A Cure for Aging?

A Cure for Aging?

28 min reading time

A Cure for Aging?

Reading Time: 28 minutes

Dr. Bill Andrews, CEO of Sierra Sciences, and Liz Parrish, CEO of BioViva Sciences, discussed “A Cure for Aging?” at this year’s 10x Medical Device Conference.

Liz starts with a statistic: 100,000 people die of aging each day, noting, until recent history humans would die from infectious diseases. As science improves, so does our ability to live longer – until we die of complications from old age.

Can we cure these complications?

Bill gives easy-to-understand insight into the role of telomeres in our death and his work with Telomerase, an enzyme at the core of his work to extend human life.

Treating biological aging as a disease, Bill and Liz combined forces to create BioViva Fiji and are building a large-scale production facility and clinic to provide a gene-therapy approach to cure aging.

They expect human trials in a year’s time.

Liz Parrish: We’re very happy to be here and we’re very happy to be presenting together because we’ve never got to do this before. Bill’s been a friend of mine for a while and we have a mutual interest in telomerase. As a matter of fact, he’s the specialist and I’m the entrepreneur. I’m the person trying to get these technologies to you.

And this morning the talk was great because we talked about an aging population, we talked about innovation, the problems with regulation. And all of that coming together is much of what I deal with every day.

So did you know that every day over 100,000 people die of aging? That’s a lot; that’s 3 million a month. It’s the biggest catastrophe; it’s the biggest epidemic on the globe.

But it’s not until recently that we’ve actually had the bandwidth to realize that in fact this is something really encumbering the human race. We’ve had our hands full. As a matter of fact just a couple of hundred years ago we didn’t predominantly die of aging at all, we died of infectious disease.

Humans naturally die of infectious disease; we don’t die of old age. Very few, very few like 1-3% of people used to die of old age. There were no names for those diseases.

So a cure for aging that sounds really science fictiony but it’s really science fact. As the video pointed out this has been done in animals, has been done in human tissue, and now we’re trying to do it in humans, and I’ll tell you why.

So these up here are the symptoms of biological aging or the diseases of biological aging. These are the things that we die of predominantly now in industrialized countries. As a matter of fact a third of this room is set to die of heart diseases, the other third is set to die of cancer, and the rest will be lucky enough to pick something else off of this map.

Sarcopenia will wreak havoc in all of our lives if we live over 65. That’s muscle loss over time. This leads to things like frailty and broken hips infirmary.

Right now we have a very reactive healthcare system. We haven’t been able to produce or generate many cures. As a matter of act the big bump in human lifespan is because of immunizations and antibiotics. That’s why we live this long to see these new prevailing diseases encumber our lives.

So how do we innovate in a very tough circumstansive regulation and start tackling these diseases now? These diseases are highly costly to society.

As a matter of fact, the costs are increasing every year of these aging diseases. So certainly we’d all like to mitigate disease and we’d like to live a long healthy life. But it’s not just solely self-importance at this point; it’s an economic crisis we’re headed towards.

So by the year 2020, this is coming up on us very quickly, there will be more people on the globe, the whole earth, over 65 and under 5. The under-5 year-olds go on to be 15 and then 25. They become the workforce for the 65 year-olds who turn 75 and 85 and up.

We actually can’t afford the cost, and most of these young children are not coming from our industrialized countries. The healthcare system looks like sometimes a hundred persons stacked on top of one 5-year-old that will be responsible for the cost associated.

And as a matter of fact by 2050 in the US it’s projected that at this rate 40% of the GDP will be spent on these aging diseases? What if we could get the health back for these people? What if we could keep them in the workforce? What if we could keep people viable and youthful and strong?

It’s a real game changer. If people are retiring at 65 but some people will live the maximum of 120 years, what will they live on? What will be their contribution? We can see here that the population over 100 years of age is going to increase by 1004%. And on one hand you might feel really great about that. You’re more likely to reach 100 than ever before in the history of mankind.

But you’re going to run into 100 being infirmed and sick and with a lot of debt. As a matter of fact we’ll spend 80% of everything we spend in healthcare in the last year of our life, and with this prolonging of what I would consider unhealthy lifespans due to the lack of therapeutics, that can actually be exacerbated up to 10 years.

So okay, we definitely want to solve this problem so what would curing aging be? Certainly we’re not talking about curing chronological aging; we want to talk about curing biological aging. And I’m going to turn to the smartest man in the room and hear from him.

