Your Genes AREN’T Your Fate—The NEW Science of DNA Biohacking for SuperHuman Health | Sharon Hausman-Cohen : 1257

The breakthrough that's happened in the field of genomics in the last 10 years is realizing that chronic diseases, cognitive decline, heart disease, diabetes, obesity, depression, anxiety, autism, they're not because of one gene. You can use your genomics to determine do they have problems with getting enough blood flow to the brain and even within that, is it because they don't make enough nitric oxide or is it because they're hypercoagulable? Do they have mitochondrial membrane issues? Do they have issues with transporting choline?

Your DNA holds the blueprint for your health. And Dr. Sharon Houseman Cohen is the scientist decoding it. Harvard trained physician, 25 years in integrative medicine. Co founder and chief medical officer of intel xdna, the precision genomics tool unlocking the future of personalized health.

This particular gene's involved in a couple of things. These are the kinds of things that you can learn about using Intellix DNA.

She's not just studying the science, she's rewriting the playbook. From cognitive decline to cardiometabolic disease, autism to the so called unsolvable cases, her work is helping top physicians crack the code on root cause medicine.

Now we're using intellects.

It gives me a more targeted approach.

We are able to really get to the core depth and the breadth of what Intellix DNA provides.

Intellix DNA isn't just a tool, It's a revolution. Dr. Housman Cohen's research is fueling cutting edge studies, including Those led by Dr. Dale Bredesen, proving that DNA driven medicine isn't the future. It's happening now.

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Longevity seekers, health disruptors. The next frontier of medicine is here, and Dr. Sharon Houseman Cohen is leading the way.

I've done gene therapy to reduce my age by about nine years. Why do you think we can't change our genetics? You're listening to the Human Upgrade with Dave Asprey. Sharon, you have a master's degree in cell biology and you're a position. It seems like we've had a genetics fetish over the past 30 years and we discovered DNA and we got into all this stuff and we all got our genetics done. And I got a report back and it said you're 0.1% strange Russian shamanic tribe and you have a 10 increase in risk of something that isn't a very big risk anyway and it was sort of a big yawn. How useful are genetics for longevity?

Well, I think you have to look at the right things and so when genetics started, people started with pharmacogenomics, people started with cancer genetics, and then nutrigenomics came along and all of them had their place. But if you're really wanting to look at longevity, you have to understand cognition. You know, what makes up longevity, heart, bones, brain. And you can't just look at one gene variant.

So it's sort of like the bucket of all of your genes is useful for longevity.

Yes. And it's I think that looking at some of the genes that are less common but clinically significant, and that's another huge piece, is if you just look at genes and you're like, okay, I have a copy of. I'm gonna pick on MTHFR because it's a pretty pop gene, right? Well, 45% of people have a copy of MTHFR, so how important can that be? You know that, yes, methylation's important, but if you have somebody that has cognitive decline, you can use your genomics to determine do they have problems with getting enough blood flow to the brain? And even within that, is it because they don't make enough nitric oxide, or is it because they're hypercoagulable? Do they have mitochondrial membrane issues? Do they have issues with transporting choline or bacteria?

Wait a minute, do you have my genetic profile with that list? Literally, I have nitric oxide genes, I have sulfation genes, I have mthfr, I have blood flow issues to the brain. And there was one other in there. So are these common problems or am I just like, Am I fucked?

Well, some. No, no. I'm pretty sure your brain's working really quite well.

Yes, pretty happy.

But I think that some of them are common. So the gene that relates to choline, for example, it does give you about a 60% increased risk of cognitive decline. And that one's fairly common.

Don't have that one.

That one's like 40% of the population. But some of them are common, some of them are less common. There are gene variants that. So the one that relates to mitochondrial membranes, it can give you more than double the risk, again, of dementia. It's 2.7 times the risk. And that one's in like 25%. But no one gene causes Alzheimer's. And I think that the breakthrough that's happened in the field of genomics in the last 10 years is realizing that chronic diseases, cognitive decline, heart disease, diabetes, obesity, depression, anxiety, autism, they're not because of one gene. They're not Sickle cell or Tay Sachs, they're because of a combination of Gene variants interacting with each other, but also with diet, lifestyle, the environment. And together, by understanding the components, you can then improve these specific things that may run in your family or, or that you're at risk for.

A friend who's been on the show and been a, an inspiration for me is Bruce Lipton, cell biologist turned biology of belief epigenetics guy. And, and some people have noted that biohacking, when I, I first defined the word, it, it's a restatement of epigenetics, particularly around longevity. And epigenetics being the environment, affects chains. Can you separate epigenetics from genetics?

Well, I think epigenetics is an answer to genomics or genetics. And so if you think of your. So genetic diseases are ones that are inherited. You know, mom has one copy, dad has one copy, you get it. But genomic issues are things that are small changes in your DNA that increase your risk for something, but they're not what we call pathogenic. They don't cause it. And epigenetics is how we respond to it. So let's take TNF alpha. So there's lots of different kinds of inflammation, but TNF alpha causes leaky blood brain barriers, it causes leaky blood gut barriers. And some people make much more TNF alpha because they have an overactive promoter. So if you have a gene variant that makes that TNF alpha promoter four to five times more active, you can't change it. Your promoter is kind of hyperactive. But what you can do is get use things, diet and lifestyle to decrease the transcription and kind of slow the transcription and the expression of TNF alpha down. And you might need that more than someone else. So lion's mane mushroom is great for TNF alpha. Even chili peppers is really good for TNF alpha. Sulforaphane. And there's many different things. And so the way that I think of epigenetics is how do we respond to our genome to say, oh, nothing I can do about it? Well, that's not the biohacker way. It's like, let's understand it and become empowered by it. Because there's so many things that can help your longevity and how do you know which ones are right for you? I mean, resveratrol can increase the expression of Clotho, which is an important longevity gene. But if you're already the high Clotho type of genotype, that may not be the most important thing for you, even though it's important for many people.

