Which Genes Impact Your Longevity The Most? How To Decode Your Genes & Unlock Key Insights To Living Longer & Aging Well (+Bonus Coronavirus Genetic Analysis Information!).
29 Jan 2026 · 81 min
Joe Cohen of SelfDecode explains which genes most affect how long you live and how fast you age. SIRT1, APOE, and telomere genes like OBFC1 matter most. You can offset genetic risk with resveratrol, NMN, intermittent fasting, and exercise.
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On this episode of the Ben Greenfield.
Fitness Podcast and this is something that we advocate as well is looking at your labs and symptoms. That's why we're integrating these things so that you don't only look at your genes. There is somewhat of a negative that if it's too high it could lower your immune system too much. Overall, it's a very good protein to have at somewhat elevated levels and yours are a bit lower there. You do have a bit of a cluster of genes that are negative genetic variants when it comes to cholesterol related genes.
And what does that mean exactly? Health performance, nutrition, longevity, ancestral living, biohacking and much more. My name is Ben Greenfield. Welcome to the show. Well, today is a full on genetics podcast. My friend Joe Cohen runs this company called Self Hacked. You may have come across them on the Internets before and they also have this really cool genetic website and we take a deep dive into everything from COVID genetics. That was pretty interesting. We kind of talk about that towards the end of the show. But especially longevity and anti aging genes. So this one's going to be fun. And when I give you the show notes URL during the show, please know that I have removed my own personal information from my genetic report, such as my phone number, my address, the name and phone number of my insurance company. But other than that, everything's right up there on the website if you want to go peruse through the results for yourself. All right, folks, I have my friend and genetics whiz back on the show today to talk about your genetics and how they relate to longevity. Plus a little bit of some bonus insight since it's a little time sensitive and relative and relevant to where we're at right now from a timeline standpoint. Because recording this in April of 2020 during the coronavirus pandemic and quarantine. And in addition to discussing some longevity related genes and some new ways to analyze those, we're also going to talk about whether or not you might be able to actually test your potential susceptibility to a virus like coronavirus. So we'll get into that as well. So lots of goodies on today's show. My guest has actually been Ben on my podcast twice. He first appeared on the episode entitled how to Decode youe Genome. And in that we delved into just like kind of kind of the general science behind genomics analysis, but in a little bit different way than what we're going to do today. Because today we're going to really focus on longevity and also just what's happened in a couple of years since I interviewed him in the realm of genetics analysis because I know it can be kind of a confusing world for a lot of people and there are a lot of myths and a lot of controversies out there about analyzing your genetics. He also was on a really fantastic episode we recorded together about your vagus nerve. We talked about 32 different ways to stimulate your vagus nerve and fine tune your nervous system and even hack your hormones utilizing a vagal nerve approach. So I'm going to link to both of those previous shows in the show notes, which for this show you can find@bengreenfieldfitness.com Self Decoded. That's BenGreenfieldFitness.com Self Decoded. My guest is Joe Cohen. Joe runs a fantastic website called Self Hacked. Wonderful, wonderful articles that he puts out. Very well researched and as you can listen to in the original podcast that I did with Joe, he suffered through a lot of health issues himself. Inflammation, brain fog, fatigue, digestive problems, anxiety, depression, kind of the genetic lottery of bad genes. And he went through a very intense journey of self experimentation and self learning to improve his health. He's a biohacker in his own right, but I respect him because he does a robust amount of research and has a pretty big research team over at Self Hacked now who are putting together articles and putting together programs like the type of genetic analysis software that we're going to talk about today. So Joe himself has been studying health sciences for 17 years. He was pre med at university, but then went on to found Self Hacked instead. And it's really become kind of a go to resource for a lot of people who want to dig into everything from the 80 billion different benefits of wild nettle extracts to the pros and cons of melatonin. Low dose melatonin, high dose. I mean he digs into everything, everything on this website. So I'll link to the website selfact as well in the show notes, which again are going to be@BenGreenfieldFitness.com self decoded. And just so you guys know, I recently turned over to Joe my 23andMe raw and we're going to use some of that as we go through our podcast today so that you guys can kind of see how you would take something as simple as your 23andMe results and glean a lot more data out of them than something like 23andMe might give you. So fun stuff. Hold on. It's going to be a wild ride. And Joe, welcome to the show, man.
Hey, man, thanks for having me here.
Yeah, for sure. You are. You just told me as we were getting ready to record, you're in. You're in Tel Aviv right now during this whole pandemic scenario. How are things over there?
It's pretty crazy. I mean, they pretty much stopped all flights coming in and out, and anyone who comes in pretty much from anywhere, you're automatically put into a hotel for two weeks and quarantined. Really? And it's. Yeah, like, everywhere else. I mean, like, a lot of places there's a lockdown, and they're taking it very seriously here. What.
What are you doing? Are you. Are you primarily just staying on the home front? Are you one of those people who's just kind of out with your hands in your pockets, whistling through the street, not afraid of anything, or. What's your take on this?
My take is that if you look at the data, it's around six times more dangerous than the flu. And if you're young and healthy, then the flu is not dangerous, and even six times more dangerous is not dangerous. So, personally, I'm healthy, I'm relatively young. I don't have anything to worry about. The people I would be worried about are people with cardiovascular disease, high blood pressure, maybe if they have a lot of variants, genetic variants and things like that. You know, obesity, COPD. Bunch of different risk factors.
Yeah, basically, like. Like 80% of the world's population, in other words.
Yeah, well, that's why governments are so afraid. It's like there's all these sick people, but if you're healthy and not sick, I. Personally, I'm not scared at all.
Yeah, it is interesting when you compare it to the Spanish flu pandemic, for example. It was a lot of the young and healthy people who got taken out by that. And so kind of a different scenario here in terms of people who have. Not to point fingers of blame, but people who may have dug themselves into a hole, so to speak. From an immune preparedness standpoint, they appear to be the people most affected by this.
And actually, even though I'm not scared at all, I decided to take out a life insurance policy. And my life insurance policy is that I bought an oxygen concentrator. So basically, the only thing that I'm afraid of is that if for some freaky reason, this thing does hit me hard. And I really don't think so, because I've already developed a strategy based on my genes and other research. But let's say worst case scenario, it hit me hard. Almost the worst case scenario Is you go to the hospital and you get oxygen. There's no way I'm going to the hospital for this thing. So I've got an oxygen concentrator at home. If my oxygen drops below like 98%, I'm putting that thing on. And I also have a pulse oximeter as well, so I can measure my oxygen. I don't even want to get anxiety about it. Like, wait, is my oxygen dropping? I don't know. So I have a pulse oximeter. I've got the oxygen concentrator. That's my life insurance for this thing.
Yeah, I think coming at it from an oxygenation standpoint is prudent. I personally have my hyperbaric chamber and I've just been using that regularly anyways. It's not like I changed my use of that just because I use that daily based on frequent dosing of hyperbaric seeming to be the best way to use that. But then from an oxygen standpoint, particularly an ozone standpoint, I, like you, made one hefty purchase when this whole thing hit. And I bought a kind of a top of the line ozone generator and have been using ozone pretty frequently and would certainly turn to that if. If I did come down with something just because of the data that I've seen on ozone. So, yeah, I think that video that I believe was released by an emergency room physician in New York City a few weeks ago, really highlighting how much of this is related to oxygenation, makes paying attention to that, in addition to just prudent antiviral strategies is a good idea. Obviously, there are 8 billion podcasts out there and probably double that of Internet articles getting into all the remedies and all of the strategies for boosting your immune system or addressing coronavirus. And I think we could probably talk until we're blue in the face about that, but I actually want to really delve into genetics. And like I mentioned to folks, we'll talk about coronavirus genetics later on. But where I would like to start is with self decode in general. When I first interviewed you, it was kind of in its infancy. And the first question I have for you is a lot of people will go and get their 23andMe tests done, or my kids, because they're doing a genealogical study right now for their homeschooling project. They just got their what is it? The my ancestry or I think it's my ancestry. They just did that to look into the pathways of ancestry, not necessarily health parameters, but those are really the two things most people are familiar with. Like 23andMe and some kind of heritage esque genealogy analysis. Now how does something like self decode differ from a tool like that?
