Mar. 11, 2016
Futurists are keen on a concept called "radical life extension."
Rather than settling for a standard life expectancy — like 78.8 years on average for an American — theorists, scientists, and investors want to find therapies to treat the age-related diseases that tend to kill us (like heart disease and cancer).
According to biologist Aubrey de Grey and his peers, once treatments are in place, the only things really killing people will be violence, accidents, and other non-natural causes. With that, de Grey says that living to be 1,000 years old will become an everyday thing.
De Grey has become one of the most vocal figures in the quest to conquer aging, between his much-viewed TED Talk "A roadmap to end aging," his book "Ending Aging," and his work as the chief science officer of the Strategies for Engineered Negligible Senescence Research Foundation.
The concern with radical longevity, as expressed by Manu Saadia at Fusion, is that wealth has a strong correlation with life expectancy. The wealthiest 20% of Americans can expect to live to 88.8 years, and for the poorest 20% it's 76.1 years. That gap would only increase with the super rich living longer than everybody else and accumulating even more assets — not to mention that billionaires like Peter Thiel are funding much of this research.
But de Grey says that extremely long lives won't just be for the wealthy.
"I'm quite sure it's going to be democratized," he tells Tech Insider, "even more democratized than anything we can think of today."
The reasons, the sometimes controversial biologist says, are twofold.
Living longer "is the thing that's going to matter the most to people," he says, comparing it to the "It's the economy, stupid," tagline that Bill Clinton used on his road to the White House in 1992.
"Ultimately, this is what people are going to vote for," he says. "If it's not available to everybody, then a party that has a manifest commitment to making it for everybody is going to get elected."
Then there are the economics of aging.
"At the moment, when people get sick, it's incredibly expensive," de Gray says. "Probably 90% of the medical budget of the industrialized world goes to the diseases and disabilities of old age one way or another. That's trillions and trillions of dollars. If we can stop people from going that way by only spending billions of dollars, it's a big net win."
Additionally, if people can stay able bodied into their 80s, 90s, and beyond, then they can keep contributing their wealth to society, he says. Adding to collective wealth rather than drawing from it — which is why the "graying" of countries like Japan puts so much stress on an economy.
"Therapies will pay for themselves in no time at all," de Gray says, "and that means from a government’s point of view, even the government of a really tax-averse country like the USA, it would be economically suicidal not to frontload the investment to ensure that everyone got these therapies as soon as possible."
So living longer wouldn't just be a luxury good; it would be, to borrow from Bill Gates, a global public good.
Sunday 1 August 2010
If we can stop the physical deterioration that comes with age, molecular biologist Aubrey de Grey sees no reason why human beings shouldn't live to be 1,000.
With his beard and robust opinions, there's something of the Old Testament prophet about Aubrey de Grey. But the 47-year-old gerontologist (who studies the process of ageing) says his belief that he might live to the very ripe old age of 1,000 is founded not on faith but science. De Grey studied computer science at Cambridge University, but became interested in the problem of ageing more than a decade ago and is the co-founder of the Sens (Strategies for Engineered Negligible Senescence) Foundation, a non-profit organisation based in the US.
What's so wrong with getting old?
It is simply that people get sick when they get older. I don't often meet people who want to suffer cardiovascular disease or whatever, and we get those things as a result of the lifelong accumulation of various types of molecular and cellular damage. This is harmless at low levels but eventually it causes the diseases and disabilities of old age – which most people don't think are any fun.
Is this the biggest health crisis facing the world?
Absolutely. If we look at the industrialised world, basically 90% of all deaths are caused by ageing. They are deaths from causes that affect older people and don't affect young adults. And if we look at the whole world, then the number of deaths that occur each day is roughly 150,000 and about two-thirds of them are because of ageing.
Why does the world not recognise this?
