or undervalued area, where 10x the resources can create the biggest leverage and impact on moving the space forward.

And then the second question is what is the craziest but exciting, recent idea, you’ve heard, that you think might just work.

Those are my questions. Thanks.

Laura Minquini: Any of our panelists, please feel free to take on this question.

Jean Hebert: I’ll take a stab. Or Liz, do you want to go first?

Liz Parrish: Oh, no, go ahead. I concede

Jean Hebert: So, I may be a bit of an outsider here, I think a lot of the approaches that are being used now or contemplated for use in reversing aging and portrayed as potentially having a big impact, might not work for example, epigenetics, right?

I think the experiments have already been done. There’s a lot of examples for at least a dozen tissues where young cells have been taken and put into an old environment. So they have a young epigenome, either have young mitochondria, they have everything going for them, but they behave like they’re old and in the new environment.

So if we don’t address the environment of the cells – the whole tissue – we’re not going to get very far. So I think that’s, to me, that’s what’s most overlooked with all the current approaches, and of course the answer is tissue replacement. So you replaced the environment of the cells with the cells and, a 10x investment in that I think would make a huge difference in terms of moving the field forward.

It’s a difficult thing like David G alluded to already, right? Making tissues is not easy, but it’s, what’s going to work. Even if you don’t understand what the aging process is, if you replace all old tissues with new tissues, you’re going to succeed in reversing aging.

So that’s my answer. That’s also what I’m most excited about because of the progress being made in these areas, including for the brain, which is the area that we work on.

Alexandra Stolzing: I have to really agree with Jean. The extracellular matrix s so unsexy at the moment. Not a lot of people are focusing on it, but it is so important for cell function and the overall structure of our body. Really improving and studying it would really help a lot.

And what is the most daring aspects of an intervention? It’s something that maybe Joao Pedro is involved in a little bit. It is instead of already fixing what we have, the idea of maybe creating a new system. So dabbling with what makes us human, and maybe daring to give us new genes or maybe you functions that could help with the anti-aging therapies. I think that’s daring, but also super exciting.

Laura Minquini: Liz. Do you want to go ahead?

Liz Parrish: Oh yeah, sure. I only know our own area, pretty much the gene therapy space takes up all of our time. Where we think that we would get the biggest bang for the buck is where we’re going next is combinatorial gene therapies, getting the basic early profile on the safety of those and probably animal models, unfortunately, and then human cells, and then going to humans.

And so I think there, we have an exponential bang for the buck because we will have a unlimited multitude of combinations. We’re looking at four genes now, but there’s a myriad more that are interesting. And then of course, George Church’s has got his huge set, and he’s an advisor of ours. I think that’ll be really great.

The unexpected areas, those are all of the areas that you just hope keep going. So no one on this call wants to block the cure for aging. And honestly we don’t know who the players will be, and what sort of technology needs to be designed. So from everything from the cribriform plate, to the basic research in very odd and strange places, or taking the genes from other species for regeneration. These are all areas that we want to see developed so that we can learn from them and make better therapies ourselves.

All of the unexpected places that I can’t imagine at this point, I just hope that everyone just puts in their passion and a hundred percent. And that’s what will make the difference.

Greg Fahy: I think one thing that catches my attention is Irina and Mike Conboy’s recent discovery that plasma replacement may have rejuvenating effect on the body. They need to collect a lot more data on this, but what they do have is suggestive and it’s consistent with what we’re doing. Which is, to change the hormonal milieu of the body.

And the point was made, I think by Alexandra before, and other extra cellular environment of the cells is very important. I think that’s true. And I think that just replacing cells and putting them into an old environment is going to produce old cells because the cells will take the cues from the old environment that they’re supposed to be old.

So if you can change the old environment either by taking out the old age factors or putting in pro-longevity factors, that would be the Conboy approach versus the Intervened Immune approach or both, then I think you can make some major progress.

Laura Minquini: Thanks, Greg. We lost you there. So I’m going to let David go.

