She Says Gene Therapy Made Her 20 Years Younger

Lightly edited from the video captions for readability.

Gary: Welcome to the 200 Year Life Project. I’m Gary Leland, I’m 71 years old, and I’m dead serious about becoming the first person to reach 200. Today I’m excited to bring on our first guest. We’ve done a lot of shows now if you’ve been following us, but this is our first guest. I had several people to choose from, and I chose Elizabeth Parrish first because I thought her story was so exciting, and she’s so pleasant to talk to. Elizabeth, thanks for coming on the show.

Liz Parrish: Thanks for having me. It’s nice to meet again, even though it’s just over the computer.

Gary: Even though it’s just over the computer. Well, I felt like we made a good tie between each other. I enjoyed talking to you, and your information was so great. I’m interviewing all the speakers who were at DaVinci 50, but I wanted to interview you first because I found your story so amazing, and what you’re doing is so amazing. Let me tell everybody a little bit about you before we get going, though.

Gary: Elizabeth is someone who doesn’t just talk about radical longevity, she puts it in her own veins. She’s the founder and CEO of BioViva, a company dedicated to the extension of healthy human lifespan through gene therapy. And in 2015 — I’m hoping I have all this right, you can correct me if I’m not — at the age of 44, she made history by becoming the first person on the planet to undergo gene therapy specifically designed for reversing aging, by testing it on herself before going to anyone else. And the results were stunning, from what she’s told me. Your telomeres lengthened by roughly 9%, your triglycerides dropped by half, and your biological markers suggested you had rolled back approximately 20 years of aging. And 10 years later, there are no specific side effects that she’s told me about, and she’s living the life. Am I pretty right on everything I said there?

Liz Parrish: That’s true. I’ve done a few more gene therapies since 2015, but that’s true. I took two gene therapies: one to lengthen my telomeres, to increase cellular divisions to get you to, let’s say, the 200 age range, and the other one was to increase muscle mass.

Gary: So you’ve done three now? Is that the deal? How many gene therapies?

Liz Parrish: Twelve.

Gary: You had to go out of the country to do the first one, I think you said. Do you still have that issue?

Liz Parrish: Yeah, absolutely. These are not approved by the US FDA. Approval takes about $50 million per gene, which is ridiculous, because the animal research that’s required is not predictive of how the gene therapies will work in a human. We feel that humans are the best model organism, and all the basic research in animals has already been done on these gene therapies.

Gary: So do you go to a regular doctor, and when they see your blood work, do they just go, “What in the hell is happening here?”

Liz Parrish: My doctor is a functional medicine doctor. She’s aware of the gene therapies I’ve taken, and sometimes she just throws my blood work results at me. She usually comments, and she says, basically, unsurprisingly I have almost no inflammation in my body, and my markers look great. So that’s been fantastic. It’s nice to have a doctor that you can confide in and let them know what you’re doing in your free time.

Gary: Very much so, especially in your situation, I guess. Explain gene therapy to me like I’m a kind of smart 10-year-old, for viewers out there who might not be familiar with this.

Liz Parrish: Gene therapy is the addition, deletion, or editing of a gene in the human genome. How we do gene therapy at our company is we take a therapeutic gene — a gene known to make humans healthier — and we deliver it to the nucleus of the cell, but we don’t modify your human chromosome. We leave it alone. Other gene therapies you’ve heard of, things like CRISPR, are delivered just like our gene therapies are, but they have the ability to modify the human chromosome. We can also use gene therapy to delete genes out of your chromosome, and we also do that with CRISPR. So it’s the modification of the genes within the nucleus of the cell.

Gary: Okay. When you started, you targeted two things: myostatin inhibition for muscle, and telomere lengthening. Why those two first?

Liz Parrish: There’s a gene with a big name, telomerase reverse transcriptase. Remember, all the genes in your chromosomes code for proteins, enzymes, or hormones, and that’s why you have the traits that you have. First of all, your whole human genome makes you identify as human, and then the differences in the way that your genes are transcribed are the differences between people — our fingerprints, our eye color, our hair color, and our disease risk.

