shanee nishry: hey, everyone. good to have you here. you may heard of him as the manwho will make you live forever, or at least untilyou get hit by a car. but here he is, aubrey de grey.
reverse aging, aubrey de grey:thank you, shanee. i like the way thatshanee introduces me. it's great. i've had the good fortune to beintroduced by her twice today.
all right. so thank you for coming. i'm going to try andtell you all about what we are doing at sensresearch foundation. i have already mademy first mistake, which to leave theclicker on my chair. so as shanee said, we areinterested in stopping you from getting sickas you get old. it has been a sourceof frustration to me
that we get sick as we getold, for quite some time. and an even greatersource of frustration that it isn't a sort offrustration for everybody. so i'm trying to change that. but also, of course, actuallychange the facts of the matter, to try to actuallydeliver medicines that will allow usto stay healthy. and so i'm going to spendthe next hour telling you all about how.
first of all, the success story. so this is, simplyfor illustration, statistics from the usashowing the proportion of the population that areover the age of 65, which was way down at 8% orso in 1950 and it's projected to be up around 22% in2050, which is pretty dramatic. and, of course, this isa cause for celebration, because it is the consequenceof a great deal of success over the past 100 or 150years in bearing down
on the diseases thatused, historically, to kill an awful lotof people in infancy, or in childbirth, and so on. and the result is thatpretty much everybody is surviving long enough toreach the age of 65 or more. but it also has, of course,created some problems. the economicproblems are perhaps foremost in manypeople's minds right now. and again, here, i'm justshowing us statistics
for illustration. but, of course, it's the samethroughout the industrialized world. we have this problem thateven though the economy has been growing nice and fast--i'm going to use this one, where you can actuallysee my pointer. i've never understood why thesescreens can't made to actually reflect a laser point oflight, even-- whatever. so, yes.
so this is the us economy,the red line going up at a nice, steady rate. and if you look at the rate ofmedical expenditure in the us over the same time period, whichis the last 50 years or so, then it looks perfectlymanageable really. it doesn't lookparticularly scary. but it's a greatdeal scarier if you take the trouble to divideone by the other, which is where the greenline comes from.
and the green line showsobviously therefore the proportion of the gdp thatis being spent on medical care. and it's gone up from5%, 50 years ago, to 18%, which isextremely scary. and, of course,is the reason why we have all these concernsabout pension funds running out of money,and medicare running out of money, and so on. so the question is,first of all, why?
why have we got thissituation in the first place? putting it in starkerterms, why have the diseases and disabilities of old age,which, of course, dominant medical expenditure today, whyhave they been so much more resistant tomedical intervention than the infectious diseasesthat we have more or less entirely eliminated overthe past century or so? this is actuallypretty paradoxical when you think about it.
and in order toanswer this question, the first thing ithink we need to do is to ask ourselveswhat is aging anyway? what is the ultimate substratefor these age-related diseases? so i'm going to give youa definition of aging now, that i'm going to beusing for the rest of the talk. and this definitionis specifically geared to trying to eliminatethe distractions that often come when aging is discussed.
there are manydefinitions of aging out there that really do more harmthan good because they just confuse the issue. but this one brings itdown to its essentials. and i think it's useful. essentially, whati'm trying to do here is to emphasize that theaging of living organisms is really no differentat the bottom line from aging of inanimatesubjects, like cars,
or airplanes, or whatever. it is simply a fact ofphysics, never mind biology, that machines withmoving parts do themselves damageas a side effect of their normal operation. and it's also a fact of physicsthat that damage accumulates and, therefore, eventuallyit exceeds the level that the machine isset up to tolerate. so that's true for a car.
it's true for an airplane. and it's true for a human being. it's true for the human body. the human body does a lotof different types of damage to itself, which i'll be gettingonto over the next while. and, therefore, we aresubject to a whole bunch of different eventualfailure modes, so to speak, of the body. and that's reallyall it's about.
so really what thatmeans is that we must address a veryfundamental misconception that is prevalent withinsociety today concerning the diseases of oldage on which we spend so much money, diseaseslike alzheimer's, and most cancers, andcardiovascular disease, and type 2 diabetes, andosteoarthritis, and so on, and so forth. these diseases are normallyviewed as diseases.
in other words, they'reviewed as, in some sense, similar to infections,and potentially amenable to the same kind ofmedical interventions that infections are amenable to. but they're not. they're actuallyall part and parcel of one single process,the accumulation of damage that the body does toitself in the course of its normal operation.
so not only arethey, as we all know, widespread and staggeringlycostly, but they are universal. the only way that you willnot get a particular disease of aging is if you diebeforehand of something else. you are going to get it. and furthermore, theynot medically curable in the strict senseof the word "curable." what do i mean bythe strict sense? i simply mean that we cannoteliminate them from the body
in the way that we caneliminate an infection. if you eliminate aninfection, then the person isn't going to sufferfrom that infection again unless theyget reinfected. but you can't dothat with things that are a side effect ofbeing alive in the first place, other than by eliminating beingalive in the first place, which would kind of defeat the object. so let's not do that.
but that does notnecessarily mean that we can't addressthe diseases of old age using medicine. it just means that we haveto rethink our starting point in designing the medicalinterventions that we might be use. i'd like to put it thisway, even more starkly. most people think ofthe various causes of ill health along the linesthat i'm showing in this table.
there are varioustypes of disease. there's infections,communicable diseases. and there arecongenital diseases that a smallproportion of us have because we got dodgy dnaof one sort or another one. and then there are thechronic age-related diseases, which are the subject ofso much concern and so much expenditure today. and then, in mostpeople's minds,
there is this completelyseparate category called aging itself,which is composed of these nonspecific, ratherpoorly defined things, like sarcopenia, whichis the decline of muscle mass in the elderly;or a gain of fat mass; or a decline in function ofthe immune system, these things that we don't reallythink of diseases. that's what most peoplehave in their minds when it comes to ill health.
but it's nonsense. this is the way that we ought tobe thinking about all of this. all the columnsare the same here. it's just where the blackline is that's changed. there are diseases andthen there's aging. but the diseases of oldage are part of aging. the only difference betweencolumn three and column four here is that columnthree consists of those aspects of agingthat we have taken the trouble
to give disease-like names to. its purely semantic and no more. that is an absolutelyfundamental thing that i'm going to be leaningon for the rest of the talk. so i wanted to make sureyou have it in your heads very clearly at the outset. now, what does thismean in economic terms? i mean we can look at it in manyterms, humanitarian of course. but let's just do itin terms of economics.