So with genes, if you have both alleles and it's mthfr, you know that whatever environmental things you do, you're not going to turn off a gene when it can't be turned off because it's all you have, right. And you can't turn on something that isn't present. So epigenetics has great power, but what you can do and what I do is, well, I know that my body will overproduce this thing or under produce it, therefore I will block it, right? And it becomes complex at one level. But if you look at symptoms like I've, for most of my life I've had really strong muscle tension between my shoulder blades, upper back to the point. In my 20s it felt like a candle burning there. It was a lot of pain, like probably 7 out of 10 just all the time. And some of it has to do with liver and toxins and I get rid of those. But ultimately for me it's a catecholamine issue. And the way my body makes things like adrenaline and cortisol and noradrenaline and I finally figured it out and some of it's genetic and if I take the right substances, I am golden. I have no muscle tension and I have no pain in my body. I could have done that, you know, geez, 40 years ago had we had the right genetic screening and understood the pathways. Now we understand those things, but I didn't do it with genetics, I just did it with symptoms. How far along the path are we of using genetics to be able to turn off symptoms? Like are we a third of the way? Are we all the way?

I think it depends on what topic. We're making great headways in certain fields because I came from a neuroscience background. We do a lot of NeuroScience with Intellix DNA, which is the company where I head the research. So we do a lot, we've done a lot with cognition, a lot with autism, a lot with mental health. But we also, in uncovering the foundations of all of health, looking at the detox pathways extensively and inflammation and many other things, we actually have surprisingly been able to help a lot with pain. We've had patients where their pain. You can have three patients. Your pain may be because you have all this high adrenaline, different genes, and there's a lot of different adrenergic receptors and compt and such. But I had a patient and she literally was limping in and she was a photographer and she said that by the end of the day she would have to crawl up her stairs because she was in so much pain.

Wow.

And she really wasn't Somebody who wanted to do 20 things. And. And in her genomics, it became really clear that she had something called Factor 2, which gives you increased fibrinogen, which makes it so you don't get enough blood flow.

I had that.

She did not transport B12 into her brain or CSF. Well, and that's pretty common. That's about 18% of the population. That's TCN2. But then she also had seven times the risk of gluten intolerance. And she had a few other things. But just by having her get rid of gluten, adding some pycnogenol and lumbrokinase to address the fibrinogen and B12 in four days, she was able to literally run up the stairs. And she hadn't done that for years. But then there was another patient and she's a makeup artist, and she would get pain in her arms and muscle cramps and dropping things. And for her, the secret was she couldn't make CoQ10, but also couldn't recycle CoQ10 to its antioxidant form, to the UBQH form or vitamin E. So for her, getting rid of her pain was vitamin E and ubqh. And again, for you, it was things that lower your cortisol.

So I think that she decreased cortisol, surprisingly.

Oh, you had low cortisol?

Yeah, I had to increase. Noradrenaline was good for me. Yeah.

So difficulty converting, like dopamine to noradrenaline and such. And so there's. Everybody is different. And so I think that genomics can take us a long way towards getting well, but the science is still in its infancy. So we have a list of a hundred different topics that we're working on that actively, but there's hundreds and hundreds more.

It feels like to me, maybe we're 10% of the way into this knowledge.

I think that that's reasonable. And so what we do is we start with the common things. You know, I'm not going to start. Someone asked me if I would work on, you know, it was something that. Oh, it was a lipidemia. And there's nothing wrong with helping people with lipidemia, but it's not common. And so I'm like, well, we're still working on fertility and heart disease and diabetes and cognitive decline, and so we'll put it on the list, but it's not happening tomorrow.

I mean, you're a longevity doctor, and I don't know if you read my longevity book or not, but I Said, look, there's these big four killers. And subsequent books in the space have called them the Horsemen of the Apocalypse. I didn't do that. Cause I'm like, that felt a little bit too alarmist. But it's heart disease, it's cancer, it's Alzheimer's, and it's diabetes. And if we just handle those things, then you get to the weird people like me who have 18 different weird genetic pathways. And I honestly think I would be disabled. I bought disability insurance when I was 26 because I'm like, so many things don't work and the doctors are useless. And maybe out of. I don't like to hurt all the time and feel dumb. I struggled my way out of it, and I'm lucky that I made a bunch of money in my 20s, even though I lost it. But I managed to figure out the combinations and to learn the pathways. I didn't do it genetically. I did it via systems biology. And understanding this leads to this leads to this. And there's a blockage here. And it was a lot of work, and no one should ever have to do that. AI is pretty good. But now that we have the type of work you're doing with genetics, I have the ability to say, well, here's the top three things that make my life not as good as I want it to be. Maybe it's brain fog, right? Maybe it's pain, and maybe it's the arthritis I was diagnosed with when I was 14. Or it's low energy, right? And when people come through at upgrade labs and they do a survey. So, well, what matters to you? Was it cognitive function or longevity? You got to pick one. And, like, why do you want both? I'm like, yeah, do them in order.

Right, I agree.

So then I could look at one of the reports that you do, right? And I could say, well, all right, I want to look at this report through the lens of let's not hurt anymore. Or I want my brain to not keep forgetting words. And how do you guide people, though, when they get a report to know this is the one that matters for you?

Well, that was actually one of my goals as well. So people would come to me bringing their 23andMe and say, I've got a family history of Alzheimer's, or I've got macular degeneration in my family or heart disease or whatever it was. And there was no tool out there that mapped out by topics that we as human beings, as well as physicians, want to think about. So the way that we use genomics is in our cognition and memory report. For example, we'll put together all the gene variants that increase and decrease the risk of Alzheimer's or cognitive decline by at least 20%. Some of them may be 200%, some may be 80%. And then we'll look at what does the gene variant do and then what can you do to modulate that with diet, lifestyle supplements, medications. But additionally, because I'm a functional medicine physician, we also look at detox, inflammation, extensive detox, extensive inflammation, lots of pathways, nutrients, gi and usually if you address those foundational gene variants and then you look at the ones associated with the specific diseases, you'll find answers. But some of the people who've been diagnosed with Alzheimer's, their gene variants aren't in Alzheimer's pathways. They're in brain ischemia pathways, things that affect oxygen or in things that affect the myelination of the nerves, white matter changes. So we went broad and then we started using it with doctors. Physicians across the country showed that we can get results of improvement in cognition. And then we went to the next topic and so we built it by topic. And so that's what I was saying. We now cover a good 40 or 50 common topics, but we don't cover every single esoteric disease state that someone could have.

And I think that's okay because most people, even if they feel really well, if you dig in, they do have several esoteric things. They just don't rise to the level of importance that it's worth dealing with.

