Does Gene Therapy Work for Longevity?

Today we take a look at gene therapy and the possibilities for longevity with someone who is not only an expert in the field but who has also tested the longevity gene therapy on herself. 

Elizabeth Parrish is an entrepreneur and founder and CEO of Bio-Viva Sciences. She is a graduate of the University of Washington. 

‘So instead of taking the drug or the protein in the form of a pill or supplement, then the gene as you say, up-regulates the manufacturing of that protein. And you avoid all the problems with drug delivery and biodistribution at all. But I guess there, there are additional challenges such as the vectors used for the gene delivery.’

Telomerase reverse transcriptase (TERT)
Follistatin (FST)
PGC-1 alpha

Mouse cytomegalovirus (MCMV) carrying exogenous TERT or FST (MCMVTERT or MCMVFST) extended median lifespan by 41.4% and 32.5%, respectively. First report of CMV being used successfully as both an intranasal and injectable gene therapy system to extend longevity. Jaijyan, Dabbu Kumar, Anca Selariu, Ruth Cruz-Cosme, Mingming Tong, Shaomin Yang, George Church, David Kekich, et al. “New Intranasal and Injectable Gene Therapy for Healthy Life Extension.” Preprint. Cell Biology, June 26, 2021.






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#longevity #wellness #antiaging #MR #lifestylemedicine #younger  #biohacking #RobertLufkinMD #genetics #genetherapy #lizparrish #KLOTHO #Follistatin #telomerase

Robert Lufkin MD 0:01
Welcome back to the health longevity secrets show with Dr. Robert Lufkin. Today we take a look at gene therapy and the possibilities for longevity with someone who is not only an expert in the field, but has who has also tested the longevity gene therapy on herself. Elizabeth Parrish is a humanitarian entrepreneur and founder and CEO of bio Viva sciences. She is a graduate of the University of Washington. Before we begin, I would also like to mention that this show is separate from my teaching and research roles at the Medical School with which I am currently affiliated. It is part of my continuing effort to bring quality evidence based information about health and longevity to the general public. Now, please enjoy this interview with Elizabeth Parrish. Hi, Liz, welcome to the show.

Elizabeth Parrish 0:57
Thank you for having me. It’s wonderful to be here.

Robert Lufkin MD 1:00
I think you and I both share the vision or the aspiration that I least I’ve seen you quoted on that, through smart genetic modification, we can reverse biological aging and unlock our potential. That’s very, very exciting. Before we get into that, perhaps take a moment and just tell us how you came to these interested in this fascinating field?

Elizabeth Parrish 1:30
Well, from 2011 to 2013, I volunteered my time for the advocacy of the use of stem cells. I was asked to join a project I created a nonprofit. And the important problem that we were trying to solve is the education around what stem cells were, how they were being used, that this area needed funding, it was regenerative medicine, it had a lot of potential benefits, but that the embryonic stem cell side of things had sort of shut the industry down and given the whole world this impression that stem cells were this awful thing and shouldn’t be used. And people thought embryonic stem cells were fetuses. And so anyway, we had a big uphill education boost to tell the public what the cells were. In the meantime, I really fell in love with what’s called epigenetics, the genetics behind why stem cells behave the way they do, every cell in your body has the same genes. But stem cells have the ability to be regenerative and differentiate into different cells and heal tissues, where as the rest of your cells kind of, you know, they deploy and they do their job, which is a good thing. That’s why your nose looks like your nose and your toes look like your toes. But I was really in love with this regenerative capacity in the genes, why the cells could do this. My stem cell advocacy work came to a screeching halt in 2013 when my son was diagnosed with Type One Diabetes. And I was thrown into the hospital and I started asking, Where are these technologies? Where would stem cells or biobanking help my son. And I was told that you know that I should look around that a lot of kids were dying of diseases, and my son had a treatable disease. And it just really never fit into my head that all of these kids were dying around me. And they didn’t have access to this technology. So essentially, they called it experimental medicine as if that was really dangerous medicine. And that just it just was not what I was seeing in the research. And it was not what I was hearing about from people who were participating in these type of therapies. So I became very encouraged to go out and try to find cures for kids. And that’s how I started my journey was going from conference to conference, to seeing where in the regenerative medicine area there were cures for kids, not just for my son’s type one diabetes, but for childhood cancers, childhood, congenital heart conditions and, and various things. And I was really, at that point, committed to genetics. I just felt like this really is, you know, where we’re going to find the medical cures. I happened into a conference called the sens conference in 2013. In the UK, the professor of genetics, George church was speaking at that conference, and I was like, Okay, I’ve got to go and I’ve got to meet this guy. And so, I did. And I learned about aging and how, you know, aging is essentially the biggest unmet medical need that the top killers in the world now by the way, are All aging related diseases, and that by treating biological aging, we could actually help people who need access to this technology now who are old enough to consent to that technology. And we could create a plethora of cures for all ages in Cuba, including curing childhood disease through gene therapy. So that’s how I got started. And you know, that it was actually a very windy road. But um, you know, basically, essentially, we found the biggest unmet ethical use of genetic therapies, and every gene therapy that we look at now would treat a childhood disease as well. So they really crossover aging and a plethora of congenital diseases or have some similar roots.

