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we can change the way things are when we stopaccepting the status quo. it’s not science fiction for us to livelonger, for each of us to be restored to the physical and mental performance of a youngadult. today’s topic is human longevity, also knownas life extension. i’m cat volz for the innovation initiative-entrepreneur tv. next to me is dr. aubrey de grey. aubrey is one of our most intelligent peoplesolving the #1 problem facing humanity- we’re all going to die, and for most of us, ourdeclining health will be unpleasant. over 6300 people die every hour.

we are holding back progress if we do notcare about aging related deaths. dr. de grey is a biomedical gerontologist,the chief science officer and co-founder of sens research foundation. he was the first person to get started onthis problem, before there was commercial opportunity, while most of the world ignoredit. dr. de grey is adding unlimited productivity,health and enjoyment to the lives of us people on the planet. this is an expensive problem. it will take a concerted application of therapiesto repair the accumulated damage that kills

us. to put it into perspective, curing diseaseis low hanging fruit. it’s attractive to investors to solve sideissues around aging (alzheimer’s, atherosclerosis, cancer), the near-term successes to returnon investment. but the sens foundation is working from acomplete solution backwards- a perfect maintenance plan so these problems don’t even occur. because there’s already funding in placeto focus on stem cell research, dr. de grey has elected to solve the harder long-termproblems that are not yet being funded. please visit sens.org to learn about theirresearch and to donate so these treatments

will be here for us to have the option ofliving longer. the sens link is below as well as a pdf toexplain the types of aging damage. welcome dr. aubrey de greythank you very much what’s the problem with society’s healthyaging stereotype? i think the real problem is that there isno such thing as “healthy aging.” i mean, of course the term aging is used inmany ways, depending on context, but most of the time, what we mean by it is a declinein performance; a decline in physical performance and a decline, of course also in mental performance—one’scognitive abilities. and nobody wants either of those things.

both of them are identical with ill health. so the idea of healthy aging is a contradictionin terms. why should we treat the system instead oftargeting the disease? the reason why these diseases are diseasesof old age is because they’re actually diseases of being alive. they are side effects of simply being alive. and for many decades they are asymptomaticbecause their early stages are so minor at the molecular level and the cellular levelthat the body just works its way around them without significant performance impact.

but eventually the accumulation of this damagethat the body does to itself reaches a level that the body is not able to just work itsway around. and that’s when these diseases emerge andprogress. so what that means is that if we’re tryingto actually eliminate and make sure that we don’t get these diseases then we have tolook at the originating cause which is the mechanisms that keep us alive in the firstplace. and clearly we can’t eliminate the mechanismsthat keep us alive because that would rather defeat the object, so the goal therefore isto identify where as to intervene, to let us be alive without the side effects accumulatingto a point that is bad for us.

you say aging is a phenomenon of physics. what does that look like? well what i mean when i say that aging isa phenomenon of physics and not of biology is that it is fundamentally the same processwhether it happens in a living organism or in a simple man-made machine like a car oran airplane. and it is the same process. the fact is that any machine with moving partssimply does itself damage. a car will accumulate rust, it will accumulategrit in the engine or whatever. and different machines of different levelsof sophistication have different ways of coping

with this damage-- either they’re designedsimply to tolerate a large amount of it or they’re designed to create the damage slowlyas a side effect of operation. but one way or another, whether they are livingor not living, these machines all at some point have enough of their, if you like, metabolismbehind them but they’ve accumulated an intolerable amount of damage. can you give an example of a side effect ofmetabolism that’s killing us? well one very obvious example is that we getcancer. cancer, most cancers, are diseases of oldage. and that’s because they result from theaccumulation of damage to our dna.

the mutation in certain genes that normallycontrol when the cell divides, that happens when the cell divides uncontrollably and that’swhat cancer is. now that damage comes from chemical reactionsthat cause mutations to occur. those chemical reactions are initiated bya family of compounds called free radicals which come out of a place in the cell calledthe mitochondrion. and that happens, every side effect, everycentral component of being alive, mainly breathing. mitochondrion is often called the power houseof the cell. what that means is it’s where the chemistryof breathing happens, where oxygen is combined chemically with nutrients to extract energyfrom those nutrients.

the details of how that happens are very intricate. and sometimes they don’t go quite rightand these chemicals called free radicals are created. and occasionally those free radicals interferewith other molecules such as dna. so the hayflick limit is a proposed finitenumber that a cell can divide. is this real and what is the work around? the hayflick limit is certainly a real phenomenonin certain circumstances. but its relevance to aging is actually rathercomplicated. the hayflick limit arises because when a celldivides the ends of the chromosome which are

called telomeres get a little bit shorter. that’s an inherent and absolute inescapableconsequence of the molecular detail of how dna is replicated during the cell division. now some cells in the body need to dividerather a lot and for that reason they need to do something about it the shortening ofthe telomeres. and they do. they have a special enzyme called telomerasewhich adds additional dna on to the end of the chromosome, on to the telomere. that dna doesn’t have any information content,all it’s there for is to compensate for

the shortening that happened during cell division. but even though this sounds a little bit badnews we have to look around a little more closely in order to determine whether it reallyis bad news. in most cells there is none of this enzymetelomerase that compensates for the shortening i’m talking about. but in most cells that’s okay because thecells do not divide, or even if they do divide they only divide very, very rarely, for examplecells that make up the heart, simply don’t divide. and if they’re not dividing then of coursetheir dna is not replicating so the telomeres

don’t get shorter in the first place sothey don’t need to have the telomeres extended. now there are some cells that do divide butonly on demand. for example, the cells in the lower layerof the skin called the dermis which divide like crazy when you have a wound, when youcut yourself. first the cut, then close the wound very quickly. but normally they’re just hanging out andnot dividing. so those cells don’t express this enzymetelomerase. because they divide so well when they areinduced to do so, they turn out to be really easy to work with in the laboratory, in thepetri dish, in cell culture.

and that is the model in which this thingcalled the hayflick limit was discovered. but if we ask what its relevancy is to reallife, we have to look at what’s going on in cell culture. cell culture is functionally equivalent toputting these cells in an infinite sized wound that they can never close. and they divide and divide and divide farmore than they would ever need to divide in the body and so it doesn’t prove that there’sactually any relevance. the cells that do divide a lot, stem cellsfor example in the gut lining or in the blood, those cells certainly do divide more oftenthan they would be able to if they didn’t

do anything about telomere shortening. but they have a little bit of this enzymetelomerase, so again, they don’t have a hayflick limit. in most cases there isn’t a hayflick problem. however there may be some cases where thereis-- white blood cells which of course, the main constituents of the immune system sometimesdivide like crazy in order to get rid of an infection. and sometimes they have to do the same, thesame cells that divide like crazy for infection have to do it repeatedly because the infectioncomes back.

