[0:00:52] About the Podcast and A Must Longevity Supplement
[0:02:39] Podcast Sponsors
[0:04:28] Today’s Guest
[0:08:37] Telomerase Activity and Lengths
[0:13:09] What Are Telomeres and Telomerase?
[0:19:32] How telomeres can be lengthened, and how to lower the rate by which they shorten?
[0:26:16] Telomeres and Treating Cancer
[0:31:42] Podcast Sponsors
[0:34:56] Telomere Testing
[0:44:15] Research on Increasing Telomerase Activity
[0:53:29] Dr. Andrews’ Personal Anti-Aging Protocol
[1:07:14] Precautions Before Taking the Anti-Aging Protocol
[1:16:17] The Telomere Clock
[1:21:52] Closing the Podcast
[1:22:45] End of Podcast
Ben: I have a master’s degree in physiology, biomechanics, and human nutrition. I’ve spent the past two decades competing in some of the most masochistic events on the planet from SEALFit Kokoro, Spartan Agoge, and the world’s toughest mudder, the 13 Ironman triathlons, brutal bow hunts, adventure races, spearfishing, plant foraging, free diving, bodybuilding and beyond. I combine this intense time in the trenches with a blend of ancestral wisdom and modern science, search the globe for the world’s top experts in performance, fat loss, recovery, gut hormones, brain, beauty, and brawn to deliver you this podcast. Everything you need to know to live an adventurous, joyful, and fulfilling life. My name is Ben Greenfield. Enjoy the ride.
So, it’s not often that I have the pleasure of interviewing someone who is as much on the cutting edge of longevity research as the guy that I interview in today’s show, but I got lucky, and you get to listen in. You’ll love this podcast with Dr. Bill Andrews of Sierra Sciences. We talked a lot about longevity. So, of course, any discussion of longevity would not be complete without telling you what I do for longevity from a supplementation standpoint. And one thing that is a daily must for me is something that you’ll find consumed both in Okinawa and in Bama, to longevity hotspots, to areas that are considered to be Blue Zones. One is called bitter melon. The other is called rock lotus.
In Bama County, which is located in Western China on the slopes of the Himalayas, they have men and women who are extremely robust and in the highest ratio of centenarians than anywhere in the world, meaning, the longest average lifespan of any country in the world. And one staple of these folks’ diet that they give a lot of credit for their longevity too is called rock lotus. In Okinawa, something that seems to act similarly to rock lotus in terms of a calorie restriction mimetic that also improves insulin sensitivity and regulates glucose metabolism is bitter melon extract. And bitter melon extract also acts kind of like exercise in a bottle by stimulating what’s called AMPK, which is one of the protein kinase that’s activated via exercise.
So, you’ll find both of these in the supplement Kion Lean. So, Kion is the company where I formulate fantastic supplements designed to do the type of things I just described to you. Kion Lean is one of the ones at the top of the totem pole. I use it every day. So, you can go to–I’m actually using it three times per day right now as a sort of experiment to see how low I can get my blood sugar. Anyways, you can go to getkion.com, getK-I-O-N.com, to get yourself some Kion Lean. Kion Lean is what that one’s called.
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Hey, folks. My guest on today’s show actually just spoke at a pretty prestigious anti-aging conference and he pretty much is at the forefront of the longevity and anti-aging movement, having written books like “Telomere Lengthening: Curing All Disease Including Aging and Cancer,” which we will talk about today. We’ll be taking a deep dive into that today. He also wrote the book, “Curing Aging.” And because he just got off the plane from that last conference that he spoke at, if you hear him walking around, it’s because he’s a man after my own heart and he’s both pacing and podcasting during this call. Just don’t clean your garage, man.
Bill: Okay. I’m in my conference room.
Ben: His name is Dr. Bill Andrews. With all the controversy these days around telomere testing, is it accurate? Do these companies that do popular telomere tests really show your so-called biological age versus chronological age? Once you get your results back, can you lengthen your telomeres? Should you lengthen your telomeres? These are all questions that I really want to explore because I get these all the time. The reason I want to get Dr. Andrews on the call is because a mutual friend of ours, Dr. Joseph Mercola, recommended Bill as being the bee’s knees when it comes to knowledge of all things, telomeres.
Dr. Andrews, who I realized I just called Bill and then I reverted back to referring to you more formally, what do you prefer, Bill or Dr. Andrews?
Bill: Please call me Bill.
Bill: I just don’t like Dr. Andrews, but Bill is great.
Ben: That’s easier on me, less syllables. Bill is the founder and the CEO of a company called Sierra Sciences, which I’ve come across multiple times and in many of the books I’ve read on anti-aging and longevity because I’m doing quite a bit of research for my own book that I’m writing on this matter. What Sierra Sciences is is they’re a company that’s focused on specifically finding ways to enhance human longevity via the telomere pathways. He’s a scientist. On his bio, he claims to be an athlete, so I’m curious what athletic endeavors you participate in, Bill. And he’s also been featured all over the place, Popular Science that today shows numerous documentaries on the topic of life extension. He was in “The Immortalists” in which he co-stars with Aubrey de Grey, a former podcast guest of ours and also kind of a guru in the longevity movement. And if I’m not mistaken, Bill, if I could drop a clue for listeners, I believe your specific flavor of athletics is kind of ultra-endurance, is it not?
Bill: Yeah, but other things too. I mean, I’ve been a professional, well, amateur competitor in snow skiing, water skiing. I used to hold the world speed record for barefoot water skiing. But running is the one I do the most because it doesn’t require a boat, doesn’t require a cart, it’s just run out your front door and go running. So, most of it is running, and I compete pretty regularly in ultramarathons.
Ben: What’s the toughest race you’d done?
Bill: The toughest would be, probably the Barkley Marathons, which is–
Ben: You did Barkleys?
Bill: I’ve done it three times but I’ve never finished. In fact, typically, less than one person on the average per year finishes.
Ben: Yeah, I was going to say not a lot of people finish that race. For people don’t know, that’s held in Frozen Head State Park near Tennessee, and it’s considered to be a fun run of 60 miles up to a full course of 100 miles, but it’s like not the average ultramarathon. It beats you up and spits you out.
Bill: That’s also my favorite.
Bill: I want to go back and do that. But I’ve also done Badwater, which is the 135 miles through Death Valley in the middle of summer at 130-degree temperatures. I’ve also run through the Himalayas at 18,000 feet elevation, 138 miles non-stop, and a race called La Ultra – The High. I love those races and I can’t wait to do them again.
Ben: Did you know there’s actually a study on endurance training and telomerase activity that actually increases telomerase activity?
Bill: There’s a ton of them. And actually, some of them, they kind of misunderstood. They actually don’t increase telomerase activity. What they do is they decrease the rate of telomere shortening. Ultramarathon runners have the longest telomeres. There are a lot of misunderstandings about telomerase activity in human cells except for the reproductive cells. It’s because telomerase assays are really difficult to do when you have really low levels of telomerase. It’s really easy to get false positives. So, there are a lot of misunderstandings there about–but nothing actually increases your telomerase activity when you really don’t have any telomerase activity, to begin with.
Ben: Well, we should get in the definitions for people shortly, but can I push back on you? I mean, isn’t there some evidence that ultra distance endurance racing can also–like short-term endurance could increase telomere length but long-term could cause some oxidative DNA damage that could imply some telomere shortening?
Bill: Yeah. It’s pretty much not the length; it’s the way you do it. Okay. So, what you got to do is, I always say, you got to keep it fun. If it quits being fun, then it’s time to quit. Save it for another day because consistent running actually decreases inflammation when measured by CRP scores and other markers of inflammation. It’s the people that are occasional runners, and when they do run, they run too hard, crossing finish lines on their hands and knees, throwing up and stuff. That is really bad for you.
Ben: Yeah. That was like me when I raced Ironman and I did test. We’ll talk about whether my test was accurate, but my biological age was significantly higher than my chronological after 10 years of Ironman.
Bill: Yeah. You know, my CRP scores are typically below detection levels. If I run a 5,000-mile race and my CRP score goes above 2, then I say to myself, “I did that too hard. I should have just taken it easy, focused more on having fun and stuff like that.” There are some times when I intentionally push myself really hard and I don’t even want to measure my CRP score because I’m afraid to. But it’s rare when that happens, and I think the benefit racial, or the benefit of training and stuff like that in a kind of fun way, keeping it going, just never pushing it is a good way to keep inflammation low, keep telomeres long, despite that maybe once or twice a year I might push myself too much during a race.