and here, for themoment, i'm going to move away from medicalexpenditure to the expenditure on medical researchbecause, unfortunately, it's the same story, perhapsin even starker terms. and again, i'm going touse us statistics just for illustration, becausei happen to have them. but again, this isabsolutely the same across the industrialized world. so the nih, the nationalinstitute of health,
is the counterpart ofthe medical research council in the uk. it's the government body thatis responsible for essentially all public expenditureon medical research. and it has a nice healthybudget of $30 billion a year. but only 3% of thatbudget is spent on aging, the nationalinstitute on aging. that is pretty badnews given that the vast majority ofmedical expenditure
and, of course, sufferingcaused by disease and so on, in the us,is driven by aging. it doesn't make sense. but that's how it is. that's bad. but it's not nearlyas bad as it gets. even within the nationalinstitute on aging, only about one sixth of thatbudget, that $1 billion, is spent on understandingthe biology of aging.
the rest goes on specificresearch on alzheimer's disease and/or geriatric medicine,or even social gerontology, studying how to preserve thedignity of the elderly, things like that. which is all very well. they're important stuff. but it's not what would actuallygive the bang for the buck. so it's a disgracethat it's so small. and that's not theend of the story.
the fact is that evenwithin the division of aging biology ofthe nia, of the nih, the amount that's actually spenton doing something about aging is way under the 10%. that number, $10million, i've got there, is a very generous estimate. really, that's amazing. most gerontology consists of--it's a bit like seismology. people who studyearthquakes, they
understand that what theystudy is bad for you, but they're not proposing toactually do anything about it. it's all about just gettingout of the way really. so it's a bit sad. i mean to put it in realperspective, what we're talking about here is that my littlefoundation, the sens research foundation that's been createdaround my work, which has only existed for a fewyears, and we only have a budge of $4or $5 million a year,
it's on the same orderas the us government. that is fairly shocking. so something betterbe done really. and that's why i go around theworld giving talks like this. this is essentiallywhere we are today. if you look at the bottom ofthis diagram, what i'm saying is what i told you already. metabolism causesdamage, causes pathology. in other words, thenetwork of processes
that keep us alive fromone day to the next, which is what biologistscall metabolism, causes various types ofmolecular and cellular change to the composition andstructure of the body, which i'm calling damage. and that damage accumulates. and eventually, when itexceeds a certain threshold, it impacts thefunction of the body. and that's when the diseasesand disabilities of old age
begin to emerge and to progress. and all of whatwe try to do today to attenuate and alleviatethe pathologies of old age consists of what i'm callinghere the geriatrics approach, geriatric medicine. it means, in a nutshell,completely ignoring everything that i've told you inthe last five minutes. it means pretending thatthe diseases of old age are just like infections andcan be eliminated from the body.
it's obviouslycomplete nonsense. first of all, for thereason i've told you, namely the damage, it'scontinuing to accumulate. so obviously,anything that comes under the geriatricsheading is going to become progressively lesseffective as time goes on and as the damage becomesmore and more irresistible. and secondly, because thepathologies of old age are quite numerous.
you're not supposed to beable to read this slide. don't worry. this is simply a nice selectionof the things that go wrong with us as we get older andthat we would rather didn't. so it's completely hopeless. but we spent a spectacularamount of money on it. now, i am by no means thefirst person to point this out. for the past 100 years, therehave been a few people out there trying to get people tounderstand that actually if we
want to do anythingabout aging, we have to intervene at an earlierstage in the chain of events, in the chain of eventsthat i've just shown you. and that's what has givenrise to what i'm calling here the gerontology approach,which is the approach favored and pursued by that rarebreed of people who study the biology of aging with aview to actually doing something about it in due course. however, that approachhas also failed completely
to deliver any kindof actual impact on the ill health of old age. why should it be? well, what is thegerontology approach? it consists of essentiallytrying to clean up metabolism, trying to slow down therate at which metabolism creates damage. and that soundslike a great idea. because certainlyif we could do that,
it would postpone the ageat which the damage reaches a pathogenic quantity. but there's a couple of problemswith the gerontology approach too. the first problem is thatit's only slowing down the accumulation of damage. so that means that thelater you start the therapy, the less benefityou're going to see. the less time you'regoing to have to extend,
before the pathogenicthreshold is reached. and that's a bit of ashame because some of us may already have the misfortuneto be in middle age or older by the time that the therapiesin question are even developed. so that's a bit of a shame. but worse than that,the gerontology approach suffers a problem that is ratheranalogous to this problem, namely-- there wego-- this problem. metabolism israther complicated.
this is a simplifieddiagram of a small subset of what we know about howmetabolism really works, about how the body works. and as you can see,it's a bit hairy. and as engineers, or as peoplewho work with engineers, i'm sure you will understandthat it's pretty implausible that we would beable to, in some way, tweak this vast networkof uncommented spaghetti code in a manner that wouldstop it from doing the thing we
don't want it to do,namely creating damage, without also stoppingit from doing stuff that we do want it to do,like keeping us alive. so it's a waste of time really. there's no way inthe world that we're going to actuallymake this work. but if that the end of my story,i wouldn't be standing here. you knew that. so what's the "get out?"
how do we extractourselves from this? well, ultimately what we dois we go back to the analogy that i started withsome minutes ago. this car is morethan 100 years old. and, of course, therearen't many cars like this. but they're not all that rare. the point i want tohighlight about this car is that it was notdesigned to last 100 years. it was designed to last maybe10 or 15 years before it would
fall apart and yougo and get a new one. and the reason it's lastedso long is understood. we all know that the way thatenthusiasts allow their cars to live a long time is bydoing really comprehensive preventativemaintenance on them, by simply repairing thedamage that the cause does to itself as a side effect ofits normal operation, a phrase that you may recognizefrom a few minutes ago. now, that means thatwe can realistically
ask ourselves, well,maybe we could actually do the same thingto the human body. maybe we could engage inpreventative maintenance. and if it was sufficientlycomprehensive, maybe it would havethe same effect. it would greatly extendthe healthy longevity of the machine that we call thehuman body beyond the longevity that it was initially setup to be able to achieve. this is what that means in termsof comparing and contrasting
with the other approaches. rather than trying to slow downthe rate at which metabolism creates damage, as thegerontology approach tries to do, or indeed the rate atwhich damage creates pathology, as the geriatricsapproach tries to do, instead the proposal is touncouple those two processes from each other. to actually go in andperiodically repair the damage so that the damage, even thoughit's still being created,
never actually reachesthe pathogenic threshold. what i'm going to be tryingto persuade you of today, in the rest of the talk, is thatthis approach is very much more favorable than the other two. that we have a realisticchance of pulling it off within the foreseeable future. so in order to goon to that, i'm going to now start talkingabout actual biology. i'm not going to get tootechnical, obviously.
