Slow Down the Aging Process: Telomere Biology in Age-Management Medicine

Welcome to the Peptides and Longevity Podcast, redefining aging and transforming health. Each week, Dr. Kent Holtorf will dive into groundbreaking science, innovative therapies, and the future of health and longevity alongside visionary physicians and experts. We'll explore how peptides, cutting-edge medicine, and lifestyle strategies can redefine the way we age. Get ready to transform your health, optimize your vitality, and unlock the secrets to a longer, healthier life. Let's get started.

Hello, this is Dr. Ken Holthorpe with another episode. Today we have the luxury of having Dr. Raphael, and he's gonna be talking about the role of telomere biology in age management medicine. Dr. Raphael, thank you so much for being on and taking the time. I know you're a busy guy extending people's lives. And, uh, so it's great to have you. I'm looking forward to learning a lot about longevity. And ways to do that.

Well, thank you, Dr. Holtorf. I'm happy to be on and happy to talk about one of my major passions in life, which is keeping people healthy and doing what they love to do as long as possible.

Yeah, I love the fact— and we'll get into this— how you, you don't just do this, you show the people and document that they are actually younger.

Yeah, I mean, we measure— one of my major focuses is to measure the aging process in people at baseline to see what their strong systems are, because we all are a mixture of weak systems and strong systems, and you have to focus on the weaker ones and try to shore up the stronger ones. Um, uh, and we really want to sort of know once we start therapies whether they're effective. It all started back in— it was 2001 when Bob Butler, if you remember him, who was the founder of the National Institutes of Aging, convened a roundtable and I had been practicing what was going under the rubric of anti-aging medicine at that time, um, doing hormone replacement therapy, testosterone for men, and then growth hormone replacement therapy. And patients were doing well, feeling well, but at the same time, the NIA was looking at studies, looking at biomarkers of aging to see whether there was any way to measure whether or not these therapies were being effective. And he invited me to a roundtable with a number of relatively illustrious gerontologist, and it was sort of like being invited as a sacrificial lamb to this thing where they're going to tell me, why are you doing this stuff? You're killing these patients. And what came out of it really was— it wasn't quite as bad as that, but what he said, look, you're a smart guy, Joe. What you're doing seems to be helping your patients. They feel well. But how do you know if you're actually— you're calling yourself an anti-aging doctor— how do you know if you're actually altering the aging process? And sort of a little light went off in my head. I've been doing this about 4 years, and I thought I was doing pretty good stuff for my patients, but that started me on this journey of looking at the literature for what was available to measure how people age, whether or not we could see whether these things that we're doing for them are actually altering their aging process in either, you know, a good or a bad way. And that's been one of my passions since then. And I, you know, thank Bob, who has since passed away, um, uh, for, for getting me started on that because it's a fascinating field. There's so much literature out there about it in one of the areas that then later, and probably about to Yeah, I can't see standard medicine moving very fast in this area.

You know, everything's about acute. But, uh, just a little formal stuff about Dr. Raphael. He received his BA in philosophy— pretty nice— in Princeton, no doubt. His MD from Drexel University Medical Center. He trained at the New York University Hospital Cornell University Medical Center, was formerly a clinical assistant professor of Medicine at Dartmouth Medical School while he practiced at the Hitchcock Clinic. Uh, he's a member of the Endocrine Society, is board-certified internal medicine, and is a diplomat of the American Board of Anti-Aging Medicine.

Or are you an endocrinologist or no?

No, I do a lot of endocrinology, but I'm not an endocrinologist.

Yeah, yeah, looks like me. I'm a member of the society, but I stopped going to their conferences because it's the same stuff over and over. It's just like they're arguing the same points that they were 15 years ago.

I would agree with you. Like, I went for probably between 1995 and 2015, I went to virtually every major meeting, every, every, every annual meeting. But I think that— and there's a lot of good science that takes place there, but they're stuck in not thinking about optimization but about disease, and that's really not what we're about. And, you know, biological variables are continuous. A testosterone of 301 is not different from a testosterone of 299. Yeah, your cutoff is 300.

Yeah, they're still arguing what the TSH normal should be. It's like, but even though with all its flaws, and I went because the top guy in terms of thyroid replacement in pregnancy was there, and I said, I can't find a study that shows that T3 crosses the placenta. Uh, he goes, I don't know, do you know? Yeah. Which we know it does because we have people on straight D3 that have great babies. But anyways, so more about Dr. Raphael. In 1997, he co-founded the PhysioAge Medical Group where exclusively practice age management medicine, uh, with a focus on personalized hormone optimization, physiologically aged age assessment. In 2007, he co-founded the PhysioAge Systems, a web-based biomarker data collection reporting system now used, used by age management functional medicine practices around the world to assess, monitor, and communicate to patients the effectiveness of their treatment. So we'll get into that about, you know, really testing people's age, not just giving them this, oh, it's good for you. You know, you could take 10,000 supplements that people say are good for you. Since 2009, he's been involved in clinical telomere biology research. He's published 3 studies on the effects of oral telomerase activators on normal aging adults. He has lectured nationally and internationally on clinical application of telomere biology. In 2015, he founded the Raphael Medical Group and blogs regularly about telomere biology, hormone optimization, and biomarkers of aging on rafaelmedical.com, R-A-F-F-A-E-L-E-M-E-D-I-C-A-L dot com, and physioage.com, S-I-O-A-G-E dot com. Yeah. Well, again, welcome and can't wait to kind of get into the meat here and, and pick your brain and share with our, our viewers and physicians and some of the intelligent lay public about all the stuff that you know and that you've been doing. So, so you've been practicing like 25 years, kind of like me. It goes by so fast.

Really does.

Yeah, it's crazy. And so you've been doing, you've been focused on this age management stuff the whole time, or?

Yeah. I mean, well, no, I, for 5 years I practiced, I've been practicing for 30 years actually. For 5 years I practiced internal medicine, as you mentioned, in the Hitchcock system up in New Hampshire when I moved up there right after residency and sort of got my doctor legs taking care of acute MIs and pneumonia and all the things you do in a primary care internal medicine practice while I was also, you know, on the assistant clinical faculty. So, but at the end of the 5 years, I had kind of aging parents. I was a little bit, uh, my parents were a little older when they had me. And so they were starting to age significantly. And I sort of wondered what I could do to help them to age better. And that started me thinking that, you know what, this isn't really the thing to do is putting Band-Aids on all these things, waiting for the diseases to occur. So that really made me sort of open up a practice, uh, move back down to New York City and open up a practice. Looking at how to slow down the aging process and keep people as healthy as long as possible.

Interesting. And just a side note, have you found— like, I found sometimes that these, like, elite athletes who you think are the, the ultimate in health, and they actually turn out to have lower or higher biological ages than normal.