Robert Lufkin MD 5:56
Yeah, gene therapy is fascinating. We’ve we’ve been hearing a lot about drugs and supplements and lifestyle changes. But this is the first presentation on gene therapy, perhaps you could give our audiences sort of an overview of what gene therapy is, and and your particular approach at bio Viva.

Elizabeth Parrish 6:16
Right, well, so what we love about gene therapy is it’s probably you know, the the most natural type of therapeutic you could do. So your genes code for proteins and proteins make you proteins and hormones are what you’re essentially made of. And in order to change how we age or the state of disease, we can actually modify genes by in our case, what we do is we up regulate what’s called regenerative genes that show capacity to help organisms live longer and healthier. And these are all human genes that we work with. Although historically, there have been genes from other organisms put in humans, there was a big study that started I think, in 2016, of the genes of light sensing algae put into a blind person’s eyes. And this year, we saw the first benefits where people were able to see light after being blind, so that’s really cool. But that’s not where we go, we work with human genes. And we use what’s called a vector delivery system. And this vector delivers these genes to the cells, and then the cells up regulate the protein, without all the nasty side effects of, you know, pills that people take that you know, might hurt their kidneys or their liver. Gene therapy goes right into the cell up regulates the protein and your cells become the gene man, the drug manufacturer, just creating the protein that you need.

Robert Lufkin MD 7:52
So instead of taking the drug or the protein in the form of a pill or supplement, then the gene as you say, up regulates the manufacturing of that protein. And you avoid all the problems with drug delivery and biodistribution at all. But I guess there, there are additional challenges about, as you say, the vectors used for the gene delivery as well.

Elizabeth Parrish 8:17
Yeah, so there have been some historical caveats in gene therapy delivery. So in the 1990s, gene therapy was like on the way to becoming the curative medicine of, you know, the the very near future, but unfortunately, a child died of delivery method of back then called the adenovirus. That gene delivery method is rarely used now. It has been attenuated in a way that causes less immunogenicity, so that means immune system reaction, but now we new use new gene therapy deliveries. And so today, the most common gene therapy delivery is called AAV. And it’s adeno associated virus. It sounds similar, but it’s a completely different virus that’s been attenuated meaning it can’t get you sick. And all it can do is deliver a gene. So what are viruses really good at? Okay, we’re definitely Living in the Time of everyone learning about viruses. They’re really good at delivering genetic material to the nucleus of yourself. So what we do is we use their ability to deliver that genetic material, and we take out their genetic material and put in the healthy therapeutic genes and so that’s what they deliver. Now, today’s AAV has some problems because it is there there are toxic doses at higher levels of the gene therapy, and there is also really limited size capacity. So they can only deliver a certain amount of gene sequence. And so, you know, our work at our company has been finding a gene therapy delivery method that is bigger and better and more immunogenetic so that patients can get a better therapeutic response.