Well, and also there's overlap. So I had a colleague who has strong family history of multi systems atrophy. Scary. Yeah. And, but there's not, we hadn't mapped that out, but when we went into his genomics, he had so many oxidative stress pathways that I, that I was then like, well, this is a big part of what's going on in your family. And then people who have autoimmune pathways. So there's different specific interleukins inflammatory molecules as well as TNF alpha that increase the risk for leaky gut barriers and autoimmune disease. So we're finding by using the principles of functional medicine, we're optimizing the human beings that even have issues that we hadn't thought of. And we'll continue to add more.

I'm actually really excited about the state of what we can do with DNA. Do you worry that if you have a 23andMe or something like that, well, you're not really getting the full human genome as far As I could tell, I was one of the first maybe thousand people to have my full human genome mapped, maybe back in 2013 or something. And it's just a big binder of crap. I don't know what to do with it. But how important is a full sequencing? And what are people actually getting when they think they're getting a full sequencing?

So that's a really great question. So a lot of people have done either whole genome sequencing or whole exome sequencing, and then they get the results and they're like, this wasn't useful. So it's not about quantity, it's about quality. Because most of the whole genomic sequencing products, they're using a tool that reports on the pathogenic gene variants because they can't report on everything. There are, you know, a few million SNPs that have been associated with something in the literature. So they're filtering for genes that have been labeled by the NIH National Health Institute as pathogenic. And that's a problem because most of the things that we care about, longevity, again, all the chronic illnesses, those aren't caused by pathogenic genes. So I feel like they're not particularly useful tools. And so with, again, with the genomics that we are doing, we don't report on a million SNPs, what would you do with it? We report on 700 SNPs, but they're ones that have been highly curated to be very highly clinically significant and associated with these common things. Because what I want to know when I'm working with the patient is if they have a family history or they have a high blood sugar, a family history of diabetes. Tell me, the five biggest contributing factors. Do they not make incretin? Well. Well, then I'm going to use the incretin mimetics, the GLP ones, whether it's the oral ones or the different injectable ones, I'm going to give them whey protein because that helps you make more incretin. Or do they have a channel that doesn't let insulin in? Or do they have a different regulator that affects their mitochondria, that affects mitochondrial biogenesis, affects insulin. So in, on and on and on, I want something that's actionable. So even though we've gotten to become a society where more is better, I actually think taking an intelligent approach to the genomics and saying, let's take the most important things, address them first, the most clinically significant, let's figure out how to address them. And that's been a lot of my area of research is going, how can we address them and then see what the results are? And we're having again, good results. So it's a different approach. I bet we'll have to do your genomics and you'll see the difference.

Oh, I'll come in. I mean, you're here in Austin, so we should have done that beforehand so we could talk about my report. But maybe we'll do another one because this is getting this. I would put this in the realm of biohacking. It's just exceptionally focused and detailed and I'm gonna look at like the NIH genes for disease. While avoiding diseases is cool, but how many superpower genes has NIH labeled?

No, that's not their goal. No, that's not their goal. So you'll find out, you know, if you're a carrier for Duchenne's muscular dystrophy or cystic fibrosis. And you'll find out a lot of rare genes, but that's not their goal to help the average person. And so if you're already 10 or 20 or 40 or, you know, whatever age you are, if you had a pathogenic gene variant causing a rare disease that was like dominant where it was causing it, you probably would have figured that out. You know, if your child is born and they're seizing and there's all kinds of funny things about them, that person needs whole genomic sequencing and a geneticist if you are, you know, I've done okay in life, but my brain's not as sharp as I want it to be. And my blood sugar is still a little bit high, even though I try to exercise and eat well. And there's a family history of heart disease. And I get depressed every now and then or anxious. That's genomics. Because genomics is the science of small changes in your DNA that by themselves are not disease causing. But together, along with diet, lifestyle and the environment can be and each other can be disease contributing and can be addressed.

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I've done gene therapy to increase my F statin levels and reduce at least on for the average person. Reduce my age by about nine years on like that. I want to change my genome to be more highly functional. How soon can I do it?

Well, I think there's two levels to that question. So unless you have access to crispr, you can't actually change your genome.

Everyone has access. I mean Jay Zayner has been on the show. I think I've known Jay for a long time. I'm one of the first people to do CRISPR editing at home. Very controversial. I mean any of us have crispr.

But what you can do. So I actually went to college with Jennifer Doudna so I'm not going to do home crispr. I'll let.

I'm not recommending that for anyone either. That sounds kind of dangerous. And I also want the jellyfish glowing gene because why not? No, I'm kidding. But for real.

But what we can do, and that's really the some of this work is really understanding that yes, you can't necessarily change your DNA, but if you understand your DNA, you can change transcription and expression. So really what we're doing is taking the knowledge of our DNA to change how much of it goes into proteins. And when part of how this work started, we were working on, we were working already on cognition and cardiac and kind of adult neuroscience and lots of other things. And I was at a conference that BLMI that Jeff Bland had hosted. That was Jeff, he's been on the show. Yeah, it was for thought leaders on genetics and genomics. And a colleague of mine from Australia who had her first degree in molecular biology and then got into genetics and Nutrition as her second PhD was because her child was born with autism. And she was like. And the child. Well, her child wasn't born with autism. Her child developed autism around age 2. And she's like, well if what we've been doing in diet, environment, exposure to inflammation, et cetera could trigger this, then we can figure out how to untrigger it.

I reverse my autism and it's a hell of a lot of work. But it's doable.

Absolutely. We have hundreds and well, thousands at this point of children that their score, their Atex score has gone from the autistic range back into the normal. Because why would a disease go from 1 out of every thousand or even 10,000 children to 1 out of every 35 in one lifetime? Well, it's because of the interactions. So I don't think you can actually change. You know, if you, if you're swabbing somebody, their DNA sequence will be the same, but you can certainly change their phenotype, how they feel. They don't have to be anxious anymore, they don't have to be depressed anymore or have brain fog.

Why do you think we can't change our genetics?

Will the actual DNA? The code?

Why not?

Well, that's kind of why usually if you're changing, how would you change the DNA in every cell in your body? That's I'm talking about changing the code, not just the expression.

Changing the code, not the expression. Well, every cell in my body gets refreshed about every seven years. Right. Maybe some stuff in the bones a little bit longer than that. And some of the cells turn over every 48 hours. So what's stopping us?

I think it's just a different. I think that we're talking about similar things, but a little different. I do think we can change how our DNA affects us, but I think that if I were to code you.

That's a low hanging fruit. Let's put on our futurist hats. Science fiction here.