So it's actually very different in the sense that we, I mean it's different in a number of ways. Number one is we focus on different topics. We actually try not to focus on anything that 23andMe is focusing on. So for example, they are not doing a longevity report, a mood report, a cognitive function report, a sleep report, or any of these kinds of topics that we're doing on. So we stay away from any topics that they're doing just to even be more different from them. But in addition to that, they don't really give recommendations except it's like very, very generic, very vague. They don't show you how it's connected to your genes and how it can improve, you know, counteract the variants. They don't really tell you, they don't do that deep dive analysis and they don't give you recommendations.
Is that because they legally can't? Like why? Or it's just not part of their model?
It's not part of their model. Now you have to be careful legally. Right. So we don't say that, you know, this is going to, when we give recommendations, just to be clear, we're giving recommend, let's say we're, we're giving recommendations for longevity or mood or cognitive function. We make, we start off with a list of what are the top ways to improve longevity. And then what we do is we prioritize that list based on your genes. So we're not telling you take this toxic pill that can improve longevity. We're not even telling you to take any drug. We wouldn't tell you to take metformin even though it's a way to improve longevity. So what we're doing is we're prioritizing the things that are already good for a specific topic.
Based on that are you actually using, you're analyzing obviously the same genes because someone can just upload their 23andMe raw results to your software. So you're using the same data set, right?
Yeah, but what we, our focus is very different. So it really has to do with the focus of a company. 23andMe is very focused on getting your genetic data and selling it to drug companies. And that's another difference, by the way, that I didn't even get into. We don't sell your data. That's extremely important because it's not our business model. It's all of 23andMe's business model. Pretty much they're doing drug discovery and that's why they got a $300 million investment from GlaxoSmithKline. And they're all about discovering drugs and they wanna get as many people's data as possible. They'll lose money on it so that they can discover drugs and, you know, make money in the future from selling your data, using your data, things like that.
Is that something that people should be concerned about, you think 23andMe actually selling data to pharmaceutical companies?
It is concerning. That's why a lot of people are not don't wanna buy 23andMe anyone I've met almost that said, you know, do you have your genetic data? Like, nah, I'm afraid of them selling it. Right. And that's why we were very strict. Like we have to have a different model and it has nothing to do with selling your data.
Okay, now, now, now, now. What about some of these heritage companies? You know, like, my kids just got tested with that. I think it's my ancestry is the name of the company or I'm sorry, it's ancestry DNA. Ancestry DNA is where they got tested. Could, like, do you think other companies are looking at, at pharmaceutical sellout of data or are those companies like the ancestry and the heritage websites just giving out beneficial genealogical information?
They, they are using your data for some purposes and I think they're trying, you know, I don't know exactly what, you know, how every company is going to sell your data, but what is clear is that their business model is very different. It's not our business model. Our business model is we're, we're giving you reports and we have a personalized blog that gives you constant updates. We're going to have a lab test analyzer. We're doing things in a way to give you constant updates so that you're constantly engaged with your genetic data. And we're also doing different topics that are very interesting. So we do charge a little more on the upfront. I mean, it's only $59 per subscription, so that's actually very cheap. And that lasts a year and you can cancel anytime. And then if you want to buy a kit from us, we don't even care if you do because we don't make a lot of money on it. It's less than $100.
Okay. Yeah, yeah. Gene testing is. Unless you're doing, doing like a whole genome sequencing, which arguably I've done that and I'm not sure that it' sit's worth the cash for Most folks, just because, you know, with a little bit of a less thorough genetics analysis, you're still getting the lion's share of the information that you want. And so gene analysis, it's pretty palatable for most people from a pocketbook standpoint. But this relates to something else that I wanted to ask you, and that is that, I mean, there's a plethora of tools out there, right? There's like Promethea, Dr. Rhonda Patrick has her Genetic Genie project. There's. There's like, what's another one? There's one up in Canada, the DNA company. There's probably like, what, over a dozen different genetic analysis tools out there that people can upload their data into. And I think it gets kind of confusing. So what, is there something people should be looking for in a gene analysis product? Are they all just kind of focused on. On different things or what's your take? Kind of what seems to be a saturated market in terms of ways that one can upload their raw data and get feedback from.
So there's a number of things that people want to look for when they want to decide which program to use. Number one is they want something with good science. And what that means is every statement is backed up, right? And also it has to be curated to some degree. So Prometheus doesn't have curation. They just, you know, throw out the signs. Their UI UX is terrible. It's almost an unusable product for most people. And so that's one set of things. Also, they don't give recommendations, right? So Rhonda Patrick, she does have good signs. She does give some recommendations. There's other things you want to look at, though. Number one is how many genes is somebody looking at for a particular topic? So I'll give you an example for our longevity report. It's 27 genes, just about longevity. That's more than anyone else is looking at in terms of longevity. And then the other thing you want to do is you want a polygenic risk score. You know, you want to account for multiple genes when telling you whether something is bad. And not only do you want to account for multiple genes, you want to account for multiple SNPs within a gene. Because you could have one SNP that's good and one SNP that's bad in a gene.
Using a popular example. Tell me what that means. Like, give me an example of a gene that someone might think they have a bad version of, which a polygenetic analysis would indicate might not be as big of an issue as they'd been led to believe.
Well, so there's two different questions. One is, if we look at a particular gene, right? You could, for example, you could take any gene as an example almost where a gene. So you know what a SNP is. It's basically a certain point and there's a variation within the genome. There's actually many SNPs within a given gene. There's not just one SNP per gene. There could be 100 SNPs per gene. Now, usually there could be like four or five important ones or whatever, and those are the ones that are going to be studied. So if you look at MTHFR, there isn't one SNP in that gene. There's actually two SNPs that people are aware of. There's actually way more. And what you want to do is not necessarily look, you don't want to look at one snp. Now, it's easier to do that, of course, if you don't have a sophisticated software, you just look at one snp. But when you're looking at a gene, you can't say that MTHFR is bad because of one snp. And that's part of the criticism there as well. But you want to look at multiple gene, multiple SNPs within a gene. And then on top of that, you want to look at multiple genes within a certain kind of trait, a certain area of a trait, let's say inflammation or oxidative stress or something like that. And so looking at multiple genes is important to understanding a general idea of am I more at risk for this or less at risk for this? And I think that's a very big difference between what we're doing in some other companies. And so polygenic risk score that's using multiple genes and using multiple SNPs for a gene to tell you if that gene is increasing your risk in some way. And then there's also. So you want to make sure that the thing gives you recommendations. Prometheus does not give you recommendations. 23andMe does not give you recommendations. You want to make sure that you're being updated with the science because the science is changing. There's new research coming out and you want to make sure that there's update updates there. And the other thing is that if they are giving you a recommendation, you want to make sure that you, first of all, you want to understand where's that recommendation coming from. I don't trust any recommendation randomly. You know, I upload my jeans. Oh, you need to do this. Just trust us, you know, and I don't think it has anything to do with my jeans. So we connect every recommendation that we give. We connect all the dots for you. And you could see, you could click on the references, we could show you exactly what, we could verify what we're saying. And the last thing is comprehensiveness. Many of these genetic programs are using like 10 SNPs, whereas we'll use 100 SNPs for a certain topic, or 150 or up to 200. Right. And the obvious thing is the topic that you're looking for, there could be one company that focuses on something very, very specific. There is no longevity report as we have it on the market. There's no cognitive function report, there's no mood report, there's no sleep report, there's no inflammation report. So we're doing these things that are simply not on the market. And we don't even have a diet report now. I mean, yet. We're gonna make one. But the point is we're staying away from things that other companies are doing because every company is doing a diet report.