Robert Lufkin MD 10:16
And I think we’re going to talk about that in a few moments, some new developments that have just come out in a preprint. But before we do that, that the, in addition to the limitations of the AAV vector delivery system, could you also talk about the current genes that your that you’re using with the company and and how their mechanisms are working?

Elizabeth Parrish 10:42
Yeah, so our next phase of, of testing these genes is to test each one of them singularly which two of them we did in the original paper, and then to start combining them. So the genes that we work with one is called h htert. It’s telomerase reverse transcriptase. And it essentially lengthens the ends of the chromosomes. So as your cells divide, the ends of the chromosomes, called telomeres get shorter and shorter with each cellular division. And this gene therapy lengthens the those telomeres so that you’ll get more cellular divisions, it’s associated with all the diseases of aging, this telomere shortening is. And it’s also associated with lifespan in you know, a lot of organisms have now been tested. And we know that the rate of telomere shortening is directly associated with how long the lifespan of those animals go. So if you want to live healthier, and you want to live longer, telomerase reverse transcriptase is the gene for you. So the next gene that we work with is a gene called klotho. And klotho is has been used in multitude of studies to show its anti aging benefits. It also protects against cardiovascular disease, kidney disease, and get this cognitive decline. And we’re going to release a paper in a couple months that shows some of the benefits of this gene along with telomerase reverse transcriptase. So they have

Robert Lufkin MD 12:18
all those effects with Oh, excuse me, but we know. Yeah, with klotho, they have all before we leave klotho to have all those effects. Is that a single protein? Or is it understood? how those all those effects on all those various diseases, including dementia? You mentioned? How does it how does that

Elizabeth Parrish 12:37
question? That’s a good question. So a lot of these genes have called have what’s called isoforms. So there are different snippets of the gene that you can use for a specific protein that you’re looking for. And so with klotho, we do use a specific sequence of the gene, the gene itself makes a myriad of proteins. And so yeah, so that that is true. And the one that we’re working with is specific to the protection against chronic kidney disease, cardiovascular disease protection, but also it’s found that people who upon autopsy after their death who had what appears to be late onset Alzheimer’s, but did not suffer from the cognitive decline of Alzheimer’s have upregulated klotho. So there’s a lot of good evidence around it. And a paper came out, actually, last year after we started our study that shows that it actually also may help with removing beta amyloid plaques, which is a symptom of Alzheimer’s, it really wasn’t our target. But that’s a great thing to do. It’s something that would be definitely beneficial in Alzheimer’s disease.

Robert Lufkin MD 13:49
Yes, and I understand there may be a paper coming out that we can’t talk about yet, but maybe look at some of these so we can stay tuned for that.

Elizabeth Parrish 13:59
Yeah, absolutely. Stay tuned, because we’re excited to give that to you. The third game that we look at is called Phyllis Staton. And Phyllis Staton is a Myostatin inhibitor of that sounds like okay, that’s too much to know. But Myostatin is a muscle regulator. So it is something that is a protein that’s upregulated to probably ensure that as you’re growing, you don’t put too much energy into muscle mass growth. There are people who are born who are Myostatin knockouts, and they’re those little super muscular babies and super strong little kids and probably grow up to be muscle man. So in this case, full of static blocks Myostatin, but it doesn’t block it entirely. So you know, there aren’t cases of people off. I suppose you could if you did an excessive amount of it. But the idea is to use this gene in order to increase the muscle Some out of an aging population there for combating frailty and metabolic disorder. So one of the great things that we see with folate status is lower blood glucose levels and HBA one sees. And we we see protection against what appear, you know what would turn into metabolic disorder. So it might protect against type two diabetes, but also just keeping an aging population from being frail and having Falls is would be super beneficial. So we know that the gene definitely affects metabolic disorder. But we want to make sure that in page people over the age of 60, or 65, it can grow muscle mass as well. So that’s a great test of that gene. That gene had been through safety and efficacy for machines and Becker’s muscular dystrophy. It wasn’t an all out cure. So muscle mass in some of the muscular dystrophies isn’t actually an issue. So but it did help some of those kids walk farther and longer and get them up on their feet, which is actually quite amazing. So it is still being used for those conditions.