David Gobel: So to answer the question, an area that I find very intriguing, and I’ve actually tried myself, is hyperbaric oxygen therapy. Adam, you could take a look at the work of Shai Efrato, in Israel. His research has shown rejuvenation in brain injury, stroke injury, massive stroke injury, where the additional oxygen in solution, and the plasma, has rejuvenated, brought back to life, areas of the brain that were fully ischemically dead. That phrase may be awkward, but there it is.

Also a recent study by them showed that it increased the length of telomeres, which they were not expecting. And it also behaves as a rapalogue, just hyperbaric oxygen. So it’s a fascinating field.

I decided to try it, since there was decades of research, done by the Navy, and continuing in the scientific community.

I had, for instance, a left eye was reaching toward a glaucoma state. I had intraocular pressure of 36mmHG in my left eye, and it went down to 25 mmHG after eight weeks of hyperbaric oxygen therapy at 1.35 atmospheres, nine liters per minute. And that resulted in an improvement in both of my eyes, and especially my left eye, to normalize it.

And neither drug, nor surgery, could have improved at that much, according to my ophthalmologist. Also, I’d just like to take the opportunity to speak for David Sinclair and for, that the research that we’re doing on epigenetic reprogramming is showing youthening, very much. So while it may not be logical, it does work. It does rejuvenate these organisms.

I’m reminded of how the Romans did not know why bridges with arches worked, but for 2000 years, that was okay. We didn’t know why it worked, but it did work.

Laura Minquini: Eventually. Hopefully we will know. Adam, great question. Thanks again for being here. Skip, if you could go ahead please.

Guest: Hi Laura. Thank you very much. First of all, thank you to the moderators for having the MVPs of age reversal here, and in living room atmosphere on a clubhouse.

I have one simple question. A yes or no question. According to the Singapore-based company, Gero.AI, maximum lifespan, if you have perfect health, would be between 120 and 150 years. Is that something that you support? Yes or no?

David Gobel: No.

Jean Hebert: David, you want to expand on that?

David Gobel: He said he just wanted a yes or no.

Guest: Yeah, that’s right. I want it to make it short because I have another question.

Jean Hebert: No.

Laura Minquini: Greg, go ahead please. Greg.

Greg Fahy: Yeah, the answer to that is, no.

If you had no aging, which, I would define as a state of perfect health then you would have the same risk of death as a 12 year old.

And if you look at the statistics of that you would have a half-life of about 960 years.

Liz Parrish: Yeah, I think the answer is it’s really complicated, because they did take a lot of data and they were just showing that – healthy for your age, I think. I think we can agree with it. They were talking about resilience with health in relation to your age, but we’re talking about ultimate health.

We’re talking about health that is not compromised by any of the deleterious effects of aging, and so in that case, you get something that we don’t talk about a lot because we talk about increasing health spans, but you probably then break the bottleneck of lifespan as well.

Joao Pedro de Magalhaes: So it’s a no for me, as well. As the others have mentioned, in an ideal scenario you will have, as Greg was saying, if you don’t age then you’re going to live potentially thousands of years.

Jean Hebert: And I would just add if you’re perfectly disease free, so healthy for your age as you progress, I don’t think you can get beyond 120 without interventions.

Laura Minquini: Thank you for that. Great question, skip. It clarifies really how far lifespan can go, I think at least for this moment.

Lawrence, welcome to the stage, please go ahead and ask your question.

10:07 – Guest: Hello. It’s an honor to be here on stage with you guys. I would like to take the second part, for example, from Adam’s question, and focus it a little bit.

So, I’m an entrepreneur that decided to have an impact in this industry a few years ago, and I spent most of it trying to learn a lot cause I didn’t feel like I could have an impact without knowing the science and then I started investing. And one crazy idea that finally got me excited and I’m actually getting involved is VitaDao, this decentralized autonomous organization that might just work to turn the whole model of funding drug development on its head.

And my question is basically, are there any big issues that you see in the industry that might just need some out of the box thinking like that, and benefit from this kind of a new type of organization?

David Gobel: Absolutely. I think that you bring up a very good point. Many people have talked about the singularity, and what we really seem to be heading toward is an event horizon where institutions themselves, and the laws that enable them, are being shredded, folded, mutilated, and spindled.

And so other things have an opportunity to arise while these other institutions are busy trying to figure out how to stay alive.