those cells have been implicated substantiallyin the declining function of the immune system during old age. and some people believe, and it’s a reasonablehypothesis, that inability to divide because of telomere shortening is a large part ofwhat goes wrong with these cells. so the short answer is, it’s a bit of anopen question. the hayflick limit is by no means as importantas some people thought it was 50 years ago. okay. but it may still have some relevance in normalaging. weren’t you just doing a crowdfunding campaignaround telomeres?

so the crowd funding campaign that we havejust done actually kind of turned the hayflick limit upside down. the thing about our campaign is that it’sdesigned to fund a project that we have that is targeting cancer. now cancer of course is a disease of uncontrolledcell division. so if cancer cells could not extend theirtelomeres, then we wouldn’t have a problem with cancer. cancers might initiate because they’ve figuredout how to divide indefinitely and escape from the immune system and break down theextracellular matrix and all the other things

that cancer cells have to do in order to divide,but then, if their telomeres were getting shorter and shorter, eventually the cellswould kill themselves just by dividing too much. they would divide themselves into oblivionbecause when the telomeres get too short all hell breaks loose. and that’s what we would like to have happen,we would like to have that happen way before the cancer got big enough for us to even noticeit. but what actually happens in a real cancerthat we do notice is that the cancer figures out how to introduce mutations that upregulate,is what it’s called, activate this enzyme

telomerase. so they kind of escape from the hayflick limitthat way. and for some time people have been interestedin the possibility of reverting that, of suppressing the activity in telomerase in cancers so asto make them divide into oblivion. divide. now what we’re doing here and what we’redoing a crowdfunding campaign for, and i should emphasize it that it’s still going. this is for a kind of complement to the anti-telomerasework that i just mentioned. and it’s needed because it turns out thatsome cancers, about 15% of cancers in humans,

actually, they do the same kind of thing,they figure out and they mutate a way into a state where they’re extending their telomeres,but they don’t use this normal enzyme, telomerase. they use a different system. (sneaky!) and that different system is not understood. telomerase is well understood. the genes were cloned a long time ago andeveryone understands what’s going on. this other thing which is called alts, whichstands for alternative lengthening of telomeres-- virtually nothing is known about it.

we don’t know the main fundamental genesthat are responsible for making it go. and once we can find those, of course we cando corresponding thing to what’s already being done with telomerase and knock it back,and thereby knock all cancers back. so you’re working on that? that’s what it’s all about. super cool. what are you thinking about introducing thenew genes from bacteria? that was something that seemed novel thatyou’re doing. sure.

so the idea here is something i first publishedback in 2002. and the concept is very simple when you hearit but a little bit left field when you first hear it. the idea here is to identify bacteria in theenvironment which have the capacity to break down substances which accumulate in the body--things like oxidized cholesterol or artificial or protein aggregates in the brain duringalzheimer’s for example. these things accumulate very slowly over time. and the reason they do so is because the celljust doesn’t have the genetic machinery to break them down.

they’re a problem when we get older, butthey’re not a problem when we’re young. evolution only cares about youngsters. evolution is all about perpetuating geneticinformation, not about perpetuating individuals. once you’ve had your offspring evolutionno longer cares about you at all. so, the idea here is, we find these bacteria,now we do not do what you might think is the obvious thing-- inject these bacteria intothe body so it can break down the substances that we cannot naturally break down. the reason we don’t do that is because thesebacteria do plenty of other things as well and there will be plenty of bad side effects.

but what we can do instead is we can identifythe specific gene or genes that the bacteria are using to allow them to break the stuffdown. and then we can incorporate that gene, justthat one gene, into the human genome of the cell so that human cell is then augmented. it has now this new ability to break downthe stuff that was previously accumulating and poisoning it. can women remain fertile longer with thesetreatments? i firmly believe that female fertility isgoing to be actually one of the easier parts of aging to deal with.

the easiest way to do that is to give womennew ovaries. now once they’re new, that can be done eitherby tissue engineering, by creating new ovaries in the lab and then surgically implantingthem or in principal it could be done by rejuvenating the pre-existing ovary in situ by introducingstem cells for example that would re-grow new follicles with new egg cells in them. either way though what this means is thatboth the fertility aspect and the endocrine aspect, the hormonal aspect of menopause andthe declining female fertility, ovary function, can be addressed by this way. essentially this is because the ovary is justanother organ, so the same kind of approach

will work there just as with any other organ. that’s fascinating. what’s the worst that could happen as faras adverse side effects from these treatments? well of course these treatments are in manycases only rather on the early stage of development. and it’s normal for any medical idea whenit’s in the early stage of development to proceed very iteratively through mouse modelsand phase 1 trials and phase 2 trials and so on so as to look for side effects. and when that happens the side effects donot actually get to completely derail the idea.

what happens is that people look for waysto get the best of both worlds—to get the effect without the side effects. sometimes that means re-engineering the wholeconcept that was being pursued, but very often it doesn’t mean that, very often it justmeans co-administering some kind of second treatment that direct, that will end thatside effect. the whole spectrum of things exists-- emphasizedreally by your question is that this does not in any way distinguish our work or workon postponing aging from any of the rest of medicine. it would happen with everyone.

of course. yeah. if you get enough funding, how long do youthink it would be until these would be accessible to the general population? i think that we will probably be able to getto the point where all of these technologies are simultaneously functioning in humans atthe same time within the next couple of decades. i think that’s only a 50-50 probabilityof course for anything even more than a couple of years away, there’s plenty of thingsthat could go wrong that would extend the timeline for any primary technology.

so i certainly wouldn’t bet on it beinga hundred years but i think the 50-50 chance is about 20 years. but as you rightly say, it is dependent onfunding. i think that if funding continues to be limitedas it has been over the past 10 years that we could add at least another decade to thatand let’s remember that you gave your number of 6300 per hour, i think it was? that adds up to well over a hundred thousandper day or you know, 40 million per year. so if we’re talking about losing perhapshalf a billion people if we actually delayed these therapies by a decade.