Science fiction. I think you would have to figure out how to get into every cell in the body. Or maybe you would just change it with some kind. I mean that's how viruses work actually is they do change our DNA. So I guess you're right. There are things that can happen that change your DNA. I'm not sure that all of them are good.

No, I'm not sure. I'm not sure they're all good either by a long shot. We know a lot of our non coding DNA came from viruses and they're like. Liz Parrish has been on the show and I know a project she's working on around using viral vectors to introduce beneficial changes to our DNA by the way, with full informed consent and not doing it to people via mosquitoes and ticks and all the weird shit that dark people are thinking about. I'm actually thinking it's possible. And I've already made temporary changes to my genetics using a mini circle technology where I've instructed the cells in my body use this new code to make this longevity protein. But that's only good for a couple years, right? And then those cells die and they don't pass it on. And I'm thinking, all right, I know that I have dysfunctional pathways here and maybe we get a signal in. So only some of my cells are better off than they were before as they get refreshed. Is this, is this even in the realm of possibility?

I'm not going to put anything out of the realm of possibility. I think that it hasn't been something that I've worked on. So my response for example, to something again, so like the number one longevity proteins, Clotho, Foxo 3, Apoe 2 is actually a benefit for longevity. So Apoe 4 is kind of a negative is to say, okay, if we know. So you take the person who feels like they're aging too fast and you do their genomics and you find out that they have. They're in the 2% of the population that's really low. Clotho. Well, we can do things to increase their expression of it, even down to exercise. Aerobic exercise is great for Clotho, but anaerobic is not. So weightlifting is not good for those people. If they're going to do it, they need to sandwich it between aerobic. That's where resveratrol works to help because sirtuins Clotho and Clotho interact. I mean even the people who are kind of hacking longevity and doing rapamycin. If you give a Clotho knockout mouse rapamycin, it won't work. No kidding. So you want to understand some of the foundations for each person. And I think that your interest in changing DNA is very interesting. I've been approaching it by going, well, what do we know? I mean there's you even, you know, we know that Clotho makes it so people it regulates all the other antioxidant pathways. So talking to someone about increasing spirulina in their diet if they are very low Clotho so that they can have more antioxidants, decreasing oxidative stress, not smoking is pretty obvious, et cetera.

It's fascinating. I looked at Clotho as one of the most important proteins when I wrote my longevity book, which is superhuman. And you couldn't buy anything to do it. We didn't know as much when I wrote that, except there was one probiotic that made a lot of it. So I legally imported that from Japan and like, okay, maybe that's the way. But now we know a lot more and soon we'll be able to increase Clotho probably with some of these gene therapies. Right, okay. In the meantime though, like you're saying, just change your lifestyle. So if, but if you don't know you're weak, you wouldn't know. And this is what your company does.

Right? Right. Because again, you and I, we could probably say supplement jeopardy and list a thousand different supplements and how they work. But what most people want to know there some of biohackers, they might be willing to do 20 different things or people who really want to optimize longevity or brain health. But most people want to know if I'm going to do five things or 10 things. What are the top 10 of diet, lifestyle supplements, nutrients.

You mean they're not the same for all of us? Yeah, I, I would argue that probably the top two are the same for, for the vast majority of people it would be broad spectrum mineral supplementation. Just so your genes have the zinc and all the other things they need to, to do their thing and the fat soluble vitamins. But even that some people have a vitamin D blockade, they need more or whatever.

Right, right, right. There could be very different levels needed. So there's about 9% of the population that don't make this carrier for vitamin D, this GC protein. And, and they need about 50,000 IUs of vitamin D a week to keep their levels in that 40 to 60. Whereas somebody else might only need 14,000 a week to keep it at the same levels. And you can test vitamin D levels, but when you understand why someone needs more, it just helps you come up with a kind of a Lifelong plan so that you're not going, why am I needing so much? Or some people. Again, their peripheral thyroid levels can look great, but it's a different gene that converts T4 to T3 in the brain than it is in the periphery. So if you know that about yourself, then, and you're hypothyroid or even if you're just kind of subclinical, you're going to want a supplement or a prescription that has T3 in it to keep your brain optimal. But for somebody else, they don't need that.

It's so fascinating. We just didn't understand this stuff for so long. And you see people walking around and their doctor says, oh, you know, your vitamin, your vitamin D, you know, take the usrda. And I would have been one of those in my early 20s. And I'm fortunate that I got invited to run a non profits longevity group. And suddenly Dr. Cannell from the Vitamin D Research Institute's there. I got my blood tests. It turns out I have the genetics. I need 15,000 IUs a day to keep my levels at about 90.

Yeah. So you probably don't make it and break it down more quickly and don't have that carrier protein and that can be huge. You had said that when you were younger you had pain. That is a huge factor for pain because vitamin D's job is to turn things off. And so one of the things that turns off is inflammation. It also turns off autoimmunity. It also turns off cells going rogue, which is why it's so important for cancer. So every single. There's so many pathways that are so important to our overall longevity, our overall health and well being.

I believe that we all have a right to any information about what's going on in our biology. And that nowhere in the constitution does it say that anyone has the right to limit my access to that information. And I didn't hire any regulators to do that or even empower them to do that. It feels like a power grasp. If you could provide the reports direct to consumers right now without somebody saying you're not allowed to do that, would you do it?

Yes, but we would also provide training.

Okay.

But it would be, you know, one of the things is even, even our physicians. So Dr. Bredesen, which many of your listeners probably know. Who.

Dan Bredesen, he's been on the show. He's a friend. Yeah.

I love Dr. Bredesen's work in their research. They're using our report, our brain optimization report because it helps them get where they're going for optimizing. But even the doctors who are at the top of their game doing research, we want to train them so that they get the most out of the report. Because most of us, whether it's a person on the street that's a computer programmer or a physician, we didn't get the study of genomics in our education. So we can really help by, by helping kind of get good education as well.

Yesterday I went to ChatGPT, the latest model, and I said, hey, if I upload my genomics report, can you help me out with MTHFR? And it said, Absolutely, I can identify all the SNPs and I can tell you what's going on and what to do about it. Isn't that enough training?

Well, let me tell you, I was working on. We are about to release our Women's Health and fertility report.

So good.

It's really exciting. It's very, very exciting.

Are you working with Anne Shippy on that?

Yeah, well, Ann is writing a book on fertility and we've talked extensively about the genomics so she can include some of that in her book and she uses our genomics. But it is exciting. We can talk about that because it's a whole. There's so many women, 13% of women are needing assisted reproductive technology.