People have been trying to claim that we can defeat ageing since the dawn of time, and they haven't been terribly successful; there is a tendency to think there is some sort of inevitability about ageing – it somehow transcends our technological abilities in principle, which is complete nonsense.
And when people have made their peace with this ghastly thing that is going to happen to them at some time in the distant future, they tend to be rather reluctant to re-engage the question when someone comes along with a new idea.
Is it that our bodies just stop being so proactive about living?
Basically, the body does have a vast amount of inbuilt anti-ageing machinery; it's just not 100% comprehensive, so it allows a small number of different types of molecular and cellular damage to happen and accumulate. The body does try as hard as it can to fight these things but it is a losing battle. So we are not going to be able to do anything significant about ageing without hi-tech intervention – which is what I'm working on.
Ageing involves the process of metabolism, and then deterioration, and then pathology – is that right?
Basically, that's right. Metabolism involves a vastly complicated network of biochemical and cellular processes that are linked and that succeed in keeping us alive for as long as they do, but they have these side effects.
The side-effects start even before we are born, they go on throughout life and they are manifested as, for example, the accumulation of various types of molecular garbage inside cells and outside cells, or simply as cells dying and not being automatically replaced by the division of other cells. Gradually those changes at the molecular and cellular level accumulate and accumulate and eventually they start to get in the way of metabolism, and that's where pathology comes.
You've identified seven particular areas of cellular decay that might be combated. Can you give examples?
I just mentioned cells dying and not being automatically replaced, that's one. Another is cells not dying when they ought to – certain types of cells are supposed to turn over and sometimes they lose the ability to respond to signals that tell them to die.
A third is cells dividing too much – they may be dying when they are supposed to but dividing too much, and that is what cancer is.
We've known what causes cancer for some time but we are a long way from being able to cure it, aren't we?
I certainly don't claim that any of this is easy. Some of it is easier – but I've always viewed cancer as the single hardest aspect of ageing to fix.
You've talked about enriching people's lives, but isn't it the very fact of death that gives our lives meaning?
That's nonsense. The fact is, people don't want to get sick. I'm just a practical guy. I don't want to get sick and I don't want you to get sick and that's what this is all about. I don't work on longevity, I work on keeping people healthy. The only difference between my work and the work of the whole medical profession is that I think we're in striking distance of keeping people so healthy that at 90 they'll carry on waking up in the same physical state as they were at the age of 30, and their probability of not waking up one morning will be no higher than it was at the age of 30.
You've said you think the first person to live to 1,000 may already be alive. Could that person be you?
It's conceivable that people in my age bracket, their 40s, are young enough to benefit from these therapies. I'd give it a 30% or 40% chance. But that is not why I do this – I do this because I'm interested in saving 100,000 lives a day.
Can the planet cope with people living so long?
That's to do with the balance of birth and death rates. It didn't take us too long to lower the birth rate after we more or less eliminated infant mortality 100 or 150 years ago. I don't see that it's sensible to regard the risk of a population spike as a reason not to give people the best healthcare that we can.
30 April 2016
Dr Aubrey de Grey, a Harrow and Cambridge-educated biomedical theorist has made a name for himself for his research into preventing ageing
Some people born already may live for up to a 1,000 years in the future. Astonishing claims came from Dr Aubrey de Grey, a Harrow and Cambridge-educated biomedical theorist. De de Grey's research team are developing new regenerative therapies. His new theories have been heavily criticised by other scientists.
A British scientist has claimed that the secret to preventing ageing may be solved in the near future and that some people born already may live for up to a 1,000 years.
The staggering claims were made by Dr Aubrey de Grey, a Harrow and Cambridge-educated biomedical theorist who has made a name for himself for his research into preventing ageing.
Dr de Grey, the co-founder and chief science officer of Strategies for Engineered Negligible Senescence (SENS) Research Foundation, based in California, says he is developing a new form of medicine based on regenerative therapies.
Dr Aubrey de Grey described the human body as being like a is a 'machine with moving parts' and that damage accumulated during its lifetime was part of life.