that really puts into perspective just howimportant this problem is. what is your response to the people that areconcerned with overpopulation? i have a variety of responses to people whoraise concerns, whether it’s overpopulation, whether it’s inequality of access, whetherit’s, you know, dictators living forever, whether it’s economic issues like the payingof pensions and so on, i have variety of answers. first of all for each of the specific concerns,i have particular ways of thinking about the problem that show that actually it’s unlikelyto occur or that we would actually be able, very straight-forwardly to avert it. so in the case of overpopulation for examplei always point out that all the other technologies

that are coming along, they’re improving,for example the use of fossil fuels and replacing them with renewable energy and artificialmeat, they’re reducing their agriculture and so on, these things are going to be reducingour carbon footprint and therefore the amount we pollute, and the same is happening forother pollutants. so of course what we already have done withcfc’s that were affecting the ozone layer. so what this adds up to of course is thatwe’re going quite soon to be in the position where we can have more people on the planetwith less environmental impact. in fact it’s precisely what overpopulationis all about, so i don’t think it’s going to happen.

so that’s kind of answer i often give buti want to complete that answer by giving you my two generic answers. these two answers apply across the board whetherit’s concerns over overpopulation or any of the others, they apply equally. the first one is sense of proportion. the same question is supposing, let’s supposewe didn’t invent renewable energy fast enough or whatever and we genuinely did have a situationmaybe 50 years from now where we will be faced with a choice of having fewer kids than wewould like because we need to make room for all these irritating old people who are notgetting sick, or instead, letting them get

sick. now, seriously which are we gonna choose? we’re going to choose to have fewer childrenand keep people healthy. so raising this as a reason not to developthe therapies is just not ethical. and the same applies to all of the other things. the other answer is the right to choose. i believe very strongly here that if we wereto say, “oh dear, overpopulation, let’s not go there” and we were not to work ashard as we can to develop these therapies, and if therefore we were to delay the timein which the therapies actually arrive then

what we would be doing, we would functionallybe condemning an entire cohort of humanity to an unnecessary early, unnecessary unpleasantdeath; the kind of death that we’re familiar with today, whereas conversely if we had goton with the job then humanity at least would have had the option with the information availableto them that isn’t available to us like whether or not they fix their renewable energyproblem and so on. they would have the option to decide whetheror when or how to use these therapies. we should have the right to have an option. they should have the right, the people inthe future should have the right and therefore we have a duty to develop the therapies andgive them that choice.

what is your inequality of access answer? so of course the generic answer to anythingregarding inequality of access to new technology which is in fact, it always trickles down,it always becomes cheaper when there’s demand and it becomes available to everybody. but i think with this particular case we havea stronger option than that, which is that this stuff is going to be enormously costsaving. the fact is today aging is ridiculously expensive. i’m not talking here just about the directcost, the cost of medicine to treat people who are sick because of the diseases of oldage.

that’s of course an astronomical cost. but even that is dwarfed by the indirect costs--the loss of productivity of the kids of the elderly because they’re looking after theirsick parents, the fact that the elderly are no longer contributing wealth to society becausethey aren’t in an able bodied state to do so, all of these things, either way you lookat it. what this means is that these therapies, evenif they’re expensive to deliver, they will pay for themselves in absolutely no time. and that means that from the point view ofgovernments, from the national point of view, it would be economically suicidal to let peopleget sick when they get old.

it would only make sense financial mercenaryeconomic sense for the federal government to actually make sure that everybody who isold enough to need these therapies does have an access to them and will therefore continueto contribute wealth to society. we’re feeling healthy and we’re workinglonger. but we have automation and artificial intelligence. so what types of jobs will be available? i used to work in artificial intelligence(before biologist) and the reason i did so was very much the same reason i now work inaging. it was humanitarian.

i felt it was extremely miserable that peoplehad to spend so much of their time doing things they wouldn’t do unless they were beingpaid for it. and the fix for that is of course automation. so you’re absolutely right to suggest thatthe advance of automation that we’re seeing right now is very likely within relativelyshort amount of time to result in the pretty virtual elimination of most of the jobs thatwe know as jobs today. and of course we’ve seen this before. we saw it with the industrial revelation whichresulted in the decimation of the size of the workforce in manufacturing and agriculture,but then the idea of maintaining a full, 40

year career with a 40 hour working week wasperpetuated because we invented new jobs. we invented this thing called the servicesector which of course expanded as the manufacturing and agriculture sectors contracted. but i don’t think that’s gonna happenthis time around because this time around as the service sector gets automated to oblivion,you know, what have we got left? what sort of sector is there, how many peopledo you need in the entertainment industry you know. so i think we really are going to bite thebullet that we kind of dodged when the industrial revelation happened.

we’re going to have to find a differentway to distribute wealth and to equitably share out the remaining things that do actuallyhave to be done. do your donors get first dibs to be studyparticipants? we are perfectly happy to try to help peoplewho help us. but you have to remember that we are doingthe biomedical research, the early stage of biomedical research to develop these therapies. and as the therapies move through the pre-clinicaland clinical stages and more and more money is required, the chances are very good thatwe will have to relinquish a lot of the control over this intellectual property, even indicationswhere we have some of that control early on.

so it’s not really, we’re not really ina position to commit to anything like that. but also i want to say if i were a wealthyindividual and i were paying for this research it wouldn’t be because i wanted to be first. it would be because i wanted it to happensoon enough. nobody really wants to be first in line forany experimental treatment. right. why do you think calorie restriction isn’teffective for humans for life extension? the ineffectiveness or the relative ineffectivenessof calorie restriction in humans or indeed in other long lived species like monkeys isactually not a surprise.

it’s something that is very straight forwardlypredicted from evolution. essentially it just come from the very simpleand obvious fact that long famines in nature happen more rarely than short famines. now that matters because the frequency withwhich a particular environmental situation occurs determines the extent of which evolutionis motivated to develop genetic machinery to be optimized for that environmental situation. if something only happens once in a millionyears than evolution just dust doesn’t care enough to develop machinery to deal with it. that makes sense.

aubrey: it’s rather like the situation wehave with vitamin c. so vitamin c is of course a vitamin, we have to actually consume itin our diet in order to get along. but most mammals don’t have that problem. most mammals make their own vitamin c internallyin their own cell. and the reason we don’t, and the reasonalso why two other families of mammals, namely guinea pigs and fruit bats… they don’t either? that’s right. the reason is believed is agreed to be simplythat in our evolutionary ancestry there was

a time when there was so much vitamin c inour diet all the time reliably that there was no selection, no evolutionary pressure,to maintain the machinery to make it ourselves. so the machinery mutated into an inactivestate and by the time the vitamin c supply became less reliable again it was too late. some of your critics have, unsuccessfully,gone out of their way to try to discredit you. this was about 11 years ago. they even offered a prize of $20,000 if someonecould prove you wrong. why would they do this?