Bill Andrews: Let me grab the mouse. So I’m going to be talking about telomeres and I want to first point out that the 1004% is not going to be because of the efforts of mine and Liz, that’s going to happen anyway. And the problem is is that everybody is going to be unhealthy because we’re not going to really be improving the health of the older people, the number one focus we want to do is we want to improve health and life extension as a side-effect of keeping people healthy.

So Telomeres is a brand new field of science, very exciting field. It’s mostly unrelated to everything else you’ve ever heard of, unless you already know about telomeres.

But what I want to do is I want to go through the basics of what telomeres are, and a lot of people already know this but I know from the cocktail hour the night before last and stuff like that, I did meet people that have no idea what these are. So I’m going to go over very carefully what telomeres are so people here is on the same page.

Telomeres are things that are very small inside of us. And they when we zoom in on a human being we first see that a human is made up of 100 trillion cells. And pretty much there’s going to be a recap of what you just saw on ‘The Immortalists’ movie.

Most of the theories on why we age say we age because these cells age. And so what we have to do is we have to find a way to prevent these cells from aging.

So most of the research that gets done in my company which is called Sierra Sciences, is to look at human cells growing in a petri dish and then this is later extrapolated to bigger things.

So we zoom in even further we see that every cell contains a nucleus as most of you already know. And the nucleus contains these blue thing called chromosomes or the genes are, they give us our hair color, eye color, everything like that.

But it’s made up of a long single-strand DNA molecule and when we look at one chromosome there are two DNA molecules and two arms: there’s a bottom arm and a top arm. And these arms each contain a very long strain of beads called DNA which typically is about 100 million bases in length, and bases are units of DNA.

And think of it like a really long shoelace except to fit inside of this chromosome is all clowered up like a slinky. Okay on your shoelaces you have these caps, and the caps protect your shoelaces from falling apart. Well chromosomes have the exact same thing, and they’re called telomeres. Telomeres shown here in yellow; those are what telomeres are.

Now as part of the DNA molecules wind up like a slinky. If we unravel that slinky in the telomere, we find that a telomere is about 15,000 bases in length whereas chromosome is about 100 million bases in length. So telomeres are pretty small things but they’re super super important. And they’re 15,000 bases at least when we were conceived.

And then here’s where all the troubles began. When your cells divide and each and every time your cells divide, the telomeres will get a little bit shorter. So there’s a lot of cell division that occurs from the time you’re a single-cell embryo to newborn baby that by that time your telomeres have shortened to 15,000 to 10,000 bases, a tremendous shortening of your telomeres.

And the problem doesn’t stop there. I mean it’s okay because it’s just like cutting the caps on your shoelaces in half, the shoelaces are still ok
ay at that point.

But they get shorter because we have to grow up, become adults and that’s going to take lots of cell divisions. So after years and years and years of cell division, your telomeres get shorter and shorter and shorter. And when telomeres get down to 5,000 bases, your cells lose the ability to function, they enter a phase called senescence. And when you have a lot of senescent cells that when you die of old age.

And let me go over that again. Conceived at 15,000 bases, born at 10,000 bases, die of old age at 5,000 bases, I think I said that right. And this is not a theory anymore, this is solid fact. My colleagues won the Nobel Prize in medicine for discovering this.

Every lab that does cell culture is aware of this problem. When telomeres get really short it induces something called the ‘Hayflick Limit.’ Or when scientists trying to work on human cells in a petri dish, they can’t work with them very long because every time the cells divide the telomeres get shorter. When they reach 5,000 bases they have to throw the cells away and get new cells. And so this is a big problem.

What’s really important is that even though I’ve been interested as said in the modulus, I’ve been interested in aging my entire life. I’ve always been uneasy, I just the twos and twos didn’t add up when I heard every theory about aging. Mostly related to the environment whether it’s internal or external.

Something was wrong because why do people who live on the north and south poles age at the same rate as people who live on the equator when the environments are very different? And why do cats and dogs age at different rates than humans when they’re in the same environment? The environment didn’t add … I’m sure environment has something to do with it, but it doesn’t explain the whole story.

I decided there had to be some kind of clock that’s ticking inside of us. And in 1992 I was attending a conference like this and I heard a scientist talk about the fact that telomeres get shorter, so I jumped on that bandwagon instantaneously.

Now it’s not just aging we’re talking about, as we said before we’re talking about health in general. But now every disease I’ve ever heard of has now been published in scientific peer review journals showing that the length of your telomeres affects your ability to 00:11:55 get them including things like the common cold.