However Dr de Grey's research team are working on a new type of regenerative therapies. It has been well backed financially with support from leading figures at Google and Paypal.
'By reconstructing the structured order of the living machinery of our tissues, these rejuvenation biotechnologies will restore the normal functioning of the body's cells and essential biomolecules, returning aging tissues to health and bringing back the body's youthful vigor,' the SENS Research Foundation claims.
However the research centres have been criticised by Dr Tilo Kunath, of the Centre for Regenerative Medicine at the University of Edinburgh, has dismissed his theories as incorrect.
Dr Kunath said that no one will be able to live past 120 at present nor will they live longer in the near future. He claimed it was only potentially possible to extend a person's life by 30 per cent if they adhere to a restricted diet. 'No one in the future could be genetically modified for a human to live longer than say 120 years. 'You couldn't even do it through diet or medicine, no not within the next 100 years,' he said, according to the Daily Express.
July 2013
Dr. de Grey’s SENS Foundation is aggressively seeking to extend the healthy human life span.
With Dr. de Grey recently being named to the Scientific Advisory Board of the Life Extension Foundation®, we thought this would be a good time for a follow-up interview.
SENS by the way, stands for Strategies for Engineered Negligible Senescence.
The ultimate purpose of maintaining a state of negligible senescence is the postponement of age-associated disease as long as the therapies are reapplied.
You have recently joined the Scientific Advisory Board of the Life Extension Foundation®. What do you hope to accomplish as a Board Member?
I’m delighted and honored to have been invited to join Life Extension Foundation’s® Scientific Advisory Board. I accepted with pleasure, because I think I can offer a range of expertise concerning biomedical research, a field that is not the sole source of Life Extension Foundation’s® business but very much does form a key component of the efforts into which Life Extension Foundation® reinvests its profits.
When Life Extension magazine® interviewed you in 2006 you were managing the Methuselah Foundation. Since then you have created the SENS Foundation. Can you explain the difference between the two foundations?
The Methuselah Foundation is still run by the person with whom I co-founded it, Dave Gobel. We split it in two (forming SENS Foundation, which we have recently renamed SENS Research Foundation) in 2009 because we came to the conclusion that it was not proving efficient, from an outreach and fundraising perspective, to have one organization pursuing two very different approaches to the same mission, namely prizes (the MF’s original focus) and direct sponsorship of research. So SENS Research Foundation now handles the research sponsorship and Methuselah is mainly back on prizes. We are still on totally cordial terms and I think everyone feels that it was the right decision: both organizations have thrived since the split.
Dr. de Grey’s book outlines seven strategies for ending aging, which are based on the seven causes of aging that he has identified. They are:
1.- Extracellular junk
2.- Cell senescence
3.- Extracellular crosslinking
4.- Intracellular junk
5.- Mitochondrial mutations
6.- Cancer-causing nuclear mutations (and epimutations)
5.- Cell loss leading to tissue atrophy.
His program of strategies is called SENS, i.e., Strategies for Engineered Negligible Senescence. Each strategy is given a distinctive “SENS” name, as follows:
AmyloSENS (extracellular junk) – Aging leads to an accumulation of junk outside of cells, the most notorious example of which is the amyloid plaque that is believed to cause Alzheimer’s disease. AmyloSENS would attempt to use the immune system to eliminate amyloid and other damaging extracellular junk.
ApoptoSENS (cell senescence) – Cells that become old and no longer divide (senescent cells) produce inflammatory substances that contribute to many of the diseases of aging. ApoptoSENS would eliminate senescent cells by inducing such cells to “commit suicide” (apoptosis).
GlycoSENS (extracellular crosslinks) – Proteins form cross-links with sugars (glycation) as tissues age. As a result of this crosslinking, tissues lose suppleness, becoming stiff and full of fibrous material. GlycoSENS seeks enzymes that will selectively breakdown these harmful crosslinks.