Ben: Yeah, I agree. And by the way, I misunderstood some of the data out there. I think, and one of the studies was in the journal of mutagenesis on the chronic and acute effects of endurance training on telomere length, and it did suggest that acute exposure to, in this case, an ultra-distance endurance trail race, could imply telomere shortening but their data suggests chronic endurance training, as you’ve just alluded to, provides protective effects on telomere length that could attenuate biological age. So, yeah, you can’t just look at what’s going on right after the event because it’s kind of like measuring yourself right after exercise. It might look like a metabolic shit storm, and then the next day, you’re actually healthier.
And so, one thing that I should mention to people before we jump into just telomeres and defining them and kind of getting into the 101 on telomeres and telomerase anyways is when Bill is talking about CRP and the heart rate and enjoying it, this is my take on endurance exercise as a whole. Our hunter-gatherer ancestors, when they were hunting or gathering or foraging or anything else, they were not pounding the pavement at a heart rate that was slightly below their lactic acid threshold. Anyone who has gone out on a bow hunting trip, for example, knows that you’re just kind of moving at a slow pace, occasionally crawling, occasionally sidestepping, occasionally hoisting some heavy packs if you’re lucky and you’ve got a kill, and you’re not engaged in the type of exercise that you see on the Hawaii Ironman on TV every year. There’s a difference between some forms of endurance racing and others, I guess, is what I want to emphasize.
Bill: If I did an Ironman, I guarantee I would finish last and cross the finish line with a smile on my face.
Ben: Yeah, yeah. If I could go back and do it again, I’d be very tempted, but I think I’m too competitive. So, anyways, let’s go ahead, and we’ve already dropped a few terms people may not be 100% familiar with like telomerase. So, can you give the 101 on telomeres, how they work, and telomerase?
Bill: We’re made up of 100 trillion cells, our bodies are, and inside of every cell is 46 chromosomes, 23 different pairs of chromosomes, and that’s where the genes are. And the best way that I’d describe it is to think of that chromosome, each chromosome, as a shoelace. And the caps on your shoelace is called aglets, so the equivalent of telomeres on your chromosomes. So, just like the aglets on your shoelace, they protect your shoelace. The telomeres on your chromosomes protect your chromosomes. Now, chromosomes are made of DNA and protein, but we’re talking about just the DNA part of it right now. And so, when the telomeres get really short, your DNA starts having some pretty negative consequences. Sometimes it starts mutating when the telomeres get really short, but it also affects expression of the genes that’s on the chromosomes. Genes are things you can turn on and off like light switches, more like a dimmer switch. The length of the telomere affects those dimmer switches. Okay?
So, telomeres, genes can turn on and off relative to the length of a telomere, and that causes aging when the telomeres get short, I don’t want to say aging per se, but let’s say declining health with age. But that’s what telomeres are. It turns out that every single time our cells divide, our telomeres get a little bit shorter, and it’s due to the fact that when you have a parent cell that’s going to become divided and become two daughter cells, everything inside that parent cell has to be first duplicated in order for–after the division that the two daughter cells become identical to that parent cell.
During the duplication, DNA is one of the things that have to be duplicated by the process called DNA replication. But it turns out that our cells lack the ability to replicate the DNA all the way to the very end. It’s like a bricklayer, putting a row of bricks on top of a wall by standing on the wall and walking backward. And when they get to the very end, they can’t put a brick in the last place they’re standing because if they step back, they fall off. That’s what’s happening with our telomeres, and they get shorter every time a cell divides. And as a result, we get declining health.
It’s known that when telomeres are 15,000 bases, which is the typical length when we’re first conceived, our cells are very healthy. By the time we’re born, because of all the cell division going from a single cell embryo to a newborn baby, our telomeres already have shortened down to 10,000 bases. Bases are units of measurement of DNA where whole chromosomes about 100 million bases in length. But 10,000 bases are still okay, still very healthy, just like if you cut your aglet on your shoelace in half, your shoelace would still be fine.
But the problems become when all the additional cell division, as you grow up, you have injuries and you have to have cell division to repair wounds and you have like diseases and your immune system has divided to fight a disease, you end up having telomere shortening occurring even at a faster rate. And when telomeres get down to 5,000 bases, everything works, and Petri dishes work from looking at people’s cells and bodies. And when cells get down to 5,000 bases, the cells essentially crash. They lose the ability to function and then eventually die. And so, people, when we calculate the rate of telomere shortening in the healthiest of people, if you had the perfect genetics and led the perfect lifestyle, your telomere shortening rate would allow you only to live 125 years.
Ben: Really? So, you can actually mathematically calculate it to be a maximum human lifespan that we currently know of, of 125 years, that we’re capable of right now.
Bill: Yeah. And that’s been published in several papers.
Ben: Well, what about all these people in the anti-aging sector who are saying they’re going to live to be 150 or 160 or not die?
Bill: They’re not going to be able to do it without figuring out how to prevent telomere shortening.
Ben: Okay. So, that’s kind of like the Holy Grail?
Bill: Well, no, because vice versa. Telomere shortening is not going to make people live longer without the other theories on aging actually being implemented. That’s the message that I just gave at Jim Mellon’s conference, is that everybody is working on all these great things and there were a lot of great speakers and we complement each other. It’s going to take a group effort to cure aging. One thing is not going to be enough, and that includes just telomere shortening. I’m hoping to see significant health advantages by lengthening telomeres, but I’m not expecting people to become immortal.
Ben: Okay. Yeah. Well, I want to talk about some of the theories as to the mechanism of action via which we could lengthen telomeres and some of the research that you’re doing at Sierra Sciences. I wanted to mention, by the way–Jim Mellon’s name was just dropped. And for those of you who haven’t looked into–well, I’ll link to Bill’s books in the shownotes for this podcast, which you can access at BenGreenfieldFitness.com/telomeres. That’s BenGreenfieldFitness.com/telomeres. And if you don’t know how to spell telomeres, go Google that.
Anyways though, the other book that I’ll link to in the shownotes is a book called, “Juvenescence: Investing in the Age of Longevity.” Bill did not write that book but that look was co-penned by this Jim Mellon guy who’s kind of a billionaire investor in the U.K. who does a lot of investing in the anti-aging sector. So, that’s also a good one to add to your list if you like this kind of stuff.
So, anyways, Bill, let’s get into the mechanism of action via which a telomere could be lengthened. And I’m also curious, as you address this, whether that’s different than just lowering the rate at which it shortens, if that makes sense.
Bill: Yeah. Those are two totally different subjects. There are a lot of things you can do to decrease the rate of shortening, but there are the things your mother always told you to do. It’s live healthy, reduce stress, meditate–those things are the best things you can do to decrease the rate of the shortening. But there’s still going to be the basal level telomere shortening that’s caused by the cell’s inability to replicate the other chromosome, actually.
Ben: Okay. So, you do all that stuff perfectly. Your maximum lifespan could theoretically be 125?
Bill: Now, the other idea of lengthening telomeres comes from the idea of the fact that when people were measuring telomere lengths and stuff like that back in the ’70s and ’80s, it was observed that in our reproductive cells, when those cells divide, there is no telomere shortening. It’s kind of important if that’s the case, otherwise, our children would be born with shorter telomeres than we have. So, there was something going on in our reproductive cells that prevented the telomeres from shortening.
So, I was recruited to Geron Corporation back in the early ’90s to figure out what this is and we ended up discovering this enzyme called human polymerase. It had been previously discovered in a microorganism called Tetrahymena, and it turned out to be very different from the human form but it was human telomerase that is actually keeping the telomeres from shortening in our reproductive cells. Telomeres still shorten in our reproductive cells, but every time a cell divides that telomeres get shorter, but then telomerase comes and re-lengthens them. So, it’s like a tug of war; pulling, shortening, lengthening, shortening and lengthening, and it’s operating in a tie.
So, after we discovered this enzyme and we tried putting it into normal cells, normal skin cells, for instance, and we produced more telomerase than actually our reproductive cells, that we actually found that the telomerase actually started winning that tug of war and the telomeres actually got longer and cells became younger–
Ben: Were you putting anything in there along with the cells to cause that to happen?