That was my first book was on fertility and Dr. Shippey's been on the show, Close friend doing preconception. I love it that you guys are working together.

Yeah. And oxidative stress and coagulation and so many things, nutrients all relate. But one of the things is we, we were working on using. We were talking about ChatGPT and so I was working on that and I thought, well, what happens if I pop this gene that's supposed to be relating to hormones and hot flashes into. And I used one of the tools that's supposed to be one of the better ones for science, for AI and it came up with completely wrong information. It thought it was a gene related to hypertension, giving me all these things enough that I was like, let me just go double check, you know, making sure I didn't type the number wrong. I didn't. So you do have to be a little careful because it might have a lot of information on common gene variants, but it thought that this gene that related to hormone transformation related to hypertension. And I'm like, we're not quite there yet. So that's, that's my comment. We're not quite there. I'm not ready to turn my health care decisions over to chat GPT yet.

I'm 100% with you. I find it's a better guide than most Americans get in the three minutes they're going to have with a gp. However, it. It's not that good. And if you were to train your own AI, which you're probably already doing, so that you could better help the physicians who you've trained. I think this is the next three years of medicine. It's going to be your doctor working with an AI that's trained on a specific set of things so that the combination of the healer and the data and the analytics and the patient and the condition becomes very different.

Yes. So if we can, and I think that is where medicine's going, where we can filter what data set we want the AI to learn from so that we know that it's so again, one of the things we're proud of@ateLix DNA is we have 20,000 references in our report. And so it's all evidence based, actionable, from what this gene variant does to the interventions. Well, if we can train a computer, of course, to help keep all those references in mind and keep the whole thing. Yes. That'll make it a lot faster so that somebody can be like, okay, well, kind of help me go through this report and find everything that relates to infertility or miscarriage and, you know, help me synthesize it. And I do think that's the future of medicine. Using personalized medicine tools, genomic tools, labs, and using computers to help us come to conclusions a little faster than our brains can work or at least than most of us can.

And then we use the computer to 3D print new DNA that we've snort that goes in and rewires all the problems. Right.

Maybe in our great grandchildren's, we can always hope.

All right, what about mitochondrial DNA? What do you do about that?

So the mitochondria are interesting. And just in case, most of your listeners probably know that mitochondria are that extra, I call it the backup power source. So you wouldn't plug an important computer into a shoddy electricity source. Food is a really shoddy energy source for a human because evolutionarily, you might go a long time without it.

Yeah.

So mitochondria can take our oxygen and, you know, different nutrients and things and make energy. So mitochondria have their own DNA. They don't have very many of many genes in a mitochondria, but there's also genes in the human genome that affect the mitochondria's DNA. And we right now sequencing the actual mitochondria's DNA is a little harder. So we do a lot of. We have a few of the mitochondrial genes. We don't have all of them, but we do have import. Some of the important ones like Cox1 affects cognition and that's mitochondrial. But we also have things like mitochondrial membrane gene variants that are actually in the human genome. One of the mitochondrial membrane gene variants is kind of the neighbor to APOE 4 on chromosome 21. And so we have some of that. But I do think that mitochondrial medicine is a huge topic not taught in medical school. I had to learn it. I learned it when I started to work with the autism world because it's really important there. But it's important for Parkinson's, it's important for people who have mold related illness.

Anything chronic ultimately seems like mitochondria are at least involved, if not causal.

Absolutely. And I think that it's because there are so many things that damage your mitochondria. So I always tell my patients that the big A's damage your mitochondria. Antibiotics, which so many of us get aging and anesthesia. And then in addition to it, we know that mold doesn't start with A, but it also is a big mitochondrial insult, causes insults and then there's many other things. So I do think that we need to pay attention to mitochondria, especially people with anything brain or energy related.

I would totally agree. That's been a big focus for me. And one of the areas that I believe that you'll end up doing is looking at the mismatch of mitochondrial DNA and nuclear DNA and for listeners and nuclear DNA is your DNA from your entire cell and then the mitochondrial DNA, I think of it like the wiring of the cell. So if you have the building plans in your DNA for a warehouse, but then you get the wiring plan for a restaurant, like they don't match very well. Is there anything where we're going to be able to do about that?

Well, again, I think that what I'm trying to do with my research is and some of it's not using genomics, some of it's using. There's other mitochondrial tests but help people understand where is the fault. So if it is. So if it's the PPAR pathways, which people think of as diabetes pathways that relate to mitochondrial biogenesis that might be pushed by alpha lipoic acid, but if it's the mitochondrial membrane proteins that might be benefited by giving things that the membranes need to repair like phosphatidylcholine and ethanolamine, different kinds of things for different causes. And so I like to say, what can I do to get the best understanding possible? Methylene blue can help with Cox One, CoQ10 can help bypass some of the electron chain. And I think that we used to kind of take a disease state. This was how medicine was. Take this topic of depression or cognitive decline or anything. And psych is very significantly does this. Okay, we'll give the. The diagnosis and then this is our first line. This is our second line. This is our third line. And what I'm trying to do, whether it's mitochondria or whether it's again, a disease state like depression is go, well, I don't care about all the components that we might address. I want to know for this person how important are these specific components? You were talking about mthfr, and that is important for depression because without it, it's not just about turning genes off. It's also about making serotonin, making norepinephrine. But a lot of people don't realize that there is a sister to MTHFR called BH4 tetrahydrobiopterin. And for people, you know, for the 4% of the population who don't have. Don't make enough tetrahydrobiopterin because of their genomics, you can't. We've had people where they're depression, anxiety, adhd, PMS goes away after years or decades because now they know how to address it.

Supplement.

Yeah.

What's it called?

It's called pterodine P, T, E, R, d, I, N. Pteridine 4, I think. Wow. Or sapropterin. I know that New Beginnings is one company that has it. There's a. Sometimes the compounding pharmacies also can make it, but then you need a prescription. But that's cool. Yeah.

The. The tetrahydro family. Guys, we're getting a little nerdy here. It seems like those quite often aren't supplements. I've been particularly interested in tetrahydrofolate. And when I wrote my. That first fertility book, I'm like, well, if you don't want a kid with autism. Because I was concerned I had it, I didn't want to pass it on to my kids. Said, you might want to supplement with folinic acid. And it's different than methylfolate and it's different than folic acid, which I don't think should be in our food supply and it shouldn't.

We can talk about that. It's. It' actually a huge detriment. But we'll, we'll go on to the felinic acid first.