Right? You mean a diet report as in you would do better on a low carb versus a high carb diet. You should have this percentage of Satur, saturated fats, et cetera?
Yeah, and not only that, it's also more complex. I wanted to stay away from it because it's actually quite a complex subject. But we are going to delve into it in the future and we're going to do it better than all the other companies. But yeah, you want to make sure all these things when you're choosing a company and when I say updated research, we have the world's only personalized genetic blog. What does that mean? It means that imagine any kind of topic that you're talking about, any supplement, any, any gene, anything, the text within the article changes based on your genetics. We give you a face that changes based on your genetics. We give you summaries that change based on your genetics. We show you snips that change based on your genetics, whether you have the variants or not, and we give recommendations that change based on the variance. So this is something that has not existed.
So in my opinion, then, based on what you've just explained, one part of this, the polygenic risk score, what you're saying is you would aggregate the contributions of a whole bunch of different DNA variants associated with some type of trait or disease risk, cluster all those together, then produce a report on, let's say, obesity risk or longevity status or inflammation potential, et cetera. And then B, you would take into account as part of that so called polygenic risk score multiple SNPs that are going to kind of more thoroughly address that particular topic.
Exactly.
There are some concerns though over genetic testing, particularly how useful this data actually is. Like literally last month the Journal of the American Medical association released an article called the need to improve the Clinical utility of Direct to Consumer Genetic Tests. And the subtitle of that article was Too narrow or too Broad. They said the narrow tests that aren't analyzing a lot of genes, they're often incomplete and only include a limited number of relevant variants which I think we just kind of addressed based on this polygenic variants analysis. But then they also say the broad tests are concerning because they, they include genes for which well established risk estimates and medical management guidelines or both might actually be absent. In other words, we're drawing conclusions based on what we think a gene might make somebody susceptible for that don't have actual data behind them. And then furthermore, related to that second point, Dr. Tommy Wood, he wrote an article really, really questioning whether gene testing does any good at all. And he got into a lot in that particular article and I'll try and find it and link to it in the show notes. But he was concerned that you know, for example, if you look at let's say like the FTO gene that would cause a lot of people to say like limit their amount of saturated fat intake or be concerned that they might have this so called obesity associated protein that if you actually look at the, the impact of FTO gene testing, it predicts risks of something like 0.4% of BMI, which is pretty much like how much weight you'd gain from a glass of water or a bowel movement. And it's really pretty much irrelevant to most people when it comes to weight loss or weight gain. And he had some other thoughts, for example on the MTHFR gene that the impact on homocysteine might be at worst 1%, which would be less than a lab error in terms of people actually needing to worry about, you know, taking a bunch of supplements to lower homocysteine because they have an MTHFR gene. So when it comes to some of, some of the questionability of these genetic analysis, have you kind of developed a response to that or do you have your own thoughts on whether or not we're extrapolating too much from this type of data?
Yeah, I think that's a great question and there's a lot to unpack There. So I'll give you an example of something, number one, about how we're doing things different, right? So a lot of people will take. I think the way that people really go wrong is that they'll say, oh, I've got this variant, I have to do X because I have this variant. If cyanide increases mthfr, I gotta take cyanide, right? That's an extreme example, of course, Right. But it's like, okay, if this thing increases mthfr, I gotta do it, right? If I have this mthfr, I'm 100% sure that I need to take folate. It doesn't work like that in real life. Number one is you want to look at multiple variants in the mthfr. That's number one. And people are only looking at one variant. So that's mistake number one. The other is you don't want to look at the gene per se, so much, focus so much on a single gene. And basically we, basically, if you are already giving the example you gave with the FTO gene, right, if you're already obese, we know that you have a problem and we know that obesity is related to the genes and we know that various lifestyle factors can improve reduce obesity. You can lose weight. There's many ways you can lose weight, right? And we know that some people are just much more prone to weight gain. Why is that? Because of their lifestyles, Right. Maybe they're not doing everything right, but obviously there is an effect from their genes. So we're not saying if you have this FTO gene, then do this right? We're saying that if you're obese and you're trying to lose weight and you can't lose weight, then obviously you're either doing something wrong or you have a problem in your genes. So number one, what we're doing is we're taking the best recommendations for weight loss and we're putting them in the report, let's say, right? And then number two is we make sure that it's connected to FTO so that it's not just random. And that allows us to sort things from highest, you know, best for you to less good. Even though everything could technically be good, right? Exercise is always going to be good, but some people exercise and it's not as good as something else that they do for weight loss. And so the same would go for anything that we would talk about, whether it's mood or cognitive function or sleep. Different things work for different people. We know that. And if you don't have a Mood issue, then don't get our mood report right, you don't have that problem.
But if you had a mood related gene and you were concerned about the potential development of that, I think that's what a lot of people are doing. They're saying, well, I may not be obese and I'm perfectly healthy. Let's use me as an example, Joe, I have that FTO gene, right? That, that would predispose me to obesity. I'm at 5% body fat. What we're talking right now. Now, you know, when, when I see the advice given to people who have that gene, you know, limit your saturated fat intake, for example, to whatever it is, I think like no more than 10% of your total fat intake or you're going to explode and become morbidly obese, that might influence me to actually say, okay, well I'm holding this dynamite. But the factor here that's important is whether or not that dynamite gets lit. So for the rest of my life I'm not going to eat saturated fats that would exceed 10% of my total fat intake. And I think that's what a lot of people are doing. People are healthy and they're saying, okay, well I want to stay healthy. So what would you say would be the correct response for me to say I'm just going to eat as much saturated fat as I want and if I start to notice a deleterious response, make adjustments or using that as an example, what would you do?
So that's exactly the wrong way to use it. Like you said. And the way that you would use it is as follows. If you're an individual who has tried to lose weight and you find it very hard to lose weight, and then we find out that you have this FTO gene and let's say, and I'll give you an example, let's say you try to lose weight and you find that higher saturated fat is better to lose weight, I would say ignore that gene. Forget it. The better you know, the better information you have is from actually losing weight, from increasing your saturated fat. Now imagine you try different things or you don't even know where to start. Like let's say you just don't know where to start. You know, there's too much information out there. And let's say it is true, right? I don't know if it is, but let's say it is true that lowering saturated fat can improve your FDO gene, right? So what you would do is you're going to say, okay, and not only that, by the way, and assuming that lower saturated fat also helped other genes related that were causing you, that were increasing your risk of obesity and you said, you know what, lowering saturated fat is actually good for these three to five genes, I'm gonna try that out and see how I feel. If it doesn't work for me, I move on. Do you notice how very, very different that approach is from what you said?
Yeah, it is a combination of paying attention to your genes, but also paying perhaps even closer attention to how your body is responding to true lifestyle factors. But it still just seems, it seems odd that there are so many recommendations currently given out based on genetic factors that when taken to the street seem to be almost like overwhelmed or overrun or reduced to a state of non importance based on lifestyle and environment factors.
Yeah, I agree. And so the thing is that if after a lot of research we found that lowering saturated fat was, you know, just forget about your genes. If it came out that the research was, you know, very good research that showed lowering saturated fat could help you improve, you lose weight, that could be a thing that you do in its own right. And then the fact that you also have this gene, it just makes it a little stronger that you're gonna do it. But don't go overboard and treat it as a religion. Of course. Right. And the other thing is, you also want to look at, and this is something that we advocate as well, is looking at your labs and symptoms. That's why we're integrating these things into the self decode platform so that you don't only look at your genes.