well actually it’s not quite that simple. the $20,000 that was put forward, was actuallyhalf of it from the magazine that orchestrated the prize, mit technology review, the otherhalf came from us, because we wanted to actually smoke out the opposition. that’s awesome. it was to solve a rather unfortunate situationthat had risen over the previous couple of years, namely that a lot of people like you,all the journalists were coming to the more established grandees of the field and theywere asking these grandees about my work and asking whether my conclusions in terms ofpeople’s potential longevity had any basis

in fact or in legitimate hypothesis. and they didn’t want to know about it becausethey didn’t know my work well enough to be able to make a cogent case one way or theother so they thought that the simplest way i can get the journalists off the phone wasto engage in off the record ridicule. because it was off the record of course ididn’t have the opportunity to rebut any of it. so essentially what i did, both with thisprize and also simultaneously in the academic literature around the same year, i was ableto essentially pick a fight with my more vocal critics and get them to set out in print thedetails, the scientific details of why they

thought that this idea of sens was unscientificso that i was able of course very easily to write very comprehensive rebuttals and theresult was exactly as hoped. it took a while of course for the dust tosettle but eventually people began increasingly to acknowledge that what i was saying didmake a good deal of sense. and the result now is that people are evenre-inventing these ideas and calling them their own, which is, you know.. it’s so true. imitation is the sincerest form of flatteringand all that. they couldn’t poke holes in your rebuttalsand then your book, ending aging, came out

and now all the things that you said then,they’re trying to do now. so, that’s pretty awesome. it is. calico is the google backed company that’stackling aging. and they claim to be funded for long termresearch. you’re obviously extremely intelligent andpassionate. why do you think they’re so secretive andwhat are your thoughts about why they haven’t brought you onboard yet? well the answer to the question about whythey’re so secretive is not something that

i’m really in a position to guess. what i can say is you know, they’re a companyand they’re being run by a guy who made his name running another company, genentech. you know they have a corporate attitude toinformation flow, i think it’s pretty normal to be secretive when you run things this wayand you want to make money. now the curiosity of that of course is thatas you say they’ve already got all the money they could possibly need from google. so it kind of makes no sense but on the otherhand they have very clearly positioned themselves so that some of their effort, a lot of theireffort in fact, is actually geared towards

actually making money fairly soon; they’vedone deals with other biotech companies including some pretty large ones that are likely tobe quite profitable within the next few years. now everybody recognizes that those deals,those projects that are collaborations with the rest of big pharma and such like are notthe ones that are going to defeat aging. and that the other part of their work whichis really targeted to defeating aging is somehow being protected, being insulated from thepressure or whatever by this kind of approach. fine so far. the difficulty, which comes to the secondpart of your question about why they aren’t working with us is that the real science part,the part where they’re really trying to

tackle aging is being dominated as far aswe can tell, and again because they’re so secretive we can only infer this from basicallywho they hire, is they’re dominated by basic scientists, by which i mean by people whoare interested in understanding nature and are good at understanding nature but are notso good at manipulating nature and the consequence of that understanding. they’re not technologists so much. this is a real problem because of course webelieve that actually aging is sufficiently understood at this point, that it is possibleto engage in the design and implementation of methods that will comprehensively postponeaging.

and it’s very frustrating that the peopleat calico, especially the decision makers at calico appear to have decided that no,that’s not true, and that more exploration and hypothesis testing and so on needs tooccur before any kind of actual technological exploitation can be contemplated. it’s a great shame. i have of course spoken somewhat to calico. i and a couple of other people here went therea couple of years ago shortly after they got going and gave a long presentation of allof our work and they were terribly polite but they didn’t call us back shall we say.

that’s so frustrating. were there any correlations in the habitsof the super centenarian population? not really. super centenarians are extremely fascinating,no question about that.any exceptional group in any sense is what is studied. super centenarians of course constitute avery, very tiny proportion of the population that have lived longer than anybody else--the definition is an age of 110. there are only about a couple of thousandof such people on record which is not very many at all.

but when you ask about the habits or anythingelse for that matter like lifestyle, diet, genetics, whatever, there really isn’t verymuch in common. i mean it won’t surprise you to learn thatjapan is over represented in super centenarians simply because japan is the country with thelongest life expectancy. but only by a couple of years which leadsto a relatively small factor, relative to other countries. so the question then is what can we learnfrom super centenarians? the difficulty is that first of all no, theydon’t seem to have very much in common except for one thing, which is they seem to be verygood at, and this applies down the list a

little bit, down to centenarians as well. they seem to be very good at handling stress. they haven’t necessarily had a particularlystress free life. but the thing is nothing bothers them. when enduring kind of stressful situationsthey cope with them very well. and so that kind of makes sense, we know thatstress is bad for you, it elevates the level of certain hormones, that accelerate the creationof damage. however the best way, the most informativeway to study super centenarians is very probably to study not them themselves but rather theiroffspring who are of course genetically very

closely related. the idea there is that then you can comparethe offspring with other people of the same age. there’s no point really in comparing thehealth or functionality of a super centenarian with someone who’s 80 because the supercentenarian is very impaired in their function both mental and physical. they’re about to die, after all. but the other thing that’s special aboutthem is that they were born a very long time ago.

if you study their offspring and you comparethose offspring with people of the same age then you’re factoring out all of that problem. so other people are now working on the problemof aging. and there’s been recent patents around removingthe intra and extracellular junk and the cross linking, will the patents interfere with yourwork at all? well first of all we ourselves are takingout ip, taking out patent protection on some of the work that we’re funding. but also one thing that is quite useful isthat we are seen as very much the nexus of this rejuvenation biotechnology, by near fellowsand the people who know everybody.

so we often have very good, a few differentcollaborations not just with other groups but even bringing other groups together witheach other so as to minimize the difficulty of competition and trade secrets and suchlike. the patent situation in some of these areasis stronger than in others. so for example with extracellular waste products,such as amyloid in the brain of alzheimer’s patients, there’s been quite a lot of workdone, lots of money has gone into the developmental of antibodies for example, they’re ableto remove this stuff. and you know, we don’t expect that there’sany real need for us to get involved. but there are other types of garbage likeanother type of amyloid that accumulates in

the heart in older people where actually thegroup that is doing the most promising work is the group that we funded and we do havean equity position in the company that spun out doing that work. it all depends on the specifics of the individualproject but the short answer is no, we’re not too worried. what can we do if we want to live longer? i’m afraid that i only have one answer tothat question and it’s not a very pleasant answer. the answer is all you can do is give sensresearch foundation large amounts of money

or possibly persuade somebody else to do so. because at the moment we simply don’t haveany medical interventions or lifestyle or diet or other interventions that are availablethat can substantially postpone the ill health of old age. therefore for any particular individual theonly thing that they can do is to change the other end of the equation. in other words bring forward the arrival oftherapies that do much more than anything that exists today. and that of course does require financialresources.

