The information theory and the eyesight result are not quite so closely intertwined as you may be thinking. The information theory, in its broadest sense, is the claim that the main determinant of the age at which we start to exhibit the chronic progressive pathologies of late life is the lifelong accumulation of epigenetic noise. Stated like that, the information theory is neither new (it was first put forward in 1982 by Richard Cutler, who named it the dysdifferentiation theory) nor, in all probability, correct, any more than any other “theory of aging” is correct: the more likely state of affairs is that there is no such single main determinant, but rather that several types of lifelong accumulating damage contribute substantially but no contribution exceeds 50%. (You might get another impression from David’s recent book - but, well, he’s not the only scientist who makes certain choices about what to emphasise.) The next question is mechanistic, i.e., how does that epigenetic noise arise? David’s key idea is that the main mechanism is that the process of repairing genetic (as opposed to epigenetic) damage, such as double-strand breaks, causes an accumulation of epigenetic damage as a bystander phenomenon: first of all the epigenetic state (methylation, in particular) in the vicinity of the genetic lesion is lost when bases are replaced, and secondly the repair process entails the temporary redistribution of DNA protection proteins from elsewhere in the genome, thus exposing those other areas to accelerated damage. That’s a highly plausible and valid theory. So is the theory of Andrei Gudkov, that the DNA damage is mostly caused by retrotranspsons. Not only that, those two theories are linked, because retrotransposon activation is itself caused by epigenetic damage. But honestly the mechanism doesn’t much matter, as I’ll explain.
So, what about the (very impressive) eyesight result? It really tests (and validates) a different theory, namely that partially removing epigenetic noise is beneficial. Note the difference: there’s no reference to the mechanism by which the noise was created in the first place, nor to whether epigenetic noise contributes more to aging than all other types of damage combined. A lot of confusion arises when people fail to make this sort of distinction - when they conflate theories about how aging happens with theories about how it can be mitigated. Indeed, it could be argued that the main thing I did by introducing SENS was to highlight the importance of keeping the two distinct.
So far so good. But the thing is, the specific method of removal of the epigenetic noise is rather critical to what is really being shown. What’s actually being shown is a very much stronger result than I wrote above, namely that whacking the entire genome with a a stupefyingly indiscriminate and non-selective baseball bat called OSKM (or in David’s case only OSK) can do more good than harm if you do it just right. The point here is that such interventions don’t have a way to distinguish between epigenetic marks that are noise and marks that are signal, i.e. are acting to make the cell do what it’s supposed to do. All it can do is remove some proportion of those marks, of both types. So what we are showing when we do this and get a desirable result is that the differentiated epigenetic state is really robust and redundant, such that we can blitz quite a lot of it and the cell still knows what sort of cell it is. Plus, the fact that the cells become more regenerative means that the marks that define what sort of tissue the cell is part of are even more robust than the marks that narrow it down to its terminally differentiated state.
So, what’s not to like? Well, as so often in aging, that comes down to one word: cancer. David’s main reason for using OSK rather than OSKM is that M is c-Myc, an oncogene. The fudamental issue here is that every adult, let alone middle-aged or older adult, is chock full of cells that have already acquired most of the mutations needed to turn them into cancer cells, and the only reason they haven’t acquired all such mutations is that mutation is stochastic - a numbers game. And that can also be thought of in terms of robustness and redundancy. A pristine cell has layer upon layer of ways to stop itself from dividing more than it’s supposed to, and these mutations progressively degrade those defences and make them more and more fragile. Not the sort of thing you would want to hit with a baseball bat, right? And what’s worse, you won’t know you’ve turned a bunch of nearly-cancer cells nto actual cancer cells until they have gone on and divided enough to become detected, which usually means someone displaying symptoms. So we can’t infer much at all about the magnitude of this problem from short-term experiments. What I’m hoping for (and yeah, I’m trying my best to make it so) is that people like David, and Belmonte (the most prominent researcher in this area), and others, will take the cancer risk more seriously than their not-necessarily-all-that-far-sighted reviewers and investors may, and devise smart ways to quantify the cancer risk of such interventions as early as possible. This won’t be easy, but it’s vital. If we hide our heads in the sand and engage in oversimplistic overoptimism about this risk, we are very likely to spend a great deal of time and money on therapeutic dead ends. I’m certainly not saying that partial reprogramming (as this is called) in general is a dead end, but I’m very much saying that it will not fulfil its potential, or at least nowhere near as soon as it could, unless we focus squarely on the cancer side-effect every step of the way.
Never gave it any thought, to be brutally honest.
Would I like to see such efforts succeed? Rapidly approaching 60, my first selfish reaction is a yes… Of course I’d love to live for thousands of years and experience the future.
But then, I think about the consequences of a world in which people no longer age and die. Is that even manageable? Would that be a good world? Would age-related death simply be replaced by more violence and war, an inevitable consequence of overpopulation? Or would we find other ways to solve this problem, spreading to other planets, eventually to other stars as a peace
Never gave it any thought, to be brutally honest.
Would I like to see such efforts succeed? Rapidly approaching 60, my first selfish reaction is a yes… Of course I’d love to live for thousands of years and experience the future.
But then, I think about the consequences of a world in which people no longer age and die. Is that even manageable? Would that be a good world? Would age-related death simply be replaced by more violence and war, an inevitable consequence of overpopulation? Or would we find other ways to solve this problem, spreading to other planets, eventually to other stars as a peaceful, prosperous civilization?
I don’t know the answer to those questions.
For the uninitiated: "the developmental theory of aging" is the hypothesis that the rate of age-related physiological and cognitive decline is substantially influenced by the continued activity of genes that were beneficial during development but are detrimental in adulthood, but not detrimental enough to have induced the evolution of mechanisms to shut them off once development is over. Thus, it is really no more nor less than the modern-day expression of Williams's "antagonistic pleiotropy" theory from 1957. It is discussed with other names too, of which the best is "hyperfunction theory" an
For the uninitiated: "the developmental theory of aging" is the hypothesis that the rate of age-related physiological and cognitive decline is substantially influenced by the continued activity of genes that were beneficial during development but are detrimental in adulthood, but not detrimental enough to have induced the evolution of mechanisms to shut them off once development is over. Thus, it is really no more nor less than the modern-day expression of Williams's "antagonistic pleiotropy" theory from 1957. It is discussed with other names too, of which the best is "hyperfunction theory" and the worst is "quasi-programmed theory".
So, what do I think of it? I think there is no doubt that SOME aspects of aging are SOMEWHAT influenced by such mechanisms. Perhaps the one with greatest relevance to aging in humans is the continued growth of bone in the cribriform plate, which appears to limit the transport of amyloid protein out of the brain and thus, potentially, to contribute to Alzheimer's disease; a company named Leucadia is seeking to address this surgically. But I doubt that effects of this sort are ubiquitous.
Perhaps more importantly, I don't think it matters how much influence hyperfunction has on the rate of aging. That's because "the rate of aging" is shorthand for "the rate at which eventually pathogenic molecular and cellular damage is created", and I have been certain for 22 years that the way we will bring aging under comprehensive medical control is not by reducing that rate, but by removing damage after it has been created. In that world, the specifics of how it is created are irrelevant - our ignorance of those specifics is sidestepped.