Yeah, I think that's what's important is you need to, you know, for example, when I take on a client, I am getting a full blood panel. I'm usually getting a nutrival analysis for micronutrients, fatty acids, you know, amino acids, et cetera, a three day stool panel, along with, if their budget permits, a microbiome analysis of the gut and then a genetic analysis and a urinary analysis of hormones and a Cyrex food allergy test. Right. So yes, I've got the genetic data, but I'm also looking at how that might be manifesting from a more clinical standpoint once you actually look at, you know, the poop and the blood and the urine and the saliva, and then also things like hrv, things like sleep cycles, you know, the actual lifestyle factors such as stress and circadian rhythm patterns that would be affected by all of this. So, yeah, I think ultimately, you know, so that we don't get too long in the tooth addressing this matter, it's that the genes can be helpful, but they're not the complete determinants of health or longevity.
Correct. And one last thing that I would add. I agree with everything you said, that for me personally, I find it to be a motivating factor if I know that I have a gene that, let's say if I'm overweight and I know I have these five genes that are increasing my risk of obesity or are having mood issues. Right. So number one is I know what to try first and different things, Right. It's changing the order, but also it gives me more motivation. Let's say I tell you that exercise can improve the ftog. I'll have more motivation to exercise because I understand my body better. And so that's the main thing.
There's some definite psychological improvements that can be had. Again, kind of with that understanding that I might have the dynamite, but as long as I don't light it, I'm going to be just fine. Case in point, I was talking to a client yesterday who has the APOE3.4 and their mom had Alzheimer's. And, and I was explaining to them all the factors that you might find in a book like the End of Alzheimer's by Del Bredesen or Genius Foods by Max Lougaeva and all the things that you can do to improve the integrity of the blood brain barrier to lower neural inflammation, not just exercise and attendance to everything from air quality to EMFs, but certain nutrients that could include blood flow to the brain or break down plaque formation. Dietary considerations, omega 3 fatty acids, some limitation of carb consumption. We just created this whole list of lifestyle factors that should just be woven into their life rather than saying, you're screwed, you're gonna get Alzheimer's. So yeah, a big part of this can just be very motivational for people to know how they can take certain action steps based off what their genes are showing. And that all being said, I do want to give us some time to dig into the topic at hand, which would be anti aging and longevity. So you guys just launched what's it called? The longevity test, the longevity gene.
It's a longevity report. So you can either upload data from a different company such as 23andMe or Ancestry, and we also accept full genome uploads from certain companies as well. You could check on the site, but if you don't have genetic data, maybe because you were scared to get it for privacy or some other reason, we can sequence your data as well and then you can download A report on the topic, along with two other reports of your choice, and then there's also an introductory one. Then you also have access to the whole platform. So you could dig deeper into the personalized genetics blog and really go into any gene that really fancies your interest.
Okay, so using me as an example here, I'd love to know what you're actually looking at as far as genes that may affect lifespan and also what you found in my results. So I'm going to kind of, kind of turn the reins over to you just a little bit as far as the direction that you want to go to how we can lay this out for people that would be beneficial for them. But where do you want to start? With what you saw in my genes.
Okay. Yeah. So we can start with, for example, something that people I feel know about, such as SIRT1. Right. And that was. That's the thing that resveratrol works on. David Sinclair. It's a popular protein and aging gene, for example.
Right. Well, it's often touted as the longevity gene. And for people listening in, that's a sirtuin gene, one of the primary sirtuin genes associated with longevity, right?
Correct. Now, guess what? Surprise, surprise. There's variants that cause your sirtuinsert one to be lower or higher. That's not surprising because there's variants that do that for every gene, but there's variants that cause it to be lower or higher. You have the variants that are relatively lower than some other people.
Meaning I would be more susceptible to DNA damage, potentially.
That's one of the things from SIRT 1. But whatever SIRT 1 is doing right, we know it's associated with longevity. We know it can improve longevity. You have relatively lower SIRT one. And, you know, as part of the big picture stuff, resveratrol could seem, you know, like an interesting thing for you, especially if it's also coming up for other genes as well.
And I'd love to hear your thoughts on this, and we'll probably rabbit hole a little bit as we go. Resveratrol, I really like what I see, especially when paired with nad, particularly for DNA damage. And I'm convinced that in people in high EMF environments, that that becomes all the more important. I interviewed Dr. Mercola about this in his book EMF, and we really talked about Sirtuin Precursors and NAD being two of the best things you can do when it comes to protecting your DNA from some of the. The more modern electrical assailants that we tend to face these days. And So I certainly have paid more attention to my sirtuin and my NAD status, although I wasn't actually aware of this gene until. Because we haven't gone over any of these results. For those of you listening in, this is the first time I've heard this. But I've been using more blueberry powder, organic blueberry powder. I have this morning smoothie I make that I call my anti aging smoothie. And so it has a lot of sirtuin precursors in there. But the other thing I've been using is pterostilbene rather than resveratrol. Because even though from what I understand that the data isn't extremely thorough on this, but it might be far more potent than resveratrol, up to 10 times more potent than resveratrol when it comes to activating Sirtuin and Sirt1 particularly.
Yeah, all these things that you mentioned are great for SIRT 1. And something interesting that I, that I realize now is longevity is actually not even if you actually just look at the data, it's not even a majority based on your genes. Why is that? Because you have somebody like Ben Greenfield who's already doing everything to counteract negative genetic variants. And so when you're taking the blueberry powder, the terror still Bean, the NAD or NMN, you are counteracting the SIRT1 gene and you're making it basically irrelevant that you have lower SIRT one. And another thing, another area of genes that I saw was perhaps a weak point was your telomere genes. There were two genes that were related to telomere length that showed shorter telomere length. But we know that there's things like meditation, astragalus, NMN or NAD that can improve your telomeres. There's a whole bunch of healthy behaviors, telomeres. I probably bet you're doing almost all of them, and you're probably counteracting those as well.
Which gene is that? That's related to telomeres, by the way?
The specific gene, it's called OBFC1 is one of them. That's one of the main genes related to telomeres that I was looking at. And so I find that at the very. Even if you're doing everything, you're already counteracting these genetic variants in the and very few people are doing everythingeverything that you're doing. Right, but you're already counteracting that. I still find it interesting that you have these variants. Right. And that you just know your body a little better right now.
Yeah, yeah. And, you know, not to shoot ahead of the sirtuin stuff too much, but lest we make people think that you're gonna get a genetic analysis and then a printout of a bunch of supplements that you should be using. You know, you mentioned this briefly, but for the sirtuin piece of things, I'm a huge fan of cold thermogenesis combined with sunlight, sauna, heat, near infrared, red light. I've seen some good data on that for sirtuins as well as this whole SMASH diet approach. Right. Like, my pantry is chock full of wild planets. Sardines, anchovies, mackerel. I don't think they do a herring. If they did, I would have it. And then also salmon. So, you know, those type of oily omega 3 rich fish, you know, along with, you know, exercise, cold, sun, heat, and then some of these precursors like nicotinamide, riboside and resveratrol or pterostilbene, these all seem to be pretty good practices for that sirtuin gene.
Exactly. And I mean, based on what you're describing about what you're doing, you sound like a sirtuin God. You know, like you're really, really doing all the things that you're increasing sirtuins. Now imagine you didn't even have this gene, right? Those things are still good for longevity, but the fact that you have it makes it slightly higher priority that you want to focus on things that increase SIRT 1.
Right, right, exactly. Same thing as with Alzheimer's, right. You might not go as far out of your way to be slightly more, let's say, strict on glycemic variability and process carbohydrate mitigation. If you didn't have an APOE3.4 gene or family history of Alzheimer's or something like that, but the motivational factor of that history and those genetic factors kind of push you in that direction a little bit more.
And by the way, just with the APOE4 gene, one thing that's really interesting is they found that. So number one is, let's say if I had the APOE4 gene, right? I don't, but let's say I did, the first thing I would do is check my LDL cholesterol, right? So not go crazy and be like, I'm going to die or whatever, I would check my LDL cholesterol because it turns out that I. If your LDL cholesterol is lower, it counteracts most of the risk from that gene. And there's other thing, other ways to counteract it. As well. You mentioned all the ways. I just wanted to go with that one. So this is another example about how knowing your genes can help. And we're also looking at the APOE4 gene, the APOE gene when it comes to longevity, it's one of the genes.