And that’s because our immune system is very sensitive to telomere lengths, when we go under immune senescence it’s because the telomeres get short. Animal studies have now shown that you can make the immune system strong again by lengthening the telomeres.

But the point is is that every disease is affected by the length of your telomeres. And some of these have been shown to be affected by the telomeres, some have been still suggested, we don’t know a cause and effect yet.

But I believe that there’s a lot of benefits going to be gained when we figure out a way to lengthen telomeres in humans.

And I want to point out at this point we’re not really a medical device group of people, okay so I assume we’re here mostly for entertainment. But I do want to say that measuring the telomere lengths is something that’s going to be a big business pretty soon. And it already is several companies doing this.

I would say personally there’s got to be tremendous improvements in the system, but this will be a big business for medical devices I think in the future of being able to take a blood sample or any kind of tissue sample and measure the length of the telomeres.

So you all keep that in mind while I focus on trying to figure out how to lengthen them, oh that’d be great.

So the question I want to ask now is, and this might help in trying to figure out how to develop a device, why do telomeres shorten to begin with? Well I said every time your cells divide they get a little shorter. Why is that? Because people think it’s something chewing them away, but it’s actually mostly not that; there’s a little bit of that but it’s mostly not.

So what I want to do is I want to use an analogy. I could spend a lot of time talking about DNA replication and Okazaki fragments and earning 00:13:46 primers and things like that. But instead of talking about all that within a replication, I just want to use an analogy of a brick wall.

So you’ve got a cell and it’s going to divide to make two daughter cells. Well everything inside that cell has to be duplicated first so that the two daughter cells have everything that the parent cell had. Well that includes this long chromosome, this 100 million base chromosome.

So I want you to think of the … So the DNA has to replicated, duplicated or replicated. Think of the DNA replication as making a new row of bricks on a brick wall. Think of the top row bricks as the chromosome, the cell’s getting ready to divide so it’s got to make a new copy of itself.

And you’ve got a brick layer in the case of the cells called DNA polymerase I and it goes along and makes a copy. So let’s get rid of the other bricks and get rid of the cat, and now the brick layer comes along and he’s laying a new row of bricks.

And this happens throughout the chromosomes, it’s 100 million bases as I said. It’s got to be accurate; any inaccuracies will lead to mutations etc. And it’s just a long tedious process even though it’s going on in several places at the same time.

What we want to really see is what’s happening over at the very end of the chromosome at the telomere. And we find that there’s a very unfortunate decision that cells made and that was to put this brick layer on top of the wall because you can’t lay a brick in the last place you were standing and you fall off the wall.

Okay, what happened here now is this new chromosome is shorter, and this is why chromosomes get shorter every time a cell divides. It’s because the new chromosome you can’t duplicate the very tip of the chromosome. The DNA polymerase I literally falls off and leaves the tip of the chromosome bare, so the new chromosome is shorter.

This happens every time. Okay, the cell’s going to divide again, again the brick layer comes along and again the brick layer is going to fall off time after time. Telomeres are getting shorter and shorter and shorter.

And there’s absolutely nothing you can do about this yet, no matter how well you eat and exercise, do everything your doctors or yourselves tell you to do, you cannot stop this. I call this basal level telomere shortening, meaning this is a rate of telomere shortening that you can’t go slower than at the moment.

Of course that’s what me and Liz are trying to figure out what to solve. Okay so this is one thing.

Now if you are so inclined that you want to accelerate your aging, that’s easy. Anything related to an unhealthy lifestyle, psychological stress, obesity, smoking, lack of exercise, name it, all these things cause degeneration of free radicals that will actually cleave your DNA and make it shorten faster.

Now I’m going to come back to this but these are things that you want to do as much as you can to keep your telomeres long. You want to meditate, you want to destress, you want to quit smoking if you’re smoking, you want to lose weight, you want to take a lot of different things like anti-inflammatories, antioxidants. All these things without them will cause you to have accelerated telomere shortening.

This is where this enzyme Telomerase comes in. This is, when I first got in the field I discovered this enzyme, or my team discovered this enzyme called Telomerase. It’s an enzyme that will actually lengthen telomeres.

So since the middle the beginning of the 1990s we’ve been actually able to lengthen telomeres and show that telomere shortening wasn’t just the result of aging, it was the cause of aging because when we lengthened them human cells in a petri dish became younger by every me
thod of measurement imaginable.