Yeah, I see that. Absolutely. I mean, there's, there's, you know, I hear about these people that have to do things like, you know, a marathon a week or a marathon a week in like every state, you know, and do 50 in a row in 50 weeks. I'm like, that's just not good for you. Um, there are people who have some in, you know, some genetics that can get them through that, but that's in the end just too much of a stress on the body. And, and you see that kind of stuff. Oxidative exercise is great for you to the extent that you then allow yourself to recover. There's damage during the exercise and the recovery builds you back stronger. But if you're breaking yourself down all the time, and this gets back to, you know, to, to really into, into telomere biology where, you know, your stem cells have to replenish those degenerated tissues. And then if they keep on, if they're being asked to divide at a much higher rate because the damage is occurring at a higher rate, then at a certain point their telomeres get too short and they can't do it anymore. So I think that I absolutely see that kind of stuff. You know, I have a guy will come in and while his cardio age, the way we measure their central arterial pressure and give them an age for how healthy their— the elasticity of their arteries is, might be great, something like their immune function or their telomere length won't be as good because they're putting a lot of stress on their body with training. And it varies. Some people have— we'll talk about the heritability of telomeres— some people have a lot more reserve, they have more money in the bank, and they can get away with that, and others don't. And there's a wide variability in what you inherit in terms of your telomere length. So giving them that kind of information is really actionable.

Yeah, I imagine it's almost harder to have them reduce their exercise than people to get them to exercise.

Like, so it does— it seems like it makes sense that they become like a chronic illness if it's just constantly under stress and breaking down.

Yeah, absolutely.

And so in terms of telomere biology, how long have you been Really interested in that. You've published on that. And what's your thought on telomere versus other methods? And I know you use a lot of things, which is the way to go. And that's like the way when we assess, let's say, a sick patient, Lyme, chronic fatigue, we love to get a ton of labs and it paints a picture. Like no one marker can just lead you astray, you know, oh, you're fine, this is good, you know. So I can totally see that.

I can see where your software program could be a big benefit Yeah, so it really— I think when I first started looking at biomarkers, and I think when the NIA and other people, you know, gerontologists started looking, they were looking for a single biomarker that could encompass the aging process in toto and, and sort of predict who was going to die younger or older based on this biomarker. And in fact, the NIH and the NIA, after 10 years of looking for that in, in identical strains of mice, said they couldn't find one like that. I think they were just setting the bar too high. And then since then, what you see is the newest kid on the block coming out, and then they say, well, okay, it's telomere biology, and then so you want to measure telomere length. And then the epigenetic age people come in, they say, no, this is more correlated with age, and so telomere biology doesn't make any difference. And then you see, you know, the proteome people coming in, or the microbiome people coming in. And the truth is, they all give information that's important and, and is useful, as you say, in painting a picture of what's going on. I mean, I think what's really happening is, is that we're understanding, for aging in particular, that systems biology is what has to be applied. And that means looking at multiple markers in multiple systems from many different angles and then applying, you know, deep learning, artificial intelligence to it to try to really understand what's happening. And to think that a single biomarker is going to tell you you know, what's going to happen and who's going to have, you know, who's going to die at a certain time, much less what state of health they're going to be in between now and then, is I think kind of silly really when you think about how complex the human body is and how it ages. So, you know, I got introduced— we were all doing hormone optimization. We had the big hiccup of the Women's Health Initiative that then actually was very good for my practice because all the misinformation out there. Um, so I was helping women sort of navigate that for a long time.

Biggest disaster, poorly designed.

Oh yeah, it caused, I think there's estimates that it caused 50,000 deaths of women because of, from cardiovascular disease for not being put on hormone replacement therapy. So it was, and it even lingers today, which is, which is insane because it's been, you know.

Oh, we hear it all the time. Don't get estrogen, you get breast cancer. Yeah, exactly.

So, so where was I going with it? So we started, I just started to, to, to get into telomere biology when I was introduced to it by Noel Patton, the founder of TA Sciences, came to my practice and said, what would you, what would you take? What would it take for you to sort of recommend this to your patients? And I said, look, you know, I'm an evidence-based doctor. I have these biomarkers of aging. The biology is fascinating. And I think the telomeres, you know, subsequently have, you know, they're one of the 4 major hallmarks of aging. There's 9 of them. It's one of the top 4. And so I said, look, if you're willing to have patients come through and get all the biomarkers, we'll track them for a year and see what happens with them. And that's what we did. And that was the, that was the, uh, the beginning of the first publication that we had for, for TA Sciences, uh, and the effect of the telomerase activator TA-65. So that got me started in looking at the biomarkers, seeing what one agent that has pleiotropic effects— because it affects stem cells and the immune system— what that has on the rest of the body. And so that's— I got started down the path that way.

Nice, nice. And so you mentioned kind of 9 hallmarks of aging. Can you talk more about that?

Yeah, so that, you know, so I think aging, the aging field has been, you know, I think at one point there was papers published that there's maybe 200 different theories of aging. I remember Ward Dean was one of the fathers of this sort of back in, back in the late '80s, early '90s. Um, and everyone was trying to figure out what exactly, you know, was what was going on with the aging process. Is there a single underlying aging process? And in 2013, I believe there was a paper published by Lopez-Otin and Maria Blasco and other people are major figures in the field, which had been predated a little bit by Aubrey de Grey's paper about hallmarks of aging as well. But I think that the field now, the sort of gerontology field, agrees that there are sort of 9 major hallmarks of aging, you know, genomic instability, telomere attrition, epigenetics—

can you go slower on that?

Oh, okay.

Yeah.

So the 9 I'm going to get them all right now. The top 4 are— the first one is genomic instability. That is, we all know about what happens, the genome gets attacked by free radicals and, and copying is, you know, there's 10,000 hits per day to, to the DNA in every cell. And that's Denham Hardin's sort of free radical theory of aging kind of thing. And then there is telomere attrition, because telomeres are what allow cells to divide. We know Remember the Hayflick limit? There is— telomere attrition occurs because the cells can't continuously divide forever. Up until 1961, most biologists believed that cells could divide indefinitely in vitro and in the body. And, you know, Dr. Hayflick showed that no, that's not the case. Um, it was little cells slipping in, in the medium into the, into the petri dishes that they were doing these things, and that's why they're able to continue propagating. So Eventually they figured out that the clock for this Hayflick limit was the telomere. So telomere attrition is a key component. Epigenetic alterations are the next one, which occurs with, you know, when the DNA methylation changes and then the access to DNA changes, so your gene expression changes, you know. Michael Fossel, who is one of the smarter guys that I know, is one of the preeminent telomere biologists, likes to talk about the fact that the genes in your nose are the same as the genes in your toes. But, you know, what makes a toe a toe and a nose a nose? It's gene expression. And so obviously gene expression changes during development, but the same gene expression takes place, changes during aging. And, you know, Steve Horvath has shown in his elegant series of studies that in fact it's so tightly, you know, when you look at certain CpGs is so tightly correlated with age that you can use it in forensics almost. But, uh, to, to figure out, you know, what, what the age is.