Being able to enable large groups of people with common cause across distributed networks is an absolutely unstoppable force. So I recommend, and I hope that you do accomplish aiming, such organizational structures at solving aging.

[01:09:10] Guest: Yeah. I would like to hear from each one of you, maybe something that you’re really frustrated by, and something that you don’t even dare usually to say that “Hey, this is a problem”, and something that might require just something completely different. That’s the sweet spot I’m looking for from each one of you.

Jean Hebert: I agree with everything David said about this mechanism being useful, I would just hope that it’s not restricted to the drug centric focus. I don’t want to sound like a broken record, but there, there are other approaches that I personally I think are more likely to work.

Laura Minquini: We’re gonna move now to Elena. Welcome to the stage, please go ahead and ask your question.

12:46Guest: Hi, everyone. Thanks for giving me the chance to be here. My question has to do with what David previously mentioned.

So he mentioned that, is working on human physiologically relevant issues, basically to improve the preclinical investigation of different drugs. And Liz also mentioned that we really, truly just can’t afford having another mouse trial that will fail later on. Having a stem cell biology background myself: my question to the to the speakers is why do you think there is no further, no wider adoption of stem cell tissues, organoids, and more physiological irrelevant human tissues, in terms of preclinical studies. Because for me, when I look at the relevance and at the utility of such models for drug discovery I think that this should be a given in every preclinical study that we have a comparison of some mouse data with some data derived from human tissues, that we can now grow in a lab. We can have organ on a chip. We can have, basically, human tissue in a petri dish. And for me, it’s actually quite surprising that despite all this advancements that we have in the stem cell field, we still don’t have a more wide adoption of this technologies for preclinical drug discovery?

Jean Hebert: I think it’s coming. I totally early that this is a model that these human tissues in a dish need to continue developing, but I think there’s a lot of growing interest and a lot of progress being made there. David, you can say more about that. And certainly in terms of safety and, their basic metabolic consequences of the drugs or whatever therapy you’re trying, that they are a little bit limited though, in terms of studying aspects of aging and the reversal of aging, again, because there’s such a young tissues, even if they are in a dish.

So a lot of people are planning on using this for Parkinson’s interventions or Alzheimer’s interventions, but there it’s very difficult to mimic the decades of development, or degeneration, that are necessary to start looking at the phenotype and phenotype reversal.

So I totally agree with you. We need these tissues, but they’re not going to be a total panacea. There might still be need for animal testing before going to humans.

Laura Minquini: Did anyone else of our panelists want to address that? Thanks for the answer answers, Jean. Liz?

Liz Parrish: I think that I’ve been in and out and I’m not sure that I fully understood the question. But, I think that the question was to the effect of ‘why we were not seeing these type of treatments in clinical trials at this point for the vast majority of what we’re talking about’?

Guest: Yeah, that’s correct.

Liz Parrish: It’s a really, actually it’s a complicated process. We just saw the approval of the first drug in 20 years for Alzheimer’s that’s a monoclonal antibody, that actually it doesn’t look like it works very well, and patients demanded access to it.

And that’s fantastic because that shows that patients still have a voice just like they did in AIDS. They demand access to new treatments, but it’s vastly because of the slow development through the FDA. So when drugs come through the FDA, they’re really 12 years old, they’re old drugs.

They’re not new drugs, they’re not the best choice medicine. And what was happening 12 years ago is the beta amyloid plaque theory, that beta amyloid plaques were the downstream effect of Alzheimer’s and therefore they must be removed. Well in the meantime, a lot of other ideas came about, but they require millions of dollars’ worth of animal studies to prove, to show evidence.

And that’s why our company has done some pretty innovative things by working with medical tourism companies to look at their data, because that’s really important data to what happens in humans. And I think we’re going to see a shift in that really soon. We’ll be releasing a paper in a couple of months about that.

But when the regulators are really stuck on a theory and the medical community is too, it’s hard to get new ideas through without a lot of money in areas that have to show evidence to new ideas working in humans. And so I think that’s vastly it, and now we’re at that switching point where funding is coming in, and the studies are being done, and ideas are expanding that maybe old ideas weren’t the best ideas.