Robert Lufkin MD 16:11
And like to say, for the elderly, the sarcopenia, or muscle wasting or muscle losses is a huge problem. So, so the fullest stat blocks Myostatin, which blocks muscle muscle growth, so it’s almost a double negative, essentially, the net effect is that we increase muscle growth. Correct?

Elizabeth Parrish 16:34
Yeah. And yeah, after certain age, you definitely want to increase your muscle growth, because you know, you’re losing it over time. Another good use for that gene therapy might be kaseya. So muscle loss with cancer treatment.

Robert Lufkin MD 16:49
Oh, that’s a great idea. Yes.

Elizabeth Parrish 16:51
So the fourth gene is very exciting. It is called PGC. One alpha. And what it does is it helps with Mio mitochondrial biogenesis. So again, now we’re out there in the weeds for some people. But your mitochondria are like the energy cells of your body. So they’re in most of your cells, they produce energy. And that energy drives you It drives metabolism, your physical output everything. And what PGC one alpha, what it does is it will get rid of it basically signals to get rid of mitochondria that are dysfunctional, and mitochondrial dysfunction is a hallmark of aging and happens in everyone over time. The cells that it transduces have healthier, and more robust mitochondria. telomerase Renu also helps with mitochondrial dysfunction, just so you know, some of these gene therapies crossover. But PGC one alpha is like the powerhouse of creating robust mitochondria. And so again, that would be gene therapy that might be used for metabolic disorder, or something, there may be gross obesity, it might show benefits there as well. It was a drug It was a looked for and looked at as a treatment for things like Parkinson’s disease as well. So far, there hasn’t been a significant outcome there. But that doesn’t mean that it was in combination with another gene wouldn’t be super beneficial. So our job is company is like looking at more than these genes by themselves. It’s like what can they actually do together and that’s, that’s really where the the cure for treating biological aging will be is in a multitude of gene sets put together.

Robert Lufkin MD 18:46
So for the PGC, one alpha, our our audience has been hearing about a tapa G and the importance of that for for healthy aging and all these chronic diseases in so many different diseases, it plays a role. So the clearing of the mitochondria would be my tafa gi sense, essentially, if I’m if I understand it correctly, and PGC one alpha up regulates my toffee G and makes for healthier mitochondria in some sense, correct?

Elizabeth Parrish 19:18
Yeah, and it’ll help with a toffee G to PGC. One alpha is one of the genes that when you work out gets naturally upregulated. So you can test humans and if they’re working out and getting in good physical shape, the gene itself up regulates. Our idea is that we need to help people because obviously, as you age, you’re going to get less and less gains from the effort that you put in to your health, unfortunately, I mean, we know right now that how everyone essentially dies from biological aging. So you know, the idea is to help people who are in the worst condition Get these sorts of therapeutics to buffer their system and people who are in the best condition to get the best gains from their efforts.

Robert Lufkin MD 20:10
And what is the fate of these injected genes and their distribution? How long do they last in the body? Do we know that?

Elizabeth Parrish 20:19
Um, you know, that’s still so gene therapy is still vastly considered a one time treatment for a lifetime cure. But the truth is, is that in the area, there it is vastly unknown. So some of the kids who were treated many, many years ago with for severe combined immune deficiency, called belt boy in the bubble disease, there’s a regulated gene therapy for that, now, it’s considered a cure, but they may need to be retreated over time. And so maybe you’ll need to take a gene therapy once every five years, or once every 10 years, it’s still vastly unknown. And it would be based on following patients and, and reporting on on all of their their blood work and outcomes.

Robert Lufkin MD 21:07
Yeah, so that’s, that’s fascinating, I think we have an overview of gene therapy and the work you’re doing. And we’ve sort of set the stage now for then this new paper, which I should say, is a preprint. It has not been peer reviewed yet. That’s in progress right now. But it’s very exciting to look at and see the results. And we’ll have a link to it in the show notes are as well. But this is a paper from the co author, the main authors are from Rutgers University, but including yourself, Liz and authors from Howard University from New Jersey medical school, from San Gen University and from Harvard Medical School. So it’s it’s quite a distinguished international set of authors. So yeah, tell us about this exciting breakthrough paper.