but i'm going to try to giveyou a feel for what this is all about. the first thing wehave to do is to define the problem in concrete terms,in down-to-earth, actual biological terms. and that is whatthis table does. here we have alist of seven types of damage, sevencategories of damage. and as you can see,each of these things
is a genuine, bona fide,physical, biological thing. cell loss simply meanscells dying and not being automaticallyreplaced by the division of other cells, avery simple concept. and this is aclassification which i have been using for thispurpose for quite some time. now, you may have acouple of questions about this classification. and i want to answerthem right at the outset.
the first question you mayhave is, well, hang on, what's so useful aboutthis classification? you recognize, as i'vealready, in fact, highlighted, that there's anawful lot of things that happen during aging. there are, indeed, an awful lotof different types of damage that gone on. so a thousand things can beclassified, can be grouped, into seven different categoriesin many different ways.
what's so useful about thisone, you may be asking yourself? the answer is that withineach of these categories there is a particular generictype of intervention that exemplifies, that illustrates,the maintenance approach. that within each categorythere may many examples. but all of them can be,in principle anyway, addressed by, broadlyspeaking, the same therapy, differing only in detailsfrom one example to another. that's the absolutelyfundamental thing
that you're looking for inany kind of classification of a problem into subproblems. so that's what thisclassification is all about. the second question youmay have is, well, hang on, how do we know thatthis is exhaustive? how do we know that thereisn't an eighth category and a ninth one? and, of course, wecan't absolutely know. but the good newsis that we have
at least a good circumstantialargument that it probably is an exhaustive classification. what is thatcircumstantial argument? here it is. it's been the sameclassification for more than 30 years. all of these thingshave been major topics of research and discussionwithin gerontology since at least the early 1980s.
now, one could say, well, that'snot really a fair argument because peopleweren't really looking to classify damage inthis way back then. and that's kind of true. but it's increasinglynot true because the fact is i've been out there,making a nuisance of myself and challengingpeople to actually come up with othercategories to add to this list for morethan a decade now.
and i do seem to begetting away with it. i am like, you know,getting away with it. so that's pretty good news. i mean it's acircumstantial argument. but it's quitecompelling really. now, i'm going to spend afew minutes now highlighting the relationship betweendamage and pathology. and this is really importantbecause ultimately it's where the rubber hits the road.
at the end of the day, we needto actually convince ourselves that if we could repair allof these types of damage, we genuinely wouldhave this effect on the variouspathologies of old age. what i want toemphasize to you here is that the relationshipbetween damage and pathology is, in some cases, quitecomplex, but it is established. it is well known. the stuff i'mgoing to be talking
about in thisparticular section, for the next couple of minutes,is not innovative ideas without portfolio, thatsens research foundation has put forward. these are things that noone working in these field would dispute. so let's start with cancer. cancer is the simplest example. because in this case, it'spretty much a one to one
relationship between thepathology and the damage. there's this onecategory of damage that i define asdivision-obsessed cells, in other words, having too manycells because there are cells which are dividing whenthey're not supposed to. that's pretty much thedefinition of cancer. so it's a nice,straightforward one to one relationship betweena type of damage and a type ofage-related disease.
but, in general, it'snot quite like that. so the heart is a good example. the heart is anorgan that can go wrong in a whole bunch ofdifferent ways in old age. and it turns out that thedifferent ways it can go wrong are driven by differenttypes of damage. so let's first of alltake atherosclerosis, the accumulationof fatty deposits in the major arteries,which leads, of course,
to heart attacks andstrokes, and therefore to the major killers,the number one killer of the western world. that comes down, at the end ofthe day, to this thing here, i'm calling intracellularjunk, molecular garbage that accumulates within cells. in particular, whathappens here is that there are a typeof white blood cell, called a macrophage,which goes into the artery
wall for the purpose ofclearing up detritus. and it's very good at it. but the macrophage getspoisoned by contaminants in that detritus,which eventually cause it to become more ofa problem than a solution. and i will come backto that at some length later on because we've donesome quite important work in addressing that overthe past few years. the second type of waythat the heart can go wrong
during old age isarteriosclerosis, which is the stiffeningof the major arteries. this is something that is veryimportant in terms of pathology because it leads to increasedblood pressure in the elderly, and therefore to thingslike kidney failure. and the ultimate moleculardriver of arteriosclerosis is this thing at the bottom,in pink, the stiffening of this lattice of proteinscalled the extracellular matrix, which essentiallygives each of our organs
their shape and physicalproperties that it has. and, in particular, theextracellular matrix of the major arteries isextremely essential in terms of giving them theelasticity that they need to dampen the pulsation ofthe heart, of the heart beat, and thereby protect the morefragile capillaries and smaller parts of the circulationfrom the blood pressure. so that's arteriosclerosis. the extracellularmatrix becomes less
elastic as a result ofchemical modifications. and we need to fix that. then there's amyloidosis,which actually has been discoveredquite recently to be a major killerof the really elderly. people who live morethan 105, 110, it turns out that most of them,certainly half of them, die of a disease called senilecardiac amyloidosis, which is essentially the accumulationof molecular garbage
outside the cell, thatthing i wrote in blue here. that's all abouta type of protein that gets into this kindof fibers that essentially weaken the joints betweenthe various muscle cells that make the heart up andweaken its ability to beat. so that's rather bad foryou, eventually, of course. and then finallythere is cell loss. the heart actually doesnot beat on its own. it only beats whenthe brain tells it to.
and the cells in the heartthat mediate that signal, they're called pacemaker cells. and it turns out that theydon't maintain their numbers during age. they die progressively. and eventually, youhaven't got enough of them and the heart stopslistening to the brain. and it just doesn'tbeat anymore. so that's another waythat the heart can stop.