[And so this is a time that we have to really look towards the future rather than moving towards the past. But patients need to demand access to this new technology, and they need to keep abreast of it. And so following non-profits and small biotech companies will definitely lighten your heart in this area quite a bit.

Greg Fahy: I might just say that if the question was “Why are studies not being done on stem cell use in preclinical models?”, I don’t have any real insight into that situation, but what I would think might be a factor is the barriers to entry of stem cell therapies clinically. So if there’s going to be a lot of obstacles to getting stem cell therapies approved in humans, that may reduce the motivation to do those stem cells studies in animal models.

But that’s just a guess.

Liz Parrish: I think that Greg hit on a good point there too. And, I think the FDA is great. I think that safe and effective drugs are what people need. I do believe that we need to use another route to getting there. But, stem cells are a great example of something that’s been around for, literally decades now, but it took the FDA over a decade to decide if they were a drug, and until then everything was held up.

So we were seeing great examples of use in Wake Forest and various universities, but, anything that was done clinically outside of the U.S was considered snake oil and what I’m guessing is there’s a halfway road in between all of that.

And what we need is just a new path in order to vet, and source, and better understand how these drugs work in humans in an open forum. Where scientists can actually view the data, work with patients, and get the access and the approval of these drugs much faster.

David Gobel: So there’s an unexamined area that is a barrier that has been caused by a pernicious adaptation by venture capital, trying to achieve the art of the possible. The key goal of a venture capitalist is to have an exit with a positive result, some multiple of the amount invested. The amount of time that it takes to get through the crucible of getting an approved drug is usually beyond the time horizon of most venture capitalists.

So how do they get their exits? It’s turned out that you can get wonderful data and results from mice, and that will encourage people to go ahead and invest. And then you can get a safety profile and a phase one at which time, somewhere in there, venture capitalists can get their exit. The public then comes in because it’s going to be the best thing since sliced bread, and usually it doesn’t work because mice are a horrible model. They almost always fail. But the venture capitalists who are good people, generally speaking, need to get out, and they do. And so we have this, I don’t know… mess, log jam. That has been organized and is financially successful, but it is not actually successful.

So to break that paradigm, if I’m right, what you need to do is to financially make it on an unenviable model for the venture capital community. And that’s something that we’ve been noodling on a lot here at the foundation. I’m sure the VC would rather that it not be that way.

Laura Minquini: It’s amazing how it always goes back to funding.

Terri, welcome to the stage, please go ahead and ask your question.

21:09 – Guest: Thank you, Laura. Thank you for your great moderation. And thank you to all of the experts that are here today on the panel. My question is actually twofold:

What do you see are the non-pharmacological lifestyle based key drivers of longevity, expanding life span and reversing aging: fitness, nutrition, sleep, controlling our environment or combination?

And, I would love for you to also to speak to the efficacy of some of the pharmacological interventions when lifestyles is taken into consideration. For example, somebody with a low risk of developing certain diseases, no history of smoking, eats well, exercises, controlling their environmental factors, would somebody like that be a better candidate for some of these pharmacological interventions? As opposed to someone who has a history of lifestyle behaviours that are not conducive to longevity.

Thank you so much. This is Terri and I’m done.

Laura Minquini: Who would like to take that? Maybe David, because of his own longevity journey. What do you think David?

David Gobel: Non-pharmacological would be joy. Our culture seems to make a lot of its money by scaring us out of our wits 24/7. And that is extremely unhealthy for us. Get outside, look at Robbins and look at oh, I don’t know, bluebirds. Walk in the forest, get away from social media, which is ironic, isn’t it?

We gave out our fourth prize, for the Methuselah mouse prize, to a mouse that lived an extra year, which was a 25% lifespan improvement. What was the cause? The animal handler turned them into a pet, always changed his cage by putting in new toys every week, loving it, petting it, changing up his kibble, and that resulted in a massive lifespan.

So that’s what I would do. And that’s what I actually do, do.

Laura Minquini: Thank you for that, David. It’s sometimes the simple things that can have the most effect. Terri, I hope that was, I think I agree, I don’t think, I fully agree with David in terms of some simple things that we all can do and then there’s the science, which is going to take us further. Thank you for your question again, Terri.