Elizabeth Parrish 21:58
Well, again, we we want to do gene therapy better. So we know some of the caveats of gene therapy. And those are based in how many genes that you can get into a vector and what the immunogenicity of that vector is. So we wanted something that performed really well got genes into the nucleus, that was something that we couldn’t find a non viral vectors not consistently. And that subverted the immune system, and could get in what we want to deliver in the future, which is like the mini mini artificial chromosome be the set of genes that are going to help you live better, longer, healthier. And so we went to the drawing board with our Chief Scientific Officer and her work had been all in the use of CMV and bcb vectors. And so we chose one of them based on a lot of criteria that were beneficial to humans, human cells, and gene therapy delivery. And we chose cytomegalovirus. So a lot of people in aging, like look at cytomegalovirus, as this, you know, benign sort of viral infection that almost everyone has, that may cause some issues as you age, especially when you get older. But what if you could take that virus take its ability to get you sick, completely out? and have it deliver therapeutic beneficial genes? Because that’s what it’s good at is is you know, ubiquitously, you know, going throughout your system. And so we showed in this study, and now we’re going on to human cell studies, that we could not only deliver the genes with the virus be attenuated. Well, not in this case, actually, with the virus, and we could get protein upregulation. But we also extended lifespan, most significantly, as seen in these genes. So the fullest and we use, we didn’t know if it would extend lifespan, it did extend lifespan by 30%. And the telomerase reverse transcriptase, actually extended lifespan on an average of 41%. And that was fantastic. I mean, really, we were just trying to see can we deliver this but we knew it was a longevity study. So this study that we thought might take like a year and a half, ended up taking almost three years from the inception of the documentation to the last mouse dying, which was we started really just sitting on the edge of our seats. And we showed a myriad of benefits, better mitochondrial function, better metabolic health, better coordination. The telomerase mice were, they looked younger hands down across the board, they were basically equivalent. to eight month old mice when they were many, many months old, they were wild type mice, they weren’t treated until they were about the age between 56 and 62. For humans, so that would be like the perfect time probably to start treating aging in humans, although probably these therapies will be used much younger in the future to keep you from, you know, taking on any of the ravages of time. It was really cool. It was so fun to be part of it was great to have an amazing team, it was great to be on the calls. Every time we were on a call, we were just like, I mean, mice are alive what’s happened. And, and then you have to realize, you know that the gains, we could have actually gained more time with these mice, but you can’t change the diet, they ate pellets of food that are like hard as a rock. As far as I’m concerned, you can’t change the diet, you can’t change anything about how you treat the mice. And the truth is the vets if the mice start to show anything that looks like sickness, they have to be euthanized because it’s considered the only humane way to handle the situation. So the lab actually said that they thought the treated mice went might have gone on for weeks, but they might have just been a little bit limpy, which humans are as when they get to the end of their life. So it was really exciting. So we’re happy with that paper?

Robert Lufkin MD 26:21
Well, with the And just to be clear, the murine CMV virus you use there is a human analog of if that, presumably would would work with humans, potentially in a similar fashion.

Elizabeth Parrish 26:37
Yeah, exactly. Oh, we’ve already chose our attenuated human CMV. And we’re going into the human cell studies. So that Yeah, so you have to, you know, you have to do your animal model, and then you do you know, your human cells. And then you go back to the animal model with the human type drug, and try to get it to work in a different model, which is kind of really strange, because, you know, the human CMV is different than the mouse CMV is different than the rhesus monkey CMV. So, there’s always things that you have to do to go around to make sure that you’re getting proper safety. And so the best way to pass proper safety is to test the the equivalent in the animal model before you start your human studies.

Robert Lufkin MD 27:29
And the other thing that struck me about the paper two was the remarkable new route of delivery that you use, instead of injections, there was an intra nasal spray that seemed to be equally effective.