Resveratrol and NMN, along with a number of other popular anti-aging supplements, have a proposed mechanism of action that revolves around making the body think it’s not getting enough calories, and thus causing it to engage a spectrum of adjustments to metabolic priorities that reduce the rate of accumulation of the self-inflicted damage that eventually makes us sick when we get old. That’s definitely a good idea. However, it’s important to keep in mind that such interventions cannot be expected to have anywhere near so big an effect on longevity in humans as in short-lived laboratory animals
Resveratrol and NMN, along with a number of other popular anti-aging supplements, have a proposed mechanism of action that revolves around making the body think it’s not getting enough calories, and thus causing it to engage a spectrum of adjustments to metabolic priorities that reduce the rate of accumulation of the self-inflicted damage that eventually makes us sick when we get old. That’s definitely a good idea. However, it’s important to keep in mind that such interventions cannot be expected to have anywhere near so big an effect on longevity in humans as in short-lived laboratory animals like mice. Also, the effect will surely vary a lot from person to person. But as a bridge to let people survive long enough to benefit from the much more powerful rejuvenation therapies that are coming, such measures will surely save lives.

Aubrey de Grey and David Sinclair have differing perspectives on aging and its mechanisms, particularly regarding Sinclair's information theory of aging.
David Sinclair's information theory posits that aging is primarily a loss of information, particularly epigenetic information that regulates gene expression. His research suggests that by restoring this information, such as through the reversal of epigenetic changes, it may be possible to rejuvenate cells and tissues, as demonstrated in studies where old mice had their eyesight restored by reprogramming their cells.
Aubrey de Grey, known for his "SENS" (Strategies for Engineered Negligible Senescence) approach to aging, emphasizes repairing cellular and molecular damage as the key to extending lifespan and improving health in old age. While he acknowledges the potential of Sinclair's work, de Grey tends to focus more on damage repair rather than information loss.
In summary, while both researchers are interested in rejuvenation and longevity, de Grey may view Sinclair's information theory as an interesting but complementary approach rather than a primary focus of his own work on repairing aging damage. Their differing views highlight the complexity of aging research and the various strategies being explored to combat it.
Where do I start?
I’m a huge financial nerd, and have spent an embarrassing amount of time talking to people about their money habits.
Here are the biggest mistakes people are making and how to fix them:
Not having a separate high interest savings account
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Here is a list of the top savings accounts available today. Deposit $5 before moving on because this is one of th
Where do I start?
I’m a huge financial nerd, and have spent an embarrassing amount of time talking to people about their money habits.
Here are the biggest mistakes people are making and how to fix them:
Not having a separate high interest savings account
Having a separate account allows you to see the results of all your hard work and keep your money separate so you're less tempted to spend it.
Plus with rates above 5.00%, the interest you can earn compared to most banks really adds up.
Here is a list of the top savings accounts available today. Deposit $5 before moving on because this is one of the biggest mistakes and easiest ones to fix.
Overpaying on car insurance
You’ve heard it a million times before, but the average American family still overspends by $417/year on car insurance.
If you’ve been with the same insurer for years, chances are you are one of them.
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Consistently being in debt
If you’ve got $10K+ in debt (credit cards…medical bills…anything really) you could use a debt relief program and potentially reduce by over 20%.
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Head over to this Debt Relief comparison website here, then simply answer the questions to see if you qualify.
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Missing out on free money to invest
It’s no secret that millionaires love investing, but for the rest of us, it can seem out of reach.
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Having bad credit
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Hope this helps! Here are the links to get started:
Have a separate savings account
Stop overpaying for car insurance
Finally get out of debt
Start investing with a free bonus
Fix your credit
The lack of such data is irrelevant to the assessment of whether SENS is likely to work on the kind of timeframes I’ve predicted. The idea that it would be relevant is akin to the idea that cars can’t work because no individual component of a car exhibits motion when burning gasoline is poured on it. Medicine is a branch of engineering, and engineering doesn’t work additively. Putting it in more biological terms: each type of damage in the body is protected against by a different set of genes (though the sets overlap), so evolution will gravitate to a quality of those genes that results in the
The lack of such data is irrelevant to the assessment of whether SENS is likely to work on the kind of timeframes I’ve predicted. The idea that it would be relevant is akin to the idea that cars can’t work because no individual component of a car exhibits motion when burning gasoline is poured on it. Medicine is a branch of engineering, and engineering doesn’t work additively. Putting it in more biological terms: each type of damage in the body is protected against by a different set of genes (though the sets overlap), so evolution will gravitate to a quality of those genes that results in the respective types of damage all becoming life-threatening at about the same age. Thus, fixing any one such type of damage (or even most of them) will not appreciably postpone the ill-health of old age.
I don’t agree that there are no indications SENS is not making positive progress. Number one below ties in directly with Aubrey’s SENS theory and there is progress in other fields too but I am 100% in agreement we need a comprehensive therapy and although removing senescent cells will very likely improve health (the most important goal) it might only add 5 years to our lives once we address all the issues identified by SENS I am confident it will be a total game changer.
- Destroying worn-out cells makes mice live longer
- Telomere extension turns back aging clock in cultured human cells, study find
I don’t agree that there are no indications SENS is not making positive progress. Number one below ties in directly with Aubrey’s SENS theory and there is progress in other fields too but I am 100% in agreement we need a comprehensive therapy and although removing senescent cells will very likely improve health (the most important goal) it might only add 5 years to our lives once we address all the issues identified by SENS I am confident it will be a total game changer.
Look at the legendary Chuck Norris’s advice since he is now a whopping 81 years old and yet has MORE energy than me. He found a key to healthy aging… and it was by doing the opposite of what most of people are told. Norris says he started learning about this revolutionary new method when he noticed most of the supplements he was taking did little or nothing to support his health. After extensive research, he discovered he could create dramatic changes to his health simply focusing on 3 things that sabotage our body as we age.
“This is the key to healthy aging,” says Norris. “I’m living proof.”
N
Look at the legendary Chuck Norris’s advice since he is now a whopping 81 years old and yet has MORE energy than me. He found a key to healthy aging… and it was by doing the opposite of what most of people are told. Norris says he started learning about this revolutionary new method when he noticed most of the supplements he was taking did little or nothing to support his health. After extensive research, he discovered he could create dramatic changes to his health simply focusing on 3 things that sabotage our body as we age.
“This is the key to healthy aging,” says Norris. “I’m living proof.”
Now, Chuck Norris has put the entire method into a 15-minute video that explains the 3 “Internal Enemies” that can wreck our health as we age, and the simple ways to help combat them, using foods and herbs you may even have at home.
I’ve included the Chuck Norris video here so you can give it a shot.
You could just google it. Allow me to copy and paste the first paragraph from the SENS research foundation website introduction:
“Many things go wrong with aging bodies, but at the root of them all is the burden of decades of unrepaired damage to the cellular and molecular structures that make up the functional units of our tissues. As each essential microscopic structure fails, tissue function becomes progressively compromised – imperceptibly at first, but ending in the slide into the diseases and disabilities of aging.”