Aaron, welcome to the stage, please. Go ahead.

23:38 – Guest: First of all, do you think aging is programmed? And then to what extent do you think aging is programmed?

Laura Minquini: Maybe we can make it a lightning round, if you want to hear from everybody.

Jean Hebert: There isn’t really any evidence for genetic programming of aging, of course, genes determine lifespan. You can just compare species to know that’s the case, but in terms of genes that are actively engaged in making us older, there really isn’t any evidence to that.

I know people point to certain examples of behaviors that lead to death. But those are encoded behaviors. It’s not really aging, like salmon, dying when they spawn, and then there’s many examples like that. But there isn’t any real evidence for genes whose purpose it is to make us age faster.

Guest: Okay. Just to focus on that, what’s your interpretation of menopause?

Jean Hebert: Yeah, Dave, you don’t take that?

David Gobel: I would say it’s a protective event to prevent unfortunate offspring, whether that is programmed or a guard rail is arguable. So when you get into the word programmed versus non-programmed, you get into some very fuzzy semantics. And I don’t plan on getting into that.

But what I would say is that there clearly are growth programs and that these are not behavioral, it’s just, your bones do get longer as you’re growing. And then somewhere around 25 to 26, that stops. There’s this theory of hyperfunction, which is that the body continues to grow in pernicious ways. And that mTOR, the mechanistic target of rapamycin, is a governor that has lost the plot and that rapamycin slows it back down and therefore aging, as we call it slows down.

But programmed versus non-programmed, I don’t think we know enough. And I think that there’s too many folks who are cheerleaders for one role or another. And I do not know. So I cannot say.

Jean Hebert: I would just add from an evolutionary perspective, most species never had the luxury of having selection for, or against, longevity because they would die, even humans, not that long ago, of things other than age or age-related diseases. So I think, that’s another argument for why it’s hard to imagine how genes could have even evolved to promote aging specifically.

Greg Fahy: I think that the idea of programmed aging needs to pause on the word programmed. It depends on what we mean by that. There’s actually a tremendous amount of evidence in support of “programmed aging”, but what is it really saying? For example, we’re all programmed to have thymic innvolution when we go through puberty.

But is that intended to shorten the lifespan or is that for some other reason it may not be evolutions intent to kill us by involuting the thymus, but that biological choice, that programmed choice inevitably makes us die eventually. Maybe not in the old days, but it does now. So for practical purposes, that’s absolutely programmed aging, but it’s not necessarily selected for specifically for that reason.

And there are infinite other examples of that sort of thing, and if you’d like to read a hundred page treatise on the subject, look at my book chapter in “The Future of Aging”, which is published in 2010. And you’ll see how actually the body ages by the existence of default processes in the adult that can be changed by various kinds of intervention.

And the example that Aubrey mentioned, of a worm that, through a single gene mutation, is able to live 10 times longer than usual, is pretty good evidence that aging is under biological control. So you can call it programmed. You can just call it physiologically controlled aging, whatever you call it, it’s real enough that we can give hormones that decline with aging to older people, and reverse epigenetic aging, improve lung function, all kinds of other stuff.

And Irina Conboy can subtract old age factors from old animals, and possibly humans, and get signs of rejuvenation of those animals as well, which wouldn’t happen if we weren’t accumulating deleterious things with aging.

And all of this is linked back to the epigenetic clock, because the epigenetic clock can smoothly predict age from all ages, from fertilization of the egg cell, until death. It’s not a discontinuous function. It’s a smooth, continuous function applying that there’s an underlying developmental process that explains not only normal development, but also aging.

So it’s a deep subject. We don’t have time to go into the details. Now there’s a lot of mythology about it, pro and con, but there’s a lot to be talked about here.

And I think that opens up huge opportunities for intervention and aging as well.

Liz Parrish: You’re right, Greg, this is like a subject of conversation for another panel discussion because it is a very interesting question. I would love to, for Alexandra to chime in, if she can Alexandra, you still there.