LysoSENS (intracellular junk) – Waste material of various kinds (“junk”) that is formed within cells is often broken down by a specialized organelle called the lysosome, which contains enzymes for that purpose. Unfortunately, some junk (proteins, fats, metals, etc.) cannot be broken down by normal lysosome enzymes, and this junk accumulates with age. The goal of LysoSENS is to develop and provide additional enzymes to the lysosomes that would break down more forms of junk molecules.
MitoSENS (mitochondrial mutations) – Mitochondria generate energy for cells, but in doing so they generate large amounts of free radicals. A prime target for these free radicals is the DNA within the mitochondria that controls mitochondrial function. MitoSENS seeks to make copies of mitochondrial DNA in the DNA of the cell nucleus, where it would be a safe distance from the damaging free radicals produced within the mitochondria.
OncoSENS (cancer-causing nuclear mutations/epimutations) – Most forms of cancer utilize the enzyme telomerase to maintain long telomeres (the caps of chromosomes that keep them functional). OncoSENS proposes to eliminate telomerase as a means of controlling cancer. Telomeres are needed by stem cells, but OncoSENS would replace this need by a program of tissue replacement (RepleniSENS).
RepleniSENS (cell loss and atrophy) – With age, cells are lost or atrophy, thereby causing tissues to stop functioning properly. RepleniSENS would utilize stem cell therapies to restore cells and tissues.
You recently inherited a large sum of money and chose to donate most of it to the SENS Foundation. Will you provide some details and explain your motives?
My mother died in May 2011 and I was her only child; the upshot is that I inherited roughly $16.5 million. Of that, I assigned $13 million to SENS (I won’t bore you with the legal details, which were tedious in the extreme). It was pretty much a no-brainer for me: I’ve dedicated my life to this mission, and I dedicate all my time to it, so why not my money too? I retained enough to buy a nice house, but beyond that I have inexpensive tastes and I have no doubt that this is the best use of my wealth. It will accelerate research considerably, and also it will have indirect benefits in terms of helping us to put more resources into raising the profile of this work and garnering more support.
Who are the other major donors to the SENS Foundation, and what proportion of the budget is covered by the money you donated?
My donation will be spent over a period of about five years, and it roughly doubles the budget we had previously, from $2 million annually to $4 million. The number one external donor remains our stalwart supporter Peter Thiel. Additionally, another internet entrepreneur, Jason Hope, has recently begun to contribute comparable sums.
What will the SENS Foundation do when your donation money runs out?
It’s hard to look ahead as far as five years, the projected duration of my donation, but we certainly have great confidence that our outreach efforts will bear fruit in that time. My hope is that five years from now we will be big enough that the expiry of my donation will go relatively unnoticed.
Do you have a strategy for raising money for research on aging?
Absolutely—lots of strategies. The brutal lecture schedule I undertake and the 100+ interviews I do each year are part of it, as they’ve always been. The research we do, and the progress we demonstrate, are of course also key. And now that we have a little more to spend in that area, we have a really talented staff that is developing various other areas.
Do you think aging is a factor that increases the risk of disease?
No, I don’t. Gerontologists will say yes, it’s a risk factor, but all they’ll mean is that there is a correlation. Non-scientists will hear the statement and will infer that with appropriate choices one can reliably avoid the diseases of old age, just as with the appropriate choices one can reliably avoid being hit by a truck when crossing the street even though crossing the street is a risk factor for being hit. As such, this is one of the most counterproductive of the many failures of communication of which I claim my colleagues in gerontology are guilty. The actual fact is that aging is the CAUSE of the diseases of old age, and we need to start saying so.
Do you think research on ending aging should be distinct from research against specific aging-related diseases?
No, I certainly do not, and this leads on from the previous question. The more we appreciate that aging is the cause of age-related diseases, the more we can get the research communities that are focused on those diseases to understand that the treatment of aging is no more nor less than preventative geriatrics. The general concept of preventative medicine already has a good rap, and we need to be making use of that.