This theory is, or so I gather, now generally accepted. What is important
You could just google it. Allow me to copy and paste the first paragraph from the SENS research foundation website introduction:
“Many things go wrong with aging bodies, but at the root of them all is the burden of decades of unrepaired damage to the cellular and molecular structures that make up the functional units of our tissues. As each essential microscopic structure fails, tissue function becomes progressively compromised – imperceptibly at first, but ending in the slide into the diseases and disabilities of aging.”
This theory is, or so I gather, now generally accepted. What is important is what he is doing about it. He first categorized causes of damage and then determined the most likely method of repairing those types of damage. You can look at their website for more information:
I read Aubrey De Greys book “Ending Aging” and said to myself “I want to learn more about that!” So I decided to study Bioscience. I am halfway though my degree.
No, it didn’t change. In 2004 (when I first started making timeframe predictions) I said that there was a 50% chance of reaching longevity escape velocity within 25 years, so long as funding was sufficient not to be rate-limiting, but that there was at least a 10% chance of not reaching it for 100 years. Now I say 17 years for the 50% cutoff (and I’m pleased to say that the only reason we have gone more slowly than I said in 2004 is lack of funding, not any scientific bad news), but I still say 10% risk of >100 years.
For clarity: this is the theory that changes in chromatin state with age cause derepression of heterochromatic retrotransposons, which insert randomly into euchromatin and mess up genes. The mechanism is qualitatively plausible, for sure, but quantitatively it suffers from the same problem as all theories involving degradation of nuclear DNA, namely that the main (i.e. first) consequence would be cancer, since only one cell needs to get the wrong changes in order to kill us. See PubMed 17588643.
Ageing can be defined as the process of accumulation of molecular and cellular damage, which are a consequence of normal metabolism. It is very important to emphasize the word 'normal', because taking it into account, it immediately becomes clear that it is impossible neither seriously slowing down the ageing process nor stopping. To do this, you need to completely redesign the human metabolism, re-writing human genome. Because processes that cause damage are the same processes that give us life! But since we can not influence the processes of damage accumulation (at least at the current level
Ageing can be defined as the process of accumulation of molecular and cellular damage, which are a consequence of normal metabolism. It is very important to emphasize the word 'normal', because taking it into account, it immediately becomes clear that it is impossible neither seriously slowing down the ageing process nor stopping. To do this, you need to completely redesign the human metabolism, re-writing human genome. Because processes that cause damage are the same processes that give us life! But since we can not influence the processes of damage accumulation (at least at the current level of science), what can we do? We can remove the accumulated damage caused by them without interfering with the metabolic processes, returning the body to an earlier, undamaged and, as a consequence, a more youthful state!
At first glance, the idea that the age reversal (rejuvenation) is not just the easiest but the only possible way to defeat ageing, seems paradoxical. But think, what is easier: to build never breaking car – or to repair it in time? To never mess in a room – or to clean it up in time? This is how our world works – eliminating structural differences (garbage and damage) is much easier than controlling the complex interlacing of various processes leading to their formation.
Moreover, we do not even need to know the scheme of the car and the purpose of things in the room! All we need is another working car and a clean room. Comparing a broken car with a working one, and a dirty room with a clean one, we will be able to find out what parts and things we need, what need to be replaced and which ones to discard. Another good news is that we need not to eliminate all the damage, for example, we need not to varnish every scratch on the car and look for every speck of dust in the room. We just need to keep their level below the critical level so that the car can normally drive, and the room is nice to live!
The first thing I think is “about damned time” - I started discussing aging with Bezos 15 years ago. But more substantively: I’m very optimistic that Altos will be far more effective in hastening the defeat of aging than its UHNWI-backed predecessors, the Ellison Medical Foundation and Calico. It has the good side of Calico in that its CEO is Hal Barron, someone who knows all about the endgame of medical R&D, i.e. the turning of proven concepts into profitable therapies. But unlike Calico, it also has a committed biomedical gerontologist as CSO in Belmonte, so the goal will be to get therapies
The first thing I think is “about damned time” - I started discussing aging with Bezos 15 years ago. But more substantively: I’m very optimistic that Altos will be far more effective in hastening the defeat of aging than its UHNWI-backed predecessors, the Ellison Medical Foundation and Calico. It has the good side of Calico in that its CEO is Hal Barron, someone who knows all about the endgame of medical R&D, i.e. the turning of proven concepts into profitable therapies. But unlike Calico, it also has a committed biomedical gerontologist as CSO in Belmonte, so the goal will be to get therapies developed as fast as possible, rather than wearing the policy of “taking as long as it takes” as a badge of honour the way Botstein does. And in addition, it has recruited enough outstanding luminaries that it will not be dominated by a single school of thought. The question of whether partial reprogramming will prove to be a (let alone the) central pillar of truly effective rejuvenation remains very open, and in particular I have considerable doubts that reprogramming using the Yamanaka factors can be made safe, but a few $B is a small price to pay to find out. So - thank you Yuri and Jeff.
Contrary to some perceptions, Aubrey de Grey has never stated that we will absolutely cure aging completely within 25 years. He HAS proposed that within 25 years, and with sufficient funding (hundreds of billions of dollars), we have a very respectable chance of developing powerful longevity therapies that will extend the healthy lives of individuals long enough for them to live to see the next generation of more powerful therapies that, in turn will allow them to live to see even MORE powerful anti-aging therapies.
Say that you have a disease that will kill you in five years, but you are giv
Contrary to some perceptions, Aubrey de Grey has never stated that we will absolutely cure aging completely within 25 years. He HAS proposed that within 25 years, and with sufficient funding (hundreds of billions of dollars), we have a very respectable chance of developing powerful longevity therapies that will extend the healthy lives of individuals long enough for them to live to see the next generation of more powerful therapies that, in turn will allow them to live to see even MORE powerful anti-aging therapies.
Say that you have a disease that will kill you in five years, but you are given a medicine that will give you ten years. Within that ten years, you are given another medicine that gives you fifteen more years. Then another more advanced medicine gives you twenty more years.
This is the thinking behind de Grey's proposition.
Ageing can be defined as the process of accumulation of molecular and cellular damage, which are a consequence of normal metabolism. It is very important to emphasize the word 'normal', because taking it into account, it immediately becomes clear that it is impossible neither seriously slowing down the ageing process nor stopping. To do this, you need to completely redesign the human metabolism, re-writing human genome. Because processes that cause damage are the same processes that give us life! But since we can not influence the processes of damage accumulation (at least at the current level
Ageing can be defined as the process of accumulation of molecular and cellular damage, which are a consequence of normal metabolism. It is very important to emphasize the word 'normal', because taking it into account, it immediately becomes clear that it is impossible neither seriously slowing down the ageing process nor stopping. To do this, you need to completely redesign the human metabolism, re-writing human genome. Because processes that cause damage are the same processes that give us life! But since we can not influence the processes of damage accumulation (at least at the current level of science), what can we do? We can remove the accumulated damage caused by them without interfering with the metabolic processes, returning the body to an earlier, undamaged and, as a consequence, a more youthful state!