Liz Parrish: The reason we chose the first two gene therapies is that one of the biggest limits to human lifespan beyond 120 would be the rate of shortening of our telomeres. Telomeres are the caps at the ends of every chromosome, and when those telomeres get short, our cells can no longer divide. We and 23 other species are limited by how fast our telomeres shorten. Dogs and cats and other organisms are also limited by telomere shortening, and that is what defines the absolute longest lifespan of the organism. Many of us die long before we get to the longest possible lifespan of humans because of our lifestyle. Lifestyle and our genes can affect us here, but our absolute lifespan would be about 120 if we were most conservative with the telomere shortening at the ends of the chromosomes. What gene therapy gives us the ability to do is lengthen the telomeres at the ends of the chromosomes, so that we have more cellular divisions.

Liz Parrish: The other gene therapy is a gene called follistatin. That one already had some safety and efficacy work done on it with children with Becker muscular dystrophy, and it increases muscle mass. Now, it does not cure muscular dystrophy. In muscular dystrophy, a gene called dystrophin is related to the breaking of the muscles. Children who don’t have dystrophin don’t have the elasticity in their muscles, and when they use their muscles, their muscles break, and eventually heart tissue can break as well. Follistatin increases muscle mass. So it did work in these children to make it so they could walk farther, and they did have bigger muscles, but it didn’t solve the dystrophin disorder. But it was considered safe and effective for increasing muscle mass. The decrease in muscle mass, eventually called sarcopenia, is the clinical diagnosis when we get older and frail. So we repurposed this gene therapy for an aging population. We felt the two together were very synergistic: one that was going to push muscle growth, which pushes cellular division, and the other one that was going to take care of the cellular division problem.

Gary: From my understanding, critics said your early telomere results were within the margin of error, and then you published peer-reviewed data in 2022 about that. What did that show?

Liz Parrish: Within 6 months of the gene therapy, my telomeres had lengthened by 20 years. If that’s within the margin of error of any of those companies, that would mean those companies were absolutely worthless. So, number one, they would have been stepping on their own toes. I think the world of these scientists was interested in stopping these tests, because they had hung their hat on the idea that lengthening telomeres could cure all of aging, and we were about to show whether or not it could. So I think they wanted to discredit what we were doing. Since the first telomere test and the last telomere test, my telomeres have lengthened by over 5 years for every year that I have lived, which is well outside of their margin of error. And we have continued to use those companies and other companies. At times we’ve used up to three different third-party companies to ensure that these telomere lengths are accurate. One of the last companies to measure my telomeres, in Israel, said that my telomere lengths were those of an early 20-year-old.

Liz Parrish: But I have to give you the disclaimer: the only cells that we test are the white blood cells. So that does not mean that the telomere lengthening has reached every area of my body, and we continue to learn how to redose that therapy to layer it into the system. So yeah, we had a big outpouring from scientists and people who make their money other ways than saving lives, and our response to that was, we’ll wait and see. If that’s within your margin of error, your test has a major problem.

Gary: For sure. I mean, 20 years is a big deal. I’ll take that right now.

Liz Parrish: That’s life or death for most people who are over a certain age.

Gary: Yeah, I’ll take that in a heartbeat, and I wouldn’t do too much complaining about it. You said a few minutes ago that, basically, the longest a person can live because of their telomeres shortening would be about 120 years. So that means you now have a chance to go 140 years?

Liz Parrish: Or more. When we do the gene therapy in a dish, it’s called ex vivo or in vitro gene therapy — vitro being the dish, let’s just picture it that way. When we do the gene therapy on those cells, they can divide an enormous number of times, and it’s called immortalizing a cell, because its ability to break past normal cellular divisions lies all within those telomeres. So if we were able to give people gene therapies, and they took these gene therapies maybe every 5 years or so, as long as we can keep those telomeres long, there may not be a bottleneck to cellular division. Now, there will be other problems that we have to solve. Lifespan isn’t all we want; we want health span, too. So we need to make sure that the rest of the cellular function is there.