Elizabeth Parrish 27:43
We couldn’t believe that. I mean, we really couldn’t believe that. So, and this was not, yeah, it wasn’t, you know, administered in any way other than just the spray, it worked just as well as the intraperitoneal injection. And that is really good news for us. Because, you know, that would be probably the route that most people would choose to do. Now, another thing that we showed with it was something that you can’t really do with a V, which is re dosing. So the paper like had, we tried to hit check every box in this paper, and the the, you know, we were, we showed that you could re infect the mouse with the virus or retreat. And they continued to have a buffered beneficial effect. So there wasn’t a rejection.

Robert Lufkin MD 28:39
Wow, wow. That’s so exciting. Now, looking at transferring this, this work to humans. We all face incredible regulatory hurdles in the United States. And there’s and costs associated with drug development and gene therapy development. There’s a, I think, a 93% failure rate for phase three trials. What you are exploring, or actually a company that you work with, is looking at exploring alternatives for this. Could you speak a little bit about that? And what the possibilities are there for people?

Elizabeth Parrish 29:24
Yeah, so we work with a company called integrative health systems. And we work with them because we’re interested in data and we’re very interested in offshore medical tourism being done correctly. And they are a medical tourism company. And they work by consensual use with patients who want to access this type of technology. And what we do is we assess the data, we see how well these drugs are actually performing, which actually gives us a huge leg up in our research and development. So This is an essential route. I mean, actually, as far as all clinical trials, over 80% of those are done out offshore the United States, even by the biggest companies in the world. So companies do like to go out of the United States to do trials or studies, because it gives less expensive access, and it gives paid customers actually, or patients more rights to access technology that they want to access instead of what’s available currently.

Robert Lufkin MD 30:35
That’s exciting. So so it’s possible to, for people to for humans, people to get access to this technology. Now, if they if they want to try it out through this through another company that you work with the the medical tourism company. Currently, the cost is very high. And like any new technology development, whether it’s Tesla or anything, usually the initial costs are very high. And then over time the costs come down. What economies of scale that can lower the costs. Do you see and and how fast will it be lowered? And how low? Do you see it becoming in the future for everyone?

Elizabeth Parrish 31:21
Yeah, so that’s a great question. So when you’re treating the biggest medical unmet need things like aging, you have the economies of scale into very expensive technologies, it’s kind of like you said, things start expensive, like the first supercomputer, no one could have afforded that. And now everyone has a smartphone that’s more powerful than that initial supercomputer. And that’s the way this technology will work. The the just making a gene therapy for one person can cost hundreds of 1000s of dollars. And unfortunately, right now, with COVID, and the reagents being vastly used for the immunizations, the cost of gene therapy is almost doubled. So I know because we’re in research and development, so I know how much it costs to make these gene therapies internally in labs. And other companies are also suffering from this who are going into clinical trials, though, might have raised a certain amount of money to go through clinical trials. And now they need double that in order to, at least on the therapeutic side to treat the patients. So right now, gene therapy is in a real slump as far as exponential costs. But we should come out of that as soon as we get COVID under control, and people have more of a herd immunity, right? I think this third bout of immunizations is probably really going to play into the cost not coming down for a while. But that’s okay. these are these are the areas that you get hit. And those manufacturers who are making the reagents should be able to bolster their gene, their capacity for those reagents that will help the gene therapy space. But right now, I you know, before I could tell you that gene therapy was getting less and less expensive, until COVID hit just like everything else sort of blew up the world.

Robert Lufkin MD 33:15
So so it’s not only the reagents, but also the customization with each patient developing the therapy. That’s that that is expensive as well correct?

Elizabeth Parrish 33:24
Oh, yeah, it takes 16 to 18 weeks to make a gene therapy for one person. This is like real precision medicine, it has to go through a lot of quality control, they make sure that you know that it is purified and ready for human use. But again, this technology is going to become more and more used all over the world. This is where the medical cures are now coming from there’s five regulated gene therapies that are considered cure, curative for the diseases. And that is just going to continue to spin out and with more manufacturing capacity, more companies are getting into manufacturing, the cost will come down. So for most people who are listening to this, the cost of gene therapy today doesn’t matter so much as it will in five years. And it should be much more reasonable and within the grasp of payers and insurers and things like that.