Right. And, and this is the only way you can get it. Unless you're eating a lot of liver or maybe a lot of romaine lettuce. A lot of romaine lettuce. So, like, what do you do? And the funny thing is, when people have a poor reaction to creatine, like they can't sleep, it's usually because you didn't have enough of this and it's an unknown supplement. But if you're pregnant or you have a brain that just, just needs it, getting that form of folate's important. How are you going to know? Probably knowing your genetics would be helpful.

Right? So, yes, so there, so in our genomics there is a gene f o l r1 a folate. And again, you. The thing is, and I don't have all the numbers memorized, I can say a gene, but they're particular variants. So, you know, you can't just go, well, do I have this gene? Everyone has every gene.

I'm sorry, you talk about cognitive function, longevity, and you haven't memorized all the numbers in the entire human genome. My gosh.

RSIDS.

Yeah.

But there are about 11% of the population that have a gene variant in their folate receptor. And to go again, I'm going to take the nerdiness and bring it, dial it back. You can't take folic acid, which is the artificial folate that they're putting in breakfast cereals and flour, that actually can't cross the blood brain barrier. In fact, it can gum up the blood brain barrier and make it so your methylfolate and folinic acid don't cross. Well, well, most people can use methylfolate and that's their best brain source for making their serotonin and norepinephrine and all of their neurotransmitters. But 11% of the population have it. A variant that makes them not transport methylfolate. Well, it's a smaller percentage, only about 2% that have two copies of the FOLR1 variant. They need folinic acid because that's the, that uses a different carrier. So there's a second carrier called the reduced folate carrier, and the folinic acid bypasses the receptor, that folr1 receptor and uses the other one. So these are the kinds of things, why genomics is so exciting. So having an FOLR1 receptor variant, even one copy of it, more than doubles the risk of Autism because getting enough folic acid, whether it's methylfolate or folinic, because they can switch back a little bit, super important to the brain. And in the autism world, one of the most common things for children who are not speaking or non, non verbal is to give them methyl B12 and folinic acid. And it can do wonders because you can also get an autoimmune brain disease, autoimmune autoantibodies against the folate receptor that creates the same kind of thing where you have then a brain, a cerebral folate deficiency. But yeah, there's so much science and when people ask me what I do, I say my job is to take everything out in the literature that all this different information in the literature that is published and make it accessible so people can use it to improve their health. Because I'm like you, I'm a nerd.

It's super cool. In fact, another guy's been on the show, another Austin guy you probably know, Brandon Crawford just posted something about, look, I'm finding folinic acid is reversing autism in a lot of the kids. And he makes the fibrous 28i laser. They'll be at the Biohacking Conference in May 28th. Biohackingconference.com Guys, 4000 people filling up the the Fairmont here in town. And I'm going, okay, this is really interesting. And I look at my own history. I have spina bifida, occultist, which about 20% of people have. And it sounds all fancy. And if you remember that movie, you know it's one of the bifidas. Remember that? Was that Ricky Bobby? Anyway, that made me laugh. But spina bifida is when there's a folate deficiency. I didn't say folic acid. A folate deficiency in mom. Which means my mom doesn't have the genes to process folic acid. They're toxic for her. Which means my spinal cord didn't fuse properly around my spinal cord. Wait, no, my vertebra didn't fuse. Whatever. So no symptoms, not a big deal. But it means that I likely have the genetics. And so for me, getting my levels correct has been a bit of hit and miss. I know I have the issue, but what happens when someone takes an excessive amount of methylfolate?

Well, you know, methylfolate has been studied in pretty high doses. So again, I don't know, it depends on if you have take a lot of methylfolate and you don't have enough B12, you may get symptoms because you're Kind of pulling from other pathways. So that's kind of the methylfolate steel type issues. And so some people don't do well when they get large amounts. But then there were studies done using 15 milligrams of methylfolate in people with depression. And not only were there no side effects, it was very effective. So I've never really, you know, again, in the autism world where you, you have to first address B12, you know, if you have someone and you give them either folinic acid or methylfolate and they get, get hyper or they don't do well, I always say take it back and look at some of the other nutrients. But some of the genes that relate to spina bifida, for example, they're homocysteine and methylation related genes. Mtr, mtrr, mthfr, there's lots of M's and T's. And so those people might need more and they also might do better decreasing the folate, the artificial folates in their diet, not using those processed cereals because again, you want to get it into the spinal cord, but they also need, some of the genes also require them to have more choline or more betaine. And so I think it's, there's, some of them have B6 as CO factors. Some people need more riboflavin. Yeah, right.

And knowing that about myself has created huge improvements in longevity, cognition, energy, health. And it's taken a lot of time and a lot of trial and error because we didn't know all the pathways now. And I like, if I could go back in time, if I could choose when to have all the crap wrong with my biology, if I was like 19 years old today, I'd be like, you know what, mom, dad, I need some help. It's going to cost me a few thousand dollars in diagnostics and I'm going to figure out I should do this and this and this and it'd take a year of trial and error and I would be done and I'd be highly resilient. I wouldn't have all the brain fog and anxiety and, and pain and just all the crap, you know, hundreds of thousands of dollars worth of crap that were unnecessary given what we know today. And that's why I think your work is so exciting.

Yeah. You know, here in Austin at our Patient facing practice resilient health, we've swabbed children as young as two or three weeks. I mean, that's not common. That's not our typical patient. But we have patients where they've Helped themselves. We had a woman who had been unable to get pregnant. She had a bad amh, which is a fertility score, failed IVF twice. She had Ms. She hired a surrogate. Her surrogate got pregnant. She actually. The surrogate ended up miscarrying. But meanwhile, we optimized her genomics. She now has two healthy children.

Good for her.

But those are many people. I think most people's children are precious children. But she then was like, I want you to tell me the roadmap for how I can raise these children to have the lowest risk of autoimmune disease and the best health. So we swabbed her kids when they were little and then came up with a plan. And I think that. What a gift. Yeah. It's ultimately, I think that we can improve the health of any person of any age by understanding some of the most important things for them to address. Some people, again, have very different needs than others. I am somebody who needs more B12 than other people. But I also. You said you're low cortisol. I'm a very high cortisol person. You probably wouldn't have guessed, you know, high energy, high adrenaline person. So for me, I wish I had ashwagandha when I was going through high school.

Right.