Gary: Right. When I tell people that I want to live to 200, which I think is possible — I know that sounds crazy to a lot of people — what they usually do is laugh, right in my face, and I have to go, “No, I’m real serious.” And then they say, “Well, I wouldn’t want to live to 200.” And I go, “Why?” And they say, “Well, I wouldn’t want to be in a walker or wheelchair that long.” And I’m like, I don’t plan on dragging a wheelchair with me. The health span is a vital part of that. Who wants to live all sickly for 50 years or 100 years?

Liz Parrish: People who generally want to live longer are people who have been diagnosed with their last diagnosis. So I take it very seriously when other people put limits on your or my or my children’s potential lifespan, because what they’re saying is that at some point they think life isn’t worth living. But if we can make you healthy and keep you healthy, then it would be worth living. And if they want to take a bet and roll the dice and decide to die at a certain age, when people may be well surpassing them in good health, let them do that. I’m certain that won’t be their choice as the science is proven out.

Gary: I think you’re correct. Let me ask a question about what I said a second ago. You said a person could live to about 120, and you’ve been able to add 20 years’ worth of time, basically, because you added 20 years to your telomeres. So in another 20 or 30 years, could you do the same gene therapy and add another 20? Could you keep doing that same therapy every 20 years, lengthening your telomeres over and over and over?

Liz Parrish: Well, I think that would be the point. I have done that gene therapy more than once. I did it a second time, and you’ll see it on that published paper — you’ll see a jump in my telomeres that definitively happened right after the therapy, and then the telomeres continue to slowly lengthen. So I think that’s the key to these therapies, until we can target every cell in the body.

Liz Parrish: Let’s differentiate gene therapies. There are gene therapies, like lengthening telomeres, that have to be put into every cell of your body, and our technology is limited. Today’s best technology cannot get a gene into every cell of your body. There are cells that sit at the ends of very small capillaries and things like that. And the gene therapy is absorbed and excreted from your body rather quickly after being administered — your liver takes it up, your lungs take it up, your kidneys flush it out. So we’re still learning how to break that bottleneck. But there are other gene therapies where you do not need to get into every cell, and that’s things like follistatin and Klotho. Those gene therapies you could just put in your muscles, here and here, and you would have a full-system benefit from them. So there are two different types of therapies, autocrine and paracrine. One of them does not share the protein outside of the cell, and that’s a limit of the therapy itself. The other one does share the protein outside of the cell and benefits the whole body, even if a smaller area is targeted.

Gary: Okay. Let’s move on to BioViva. Where is BioViva today compared to where you were in 2015? How far has the science moved?

Liz Parrish: I think that we are actually the fastest-moving gene therapy company in the world. We just came out with a dual gene therapy for liver regeneration, and it’s already in two people, and that was this year. And we have patents. But as far as how fast we’ve moved, I think we’ve moved incredibly slowly. When people look at us, they say, “Wow, you guys are like biohackers. You’re moving so fast.” It’s really not true. It took us two years to decide to use the first two gene therapies in my body in 2015. It took five more years to make the dementia therapy that we published on and got the patent for this year — that paper came out around 2021–22. It took us six more years to do the next two gene therapies to regenerate the human liver. So we are working at a pace where, if you had institutions and largely funded companies, you should be able to work at three or four times that pace. But we are the fastest-moving gene therapy company in the entire world, working on a fraction of the resources, just moving on a humanitarian mission to move these technologies as fast as we can with as little as we have.

Gary: Wow. So it’s not fast enough, in your opinion, but that’s just how much time it takes?

Liz Parrish: No. When the story launched in 2015 that I had taken the first two gene therapies to treat biological aging — that’s over 11 years ago — people rushed to us to help solve the aging problem. And since then, 36 million people have died of aging every year, because we need funding, we need support, and we need advanced research in larger institutes. And the system has been vastly resistant to that, because it’s a pharmaceutical system. Going to this system and asking it to cure disease is like going to big oil and asking it to put in renewable energy. It’s not their business.

Gary: Like saying put in electric cars.