Alexandra Stolzing: I don’t have really much to add, like Greg summarised it so beautifully. There are so many examples where an intervention led to a longer lifespan, and I think that gives a lot of indication that it’s not programmed.

Laura Minquini: Thank you for that Alexandra. We have two more questions before we’ve finished the panel today.

Sean and Jordan, you’re the last ones on stage. Sean, please go ahead.

Guest: I would Jordan want to go ahead of me?

29:23 – Guest: Thank you. First of all, thanks to all the speakers and the organisers, this has been really very interesting.

So a lot of you have criticised mouse models for good reason. And one big, knock against them in my mind, is that lab mice have artificially long telomeres, or at least most of the mice used in the U.S, but given all the data that’s already been generated in mice, what do you think the best way is to interpret these studies. Knowing that they very poorly mimic like key parts of aging, such as exhaustion of like proliferative capacity? Any of the speakers I’d be interested to hear your opinion.

Greg Fahy: Are you referring specifically to the telomere story? Or, to the mice as a model in general?

Guest: More specifically to telomeres as it relates to aging. But I guess mice as a model for longevity to work

Greg Fahy: I’ll just very briefly say that the models in which the telomeres were artificially shortened in mice and then re-elongated does provide a lot of evidence that telomere shortening can be relevant in aging models, depending upon how much shortening actually takes place in a given organism and its normal natural lifespan.

Guest: Not as much talking about that story. I have seen that firsthand and worked on lengthening telomeres in mice, I guess just more talking about, for example, you talked about the heterochronic parabiosis. The Conboys’ have done is, and just removing old plasma.

So like studies like that are in mice. They’re really exciting, really awesome. But there are a lot of problems with the mice models. So I guess what is your framework for thinking about those studies and translating them to a more relevant model or like humans?

David Gobel: The Methuselah foundation does not engage in any telomere research or at any companies involved in telomere research.

We’re not against it. We just think that there are areas that have much higher probability of having disproportionate impact. As far as mouse models in general, we think that my mice have served us well. We have used mice to prove that human lifespan extension is plausible by giving the  prize out four times, for 25% on average increase in lifespan.

They’ve done yeoman work. It’s time to move on to something that will actually work for humans. And that’s our view.

Greg Fahy: I would say mouse models are good in some respects and not so good in other respects. I think the mouse and the rat are good models of immunological aging in people, so I liked them for that reason. I think they could be very misleading when you start getting in the transgenic animal models, because unless you express the transgene only in the adult state, I don’t think you have a valid model.

For example, the growth hormone, knockout, mice are physiologically horrible. They live longer because they’re raised under artificial conditions. And part of the reason that they work is that you’re reprogramming the way the brain is wired to prevent late life brain inflammation, which is nothing that benefits us as already existing adults.

So I think that depends on the model. There are good models, there are models that are not so great.

Alexandra Stolzing: The advice is always choose your model wisely and know what the condition of your model is. But the mice have been used a lot, but basically I seen more and more dog work. There’s the work on rapamycin in companion dogs. And I think we will be seeing more of this. Large animal models might be better, but I think we don’t have a lot of experience with it yet. But there is a variety out there and I think they will become more useful in the future.

Laura Minquini: Thank you, Alexandra. Thanks for your question, Jordan. And last but not least Sean, please go ahead and ask your question. The last one of the day.

33:10 – Guest: Thank you so much, Laura. And I just want to say everyone on here is an absolute fascinating, and I think there’s one common goal: how can we live longer and more productive lives? And I think it’s amazing that people are working very hard towards obviously this objective.

I wanted to share a little bit information and then follow up with a question. I look at aging and longevity more from a physical standpoint, more from a posture, I believe that there is a design to the body based on gravity.

And, I think there’s a riddle of the spring switches, thousand years old, where eventually man does head to the cane. And I’m very curious on the impact of posture against the cellular level, as far as your research, and what we’ve noticed in our founder actually discovered was actually the exercise that he was doing at a younger age was actually training his body away from the design of the body actually causing his pain and injury.

You look at 80% of the world’s population have lower back issues. And most of the time, once you have a lower back/ shoulder/ hip related issue, you’re eventually either going to get it replaced or you just stop moving, right? You basically say I’m no longer going to play the sport or things that I enjoy. I’m not going to walk as much or run or whatnot.