You know, it made a huge difference to me as an adult because it let me lower my cortisol 30%. But you can't do everything with trial and error. And so people are getting diagnosed with adhd, they're getting diagnosed with anxiety. Instead of labeling children adults, let's look at what's going on and just address it.

There's always a reason for it. It's funny, I actually just take cortisol, like, just the way some people take thyroid. My body literally makes very little cortisol, and knowing that about myself is just amazing. But the genetics behind that are not ones that normally get tested. It's. It's most likely in the RCCX thing. Have you looked at rccx?

So we. We have. So that also can relate to mold. And we do have some early research with that. It's not one that we have odds ratios for yet.

I don't think anybody does.

And I think that that's one of the problems when you're creating. So we're trying to start with the things we do have, like the ability to kind of like a research tool. But in our formal report, we haven't put RCCX yet because we don't have odds ratios yet.

Yeah.

But we do have it on our radar.

And for me it was, oh my gosh, I have this, this one gene that stops, what was it? Dehydroxyprogesterone, from converting to cortisol. My liver doesn't do that. Like, oh, that explains a huge number of things that have happened in my life. And that's just one thing. Not to mention all the other things. Now if you're listening to this, you'd be like, Dave, you sound like you're a train wreck. Pretty much biologically, yes. Which is why if I can extend my life and I can be 5% body fat with a highly functional brain and do all the stuff I've done as a 300 pound autistic, you know, pretty broken human as a young person, it should be easier for you and it should be a lot more affordable for you. And now that we have tools like films, we're talking about today, it's kind of the golden age to have a chronic illness because there are specific things you can do. Because we even 10 years ago we didn't know these pathways, did we?

No, no. And one of the things to take, put it in perspective, the human genome wasn't sequenced till 2000. I think the final was 2003 was we got the human genome sequenced and it was a cost of close to $3 billion. And so even after it was sequenced it took a couple decades because for these genes, like when I was talking about the one that relates to tetrahydrobiopterin, and we're about to publish a paper, cause we have enough cases of people that have benefited from this that two copies is 4%. So how many people would you have to screen? Well, if it's gonna cost thousands and thousands and thousands of dollars to run someone's genomics, doing studies on the less common genes was cost prohibitive. And that's why the literature is exploding now. So we started out, I remember teaching about MTHFR 15 years ago. I was talking about it to people with depression and all kinds of things because it was easy to find people who had it. And it was, you know, it was so common. But now the literature's exploding. And what I want to know is I want to know some of those gene variants and that I have that are only in 2%, 5%, 7%, because sometimes they're the most impactful. And that's what's so exciting about this decade, is that literature is exploding.

It's exploding and I think AI is going to make it take less time than we all think it will in order to Find like that weird thing. And it could be even worse saying, well, I have the COMT gene and I have an MTHFR gene, but the combination of those two with this other thing that no one ever thinks about, like that gives you third eyeball syndrome or whatever, no one's ever going to see that, but I think AI will.

Well, and that's some of what our research has done. And now AI helps our research team now because we still have to vet everything. But we started in 2016 and we were the first tool that I know of that looked at combinations. So let's talk about Apoa 4 combinations, because that's huge.

Oh yeah, I want to go well first, what is APO versus APO two, APO three, APO four.

So, okay, so APOE is the gene name apolipoprotein E. And it is a, it's a lipid carrier, but it also relates to amyloid processing. But the APOE protein also interacts with 1700 promoters. That's a big deal given that we only have about 3,000 genes that have been identified. This interacts with all these other genes, genes that relate to your bdnf, brain derived, you know, what I call the fertilizer for the brain, genes that relate to inflammation, genes that relate to hormones. So people who have apoe too, they're the lucky ones that make more apoe. It's a, it's really a gene that just kind of upregulates your APOE production and they're going to have actually 40% lower risk of getting Alzheimer's and cognitive decline.

Okay.

APOE 3 is what most of us have two copies of. And that's the normal amount of APOE. And then APOE 4 individuals, their APOE is funky and there's less of it. So the APOE protein should look like this because of this one molecule that got that one amino acid that got changed. It gets a cross link so it looks like an A instead. So it doesn't work well, so it doesn't turn on and off all the genes it's supposed to. And it causes again, problems with longevity, with sirtuins, it causes problems with growth factors for the brain with inflammation. However, in overall, if you look at all Apoe 4s together, it gives about 3.2 times the risk of Alzheimer's with one copy, 14 times the risk with two.

What is the normal risk of Alzheimer's?

That's a good question because it gets muddled with so many other kinds of dementia. But ultimately it is the most, a very common Cause of death.

Like, 20%?

Yeah. About 20% of people will have cognitive decline when they get into their late 70s, 80s.

14 times. 20% is more than 100. How does that work?

No, 14 times the risk compared to someone who's an APOE 3. 3.

Oh, okay.

Got it. So everybody, there's a lot of people who, they learn, they have APOE 4, they get all scared. Well, that's what drove us to better map out the combinations, because if you have APOE 4, and 75% of people who have APOE 4 also have the mitochondrial membrane issues, that together gives part of the risk. But then there's a gene, it's called butylcholinesterase. If you don't have that and 30% of people who have APOE4 don't have that BCHE gene variant, then your risk gets cut in half. So it's really only. So it's really 1.7 times the risk instead. Well, that's a huge difference. And then there's ones. There's a TNF alpha. There's things that interact that make you have six times the risk. There's estrogen receptors. There's things that relate to detox. There's all kinds of genes that interact. And one area of our research is to empower APOE4 individuals to say, Hey, I might have APOE4, but it's not only about APOE4. What do I have with it and what do I not have? So they can truly decide what makes sense to help optimize their brain health. And I have APOE four. Four patients in my practice. One who's 81 years old, who's still in the 92nd percentile for cognition.

Oh, wow.

And so it doesn't have to be this, oh, my gosh, I'm gonna not have my brain when I'm 80. You just have to work at it.

She works at it so you know what it is. And then you block all the appropriate pathways.

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When people get a blood test and they say, oh, you have high apolipoprotein levels, that's dangerous, it's a genetic thing, you should go on drugs. What do you think about that?

So I think there's a lot of different apo proteins and I think you're talking a lot about the lipidology with cardiac and some of those as well. And I think that we're getting more knowledge than that. So it's not just what your LDL is, whether or not you have cardiac risk. It's is your LDL oxidized? What are the size of your particles? And so I Think that we need to throw out medicine from 30 years ago.

Oh, yeah, all that.

And bring it into the. The current century.