one of the most important things i alwayshave to emphasize about this work is that out of the three problems that i had to solvewhen i first entered the field 20 years ago, two of them were solved pretty quickly. number 1, after only about 5 years i figuredout the sens plan, the idea of damage repair being a more practical approach than inhibitingthe creation of damage by the body. and then one being the personnel, gettingworld leading scientists in all the various relevant disciplines on the side, gettingthem enthusiastic about doing all of this work, that has meant that at least for thepast decade, the only problem that remained is the lack of resources with which to letthose scientists get on with the job.

i take it you want me to open this box. yes. hope i can keep the skull. alright well this is one of the best beersknown to man. so this is pliny the elder, and it’s kindof a famous cult following microbrew in northern california and the “elder” is kind ofpun intended. but i wanted to ask is it true that you drink3-4 pints of beer a day? i suppose that’s a pretty good average. how many hours do you sleep?

i actually don’t get enough sleep. this is the one big thing that i do that isprobably bad for my health and my longevity. i figure it’s kind of a good trade off becausei’m bringing forward the defeat of aging by my work and maybe i’m shortening my lifebut not by such an amount as the amount that i’m hastening the defeat of aging so it’sa net win if you like. you’ve got a lot of confidence that you’regoing to pull this off. it’s all probabilities but yeah i mean idon’t have enough sleep that’s for sure. do you have hobbies? i used to have hobbies.

i’ve pretty much given hobbies up. many years ago i used to play competitivelya board game called othello which is actually not very well known in the west. it’s quite well known in japan where it’squite popular. it’s very, very simple rules and it’sgot a very simple strategy. there are world championships in it, has beenfor 40 years almost. but yeah i used to be the chairman of thebritish othello federation. i used to be play it quite a bit. but i haven’t been able to do so for atleast a decade now.

that’s entrepreneurship. you married pretty young to an older womanwho was already an established biologist and geneticist. was love an impetus to get up to speed inyour field? a lot of people have suggested that maybei got into this business because my wife is 18 years older than me and i wanted to saveher life so to speak. and of course i would not object to savingher life, that would be very fine. but, no, that is absolutely not what getsme out of bed in the morning or whatever has. in fact saving my own life has not been thething to get me out of bed in the morning.

what really energizes and drives me is purelythe humanitarian aspect-- the fact that i’m gonna be saving so many lives every time ibring the defeat of aging even one day forward—that’s 100,000 lives. it’s pretty easy to get excited about that. yeah it seems your pursuit of something importantmakes you happy. millennials can respect and relate to thefact that you’re not motivated by money. you could have had a luxurious life with yourmother’s inheritance but you assigned $13.5 million to your sens foundation. how did she amass her fortune?

so my mother was i guess both very wise andvery lucky. she inherited from her parents a small amountof money about 30,000 pounds which was you know, a respectful amount back then in the50’s and 60’s. but still not a ridiculous amount, but sheinvested almost all of it in two houses in chelsea, in central london. so the amount of income that she had and thatwe lived on thereafter was pretty limited because very little was left after the investmentin the houses. but the result was in the end extremely fortunatebecause that area of london continued to appreciate, the property prices right through the restof her life.

and the result was that when she died in 2011and we sold the houses, one of them we had, which originally cost 6 and a half thousandsold for 3 million, and the other one which was originally 23,000 sold for nearly 8 million,and that’s all in pounds. so yes, so the result was i inherited i thinkwe came to a total of 17 million and as you say i was able to donate 13 and a half millionof that to the foundation. it was complicated because my mother of coursewas british and the foundation is a us charity so it has to be done by an affiliate charitythat we created in the uk but it all worked out. that must have been a pain.

well it was okay, it was worth it. of course we knew in advance of my mother’sdeath what was going to be needed so all of it was in place by the time that happened. and i hold on a little bit so i did, i wasable to buy myself a nice property in the santa cruz mountains, which is as far as i’mconcerned, all i really need. you’ve made such visible progress in yourfield. has your father ever tried to contact you? no. you signed up to do cryopreservation withalcor.

can you tell us about that? so i think that pretty much the only tragedyin the world that compares in severity with the hesitance of humanity to embrace and pursuethe anti-aging mission more aggressively is the reluctance of humanity to embrace cryonicsmore aggressively. because cryonics is a massively valuable componentof future healthcare. and therefore of today’s healthcare, ifonly it were understood what cryonics really is then i believe that first of all, the actualquality of cryopreservation that can be achieved will be far higher now than what actuallyexists because more investment would have gone into the research.

and secondly, that vast numbers of peoplewould be cryopreserved. what we have to remember about cryopreservationis that it is just healthcare. we take someone who has just become legallydead and we learn to lower the nitrogen temperatures so that they don’t become any more deadthan they were before. the idea of someone being partly dead of courseis the problem here because most people, society in general doesn’t like to think that way. they like to think of people being eitheralive or dead and nothing in between. but that is that is biologically nonsense. death is absolutely not a process that happensinstantaneously.

it’s a process of steady and certainly acceleratingdecay in the body, accumulation of damage. that rate of accumulation accelerates verysharply at the point that we stop breathing and our heart stops beating. but it’s still only finite. so if you take someone who has just undergonecardiac arrest and may even have not any brain function anymore but still they don’t havevery much more damage than they had previously when their heart was still beating. if you can stop any further damage from accumulatingwhich is what freezing someone does than they’re still in a state where there’s a substantialprobability that they can be revived from

that state using the benefit of medicine inthe future that is first of all better at keeping people healthy with minimal amountof damage and second of all capable of repairing the damage and getting them back to theirtruly healthy, youthful state. now the catch in all of this that everyoneis quite well aware of, of course, is that the process of cryopreservation itself createsdamage. take someone who has just become legally deadbut they’re warm and you cool them down, if you cool them below freezing, they’regoing to become, they’re going to crystallize and that’s gonna rip the tissue apart. and it’s extraordinary to me that stillhardly anyone realizes that this problem was

completely solved, more than 20 years ago,with the development of a rather elaborate cocktail of cryoprotectants that essentiallystop this from happening at all. the body doesn’t form crystals it formsa glass, it can amorphousize and that’s why it’s called vitrification. there are further advances that are certainlyneeded in to eliminate even other types of damage from cryopreservation but even withthe current situation people who are cryopreserved in the best possible state have, in my view,a substantial chance of being revived. and another thing about cryobionics is cost. people always think, oh my god, alcor charged$200,000 to cryopreserve someone, we think