At first glance, the idea that the age reversal (rejuvenation) is not just the easiest but the only possible way to defeat ageing, seems paradoxical. But think, what is easier: to build never breaking car – or to repair it in time? To never mess in a room – or to clean it up in time? This is how our world works – eliminating structural differences (garbage and damage) is much easier than controlling the complex interlacing of various processes leading to their formation.
Moreover, we do not even need to know the scheme of the car and the purpose of things in the room! All we need is another working car and a clean room. Comparing a broken car with a working one, and a dirty room with a clean one, we will be able to find out what parts and things we need, what need to be replaced and which ones to discard.
Another good news is that we need not to eliminate all the damage, for example, we need not to varnish every scratch on the car and look for every speck of dust in the room. We just need to keep their level below the critical level so that the car can normally drive, and the room is nice to live!
In a nutshell, we’re not all that far apart. We differ somewhat as regards what can already be done today (what he calls “bridge 1”), but regarding future advances we are on very much the same page.
The first person to live to the age of 200 is probably alive right now. Beyond that, you can say little definitively.
As you age, you are subject to an increasing number of diseases. We must eliminate all of them as well as the many causes of aging before anyone will be able to live for centuries. The treatments may have side effects. Each breakthrough in aging research will be more difficult than the last one. Medical breakthroughs are almost impossible to predict. Just look at the predictions for Alzheimer’s two decades ago.
You should take these predictions (from de Grey and Kurzweil) with a
The first person to live to the age of 200 is probably alive right now. Beyond that, you can say little definitively.
As you age, you are subject to an increasing number of diseases. We must eliminate all of them as well as the many causes of aging before anyone will be able to live for centuries. The treatments may have side effects. Each breakthrough in aging research will be more difficult than the last one. Medical breakthroughs are almost impossible to predict. Just look at the predictions for Alzheimer’s two decades ago.
You should take these predictions (from de Grey and Kurzweil) with a large handful of salt. There is an outside chance that they will be right about this one. It is more likely that they are exaggerating what will happen. We are on the verge of extending human lifespans by 30 years for healthy people. We are close to finding cures for SNP diseases. Medical research plods. It must. Testing and releasing a new treatment takes a long time. They do not always work the same way on all people.
If a 20-year-old today takes good care, then there’s a good chance of living to 100 years as things stand. Senolytics could add one-to-three decades to that. If that person lived as most do, the expectation is living to about 80, and senolytics may only add one decade. Future advances could add to those numbers and even produce the first person to live to 200 years, but few will make it that far just as few make it to 110 today. Do not count on you being one of the lucky ones.
What he actually proposed was a series of steps, each of which would increase life expectancy by 30 years. As long as the time between steps stays less than 30 years, the process can extend life expectancy for people living today.
It's a work in progress. He set up a foundation that is sponsoring research in the areas he (and co-workers) believe are most important. So far, no breakthroughs have increased life expectancy by that first 30 year increment.
When a breakthrough occurs in one of his key areas, we'll know more about the feasibility of the whole process.
- Will the first breakthrough extend
What he actually proposed was a series of steps, each of which would increase life expectancy by 30 years. As long as the time between steps stays less than 30 years, the process can extend life expectancy for people living today.
It's a work in progress. He set up a foundation that is sponsoring research in the areas he (and co-workers) believe are most important. So far, no breakthroughs have increased life expectancy by that first 30 year increment.
When a breakthrough occurs in one of his key areas, we'll know more about the feasibility of the whole process.
- Will the first breakthrough extend life for people who are already 90 years old? Or maybe only for kids? Or maybe only for future generations who can benefit from genetic interventions?
- Will the first breakthrough really extend life expectancy by 30 years, or only eliminate one of many parallel processes that now limit us?
It's research. Success is not guaranteed. We don't even know how long it will take to know if success is possible. But I've looked at the site (see some of my other answers to questions about De Grey) and I don't see anything obviously wrong with the approaches. I'm hopeful.
EDIT(January, 2023) I wrote the above a few years ago. I want to add one sense in which De Grey’s program is already succeeding:— Other medical advances have already increased life expectancy by something like 20 years during my lifetime. In the last 23 years I’ve had two hernias repaired, both hips replaced, two vertebrae fused, and three joints in my left foot fused. The combination has kept me walking and active. I’m 75 and without them I’d probably have been in a wheelchair before 65.
I also have three friends who have survived cancers and one friend who survived a very serious heart attack. Without modern medical advances, at least two of them would have been dead.
So medical advances (although not part of De Grey’s program) have given me an extra 10-20 years of active, quality life. And some further advances are likely to get me another 20. So I may be able to benefit from further advances by 2045.
Time has proven that Aubrey de Greys SENS theory has a high likelihood of being correct and whilst can't yet fix the damage which arises as we age but we are getting close and the path ahead is already quite clear because we already pretty much know what we need to do, this is because we have rapidly increasing knowledge in all of the required areas in which we need to intervene so things are looking very positive generally in terms of timeframes. In my opinion we should be able to address the problem of aging quite comprehensively within a timeframe (65% or better probability within under 20
Time has proven that Aubrey de Greys SENS theory has a high likelihood of being correct and whilst can't yet fix the damage which arises as we age but we are getting close and the path ahead is already quite clear because we already pretty much know what we need to do, this is because we have rapidly increasing knowledge in all of the required areas in which we need to intervene so things are looking very positive generally in terms of timeframes. In my opinion we should be able to address the problem of aging quite comprehensively within a timeframe (65% or better probability within under 20 years) which will benefit the majority of people currently alive.
Although I don't think we will find an actual CURE for aging in the foreseeable future, there is a middle path that is likely to succeed based on our current and near future technology. In my opinion, we must work from where our knowledge stands currently, this is that although we understand the reasons why the body deteriorates with age, we do not have the requisite knowledge to intervene in a way that influences the actual ongoing metabolic processes.
I am often asked "how long before we can cure aging?" I would hazard a guess that it is at least 100 years away. The alternative approach is to aim at controlling aging and repairing the accumulated damage and this should be our primary goal because we understand how the damage is laid down even though we understand very little about actually slowing aging or influencing metabolism. This is the essence of Aubrey de Grey's SENS theory regarding the engineering approach and most other theories follow much the same way of thinking with a few variations regardless these routes offer the best prospect of success in the first half of this century.
Personally I am pretty confident that with SENS and other routes being explored such as Telomere research, Stem cell treatments , cellular reprogramming and Senolytics among others that we do not have to find a cure for aging itself, therefore, we bypass the problems that our lack of knowledge in the area of metabolism and its impact on the aging process creates because what Aubrey de Grey terms “engineered negligible senescence" can potentially extend life indefinitely while not actually curing the underlying aging process which is allowed to continue as normal.