What is advantageous and what is disadvantageous about the money spent on aging research by the National Institute on Aging (NIA, a branch of the US federal government’s National Institutes of Health)?
It’s pretty much all advantageous - just not nearly as advantageous as it could be. There is pitifully little money going into the search for interventions to postpone aging, and of what there is, pitifully little is focused on late-onset interventions.
What do you think of the way the Ellison Medical Foundation spends money on aging research?
Exactly the same as for the NIA. The Ellison Foundation was set up with a remit to fund work that complemented the NIA, but I’m afraid to say that in practice it has merely supplemented it.
Do you think it is more important for aging research to raise money from wealthy individuals than would be the case for research on cancer or heart disease?
I think wealthy individuals have a key role to play across the whole non-profit world, but probably even more in fields that so far lack widespread public support, of which the defeat of aging is unfortunately still one.
For which of your SENS strategies would success achieve the most additional healthy years?
No one strategy would achieve very much on its own - certainly not as much as ten years, probably not even five.
Which of the SENS strategies has the best prospect for success first?
A couple of the strategies are already in clinical trials for some relevant conditions - stem cells for various things, including Parkinson’s disease, and vaccination against extracellular debris for Alzheimer’s.
Which of the SENS strategies would be the most difficult to achieve?
I think it’s pretty clear that the approaches for defeating cancer and for obviating mitochondrial mutations are the hardest, because they will both involve gene therapy, something we’re not at all good at yet. Out of those two, I would say that the OncoSENS (the elimination of telomerase enzyme) is the harder, because it is much more complex and also because it involves gene targeting rather than just insertional gene therapy.
Will you make a general statement about the goal of SENS research?
SENS is based on the appreciation that there is a continuum between (a) the initially harmless, progressively accumulating damage that accumulates in the body as a side-effect of its normal operation and (b) the pathologies that emerge when the amount of that damage exceeds what the body is set up to tolerate. We want to treat (remove or obviate) the damage and thereby prevent the pathology.
How difficult would it be to eliminate lipofuscin (the cellular junk that particularly accumulates in neurons and heart muscle cells) compared to eliminating 7KC (an oxidized derivative of cholesterol that accumulates in atherosclerotic plaques) or A2E (a substance accumulating in the retina with age that causes macular degeneration and blindness) as a lysoSENS project? How much difference do you think elimination of lipofuscin would make in terms of rejuvenation?
This is a big question right now. We have a PhD student in our funded group at Rice University who is working on lipofuscin, but he is just starting. Lipofuscin is indeed harder, but what makes it harder is not the aging-versus-disease distinction but simply the nature of the substance. Lipofuscin is very heterogeneous in its molecular composition, and moreover it is mainly made of proteins, so it is hard to distinguish from material that we don’t want to break down. I should note in passing that the material whose accumulation causes macular degeneration is often called lipofuscin but really should not be, because the only thing it has in common with bonafide lipofuscin is its subcellular location (the lysosome) and its fluorescence properties: its molecular composition is entirely different.
In the 2011 report of the SENS Foundation, progress on mitoSENS (making copies of mitochondrial DNA in the nucleus to protect them from free-radicals generated by mitochondria) was restricted to 5 of the 13 protein-encoding mitochondrial genes. How confident are you that all 13 such genes can be copied into the nucleus in the foreseeable future? Are some of those genes more important than others, or are you simply going after the easier targets?
We’re pretty confident. Some of the genes we’ve chosen to work on first are easy targets in the sense that other researchers have demonstrated some success with them already; other genes are chosen more because success would be high-impact, in that it would allow more clear-cut assays of efficacy. In the end, all 13 are equally important.