Yeah, that's a very interesting point. It's because, yeah, you do have the same genes everywhere, right? But yeah, all the different parts are doing different things and, and, you know, the basically epigenetics. And that's like where a lot of peptides, they'll show, they'll turn on 45 genes and turn off 26 genes that they know of and A lot of things work very well for flavonoids, you know, which I, I love. But yeah, keep, keep going.

Yeah, I mean, so I mean, that's— I think the same thing that takes place during development takes place with aging. And, and, and so there's an aging— a youthful gene expression, and there's a more aged, and then there's an old gene expression. And, you know, that shows that there is malleability to the aging process if you can turn back. And there's, you know, there was an early study, a recent study looking at Turning Back the Epigenetic Clock with Growth Hormone, DHEA, and Metformin, the TRIM trial.

So I think that obviously gene expression is a major question for you, just about, you know, growth hormone. The anti-age people use growth hormone, but shown to help. Like, no study has shown giving growth hormone causes cancer, which everyone brings up, but the longest-lived people seem to have like low IGF-1 uh, how do you reconcile that?

Yeah, that's a very complex area. I mean, I think that, you know, if you look at— if you talk to, uh— and those are very good points— there's a— I think there's a little bit of a trade-off between function, performance, and potentially aging. And some of these, you know, the old, old that they study, and they show some of them have lower IGF-1— I mean, I don't necessarily want to be like that when I'm that age. I mean, I think that the animal models that they look at where IGF-1 is— growth hormone is way overexpressed in these transgenic mice. I mean, we know what happens when you have way too much growth hormone. That's acromegaly. Those people don't live long. They get big hearts, big jaws. They have other issues. So we don't want that. The real study that no one has done—

no one's rich enough to have that happen to them.

Right, exactly. You need a lot of growth hormone to have that, and you don't want that. I think what— but then they do look at these studies in the mouse models and they, and they say, you know, that IGF-1 turns up is a pro-aging form. It's also a pro-performance. I mean, we know that higher levels of IGF-1 are associated with better levels of cognition. So the question is, is, is, is in the aging adult, is keeping growth hormone and IGF-1 levels in the more youthful physiologic range in the aggregate beneficial? There's no study that speaks to that. We just you know, the NIH did short-term studies and there wasn't any increased risk of cancer. You're not going to see that in, in a year-long study. There was some improvement in lean body mass, but that wasn't long enough to know whether overall it's going to affect the aging process. One of the reasons growth hormone is long-term— is approved for long-term therapy in growth hormone-deficient adults is because of the 2- to 3-fold increased risk of cardiovascular disease that you have if you are— if you have a very low IGF-1 for a long time. So the growth hormone story and IGF-1 story in aging is, is just another— is a sort of evidence that you have to look at the whole picture. You have to look at—

all right, so you're diving deep into peptides and longevity on this podcast, and we're right there with you. Integrative Peptides stands out, trusted by over 10,000 doctors to deliver real results for their patients. These premium peptides are your key to unlocking vitality, recovery, and a long longer, stronger life. Visit integrativepeptides.com and use the code PODLIFE for 10% off your first order. Again, integrativepeptides.com, use the code PODLIFE for 10% off. It's time to elevate your journey starting now.

Like, look at all the studies and sick patients and just aging. When you look at even involution of the thymus, like it, you know, everyone has hypothalamic pituitary dysfunction. So really in the modern world, toxins, pesticides, stress, chronic infections, gut dysbiosis is going to suppress that. You know, we have now, you know, kids coming in at, you know, 25 and their testosterone levels like 200, which is like that of a 90-year-old. Growth hormone is super low, you know, so like, how can that be healthy?

You know, it's not.

I mean, if you look at them and then, you know, I, been treating patients with growth hormone for, like I said, 25 years. And, you know, you have to look at each patient individually, and you have to— you say, look, okay, if your IGF-1 is, is below 150 and you're having trouble with abdominal fat even though you're exercising, giving growth hormone fixes the abdominal fat, brings the IGF-1 up, then you set into motion a whole bunch of beneficial things. The insulin resistance reduces, um, And, and so it's, it's gotten a lot of hype both in the negative and in the positive. And the truth is it's just another one of the hormones that's important. Not everybody needs it. Some people do, some people don't. And that's the way I practice.

The problem too is you look at, you know, reference ranges.

So they'll take 95% of the people, like take testosterone for instance. It's like, you look, decade ago ranges were higher, and decade before that they were higher. So now It's like they let— especially with growth hormone, like the lower limit of normal is like the person would be— seems like they're going to be dead, you know? Yeah, I mean, it's crazy.

Yeah, so but to sort of bring it back to telomeres, I mean, growth hormone is important because it, you know, what it does in muscles, it stimulates muscle satellite cells, which are the stem cells in muscles, to divide, which then can be worked on by testosterone to get bigger for hypertrophy. So you have hyperplasia and hypertrophy. But if you're stimulating the muscle stem cells to divide more rapidly with growth hormone, you got to make sure they got telomeres that can do that. So that's why I think that telomere biology dovetails very nicely with hormone optimization, and knowing whether or not someone has an adequate telomere reserve to be able to take the, the increased stimulation for cell division that the hormones give you is, is important. I mean, I haven't done the study, but hypothesis is that perhaps, you know, some of the risk, which in aggregate is either none or very, very, very little of increased risk of breast cancer may be localized in those women who have very short telomeres, because very short telomeres are unequivocally associated with increased risk of cancer of many different kinds of epithelial cancers. So, so that's why I now, when I measure hormone telomere length in all my patients, and I want to know what's happening, because if the telomere lengths get too short, the cells then then they get genomic instability and they become much more likely to become cancerous cells.

Interesting. And yeah, BPC-157 actually increases growth hormone receptors on the cell. And now in terms of telomeres, what's more important, the average length or the percent of short telomeres? Or can you discuss?