Robert Lufkin MD 34:21
Now, this is such an exciting time in this space. Well, in our last few minutes. Maybe you would if you wouldn’t mind sharing given your deep expertise in this knowledge in this area. What what lifestyle choices have you have you use this knowledge to inform your own lifestyle choices and in what you’ve done and I should say at the outset that you are in a unique position that you also actually tried all four of these gene therapies on yourself in 2015.

Elizabeth Parrish 34:57
So when we started this company, the idea was to make the biggest impact with the company possible. And what was really lacking was human data. There were these great genes that had the propensity to do amazing things. But there wasn’t human data, especially on telomerase reverse transcriptase, the ones that the one that lengthens the ends of the chromosomes. And so we thought to start the company, we should have some human data. Because these gene therapies, it’s set on the shelf for far too long, you guys. I mean, this technology has been around for decades, it’s not new, it really has the the evidence that it would have the biggest impact on all over health. And yet, no company has been able to raise the amount of money that it would take to get these into proper clinical trials. And we really wanted to do that. So I took we started the company with me taking two of the gene therapies, Phyllis Staton and telomerase reverse transcriptase. And I mean, it I, I’m 50. Now I feel great. We haven’t seen any drawbacks from it, we saw increased muscle mass, we saw lengthening of telomeres have had better metabolic health. And in 2020, I tried a few more of the gene therapies, a couple more the the klotho, and the PGC, one alpha. And I mean, I, I’m a huge proponent of that this is the future of technology, and this is where we’re going. And this is going to benefit everyone in the world, significantly, at least enough to the effect that you can then make lifestyle and diet and exercise changes, listen to your doctors take the right supplementation, that’s then going to cap off, what we can do genetically, and we’ll consider will continue to accelerate the development of these type of technologies. For instance, the work that we’re doing, where we’re combining genes now to see if the multitude effect that we can get, you know, one of those sine wave monsters where we, we actually blow biological aging out of the water and create ultimately healthy bodies that stay in homeostasis. And that sort of myriad of common tutorial, gene therapies will continue to grow. So I 100% believe in gene therapies, I think that we’re one of the companies one of the very few companies that take our own medicine. And, and will continue to grow that now. You should get out and do your diet and exercise and make sure that you’re making the right choices. But you know, everyone’s small, you got to slip and have some fun and and your gene therapies will be there to catch you.

Robert Lufkin MD 37:56
Absolutely. How about supplements, anything with that or anything along those lines?

Elizabeth Parrish 38:04
Yeah, so I’ve recently been suggested to take some na D supplements. And so I’m going to do some pre blood testing and some post blood testing to see how that goes. I do occasionally not everyday, but occasionally take a multivitamin. I think that that’s really important. Just make sure you got your bases covered. I’m a huge believer in the omegas the omega threes that those are, those are probably good for you, you’ll have to tell me if they’re not, um, I don’t have a lot of help on that side. So of course, I’m a vegetarian are a veer towards vegan, and I’ve been a vegetarian for I mean, decades and decades now. So I adhere to a more of a plant based diet, which suits me, I’m trying to think of what else is in there. Because like, sometimes I get sent lots of pills, like you know, nutraceuticals and I really love it and I start b 12. I take a b 12. being vegetarian, so I don’t know I think that there’s fabulous stuff out there. But I really need probably a medical doctor to tell me exactly what I need to take. I tend to just get shot information you need to be taking this and

Robert Lufkin MD 39:27
with your vegan with your vegan diet. Do you practice any type of intermittent fasting or time restricted feeding or pretty much ad lib?

Elizabeth Parrish 39:38
I have done that before. When I’m really busy. I naturally do a calorie restricted eating because I generally will be like so busy during the day that I only eat in the evening. But I gotta say that lately I’m kind of eating all over the place and yeah, I I need to get a better pattern I’ve spent I’ve been doing my MBA while I’ve been running this company. And we’ve got several papers, like I said, coming, I’ve got my my thesis is due in, I think two weeks from now. And I’ve just got to say, it’s just been a crazy, last eight months or so. But I’m committed to getting back on top of everything and organizing my life more rather than my paperwork very soon.