so, as you can see,the relationship here, between damage and thisparticular type of pathology, is quite a complicatedone, a many to one relationship for sure. but, like i said earlier,it's really well understood. and that's the importantthing i want to get across. the same withalzheimer's disease. alzheimer's disease was definedabout 100 years ago or more, as the combinationof these two things
here, a type ofjunk inside neurons called tangles and anothertype outside called plaques. and now, of course, wealso know that there's a lot of cell death inalzheimer's disease. so again, a complexrelationship, but a well understood one. the big thing to take intoaccount here and to emphasize is that thesenonspecific aspects of aging, that we don't givedisease-like names to, the same
applies. most of these things--pretty much everything except division-obsessedcells-- ultimately can be linked causally tovarious types of decline in function, likeloss of muscle, or loss of immunefunction, and such like. so this is really good news. we have a very clearidea of this linkage. all right then, enoughabout the problem.
let's go to the solution. so what is the preventativemaintenance approach? it falls into thesefour types of approach, replace stuffthat's gone missing; remove stuff thathas accumulated, that you don't want;sometimes in situ repair of stuff that you don't wantto remove or to replace; and sometimes reinforcement. that means essentially breakingthe link between damage
and pathology, somehowdoing something to the body. that means that the damagecan still accumulate, but it no longer actuallyhas any pathogenic effects. and when we come down tospecifics, it's all about this. so i won't go throughthis in detail. i'm going to touch on acouple of the examples here in a moment, to look atthe details of the pathologies. but essentially whati'm showing here is that we know exactly howto do this in principal.
some of this, muchmore than in principle. lets take cell loss. the main way-- the generic wayto restore cellularity, cell number, to a given tissue is,of course, stem cell therapy. that's true for cellloss during aging, just as it is in terms ofany kind of acute trauma or injury for which stemcell therapy may originally have been developed. parkinson's disease isa great example of this.
it's a disease in whichcells in one particular part of the brain dieunusually rapidly. and stem cell therapiesfor parkinson's, they were first attemptednearly 20 years ago, when we really didn't know whatwe were doing with stem cells. but even then, they sometimesworked really, really well. and now, there's agreat deal of resurgence of interest in this and newclinical trials going on. and i think there's quite agood chance, at least 50%,
that within as littleas 10 years from now, we will be able to say thatparkinson's disease has been cured. so i won't go on to theothers now because i'm going to touch on someof them in detail. what i'm going to dois talk about how far advanced they are. and i'm going to start with theones that are most advanced. so i'll just mention clinicaltrials for stem cell therapy.
these are already inprogress, in certain cases. and that's great. that's wonderful. and actually, it'sthe main reason why sens research foundationdoesn't do anything to speak of, hardlyanything, in the whole area, because our contributionwould be a drop in the ocean. another case thati want to highlight in a little more detailconsists of this business
of molecular garbage outsidethe cell, which in general comes down to this thingcalled amyloid. amyloid, as i mentioned earlier,accumulates in the heart and it also accumulates in thebrain during alzheimer's. that's what female plaques are. and 15 years ago, or so, it wasdetermined, at least in mice, that one could get rid of thisstuff just by immunization. essentially, one couldtrigger the immune system to engulf the material,get it inside the cell,
inside phagocytic cells. and this was enough to getrid of it, to remove it, because the machineryfor breaking things down inside the cell ismuch more powerful than what exists outside. and this moved, in the caseof alzheimer's disease, very rapidly to clinical trials. and those clinicaltrials got to phase iii and reported just a year ago.
and the reactionwas frustrating. the trials did not achievetheir clinical endpoints. that isn't what was frustrating. i would have beenabsolutely amazed if people, given thesetreatments to get rid of plaques, hadactually exhibited any significant restorationof cognitive function. why? because it's not the wholeof alzheimer's, dummy.
i mean alzheimer's is thesethree things that happen. it's not justamyloid accumulating. it's also tangles accumulatinginside the cell, which was not targeted by the therapy. and so there wasno reason why we would expect them to go away. and similarly,the cells that had gone missing, that had died,were not being replaced. there's no clearchain of causation.
it's not as if wealready had any reason to believe that ifyou remove plaques then the tangles wouldgo away on their own or the cells wouldsomehow regenerate. i think it's a bit like whati'm saying at the bottom there. it's a bit like saying let'stake a car apart and put the individualcomponents out in a line. and then let's pourburning petrol over them and we'll expect to seesome kind of motion.
it wouldn't happen really. so it's frustrating that medicalresearchers and scientists are often rather carelessin their evaluation of how technology is supposed to work,especially divide and conquer technology of this kind. let me talk about another case. and here i'm going to emphasizethe role of the private sector and especially the rolecalled of venture capital. because obviouslyin the it world,
you guys are quitetuned into all of that. and you may bewondering already why does a nonprofit, such assens research foundation, really need to exist, ifall of this is so clear? so i'm going totalk about this case because it's aninteresting, kind of intermediate,transitional case. it concernsdeath-resistant cells, which is a categorythat i've defined,
that simply means "the otherway of having too many cells." you can have too manycells because cells are dividing whenthey're not supposed to. that's what cancer is, asi mentioned a moment ago. or you can have too manycells because cells are not dying when they are supposed to. people often overlook thatbecause they think, well, cells are not supposed to die, right? but that's not true.
it turns out of thereare certain parts of the body in whichcells are absolutely required to die in order forthe whole system to function. so we'd like to be able toget rid of these things. and for a longtime now, i've been saying that the way todo this is with something called suicidegene therapy, where you use engineeredviruses to introduce a toxic gene into cells.
this gene creates a protein thatwill actually kill the cell. and the way you do it is byensuring that the protein is only synthesizedwithin the cell, in the case where the cell hasgot into this bad state, where you'd like to get rid of it. so this is something thatis routine in the lab, in mouse experiments. but it's verydangerous and so it hasn't got to primetime for the clinic yet.
but it will. it will. so that was the thing i wasinterested in making happen. and the good news is thata couple of years ago, a group at a very prestigiousinstitution called the mayo clinic, actually had ago at pretty much that. what they did was, sincethey were working in mice, they didn't actually need toresort to this engineered virus business of suicidegene therapy.
they just introduced thesuicide gene transgenetically so that it was inevery cell in the mouse from the time themouse was conceived. and what they did was they madea combination of two things. first of all, theyintroduced a second mutation into these mice, adifferent mutation, which caused thesedeath-resistant cells to accumulate much,much more rapidly than they normally would.
but which did notcause any other aspect of aging to be accelerated. so these mice basically died ofhaving too many death-resistant cells. and they died pretty quickly. they died at less thanhalf the normal age. this mouse at the bottomhere is such a mouse. it's less than a year old. and it's only got about amonth to live, if it's lucky.