You have been demonstrating an increased appreciation for the role of neurofibrillary tangles (tangled aggregates of tau protein) as a potential cause and treatment target resulting in the cognitive decline of Alzheimer’s disease. Are you planning any SENS Foundation projects to remove tangled tau to better prevent Alzheimer’s disease than simply removing amyloid? Would this be distinct from LysoSENS (elimination of intracellular junk by more powerful enzymes in lysosomes)?
I’ve always said that (tau) tangles are likely to be just as important as (amyloid) plaques in Alzheimer’s disease, and indeed that cell loss must also be addressed. Absolutely we want to remove tangles. Tangles are an unusual type of intracellular aggregate in that they are not normally eliminated by lysosomes, but they are still a target of LysoSENS because we believe that they are the visible manifestation of a “traffic jam” caused by lysosomal dysfunction, which is itself caused by other molecules, maybe the same ones that cause atherosclerosis. (This suspicion arises from, among other things, the fact that apoE genotype is the most significant genetic contributor to risk of both Alzheimer’s disease and atherosclerosis.) At the moment we have no project in this area but we are in detailed conversations with people focused on it.
Is AmyloSENS (elimination of extracellular junk, mainly amyloid) now primarily focused on transthyretin amyloid, rather than the amyloid plaques believed to cause Alzheimer’s disease? (Transthyretin is a form of amyloid that accumulates outside of the brain, especially in the heart, and has been found to be the frequent cause of death of persons over 110 years of age.)
Yes, our only AmyloSENS project at present (a collaboration between labs at Harvard and at University of Texas, Houston) is focused on transthyretin amyloid. We are leaving the research on Alzheimer’s disease amyloid to the many well-funded groups that already have it in their sights. The other main amyloid identified as having a role in Alzheimer’s disease is islet amyloid in the pancreas, and we may get into that area soon.
SENS Foundation has been investigating the possibility that mutation and epimutation (changes in gene expression rather than alterations of the genes themselves) may be deleterious in ways other than cancer. If that proves to be true, what strategies do you envisage to address that problem?
Our current work is focused on epimutations; we feel that the work of experts in the field of the genetics of aging (Jan Vijg’s group at the Albert Einstein College of Medicine in particular) has already shown really conclusively that mutations accumulate far too slowly in most tissues (notably the brain) during adulthood to have any chance of contributing to age-related ill-health. If epimutations don’t come out the same way, we will need to look at ways to mildly accelerate cell turnover, combined with autologous stem cell therapy, which uses one’s own stem cells for cellular therapy. But that’s awfully hard, so let’s hope we don’t need to go there!
In the November 2, 2011 issue of Nature, Darren J. Baker, et al. described success in rejuvenation of an accelerated-aging model of a mouse.* Do you think that Baker’s group is more successfully fulfilling ApoptoSENS than the SENS Foundation is likely to achieve?
The Baker paper was a huge validation of the idea that death-resistant cells are bad for you, but it didn’t actually put forward any particular approach to eliminating such cells in genetically unmodified organisms, so it in no way “fulfills ApoptoSENS.”
The 2011 research report of the SENS Foundation contained only a brief mention of RepleniSENS, the use of stem cells to restore and replace cells and tissues. Given all the interest in stem cell therapies by others, is there really a need for SENS Foundation to be doing research in this area?
You’ve got it - this is the clearest example of a theme of SENS which is not being pursued aggressively by SENS Research Foundation, and that’s precisely because it’s being supported so well by others. That said, we still keep our eyes very open for specific projects in the RepleniSENS space that might need a leg up.
May 23, 2014
Aubrey de Grey has been called many things. “Transhumanist” is one of them, but one he dislikes. “Immortalist” is the tag used to describe him and his colleague Bill Andrews in a documentary shown at South by Southwest this March, though de Grey rolls his eyes when someone drops the word “immortality.”
The British gerontologist considers himself a “simple medical researcher,” but his research is about fiddling with cells to stop ageing in human beings, and potentially postponing death indefinitely. If it’s not immortality (in de Grey’s world, you could still be dispatched by an infectious disease or a shotgun), it’s quite a close beast.