What about the APO C1 gene, have you looked at that one?
Yes, it's also in our report. And basically what I found with you is that that thereyou do have a bit of a cluster of genes that are negative genetic variants when it comes to cholesterol related genes.
And what does that mean exactly?
One thing I would look at is to measure your cholesterol, triglycerides, ldl. My bet is that your triglycerides are very low, your HDL is probably high, and I would just also look at your ldl. But you're probably doing a lot of things that are already counteracting these things. Right. But have you ever checked your LDL cholesterol?
Oh, oh, well, many times. And you are correct. You know, the so called atherogenic index, which I think is far more important to look for or look at than total LDL cholesterol. You know, my HDL levels are nearly three times that of my triglycerides. And really, if you're looking at trig to HDL ratio, you would want that preferably, you know, many people say lower than 4, I say lower than 1. Mine is 0.25. And so yeah, absolutely, I've looked at it and this Apoc1 protein, not a lot of people talk about that, but that is one that it appears that I actually have the genetic factor for that would allow for blocking of the lipoprotein receptors, which would ultimately increase cholesterol and fat levels in my blood. So for me to do something like keep my eye on LDL cholesterol would be prudent. But I think more importantly, I should keep my eye on anything that would increase the ability of cholesterol to become atherosclerotic, like long transit time in the vessels or inflammation, particularly high blood glucose, crp, cytokines, fibrinogen, homocysteine, and then that HDL to triglyceride ratio. Those are things I pay attention to far more than LDL because frankly, I try to keep my LDL a little bit elevated just because of some of the data I've seen on the benefits of that for cognition or for longevity or for hormones.
Yeah, I think the way you're going about this is in general great. I mean, like you said, if Everything else is good and your LDL is higher, I would not worry. Right. But most people don't have everything else good. And so it's one of the things you want to. You should just keep it on the radar. You don't want it too high, but it's something that is not the be all end all. You want to look at all the other factors that you mentioned, especially if your LDL is high, but that particular.
SNP, that, that APO. Am I using the correct terminology? And I say SNP? I guess I should be saying gene. Right? The APO C1 gene.
The APO C1 gene, yes.
That's one that you guys are testing for when it comes to a cholesterol related gene that may be impactful for lifespan.
So we're looking at SNPs within that gene, correct?
Okay, got it. Alright, so we've got the sirtuin genes that you're looking at. We have the cholesterol related genes that you're looking at. What's another one that you investigated or that you found relevant for me?
So then there's TP53, which is a DNA repair gene. You know, it's most associated with cancer, let's say. Right, okay. It's a really important gene when it comes to cancer because we know DNA repair is important for cancer, but it also not surprisingly has an impact on longevity. Right. You want to repair your DNA. Well, if you don't, you're probably not going to live as long. Now there's things that you could do to counteract it like tea and the polyphenols like EGCG and things like that. I'm assuming that you incorporate that into your regimen in some way or another.
Yeah, I certainly do. Have they done studies for this particular gene on the polyphenols in something like coffee versus say the EGCG from green tea?
Well, what we've seen is that we have the research in the post that it's EGCG can increase TP53 which will help DNA repair. I'm not sure of all of them, but I know that I'm assuming that other ones also. But I know that it could be that there's no research on it.
I'll see if I can pull up this section. Okay, so P53, this one related to DNA repair. So this would be separate for those of you listening in, separate than the sirtuin and then the NAD factors. This is one that isn't discussed as much. It looks like a lot of the same things though. That would act to be helpful for something like sirtuin or NAD would be helpful for this. Because you are correct. EGCG is listed as one of the primary factors, but so is quercetin and fisetin. You know, like red apples, onions, wild strawberries. Yeah. Flavonoids, curcumin, resveratrol again, and then apigenin, which I believe is actually apigenin, I think is found in pretty high concentrations in chamomile tea. And so, yeah, this idea of almost like a Mediterranean esque approach to addressing DNA damage, the inclusion of a lot of, you know, bitters and herbs and spices seems prudent. And, you know, kind of where my mind goes on this when I look over some of the components that may help to protect DNA is what do you say to people who will, for example, point out in vitro cell studies of these compounds and found them to be cytotoxic? That's something that Paul Saladino talks about in his book the Carnivore Code. Is a lot of these bitters and herbs and spices that we feel could be protective based on their hermetic effect are in fact cytotoxic and that you don't need them and they might even be doing more harm than good. Do you have any thoughts on that?
I completely don't buy that. And just to say it simply, and he could find, you could always find one study saying whatever you want it. But if you actually look at the totality of research and I'm looking at different genes, I'm like, oh, this helps this gene, it helps that gene. It's helping all these genes that are increasing the risk for different things. Right. But when it comes to the toxicity, I'm sure you could find a study that's using some crazy amount in a cell study that you're never using in real life. Right. And so the idea is to vary it up. You're not taking, you know, a billion grams of curcumin or resveratrol. If you take too much, I don't think it's good. I've taken as experiments, megadosing experiments. I've taken 10 to 12 grams of curcumin and I didn't feel healthy.
Yeah. And actually if you look at animal models, like there's a really good book about this called Nor, and I'll link to it in the show notes. I read it last year. Typically, for you to get to the amount to where cells like cultured cells or in vitro would be saturated with the amount necessary for toxicity Nausea kicks in far before then, like in animals nausea. And when they give animals anti nausea drugs, they actually feed on a high, high amount of bitters and herbs and spices and a lot of these younger plants that are more concentrated in those as a plant defense mechanism because their nauseous mechanisms don't kick in and thus their natural self protection does not kick in. So I think there's something to be said, you know, as you've just alluded to, for intuitive eating, like, do I feel like crap, does my stomach hurt? Do I get nauseous when I'm eating this amount of turmeric or curcumin or something like that? Because it appears that we may have built in like self defense mechanisms ourselves that just based on something like a nausea signal or a stomachache signal would keep us from say poisoning ourselves with plants.
I agree 100%. Yeah.
Okay, so, so T53, TP53, that's another one that you guys work in.
Yeah. And I can go through a few more if you'd like.
Yeah, I actually wanted to return to one that, that you kind of briefly went over and that was the, the telomere. What did you say that was? The OBF C1.
Correct.
Tell me a little bit more about that one.
Basically that one. And it basically works with telomere protection. It's basically like a, it's this complex, it's part of a complex that helps protect telomeres from DNA damage and things like that. And if it's not, if the variants basically make it that it's not working the way it's supposed to, and people with shorter telomeres have those specific variants.
Okay, got it. So for this, you know, we hear a lot about these, these so called telomere increasing compounds. I guess one that you had mentioned earlier, astragalus is probably the one that's mentioned most often. Are there others that you think? Because obviously you could probably fill an entire book. As a matter of fact, I think entire books have been filled with how to increase your telomere length. But is there anything particular, just based on the research you guys have done at Self Hacked that you think would be surprisingly effective at mitigating an increase in telomere shortness.
Yes, definitely. I mean, so I think psychological stress is a big one. And you know, meditation and yoga have been found to help that even in clinical trials. Mediterranean diet has been found to help. There's green tea, intermittent fasting is a big one. And then there's things like we said stragalus, nmn there's a number of things, but I'd say these are the main ones that I would look at. And in your case specifically, you actually have four variants that are causing your OBFC1 gene to increase the risk. So it's actually a significant gene for you, I would say.