I’ll come back to how we’re doing this but this is an important enzyme so I want you to, as I said in the modulus there’s two things: telomeres and Telomerase. Telomerase is the enzyme that lengthens the telomeres. This is just showing a cartoon, the Telomerase enzyme is shown as a factory here adding bases onto the very tip of the chromosome.

So you’ve got the lengthening and the shortening going on, so let’s go back to this brick-laying model and what is happening here is in cells that produce Telomerase that brick layer is still going to fall off at the end of the wall. But shortly thereafter like an angel Telomerase comes in and replaces that brick.

So this is happening inside of any cell that’s producing Telomerase. Now I want you to think about the fact that if you have low levels of Telomerase, then not that brick won’t be replaced every single time it’ll just be replaced some of the time. So telomere shortening will still occur but just at a shorter rate.

And then we’ve also found that if we actually produce lots of Telomerase inside of a cell, every brick gets replaced but even more so that angel starts making that new row of bricks longer than the old one. And that’s when age reversal starts occurring. That’s what we’ve seen in mice studies and human cells, and I’ll come back to that in a minute.

So I want you think of this as tug of war. You’ve got shortening and lengthening going on at the same time. So even though the cell’s producing Telomerase, that telomere still gets shorter but then Telomerase later comes in and re-lengthens it, so you’ve got this tug of war shortening and lengthening, shortening and lengthening. So you have the shorteners on one side and lengtheners on the other side.

Now in all of us the normal thing is we don’t have any lengtheners. Every cell in our body just has these shorteners so we have this tug of war going on that’s continually getting shorter and shorter. And shorteners win and we die of old age, or we get cancer or heart disease or all these other diseases that have been associated to length of your telomeres.

Now there are things that I’ve mentioned, antioxidants, Vitamin D, exercise, things like that. Well you can reduce the number of shorteners, but you can’t reduce it more than what I call that basal level telomere shortening where there’s still like two people pulling, slowing down the rate of shortening but it’s still occurring.

And it turns out that if you do, if you have the perfect genetics and live the healthiest of lifestyles, you can slow this down to about 50-100 bases per year. And that will allow you to live to be 125 but not any longer. There’s no way that, there’s no recorded, in recorded history that anybody has ever lived longer than 122 so far.

So you are still limited and your health declines. Even the 122-year-old person was very unhealthy. My goal is to make certain that we all are playing tennis, dancing and having the time of our lives when we’re 150 and older.

So that’s one way to reduce the shortening. Now the way that we are working on is to add lengtheners and that’s the enzyme Telomerase. It’s the only normal way to do it, there’s other procedures called ‘old pathways’ and things like that has have occurred in some type of cells. but the way we can do it without causing mutation through to our cells is do adding lengtheners and that’s by the enzyme Telomerase.

So there are products already in the market that do stimulate a little bit of Telomerase, and it’s essentially to having one lengthener against two shorteners. Well the shorteners are still winning. There isn’t a product on the market right now that will lengthen telomeres, cause the net result of your length. They do lengthen them but not enough to overcome the shortening.

So it just lowers the shortening rate down, which is still good, so I encourage everybody to do everything they can to get there. To decrease the number of shorteners and increase the number of lengtheners.

Now what my company is doing research on and Liz’s company is doing research on is trying to add more lengtheners. And eventually when we can get to a tie that should stop aging if humans are anything like their cells in a petri dish because it’s worked really well in human cells in a petri dish and some other things I’ll mention in a minute.

Now what we really like to do is add even another lengthener, and this way lengtheners win. The telomeres get longer and the shorteners lose, and this is when we expect to see age reversal.

And the only way so far that everybody, and any scientist in the whole world has been able to solve to be able to do this is through gene therapy. My company’s working on other approaches and hopefully one day we’ll have that there too, but right now the only way to get your telomeres longer is through a process of gene therapy.

And we’ve been doing gene therapy in my lab since the 1990s and we have 00:23:12 one case … So I’m not going to go into a lot of detail about all this stuff but I want to make it clear that anybody who’s doing anti-aging research consider these major milestones, major problems that have to be solved if you actually want to cure aging.

One is extend the Hayflick Limit. I could spend half an hour talking about what that is but it’s … We actually with gene therapy delivering Telomerase to cells actually have exceeded what’s called the Hayflick Limit which is a major milestone in aging. We did this actually in the 1990s.