Bill: Just the telomerase. All we did was insert–so you have–let’s say fibroblast cells are the most common cell that’s used because they’re the easiest to grow that has been tested on every cell type in a human that I cannot remember about right. When you grow fibroblast cells in a petri dish, and there are human fibroblast cells, they will grow for a certain amount of time and then stop growing. Okay. They enter a phase called senescence. This was discovered in 1960 by Leonard Hayflick, and so this is called the Hayflick Limit. For some reason, human cells can only divide a certain number of times.
Same with mouse cells but it turns out mouse cells do it for an entirely different reason. What we discovered at Geron Corporation is after discovering telomerase and put it into these cells, the cells never actually reached senescence. They kept on dividing because the telomeres didn’t get shorter. I think of the telomeres as like ride tickets at an amusement park. Your telomeres are these ride tickets and every time a cell divides, you lose a ride ticket, and after you use up all your tickets, the ride is over. And so, telomerase is essentially just giving you more ride tickets or giving you more telomere lengths.
Ben: Well, geez, start making some applesauce with telomerase in it and you’ve got your next billion-dollar product.
Bill: Unfortunately, telomerase is too big to get into cells.
Ben: I knew there had to be a catch here.
Bill: You have to engineer the cells or do something to the cells to get them to produce their own telomerase. We also have delivery methods that will deliver the gene to telomerase and we’re doing those kinds of things too. Since I mentioned mouse cells, when we lengthen telomeres in mouse cells, it has no effect on that Hayflick Limit. The mouse still goes into this senescence phase. But you can get them to overcome senescence by antioxidants because oxidative stress and mitochondria dysfunction are the key problems in mice. But in humans, when you treat human cells with antioxidants, it has no effect on the Hayflick Limit.
Even though they appear to be the same, mouse senescence and human senescence are very different. But that’s what we did. We showed that we could turn the old cells into young cells by every biomarker of aging that existed at the time. I left Geron Corporation to start Sierra Sciences at that point. Dr. Walter Funk continued some of the research and he actually tried human skin grown on the back of a mouse. And when he took old human skin and grew it on the back of a mouse, it looked old. But when he put telomerase in, the cells became young in every way imaginable that you could measure.
And then Dr. Ron DePinho in 2010 did this with adult mice. I just got finished saying that mice don’t age the same way, they don’t have senescence in the same way, but he did engineer mice so that they did. And so, he could see that mice–
Ben: He engineered a mouse to be more of a model of what a human being would look like when it comes to the eventual conversion of a cell into a senescence cell.
Bill: Yes, exactly. So, he made it so that the cells would have telomere shortening and the telomerase would get really short and the mice would suddenly start showing all the same signs of aging that humans do. But then he lengthened the telomeres and those mice got younger and–what did he say? There was a quote he–when he was interviewed by Barbara Walters, he said it was a remarkable reversal of the aging process. He saw brain function come back, he saw the hair color come back, he saw hair come back, he saw ability to reproduce come back, all these kind of things. I don’t call it a proof of concept because mice and humans are very different, plus these are engineered mice, but I think it’s a strong supportive concept. It’s one of the things that keeps me motivated to keep moving on with my research.
Ben: Now, one question I have about this whole senescence cell thing is, you know, cells operate in cycles, and cellular senescence, at least in my understanding, has kind of historically been viewed as like this arrest mechanism that acts to protect against cancer. And so, the first thing that comes to mind for me would be if you shut down the formation of senescence cells, couldn’t you theoretically be at the same time inducing increased risk of cancer?
Bill: The answer is the exact opposite. It actually decreases the risk of cancer because one of the main causes of cancer is mutations caused by short telomeres. Just like on your shoelaces, as I was saying, when the caps on your shoelaces get really short, your shoelaces start falling apart. Well, the same thing happens with your chromosomes. When telomeres get really short, there are so many massive mutations that you can actually see them in the microscope. Okay. You see what’s called chromosome rearrangements.
So, that’s usually a precursor to cancer. So, the telomeres get really short, you get all these mutations, the mutations cause the cancer, additional mutations cause telomerase to turn on. Next thing you know you’ve got a cancer that’s immortal. You look it in the microscope and you see the chromosomes are all rearranged. You sequence the DNA, you find that there are a tremendously even more number of mutations that you can’t even see by the microscope, and that all could have been prevented by just keeping the telomeres long. But that doesn’t mean that that’s going to eliminate cancer because there’s still risk of cancer from other things like exposure to toxins and you–
Ben: Yeah, yeah. And I should also clarify for people because I know there’s a lot of people who kind of think–they have this myopic view based on the Warburg hypothesis that, “Oh really? It’s not a problem with cell mutation,” or really, genetic anomalies that you’ve just referred to but rather it’s an acidic environment within the cell, non-oxidative breakdown of glucose causing tumor growth, and that’s generally due to mitochondrial deficiency and lactic acidosis, lactic acid buildup in a hypoxic condition. But there actually has to be, to my understanding, some type of mutagenic occurrence that happens for the cancer to occur in the first place. And then, the presence of lactic acidosis is what causes that to be able to continue on.
Bill: Well, I’ve done a lot of cancer research. In fact, I was second place for National Adventure of the Year in 1997 for my cancer research, and I’m the first one that’s going to say, “We still don’t know really what causes cancer.” But I will tell you that there’s never been a cancer that’s been studied that wasn’t shown to be caused by a mutation. So, mutations are something that has to happen, otherwise, the cells are already designed not to be cancer.
Ben: Yeah, yeah. I feel like we could probably have a pretty lengthy discussion on cancer alone, and perhaps, that might be a good one to tackle for round two. But ultimately, what you’re saying is that decreasing the ability of a senescence cell to form is actually going to impact the level of mutation that occurs on the telomere level, and thus, decrease the risk of cancer while at the same time increasing lifespan.
Bill: Yeah. It also decreases the chance that a cancer is going to survive. So, if you let the telomeres get short and it becomes a cancer, and then you treat it with a chemotherapy that kills the cancer, the mutation rate is going to be so high, that it’s because of the short telomeres that that cancer is going to survive the chemotherapy and come back. And then, any roadblocks to keep it from metastasizing are going to be overcome by the short telomeres. So, keeping telomeres long, even in cancer cells, is what I promote mostly as the best thing to do.
And if I could choose an analogy here, this is–see, I’m not going to say that keeping telomeres long is going to prevent you from getting cancer. You can still get cancer. But I think of it like if I’m going to go across country, should I drive or should I fly? Okay. And both ways I could be killed in an accident. But so many people are afraid of flying that they drive, but driving is way more dangerous than flying, but they still do it. So, here, should I lengthen my telomeres or shouldn’t I lengthen my telomeres? People are saying if you lengthen your telomeres, you’re going to have a chance of getting cancer. Well, if you don’t lengthen your telomeres, you’re going to even have a higher risk of getting cancer. But some of the rumors and hearsay is going around us saying the best thing to do is don’t lengthen your telomeres, and there’s no data supporting that whatsoever. It’s completely rumors and hearsays.
There is a video on my website where I spoke at a conference in Tokyo with about 500 doctors. It’s in 2017, and if people listen to that video, beginning about 26 minutes into the video, I just nailed that subject completely.
Ben: Where do I find that video? I’ll link to it in the shownotes.
Bill: Go to my website, which is www.sierrasci.com.
Bill: Then, just look for Tokyo 2017 video.
Ben: Okay. Alright, cool. I’ll find it.
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I mix it up with a little bit of almond milk or coconut milk with a latte frother or a blender, so it gets all foamy. Sometimes I put a little CBD oil in there at night. Do all sorts of recipes with it. It actually blends up pretty well with ice too, like ice and bone broth. But anyways, it’s called Organifi Gold, and you get a 20% discount on this or anything from Organifi. They even have a chocolate flavor of gold, which I think makes it more like brown gold, which is what I would have named it but that’s why I’m not in branding because they called it gold chocolate. You go to BenGreenfieldFitness.com/Organifi and use the discount code mentioned there. That saves you 20% off of all of the fine, fine fair at Organifi. It’s BenGreenfieldFitness.com/Organifi, Organifi with an I, and use the code mentioned there.