Yeah, that's a good— that's a great question. I mean, the vast majority of the data on telomere length and health and disease is using mean telomere length. And so that's still a useful, a useful measure for, for looking at where somebody is. But it is pretty well established that it is the critically shortest telomere within the cell that causes the cell to go to become senescent or to go into apoptosis and into crisis. And, and you have— it's going to be 2 or 3 short telomeres within the cell that causes that. So, and we know that telomerase preferentially goes and tries to lengthen telomeres that are shorter. So in the actual biology of telomere length, it is the critically short ones, but we have to remember when we're measuring telomere length in blood, we're measuring telomere length in the white blood cells. And depending on the technology, it's, you know, PBM, or if you're using the technology that I use, we can break it down to the granulocytes and lymphocytes. That's a surrogate marker for what's going on in other tissues. And there's concordance between what's happening in the white blood cells and what's happening in other tissues because of, you know, that's been studied. But you want to look at the data which shows that— I think that looking at the average telomere length does help you know whether or not a person's at risk and also whether or not the telomerase activator is working. There isn't a really good commercially available short telomere assay. Lifelength does have you know, they give a 20%, but that's really more correlated with the mean telomere length than it is with the critically short telomere lengths, which are under 3 kilobases. Just to give you sort of an idea for your listeners, telomere length by, you know, by what we call Flow-FISH is usually somewhere between 8 and 12 kilobases, or 8,000 to 12,000 base pairs in length at birth, um, and, and then you rapidly lose some during the growth phase, and then after that it's about 0.05 kilobases or 50 base pairs per year. So that is kind of just sort of an idea about where you are with telomere length when you're measuring.

And you kind of answered the question I was going to ask you, like, you know, you're checking telomeres and, you know, white cells, like, what's going on with whatever, all the things of all different cells in the brain, heart, whatever. Um, they tend to correlate. Is that— yeah, studies on that?

Yeah, limited studies. I mean, not as extensive as you'd like, because you, as you can imagine, it's not easy to get biopsies of liver and lung and brain. But the studies that have been done show that there is pretty good concordance. And the reason for that is because one of the major determinants of your telomere length in all your tissues is what you, what you inherited from your parents. Um, and so that's about 70%. That's a it's a very highly heritable trait, which we call a telotype. So you, when it comes to telomeres, lifestyle is very important and everything else you're doing, but you really want to choose your parents wisely. That's really what happens there. I mean, the difference between 8 kilobases and 12 kilobases of telomere length inheritance is about equivalent to the amount of loss that occurs between young adulthood and death. So if you start out, you know, at 8, you're like pretty far along. As compared to somebody who starts out at 12. And that's why people have quibbled about whether or not telomere length is a useful biomarker of aging, because a 70-year-old can have the same telomere length as a 40-year-old. And so why is that useful? Well, it's useful because we still know that once you get down to a certain telomere length, all hell breaks loose, and that's around below 5 kilobases. So, you know, it's a matter of what you inherited and then what your attrition length is. You can't change what you inherited, but you can change the attrition length by— that's why telomere length is, is telomere length is so interesting, is that pretty much every healthy behavior from lifestyle to exercise to diet to supplements, etc., has been shown to slow down telomere length loss. And pretty much everything that you do is bad— smoking, high fat, being overweight, not exercising— all those things are associated with shorter telomere. And so it's kind of an integrator of many different what we call allostatic load on, on the body. Um, and so if you're doing all the good things that are healthy, you might have a slower attrition. But if you start out with really short telomeres, it's still going to be a problem. I mean, you could have a healthy person, and I have like people that do everything right, and, and I see that because I track them over time. They're not losing telomere length at a very— but they didn't start out with very good telomere lengths, and so they have to be more careful. You know, don't smoke. I mean, and it's very behavior-modifying as well. When you tell somebody that, you know, your telomeres, you're 40, and they're more like a 50 or 60-year-old, then they're more likely to be more proactive about healthy behaviors because they know that their 401— I like to call it the biological 401— or, you know, their biological IRA is, is just not as full for their retirement of healthy aging as they get older.

And does sleep affect Telomere length?

Yep, it does. In the same way in which, I mean, I would say that it's not a good biomarker of aging if sleep doesn't affect it. So epigenetic aging, DNA methylation has been shown to be highly affected by, by poor sleep because that's when your body gets into a reparative state and fixes things. So it's definitely associated with that.

Like, do as I say, not as I do. And I know, like, I stay up all night to get projects done. That's when I work well. And I feel like it's aging me, you know. And I don't— studies on like night shift workers and telomere— do you— is there anything like that?

Yeah, they're shorter. And also, uh, night shift. And, and of course it would make sense that night shift workers have increased risk of cardiovascular disease and cancer, you know. And it's probably not solely because of their telomere length, but certainly, uh, there's other things that occur. I mean, vitamin D is associated with telomere length. And so if you're a night shift worker, you're probably not getting as much vitamin D, and your vitamin D level is low. Um, it's really— it's a very good integrator of many different things, but also with the caveat that it depends on what you inherited. So one, one telomere length measurement gives you some information, particularly if it's very short, or— and also it's very long. But what really gives you information is serial measurement over time.

You want to see where you're going.

Yeah. Where you going?

And so how much of an increase can you see with like TA65 over what period of time? Or with other interventions, what are some of your like major things? Say like, this is the number one thing. I guess it matters what they're also— people are doing, like what's the worst thing they're doing. But like, let's say we give someone TA65, when do you recheck? And what type of response have you seen?

Yeah, so let me start with, um, the, the clinical studies that we have. The— in the cohort study that I mentioned, we didn't see an actual increase in telomere length, but we saw all sorts of improvements in immune system function, that reduction in senescent T cells, which we think had to do with perhaps decreasing the number of shortest telomeres within the cell. But that spurred the company on to do a randomized controlled trial looking at the effect of TA-65 in CMT-positive patients. And we found that there was a 533 base pair increase after a year of TA-65. So that's, that's a pretty big one. Now that was using the technology that is where the average telomere length is about 40% longer using that technology. So have to take that 533 and make it more like about 300 base pairs, or 0.3, which is still quite a significant increase. And it was highly statistically significant in comparison to placebo, which lost telomere length, which of course you would consider. So we do have randomized controlled trial data showing that, that there is an increase in telomere length with TA-65 at the doses that are normally used, 250 IUs to 500 IUs. Now, in my practice, I have seen patients have actual increase in telomere length over time, going up as much as half a kilobase or 500 base pairs over a couple of years. But what I see most often is, is that the loss stops and you get, you know, so, and I myself have had telomere length of about 6.4 kilobases for the last 13 years, which is, you know, I would expect over that time period to have lost about 0.8 kilobases have gone down to below 5. And, uh, and that's— and if you can maintain your telomere length, as I said, this is when they get critically short that it's a problem, then that is really, you know, is, is quite good. Just like a coronary calcium score. I mean, you don't have a coronary calcium score too high, but if it stays at 200 or 400, you're unlikely to have a coronary event. Because—

and do they do CME-infected patients kind of like speed up that aging, the telomere loss, so you get a better— like, so you can do a shorter study, uh, not wait 20 years?