We also reversed aging in human tissues. We grew human skin on the back of a mouse and treated it with Telomerase and found that the skin became younger in every way imaginable, every method of measurement imaginable.

Dr. Ron DePinho at Harvard using gene therapy turned extremely old mice into young mice. You can Google this you can find … In fact there’s a lot of information I’ll be talking about more where you can find more information about this.

But this has actually be successful so far. And what was surprising in all this he was able to show that every other theory about aging ended up being reversed just by lengthening the telomeres. Oxidative stress, mitochondria dysfunction, you name it, all these other things disappeared. He called it telomeres are the kingpin.

Now Dr. Ron DePinho is not just any kind of cracker 00:24:44 because the field of anti-aging is just filled with them, he’s the head of MD Anderson at Texas. He’s a very respectable scientist.

So now he’s done … What we and he had done all this but nothing else has ever done this. You keep hearing theories about people are saying they’ve cured aging but all they’ve is like increase the energy of the mitochondria inside of a mouse cell or something like that. That’s not reversing aging, we’re not reversing aging until we see a 90-year-old person walk in a room here and look 24 and act 24 again. That’s when we’ve cured aging; that’s what Liz and I are trying to do. So nothing else has ever done this.

And with that point Liz, tell us how you’re going to make us all benefit from this.

Liz Parrish: Okay. So let’s talk a little bit about what gene therapy is. Is anyone familiar with gene therapy? Yeah it’s been in the news a lot more lately than it had been for quite a few years. With gene therapy today we take a human gene, our target gene, in this case the gene that creates Telomerase and we put it into a vector. And that vector then is injected into you and it delivers the genes to the cell, and then the cell starts making the target enzyme, the Telomerase.

And so it’s a very elegant science. This is the wave of the future. I believe that this is the how we will get most of our medicine in the future. Much like immunizations and antibiotics we’ll be going for gene-boosting therapies and they will be real preventative medicine.

So how are we going to do this? This
is my company’s logo here, my company is BioViva and we’re a gene therapy company that treats biological aging as a disease. We are teaming up with Bill at Sierra Sciences and his many years of science behind this therapy. Actually essentially founding the science behind this therapy.

And Chase Life Extension Foundation, these are colleagues of ours in New Zealand. And they are very ambitious and motivated to help us create the technology and the platform of the future where you can come to get therapeutics.

We are coming together to create BioViva FIJI. So this is our new strategy. For opening a clinic to the world to give them access to these therapeutics. This is a place where we can run trials on Telomerase-inducing gene therapies and see how they mitigate the diseases of aging and hopefully restore the human body to a youthful state. And move the therapeutics into consensual care and preventative medicine.

So today gene therapy is raising millions of dollars and there’s actually no wonder why. Pharmaceutical to-date in the last 50 years have created 97% of amelioration of diseases through their products. That means we’re just treating symptoms.

The last speaker was talking about a reactive healthcare system. We wait until people get sick and we give them drugs that only moderately help their disease. As a matter of fact the efficacy of most drugs that go through the FDA is rather low, with some of our most promising cancer therapies only affecting 30% of the population.

I don’t have that slide on this reel but I do have it if you want to see it. 97% of non-cures and yet in the last year we have six potential cures for disease in the pipeline using gene therapy; in one year. We find the gene, we target it, we put it in the cell. The cell becomes the drug factory creating what you need to be healthy.

And right now most of the drugs going through are actually for treating cancer, which is fantastic 42% of them, and the rest are generally for monogenic orphan diseases. Monogenic means that there’s one gene that’s the target issue, like Adrenoleukodystrophy. This is the one that says “Lorenzo’s Oil” Disease.

This is a disease in young males about one in every 21,000, but it’s fatal. And by delivering the proper gene, these kids live. It’s very exciting. This industry by the year 2025 will be an $11 billion industry in the US alone. It’s fantastic. The future looks bright, the future looks beautiful.

A lot of the questions that I get is doesn’t Telomerase cause cancer. And of course I don’t believe that it does but we’re going to again defer to the expert.

Bill Andrews: Thank you. Let me start off with I think one of the main reasons why there are people out there that think that Telomerase causes cancer is because when I, my team first discovered Telomerase we first put it into human cells, skin cells in a petri dish and showed that they got younger.

But we also put what’s called the antisense into cancer cells and showed that we could kill every cancer cell by causing it to die of old age. I was actually awarded second place for National Inventor of the Year for that discovery.