and you can see, it'svery unhealthy already. so what they did was,this research group, they engineered this suicidegene into these mice. and they engineered this in whatwe call a drug inducible way. in other words, in sucha manner that they could activate that gene,but only, of course, in the cells thatthey wanted to kill, by giving the mice some simpledrug in their drinking water. until that time,even the bad cells
would not actually diebecause they would not express the suicide gene. so what they did was theywaited until, let's say, halfway through these mice's lifespanbefore giving them the drug and activating the suicidegene, so that a whole bunch of these cells wouldalready be in existence. and the result was very nice. the top mouse thereis one like that, same age as the bottom one.
and as you can see,it's perfectly healthy, doing very fine. and they measured therelative health of these mice in all manner of different ways. this graph on the right isjust one of the dozen things they did. it's to do with muscle mass. so this was all very good news. now, here's theinteresting thing.
they did this in anacademic institution. but they decided to go outand start a startup company. and they got vc moneyreally pretty fast. why is that interesting? the reason it's interestingis because the experiment was extraordinary preliminary. first of all, it was in mice. and we all know thatstuff that's in mice often takes quite a long time totranslate to the clinic.
second of all, they were workingin this artificial system where they had acceleratedone aspect of aging very, very dramatically. so there's no evidence fromthis experiment showing that the senescent cells,these death-resistant cells, are actually all that badfor you in a normal mouse, in a normal lifespan. so this was really abit of a leap of faith. the third thing thatwas very preliminary
about this experiment was thatit was a transgenic experiment, where they introduced this geneinto the mice that allowed them to kill the relevant cellsat a point of their choosing. now, tells us absolutelynothing about what the actual plausibility isof the company's business plan, which is to createan actual pharmaceutical, a small molecule drug thatwould do the same thing. there's absolutelyno way that there's any evidence fromthis experiment
that that is even possible. and the fourth thing is thateven if you forget all this and you just presume investorswere stupid or at least they thought that their eventualcustomers would be stupid, that they might be goingfor some kind of very superficial bottom line, thatbottom line would be longevity. there's one thing i haven'ttold you about this experiment so far. you probably think thatthese mice at the top, right,
probably lived a normallife, like 2 and 1/2 years, as it gained certainly a yearfor the mouse at the bottom. that turns out not to be true. it's actually the casethat the mice at the top died after a year, sameas the mice at the bottom. because it turned outthat was something else than the gene did,that the mutation did, that caused theaccelerated accumulation of death-resistantcells, that was not
to do withdeath-resistant cells. it just basicallymade the heart unhappy and so they died anyway. so on every single measurethat you could think of, this is a massivelypreliminary experiment. but they got their money. how did they do it? i think that the answer isa very encouraging answer. namely, that investors,smart investors,
who are looking at things todo with the eventual delivery and development of anti-agingmedicine that actually works, have been payingattention to the numbers. they've started payingattention to the fact that the real anti-agingindustry to come, the anti-aging industryconsisting of therapies that work, is going to bethe biggest industry ever, by a very large margin. it's going to be theindustry of all time.
so that, of course,means that if you want to get into it, ifyou want make money, then your calculations of decisionsabout whether to go for it or not will usedifferent numbers. you will be willingto accept higher risk. you will be willing toaccept a longer time-frame before access, all those things. that seems to be happening now. that's why this kind ofthing is actually occurring.
and it's veryheartening, indeed. so you may think,well, ok, that's great. so even somethingreally preliminary is getting funded bythe private sector. why does sensresearch foundation need to exist as a nonprofit,funded by philanthropy? well, i'm afraid theanswer is that even though some things are movingforward nicely like this, and they are in the positionalso being able to get money
out of venture capital, a lotof things that need to be done are still at an earlierstage than that. at early enoughthat i don't think the calculations aregoing to fly for a while. the mission statement ofsens research foundation is that we want to create arejuvenation biotechnology industry. don't get me wrong. we definitely wantthat to happen.
but there are some things whereit's not ready for prime time yet in the private sector. and i'm going to give youan example here because it's a good example of the stuffthat we've been doing. it's showing verygood proof of concept. but it still has alittle way to go. and it's do with thisthing, molecular garbage inside the cell. and it comes back tothe number one killer
in the western world,atherosclerosis. atherosclerosis, asi mentioned earlier, starts with white bloodcells, a particular type of white blood cell calleda macrophage-- excuse me-- going into the arterywall and clearing up garbage, clearing up detritus. it basically recyclesvarious materials and exports themback out for reuse. but there arecertain contaminants
in that detritus whichthe macrophage is not equipped to handle. and those contaminantspoison the macrophage. and eventually, it doesn't work. the particular part of themacrophages that stops working is this thing calledthe lysosome, which is kind of the garbagedisposal machinery of the cell. and it's reallyan important part. so when the lysosomestops working,
the cell stops beingable to do things that it used to be able to do. and eventually itturns into this kind of undead thing calleda foam cell, which is what we have showing here. this is the first visiblestage in atherosclerosis. and actually, all ofus have foam cells in our major arteries,even as young kids. but we don't havevery many of them.
and when we don't have verymany of them, lo and behold, they're not harmful. but eventually there's too many. and the environment,the other cells around, start to get a little angry. they get inflamed and badthings start happening. more white blood cellspile in, in an attempt to solve the problem. but they got poisonedas well, so they
become part of the problem. and the plaque grows and grows. and eventually you end upwith the plaque bursting. and that's when you gotheart attacks and strokes. so what could we do about this? well, about 15years ago i proposed that what we really need todo to stop this kind of thing happening-- and asimilar kind of thing happens with different toxicmolecules in, for example,
macular degeneration,the number one cause of blindnessin the elderly. the thing we needto do is simply equip the relevant cellsthat are being poisoned with additional machineryfor breaking things down. so that, in particular,they can break down the things thatare poisoning them. and it turns out that that'snot so hard as all that. in the case ofatherosclerosis, there
is just one particular compound. it's called7-ketocholesterol, which appears to be responsible forat least most of the problem. it's not by anymeans the only thing that accumulates inmacrophages over time. but it does seem tobe the most important in terms of its abundanceand its toxicity. and what we decided todo was to take a leaf out of the book of environmentaldecontamination, not even
a biomedical field at all. so, of course, no oneworking in gerontology knew anything about this. but what we did was wesimply used the idea that you might be able to findbacteria in the environment, in the soil, that couldbreak down the material that is poisoning thesemacrophages, this compound 7-ketocholesterol. now our idea was not,i should emphasize,
that having foundsuch bacteria, we would inject them into the body. i have to think thatmight have side effects. but what we decidedto do instead was, once we foundsuch bacteria, we would identify the geneticbasis for that capability, the genes and enzymesthat they had, that allowed them to breakdown these compounds. and then we would introducethose genes and enzymes
into human cells,thereby augmenting the capacity of thosecells to break things down. so here's the first step. and as you can see, thispaper came out in 2008. it was actually thefirst paper that was published out ofwork funded by us. and it went very nicely. we found bacteriathat did the job. what you're seeinghere is what's
called an enrichmentculture, where we take a whole bunch ofdifferent bacterial strains and we give them thisstuff, 7-ketocholesterol. and we don't give themanything else to live on. the idea here is that ifthey can break down 7kc, then they can grow because theycan extract energy from it. and if they can't, they can't. so most of these strains can't. they just there like lemons,doing exactly nothing.