Okay. Well, I don’t mean this to be fabricated suspense because I do want to return to this idea of, “Okay. Well, if telomerase does all this, what are the kinds of things that we can do? What are the compounds, for example, that could theoretically lengthen telomeres?” But before we do, I want to tackle one of the elephants in the room, a question that I get over and over again about telomere testing. There are a lot of different companies out there, from SpectraCell to TeloYears to–heck, there’s probably a dozen different companies now testing telomeres, coming back to you with what your biological age versus your chronological age is. Usually, this is like a blood drop test that you do. I’m curious, if you could kind of take us through how these tests work and what their accuracy is.
Bill: Let’s go in reverse order. The accuracy is extremely low, okay? I’m not a big fan of using telomere length measurement to measure your biological age right now because of the fact that they’re very inaccurate and very inconsistent. I will say that the best, in my opinion, is the fluorescence in situ hybridization approach. Life Length and Repeat Diagnostics are two companies that use that protocol. So, I think those are the most accurate.
Ben: Life Length and what was the other one?
Bill: So, it’s Life Length like L-E-N-G-T-H, and the other one is Repeat Diagnostics.
Bill: Life Length, in addition, will actually not just measure the average telomere length; they’ll measure the percent of telomeres that are critically short, which I think is a much more important measurement than the average telomere length. It’s like as I was saying when you cut the aglet on your shoelace in half, your shoelace is still perfectly fine. The thing you got to measure is how many shoelaces do you have that have critically short telomeres. And that’s really the big measure of overall health.
Ben: Okay. So, one more time, why are these other tests inaccurate then?
Bill: Well, first of all, PCR, which is what a lot of the companies do, because it’s the cheapest way to do it, is just very manipulatable, okay, let’s say without knowing it.
Ben: So, PCR meaning polymerase chain reaction that’s used to make a bunch of copies of a DNA segment.
Bill: Yeah. You know, I’ve been doing PCR since PCR was invented. In fact, I worked with Kary Mullis, the guy who got the Nobel Prize for it and actually hired one of his people to be head of my PCR operation when I was at Berlex Biosciences. We learned that, boy, you can get any kind of result you want by just making slight different changes in temperature or salt concentrations and their reaction. When you take samples from blood, it’s really hard to make every blood sample end up having the exact same kind of concentrations of salt and other things in there. So, PCR is very less–I don’t know what the word is, is manipulatable, sounds like intentional, but I’m talking about uncontrollable kind of changes and stuff like that.
Ben: Right. Yeah, that makes sense.
Bill: But in situ hybridization is where you take like a fluorescent DNA probe and actually bind it to the telomeres. That’s a lot more accurate, but it’s still not 100% accurate. And one of the big problems with measuring telomere lengths is that it’s random. So, even a 95-year-old person is going to have long telomeres in some of their cells, or even some of the cells with short telomeres are still going to have some chromosomes with long telomeres in it. So, you actually get a whole range of telomeres, and that’s why people always report on the average length because the distribution is very wide.
Ben: Yeah, yeah. By the way, what about SpectraCell? I know a lot of anti-aging facilities now are using SpectraCell. Have you looked into that clinical test for telomeres?
Bill: Yes. Well, that’s PCR.
Ben: Okay. So, that’s also PCR.
Bill: Same with TeloYears, that’s PCR too.
Bill: I’m not going to discourage people from doing them but I would say, boy, get yourself tested a lot of times, okay? And I would actually recommend, just in case, there’s somebody at those companies that might be kind of keeping track, I would say, send in your DNA, send in your blood samples using different names or some–
Ben: Anonymously, yeah.
Bill: Yeah. I do know one billionaire that actually did that, and he sent in four blood samples, and one of them said he was at the top 90 percentile, and another one said he was at the bottom 90 percentile. So, the variance that you can find in these protocols is very high. Now, I want to say that there is one protocol called terminal repeat–what was it? Telomere restriction fragment. It’s where you actually chop off the telomeres and run them on an electrophoresis gel, and you can actually look at the–you can actually see them. You’re not just measuring a signal from it; you’re actually seeing them distributed from small to big.
And so, you can see that it’s–one, you see it’s a big, big range, but the good thing is is that when you see this, essentially like a bell curve–okay, there’s short telomeres and then there’s very long telomeres. And somewhere in that is the average telomere, which is more intense on staining. But when you take two different cells that are from different ages, you can clearly see unambiguously that one has a longer distribution of telomeres than the other. That’s my favorite method but it’s only qualitative. We do quantitate it but even in some of the studies we’ve done, we had five different people independently try to quantitate the same thing and they’re all really good and they get different answers.
Ben: Okay. Are there differences in costs that are significant between a telomere test from a company like TeloYears versus Life Length or Repeat Diagnostics?
Bill: Yeah. I mean, the more accurate is the more expensive. Life Length does do this test that I just mentioned, the telomere repeat or terminal restriction fragment thing is going to be the most expensive. Their measurement of short telomeres is the next most expensive. And I think if you would insist, they’ll even do PCR, which would be probably the least expensive.
Ben: Give me a ballpark on numbers in terms of the expense of a TeloYears’ test, if you know, versus a Repeat Diagnostics or a Life Length.
Bill: Well, TeloYears is under $100 now. Last I saw, they were $99. The Life Length I think is $200 plus. I can’t remember their price.
Ben: So, it’s perhaps a factor of two or three, let’s say, which is not significantly expensive. The reason I’m asking this too is because I have done a podcast prior to this with TeloYears and mentioned other companies as well who I believe are all doing more of a form of this PCR-based analysis, which you’ve elucidated could be inaccurate. And I know people are going to be writing into the show and commenting on the show, and of course folks, if you’re listening in, this is why I do these podcasts, this is why I’m intensely curious and consistently curious, is so that I can prove myself wrong in certain scenarios. And it’s sounding, in this case, like potentially, even the TeloYears test I’ve been doing on myself may be questionable in terms of accuracy.
I can tell you one of the first things I’ll do after this show is probably order a test through Life Length or Repeat Diagnostics to see how the numbers compare, but it’s very interesting. And again, for those you who are confused and saying, “Oh, but Ben, you said this before,” this is why I do this to give you guys the most cutting edge knowledge that I can get my hands on. One other question on this, Bill, and I have to ask this, and please don’t take offense, are you financially affiliated at all with these other companies that are doing different forms of telomere testing than the PCR testing?
Bill: Not at all. In fact, I pay them.
Ben: Okay. This is unbiased then. Okay, good.
Bill: I am totally researching. In fact, if you knew me, I am so opposed to marketing. In fact, the only time you ever hear me do anything like market anything is when, under contractual agreements, I have agreed to do some marketing like in a video or something like that for a company that’s actually paying us a royalty to fund our research. So, those are the only times I’ve ever–I just stay away from market. I focus on really what’s best for doing our research.
Ben: Yeah. And that’s actually what I want to talk about is your research because–and we talked about telomerase and the Magical Unicorn Tears that it seems to induce on longevity. So, now I’m curious, what kind of research are you doing now at Sierra Sciences now that you know that telomerase can do what it says it can do? What’s the research like right now on how we can actually increase our telomerase activity?
Bill: Well, there are two ways to produce telomerase inside of your cells. One is to find a way to turn the gene on in your cells that are already there. All your cells contain the gene. The genes just shut off. So, figuring out a way to turn that gene on is one way. The other way is to deliver a brand new gene to the cell that’s turned on completely already, in fact, turned on even higher than the regular gene would turn it on.
So, we’re focusing on both those approaches. And our main approach is the first one I mentioned, trying to turn the gene on that’s already inside of our cells. Nobody has yet figured out truly how that gene is regulated, how the telomerase gene is regulated, how it’s turned on and off. I believe it’s very complex, probably has multiple repressors that shut it off. So, we do what’s called high-throughput screening, testing chemicals and natural products. Just look for anything that actually causes that gene to turn on. So, when we were taking like human cells grown in a petri dish, we’ll add a chemical to it, and 24 hours later, the chemical will cause the telomerase gene to get turned on.