But what if it was as simple as actually training. The pull the body back into design and there’s no longer pain. There’s no longer that rubbing or what’s actually causing the recurring issues at that joint. We actually worked with major athletes around the world, that have relied on PRP and a lot of the different things that you can do to give you a temporary relief.

But I don’t see anyone really talking about how do you permanently get back to a position where the body can work, imagine walking into a mechanic with a car and they don’t return your wheels at the right angle, and you continue to have the same problem over and over again. You’re really not addressing the root cause of what is aging us.

And I guess we discovered that exercises themselves are actually pulling the body out and we reinvented it with a leveraging system that can pull the body back in position within a handful of days. It’s not perfect, but it just heads you in the right direction, and we worked on a lot amazing athletes with amazing results.

I guess my question for the panel is, have you guys seen any correlation between posture and the design of the body and what the impact that it has at the cellular level? Because I do believe that once you do return the body to a certain position, that the body can now heal itself and more importantly, actually head in the right direction. And I’m curious the impact of that as far as lifespan and whatnot.

Jean Hebert: No, we haven’t looked at that.

Greg Fahy: It seems that this was not a well investigated area. The only thing that I would say is that there have been studies on regeneration as induced by very weak electromagnetic fields. So as you apply stress to cells, they respond to the stress. So it’s conceivable that that posture and other mechanical factors might influence cellular health at some level.

But I would have to say this is not an area that anyone has really looked into from a standpoint of fundamental biology of aging.

David Gobel: I would say that we, when we’re young, when we’re children, we like to climb trees and get into jungle gyms and hang upside down and swing from ropes.

And that as we go to older, we tend to do that less and less because it hurts more. What I would say is that it is not likely to reverse aging and that reversing aging is our goal. And that if you take care of the fiddly bits, the tiny things, and they scale up, you’re likely to do better. But also I agree that there is a very strong element of having your body in alignment.

But there’s not a lot of money in that. It’s unfortunate that the capitalist system looks for places that it can make money and just doing things right, and better, doesn’t seem to attract a lot of them of attention. I think that shoes are one of the worst things that ever happened to humans.

Once you can clean up all of the roads and stuff, because they malformed feet, you basically put your feet inside of foot coffin and deprive your foot, with all of those wonderful muscles and arches and nerves, you deprive it of any kind of feeling it’s got to be there for a reason. But as far as a program of a well-thought-out program, that head that way. I applaud that you’re working on it and I wish you success.

Guest: David, I appreciate the feedback. And it’s so sad that from a capitalistic standpoint gets in the way of us trying to figure out what is best for the human body, for us to live productive lives. I think what’s good with longevity.

If you can’t move around or you have to get a hip replacement, or it’s funny, I’m sure people in this panel can recognize plenty of people in their lives that do get back surgeries. You look at Tiger Woods, five back surgeries and still has back issues. And so if you prolong someone’s life and they still are unable to enjoy it or move around, what’s the purpose?

And what’s sad is that I do agree with you. There is a challenge in making money. There is a challenge in actually recruiting people that care about actually changing the world from a sense from exercise. And we’ve given back a lot of major athletes, their careers within a week, two weeks, worth of training, and so we know how powerful it is.

The challenge is how do you find the investors that for the long haul, do you want to do good for the human race and figure out what is best. But I think working side-by-side with scientists like yourselves will super important because we do believe that there must be some correlation between posture and the alignment with gravity and the impact it has at the cellular level, because I do believe that as your body, everything we do is in front of us. And it actually pulls our bodies forward with all of not only our day-to-day life and sedentary aspects, but also what we do from a training perspective. And if we don’t learn to do the opposite we’re basically heading in the wrong direction very quickly.

And so we are looking for people that are looking to try and change lives, and it is a challenge because I think people want it for themselves, but not necessarily the betterment of people around them. And that’s definitely a big challenge. I’m sure that you guys are faced with as well.

We would like to say a huge thank you to all of the panelists for giving us a portion of their busy schedules, and providing such an enlightening and thoroughly fascinating conversation.

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