So you're saying I should go out and spend the 800 bucks on what's his name? Bill Andrews. I interviewed him a couple of years ago on his telomere enhancing supplement TAM818. His other one that's also well known is TA65. And those, based on what they say at his company, Sierra Sciences, are just like the bee's knees when it comes to limiting telomere shortening. But for me, this is related to that idea of do you want to live to 120if 35 of those years are spent inside a sauna or a cryotherapy chamber or hungry because you're fasting all the time? It's kind of like me, do I want to increase my telomeres to the level where for $1,400 a month, month, I'm skipping out on ribeye steaks and cool new books and Legos for my kids? And for me, I did a short stint of that stuff. But yeah, I agree. Meditation, yoga, intermittent fasting, some elements of calorie restriction, a well formulated Mediterranean diet that might be adapted to be specific to your needs and your exercise levels and even your genetic factors like this. I think that's more palatable to a lot of people from a budgeting standpoint. But what about NAD or nmn?
So NMN is also one of the things that would be recommended for that. And just to be clear, if I were to make a wager of, you know, if you tested your telomeres, and I would wager that they're higher than the vast majority of people even with this variant, because as you could see, you're already doing basically everything on this list and many other things that, that are not on the list and that I didn't speak about and other things that we don't even know improve telomeres. But we know that a lot of healthy behaviors are increasing telomeres and I would wager that you probably have very good telomeres compared to the rest of the population, even with this gene and the negative variants.
Well, I test my telomeres twice a year and currently I'm using Spectracel, which I think is one of the more accurate telomere measurements out there, although I don't think it's it touches these newer Horvath clocks for methylation and aging predictiveness. But they do measure telomere length and I can tell you the one thing that lowered it most significantly. Meaning that the last time I tested my spectra cell analysis indicated that my telomere length was that biologically of nine year old boy and that was about. Of Epitalon, the Russian peptide Epitalon. I did a. I think it was, I don't recall if it was a 10 or a 20 day injection protocol of that. It was, it was the basic covensin protocol. I'll link to that protocol and that peptide or a page where you can learn more about that peptide in the shownotes. But that above anything that I did. I'm not saying meditation and yoga and everything aren't great, but there's something that that Russian Epitalon peptide did that was absolutely staggering when it came to my telomere line length.
Maybe it improved your OBFC1 gene.
Could be. Yeah, could be. But, but you know, I'm, I'm not quite sure. You know, currently the legality of peptides is going back and forth. But what I'll do is I'll, I'll just link to the, to the Wikipedia page for Epitalon for those who want to dig more into it. And I can tell you right now that if you're going to get a peptide, don't just order something like this from some random website. You, you want, you want to be careful because these things are interacting with cell surface surface receptors. And I'd go through a physician, preferably one through the International Peptide Society or a good peptides company like Taylormade Compounding or something like that if you're gonna get a peptide protocol on board. Okay, so that was the telomere gene. And then in glancing at my report that you sent over to me, it looks like there were actually a few other genes that you looked at. So, so what else?
So I noticed some genes related to oxidative stress and I can quickly list them like PON1, VOXA1, GPX1 and SOD3. Right? Those are genes. And I could just like for example, PON1 helps detox toxins, especially organophosphates. But guess what, you're already eating organic and you're doing a lot of other things that increase PUN1 when it comes to FOXO1 things like intermittent fasting, resveratrol T also improves it when it comes to GPX1. That's glutathione peroxidase. Things like Having enough selenium or getting enough sulfur amino acids, that can increase that as well. And you know, taking, having enough antioxidants in your diet from vegetables and other things that will also improve the SOD3 genes. So those are some related to oxidative stress.
There's a lot of talk out there in the functional medicine community that one of the better things to do for glutathione status and also superoxide dismutase is not necessarily like high dose supplementation or intramuscular injections or any of these other higher dose delivery mechanisms of glutathione, but rather supporting your own endogenous glutathione status via some of the lifestyle strategies that you just mentioned, along with intake of things like, like cruciferous vegetables, practice and attention paid to the health of your liver, perhaps even the use of things like coffee or coffee enemas or things that would spark your own glutathione or superoxide dismutase activity versus high dose supplementation of glutathione. That all being said because I was already aware of these genes based on another genetic analysis I'd done and aware that my children also are very deficient in a whole host of genes related to glutathione and superoxide dismutex case. Me and my boys do use small amounts of glutathione on a daily basis. We just use like a liposomal glutathione. So I think that sometimes the, you know, your take on your, how much you're going to go out of your way to get extra glutathione on board could be influenced by, you know, how many factors related to glutathione and superoxide dismutase are popping up on your genetic labs. So again, again, just something that's going to be personalized from individual to individual. We talked briefly about cholesterol, Joe, and there was another gene you looked at called the cholesterol ester transfer protein CETP and specifically related to longevity. How does that one work?
That one works basically it transfers cholesterol from HDL to ldl. That one is a little less clear, to be honest. There is some like, basically when there is conflicting research for something, we give you the conflicting research and in this one in particular there is conflicting research. But in terms of overall you still have two risk variants, two out of two risk variants in that gene and basically they're not associated with longevity. So in general you want to think of the bigger picture in that regard, such as making sure your Cholesterol level levels are at a healthy point. Including your hdl, ldl, things like that.
Yeah, probably most particularly for this scenario, HDL and triglycerides would be the two to pay the most attention to. Again, that atherogenic index. And that's something that I bring up over and over again with folks when they're looking at their LDL levels. Just because you're taking into account not only HDL and triglycerides, but the ratio between them. And again, paired with looking at glucose and inflammation levels, I think that's as important or more important than what annoys me when I see articles that refer to LDL as the so called bad cholesterol, when in fact that's not a sufficient factor for induction of heart disease. It's certainly present, but it's not sufficient in and of itself to be a cardiovascular risk factor. What about any inflammatory markers? Did you look at much related to that aside from glutathione and superoxide?
Yeah. So you have one inflammatory marker in particular that I would look into and that's interleukin 10. So interleukin 10 is a cytokine. Normally we think of cytokines as inflammatory cytokines, but in your case Interleukin 10 is actually an anti inflammatory inflammatory cytokine. And I actually have the same variants. And I noticed, you know, I noticed that, I mean I have a lot of autoimmune problems as well. And that's like a cytokine that's really good for autoimmunity, bringing down autoimmunity, increasing T regulatory cells to basically balance the immune system from not overreacting. And sometimes viruses can, you know, there is somewhat of a negative that if it's too high in certain states, you know, it could lower your immune system too much. But overall it's a very good protein to have at somewhat elevated levels and yours are a bit lower. And so when we wanna look at the things that are really good for that, one of the best things in my opinion based on the research and what I've seen is bioavailable curcumin, which I'm sure you're already taking. Right.
I do get curcumin in my diet, although I have to say that probably my primary source of that, that or compounds related to that is my own company, Kion. We make a product called Flex to support joint health and that actually has a whole bunch of isolated tumorosaccharides in it which are actually different than curcuminoids, but act similarly on A lot of these cytokine pathways. And then I also drink a ton of bone broth and typically have a little bit of extra fat. A lot of times with lunch, I'll mix a little bit of extra fat, like an olive oil or ghee in there. And then turmeric. Turmeric and black pepper I don't use too often, like a higher dose curcumin product. Not that I'm opposed to that, but just because I'm getting turmeric in here and there and some of the natural curcuminoids in that, along with the turmerosaccharides from Kion Flex, which I probably take four or five times a week, just on an empty stomach at night. I would imagine I'm probably decently equipped. Unless, you know, that higher dose curcuminoids could be something that wouldthat would push this in an even better direction. I'm just, you know, it's not something I do a ton of.
I think bioavailable curcuminoids havetheit's really very hard to get that you really needi personally think you need a bioavailable curcuminoid rather thanbecause the turmeric, even with the black pepper, very little of it gets into the bloodstream, and almost none of it gets into the brain. And. But you're doing other things that also help. If you don't want to take curcumin, for example, exercise increases interleukin 10 and a lot of other healthy behaviors and a lot of other things. It's just, I was just saying one of the best things is bioavailable curcumin. Now, if you're doing, you know, 20 other things, like you said, you're taking these supplements, I'm sure that a bunch of these things are increasing interleukin 10, and it' syou're probably counteracting the negative effects of that. But I do think bioavailable curcumin is probably a good supplement for you.