The key lies in the fact that we have a sufficient understanding of genetic and biochemical processes that lead to metabolic damage that we can already envision what the repair strategies will be. Aubrey frequently used the question "how long will a house last?" Of course, the answer is that, if you look after it, it can last forever! The key here is that Aubrey proposes that we find a method to undo the damage that has accumulated over the first 50 or 60 years of a person’s life. Repairing the damage means we do not need to understand all the processes of aging, only that we need to know enough to extend healthy lifespan by let us say 25/30 years. We are making rapid progress in many areas and when you look at the research into senolytics which kills what are termed zombie cells, gene editing technologies such as CRISPR-Cas9 and cellular reprogramming progress all are moving very fast. An area which looks very interesting at the moment focuses specifically on cellular reprogramming. An organization called Altos Labs has recently secured $3 billion in initial financing via billionaires such as Jeff Bezos to concentrate specifically on this research, the process consists of applying Yamanaka factors to cells for long enough to reset the clock effectively reversing cellular aging and repairing cells and tissues but without inducing pluripotency, to explain this difference iPSC (Induced Pluripotent Stem Cells) are created from blood or skin cells that have been reprogrammed turning them back into an (embryonic) pluripotent state which enables the production of all kinds of human cells which can be utilized for therapeutic purposes, iPSC’s were first discovered in 2006 and CRISPR-Case 9 in 2015, now that the two technologies can be combined we potentially have some very powerful anti aging and rejuvenative technologies in early development, it's the synergy between the two technologies which is the key because cellular reprogramming requires CRISPR-Cas9 in order to insert the Yamanaka regulatory factors into a cell's genome. Whilst we are currently only in the very early days of this research it's moving extremely fast and results are looking very promising because we know that epigenetic information deteriorates over time and clearly restoring the epigenetic information has a very good chance of managing or potentially even reversing aging.
So the big question you are likely asking is “how would it work in practice?” This is actually quite easy to follow once you get your head around it, in essence its this, let’s say you are 60 years old at the time of the first intervention and that this early and fundamentally imperfect treatment repairs 75% of the accumulated damage and winds the clock back by 25 years. Then 10 years later you would reach the chronological age of 70 but would be biologically only 45 years old and look and feel like a 45 year old. We now come to the vital key to the whole theory which is this, let's say 20 years after the first treatment, when you are chronologically 80 but biologically 55 years old, both your doctor and yourself will realize that the damage that was not repaired in the first treatment combined with the further damage accumulated over the 20 years since is again posing a health risk. At this point it is time for another intervention. It is now that the progress in medicine comes into play because, by the time 20 years has gone by, anti-aging medicine will have moved on significantly and, whilst the first treatment bought you an extra 25 or 30 years by repairing a fair amount of the damage accumulated over your first 60 years, it did not repair it all. 20 years later medical progress will mean that the latest treatment will not only repair all the damage corrected by the first intervention but also some of the damage that was not able to be repaired 20 years earlier, so in essence you are now chronologically 80 (but biologically in your 50s). This means that, whilst you will have aged 20 years chronologically, you will be biologically younger after the second intervention than you were after the first.
This is the essence of Aubrey de Grey's SENS theory and pretty much any other theory based on rejuvenation and damage repair, essentially, it's a shortcut to radical life extension. It is not a cure, but it acknowledges that it does not need to be because it simply buys time and leads to a situation where regular interventions at say 15/20-year intervals with increasing effective treatments could extend life virtually indefinitely.
Will it happen? My opinion is that we are well on the way in a number of areas. Of course the exact impact these future enhancements will have is hard to judge, but we are close enough to the stage where they can be deployed to know what the likely impact will be, we also know that these technologies are all experiencing exponential growth bringing the time when they will be employed rapidly nearer, of course some therapies are already in use such as stem cell treatments, but others are only in the early stages of development, even the treatments we have currently are nothing like as effective as they will be in the future when all of them can be potentially combined, in summary these technologies encompass AI, biotechnology, stem cells, nanotechnology, tissue engineering and gene therapies, ultimately they will offer us the opportunity to transcend our biological limitations and create a situation where we may even have to evaluate what it means to be human
Big Pharma is getting increasingly interested and money is starting to pour in because it is clear we can see the light at the end of the tunnel which to investors equates to return on investment. A number of factors will drive things forward and interest is increasing rapidly among both Scientists, researchers and the general population as well as wealthy philanthropists. The greatest driving force of all is that the baby boomers are aging and this will place increasing demands on healthcare systems. Keep in mind that the average person costs more in medical expenditure in the last year of their life than all the other years put together. Also, the number of workers is declining in most developed countries, which means that we need to keep the existing population working and productive as long as possible.
These are just two reasons, but jointly they pose a catastrophic and rapidly looming economic problem to many governments worldwide. So what time-frame do I put on it? I made a projection some time back and, based on current research, I feel we will be pretty much able to treat and manage aging within under than 20 years but probably not sooner than 10, the important factor is that given sufficient motivation, appropriate research and rapidly increasing funding more and more institutional investors and wealthy individuals will wake up to the fact this is something which is possible and will inevitably happen because it’s no longer in the realms of Sci-fi, the only question is the timeframe in which it will arrive. Many of the therapies are progressing well already such as stem cell therapies, senolytics, gene therapies and tissue engineering but without a comprehensive intervention targeting all the types of damage that arise due to aging the treatments individually will most likely just allow a person to grind on foray extra 5 or 6 years.
Of course there are other routes other than engineering approaches such as SENS and I think even Aubrey de Grey knows SENS is only a means to to get a foot on the ladder but clearly once SENS strategies are perfected they will certainly save millions of lives and prevent a great deal of suffering. As I see it there are five technologies which will ultimately lead to radical life extension during the course of this century, these are advanced Biotechnology, Nanotechnology, Advanced Robotics, Genetics and Robust Artificial Intelligence often just referred to just as AI, the effect these technologies will have on life extension differs greatly, but my guess is that there are three potential approaches which are likely to come to fruition first, one is SENS which is biotechnology the second is nanotechnology which will enable us to repair the body at a cellular and molecular level though this will probably come after SENS - though it's possible that it could arrive in the 2030s or worst case 2040s - because this one is more difficult to predict I tend to be very much of the mind that SENS is much more predictable than the second and third routes simply because our knowledge of biotechnology is currently significantly greater than nanotechnology. The third route which I consider to be a likely success is whole brain emulation or mind uploading, whole brain emulation is where the brain is uploaded to a digital medium and increasingly enhanced and replaced with non-biological components until it reaches a stage where the non-biological components can model the biological part so accurately the original brain's loss would be irrelevant from a functional perspective, this is a technology which is hard to put an exact time frame on though we may reach this point much earlier than expected based on current progress with technology such as Elon Musk's Neuralink which seems to be at a stage we had not expected to reach yet, whilst this has the potential to encounter significant difficulties which are unforeseeable from where we stand at the moment it's quite possible that nanotechnology will speed up the development of whole brain emulation and if not computer brain interfaces will get us there to some degree.
Personally, I feel the outcome long term for life extension will ultimately be a combination of the five routes outlined above, the crucial point is that each of these technologies individually has the potential to get us to where we need to go. What this means is that for the development of radical life extension to fail all of these technologies must also fail and that simply won’t happen, so my guess is we will reach the stage of having a decisive level of control over the aging process within under 20 years although maybe not all the technologies I describe would be sufficiently developed at that point the road ahead for those that aren't will already be very clear. We must also factor in that there is also a possibility that we could find a faster route if a few more technologies like CRISPR were to be developed, things could move very rapidly.