oh well that means it’s only for wealthypeople. but that’s nonsense too and the reason it’snonsense is because society doesn’t understand death. society doesn’t understand death. so when someone is pronounced legally deadtheir life insurance can pay out, even if the cryonics company and the patient beforethey were legally dead, don’t think they’re dead, and they just were in a coma effectively. so life insurance pays out which means thatif you have a life insurance policy, whose payout is let’s say $200,000, then if youstart it when you’re in your 20’s or 30’s

or 40’s the monthly premium is going tobe perfectly manageable just like any other life insurance policy, the only differencefrom the regular insurance policy is who the beneficiary is, rather that the beneficiarybeing the next of kin, it’s alcor, or whichever. so it’s really very affordable and it’sa scandal that even though people like myself and the people who run alcor and so on havebeen telling journalists this since forever, nevertheless it still isn’t getting throughto people’s consciousness. do you believe we have eternal non-physicalsouls? aubrey: i have no idea whether we have anykind of non-physical attribute to the body. however what i will say is that if we do thenvery clearly it is intimately associated with

the physical body for as long as the physicalbody keeps functioning, and therefore it doesn’t really matter. we want the physical body to keep functioningand if there’s any soul around that’s inside it or tied to it in some way, thenso what, really. until recently your beard had a facebook fanpage. if the reserve was set really, really high,would you consider auctioning your beard to raise money for sens? i have indeed been on the record for sometime as saying that a million dollars will buy you my beard.

what about peter thiel? peter thiel is awesome. he is one of very, very few wealthy individualswho are not only visionary but are also rational enough to understand that not everything canbe driven by capitalism. so he definitely likes making money and he’sdone very well investing in innovative technology but he’s also donated very substantiallyto our research and to other research that was at a pre-competitive stage. he is awesome. what about ray kurzweil?

ray kurzweil is pretty awesome too. he’s definitely been the kind of thinkerwho has been able to see well outside of the box and he’s invented a number of technologiesthat have been very successful. so he’s definitely very much earned hisnational medal of engineering or whatever it was that he won a number of years ago. his work in longevity is also perfectly reasonableby in large. i believe that he is somewhat over optimisticwhen it comes to what we can do today using just vitamins and supplements and such liketo postpone aging. he takes a lot.

but his attitude to future technology is prettymuch spot on. he believes just like me that the next coupleof decades will see the development of really powerful regenerative medicine, rejuvenationbiotechnology. and his longer term vision of the use of nanotechnology,in particular a variety of different non-biological solutions to the medical problems, all ofthat is also very reasonable. it’s not an area i’m an expert on so idon’t want to say that whether it’s right or wrong but it’s not crazy. what about dr. craig venter? so craig is another guy who’s achieved agreat deal by not being scared to be different.

he has of course been extremely prominentin biomedical technology for quite a long time. he was responsible for sequencing the humangenome and more recently he has taken that technology, high-throughput sequencing, intoa variety of other areas including environmental protection and such like. of course at the moment, his main claim tofame that’s relevant to our work is that he along with, peter diamandis, a great friendof ours, started a company called human longevity incorporated which is, well as the name suggests,interested in doing something about aging.now the general value proposition of that companyas it currently seems is somewhat short-termists--

they’re more focused really on using genomicinformation to optimize personalized medicine, but as time goes on i’m quite sure thatcraig will, because he is ultimately a really heroic pioneer, will be at the forefront ofdeveloping other technologies that will help make a big difference. what do you think about modern meadow? modern meadow is a great company trying todevelop artificial meat that is good enough to eat and therefore can significantly reduceexpenditure on agriculture and of course the pollution that comes with that. modern meadow is actually a spin out froma company named organovo which is interested

in the rather more difficult problem of developing3d printed organs. the reason it’s a more difficult problemis because with meat you don’t need the circulation to work, the vasculature, whichis the main physics problem, the main real material science problem with creating organs. however, i feel that both of these companiesare very palatable, in fact we, in our previous forum at the methuselah foundation were thefirst investor in organovo. what do you think about eliminating sugarfrom the diet? i really don’t think that there’s enoughevidence to suggest that completely eliminating sugar is a particularly good idea.

i’m not saying it’s a bad idea. i just think that either way the differencethat you’re going to get is relatively mild. of course we are not comparing normal sugaruse to high sugar use, excessive sugar use. excess of anything is definitely bad for you. but going from normal amount of sugar to zerosugar, i think it’s rather like any other area of dietary manipulation. we see sometimes we see mild beneficial effectsin some people. you don’t know whether you’re gonna respondbecause every person is different. so you know, for me it’s not really, it’snot the real mccoy.

it doesn’t really rise to the level thatwe are interested in. what about vegan, raw food or ketogentic diets? really i have exactly the same thing to sayabout all of these other dietary approaches that i do to, with regard to sugar. i think that any diet that is reasonably balancedin terms of its nutrient intake, both micronutrients and macronutrients is gonna be okay. you can always have too much of a good thing,so one mustn’t get overweight or anything, but the difference between one reasonablediet and another reasonable diet is very unlikely to be enough to get us interested.

we at sens research foundation are all aboutdoing things that will postpone the ill health of old age by a far greater amount than anythingwe can do today. what about drinking deuterated water? deuterated water is very unclear as to whetherit’s got any interest. but since you mentioned deuterated water whati would like to mention is an alternative use of deuterium which seems to be very beneficialand indeed the benefits that it seems to confer make a lot of biological sense. so i believe this both theoretically and practically. the idea that is being pursued by a companyactually local to here called retrotope is

to create versions of fats that have deuteriumreplacing the hydrogen atoms in certain judiciously chosen places in the molecule. and the purpose of this is to slow down therate at which these fats actually react with free radicals, as i mentioned earlier. do that, then because of some of the detailsof how free radicals react with fats and how fats then react with each other, because ofthe details, it turns out that even a relatively small amount of deuterium incorporated inthese judicious locations in molecules is enough to make a big impact on the oxidativestress of the organism on how much free radical damage occurs.

and eventually that includes damage to dna,which i mentioned earlier. so this is a radical and very innovative approachto dietary manipulation to postpone aging. it involves a lot of chemical sophisticationas i’ve already indicated. but i believe that it definitely has a lotof merit. what about omega 6, vitamin e, and other anti-antioxidants? vitamin e is a bit of a mixed bag and thishas been understood for a long time. the thing about vitamin e is that it transferselectrons from one place to another. in particular it’s what’s called a lipidsoluble antioxidant which means that it can protect fats from arterialization i was describinga moment ago.