Okay. Yeah. Sometime back, I interviewed Tom. What's his name? He's like a magazine cover model, big ketogenic guy, Tom. I'm blanking on his name, but he talked about something called Purathrive. Thomas DeLauer. Thomas DeLauer is his name. He had a product called Pure Thrive that they make that's apparently a extremely bioavailable curcumin. He had sent some to me. It tasted like an orange creamsicle. So I wouldn't complain about getting some more of that stuff, but I'll see if I can hunt down that podcast and toss it in the show notes. But I think that stuff was curcumin gold, I believe by Purathrive. So maybe I should just put a few squeezes of that into my bone broth and turn my bone broth into a bone broth creamsicle.
The most bioavailable curcumin that I've seen on the market. And there's new ones coming on the market now. There's a bunch of them, but. But the two ones that I like the most are Longvida and there's a bunch of different brands there. And then also Thera Curcumin. Those have very good bioavailability.
Okay, got it, got it. All right, cool. Taking notes. And I'll put this stuff in the show notes for you guys. Okay, so that's that gene there was. Because I want to make sure we have enough time to briefly address what you're doing when it's related to coronavirus. But I would be remiss not to ask you about growth hormones hormone, because obviously there's kind of a sweet spot for growth hormone. And I know there's certain genes related to the IGF1 receptor that could be related to longevity, and I know that you're looking at that as part of your longevity report. So I'm curious, were you able to feed any of my results in and look at any growth hormone or IGF1 factors?
There was a gene that came up that was related to IGF1 receptor. The problem is that it wasn't very clear in the research exactly what the issue was. And also there's conflicting research on whether higher IGF1 or lower IGF1 is better. Now, that's probably because it's good to get cycles of it, right? And so because you have that variant, you do want to go through periods where you decrease your IGF1. Intermittent fasting, lower protein, things like that. I don't recommend always doing it right. But you go through cycles of lower IGF1 to higher IGF1. And we know that the IGF1 and growth hormone are very connected in those pathways. But at the very least, I wouldn't take growth hormone. If you're having that variant, then you want to live longer, maybe unless you have, like, very low levels. But IGF1 is actually a good proxy of growth hormone levels. And one thing you might want to do is just check your levels. I mean, this particular gene is affecting the receptor, but you want to check your Levels. And the other thing is to do healthy practices that kind of, you know, go from lower IGF1 to higher IGF1, you know, going through some periods of fasting or intermittent fasting or somewhat calorie restriction and then increasing your IGF one as well when you want to focus on performance and things like that. Because there are a lot of benefits to IGF1, right?
It's that whole trade off between growth and longevity or between performance and longevity. And kind of related to what I was talking about earlier when it comes to enjoyment of life versus just living as long as you possibly can. And certainly lower levels of IGF1 and a lower metabolism and lower oxygen consumption overall all seem to be correlated with longevity and this idea of frequent periods of hibernation, a lower metabolism, you know, things like advice from Patrick McCown who says, you know, take very small breaths in and very small breaths out through your nose. I think that, that all of that is somewhat prudent. But at the same time, you know, I, I think that being strong, being hard to kill, being able to chop wood, being able to like have libido and strong sexual performance, being able to have like a competitive drive when you're out on the tennis court or the basketball, basketball court. I mean, you throw a lot of that stuff out the window if you're just trying to lower IGF1 at all costs. And, and I do test IGF1. I, I personally feel pretty good at a sweet spot of about 100 to 150. And that, that's a nanograms per milliliters I think is how that's measured. And so, yeah, I don't keep it low, you know, at the sacrifice of everything else. But I certainly do, as you've just alluded to pay attention to having periods of time where like, for example, four times a year I implement more of a fasting mimicking diet where for five days I eat about 40% of the number of calories I would normally consume. And I do intermittent fasting 12 to 16 hours every day. Twice a month I do a 24 hour dinner to dinner fast. I exercise, which in and of itself is going to naturally lower IGF a little bit, along with some amount of carbohydrate mitigation. And so, so yeah, I certainly pay attention to it, but I also want to impress upon people that lowering it at all costs. Yes, you'll live a long time, but you also might be kind of miserable, right? Because if we really wanted to live a long time, we should be like a bear and just climb into a cave and hibernate and not eat any food and lay there breathing as little as possible. And we'd probably live a long time, but it wouldn't be that great of a life.
Yeah, and I'm not even, I think what you're doing is really smart with those periods of reduced calorie consumption. So I think the way you're going about it, it really strikes a very balanced note and I think it's really good and other people can mimic that. But I actually am not convinced that lower levels of IGF1 just, if you were just going gung ho on that, you would even live longer. And the reason is because biology is complex. For example, it's very good for your muscle and your brain. And if your brain function declines or you're losing muscle, I mean, your muscle mass in older age is a predictor of how long you live also. Right. So there's this trade off. There's always a trade off. And even within the longevity space, there's a trade off within longevity because some things could be good and then some things you can repair injuries more. There's a lot of benefits to IGF1 and it's not clear that just going crazy on low IGF1 is a good idea even for longevity right now.
I think there's some interplay here with insulin as well, meaning that lower levels of IGF1 in a state of insulin sensitivity allow you to actually get the benefits of insulin like growth factor with, well, being more sensitive to lower amounts. So I would say, if anything, perhaps pay more attention to insulin resistance and glycemic variability. And even if you, if you do have lower levels of free plasma IGF1.1, you're probably going to be more sensitive to those and thus you'd need slightly lower levels anyways. So, you know, I think if you go higher up and just look at insulin signaling and glucose stability, that's probably a smarter way to approach things than just saying, okay, I want to keep my IGF one low. You should instead say, well, I want to be as sensitive as possible to the signals that that's sending or receiving in this case. All right, well, that is a lot for people to think about and what I'm going to do because I think folks are aware that I have pretty much every piece of public health data on my entire life out there on the Internet anyways and have yet to have my hand slapped by my insurance company. So I'll put a link to my results in the show notes for those of you who want to dig a little bit more into my own genetic longevity analysis. But then I will also link to this longevity report. If you want to get your own report from self decoded, I'll put a link in there.
There.
I'll also link to a lot of the books and the resources that we discussed as we were delving into longevity. And that's all going to be over@BenGreenfieldFitness.com self decoded. But I did want to ask you, Joe, about this coronavirus piece because I'm curious. You had mentioned that you guys are doing some kind of genetic analysis for coronavirus risk or something like that. I'm just curious what you're looking at.
So, yeah, we're doing a genetics report on coronavirus and its related complications. And that's actually super interesting. And it's going to be released. I mean, it's released now, essentially, and it's just, you know, by the time this podcast is published, it's going to be released. And there's quite a lot of interesting things when it comes to coronavirus, quite a lot of interesting genes. So what we did was we broke it down in a few ways. We looked at what are people dying from when it comes to COVID 19 or what are they getting complications from. And some of the worst complications have to do with ARDS and cytokine storms. The ARDS is acute Respiratory distress syndrome. And that's basically when the lungs start shutting down from very high levels of inflammation. And what happens is that if the immune system is poor in the beginning, then the viral load builds up and that causes an opposite response. Basically you have a, let's say if someone has a poor immune system or they have genetic variants that make it very easy for the virus to latch onto cells. And so that causes the viral load to go crazy and that causes an overactive response later on. And if they also have genetic variants that, that cause this response to go overboard, they will get this respiratory distress and acute respiratory distress syndrome. And that's how people are pretty much dying. Their inflammation is overloading the lungs. So we were looking at some of those things in terms of what are the genes that are related to that. And we looked at around 29 genes and it's quite interesting. So, so the way that we break up the genes is, for example, viral entry. And so some of the two genes that people are really, really interested in now are called ACE2 and TMPRR. TMPRSS2. That's, that's pretty hot on the conversation list. Right now?