He believes that tackling the individual illnesses that haunt old people’s lives is a fundamentally flawed strategy; the right course of action is to act at the cellular level to prevent ageing from setting off those illnesses in the first place. His Silicon Valley-based foundation-cum-laboratory, the SENS Research Foundation, is completely devoted to this feat.
In the past, de Grey’s views were often met with skepticism or hostility, when not openly guffawed at. That has not completely changed, but the idea that ageing should actually be regarded as a disease, and that it might even be treated as such, is increasingly gaining ground. Recently, that's been given a boost by research into tackling ageing on a genetic level.
I wanted to ask de Grey how things are going at the frontline of the anti-ageing battle, so we exchanged some emails (he doesn’t carry phones, “ghastly, horrible things that deprive people of essential solitude”), and we finally met in Cambridge last week.
Drinking a pint of ale and tormenting his greying Old Testament-style beard, he initiated me in the science and doctrine of which he’s the standard-bearer, most of which can be summarized in one question: If we could really wipe old age and death off the planet, why shouldn’t we?
First of all, let’s look at some recent news. A couple of weeks ago, scientists at Harvard linked the circulatory system of a young mouse to that of an older mouse. The result was that some tissues of the old mouse were rejuvenated. What’s the significance of that?
Aubrey de Grey: It’s very important. This whole idea of linking two animals of different ages—it’s called heterochronic parabiosis—to study ageing has been around for a little while now. At SENS, we work very closely with some of the guys who did that at Harvard. Of course, we’re not going to do the same thing to people.
In general, the experiment has led to a very useful discovery: There’s a particular protein in the bloodstream of young individuals, called GDF11, that helps to reactivate certain aspects of cell division in certain parts of the brain. Now, that’s only a small piece of information; there’s lot more that is not yet known. But I expect that, within the next five years, at least another half a dozen similar rejuvenating factors will be discovered.
So is this mice thing the first step to defeat ageing?
I don’t want to quite say that. All we know is that GDF11 can stimulate certain types of cells to divide when they would not previously divide due to old age. Now, cell division is not the whole story of ageing. In fact, sometimes it can be a bad thing to make cells divide more often, because they may be more exposed to cancer. But still, it’s a whole new tool, and it’s very important.
Do you think that people may be starting to think that ageing is the real enemy?
I do think so, yes. The things that I’ve been saying for years are finally beginning to get understood. People are understanding that diseases of old age are not really diseases: They are aspects of ageing, side effects of being alive. If you want to cure them, what you’ll have to cure is to be alive in the first place—but you can’t actually do it. So we’ll have to take a preventative maintenance approach. That means that we’ll have to identify the various types of molecular and cellular damage that the body does to itself as a side effect of its normal metabolic operation. Once you’ve identified them, which has already been done, you have to find a way to repair that damage and prevent it from developing into a pathology of old age. That’s what I’m working on.
What are you really trying to achieve? Longevity or immortality?
Well, first of all, any longevity benefit that I may achieve would be a side effect. I don’t work on longevity, I work on health. And it just happens that, historically, the main thing that kills people is…not being healthy. So healthier people will likely live longer.
How much longer? It depends on how much longer we can keep people healthy. The best we can say at the moment is that the human body is a machine. Therefore, it ought to be the case that we can have the same kind of impact on the human body that we already have now on simple manmade machines, like cars. So, as I said, we can rely on preventative maintenance: repairing any damage before it makes the doors fall off. It seems to work really well with cars; we've got one-hundred-year-old cars around now. So, if you do sufficient maintenance, the sky’s the limit. We should be able to maintain the human body in good health indefinitely, however long we like.
So…it’s immortality, right?
Don’t use the word immortality when you talk about my work. It’s taken; it’s a religious word. Immortality means zero risk of death from any cause, but I don’t work on stopping people from being hit by trucks. I work on keeping them healthy.