But when people started hearing this they started saying, “Well if inhibiting Telomerase kills cancer cells, then Telomerase must be the cause of that cancer.”

But it’s not, and I can actually spend an hour talking about this. And I do speak at cancer conferences and stuff like that and go over this great detail with doctors explaining exactly this. And believe me every one of them knows after I get done talking that Telomerase doesn’t cause cancer.

But I just want to quickly just summarize a few key relevant points. There is no clinical data whatsoever published anywhere that shows that Telomerase causes cancer. The data all shows that lack of Telomerase causes cancer.

Where do we get cancer? And it’s because our telomeres get really short and when our telomeres get really short it induces chromosomal rearrangements. We can have tens of hundreds of mutations, rearrangements in every cell in a cancer population because of the short telomeres. This has been published a lot in 2015 and 2016 that short telomeres cause all the mutations that lead to cancer. So keeping telomeres long is the really important thing.

And let me just say that for every study that’s ever suggested … In fact no study, except maybe sometimes you read in the discussion section where they’ll just refer to an old study, no study has been published that even suggests that Telomerase causes cancer since before 2005. But for every study that suggests that Telomerase might cause cancer, there are hundreds of studies that show that the lack of Telomerase does cause cancer.

And this is something so we now know and there’s lots of literature supporting that … I’m bringing this up because some of you may have heard somebody say Telomerase causes cancer. I want to tell you there’s no data, nothing suggesting, and actually all the data suggests exactly the opposite. If we produced Telomerase inside of our cells we’re going to decrease our risk of getting cancer, we’re going to increase our ability to fight cancer if we already have it by lengthening the telomeres in our immune cells.

And we’re also going to be able to allow our bodies or our cancers to not adapt to any kind of change. When you treat a cancer with something like a chemotherapy or whatever kind of thing, with all these mutations occurring, one or two of those cells are going to figure out a way to survive whatever you’re hitting them with. But if you keep the telomeres long they won’t.

So three things: one is it decreases the risk of getting cancer, increases your body’s ability to fight the cancer, and increases your chances that the cancer will not come back.

So these are really really important and …

So do you want to talk about anything else because I can talk hours on this one? Do you want to talk about anything that people say we shouldn’t be doing this?

Liz Parrish: I just think that there’s been a lot of critiques and concerns about healthy lifespans. Our job is health, the other issues we certainly can solve with time. I think that that’s most of what I want to say. Of course I want you to consider your most important currency, one that you’ve probably not considered before and that is time and we hope to lengthen yours; your lengthy time here on earth.

Let’s see, what sort of information do we have?

Bill Andrews: Well there are people that say things like, “Won’t the world be overpopulated if we cure aging?” And then there’s others that say, “How will the young ever get jobs if the old never get weak and feeble? The old people they’re just going to get better and better and better because they’re still going to be really young, and the young will never be able to get jobs.”

There’s all these kind of problems. There’s also people that are saying that religious groups might be very opposed to this. Turns out that the Catholic Church actually published a chapter in my book supporting it, saying this is part of what they want to see happen.

But there’s a lot of these kind of things going on, and I don’t know, my personal belief on the thing is that if we win, let’s not say if, when we have a cure for aging, 100 years later the world’s suffering from every kind of problem that you can imagine occurring, nobody’s going to say, “Let’s vote to ban the cure for aging.”

Because the cure for aging is going to be good. And if it’s going to be good then I’m thinking it’s going to be good now. It’s worth doing. We already have major problems and a lot of the problems like what Liz was talking about something called the Silver Tsunami where we’re just getting a lot of old people.

Those are really big problems because who’s going to care for these people? I think the number one profe
ssion 30 years from now is going to be taking care of the old people unless Liz and I succeed at what we’re doing, when we succeed at what we’re doing.

Liz Parrish: Exactly.

Bill Andrews: So to learn more I do have a book called ‘Curing Aging’, it’s available on Amazon.com. It mostly is answering all the kinds of questions that people ask when we get done talking.

You can also watch ‘The Immortalists’ as you saw, it’s actually like two hours long I think. It sort of goes into a lot more detail than what you just saw.

And then there’s our individual websites that you can go to: BioViva-Science.com and Sierrasci.com to learn more.

So thank you very much.

Liz Parrish: Thank you.

Bill Andrews: If you have any questions.


Joe Hage: Your first review comes from my mom who found you fascinating, no offense Joe but yeah she was all over this.

So having seen your movie and getting to know you a bit, I know that funding has been challenging for you with all this promise. Can you talk to us a little bit about that struggle and dot dot dot.