but a couple of themare doing very fine. you've got a couple of strainsthere which after only 10 days, have consumed theentire material. so that's great. then we're got to, as i say,find the genes and enzymes that they're using. and that turned outnot to be too hard. this is one waythe way we did it. it's called mass spectrometry.
we essentially identifiedthe breakdown products that the bacteria are creatingin the process of breaking down the original substance. and that allows us to infer whatenzymatic reaction is occurring and used by informatics toidentify candidate genes. there are other approaches. we also used expressionanalysis to find which genes were being activatedwhen we gave them the 7kc, and so on.
all these methods seemedto work pretty well. the long and short of itwas we had a few candidate genes by about 2010. that's when thingsstarted getting tricky. step three in thisprocess is the hard one, which is to actually getthese enzymes to work in a human cell. the reason that's hardis because humans cells are very differentfrom bacteria.
bacteria doesn'teven have lysosomes. but we managed it. first of all, we actuallyhad to do the localization. we have to get our enzymesto go to the lysosome. and this shows thatwe could do that. the red on the left is a stainfor the lysosome in cells. the middle one is ourengineered protein. and the fact that they'reoverlapping reasonably well shows us thatplenty of our enzyme
is going to the right place. so that's all good. but at the end ofthe day, we also had to show that it worked. and that was what we were ableto show maybe 18 months ago. this graph is asummary of the results. essentially what it saysis that if you give cells a completely insupportableamount of 7kc, on the right-handend here, then it
doesn't matter what you'vedone to them in terms of giving them extra enzymes. they die anyway. but if you give them arelatively modest amount of this toxicmolecule, then the fact that the right-hand barof each of these groups is higher than the otherbars, that basically says that the cells whichhave the enzyme seem to be targeted to theright part of the cell,
the lysosomes are projected. they survive better than othernegative control cells, cells that don't have an enzyme, orthey have the wrong enzyme, or they have the enzyme nottargeted to the right place. so this is a extremelygood proof of concept. we're very happy about it. we have a couplemore steps to go before we think we wouldbe able to take this to the private sector.
first of all, wewould need to get this working in adifferent cell type. we did this infibroblasts, which happened to beeasy to work with. but we need to get itto work in macrophages. then we need tomove to mouse models of cardiovasculardisease and show that it's protectivethere as well. but we're well on our way.
i think i can probably trust youto understand that this really is a very effectiveproof of concept. and we learned a lot more. we only have $4 milliona year, or thereabouts. but we are spendingit very efficiently. we have a headquarters inmountain view, california, just a couple of milesfrom the googleplex, that has a few thousand squarefeet of lab space, where we do three of ourmajor projects.
and we have more thana dozen other project at various universitiesaround the world. that one i justdescribed to you happens at rice university in houston. we also have an educationalarm, which i always like to mentionbecause i think it's very important to understandthat we're trying to grow the next generation ofrejuvenation biotechnologists. so that's somethingthat you can read
about at the website, of course. now, i thought i should mentiona little bit about credibility. because maybe 10 yearsago-- some of you have already come acrossme-- it was actually pretty tough tosell this concept. i think you already got theidea from my early remarks that the wholemaintenance approach is a big departure from what peoplehad previously been thinking. people who wereworking in gerontology
viewed this whole idea of damagerepair as a complete solution, as a very, veryimplausible idea. it was as far away fromthe historical thinking as the geriatricmedicine approach was. so i had to do alot of education. and it took a while. but the good news is that itreally has been very effective. we are now in the veryheartening position of having this kind of researchadvisory board, of very
obviously explicitendorsers of our approach. every single one of these peopleare really, really prestigious dignitaries in their variousbiological disciplines. now, there are obviouslystill a few people out there who just refuse to beeducated about this. but by and large, thecredibility barrier has been breached, whichis very nice to know. but still, we're got to do more. one thing we have to do,of course, is publish.
we have to demonstratethe validity of what we're doing in the traditional manner. and that's, of course,what we're doing. so these are just a smallselection of the papers that we've published recently. that one at the top is the onei've just mentioned, of course, the rescue of cellsfrom 7-ketocholesterol. but we've done alot more than that. a couple months ago,we had a lovely paper
in a very prestigious journal,"the journal of biological chemistry," showingthat we could address senile cardiac amyloidosisusing antibodies that would break the stuff down. a couple of otherexamples there. so things are going nicely. but, of course, there'sstill a very long way to go. i'm pretty much done. and i'm just going to spend afew minutes on other matters.
the first thing i'mgoing to tell you is what i'm notgoing to tell you. in other words,i don't really do the sociological considerations. i do have to. some of you probably know thati do a brutal amount of media. i do probably 100interviews a year. and the bulk of my timein those interviews is spend answering questionsalong the lines of, oh, dear,
where are we going toput all the people, or won't dictators live forever,or won't we all get bored? shall we say, i havebecome a little bit bored myself of these questions. i regard them as beingultimately founded on a degree ofmyopia with regard to the importance of thiswork, a degree of ability to put out of one's mindthe fact that we have quite a bad problemtoday with aging,
namely a problem of 100,000people every single day dying of it. that's 2/3 of all deaths. in the developedworld, it's something like 90% of all deaths. and, of course, it'snot just the death. it's also all thesuffering that most people have for a long period oftime before they die of aging. so it's fairly obvious thatthis is not really the right way
to think about it. we shouldn't be thinkingabout these problems. we should be thinking aboutthis, that if we were actually to move to apost-aging world, we would have noage-related ill health. people's health wouldnot be a function of how long ago they were born. the elderly would still becontributing wealth to society, so these therapies wouldpay for themselves.