By the way, what’s your relationship with religion?
I personally have no religious views, but I have sometimes been attacked by religious people, who said that I was playing God. But it’s quite interesting that it’s really easy to get people coming from a religious background to understand that it would be a sin not to work on this. That’s because ageing causes a lot of suffering, and alleviating suffering is something the scriptures told was our duty. I had some success with that argument.
Ok, what about the social and political consequences of this potentially indefinite extension of life you’re aiming at bringing about?
I’ve addressed this issue once or twice, and I noticed that the mistake that people always make is that they think I’m saying we would live much longer in a context where nothing else changes. They think like, “The rest of the world will be just like now but everybody will be biologically 25 forever.” That’s obviously complete nonsense. If we just look at the mathematics, before we’ll have anybody living until the age of 200, a lot of things will have happened, and changed. For example, people always panic about paying pensions to people that live longer. But why would you need a pension if you’re healthy? Even the very concept of work won’t exist in the same way, because we’ll probably have more and more automation. Look, we have at least one hundred years before we’ll have any 200-year-old people.
But we should probably start planning everything in advance. Right now, nobody is going to behave as if it’s going to happen. If you actually managed to do it, one day, society would be completely off-guard.
That’s true, but I am not going to tackle each individual problem—pensions, kids, resources—that might arise in a post-ageing society. I prefer to help people focus on the fact that we’ve a problem today, a really rather bad problem. That is that 100,000 people every fucking day are dying of ageing. That’s the important thing, not worrying about hypothetical problems.
Unfortunately, people are programmed to find reasons why it would be a bad idea to defeat ageing. This is mainly because they fear the unknown, since the world would be very different without ageing.
Aren’t you afraid that living for, say, one thousand years, may be boring?
I find this a very sad question. Of all the ridiculous questions I get about defeating ageing, this is the saddest. Anyone who asks that question must have such a miserable life.
I’m not very happy with my life right now, I must admit.
How could you possibly imagine that you could run out of things to do?
I have a long list of things to do if I was to live 1,000 years: just think about all the films you haven’t seen, all the books you haven’t read. And by the time you’re through them, you would have at least another thousand years of backlog.
Apart from anything else, the main thing that people enjoy with life is other people, mutual interaction. And we have seven billion people to interact with. But even if there were only seven million people worth talking with, people don’t stay the same; they change over time, so you’ll never actually get bored.
Do you define yourself as a transhumanist?
I don’t really like to be called “transhumanist,” it sounds like I’m doing something weird. I’m not doing anything different from any other medical researcher, except that the consequences of what I’m doing might be quite big. I think it’s a mistake to label visionary technologists with something that starts with “trans.” It creates a kind of psychological separation that is really counter-productive.
But would you do some of the things that some transhumanists advocate, like uploading your mind on a computer?
I’m enjoying my body of meat, but if I had no choice I’d certainly be just as happy to continue my existence in another form of hardware, rather than not continuing my life at all. It remains to be seen what’s actually gonna happen. My current suspicion is that uploading, if it’s possible at all, is still a lot harder than the medical approach that my team and I are taking. But I could be wrong, so I’m very happy that there are people exploring alternative methods.
Are you experimenting with any life-extending practice right now?
Sure: I’m doing this interview. I mean, I’m not following any particular diet or practice, because what we have today is quite useless. The most important thing is getting the word out, getting the things to happen sooner, hastening the development of the therapies, rather than trying to use the little we have today.
What are the chances that the two of us are gonna live to a thousand years?
I don’t know, but I’m working on it. It’s going to happen, it’s just a question of when. The work I do is simply speeding up the inevitable.
But it is very important to me, because for every day that I bring forward the defeat of ageing, I’m saving 100,000 lives—100,000 lives: thirty World Trade Centers. And I’m very happy about that.