Yeah, so the reason— I mean, CMV is a whole other fascinating thing that, uh, that there's whole conferences that are convened on CMV. Just to— for the— for everybody that knows, CMV is herpesvirus 5. And in immunocompetent individuals, most doctors are like, you know, it's not going to do anything to you, don't worry about it. And about 60% of the U.S. population is CMV seropositive, and it goes up 1% per year starting at 10 years of age. So by the time we're in the 8th or 9th decade, it's virtually 90 to 100% CMV positivity.

Um, it doesn't mean active, right?

Well, so that's the interesting thing. As with all herpesviruses, they sit latent. You know, it's the gift that keeps on giving, doesn't ever go away. And to the extent that there are reactivations, there's a problem. So when you get a culture that comes out, that's herpesvirus 1, you feel systemically kind of crummy. It's not just the culture, because there's a whole reactivation of it, and that makes your immune system have to rev up to then make it latent again. That causes your white cells to have to divide more, your lymphocytes to have to divide more, and that shortens your telomeres. Same thing happens with CMV, except when those reactivations occur, there's no real symptoms. You might feel a little crummy, maybe a little something, but most people don't have any idea that they're having a reactivation. And if that occurs over and over and over again, that accelerates telomere loss, increases the accumulation of senescent T cells, which we know are bad for you because they secrete the— what's called the senescence-associated secretory phenotype— all these inflammatory markers like IL-6, TNF-alpha. They reduce their production of interferon gamma to fight off viruses. So it increases what we— it causes this state of what we call inflammaging. So CMV, even in an immunocompetent adult, it causes over time an acceleration of aging of your immune system, and we think most other tissues in your body as well. You know, there might have been some benefit to it in our ancestral environment because it allowed us to, to potentially have a more robust immune response to pathogens, and nobody lived long enough to have the adverse effects. Something called antagonistic pleiotropy, where something is good for you when you're young but may have other adverse effects when you get older. That's true of CMV. We chose CMV for that trial because there is a more acceleration of loss of telomere length in them, and because we saw in our cohort that a lot of the benefit was in the individuals that were CMV positive within that cohort. So subsequently, there's a trial that is pending right now, submitted to OBM Geriatrics, to look at the effect of TA-65 on senescent T cells. And that's, you know, in both CMV positive and CMV negative, and we see a beneficial effect in whether CMV positive or CMV negative.

Yeah, because I rarely see anyone and like, well, what test do you use? Because you see, I, you know, IgG, they don't make even a reactivate IgM. It's not a new infection. And the PCRs from standard labs are so insensitive. That's kind of like HHV-6, you know, at least Montoya showed a little bit of a good study where, you know, the reference range is like 1 to 20, but really a positive is like 1,200, you know, because that's what it doesn't mean. It's reactive, but it's more likely the higher it is. Is that what they did, or they do a PCR, or what would they do for, for looking at the CMV?

No, so it's just whether you're CMV positive or negative. That's okay. We didn't look at the titer. What you're talking about is the titers. And, and yes, those in— actually, in CMV, if the higher titer you are, you have, the, the more you have senescent T cells because there's more reactivations taking place. I mean, I think that CMV is, is not unique, but it's probably the most immunodominant in terms of stressing your immune system. But pretty much anything that causes you to have to mount a response. Intracellular pathogens like Lyme and babesiosis, the other things that you're mentioning. I have patients that come in that are being treated by Lyme doctors and for chronic Lyme, and their telomeres are shorter. And what's interesting is there's something called the lymphocyte to granulocyte telomere length gap. So granulocytes, which are neutrophils, are, are, come from the bone marrow, circulate for a day, and then they're gone. Their telomeres, they don't divide again, and telomeres don't get any shorter. They're a good reflection of your bone marrow stem cell telomere length and of your inherited telomere length. The lymphocytes, however, as you know, fight off— released from bone marrow and then fight off the infection that they need to, or the tumor that they need to fight off. And then memory cells are left behind, and if that— they're challenged again, then they come out again. And that's what's happening with CMV, that's happening with other herpesviruses, and that's what's happening with, with other chronic infections. And so anytime you have a chronic infection that is asking the immune system to keep it at bay, you are going to cause telomere attrition. In fact, a nice study was done looking at the number of herpesviruses that you have in addition to CMV, from 1 through 4, EBV, HSV-2, HHV-6, which I think is a big immune stressor, and I know you work with that in chronic fatigue. The more they have, the much shorter, the much faster the telomere attrition is. So there's a slope that's relatively shallow, about 0.05 kilobases for one herpes virus infection. It gets steeper for two, even steeper for four, and at four it's very steep. So it's like a 50% steeper slope. So you want to try to avoid, avoid these, uh, these things. That's why I tell patients, you know, the way we're treating COVID right now, you should try to keep other pathogens away from you. When you're young and you're trying to teach your immune system, maybe getting a few things to help tolerance, but when you're older you want to stay away from these things.

Yeah, and even like, you know, HHV-1, you know, herpes virus 1, okay, you get a cold sore, but they find it travels up the nerves into the brain and is associated with Alzheimer's. And, and so these things are not benign, you know.

They are not. No, yeah, that's a nice series of studies that's, I think, just starting to get the recognition that it should get, that HSV-1, herpes, human herpes virus 1, is a bad actor for increasing risk of Alzheimer's disease.

So yeah, everyone's chronically infected, and I think it's so much higher than, you know, 20 years ago. Now I can't go to a party where, oh, you know, I'm so sick, or my brother's so sick, or family. It's— and you didn't hear that 20 years ago. Everyone has these chronic illnesses that just standard medicine just doesn't know what to do with, and everyone's immune system is shot.

You know, yeah, so that's where, you know, some of the peptide therapies you talk about, you know, thymosin-1 alpha and that kind of stuff. And then I think even potentially growth hormone, which can rejuvenate the thymus in, you know, some smaller studies. You know, the focus when you're talking about these chronic immune stressors should be on the host, on shoring up their defenses through immune system rejuvenation and then through maintaining telomere length so the cells can continue to divide. Because once they become senescent they can't do their job. And not only can they not do their job, I kind of liken them to an old watchdog which not only doesn't go after the burglar but bites the owner and snarling all the time, um, causing problems. So I think that, that keeping your immune system youthful is, is, I think, not only for fighting off infections and cancers but also chronic degenerative disease like osteoporosis, cardiovascular disease, and Alzheimer's, because of the reduction in inflammation. You know, I follow C-reactive protein in everybody, IL-6 in everybody. People that have a lot of inflammation—

you have a good lab for IL-6?

Yeah, I mean, Quest does a good job, and LabCorp, they, they have a good assay for that.

Because we find it— I think it matters the draw station, you know, how they, you know, they hold it. And a lot of these like key tests, like, they'll come out zero, you know, and and they, you know, hold them, are supposed to be, you know, frozen or whatever immediately, and they're sitting out. We find that's a big problem. But yeah, FDA is coming after thymosin alpha 1 because people are using it for COVID, and it's such a great COVID, you know, and it's reversing COVID quickly. And but God forbid, they don't want that, and so they're coming after it.