Liz Parrish: Exactly. So we have moved as fast as we possibly can on a humanitarian mission to help as many people as possible. What we’ve done is quite amazing, but what we could do would be exponential.

Gary: I believe when you were talking at DaVinci 50, you said you’ve had test subjects — you aren’t the only person now who’s done this — but it’s super expensive at the moment. For some reason I’m thinking you said like a million dollars to do this, but I could just be daydreaming.

Liz Parrish: It’s less than that. Over 300 people have participated through licensing partners. As a US company, we cannot treat patients, but we can license the technology out to where they can legally treat patients, and over 300 patients have been treated. It runs under half a million for a full large-dose gene therapy, but most people want multiple gene therapies, so that can climb in price quickly. Right now we’re opening up funding to buy a GMP facility that would be able to make a large-dose GMP gene therapy for $20,000. I know that sounds like a lot to people, but for us that’s almost a miracle.

Gary: Well, compared to $500,000, it sounds like it’s on sale to me.

Liz Parrish: Yeah, and if you look at the US-approved therapies, they run from two to seven million dollars. So we’ve already gotten the prices way down. With this, we might be at a point where even insurers would start approving unapproved therapies for payer use, meaning insurance companies could start covering them, because there would be enough human data to make them a better alternative to other therapies.

Gary: If you were not on your deathbed, but say you were pretty sick and you knew you had a year or so left, would this help in that situation, or is this something you have to take while you’re still healthy?

Liz Parrish: We would hope that it would help. Our licensing partners are open to all scenarios, because people with all different degrees of health concerns need access. I believe that the best use of the medicine in the future will be prophylactic. It’ll be used like an immunization after the age of 45, and you’ll start getting your gene therapies to protect you from the ravages of time.

Gary: Okay. What do you think is the single most exciting thing you’re working on? Because it sounds like you’re working on a lot.

Liz Parrish: Right now we’re really excited about liver regeneration, because it would qualify a lot of people who otherwise could not get access because they have fatty liver disease. It also could be a replacement for GLP-1 agonists, which we greatly need. People are going to have muscle loss and bone loss from these extreme diet solutions, and we would like to be able to meet that. But I really can’t say that one gene is more important than another. We can’t really pick a team; we have to realize all the genes are on the same team to treat aging. And obviously raising the money to get the cost of the gene therapies down is super exciting, so that more people can access them. That would probably be up there with something I would consider very, very important.

Gary: That sounds pretty exciting to me. I know you don’t know a date, but is that a 2-year deal or a 10-year deal?

Liz Parrish: If we could get the right investor, we could have the affordable gene therapies within a year of making the investment. So it would actually work quite quickly.

Gary: Okay, so once you get the capital, you can do it quickly. Right now AI is into everything — literally everything — and it’s only been out a short while. I don’t know where it’s going to be in 10 years. Is AI helping accelerate what you’re doing?

Liz Parrish: We have built a system of all known gene therapies, and we’re building a system that incorporates all of the GWAS data, and then we will build a system to interpolate human genomes person by person to create precision medicine. So we’re actually working on our own AI system so that we can more quickly identify the combinatorial gene therapies each person would need to treat their biggest disease risk states and treat biological aging. That’s been exciting. And in order to do that, we had to prove that we could build an AI system. You might remember I shared something called trialatlas.ai.

Gary: Yes, I’ve gone on that several times.

Liz Parrish: That just helps people get access to clinical trials, which could be life-saving in the interim while we bring the prices of these gene therapies down and get more safety data.

Gary: And that’s at trialatlas.com, right?

Liz Parrish: Dot AI.

Gary: Dot AI, okay. That was pretty good.

Liz Parrish: Yeah, it is, and it showed us what we could do. Now we’re doing internal LLMs and a whole locked-down system so that researchers will also be able to access the ability to create combinatorial gene therapies. We never started with a single gene therapy; we were always a combinatorial gene therapy company, and that’s what is going to be important to treat complex disease. In the world of monogenic disease — mono meaning one, genic meaning genetic, people with a single gene mutation — there are a lot of treatments out there now, 13 approved treatments through the FDA to treat those conditions. That was a great testing ground, but in order to treat biological aging at the core level, we need combinatorial gene therapies. So maybe this can take that first two years, the next five years, and the next six years and turn it into a six-month on-ramp. We’ll still have to double-verify with human eyes that what it’s come up with would be beneficial to humans, but having that system is going to help us a lot.