but a given bit of a vitamin e molecule canonly do that once and then it has to be recycled by reacting with vitamin c. now vitamin cis, it’s not a lipid soluble antioxidant, it’s a water soluble one which means thatthe rates for these reactions between vitamin c and vitamin e and between vitamin e andthe fats are dependent on details of where the molecules are. for example if the vitamin e is in a membranewhich is a very flat thin surface then it may be able to get greater rather rapid accessto vitamin c than if the vitamin e molecule is in a kind of a spherical globule of fat,like a lipoprotein in the bloodstream. and this means that sometimes vitamin e canactually not be an antioxidant at all but

a pro-oxidant. now you mentioned earlier, 6 and omega 3 fattyacids, this is again part of what i was saying a moment ago about deuterium in fat. it turns out that different fatty acids havevery different roles to play and very different susceptibilities to oxidation and thereforeto contributing to oxidative damage throughout the body. what about liposuction of abdominal fat? they say that’s the most problematic fat. so abdominal fat is indeed often mentionedas a big problem because a lot of it gets

into a state where it secretes toxic moleculesthat will accelerate aging in other places. and there was some very exciting work donein new york probably as long as 15 years ago now showing that removal, surgical removalof that kind of fat from rats perhaps were diabetic could almost instantly relieve thediabetes. so that was pretty exciting and that kindof work has proceeded. people of course have looked at ways in whichthe fat can be removed non-surgically. but there’s still plenty of interest inthis area. it’s got promise. and there’s another thing about removalof abdominal fat that i should probably highlight

as well which is that the abdominal fat youremove doesn’t only contain fat cells, it also contains fat stem cells. those stem cells can in today’s world whatwe understand about stem cells, stem cells can be manipulated and turned into other typesof cells and reincorporated into the body in beneficial ways. yeah they’re starting to do that a lot. what do you think about exercise? exercise is a bit like diet really. you better have enough of it but having morethan enough probably isn’t gonna help you

very much. hyperbaric oxygen therapy. so people have been playing around with theoxygen pressure and indeed oxygen concentration in what you breathe for quite some time andthere is some tantalizing data out there showing that it may have beneficial effects of a varietyof types. i think tantalizing because i don’t thinkthe date are conclusive yet. there’s plenty more to do but luckily enoughpeople are tantalized that that data continues to accumulate. and so i think we will progressively learnmore about this, again though, i would bet

good money that it is not going to be thefountain of youth. what about metformin increasing lifespan? the metformin is originally an anti-diabetesdrug and of course diabetes is a prevalent disease of old age-- type 2 diabetes. so we would expect that there would be somebenefit but the reason you bring it up of course is that there have been a number ofexperiments in the laboratory that have indicated that metformin has a more widespread effecton processing the damage accumulation in aging than nearly the anti-diabetic effect. and the result is at this point that a numberof researchers including incidentally the

guy who did the work i mentioned on gettingrid of fat from rats earlier. i have got together and have actually successfullypetitioned the fda to allow for a clinical trial of metformin against aging. now this is a real breakthrough, the firstof its kind, because until now the fda were unwilling to recognize aging as a conditionfor which there could be clinical trials and approval of a drug or anything like that. and in this case, this is really just a proofof concept firstly because metformin is of course a very old molecule and no one’sgonna make money out of finding that metformin works against aging.

and secondly because, to be honest, i don’tthink metformin is going to have much effect in terms of overall impact on… it’s negligible. i could be wrong about that so glad the trialsare being done but the big thing here is that the negotiations between the researchers andthe fda have resulted in a definition of aging that everybody can work with. essentially it’s all about multi-morbidity,all about having more than one defined thing wrong with you at the same time. and the design of the clinical trial thereforeis absolutely certain to be copied again and

again and again for other drugs now that theprecedent has already been set and now that drug companies can make money out of a drugthat actually achieves these ends. liz parrish. i know liz very well and i wouldn’t do myselfwhat she’s doing but that doesn’t mean i think that what she’s doing is wrong. she has taken good scientific advice froma number of people including myself and she has decided to volunteer as patient 0 to receivegene therapy for a couple of genes that may postpone aspects of old age. now the results of that are of course difficultto evaluate for a variety of reasons.

number one it’s only one person. number two she’s actually in the prime ofhealth. she’s in her forties and most people wouldnot guess that she was as old as that, so it’s unclear whether the can be any realperformance indicators. however that still allows for the possibilityof tentative preliminary indications at the level of blood work for example in terms ofwhat effects these genes might have. and importantly the effect is supposed tobe rejuvenative. it’s not just supposed to be slowing agingdown. so the effects may therefore show up quitequickly if they exist at all.

so along further is you know, i mean she’snot trying to make money out of this. she’s just experimenting on herself andself- experimentation has a long and distinguished history in medicine. so you know, it’s really her choice andi am very pleased that she’s not being given too hard a time for it. certainly her choice to do this and the publicityof it has attracted a lot of controversy but it hasn’t been particularly vicious. what about gensight? gensight are a very interesting french companywho are doing a few things but the main thing

that’s relevant to our work is that theyare trying to do something called allotopic expression which is the copying of or theinsertion of back-up copies of the mitochondrial dna into the nuclear dna. the idea here is that 13 proteins which areoccurring in the mitrochondrial dna are essential components of the mitochondria but there aremore than a thousand proteins that are also essential components of the mitochondria andthey are encoded by nuclear genes naturally. so if we can kind of co-op the same machinerythat transports the nuclear coded proteins back into the mitochondrion then what we wouldhave is a system where it wouldn’t matter if you got mutations in the mitochondrion.

and that’s really useful because mitochondrialdna turns out to be vastly more prone to mutation than nuclear dna. now gensight are pursuing one particular applicationof this, which is a type of blindness called leber’s hereditary optic neuropathy andthe reason they’re doing this is because unlike the mitochondrial damage that you seein normal aging the damage that is the cause of this particular neuropathy is just a supermutation in one of us those 13 genes. so they’re trying to put one of these backupcopies in to correct that and they have pretty good initial data well good enough to getinvestment anyway. but the reason we’re interested in thisof course is because we’re trying to do

exactly the same thing, though we’re tryingto do it for all 13 of these proteins because that’s what you need to do in order to havea good effect in normal aging as opposed to this one type of blindness. i have some questions about dr. aubrey degrey as an entrepreneur. you started off in computer science. if somebody would have told you: you’regoing to be the first to work on the problem of aging, you’ll be a famous author andpioneer and you’ll be solving the hardest and underfunded problems, you’re going tomap a concerted set of therapies… did you feel back then like you know, i’m that guy,i could be that guy when you started?”