Yeah, well, you can't get— you can't make those claims. That's the problem without going through the trials. Um, but, but, you know, look, we know treating patients— and that's why we're allowed to do off-label stuff— that, you know, things work. That's how medicine progresses, through doctors treating patients. And you have to look at the risk-benefit equation. I mean, what's, what's the risk-benefit equation here? It's, it's, you know, we know it's highly in favor of benefit because the risk is so low.

Um, so yeah, so that's the same thing with COVID Why aren't we giving everyone, you know, vitamin D and zinc and vitamin C and flavonoid, you know, even ivermectin, even Hydroxychloroquine. Oh, the black helicopters are coming after me, you know. And we don't even need the vaccine.

I—

no one should be dying from COVID The hospitals aren't giving people anything. Like, a study just showing people on ventilator, they gave them half vitamin D, 5% mortality. The other half without it, 50%. Like, and there's no downside.

Yeah, and then that all speaks to— I mean, look, I just did a talk for the Institute of Functional Medicine on on the virome, telomere biology, and the effect. And what you need to do is to shore up the host, because COVID has shown us that, you know, the age association of COVID is so strong that it's the aging process and the debilitated host that's the problem, and the cytokine storm coming from the senescent-associated secretory phenotype um, but the fact that it happens to younger people is the really interesting thing. And what markers of, of, of risk are there? And I, I believe that— and other authors that are in telomere biology— that probably these people have short telomeres. The younger people that are getting really sick, they either have short telomeres or they have much higher accumulation of senescent T cells. And it may be that that's what's putting them at risk.

Now, we don't have the data for that, but I bet you're right on that.

Physiology works out.

I, I would, I would bet a lot that you're correct. Is there a racial difference in telomere length?

There is. African Americans have slightly longer telomeres, um, um, and that's, that's the only major one. But then on top of that, there is the senescence T cell stuff comes in because there's a higher incidence of CMV in, in, in non-white ethnic populations in the United States. And so that stresses the inheritance that they got. And over time, I think their risk increases.

It becomes so difficult to, you know, so many of these things, they all— these people have this, but why is the real reason, you know? And so there's other things like, you know, DNA methylation, proteomics.

What— so just going back to the, uh, to the, uh, to the biomarkers, the Hallmarks of Aging, the mitochondrial dysfunction you know, it's all linked. You know, what I found fascinating, when a paper came out in 2011 which looked at the effect of short telomeres on mitochondrial biogenesis and mitochondrial efficiency, and it's through that master regulator, those master regulators, the PCG-1 alpha and beta, they are turned down when telomeres get short so that you get less mitochondrial biogenesis. So keeping your telomeres longer helps your mitochondria, and vice versa, because having efficient mitochondria decreases reactive oxygen species, which then don't attack telomeres as much. So dividing cells lose about 100 base pairs per year, but then while you're dividing, if you have a lot of oxidative stress, you know, a telomere, which I didn't, you know, say for the audience, is TTAGGG, TTAGGG. So repeats of those, of those 6 nucleotides, and the GGG is very susceptible to free radical damage. You maybe, maybe using your practice or have heard of the, uh, the DNA damage test which looks at 8-hydroxy-2-deoxyguanosine in the urine. That's those base pairs getting repaired because they've been attacked in the DNA and end up in your urine as a good measure of it. So, so it's all, you know, what I like about where the field has gone is we now have sort of a unified— the equivalent in physics of a unified field theory in, in aging, where we're really starting to put all the pieces together. You know, it's not just this or just that. It's like the, the free radical damage affects telomeres, that affects epigenetic DNA methylation, and, and, and then, you know, we're just learning. It's all coming together, and it's a really fascinating field. Um, and then, you know, then we have other hallmarks of aging— cellular senescence, stem cell exhaustion, and the list goes on. Of all these things that you look at as the major things. And I actually, my— in my practice, I target the hallmarks of aging. I look at ways to measure them. Um, you know, we have DNA methylation, we have telomere length, we have, you know, ways to look at DNA damage. You can look at senescent T cells. And I focus my therapies on, you know, certain things like flavonols. Flavonols can have a beneficial effect. Hormone replacement therapy can have another kind of effect to try to make your hallmarks of aging as healthy as possible, and then put it all together. That's at the molecular level. Then you look at things like arterial stiffness, pulmonary function. These are tried and true biomarkers that are, you know, hard endpoints for mortality and cardiovascular disease. Most people don't know that FEV1— I mean, they know it's associated with age, but they, they don't know that it predicts mortality 25 years later from all causes, not just pulmonary and respiratory causes. If you have a lower FEV1 relative to others in your age group. So, so looking at all these different biomarkers, we get a, we get a feeling for what's happening to the aging process. And, uh, and, you know, things like TA-65, which helps keep telomeres longer, has effects in pretty much every system. I haven't talked about cardiovascular disease. There's a trial going on right now in the UK looking at the effect of TA-65 on senescent T cells in people who have had an MI, and whether or not through reducing senescent T cells and the inflammatory response of T regulatory cells, will we have a reduction in repeat MIs? Because we think that, and there's very good data showing that short telomeres are associated with cardiovascular disease as well. So, you know, that's what I like about it, is that you're fixing many things when you're fixing the telomere length. We all know the power of hormones. I mean, a postmenopausal woman comes in and you fix your hormones and she feels 100% different, and it's very gratifying.

Oh sure, you can. And I don't want to offend anyone, but a woman is not on estrogen, you can pick them out.

Like, yeah, I mean, it's, it's, you know, and I, I've been doing it for 25 years. I have patients that have been going along and they tell me, you know, my girlfriends are saying, you know, they're just looking different and feeling different from me, but But, you know, so, but then you want to make sure that their telomere lengths aren't getting shorter. Uh, so you want to, you know, optimize all aspects of their aging process.

Uh, that's great.

And do you have a test, good test for mitochondrial dysfunction?

I don't really have a great one right now. I think that, you know, your, you know, your VO2 max might be a beneficial one to a certain extent, but that a lot of that is built in genetics. I, I, I've been looking for one. And if anybody—

Yeah, I've been looking for a long time. There was the Mitoswab, but I don't think it— yeah, it's, you know, it's pretty hard. Yeah. Well, we'll check people's basal metabolic rate, which I think, you know, correlates. They don't have mitochondrial function, but because so many diseases are associated with mitochondrial dysfunction, you know, you know, most everything, disease of aging especially. And then let's see, what was my other— oh, EMFs. Do you know anything about EMFs and telomeres?

I, you know, I don't. I mean, I, I've looked for data on that, and off the top of my head right now, I can't tell you that I found anything. But one would think that there's— I mean, look, low-level EMF could be beneficial potentially, you know, as some people use as therapeutically. Let me get my screen opened up again. But I don't have any.