Gary: Got you. Let me tell you — because of AI, when that came out last year, that’s when I started on this 200-year deal. I always thought my kids, who are 38 and 39, would live a long time because of technology. But I thought Kathy and I had completely missed the wagon. We were the generation before longevity came out. But with AI, I thought that changed the speed at which stuff would come out. And I’ve heard this repeated by other people now, and every time, Kathy nudges me and goes, “Hey, that’s what you’ve been saying.” I feel like I’m not going to go from the average lifespan of 80 or whatever straight to 200, but it would come in waves. A wave comes through and all of a sudden it goes from 83 to 103. And then in that 20 years, stuff happens that takes you from 103 to 120. So it’s really important to get on that first wave, because if you get on the wave, then it’s like surfing. You can go a long ways. But if you don’t get on the wave, the wave’s gone by, and you have to wait for another one and hope a good wave comes by. Is there anything to what I’m saying, or am I just talking from crazy town? What do you think of my hypothesis?

Liz Parrish: I think that’s absolutely true. I know that Aubrey de Grey also said it — someone said it before him, I can’t remember who — but there’s something called longevity escape velocity, and that just means that you live long enough to catch the ultimate wave into exponential longevity. It probably sounds counterintuitive to some people, because people used to loathe birthdays, but we want you to have as many birthdays as possible — in good health. And actually, the data really doesn’t show that you can live in bad health very long. Just to put that out there for people watching who think that ultimate longevity is just living longer in bad health: the data does not show that you can live in bad health for very long. So if you’re in bad health now, you need to do something about it. The data shows that in good health, you can live a long time. And that’s what we’re trying to do with genetics.

Gary: That has been my thought also — not that I’m a scientist or anyone smart. I’m just an old boomer having a good time trying to live a long life. But I had to quit drinking when I saw how bad drinking was for you. I quit smoking years and years ago, but I quit drinking now. I work out every morning. I’m not pumping 500-pound weights, but I’m doing exercises — things I never did before. And I was telling somebody the other day, if people knew how much better it feels to be healthy than unhealthy, they would all get on the wagon automatically. They just don’t know, I think. And it doesn’t take that much. I don’t really do that much, but it’s a lot of little things I need to do. So you need to stay healthy if you want to have a shot at getting on this first wave.

Liz Parrish: Yeah, and you’re doing everything right. The data would tell us that lifting really heavy weights is bad for your heart. You do not want to blow your heart valves out, and we’ve seen that time and time again with extreme athletes. Keeping your muscles active and keeping your body active are important, but high-impact sports are not necessarily great. Being super skinny is not great for longevity. Being grossly obese is not great for longevity. You want to find that middle spot. Certainly one of the greatest expansions in lifespan you can get: if you want to expand lifespan, you do not want to smoke or drink alcohol. There was a study in Wales, and the greatest recent lifespan expansion was from the cessation of smoking. It was 6 years for the average person — 6 years. If you cured all cancer for people who are old, all cancer, they would only live 2 to 4 years longer, because you haven’t cured cellular aging. Just think about that. If you want this great expansion of lifespan in your middle years, and health span along with it, do not smoke and do not drink alcohol. I wish somebody had told me that when I was younger. I certainly had fun with it, but it’s actually very detrimental to your health. They’re both poisons.

Gary: I just got through with — what is it — Dr. Roizen, who was at our event?

Liz Parrish: Yeah, fantastic.

Gary: Yes, he’s a great guy. I just finished the first book he wrote, and I love that book — and he’ll be on the show in the future, by the way, everybody. I love his book because he does what you just did. He lists all these things: if you quit smoking, you add 6 years to your lifespan. If you brush your teeth and floss every night, you add 2 years to your life. That’s not necessarily the exact number, but he has all these things. If you wear your seat belt, you live an extra year on average. It’s crazy all the information he has there, and it’s in such a short, simple-to-read book. So when you said 6 years from smoking, I think that’s the number he has, too. Gosh, I’ve really enjoyed talking to you. I’ll give you a chance in a minute to tell people where they can follow you or find out more about you, but before we go to that, is there anything that I might have missed that you wish we covered?