Bill Andrews: Let me go first here. You know, we were very well-funded before the 2008 economic crisis and we made major progress and stuff like that. This gene therapy is coming along really well but it’s not going to be affordable by everybody. And my company’s mission is to find something that’s affordable by everybody and which would be a small molecule of drug or natural product.

And so we’ve been struggling trying to do that but since 2008 it’s been really difficult. We actually spent $33 million on our research up until 2008, and then we haven’t gotten any investors. We’ve actually taken some of the discoveries that we had, licensed them to other companies and they turn them into products.

And we get our funding now from the royalties from that, but it’s not enough to get ourselves back to where we were before 2008. And I’ll tell you, we would be one year away from having a pill ready for people to take that would actually lengthen telomeres and then we can see what happens within a year after we get the amount of funding that we need.

But you’re the entrepreneur, you tell more about it because you’re more really closer to the problem.

Liz Parrish: Right, so we brought in early money very quickly and then we shut down our search for money and we ran the first human test with these therapeutics. As a matter of fact I was the first person to take a what would be considered a lower dose of the human telomeres activating gene therapy and a myostatin inhibitor.

I took two gene therapies to treat biological aging to prove that they were safe and that we were ready to embark on treating the world.

We have now come back up, we’ve breached, and we’ve partnered with a company called Deep Knowledge Life Sciences who will be our funding mechanism. And there’s a lot of interest in what we’re doing now because we’ve certainly proved some amount of safety. I certainly have been continue to be in fantastic health.

We have some preliminary data that we’re weighing out the benefits of Spectrocell imaging of my white blood cells that then show potential small increase in telomere length. So this is very exciting news for us and it has created a big buzz but of course we want to deliver on the promise and not just talk about it.

So we have partnered with DKLS. And the second thing that we’ve done is I’ve been globetrotting around the world and this kind of comes back to the first speaker. We’ve been going around the world with world leaders, a global consortium of top personage, even people from the UK government that are trying to help companies like mine find a regulatory zone where we can prove safety and efficacy in short order and get these therapeutics to humans.

This is it’s called the Global Longevity Initiative, the GLI, and we have met with presidents and prime ministers and we continue that march. And these people are actually very receptive. They want to be innovative companies and innovative countries that actually bring therapeutics to the world that show the biggest promise over anything that we’ve offered before.

Of course we would like to start in compassionate care and then move back to preventative treatments. So we have a game plan. We’re very hopeful about it, and DKLS is determined to help us as a company find the investment that drives the costs down on these therapeutics so we can treat more of the world within the next five years.

So that’s a very long answer to a very short question.

Audience 1 (Male): So hi, it was very fascinating. I just have a technical question about how you are getting your genes into the cells and what do you need to get it into all the cells. Otherwise I expect you would get some old cells and some young cells and what is that going to look like.

Liz Parrish: Right, so Bill can you answer the science questions?

Bill Andrews: Well we already have some young cells and old cells. Everybody because of the fact that only one chromosome, the new chromosome gets shorter and the older one stays longer means as a result you’re going to have a whole population mixture of different things. So you’ve got young cells and old cells in every person, it’s just the percentage of old cells over the young cells that really makes the difference.

So our goal is to get every cell infected and hopefully delivery through the blood is the best way to do that. But even if we don’t we think that we’ll still get most of them and the old cells will end up dying and the young cells will take over.

Then there’s also of course the cells that don’t divide, those cells actually do have telomeres shortening too mostly by the accelerated telomeres length measurement that 00:40:55 saw. But they’re more affected like the nerve cells they’re affected by Schwann cells or other types of glial cells. They protect them, but those cells do divide and those are affected by telomeres length, but they’ll die off and other cells replace those as long as we have the telomeres long in some of the cells.

Jon Speer: I appreciate all the details and the information that you shared, it just really is fascinating. And you touched on it a little bit but the socio-economic factors that the problem you’re trying to solve that it has on jobs, you mentioned that.

But also things like social security and just overpopulation and things like that. Can you go into a little more depth into that because I can imagine that would be an area of a lot of resistance too.

Liz Parrish: Yeah absolutely, it is very important and on this presentation we didn’t really talk about that and we do have many of those answers because it’s part of being in this profession.

There’s not only the savings of keeping people working and active, there’s actually the savings of mitigating these diseases. So the US government would save $4 trillion in one presidential term by curing these diseases. So it’s kind of money in the bank that’s just not having to be delved out to begin with.