Well, the Ace 2 I'm pretty familiar with because obviously that's the receptor that the virus is interacting with in the lungs. What was the other one?
TMPRSS2. It's actually also one of those genes that people are really looking at in terms of risk, in terms of how susceptible someone is to the infection. So this TMPRSS2 basically it interacts with the virus in a certain way that it makes, it allows the virus to spread more quickly. Okay, yeah. So these two genes are very important for, you know, if you have these kinds of variants. And again, I wouldn't only look at these genes. You want to also look at, there's lab tests you can look at. There's also, even more importantly is if you have any of the conditions that are increasing your risk. And we're also doing something there to give you a risk profile. You put in your symptoms and it'll tell you what your risk is just based on your symptoms. And so, for example, if you have high blood pressure, if you're overweight, if you have a lot of these risk factors, that's even more important than these genes. But if you have those, then you even want to look at your genes even more because you already have these risk factors, you want to try to improve them, but you also want to try to look at your genes and see what you can do with that regard. And so we're looking at the viral entry genes, genes, and then we're also looking at inflammation related genes which are related to this respiratory distress syndrome and cytokine storm. So you'll find all kinds of inflammatory pathways and genes that are increasing risk for this complication. Basically the immune system turns on, but it turns on way too much. Even though you could have a low immune system and then not get this respiratory distress, but you could have variants that basically after your immune system is low and they start attacking your lungs, it goes overboard and it attacks it too much, which increase the risk of ARDs.
Okay, so let's say theoretically that you had the ACE2 gene factor that would make you more susceptible to a coronavirus infection. Are there certain things that you've investigated, and again, I want to be very clear here that I in no way want to position this as saying, oh, here's a cure if you have higher susceptibility for coronavirus, but are there certain compounds that for example, would somehow affect those ACE2 receptors in a manner that would inhibit the binding of the virus to those receptors?
So there are things that you can do, for example, to block the ACE2 receptor and things like that. And you know, that's something that you would want to focus on. And so the things that, for example, that would do that. And this is something that's very popular in general. So number one is I would say it's a good thing to take, right? If you have, if you're afraid of respiratory infections in General and specifically COVID 19. And again, I want to say the same thing. There's no, this is not 100% right. It's just, just if you have genetic variants that are causing this virus to enter more and then you also have a bunch of risk factors, it's something you want to look at. And so one thing is zinc, right? And that I would say is one of the most important things. And there's other things, for example, like Ashwagandha that might help. For example, one of the compounds in there with an owner is it may help SARS CoV2 from binding to the ACE receptor and entering cells. But we also want to look at studies, right? We don't just want to say, oh, there's some cell study or something that shows that it could block the receptor. So what we do is we want to see is this a good supplement anyway. And it turns out that for example, Ashwagandha could potentially help with lung function, for example, in a clinical trial of, of 40 elite cyclers, which your fan base would be one of them. Eight week supplementation with Ashwagandha improved respiratory endurance. And we also know that it has some antiviral properties also. One thing that's very important is vitamin D deficiency. Vitamin D does interact with these ACE2 receptors. The interaction is complex. But what you want to make sure is that you're not deficient in vitamin D. And so the two top recommendations would be zinc, vitamin D. And there's other things as well. But like I said, it depends on what else is going on with your life. You really have to look at these things in a comprehensive way. But I personally think zinc is a great supplement anyway. And if I had this ACE2 receptor gene, I would 100% take zinc.
Yeah, I think that zinc's pretty prudent anyways. The life extension zinc acetate lozenges that I usually keep on hand sold out within about the first week that this pandemic struck. But I actually, in my teas or coffees I quite often put a teaspoon of, don't laugh, black ant extract which is extremely high in zinc. I made the mistake, unfortunately. I mentioned that on a podcast a couple weeks ago and you can't get it anymore. I was getting this stuff from Lost Empire Herbs, their black ant extract, which is amazing pre workout as well, which is how I was originally using it. But yeah, I was using that blackor. That Lost Empire Herbs Black Ant for that same reason. Just because of what I've seen as far as the potential for zinc to reduce the binding capacity for the virus on these ACE2 receptors. But again, I would say that it seems to me that the big story here is if you get your genetics tested and you happen to have some of the. And again, like I'm always careful with my terminology here so I don't get torn to pieces the SNPs that would be associated with expression or upregulated expression of ACE2. It might be prudent to keep some zinc on hand and use that as a supplementation during this time along with other things that could help with Dh2. I think some of the ones you list on your website would be sunlight vitamin D. Ashwagandha you talk about like you just mentioned, I think there's another one called Japanese Japanese knotweed. Yeah. And I think that one's, that one's currently under investigation. Right. For ACE2 receptor binding.
Yeah. And you know, if you take a resveratrol supplement, most of them are coming from Japanese knotweed and probably half of it is Japanese knotweed.
No kidding. Okay, cool. Well that's good to know for people who are already taking resveratrol and then ashwagandha. It's kind of funny because that's something I take pretty regularly anyways. My wife and I have a, have a tincture from. We, we love to go to Kauai and there's an organic pharmacy down there that we visit called Kauai Organic Pharmacy. And they make like this chewable Ashwagandha root and then this super potent Ashwagandha tincture. We, we keep that in the bedroom and we have that before sex. And it just like your, your stamina goes through the roof sexually with, with, with Ashwagandha. When you both use it. It seems to kind of, I don't know if there's something, something spiritual or energetic going on there, but that one's great for lovemaking as well, Ashwagandha. So you can basically bang it up pretty hardcore in the bedroom virus free with a little bit of Ashwagandha extract. So if you learn nothing else from this podcast, there you have it. Support your immune system and have a good time in the bedroom. As well. Well, this is quite fascinating. And what I'll do, Joe, is if you send me over a link or whatever, I can include a link to not only the longevity report in the show notes, but I can link to that coronavirus report if people want to test, for example, their ACE receptors or any of these other receptors associated with possibility for increased susceptibility to viral infection in case they're curious. Again, neither Joe and I are physicians. We are not saying that this is something that's going to be able to test or diagnose a disease, nor are any of the recommendations something that we would consider to be a cure. And so I just want to make sure I highlight that we're not telling you to go rush out and get a genetic test and then take a bunch of stuff based on that genetic test to cure yourself of coronavirus. But some of these things are at least interesting to look into. And learning about your body, your unique body, I think in any manner is just always going to make you better informed for your own immunity, your own health, and of course, your own longevity in the future. So, Joe, thank you so much for coming on the show and sharing all this stuff with us, man.
Hey, it's my pleasure.
Yeah, this has been fascinating. And again, the show notes, for those of you listening are@BenGreenfieldFitness.com Self Decoded. Self Decoded. And I'll link to everything over there, all the books mentioned, the products mentioned, the reports that Joe is running. And I believe after this podcast Joe will get me over like a special code or a special discount that you guys might be able to type in to save on the longevity report. And I'll put those in the show notes as well. So again, BenGreenfieldFitness.com selfdecoded until next time, I'm Ben Greenfield along with Joe Cohen, three peak guest now on the BGF show, signing out from BenGreenfieldFitness.com have an amazing week. Well, thanks for listening to today's show. You can grab all the show notes, the resources, pretty much everything that I mentioned over@BenGreenfieldFitness.com along with plenty of other goodies from me, including the highly helpful Ben Recommends page, which is a list of pretty much everything that I've ever recommended for hormones, sleep digestion, fat loss, performance, and plenty more. Please also know that all the links, all the prompts, promo codes that I mentioned during this and every episode help to make this podcast happen and to generate income that enables me to keep bringing you this content every single week. So when you listen in, be sure to use the links in the show notes. Use the promo codes that I generate because that helps to float this thing and keep it coming to you each and every week.
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