If you are unsure whether this is a war worth fighting, consider this. When the war on aging is won (and it's a case of when not if) 100,000 people per day would be saved! This is because, of the 150,000 people who die each day, two thirds die from aging. This is a staggering figure and what this means is that, of nearly 60 million people who die each year, 40 million die from age related issues. I believe we will achieve significant positive results within the 5 years in research on mice and that the knowledge acquired will then be transferred to humans and, hopefully, end the horrific descent into senility and old age of the millions of people who linger in retirement homes and suffer the indignities that come with the passing years.
Conquering aging is pretty much the same as beating any other disease, albeit aging is a complex issue involving many processes but that does not mean that it is not a realistic goal with odds of over 65% to render it a chronic albeit manageable condition within a 10-20 year timeframe.
As far as how long I want to live, 500 years would do for a start if I could keep running my businesses or new ones, riding my motorcycles, jet ski and eating and drinking everything I like - why wouldn’t anyone go for it?
At the time of publication things were very different to now because the book is probably around 8 years ago and I have a copy but am away from home currently so can't check. The vital point is that 10 years ago Aubrey de Grey was seen as being an outsider and on the fringe but as his theories have become more mainstream and the evidence points increasingly to him having been very much on the right track from the start. I have followed Aubrey de Grey among others in this field pretty much since the start but Aubrey's role was crucial because he has raised the profile of anti aging research gen
At the time of publication things were very different to now because the book is probably around 8 years ago and I have a copy but am away from home currently so can't check. The vital point is that 10 years ago Aubrey de Grey was seen as being an outsider and on the fringe but as his theories have become more mainstream and the evidence points increasingly to him having been very much on the right track from the start. I have followed Aubrey de Grey among others in this field pretty much since the start but Aubrey's role was crucial because he has raised the profile of anti aging research generally and progressively (along with many others) moved it from very much being on the fringe toward the mainstream where even Google with the Calico project are looking at things very closely. I am sure we will look back in 30 years and say "that de Grey guy was right" I also believe there will never be a single magic pill that cures aging but there doesn't need to be because the incremental gains year on year will mean that many alive now will ride the wave because their life expectancy will be increasing faster than 12 months per year. Once that stage is reached we won't have actually cured aging but the result will be essentially the same because each year our appointment with the Grim Reaper will be moving further and further away rather than edging ever closer.
I share Aubrey's opinion that aging is essentially no different to any other disease and like all diseases is ultimately treatable given the resources. We cannot afford to sit back and accept it. Everyone in history has lived and died but it is a mistake to view aging as a fact of life set in stone when science has progressed to the level where we have a pretty good change of bringing under a decisive level of clinical control within 25 years and maybe less.
Personally I donate to the SENS Foundation see SRF Home | SENS Research Foundation which I think is the best route to assist in bringing the date closer when everyone no longer needs to fear ill health in later life through Atherosclerosis, Alzheimers, Arthritis, Cancer, Diabetes or Stroke because these are all essentially diseases of aging which rarely strike young people but where the risk rises for all of us with every passing year.
Yes I tend to agree with them but I think anyone born after 1980 has a very good chance (80%) and even a person born in 1960 has reasonable odds because if you can survive another 20 years you could be home and dry. We only need to add 20 years and the majority alive will cross the line.
Although the question is speculative we can nevertheless pretty much figure out how things are likely to go based on current rates of progress. I think if the first generation treatments repair 75% of the accumulated damage (a reasonable estimate based on where we currently stand) that has built up over a perso
Yes I tend to agree with them but I think anyone born after 1980 has a very good chance (80%) and even a person born in 1960 has reasonable odds because if you can survive another 20 years you could be home and dry. We only need to add 20 years and the majority alive will cross the line.
Although the question is speculative we can nevertheless pretty much figure out how things are likely to go based on current rates of progress. I think if the first generation treatments repair 75% of the accumulated damage (a reasonable estimate based on where we currently stand) that has built up over a person's lifetime they will be good enough to reset the clock by around 25 years. The really interesting part occurs 15 or 20 years later when the second intervention is needed because it's now that the progress in medicine really comes into play, this is because anti-aging medicine will have progressed significantly, and whilst the first treatment bought you an extra 20 or 30 years by repairing the bulk of the damage, it did not repair it all. Now 15/20 years later progress will mean that the latest treatment would not only repair all of the damage corrected by the first intervention plus further accumulate damage but it will also fix some of the damage that was not able to be repaired 15 or 20 years earlier so in essence athough you are now chronologically 15 or 20 years older when you receive intervention number 2 you will be biologically younger after the second treatment than you were after the first.
My guess is that with the number of Biotech companies getting involved the first therapies might also be such that various treatments could be administered in a multi pronged approach. I see the whole thing in the early days as likely involving biotech such as senolytics, gene therapies, stem cell treatments, protein crosslink breakers and treatments stimulating the immune system to remove accumulated waste products which build up in the tissues such as plaque in the arteries as well as other waste products the body can’t dispose of, potentially tissue engineering involving surgery might be required too but hopefully rejuvenation is situ will be sufficient. Clearly the first therapies might be pretty unpleasant (maybe laying people low like chemo does today) but for many of the older people alive now that will be a price they would accept paying when confronted with the alternative. I work on the basis I will be in my 70's or maybe early 80's when the first interventions arrive and will have to avail myself of whatever is available. I feel the risk will be a factor too and maybe a small percentage of people will suffer side effects and possibly not make it but again the risk/benefit ratio will mean that the early treatments will still have lots of takers.
The result is important, and the “DRI” technology used to do it is potentially even more important because it is so broadly applicable. We’ve known for a while that the elimination of senescent cells is a major plank of rejuvenation, and this is a further confirmation, with the advantage that it is underpinned by good scientific understanding of the mechanism.
I’m very much on the fence. The question of whether telomerase activation will have decisive long-term negative consequences in terms of cancer is one that we cannot currently answer with confidence. Therefore, I very much endorse and support the research and clinical trials currently underway on telomerase activation, while at the same time SENS Research Foundation itself is heavily engaged in research to do the opposite, suppressing telomere elongation as an anti-cancer strategy.
In the early days many were sceptical (we are talking 10+ years ago) but the evidence now leans very much toward him being on the right track because we now know a lot more about stem cell treatments and also senescent cell clearance among other areas both of which were highlighted by Aubrey de Grey nearly 20 years ago when he devised the theory of SENS. I have to say I always disliked oncoSENS Aubrey’s original theory to tackle cancer and the reason was is sounded horrific but even Aubrey now accepts things have moved on and there are now other routes as far as the rest of the theory of SENS
In the early days many were sceptical (we are talking 10+ years ago) but the evidence now leans very much toward him being on the right track because we now know a lot more about stem cell treatments and also senescent cell clearance among other areas both of which were highlighted by Aubrey de Grey nearly 20 years ago when he devised the theory of SENS. I have to say I always disliked oncoSENS Aubrey’s original theory to tackle cancer and the reason was is sounded horrific but even Aubrey now accepts things have moved on and there are now other routes as far as the rest of the theory of SENS which consists of 7 areas I was always 100% in agreement with those.