Liz Parrish: Well, I guess I could briefly talk about the different genes that we use, how they work, and what they work on. That might be interesting.

Gary: Sounds great. Tell us about the different genes you use and what you work on.

Liz Parrish: Telomeres, we’ve talked about. That’s to lengthen the caps at the ends of the chromosomes to give you more cellular division. Follistatin is to increase your muscle mass and help your metabolic system. It increases insulin sensitivity, and it has a myriad of neuroprotections. It helps with brain plasticity. Then Alpha Klotho — Alpha Klotho is a gene we just got a patent for. It is typically for neurocognition, so we use it in cases of dementia, but we also use it to help protect the cardiovascular system and the kidneys. PGC-1 alpha we use for mitochondrial biogenesis, so it increases the number of mitochondria in your cells. And then we just used two new genes that we can’t talk about yet until the provisional goes in. They regenerate your liver. One of them actually connects to a feedback loop in your brain that helps you with food satiation, and it also metabolizes fat. That’s instead of GLP-1 agonists, which could be very unhealthy for your body, because they keep you from desiring food — and when you don’t eat, your body eats anyway. It will eat your bone and your muscle. This gene specifically helps you burn fat and maintain muscle and bone. So those are the different genes that we’re using and the different reasons that we use them.

Gary: You’ve got a lot of stuff you’re working on. How many patents do you have?

Liz Parrish: We have several pending, and we have two that have been awarded. Follistatin, telomerase reverse transcriptase, and Klotho are all covered within those patents.

Gary: Wow, that’s exciting technology.

Liz Parrish: Yeah, it is exciting technology.

Gary: Very exciting. Now, where can people follow you or keep up with you and BioViva? What’s the best way for them to do that if they’re interested?

Liz Parrish: You can find BioViva at bioviva-science.com. We have social media. Personally, I have a LinkedIn under Liz Parrish. I’m on Instagram and Facebook, but not very much, and usually on my personal pages I just share my personal life — and not very much of it. I’m not an influencer. I don’t need you to hear my opinion all the time. I’m just trying to create drugs that extend your healthy human lifespan. But I do share a lot of value-added pieces. If you follow me on LinkedIn, or my professional account on Facebook, or BioViva, you will get almost everything that’s up to date — what’s happening this week, next week, or last month in gene therapy, from all the companies working on this and all the research. And you will really find a world that you love, I believe, because in those papers lies your human enhancement and your future.

Gary: I’m excited about that. I’m going to follow and share, and I recommend everybody else do the same. Well, Liz, I really appreciate you coming on the show. I’ve enjoyed seeing you again. I hope that we run into each other again at a conference in person.

Liz Parrish: Somewhere. Yeah, I’m sure we will.

Gary: Now that I’m into this full-time, it’s like my job now. But being healthy is a job, though.

Liz Parrish: Yeah, it is. And I hope that you go through one of our licensing partners and become a patient, if you decide to do that. Nobody has to do that. I’m not here to pitch anything.

Gary: I’m definitely planning on doing it.

Liz Parrish: That’s fantastic.

Gary: Especially if it hits that $20,000 mark — then I’m probably going to be there the first day, flying into wherever it is. So yeah, I’m definitely interested.

Liz Parrish: It’ll be that plus hospital and doctor’s fees, but it’ll be the most affordable gene therapy on the planet, for sure.

Gary: At our age, we can’t mess around and wait for it to get much lower than that. We’ve got to go for it when it gets to that kind of pricing. Half a million is kind of hard to stomach. I think I’ve definitely got five years — that’s why I asked how long you think it’s going to take. So hopefully you find a big investor soon. I appreciate you coming on the show so much, and thanks.

Liz Parrish: Thank you so much for having me.