the elderly would not be aburden on their kids anymore. this is obviously somethingthat a lot of the elderly worry about a great deal. so that's kind ofthe way i think. all right then, so thefinal point, call to action. what can you guys do? as far as i'm concerned,this is really where i want to placeemphasis because whenever i give a talk likethis, or an interview,
i feel i do get people inside. i do get people tounderstand that, yes, this is a really importantproblem, and yes, we do have a respectablechance to actually solve it. but i need to actuallymake sure that we solve it faster than we otherwise would. and at the end of the day, itall comes down to these things. the first thing is,ultimately it all costs money. 10 years ago, 15 yearsago, when i started out,
i had three problems to solve. i need a plan forhow to solve aging, and that's what i'vebeen telling you today. i needed people. i needed theworld's best experts in the variousscientific areas to be enthusiastic aboutworking on this. and that, i have demonstrated. we already have now, very much.
but, at the end ofthe day, these people are still, by and large,sitting on their hands, waiting for the resourcesto actually get on with it. because we only have perhapsone tenth of the budget that we would need to beable to fund everything that really needs to be funded. and that is absolutely thenumber one problem right now. obviously, i'd likeyou to learn more. i've only had an hour.
that's not nearly enough timeto do justice to all that we do. anyone who wants to get involvedin terms of actually learning more about it through oureducational initiative, please go and have a lookat that at the website, at sens.org. but ultimately, it'sall about advocacy. hands up. anyone here whodoesn't know anyone who's richer than you are?
so it's all about changingpeople's minds, right? it's all about changingpeople's minds. the more people wehave on-side, who understand about theimportance of this mission, the faster it's going to happen. and i spent a lot ofmy time getting people to understand howimportant this is. if the people that i wereable to bring on-side, were to go out and bringother people on-side,
and so on and soforth, we would solve this problem agreat deal faster. i wrote this bookseveral years ago. it's very comprehensive. i call it semi-technical. what that basicallymeans is you don't have to be a trainedbiologist to understand it, but you probably won't bereading it in one sitting. it's quite dense.
it doesn't cut any cornersat all on the science. and it was writtenseveral years ago. but it's stillfairly up to date. that is not becausethere has been inadequate progressin the meantime. the progress has been wonderful. but what it is isbecause the progress has been pretty much the typeof progress that we predicted would happen.
in other words, this is, again,another piece of evidence that the sens paradigm isstanding the test of time. so that's all very heartening. i think i shouldalso mention this. incidentally, if any of youare going be in california a few weeks from now--but i guess you probably have friends who are-- andanyone that you might want to recommend to cometo our conference, i would very muchencourage you to do that.
this conference is happeningjust-- maybe 10 miles south of the googleplex,august 21st to 23rd. and, of course,it will cover all of the science ofwhat we're doing, of rejuvenation biotechnology. but also we'll haveextensive participation from industry, fromregulatory people, from policymakers, and so on. so it's going to bequite a gathering.
and, of course, lots oflaypeople there as well. and i very much encourageyou to encourage other people to do that. i'll stop there. and i think there's probablya bit of time for questions. thank you very much. [applause] audience: hi. so in the fieldof cancer, we see
that there are some cancersthat have been very-- well, have been tackled extremelywell in the last 100 years, others that becomevery resistant and very difficult to deal with. do you see the same thingslikely to happen when we tackle aging more generally, inthat some diseases will be eradicated quickly andothers will take a much longer time to get ridof, and a long tail. aubrey de grey: yeah.
that's a really great question. so first of all, let me giveyou my take on where cancer sits within the whole universeof problems of aging. my view is that conceptis by far the hardest aspect of aging to fix. it's the one that has naturalselection on its side. and that makes it--any cancer that's big enough to beclinically relevant has a trillion different individualengines of genetic creativity
in it. it's really atough nut to crack. now a lot of people, becauseof largely the kind of evidence that you described,they don't like to think of cancer as asingle disease anymore. they like to think ofit as family of diseases that we just happen to givesome collective name to. but the fact is that'snot really fair. because there are some thingsthat cancers have in common.
and in particular,there's one thing that absolutely all cancershave in common, namely the fact that they needto figure out a way to grow the ends oftheir chromosomes. chromosomes get shorterwhen a cell divides and there needs to be away to compensate for that. there's only two ways thatcancers ever use to do that. and we're well onour way to being able to stop thatfrom happening.
so that's essentially the waythat we're going about it. in general when you talkabout the relative degree of difficulty of copingwith aspects of aging, i think you're right. there are definitely thingsthat are harder than others. and actually, the lastpart of the reason-- well, in fact, most of the reason whysens research foundation was set up, was precisely tomitigate that problem. to ensure that we workon the hottest things
and that they don'tget left behind and we just fix the easy thingsand end up where we were. audience: thank you. audience: if you hadlike a crystal ball, how long do you think it willtake until you've got something that you say actually we'llbe able to live for 100 years? you ask that questionin exactly the way that an engineer should ask it. in other words, i haven'tthe slightest fucking clue
because it's a long way away. but, of course, youwant an estimate. and actually you're quiteright to ask the question. because a lot of gerontologistswould just refuse to answer. they would say it'sirresponsible to get people's hopes up, orsomething like that. and i say, on the contrary,it's irresponsible not to give an estimate becausehowever bad my estimate is going to be, yours is goingto be even worse, right?
and therefore, i'm got to giveas good an estimate as i can. so my estimate is this. i think we have atleast 50/50 chance of getting the technologiesthat i described today working reasonably well withinthe next 20 to 25 years. audience: yes. aubrey de grey: right. and the technologies thati describe today i think will probably give about30 additional years
of healthy life. and, of course, theywill give those years to people who are already inmiddle age or older, 60, 70, or even maybe 80, at the timethat the therapies arrive. so that means mostpeople in this room have a relatively goodchance of benefiting. two caveats. the first caveat,everything i just said is only going to be true ifresearch in the next five
or 10 years goes a lot fasterthan it's currently going. the funding limitationthat exists at the moment, i estimate isslowing things down by roughly a factor of three. in other words, over the past10 years, the amount of progress we've made towards gettingproof of concept of these things in the lab and so on, hasprobably only advanced by about three yearsrelative to where it could have gone if onlyscience had been limiting.