So, we don’t do this in actual Petri dishes, we do it in what’s microtiter dishes, and we do up to 4,000 a day testing and using our robotic systems that can do high-throughput testing. And high-throughput meaning it tests a lot of samples very quickly, and this got to be a robotic because a human could never do that many without errors. So, we’ve been doing that and we’ve identified a lot of natural products and a lot of chemicals that do turn the gene on. But they don’t turn it on enough to win that tug of war that I was mentioning. Okay? What they do is slow the rate of that tug of war down. Let’s say a telomere shortens 100 bases. The telomerase will lengthen 20 bases, then it shortens another 100 bases, then telomerase lengthens 20, another 20.
Ben: So, again, to clarify for folks, you’re still not decreasing the rate at which the telomere is shortening; it’s shortening, you’re lengthening, then it’s shortening, then you’re lengthening?
Ben: Got it.
Bill: In fact, you are just really decreasing the rate of shortening but you’re doing it by lengthening. Okay?
Ben: Right. You’re not doing it via the method that say like some of those other things that you alluded to earlier such as meditation or yoga or low stress or sleep might be doing it, instead, you’re directly lengthening it but then it’s shortening. And so, it’s a different way to decrease the rate of shortening really.
Bill: Yeah. And using the tug of war analogy again, meditation, healthy diet and stuff like that is decreasing the number of people that are pulling on that tug of war rope to shorten.
Bill: Okay. So, you decrease, whereas the other approach, lengthening is adding people to the other side to lengthen.
Ben: Yes. That makes perfect sense. Okay.
Bill: So, we’ve been actually on a pretty good trajectory of finding hits. Our strongest one so far produces 16% of the amount of telomerase inside of a cell that wouldn’t be needed to tie–have that tug of war be a tie. So, 16% is actually pretty good. I mean, I highly recommend people to do anything they can to get that much telomerase produced. But it’s not enough to actually reverse aging. It could slow it down though it would be hard to measure that, but it definitely won’t reverse aging.
We think that we’re about maybe one to three years away from finding something that actually will lengthen it. And when I say finding, we’re not just randomly screening. We did, maybe for the first 200,000 different chemicals, we tested that was random because we had no idea what to expect. But after finding 30–I guess we found like 900 but we could classify them into 37 different families. By looking at their structures, we get to classify them into 37 different families. And from that information, we were able to now start designing new chemicals, and that caused our success rate to increase because now we weren’t just doing random, we were actually designing new chemical old data that made it even better.
Ben: When you say new chemicals, what are you talking about?
Bill: Well, every pharmaceutical you’ve ever heard of has been tested, but also just random chemicals. There are actually companies out there that actually, all they do is produce, design chemicals, and they produce novel ones all the time just so that companies like us can test them in our high-throughput robotic screening.
Ben: So, you’re pretty much just like throwing a bunch of stuff at telomerase in a cell medium and seeing what works and what doesn’t?
Bill: Yeah. That was the original place. Now, we’re not just throwing anything in there; we’re designing things and testing them, and we’re finding that our ability to design better things is actually far more productive than just randomly screening. But we’re about one to three years away from having something that would be potent enough to cause that tug of war to be a tie. And then I think the exciting things happen when we get something even more potent than that, and telomeres actually start getting longer. Then we can start asking a question. Well, Betty White becomes a 24-year-old again, you know, in every way imaginable. That’s the kind of things that I’m–
Ben: Now, when you do this, once you find a chemical, is this a chemical then that a pharmaceutical company would have hired you and then the pharmaceutical company will purchase that from you? Well, Sierra Sciences simply create this and sell it. I mean, this seems like something that would be highly profitable for whoever gets their hands on it if we’ve found something that can actually induce an increased activity of telomerase.
Bill: Yeah. My policy is that we only do research. And so, even after we do discover something that’s potent enough to win that tug of war, I’d still want to license it to some other company and let them do all the marketing and stuff like that. I still want to find even stronger things or further do testing. It’s just, if there are any side effects, how to get rid of the side effects and things like that. So, I want to continue with the research and let other people do the marketing and all that kind of stuff, which I hate.
Ben: Now, when I visit the front page of your website, at the very top on the upper right-hand side, it says, “TAM-818, most potent telomerase inducer on the planet.” Is that an ad or is that something you guys have created?
Bill: That’s a contractual agreement between a company called Defy Time and us. Defy Time sells TAM-818 and they pay us a royalty that 100% goes into research. So, we have that there so that people can click on that to go to Defy Time’s website, which is a totally different company from us. The only association between us and them is that they sell it and pay us a royalty off of their profits.
Ben: Alright. So, what’s TAM-818 then?
Bill: TAM-818 is that chemical that I mentioned that is 16%. We called it C0314818 because that was the 314,818 chemical we tested. They didn’t like that name so they changed it to TAM-818.
Ben: Okay. On that website, for $800, it appears I can get a bottle of capsules that says, “TAM-818,” and that’s basically the going rate to do something like purchase a bottle that would do this to telomerase in the way that you’ve described based on your research?
Bill: Yeah. And $800 sounds bad but it’s a three-month supply.
Ben: Hmm. Now, for a lot of people who are spending a lot of money on stem cells and peptides and things like that, that’s actually not that expensive, whereas, for the general population, it’s a shocker compared to your average supplement budget. But basically, companies now are purchasing things like this and licensing them. And pardon me if this is too personal of a question, you don’t have to answer, but do you take this, this TAM-818?
Bill: I’m so obsessed with trying to slow the aging process down my own aging that I do everything. I take every single telomerase activator that has been shown to work by testing in our labs. Even the ones that we didn’t discover, I take, I pay for, I pay for them, too.
Ben: Do tell. I would be curious to hear as much as you’re comfortable sharing on your personal anti-aging protocol.
Bill: Oh, well, that would take an hour but I mean–
Ben: Give us the short version.
Bill: Well, so let’s just focus on the lengthening of telomeres, okay? I take TA65, IsaGenesis, and TAM-818. All of those have been shown, at least in vitro to our lab, to actually induce some level of telomerase activity.
Ben: TA65, I’m familiar with but a lot of people say that you could just get that by megadosing with astragalus, is that true or not?
Bill: I don’t believe so. We’ve tested astragalus roots, extracts, and we cannot get any detectable activity. The surprising thing is there’s a lot of people out there saying they know what TA65 is, but when we test those compounds and compare it to TA65, we don’t get any activity too. So, I think TA Sciences is doing a really good job to really protect the identity of TA65 even though they’ve sometimes admitted that it might be something, but when we test it, we can’t get it. We can get TA65 to–
Ben: Okay, fair enough. Well, what is IsaGenesis?
Bill: IsaGenesis is another natural product. So, TA65 is a natural product. IsaGenesis is a natural product that’s actually a mixture of different extracts that were–we were contracted by a company called Isagenix to test 10,000 different natural products, and we found several that actually induced telomerase and the most potent ones were mixed together and are called IsaGenesis. Now, it used to be called Product B, B as in boy, but then they changed the name to IsaGenesis.
Ben: Is there an actual ingredient list somewhere for IsaGenesis or is that kind of a proprietary blend?
Bill: No, that’s on their bottle. The list of extracts and stuff like that are written right on their bottle. But they don’t say which ones are the inducers and which ones aren’t, and I will confess that when Isagenix sent us these 10,000, they sent it to us blind. So, we tested one through 10,000 without knowing what was what.
Ben: Geez, yeah.
Bill: We found 30 something that actually did work and just told them what numbers they were.
Bill: So, I can’t even tell you which ones on that list are the true telomerase inducers, but they did file a patent too on it and they listed a bunch of things. I do know that some of those things that they list there are not telomerase inducer. So, I don’t know what to believe. But my business isn’t to come up with this kind of things. My business is to find a way to reverse aging, and these are just things that fall out on the way. And so, I’m not interested in following up to find out how IsaGenesis works or TA65 or even TAM-818. TAM-818 is not a natural product, it’s a pharmaceutical. And the problem is that natural products, you can’t design them to be better because if you did, they wouldn’t be natural products anymore. But in construction of TAM-818, we were able to design better and better molecules to get to the point of TAM-818. But we’re also continuing to search for even more potent things and the finite product will probably be the ones marketing those too when we find it.
Ben: Okay. So, you take TA65, you take TAM-818, and you take IsaGenesis. Are there any other biggies that you would consider to be maybe things that fly under the radar but that you incorporate into your personal anti-aging protocol that you think are especially important?