Yeah, Promozek has shown that— I started looking into it very skeptical, like, oh, it's got to be safe, and dramatic increase in IL-6, and they activate the calcium voltage-gated channels, and, you know, the calcium—

this is in vivo, in vitro though, right?

Both.

And then also, like, one study they put just a cell phone in the middle of a box of rats for 9 days. And then they sacrifice them. They look, they got hippocampal degeneration.

Wow.

It's, it's crazy. I'm, I'm worried. The more you dig into it, the more you're like, oh my God. But that's a whole nother, another topic. What were some pearls? Like, what are your favorite treatments? I know, you know, TA65, of course. Other things. What are your like top 5 things, or—

I mean, for me in my practice, I do a lot of hormone optimization. I don't think that people without sort of more optimal hormones are going to enjoy life as much as people that don't have optimal— as people that do have optimal hormone levels. I mean, I do use TA65 a lot. I have a whole pack of supplements that I think the omega-3 fatty acids, I think, are very, very important. There's a lot more coming out on that, particularly in Alzheimer's disease. And then, you know, the plasmalogens, which you, you may have seen some of that work that's been done, um, uh, where— by Diane Goodenow— where, you know, you're looking at, um, um, you know, APOE genotype and risk being abrogated or almost completely mitigated by, by having good plasmalogen levels. So I try to— I saw your Boston Heart up there in the corner. I do the Boston Heart Fat essential fatty acid analysis, and I have everybody want to get their omega-6 index in optimal range. So I use them. If they don't get it through fish, you know, I get it through the fish oil.

And the plasmogens, I mean, I have some here, I like to say, and then I've also heard though, oh, they just get broken down.

No, so plasmogens do, but what you're seeing there is a precursor that then makes it through the gut and then is is used to build plasmalogens. At least that's how it's been explained to me. I've done my first baseline. I have to do some follow-up ones to see, you know, whether or not it's effective. But I'm just— that's an area, just in general, fatty acids, I think, and plasmalogens are, you know, an area that I think is really up and coming for data supporting, you know, optimizing those levels for healthy aging and disease prevention. I would say, you know, we talked about senescence of the immune system, you know, if— for people that can't necessarily send their stuff to UCLA where I send it for looking at naive T cells and senescent T cells, which are specific markers, CD95 and CD28, if you have a CD4 to CD8 ratio, which is available at, you know, Quest or LabCorp or any lab that does, you know, lymphocyte subset panel, if it's less than 1, there's a, there's a, there's a good body of data that shows, particularly in older individuals, those are 80 and above, and then even 60 and above, that they're starting to collect more senescent T cells because the denominator is the CD8s, and it's the suppressor cytotoxic T cells that get senescent, not necessarily the helper cells as much. So the top stays fairly stable, the CD4, but you get this accumulation. They don't die and go away, and it's not because you have a lot of healthy senescent suppressor, a lot of healthy suppressor cells, you have accumulation. You know, of them. And if that gets below 1, then you really want to look at, you know, trying to— I would then measure the telomere length in that patient. And, and, and if they're not, you know, if they're doing— if they're not doing everything you can do from a lifestyle standpoint, then do it. Quit smoking, make sure, because they're at significant increased risk of, of disease and mortality when that ratio gets inverted. It's normally around 2 to 2.5, and when it gets below 1, things, things get really pretty bad.

Because I'm thinking of Lyme patients, we see their CD8s drop much more than their CD4s.

Drop? Oh, with the total CD8 population?

Yeah.

I'm not sure about— I mean, that I kind of— are you sure? I'm not sure about that because what would happen, I would think, is that you would increase the number of senescent T cells because the Lyme is trying to be fought off by that. But in the patients that I have come in, I see, like, I have a number of them, they have large accumulations of senescent T cells. Just to give you an idea, I mean, you typically have zero senescent T cells when you're born, and then, you know, they thought that you should— used to accumulate them with just the aging process, but it's really whether— it's really your viral load, and particularly CMV, that causes that. And also other, as we talked about, other immune stressors. So I have patients that are in their 60s that have, you know, 20, 30 senescent T cells, uh, you know, on a measurement. And then I have patients who have 800, and that's like 75 to 80% of their CD8 compartment is senescent and secreting all sorts of inflammatory cytokines. What test do you use for that? Yes. So that's the CD28 negative, is the senescent T cell that you can get at UCLA. And you can get it through PhysioAge. You know, you go to physioage.com and you have a licensee, you can get it through that. Or TA Sciences also offers that at tasciences.com to get the test through UCLA as well. But as I said, the less, you know, the one that can go through insurance and is less expensive is to just look at the CD4 to CD8 ratio. And if it's under 1, then you almost assuredly have a high accumulation of senescent T cells.

And how about CD16?

You mean that's a— there's not a CD16, there's CD19, which is the B cell.

CD— I remember because I haven't done my labs in a long time and mine was just so low when I was sick.

Um, CD56, CD16 you're talking about for the natural killer cells?

That's it.

Yeah, no, CD56 or CD57. But anyways, it's interesting. It's what also— so the immunosuppressants suppress for autoimmunity, but they tend to be really low. Um, but in some patients, it's weird, a subset of patients.

Yeah, I, I don't measure that one. We look at, then we look at the natural killer cells, which is the CD56, CD16 positive, and then we look at the, the CD4, CD8s.

And did you measure function?

No, it's, it's the lymphocyte subsets because there's a very large body of data showing the association between those and autoimmune disorders. The viral load, mortality. Um, functional assays would be interesting. There haven't been as many studies with those, but you know, you get very good information in just looking at the markers on the, on, on the, uh, yeah.

And for instance, like natural killer cell function, you know, it's a hallmark of chronic fatigue syndrome, that about 70% are low natural killer cell function, about 30% are low natural cell number. So a lot of them like their gifts, and that's a not working. But the problem is, like, Quest does the function, and Quest's so difficult to deal with. They, they're all messed up. And LabCorp, much easier to deal with, but they're— I don't know, their tests, a couple of their key tests that we like, uh, Quest does a better job. But overall, Quest is a pain in the ass.

But yeah, they've been going through the last 2 years and trying to become a true national lab, and they're just not They're not there right yet. Yeah.

Yeah.

I'd love to see someone else come on, you know, come online. And let's see, wrote a number of papers on the TA65. And so imagine that's a core treatment. And do you— so hormones, you do thyroid, by the way, do you?