Robert Lufkin MD 40:28
Yeah, as far as we’ve got your sirtuin genes covered with the NA D supplements for presumably, how about a MP kinase with any Metformin do you do you prescribe take that.

Elizabeth Parrish 40:42
I do not take Metformin, as I understood, so I took full of Staton for my muscle mass and not see it. But anyway, there’s a little bit of a balance there, where when you when you’re sort of growing muscle mass, and the Metformin had been shown to maybe inhibit that a little bit for if you’re being super active, I think that Metformin is generally great for all people outside of maybe if you’ve taken a gene therapy for muscle mass, I do have to tell you that klotho is an mTOR inhibitor as well, it may be that that gene itself mimics calorie restriction. And so it there’s a lot of good scientific evidence that shows that it might be the equivalent to taking something like Metformin. So I can’t say that I’m not taking an employer inhibitor.

Robert Lufkin MD 41:37
Yeah, it sounds like and then wrap on mice. And also then the klotho might, if it is inhibiting mTOR, then rapamycin wouldn’t be necessary either as well. So that’s, that’s fascinating. Yeah, some of our some of our audiences taking rapamycin and Metformin, as well as the the sirtuins, the resveratrol, and the NA D supplements as well. But it’s, we’re all learning and it’s it’s all a new space, and nobody really knows the answers yet. Anyway,

Elizabeth Parrish 42:11
you know, we will know the answers down the road. And I have to say, like gene therapy was for me, because as you can tell, I’m like taking pills. And having that sort of a schedule is not sort of my thing. I’m sort of set it and forget it person reminds us of an old night, late night commercial, but I’m definitely a set it and forget it, kind of person. And that’s why I like the gene therapies is you know, you take them and then you have them and then everything else that you’re doing, hopefully is a beneficial supplement to that sort of baseline. Yeah. Me a list of things that I really need.

Robert Lufkin MD 42:54
It’s such exciting work you’re doing how can our audience get in touch with you and follow the work you’re doing? So sure, yeah. And and maybe you could just give us give us your website or your link, if you don’t mind?

Elizabeth Parrish 43:10
Yeah, so we’re at bio, Viva dash science comm you’re gonna see a lot of really groovy tests there, you’re gonna see we’re selling an epigenetic test. That’s amazing. It’s saliva based, it runs multiple clocks, it gives you an assessment of those that data. Pretty soon, we’re going to have telomere associated length as part of the test, and rate of aging. So as you you only spit once and you continue to get more and more data off of that, that one sample, of course, we do suggest that you take it about every six months. And then there’s other tests there like na D testing, senescent cell testing, which is really quite cool. And immune testing. So bio, Viva dash science calm. We’re on Facebook, Instagram, Twitter, where we’re kind of just out there in the social world and vastly that that’s done by team members who do the marketing. So I am not as social media savvy as they are. But I occasionally pop into social media. And if I do, if you see me, I usually for 24 hours, we’ll follow up on comments and questions. And so look for me too.

Robert Lufkin MD 44:22
That’s great. And we’ll include links to those, those products also. And we may even have some discounts for them discount codes if you want to use them as well. But thanks. Thanks again, Liz so much. I really enjoyed spending this hour with you today. And I look forward to hearing hearing from you again soon.

Elizabeth Parrish 44:42
Oh, thank you for having me. I hope it was informative. I hope people got really excited about the future. Gene therapy isn’t just for me, it’s literally for you. And hopefully in the future you’ll be able to say I don’t want biological aging. I want bigger muscle mass. I want to eat more of what I want to eat. Without the the caveats, and I don’t know I want purple eyes. I wouldn’t be for the future. Not for today and hopefully we’ll be able to get that to you.

Robert Lufkin MD 45:10
I love it. Thanks again and we’ll, we’ll hopefully talk again soon.

Elizabeth Parrish 45:15
Okay, thank you for having me.

Robert Lufkin MD 45:19
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