Bill: Oh, lots and lots of things. But those are the only things that lengthen telomeres. Even though there are books and publications saying that exercise and things like that would lengthen telomeres, it’s all misinterpreted data. But they do decrease the rate of shortening. And so, for instance, I would say the biggies are to take vitamin D, to get your blood levels of vitamin D up to 60 to 100 nanograms per mil. Your telomeres are protected a lot from inflammation and oxidative stress.
The next one is omega-3 fatty acids. I’m a big proponent of omega-3 fatty acids. And even though I’m a vegan, I still take fish oil because DHA and EPA are extremely important omega-3 fatty acids, and they really help. And I always say you want to take about 1.4 grams of EPA and one gram of DHA, but you also want to take at least a gram of ALA, which I get from flaxseeds.
Ben: Yeah. The way that I do it is there’s a product called SuperEssentials fish oil, and that has a lot of your parent essentials in it like boric acid, it’s got astaxanthin, and then the ratio is close to a one to one DHA/EPA on that one. And so, I’m comfortable recommending that one to folks. Is there one that you like for fish oil?
Bill: Yeah, but yours is probably just as good. I forget the name of the company, EFA-Sirt, S-I-R-T. I forget the name of that one, but I take more than what they say on the bottle because I want to get the 1.4 grams of EPA. But yours that you just mentioned doesn’t contain ALA, which is–I forget what the letter stands for, alpha-linolenic acid.
Ben: Yeah. It’s got gamma-linolenic acid from borage seed oil and then some mixed tocotrienols in there. It does not, I believe, have the ALA in it. Are you getting that from an additional dietary source or simply supplementing–?
Bill: Yes. No, I’m getting that from flaxseeds, well, from flaxseed capsules. You need a lot more than what simply putting flaxseeds on your cereal is going to do.
Ben: Is there a particular brand of flaxseed capsules that you like?
Bill: Yeah, but I can’t remember. I buy it from amazon.com. It’s a brown bottle but I can’t remember the thing. So, vitamin D, omega-3 fatty acids, and then antioxidants. And so, I take a lot of different antioxidants. My favorites are alpha-lipoic acid, and I take vitamin C and vitamin E. I’m a big believer in the possibility that a lot of people say that vitamin C from capsules and stuff like that isn’t real vitamin C. The only true way to get good vitamin C is from eating fruits. And I stay away from fruits because of the high sugar level.
Ben: Yeah. And I’m pretty sure ascorbic acid is ascorbic acid.
Bill: Yeah, and maybe not enough. Vitamin C is probably more than just ascorbic acid. So, it turns out the fruit that has the highest allowed amount of vitamin C and the lowest amount of sugar is actually yellow bell peppers. So, I eat a yellow bell pepper, the whole thing. That should take–
Ben: Wonderful for the eyes as well, very, very high in carotenoids.
Bill: Every morning and every night, I eat one. But I still supplement with vitamin C from powders. And so, I do take a lot of that too.
Ben: Yeah. I should name though, by the way, less we’re leading people astray, a lot of manufacturers extract their ascorbic acid from GMO-based corn or rice starch and they use some pretty volatile acids to do that. You do want to make sure that you’re at least looking for a brand that doesn’t do that. I know there’s one that I’m aware of, even though I just do vitamin C IVs now, one that I’m aware of is American Nutriceuticals. I think they have a powder on Amazon. I’ll find it. But I know they don’t use a GMO source to my knowledge for their vitamin C.
Bill: Yeah. People email me on stuff like that, I can tell them what I take, but I do take a powder of vitamin C that I did a lot of due diligence on, yeah.
Ben: Yeah. Back in the day, I did due diligence, and I recall this American Nutriceuticals, and I used it for a while before I kind of switched over to just doing IVs of vitamin C. A couple of times a year, I even go down to the clinic of Dr. Jason West in Pocatello, Idaho and get about 100 grams. But for the powdered form, I’ll find a list for you guys and put it on the shownotes over at BenGreenfieldFitness.com/telomeres. So, it looks like kind of your protocols, omega-3 fatty acids and vitamins, and antioxidants, vitamin C, TAM-818, TA65, IsaGenesis, is kind of like the crux of your program?
Bill: Yeah, but I take 80 supplements.
Ben: Okay. Yeah, it’s funny. A lot of people I talk to in the anti-aging industry, they take that. I mean, if you ever wanted to share, by the way, if you were to ever email me your protocol, I’m happy to publish it in the shownotes for people because I know a lot of folks like to see what the people who are at the forefront of this are actually doing. And you can feel free to share that with me.
Bill: Well, let me recommend one thing, and that’s because much of my supplement protocol actually comes from Dr. Sandra Kaufmann, and she’s written a book called, “The Kaufmann Protocol,” which is available on amazon.com. I just read that book and I thought it was the best book I’ve ever read on the subject of what to take, how much to take, why you take it, and things like that. I pretty much have just fallen exactly into that protocol. So, I highly recommend that book–
Ben: Free on Kindle Unlimited as well. I’ll link to that one in the shownotes, “The Kaufmann Protocol.” You think it’s pretty up to date?
Bill: Oh, this is a brand-new book. I think Sandra Kauffmann is brilliant. So, I highly recommend it. But as I said, I do take other things, but also I do yoga all the time. I’m a big believer in meditation as a good way to decrease the rate of telomere shortening. There are publications saying that yoga and meditation actually induce telomerase, but that’s actually I think, again, misinterpreting their own data. It doesn’t induce telomerase, but it does decrease the rate of telomere shortening.
I’ve actually been a keynote speaker at yoga conferences because of this and stuff like that. Yoga and meditation is, I think, a really great way to keep your telomeres long, and also, running it. And what I like to do is I like to call running moving meditation, because when you focus on your running that way, it actually is very beneficial to you. Just enjoy it. Have fun. Running around a track is never going to be a way to actually make things happen. You combine running with a denture and exploring and stuff like that and it’s a relaxing, very meditating, very healthy thing to do.
So, let’s see. What else do I do? I mean, I just decrease stress every way I can. Oh, and you know, inflammation is the really cause of most of age-related things. I think everybody in the anti-aging field, let’s say, inflammation is the number one thing.
Ben: I’d say inflammation and glycemic variability. I would say those would be the top two.
Bill: No, I agree with you 100%. It’s a lot easier to reduce your glycemic variability, I’m trying to use the words you did, by doing foods that have little glycemic indexes and stuff like that. But also, inflammation is a little harder to deal with because everybody is different. So, I get blood tests. Every six months, I get my blood analyzed by a company called Alcat, A-L-C-A-T. Actually, that’s not the name of the company, that’s the name of the test, but Cell Systems. I think that’s the name of the company, but I sent them a blood sample. They tell me what foods and what medicine–
Ben: I’m familiar with that test. I’m not super happy with the accuracy of the Alcat versus–I don’t know if you’re familiar with the Cyrex panel?
Bill: No. In fact, I’ll try the Cyrex panel if you recommend it.
Ben: Yeah. The Cyrex panel tests the reactivity of both the cooked and the raw protein in terms of the white blood cell reaction. They also have some very interesting arrays for like gluten-cross reactivity and mold and mycotoxin sensitivity. But if you look into their labs, you tend to get a smaller laundry list of false positives, and a smaller list of simply antibodies that are present in the bloodstream because you’ve been eating a food versus it being kind of a true food allergy. That one’s called, yeah, Cyrex Labs, C-Y-R-E-X.
Bill: I’ll check them out. Knowing my background as a scientist, I will get two blood samples at the same time, send one to Cyrex and one to Alcat, and see.
Ben: I would love to see the results if you do that. It’s something I have yet to do even though it crossed my mind a few times. So, yeah, if you do that, keep me in the loop and I’ll keep our listeners updated as well. This is fascinating.
Do you think there are any other potential deleterious effects to lengthening the telomeres aside from the cancer issue that we brought up? Is there any caution that we should take before rushing off to buy $1,000 worth of supplements and incorporate all these fancy protocols? Could we be shooting ourselves in the foot in any other way that you can imagine?