well only in part. i mean when i was in my twenties, my earlytwenties or my teens and i was making career decisions i had given up biology already. i only went back into biology after i metmy wife. so i definitely never thought that i wouldgo into biology per se but i certainly did think that i would wanted to spend my lifetrying to change the world, where could i make a big difference? and i went into artificial intelligence researchsimply because i found, at the age of maybe fifteen, sixteen, that i was a pretty goodprogrammer.

and so i thought well this is an area wheremy talents can be applied for good humanitarian benefit. then the progress i made when i was doingthat was really very specialized—i was working in a particular area called software verification. however, you know, it was an important areaand i certainly had a strong belief that my work there could translate and generalizeinto full blown artificial intelligence of one kind or another in the long run. but more to the point it also taught me thati was not just good at programming, i was also good at working on really hard problems,breaking them down and figuring out how to

solve them. so when i started to talk to my wife and otherbiologists about aging at the age of about twenty-seven, twenty-eight, twenty-nine, itwasn’t too much of a struggle for me to start to realize that maybe this was an evenmore important target than the problem of tedium and having to work on all these thingsthat we don’t really want to do and the fact that i knew i was good at working onhard problems was a big start. so by the time i switched, most of what youjust said really was true. i felt that i have a respectable chance ofmaking a big contribution if i switched field. wow.

you founded your first company within a yearafter undergrad. is that true? kinda yeah. so man-made minions, which was the companyyou’re talking about that was the company within which i pursued this software verificationwork. and but it’s not really fair to say thati founded my own company. first of all i co-founded it with anotherguy from the same company where i was working in that intervening a year. and that other guy with whom i worked was2 years older than me, 2 years more experienced,

generally he was the person who really foundedthe company. and i was really the back room guy doing research. second thing i want to mention is that thiscompany wasn’t selling anything. it was a company that was really a companyonly in name with my colleague going out and doing contract programming work that paidthe bills and me just doing full-time research. so i think it would be misleading to say thati founded my own company. that was very honest answer. how did you get a publisher in 2007 for endingaging? it wasn’t too hard actually to get endingaging published.

the reason it wasn’t too hard was becausei went to ted. ted was not quite so glitzy as it is now backthen. they didn’t even have ted talks let aloneted x. but it was still pretty glitzy, and i wasinvited as speaker in 2006 and of course the book was in gestation by then, it was largelywritten and one of the people i met there was a very famous literary agent named johnbrockman who has handled books for a general audience for pretty much every scientist youcan think of who has written a popular book. and he, having seen my talk, and having talkedto a few other people, he didn’t have too much difficulty persuading himself that thisbook was going to be worth taking on.

so once brockman’s on board, the rest iseasy. it’s all downhill from there. so brockman found us st. martin’s press,which took on the actual publication. you have a 25 member advisory board and aton of very talented people working for you. how do you onboard reputable people? the main way in which one gets scientiststo associate themselves with a particular project, whether it’s senior scientistswho are working with advisors or professors or whether it’s community people who aredoing the actual grunt work at the bench, the main way you get good people is by doinggood work.

and that means, that comes down to two differentthings. first of all it’s what you’ve alreadydone, the track record of grants and publications you put out and so on. and second it’s just how it feels, how legitimate,how exciting it feels. you can look at, someone would look at ourwork for example and will say oh a lot of this seems very speculative, but the morei get into it the more they see that any initial skepticism they might have about the feasibilityof this or that, actually we’ve already thought of their objection and we’ve gota good answer, and the more times you get around that cycle the more your confidenceincreases that actually the objections are

invalid and the excitement is what’s valid. in light of what happened with theranos, arethe sens studies published and peer reviewed? we do publish our work in the peer reviewedliterature and we think that’s very important. we think that credibility of our work needsto extend across all audiences and there are many scientists who simply aren’t goingto pay really good attention to any work unless it’s been published in peer reviewed academicliterature, which is fine. what we don’t do is submit to what’s oftencalled the publish or perish paradigm. in other words essentially the philosophyof publishing as much as we possibly can and indeed choosing what work we do in order tobe able to publish as much as possible.

this is very, very prevalent in academia,in fact i would say that it’s absolutely ubiquitous in academia, simply because it’sthe only way for people to distinguish themselves in competitions for grants and promotionsand tenure and so on. but it’s immensely damaging to the longterm progress of science because it means that people aren’t actually working on themost important problems, they’re only working on the easiest problems so they can get publicationsquickly. so we do publish but we don’t publish nearlyas much as a grip of our size of our total budget would publish if we were doing thingsthe normal academic way. what’s the best and worst part of your job?

the best part of my job is the achievements. every time that we make a breakthrough, weget something working, i know that we are one step closer to ending the biggest problemof humanity. and also even when people come to me and theysay that i’ve inspired them to move into the field for example or it works out financiallyor anything like that, again it’s a sense of achievement. the fact that i really am being given externalvalidation, that i really am making a difference that i wanted to make. the worst thing about the job-- hard to say.

i mean i feel very fulfilled by the job. the fact that i’ve made such a differencealready and the fact that i continue to make a difference of course is huge. i guess the worst part of the job really isthe frustration that it’s not going faster. the frustration that despite my best efforts,and spending an awful lot of time on camera and on stage trying to get the word out, tryingto explain to people that this is both feasible and desirable, nevertheless it remains a reallyhard sell. you have an operating budget of about $4 milliona year. how does the research break down- what coststhe most?

at the moment our budget which, as you sayis about 4 million a year, is mostly on research itself. we also have a minority that is spent on outreach,on you know, conferences for example and then a minority that is spent on education, onfunding internships in this facility and also in various extramural labs that we support. the research breaks down into the obviousthings really, personnel, salaries and reagents and consumables and equipment and that variesenormously from one project to another, there’s no single path. do you have any regrets?

honestly i don’t have any significant regretswith regard to how this whole process has gone. i don’t even regret the fact that i startedout in one field and then didn’t discover the utility that i might have in the anti-agingeffort until relatively late in my life. i don’t regret that because i think thatmy work in artificial intelligence per se equipped me very well to make more of a differencethan i could have otherwise have done after i switched fields. with regard to how i’ve actually conductedthis whole thing going about learning and thinking and coming up with ideas and gettingthe ideas out there and so on.

again i don’t really look back and say tomyself that i really made a bad mistake here or there. i think by in large any mistakes i’ve madehave been pretty minor. what’s the most important thing a humancan do in this lifetime? so that is probably the most unanswerablequestion it’s possible to ask because for sure in certain what’s important is a valuejudgement and what any given human can do varies very much from one human to the next. so it seems to me that the main thing, themain way to think about that question is to think about how many things we can do in alifetime which of course is somewhat limited

by how long our lifetime is, and that’swhat we’re trying to fix.