Personally I am pretty confident that with SENS and other routes being explored such as the Telomere research plus the breakthroughs in Senolytics show that we do not have to find a cure for aging itself, therefore, we bypass the problems that our lack of knowledge in the area of metabolism and the aging process creates because what Aubrey de Grey terms “engineered negligible senescence". Theoretically this approach could potentially extend life indefinitely while not actually curing the underlying aging process which is allowed to continue as normal. Repairing the damage means we do not need to understand all the processes of aging, only that we need to know enough to extend healthy lifespan by let’s say 25/30 years each time the treatment is administered.
Many people say to me “so how would it work in practice?” It’s actually quite easy to follow as I will explain, let’s for the sake of argument assume you are 60 years old at the time of the first intervention, this early and fundamentally imperfect treatment will probably repair 75% of the damage accumulated up to that point. What happens now is that 10 years later you reach the chronological age of 70 but are actually only 45 years old from a biological perspective and also look and feel like a 45 year old. We now come to the vital key to the whole theory which is this, let's say 20 years after the first treatment, when you are chronologically 80 but biologically 55 years old, both your doctor and yourself realize that the damage that was not repaired in the first treatment combined with further damage accumulated over the 20 years since it was administered are again posing a potential health risk. At this point it’s time for another intervention. It is now that the progress in medicine comes into play because, by the time 20 years has passed by, anti-aging medicine will have moved on significantly and, whilst the first treatment bought you an extra 25 or 30 years by repairing a fair amount of the damage accumulated over 60 years of living, it did not repair it all, 20 years later progress will mean that the latest treatment will not only repair most of the new damage that has built up since the first intervention but also some of the damage that was not able to be repaired 20 years earlier, this means that although you are now chronologically 80 (but biologically in your 50s) after intervention number two whilst you will have aged 20 years chronologically since the first treatment you will be biologically younger after the second treatment than you were after the first.
The above example is the essence of Aubrey de Grey's theory and pretty much every other theory based on rejuvenation and damage repair, essentially, it's a shortcut to significant life extension. It isn’t a cure but it acknowledges that it does not need to be because it simply buys time and leads to a situation where regular interventions at 15/20 years intervals with increasingly effective and comprehensive treatments could potentially extend life virtually indefinitely.
One thing I am often asked "How long before we can cure aging?" I think the time span for a true cure is at least 100 years away hence Aubrey de Grey’s path offers a viable alternative.
Q: Is David Sinclair's recent announcement that he's reversed aging in mice real?
Answer: Not only is David Sinclair's recent announcement that he's reversed aging in mice is real, but he has developed and published an anti-ageing “protocol” (= prescription for reversing the rate of ageing) for people. But it does not completely provide ageing in all physical departments. See
I assume you mean this:
In a word: meh. There's nothing particularly wrong with it, and they have corrected the most glaring omissions in Lopez-Otin 2013, namely the stiffening of the extracellular matrix and the restriction of intracellular waste to proteins, but they've retained the main conceptual shortcoming of that paper, namely the failure to classify aspects of aging according to the ways in which each can in principle be medically addressed. The actual first paper to describe aging as a collection of damage-accumulation processes - here I of course ref
I assume you mean this:
In a word: meh. There's nothing particularly wrong with it, and they have corrected the most glaring omissions in Lopez-Otin 2013, namely the stiffening of the extracellular matrix and the restriction of intracellular waste to proteins, but they've retained the main conceptual shortcoming of that paper, namely the failure to classify aspects of aging according to the ways in which each can in principle be medically addressed. The actual first paper to describe aging as a collection of damage-accumulation processes - here I of course refer to PubMed 11976218 - remains, in my entirely unbiased view, the gold standard for such a classification, largely because it describes an intervention strategy corresponding to each category. Back then I listed nine categories, but not long thereafter I realised that immune and endocrine aging were better described as aspects of the other seven. The rest is, well, history.
I have no idea why I would have been asked to answer this question - but I see Victor’s answer and I will reply.
I mean simply that the underlying reason why complex living organisms age is the same as why man-made machines with moving parts age, namely that the laws of physics dictate that wear and tear happens and that it takes work to reverse the accumulation of that wear and tear.
10 years ago Aubrey de Grey was seen as being an outsider and on the fringe but as his theories have become more mainstream and the evidence points increasingly to him having been very much on the right track from the start a typical example is the removal of senescent cells which is one of the cornerstones of the SENS theory see Destroying worn-out cells makes mice live longer . I have followed Aubrey de Grey among others in this field pretty much since the start but Aubrey's role was crucial because he has raised the profile of anti aging research generally and progressively (along with many
10 years ago Aubrey de Grey was seen as being an outsider and on the fringe but as his theories have become more mainstream and the evidence points increasingly to him having been very much on the right track from the start a typical example is the removal of senescent cells which is one of the cornerstones of the SENS theory see Destroying worn-out cells makes mice live longer . I have followed Aubrey de Grey among others in this field pretty much since the start but Aubrey's role was crucial because he has raised the profile of anti aging research generally and progressively (along with many others) moved it from very much being on the fringe toward the mainstream where even Google with the Calico project are looking at things very closely. I am sure we will look back in 30 years and say "that de Grey guy was right" I also believe there will never be a single magic pill that cures aging but there doesn't need to be because the incremental gains year on year will mean that many alive now will ride the wave because their life expectancy will be increasing faster than 12 months per year. Once that stage is reached we won't have actually cured aging but the result will be essentially the same because each year our appointment with the Grim Reaper will be moving further and further away rather than edging ever closer.
I share Aubrey's opinion that aging is essentially no different to any other disease and like all diseases is ultimately treatable given the resources. We cannot afford to sit back and accept it. Everyone in history has lived and died but it is a mistake to view aging as a fact of life set in stone when science has progressed to the level where we have a pretty good change of bringing under a decisive level of clinical control within 25 years or maybe less.
Personally I donate to the SENS Foundation see SRF Home | SENS Research Foundation which I think is the best route to assist in bringing the date closer when everyone no longer needs to fear ill health in later life through Atherosclerosis, Alzheimers, Arthritis, Cancer, Diabetes or Stroke because these are all essentially diseases of aging which rarely strike young people but where the risk rises for all of us with every passing year.