Bill: Well, I could imagine, but I can’t–I’m really grasping for straws, but I am not aware of a single negative impact of long telomeres. And there’s been papers published called the “Goldilocks effect” saying that there is such a thing as telomeres that are too long. But when you read the actual paper, you find out that the only thing that they saw was when telomeres got really long, their rate of shortening actually got higher, okay? So, they got back to the original length a little bit faster than they would have, but just a little bit. They said that means something is bad that’s happening. But I think the longer telomeres just become more susceptible to like poor genetics and poor lifestyles.
But it doesn’t say that the long telomeres were bad for your health. There’s nothing. We’ve, many times, made telomeres in human cells so long we can’t even measure them, and we’ve never seen any health issues with–I mean, of course, this is only in vitro because we’re dealing with human cells grown in a petri dish. We’ve never actually made telomeres really long in humans because that hasn’t been done yet, which by the way, we haven’t even discussed yet our other whole research area. But the people have made telomeres extremely long in mice and have seen no negative side effects of that at all. In fact, the publications have shown a decrease incidence of cancer when they’ve done that.
Ben: What’s the other whole area of research you just alluded to?
Bill: Well, that’s the delivering a new gene to the cell. I call it gene delivery. It’s also called gene therapy. But we’ve been doing gene therapy for 25 years on telomerase. And the reason why this hasn’t been made more public before was because the techniques of gene delivery have only recently become safe. Delivering a gene to a mouse actually, any kind of mouse, actually kills a lot of the mice, just trying to get the gene into the cell. And then what you do is you study the survivors. So, we don’t want to do that with humans. I don’t want anybody to die from just the delivery method.
But now some recent–probably about eight years ago, we started working with a new system called adeno-associated virus. I used the word virus but I don’t like using virus for gene therapy because it insinuates health issues. But viruses are only dangerous because of their payloads. And in this case, we’re putting a telomerase gene. So, the only thing that gets delivered when we use this AAV is the telomerase gene, and it gets put into your cells. When we do that, that more than wins the tug of war. It produces 30 times as much telomerase activity that’s needed to tie that tug of war. So, it actually wins that tug of war.
And we’ve been working on that and we licensed that to a company called Libella, L-I-B-E-L-L-A, Libella Gene Therapeutics. And they are now getting ready to their first clinical studies. They’ve actually got the first patient identified. First patient will be probably treated on May 1st of 2019. And unfortunately, another reason why I’m not 100% focusing on this is because it literally costs like $3 million for us to produce enough of it to treat one person once. So, it’s not going to be something that everybody’s going to be able to afford. Billionaires are going to be able to afford that, and I sure didn’t get in these businesses that make billionaires live longer, but at least it’s a proof of concept. Okay. It’s going to be a proof of concept. And, again, I’ve licensed it in exchange for royalties that they’re going to get that’s going to be used to fund our research that will eventually put them out of business and they know it.
Ben: Yeah. But that’s [01:11:45] ______. So, you’re essentially using a gene therapy delivery mechanism as a form of like telomerase therapy, but you’re actually able to target the treatment, and even target it specifically in situations such as Alzheimer’s.
Bill: Yeah. Well, we don’t need to target. We just deliver it to all the cells of the body that we can. In some cases in gene therapy, you do want to target. And so, there are ways of doing that but our focus is to not target. Our focus is to go everywhere because there are no negative impacts of all of having telomeres that are too long or having telomeres that are really long. And so, we’re targeting everywhere but we’re–and when I say we, I mean Libella Gene Therapeutics. I’m actually very much consulting for them, so I kind of include myself in that. But they are going to be delivering the gene therapy into the blood, and also into the cerebral spinal fluid.
Ben: Interesting. And that’s the actual telomerase gene that they’re delivering?
Bill: Yes. It’s an engineered gene, but it’s only engineered so that it produces more telomerase. The telomerase that gets produced is identical to human telomerase but it produces a lot more.
Ben: This is fascinating.
Bill: Yeah. I’m fascinated. I can’t wait to see the results. The first patient is a guy, 70 something-year-old guy who’s been diagnosed with Alzheimer’s about six years ago. By the way, this is being done through the FDA using a program called RMAT, R-M-A-T. And RMAT allows you to do the first testing in other countries and stuff like that, all approved by the FDA. And so, it’s actually a really great study going on, which has been an incredible amount of work to get going, only because making the gene therapy was the easy part. Making certain that everything possible gets tested for has been a really big challenge.
And so, we have something like 100 different biomarkers of aging in general. We got a whole bunch of markers for cognitive disorders and things like that to look at the Alzheimer’s, but we’re also looking at every aging biomarker. And we also are very interested in immune responses. For instance, we’re not worried about the telomerase causing any problems, but we are worried about the delivery method actually causing an immune response in people, which isn’t going to be that bad but it destroys the ability of the gene therapy to work.
So, we’re doing extreme measures to prevent the immune responses too, which–to do a study like this requires hundreds of different people, all specialists in certain areas all working together to try to–it’s like one big orchestra. You got to have everybody in place, and getting that all set up has been a miracle. And I’m so impressed with Libella Gene Therapeutics. They pull all that together.
Ben: Well, I will link to their website as well in the shownotes. I will also link to everything we talked about, your books, all the ingredients that we discussed, albeit the expensive ones, and I realized that’s quite a punch in the wallet for a lot of people, but for those of you who are interested, I’ll just lay it all out there on the site and you can go to town if you want to kind of use some of these similar protocols. I just want to caution you to pay attention to some of the other things that Bill was cognizant enough to mention, like yoga, meditation, low-level physical activity.
Please do not go out and purchase $1500 worth of supplements for your next three-month protocol and neglect the other important areas of life. We know that there are plenty of centenarians who have smoked cigarettes their whole life but have wonderful relationships and family lives, and frequent sex, and drink tea and red wine, and do a lot of what we see the Blue Zones do, and they also survive. So, do not neglect the natural low-hanging fruit. But at the same time, if you’re ready to take it to the next level, this is some pretty damn cool stuff.
And Bill, I want to thank you for coming on the show and sharing all this with us.
Bill: Yeah. There’s one other thing that I’d like to talk about, and I think Joe Mercola would appreciate this.
Ben: Fair enough.
Bill: It’s the discussion about–there’s another–I always talk about the telomere clock. People are saying you can measure telomere lengths and figure out how old you are, and more important, how long it’d be before you die of old age. I’ve already said they’re not all that really great. But I do believe telomeres are something that eventually are going to be a good marker of overall health and declining health and stuff, but not yet.
Now, the epigenetic clock, which is looking at methylation–there are two different clocks that have been looked at a lot; one is the Horvath clock and the other one is the Hannum clock, I think both of those are pretty good too, but I don’t think there’s any way of comparing. A lot of people are saying one clock is better than the other clock, and I personally have no idea. I think that studies haven’t really been done. There are a few people claim they have done some studies. But at this particular moment, I would not even venture a guess as to which one’s the more accurate. I think they both need a lot of work.
This whole methylation stuff, that’s not a new science. I was looking at methylation and gene regulation back in the 1970s. So, methylation, that’s a long-term science. People ought to think this is brand new but it’s not in–the word epigenetics, by the way, is just a new word for an old subject. I’ve been studying epigenetics since 1970s but it only became called epigenetics recently. But those two clocks I think have the potential of eventually being really, really accurate if more work is done. But there’s I think a really good chance that the epigenetic clock, the methylation, is a result of telomere length and not vice versa. Very unlikely, methylation is a cause of telomere shortening.
But it might be that telomere lengthening might become the holy grail of markers. And Ron DePinho actually published some stuff on that. He’s the one that extended lifespan in mice by lengthening telomeres. He’s also looked at oxidative stress and mitochondria dysfunction and found out that lengthening telomeres had a tendency to make those pointless because telomeres actually were the roll. But again, we can only best guess at the moment, and that’s all I’m doing and until there’s better data, I just can’t really answer that question even though a lot of people are out there trying to say they can answer the question. The data is not there yet.
Ben: Yeah, yeah. I do know one thing that these human embryonic stem cells and potentially even some of the exosomes that folks are using now do express some pretty high telomerase activity. So, there may be something to that as well, this whole idea of stem cell therapy or even, I believe they call them induced pluripotent stem cells. It’s kind of a way to fill your body with cells that may have enhanced telomerase activity.