And I believe that Bill also addresses this in his book that the economic savings on mitigating the diseases of aging could create actually sabbatical, a 10-year sabbatical in the mid-term of your life that the government could pay you to have to reeducate, to relearn or go and travel the world and be ready for that second half of life work that you’re going to be doing. So there are a lot of benefits.

Also we are working into a burgeoning society that’s looking at doing very many new things, space travel and things like that that seem like a technology of tomorrow. Where companies are alrea
dy being funded for mining asteroids and things like that. We’re looking at workforces to start to go to Mars. It seems a long ways off but it will be here before you know it.

I’d like to talk about the overpopulation issue because in 1960 the club of Rome got together and they decided that by the year 2000 we’d actually be eating each other.

This didn’t happen and as a matter of fact we’re coming in to more abundance with technology as it comes, but they created a catastrophe scenario for the human race but they were something that they overlooked and actually none of us could see it. And now we do we see it actually very clearly.

It doesn’t matter where on the earth a population or culture is, it doesn’t matter if they’re in the middle of the jungle and you’ll never meet them or they’re your next-door neighbor. As lifespan increases birthrates go down, everywhere on the earth. This is reflected in every single place.

There’s a beautiful graph again that I don’t have to show you but I can get you if you’re interested, and it shows the decline in birthrate over the last several about a hundred years; it’s staggering. This is a natural consequence of living longer we have less children.

And of course I love children; I actually got involved in BioViva to cure childhood disease. I didn’t know about things like longevity science when I got started, but this creates a world where maybe every child would have a better opportunity in the future.

So that’s just a few things touched on. People will certainly still have accidents, infections disease will certainly still nail our populations read hard. So when I was talking about how we used to die, how we naturally die as a society is before the age of 30 of infectious disease. That was about 90% of what happened to everyone outside of accidents and the very few that died of old age.

In 2010 we got infectious disease down to 3%; only 3% of the population dying from it. It’s considered so abnormal, and we’d just like to take the next step in science and that is to knock off the next big killers, reduce the amount of suffering.

And I’m sure that many of these problems that will arise from this that many of them that we already have will be solved with more time, with more manpower.

As a matter almost every big industrial revolution did not just happen by human ingenuity, it actually happened by lifespan. Did you know that? As we increased our lifespan we went into the first big industrial revolution that changed everything.

So take that into consideration and hopefully we’ll create a better world.

I see that Joe is like, “Please stop.”

Joe Hage: Well we do, I regret that more hands went up than we can accommodate so we’ll take one more question from David Cassak.

David Cassak: Well maybe this is not the best question to ask. I was just wondering your lab work how are you measuring the effect of practically of reversing of aging. Do all organs age at the same rate? And might we wind up in a society where brains deteriorate fast … The physical body reverses aging but brains don’t. Are there long-term implications? Do you have any evidence that everything in the body will reverse aging at the same rate?

Liz Parrish: What’s interesting is of course we are interested in aging all the way through. And of course most of the questions we get are from more of the vanity industry of anti-aging. A lot of people say, “Will my skin look younger? Will my hair not be as gray?”

And it’s really important, this is a very important conversation because we want you to be youthful all the way through. We do have a plan to embark on. This would be almost like the 100,000 Genome Project. This would be a plan where we actually MRI our patients before and after treatment.

We create a database of thousands of patients of all very ages because there’s actually biomarkers just in that. We obviously do blood work, we do telomeres length testing, we have a protocol for all of that, for kidney function and body function.

But believe it or not whole-body imaging of what the organs look like, what the brain looks like, I have a fantastic slide of a 27-year-old with what we consider a healthy brain and next to an 87-year-old who doesn’t even have any signs of dementia and the brain is different.

So yes, we want to go through the whole, slice through the whole body and see what looks like. And that was what Bill was talking about with Ron DePinho, the mice did show increase in every organ including brain size.

Joe Hage: Bill, some closing thoughts.

Bill Andrews: I just want to say I want to answer everybody’s questions, I usually am the last person to leave the room, but I won’t be able to right now because of time. But I do have business cards, if anybody has questions you can contact me but I’ll be here for a few hours too but I don’t want you to come and ask me questions when somebody else is speaking.

So get my business card from me and you can contact me I’ll answer your question.

Joe Hage: Very generous with his time. Dr. Bill Andrews, Liz Parrish.

Liz Parrish: Thanks.