With todays technology it is completely out of the question but because we know the 7 types of damage which arise due to aging and are rapidly making progress in all of these areas we have a reasonable chance (better than 50%) of bringing aging under a decisive level of clinical control within 20 to 25 years. These types of damage are as follows (1) cell loss, (2) death resistant cells, (3) nuclear DNA mutations, (4) mitochondrial DNA mutations, (5) intracellular junk, (6) extracellular junk, and (7) extracellular crosslinks. This might sound rather daunting but the key is that we don’t need t
With todays technology it is completely out of the question but because we know the 7 types of damage which arise due to aging and are rapidly making progress in all of these areas we have a reasonable chance (better than 50%) of bringing aging under a decisive level of clinical control within 20 to 25 years. These types of damage are as follows (1) cell loss, (2) death resistant cells, (3) nuclear DNA mutations, (4) mitochondrial DNA mutations, (5) intracellular junk, (6) extracellular junk, and (7) extracellular crosslinks. This might sound rather daunting but the key is that we don’t need to actually stop the damage accumulating we just need to control and repair some of it periodically - what Aubrey terms the maintenance approach. It is this approach which potentially gives us a shortcut to radical life extension via technologies such as stem cell treatments, tissue engineering, immuno and gene therapies ultimately nanotechnology. Regardless of what some people believe I am pretty confident that an actual cure for aging is at least 100 years away but we don’t need a cure as such what we need is a solution that is within shooting distance, this is why controlling aging and repairing the accumulated damage is another matter entirely to achieving a cure and this must therefore be our goal because we understand the nature of the damage and its effects whilst understanding very little about actually slowing aging, how its laid down or influencing our metabolism. The key is achieving the crucial first step of adding 20 to 25 years of extra life which buy’s time until the next treatment 20 or so years later which in turn adds a further 25 or more years. By this route we can ride the wave of increasingly advanced technology and effectively live forever without actually curing aging itself. So to answer the question "how is it going?" the answer is no we don’t have the technology yet but to live for hundreds of years but by receiving periodic maintenance treatments we have a potential shortcut which takes advantage of rapid progress in technology. The key to the maintenance approach lies in ever improving treatments which repairing more and more of the accumulated damage as the interventions evolve this means that whilst in treatment one a fair amount of the damage accumulated over say 60 years of living is repaired it did not repair it all. Twenty years later progress would mean that the latest treatments will not only repair all of the damage corrected by the first intervention but also some of the damage that was not able to be repaired twenty years earlier. This means that whilst you are now chronologically 20 years older than at the time of the first intervention you might well be biologically younger following the second treatment. Whilst not a cure for aging this offers a shortcut to radical life extensions using technologies which to varying degrees are already developed and will potentially act as a lifeboat until aging is curable somewhere by my estimate in around 100 years time.
DNA damage is just as important as the other things you list. What you’re missing is that I think the only reason WHY it’s important is because it causes cancer, because of the concept that I’ve called “protagonistic pleiotropy”.
Yes I think anyone born after 1980 has an 80% chance of living a very long time but exactly how long is hard to say.
We pretty much know already what is needed to significantly extend both lifespan and healthspan, in essence it’s a question of putting everything together to achieve a comprehensive level of rejuvenation, the reason it needs to address all the areas is that there is little point in partially rejuvenating the body just by treating some of the issues caused by aging only to then to suffer a life threatening event due to one of the remaining areas letting the side down!
As far as the
Yes I think anyone born after 1980 has an 80% chance of living a very long time but exactly how long is hard to say.
We pretty much know already what is needed to significantly extend both lifespan and healthspan, in essence it’s a question of putting everything together to achieve a comprehensive level of rejuvenation, the reason it needs to address all the areas is that there is little point in partially rejuvenating the body just by treating some of the issues caused by aging only to then to suffer a life threatening event due to one of the remaining areas letting the side down!
As far as the areas of progress and the timeframe I would say we have a 60% chance in bringing aging under a decisive degree of medical control within not less than 10 years but not more than 20, and a 90% or better chance this century. We only need a few more breakthroughs such as CRISPR-cas9 (first used for gene editing in 2013), Stem Cell therapies such as induced pluripotent stem cells (iPSCs) which can now be created much more easily due to major progress in 2012, if we now factor in recent developments in senescent cell clearance (another area of rapid progress) it becomes clear we are well on our way to mitigating the nightmares of old age. The big key to this is that medical knowledge is continuously doubling in less than 90 days vs. every three and a half years as recently as 2010 although it’s hard to look as far as 20 years out many researchers believe that with AI and other technologies medical knowledge could then be doubling every 7 days, this situation would obviously be a total game changer. This trend was foreseen by IBM in 2017 as mentioned in the link (1) at the bottom.
One thing I am often asked is "How long before we can cure aging?" My answer is that a cure is not likely before the end of the century hence our need for a short term alternative to get us from here to there. The approach to dealing with aging therefore has to be control and not cure, it will be achieved by repairing the accumulated damage, this is because we understand how the damage is laid down even though we understand very little about actually slowing aging or influencing metabolism, using this path we are within striking distance of reversing the effects of aging whilst being unable to stop the ongoing process. This strategy is the essence of Aubrey De Grey's SENS theory (2) and is often referred to as the engineering approach, it is this route which holds the best prospect of success in the first half of this century because we bypass the problem of our lack of knowledge regarding metabolism Theoretically this approach could potentially extend life indefinitely while not actually curing the underlying aging process because we do not need to understand all the processes of aging, we only need to know enough to extend healthy lifespan by let’s say 25/30 years each time the treatment is administered.
Many people say to me “so how would it work in practice?” It’s actually quite easy to follow as I will explain, let’s for the sake of argument assume you are 60 years old at the time of your first treatment, this early and fundamentally imperfect treatment will probably repair 75% of the damage accumulated during your life up to that point. Now looking ahead say 20 years after the first treatment, when you are chronologically 80 but biologically 55 it’s time for another treatment. It is now that the progress in medicine comes into play because, by the time 20 years has passed, anti-aging medicine will have moved on significantly and, whilst the first treatment bought you an extra 25 to 30 healthy years by repairing a fair amount of the damage accumulated over 60 years of living, it did not repair it all, 20 years later progress will mean that the latest treatment will not only repair most of the new damage that has built up since the first intervention but also some of the damage that was not able to be repaired 20 years earlier, this means that although you are now chronologically 80 (but biologically in your 50s) after intervention number two whilst you will have aged 20 years chronologically since the first treatment you will be biologically younger after the second treatment than you were after the first. This is the essence of every damage repair strategy related to aging and offers the best and most realistically achievable route to address degenerative aging, frailty and infirmity within the near future.
I am not sure of de Grey’s answer, and I have not read the article in BBC News. I can comment that FOXO gene, especially FOXO3a has been linked and replicated in a number of studies to be associated with exceptional human longevity.
The important question of how much genes, or combination of genes, could be accounted for variability in longevity is quite controversial. Current literature tended to say that genes could account for no more than 30% in humans. This may or may not be true with added and new research in the future. If it were true, the question of whether influencing this 30% is mea
I am not sure of de Grey’s answer, and I have not read the article in BBC News. I can comment that FOXO gene, especially FOXO3a has been linked and replicated in a number of studies to be associated with exceptional human longevity.
The important question of how much genes, or combination of genes, could be accounted for variability in longevity is quite controversial. Current literature tended to say that genes could account for no more than 30% in humans. This may or may not be true with added and new research in the future. If it were true, the question of whether influencing this 30% is meaningful or not in changing or impacting longevity.
My pet peeve is that the media (and some people) tended to jump the gun too much in predicting some discovery, minor or not, could change the world. Most of the time, it remains to be seen. In the areas of longevity, there are discovery of pills that would increase longevity, and most of the time we don’t hear about this discovery in a year or two.