Oh yeah. Yeah. Thyroids. I mean, what you were talking about with getting women pregnant with the T3, I mean, it's very gratifying. When they, you know, their fertility doctor's telling me your thyroid tests are normal and, and, you know, they've done 3 rounds and you get their T3, you know, above 3.8 and all of a sudden they're pregnant. So I do, I do, I do a fair amount with thyroid. I find it to be—

yeah, and that's like I spent most of my medical work convincing people that TSH is not reliable, you know, because all these sick patients, they get suppressed, you know, hypothalamic-pituitary-thyroid axis, and they're not making TSH. And, but that's just the way it's an easy test and, you know, controversial. So I've been working on an assay that will show that, but we're on for 15 years and I get to a certain point and something happens. So now I'm going to some big guys and see if I can get that done, but kind of prove that all these people with normal TSHs, you know, and they come in and normal TSH, and they're— we check their basal metabolic rate and super low, and they're, they're basically relaxation phase of their reflex super low, and their pulse is like 50, and they're gaining weight like crazy. And then you give them some thyroid and say suppress the TSH, like, oh, they're hyperthyroid. And like, oh, they can't get out of bed, pulse is 48, and they're freezing cold. And, you know, anyways, but another thing, I imagine thyroid has lots of increased mitochondrial function and does so many things.

Yeah, absolutely. I mean, it's just, you know, it needs to be optimized as well. I mean, thyroid analogs have been looked at to lower cholesterol. I mean, we all know the cholesterol shoots up when you're hypothyroid, and patients that have good thyroid function, the cholesterol can come down quite significantly.

So yeah, I mean, it's like the safest way and Or the STAR report, largest study ever done on antidepressants, showed that T3 was a better antidepressant than antidepressants with less side effects. But it didn't make the abstract because they didn't pay for part of the study.

You know, you have to deal with that in our field.

There's so much biases that, that's just, you know, basically driving me crazy. But yeah, your, your whole program sounds very interesting. And, and looking at all these things, I think, is the key to so many ways of approaching so many illnesses. And I think that's the problem with modern medicine, is you get sent to, you know, gastroenterologist for this, you get neurologist, and you don't go until something's really bad, right? You know, and, and people say, oh well, I can't, you know, out of network, you know. And how much is it worth not being in a nursing home for 20 years? Living longer, being longer with your kids and your grandkids, and having a better quality of life. You can't put a price on that. And, you know, when I had Lyme and was bedbound, you know, I would trade everything for— just take everything. I just want to be healthy because you can't— doesn't matter how much money you have when you don't have your health. And so I think you're doing some amazing work and helping so many people because we take it for granted. That we're healthy until we're not. And shit happens, you know.

Yeah. And, and the key, the key thing that I would drive home is that you can measure how healthy you are, you know. And you may not be as healthy as you think you are, even though you feel good, because a lot of this stuff smolders at a subclinical level until it breaks through. Uh, and the idea is to pick it up 10 to 15 years before then. And that's why we look at—

yeah, when you can do something about it.

Yeah, exactly. There's old phrases that, you know, at first a disease is easy to cure but difficult to diagnose, but as time passes it becomes easy to diagnose but difficult to cure. That's Niccolò Machiavelli.

And that's a good, a good summary right there. Hey, I think this is fascinating stuff. I think you're doing great work. And, you know, I think the way showing people all these different, you know, markers, I, I think is, is just huge. And you're very obviously evidence-based. And hey, and as patients, you're proving to the patient this therapy works, not just, hey, take this. Oh, one question I want to ask you: what's your thought on statins?

You know, I think that statins, interestingly, look, this— the world is kind of— it's gotten really divided. There's people that are pro-statin and people are anti-statin.

Everything becomes like a political argument.

Exactly. I think that the statins— my quick take on it is that in certain correct populations, they save lives. I don't— I mean, there's strong data for that. They're overprescribed in people that don't need them. And, you know, most people tolerate them, but a lot of people don't tolerate them. Interestingly, statins do have a mild telomerase activator. And maybe one of the reasons that they're effective by turning on telomerase and lengthening telomeres. That's part of the work that's being done by Kim Spyridopoulos out in the UK, and the same one that's running that trial that I talked about with telomere biology. But I think that the problem is, is that cardiologists and internists sort of don't give patients a chance and say, look, you can get your cholesterol down if you make these changes in your diet, get exercising, do all these things. And I have patients with cholesterol of 300 because everything else is working well. They got clean coronaries and they're 75 years old. So, you know, that person doesn't need a statin. A person with a cholesterol of 200 with a coronary calcium of 1,000, I think, you know, you're probably— it's malpractice not to give them a statin at that point if they're not doing everything else. Because of the anti-inflammation, probably doesn't have that much to do with the cholesterol.

Yeah, I think the whole cholesterol theory of heart disease is, you know, it's getting its legs knocked out over and over. And it is anti-inflammatory, but also it's a it's a mitochondrial inhibitor, you know.

Right, yeah, so yeah, and that's the problem, right, exactly. So I think there's a better way, you know, to, to do it, you know, in, in certain patients, you know.

For instance, the study came out and showed basically, it seems, the ideal patient, diabetic patients with heart disease, they showed an increased mortality. Like, okay, it doesn't work for these people, why? And I think anytime you try to give it to everyone you know, they want to put it in the water. That's when you get into trouble.

That was a big problem. I mean, the polypill back in, back in the day when they wanted to put a beta blocker, a statin, an ACE inhibitor, aspirin, I think one other thing in, in a pill. That's the opposite of personalized medicine. You would probably get an overall beneficial effect on mortality, but you'd have a lot of people being treated that don't need to be treated, have side effects. N of 1 is really, you know, where medicine is going because we're all very different in many different ways. And unless you're exactly like the average person in that large clinical trial, the data may not be applicable to you. Yeah.

And it's totally true. And I tell patients, look, we go by the studies, but you're not a study, you're a person. And, and they usually take people that don't have anything else, and which— so they're a rare breed, you know, finding those people. And, and so we're, you know, doing studies and thinking like, how do you find a healthy person?

You know, and it's—

everyone's exposed to toxins, pesticides, plastic, stress, you know, all this stuff. And like, you know, BPA, you know, and all the pollutants, but chronic infections. Like, I don't know, there's healthy people out there to do the control. But yeah, hey, fascinating stuff. I, I, I, I think this is great. I think you're doing such a great service and Happy to help get, get the word out. I'm gonna give you a buzz this week and, and about your software. I'd love to.

Okay, sure.

Yeah, I'll be around. Absolutely. Great talking to you. Thanks for having, thanks for having me on.

Great.

Thanks so much. All right.

Take care.

Have a great day.

Thanks for joining us on the Peptides and Longevity Podcast. If you enjoyed today's episode, don't forget to subscribe, share, and leave a review. It helps us reach more listeners passionate about optimizing their your health. For more insights, resources, and updates, visit our website at www.holtorfmed.com. Together, let's embrace a future of health and vitality. Until next time, stay inspired and keep thriving.