Bill: And that’s what we’ve been doing for the last 10 plus years, almost 20 years, looking to find out how telomerase gets turned on in those cells. PubMed would show that I’ve authored some papers on induced pluripotent stem cells and human embryonic stem cells and looking at what causes telomerase to turn on in those cells so that we can learn the same mechanisms to do with normal cells. But unfortunately, when you induce pluripotency in a cell, that’s actually de-differentiating the cell back to an embryonic state.
That’s giving some good data in my showing possible rejuvenation, but their side effects are tremendous because you’re actually turning differentiated cells into undifferentiated cells. And if you push that full process forward, you’re going to find out that you’re going to turn a whole mouse into embryo, not into an embryonic cell instead of a young mouse of it. But still, rejuvenation, let’s say the youthfulness is actually probably totally due to the telomerase lengthening telomeres. But we still have not been able to figure out after years exactly how the telomerase gene is turned on. There are like six different factors that you can add to cells. Sometimes just four at a time or all six at a time that will induce pluripotency, and we find out that we need all six. If we leave one out, we don’t get telomerase activity.
So, it’s a big, big process, some very complex protocol that’s causing telomerase to turn on. So, I don’t know. I think stem cells and exosomes and everything else is a great thing to do. I highly recommend it. I’m even getting ready to possibly try some stem cells on myself. I think of them as just a way to provide your body with cells that have long telomeres. And in the near future, hopefully five years from now or less, we will be able to lengthen the telomeres and all the cells that you already have, instead of just adding new cells with long telomeres. So, I could go on and on.
Bill: By the way, I could talk for 10 hours.
Ben: I know. I could talk to you for 10 hours. I know you’ve just gotten back from that conference though, so I’ll respect your time and mine, as I have another interview I’ll have to get off to here pretty soon. But what I’ll do–again, for those of you listening in, BenGreenfieldfitness.com/telomeres. That’s T-E-L-O-M-E-R-E-S, there, I spelled it for you, BenGreenfieldFitness.com/telomeres. I’ll link to everything there. And then I’ll follow up with an email, Bill, and give you my email address, should you want to send over any other little research papers, videos, personal protocols, anything like that, and I can always include those things in the shownotes before this episode is released. So, thank you so much for coming on the call, man. This is fascinating. I love this stuff.
Bill: Well, thank you very much. I enjoyed it.
Ben: Alright. Well, I’m Ben Greenfield, folks, along with Dr. Bill Andrews of Sierra Sciences signing out from BenGreenfieldFitness.com. Have an amazing week.
Want more? Go to BenGreenfieldFitness.com or you can subscribe to my information-packed and entertaining newsletter. Click the link up on the right-hand side of that web page that says, “Ben Recommends,” where you’ll see a full list of everything I’ve ever recommended to enhance your body and your brain. Finally, to get your hands on all of the unique supplement formulations that I personally developed, you can visit the website of my company, Kion, at getK-I-O-N.com. That’s getK-I-O-N.com.
There’s plenty of controversy these days around telomere testing.
Is it accurate?
Does it really show your so-called “biological vs. chronological” age?
And once you do get your results, how can you lengthen your telomeres?
In today’s episode, I interview one of the world’s leading experts on telomeres: Dr. Bill Andrews. Dr. Andrews is the Founder and CEO of Sierra Sciences, a company focused on finding ways to extend the human lifespan and healthspan through telomere maintenance. As a scientist, athlete and executive, he continually pushes the envelope and challenges convention. He has been featured in Popular Science, The Today Show and numerous documentaries on the topic of life extension including, most recently, the movie The Immortalists in which he co-stars with Aubrey de Grey.
Bill has been a researcher in biotech since 1981, focusing on cancer, heart disease and inflammation research; though his passion has always been aging. In the early to mid-1990s, while at Geron Corporation, Dr. Andrews led the research to discover both the RNA and protein components of human telomerase. He was awarded 2nd place as “National Inventor of the Year” in 1997. After earning his Ph.D. in Molecular and Population Genetics at the University of Georgia in 1981 he then served as Senior Scientist at Armos Corporation and Codon Corporation, Director of Molecular Biology at Berlex Biosciences and at Geron Corporation, and Director of Technology Development at EOS Biosciences, before starting Sierra Sciences in 1999. Bill is also a named inventor on over 50+ US issued patents on telomerase and author of numerous scientific research studies published in peer-reviewed scientific journals.
Bill is also an avid ultra-marathon runner. He regularly competes in 50 and 100+ mile races often finishing at the top of his age group. These grueling races have taken him all over the world to race in some of the most extreme environments, from Death Valley to the Himalayas. His running is presently featured in the movie “The High.”
During our discussion, you’ll discover:
-The differing effects of short vs. long distance running on telomere lengths…9:25
- Not the length per se, but how you do it.
- If it quits being fun, it’s time to quit.
- Consistent running actually decreases inflammation; inconsistent or sporadic running is problematic
-What are telomeres and what is their role in our physical mortality…13:15
- Think of each chromosome in the body as a “shoelace”; the little caps on the end of the laces are the telomeres
- Telomere shortening results in declining health with aging
- Each time our cells divide, our telomeres get a bit shorter
- DNA and cell replication
- Cells can’t replicate DNA all the way to the end
- Cells eventually “crash”; lose the ability to function
- It’s possible to calculate the maximum lifespan of a human based on telomere shortening rates
- Attention anti-agers: you can’t do it unless you can figure out how to prevent telomere shortening
- Book by Jim Mellon: Juvenescence: Investing in the age of longevity
-How telomeres can be lengthened, and how to lower the rate by which they shorten…19:30
- Telomeres are not shortened when reproductive cells replicate
- Telomerase prevents the shortening of telomeres
- Telomerase is too big to get into cells
- Senescent cell: a cell that has lost the ability to divide
- Shutting down senescent cells actually inhibits cancer cells
- “Chromosome rearrangement”: a precursor to cancer
- Shortened telomeres hinder cancer treatments such as chemotherapy
- Keeping telomeres long is the best way to treat cancer should it enter the body
-Whether or not telomere tests work and how accurate they are…35:10
- Accuracy is extremely low in measuring biological age
- Best available is fluorescence in situ hybridization
- PCR, a popular means of testing, is “manipulatable”- uncontrollable changes
- Test yourself multiple times; use different names
- Telomere Restriction Fragment is Dr. Andrews favorite test
- Difference in costs:
- More accurate = more expensive
- Range: $100-300
-The research Dr. Andrews is conducting on increasing telomerase activity…44:20
- Two ways to produce telomerase inside the cells
- Find a way to turn the gene “on” in preexisting cells
- Deliver a brand new gene to the cell; turned on more than a regular gene
- Decreasing the rate of shortening the telomeres
- “Tug of War” analogy
- Not currently possible to reverse the aging process
- 1-3 years away from having the tug of war a “tie”; meaning the aging process comes to a halt, then possibly we’ll see aging process reversed
- Real life products in the marketplace based on Dr. Andrews’ research at Sierra Science…50:30
- Dr. Andrews focuses solely on research; partners with pharmaceutical companies for marketing, distribution, etc.
- TAM-818: a supplement that increases telomerase levels
- Dr. Andrews takes every supplement that’s been shown to increase telomerase levels
-Dr. Andrews’ personal anti-aging protocol…53:45
- You can’t design natural products to be better; they would cease to be natural products
- Elements of his protocol that may fly under the radar:
- Vitamin D/K Blend
- Omega 3 fatty acids (Superessentials Fish Oil)
- Barlean’s Flax Seed Oil
- Vitamin C from American Nutraceuticals
- Yellow bell peppers: highest amount of Vitamin C and lowest amount of sugars
- Book: The Kaufman Protocol
- Yoga, meditation, running, don’t increase telomerase, but limit shortening of telomeres
-Precautions to take before diving headlong into an anti-aging protocol…1:07:35
- No known negative effects of long telomeres
- Gene delivery/therapy
- Libella Gene Therapeutics
-About the “telomere clock”…1:16:15
-And much more!
Resources from this episode:
-Book: The Kaufman Protocol
–Kion Lean Support for normal blood sugar levels and healthy energy metabolism, even after large, carb-rich meals.
–JOOVV After using the Joovv for close to 2 years, it’s the only light therapy device I’d ever recommend. Give it a try: you won’t be disappointed. Use my link for your purchase and score a sweet bonus gift!
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