the second caveat isthe probabilities. so i can tell youthe 50-50 estimates. but i want to tell you rightnow the variance is high. i think there's atleast a 10% chance that we won't getthere for 100 years. but who cares? a 50% chance is perfectlyenough to be worth fighting for. audience: yeah. thank you.
audience: thank you very muchfor this very interesting talk. aubrey de grey: thank you. audience: actuallyabout a year ago, we set up this company calledcalico, the california life company. and we set it to upwork independently. and i was justwondering, first of all, how do you viewthis development? and secondly, if youalready had the chance
to work with them so far? actually, i was verysurprised that no one at the talk i gave atlunchtime asked about calico. but, yes, calicowas, as you say, set up my larry andsergey about a year ago. well, my view ofthat development was expressed in"time" magazine, which was where the thingwas announced. "time" got me to write thereaction piece, so to speak.
and i was pretty effusive. i was overjoyed. and i am still am. i think there is a veryrespectable chance that they will make a really bigdifference, but only a chance. it just remains to be seen. they are taking theirown really good time to decide exactlywhere they're going to be prioritizingtheir efforts.
and in a way,that's a good thing. the worst thingthat could possibly would have been a repeat ofwhat happened 15 years ago when another very wealthyindividual, larry ellison, decides to do essentiallythe same thing, albeit in a foundation,rather than a company. he basically went outand promptly hired a veteran gerontologistfrom the nia. and the result wascompletely predictable.
15 years and $400 millionlater, absolutely nothing had been done that wouldn'thave been done anyway. and he's given up now. so calico is potentiallya really good thing. they've got people at thetop who are, by and large, not trained gerontologists. and therefore, they knowwhat they don't know. they're makingtheir own decisions. they're not talking to us nearlyas much as we'd like them to
and as we think they should be. but that may change. so i'm hopeful. audience: hey, aubrey. if, as you describe,this might become one of the biggestindustries ever-- aubrey de grey:the very biggest. audience: and if,as you describe, you've done a great jobof convincing people
that it is worthwhilefighting for it, what are, in your opinion, the threemain obstacles to actually get the necessaryfunding going, which seems to be one of thebiggest problems on the way? i will actually just stickwith one main obstacle, which is something thati historically used to call the pro-aging trance. but my marketing people tellme that that's too derogatory. so i'm not allowedto say that anymore.
essentially it's fear. it's a combinationof two types of fear. number one, fear of theunknown, recognition that a post-aging world wouldbe very, very, very, very different. and therefore, maybe we oughtto stick to what we know. kind of essentiallythe same as what happened to resistance tothe industrial revolution. and secondly, fear ofgetting their hopes up.
people just are not willingto reengage this battle. people, in general, havemade the peace with aging. they have accepted defeat. and when you've accepted defeat,the last thing you want to do is go through allthat stress again. so that's basicallywhat it's all about. people who are otherwiseperfectly well educated and perfectly rational inabsolutely every other walk of life, will saythings and think things
that they would be embarrassedto say to a small child to shut them up, when it comesto this particular topic. and, of course, theproblem is that i don't get to talk to everybody. time and time again, i willbe in the company of people who are not only getit, but say they get it. and they will tell otherpeople that they get it and that things are good. but do they actually runme a check, not as such.
why do they notwrite me a check, probably because theirwife doesn't want them to. the cost of gene sequencinghas decreased kind of massively over the last 10 years. and i've seen variousdepictions of people saying that in fiveyears' time, we'll all be getting our genesequenced for the cost of $10, or whatever. do you think it's ahigh chance that we
might find genetic causesfor all these problems, like alzheimer's,before we find solutions that involve damage limitation? great question. so i'm going to answer it ina slightly complicated way with two definitionsof the word "solution." there will be thepossibility of identifying genetic factors that areresponsible for the age of onset of certainage-related conditions,
whether it be alzheimer'sor anything else. and then also the possibilityof genetic conditions that are simply responsiblefor it in a binary way, for it happeningor not happening. so what i can tell youis that it's very likely that we will find the former. albeit, it's not nearlyas easy as people were thinkingmaybe 20 years ago, when [inaudible] was discovered.
and it looks likeit will involve a lot of differentgenes combining in different people, eachindividual one of which only makes a small contribution. however, we can saydefinitively at this point that the answer to thelatter question is no. that the aspects ofmetabolism that ultimately drive the accumulation ofthese various types of damage. and therefore the eventualarrival of these pathologies,
are non-negotiable. now, the number oneworse thing that we have, that drives all thesethings, is breathing. breathing is really bad for you. but there's not a lot ofchoice that we have about it. audience: thanks. you talked a lotabout sort of funding and where you getit from and also bringing in theprivate market narrows
the diversity of the research. so at what stage do yougo to the private markets and the venture capitalists? aubrey de grey: yeah,a great question. i'm not really sure aboutnarrowing of diversity. i mean in a sense thecontinued existence of nonprofit participationin all of this is a good protectionagainst that. so individualcomponents of the range
of things that needto be done might go into the private sector,without necessarily restricting the ability of other componentsto continue being developed in the philanthropicsector, so to speak. that's kind of how it going. i think we may be done. more? this may not be ofinterest to you at all. but sticking you with yourcar analogy, if you take a car
and you drive iton a smooth road, and you keep it away from sun,and you put in the right stuff that it needs in the engineand what's in everything, it probably accumulatesless damage. if we look at thatfor a human being, in the meantime, before yourresearch is going to save us all, what can we bedoing to damage limit? aubrey de grey: that's anabsolutely excellent question and an absolutely excellentway of expressing the question.
because you're absolutelyright, in the case of simple man-made machines likecars, lifestyle matters a lot. you can drive a car carefullyand well and it will last a lot longer-- quite a lotlonger than if you don't. the unfortunate factis that it's not quite like thatfor the human body. when i mentioned amoment ago that breathing is really bad foryou, breathing and the other non-negotiableaspects of being alive,
like eating-- eating anything,not just eating badly-- are the overwhelmingmajority of the drivers of the accumulation of damage. of course, there are things thatyou can do that are obviously bad for you, like smoking orgetting seriously overweight, but nothing you motherdidn't tell you. if you're basicallyaveraging healthy, then the amount ofadditional postponement of age-related illhealth that you
can achieve by any kindof lifestyle, or diet, or exercise modifications,or whatever, is, as far as we cantell, really tiny. and therefore,there's only one way out of this, which is to hastenthe development of therapies
that we don't yet have. in other words, give melarge amounts of money. [laughter] thanks very much everybody.
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