Yeah. Let me. I'm going to look at my levels really quick here and we'll just talk about that because. Yeah, I don't care about the cholesterol stuff unless it's oxidized or there's evidence.

Small particles. And. And it also depends on what quality your endothelium is in. And so many other things. There are people who get more vascular inflammation. There's people who build up calcium. So again, with heart disease, there's really like 10 things I like to know at least.

What are they?

I like to know if somebody has like LP because it can affect micro clotting. There are gene variants that affect calcification. I think that's really important because if calcium builds up in your arteries, that's. That increases your risk of abdominal aortic aneurysms, but also premature heart disease.

Okay.

I like to know some of the stuff, a couple of inflammatory pathways that combined with each other can make you have up to four or five times the risk of heart disease. I like to know compti actually, because those people who have the super high. The slow compt. That get the high adrenaline, they need to be a little bit careful about the super high adrenaline if they have other cardiac risks because they can have more sudden cardiac death. Those are some of the ones. There's things that relate to haptoglobin type, which is important.

If you have sugar, what big is a haptoglobin? I know a lot. That's a new one on me.

So haptoglobin was first popularized by a cardiologist and another physician named Bale and Doneen. And they showed that if you're this certain haptoglobin type 2, 2, and you have high blood sugar, it gives you a dramatically higher risk of heart disease. And the reason I care about it is one, keeping those people's blood sugar is really important. But vitamin C is super important for people who have the more detrimental haptoglobin type. So there's just so many fun things. And even APOE can affect cardiac risk.

There's a marker in blood that just. They call it apolipoprotein and it's. You want somewhere between like 50, it goes up to like 200.

You're talking about apolipoprotein B. Yeah, yeah.

So talk about that in the context of risk because there are people out there. One person in particular, I'm thinking of who Says you can't extend human life. But I'm a longevity doctor. And it's like if you have that, you have to go on drugs right away. Go on statins. Go on statins. And is that a risk factor or is it causal or is it just there?

It's a marker for small protein, for a small ldl. So I think of our lining of our arteries is called the endothelial lining. And there's a lot of things that affect making it healthy. But between the cells, because they're kind of like pavers on a sidewalk, there's cracks. And if you have lots of small particles, especially if they're oxidized, they can go between the cracks. So if you have a very high apob, that means you've got lots of small particles. So if you imagine a one cup measuring cup and you have little teeny pebbles in it versus marbles, you can fit a lot more pebbles. It's more dangerous. So it's a marker that you might pay more attention to your other cardiac risk factors. And it's a gene variant, if you have the gene variant that makes you have the smaller apobs. And again, there are things you can do. One of the things is to keep your endothelial lining healthy. There's different things that you can do. So the cholesterol, so the macrophages don't take up the cholesterol that have to do with inflammation. And to me it's just one piece of knowledge. I wouldn't have thought of that as someone's main cardiac risk, to be honest.

I wouldn't either. And Paul Saladino and I talked about it when he was on the show and, and there's one person out there who's like no, you have to go on statins right away if you have that. And it, it seems alarmist.

I think that the more tools we give patients, that we give clinicians, that we give cardiologists, the less they'll focus on cholesterol. There's, there's a molecule that most people have never had checked in their blood, in their blood that's soluble ST2 and it's kind of the anti inflammatory marker for the heart. And I'm much more concerned about the person who instead of having their anti inflammatory cardiac pathways attached to the heart muscle, has it floating. That's due to a gene. We look at that. I'm more concerned about that than I am about cholesterol typically because that's been associated with 4.9 times the risk of heart disease and heart Failure, and you're gonna work on it with inflammation, you know, So I think it's about, let's take a personalized approach to human health and longevity.

You said something really important. I take 150 supplements a day. I've disclosed a bunch of stuff on myself. I've had people offer me tens of thousands of dollars to go into my supplement room where I have all the shelves of stuff I take so they can copy me. And I'm like, don't. You'll probably get a headache and disaster pants. Right. This is carefully designed for my biology with dozens of longevity doctors and functional medicine doctors and years of research. And it, it seems absurd to recommend that. So you have to say, well, what are your goals? What are the problems you have? Do you want to live a long time? Do you want your brain to work better? You want both? How do you want to balance it? What is your lifestyle like? And based on that, you come up with almost like a counterbalance. Like it's a, it's a dance. So I see people out there saying, well, here's my 55 ingredients and my longevity thing. And they're not even targeted at one pathway. I love multi formulas that do one thing. But what do you think about this? Are these.

What's so. So when someone comes into me on 100 supplements or 50 supplements, or even 25, I say, let's start with your genomics.

Yes.

And let's get a better understanding of you. Let's get an understanding of what things you've noticed about yourself and your body, what is in your family and your genomics. And let's build a protocol and starting from scratch, not that there aren't going to be things that you're already on that we would, but let's at least start by going, what's the most important that way? And again, somebody who has, I mean, I have some patients that have, because we do, we do quite a bit of brain at our practice who have pretty bad genomics for cognitive decline. And I tell them, if you're an APOE 44 and you're already having some memory problems, we can help you, but we're not helping you with three supplements. You are going to have to do more with diet, lifestyle and supplements. But I think that depending on someone's health, being able to prioritize can be very beneficial because you are a very disciplined person. There are a lot of people who are like, I'm happy to do seven things, I'm happy to do 12 things. I'm happy to do 20 things, there are very few that can do a hundred. So I feel like genomics as well as labs and history is a tool that can help you say, okay, what if I were only going to take a certain number of things and not just supplements. Also, if what foods should I add? I mean there's definite, as I mentioned, like chili pepper is really great for TNF alpha, but for someone who's got all this oxidative stress pathways with catalase, then we might be doing more of the antioxidant foods with spirulina and the algaes. For somebody else with some of the detox pathways, some of them you regulate with pomegranate juice and some you regulate with vitamin C. So I tell people that genomics can be really helpful as somebody who wants to optimize longevity because it lets you take your desire to optimize longevity and make a more focused protocol. And then you can use testing. There's a lot of biomarkers that you can use to look at your overall health, your, you know, whether you use glycanage or telomere length or on and on and on. There's so many markers. I use a lot of CNS vitals, which is a cognition test that also looks at processing speed, visual memory, verbal memory. Do a baseline, then let me optimize your brain or work with a doctor that can use genomics to optimize your brain and see how the numbers do. Let's get data.

I love looking at outcomes there and I just, I worry that you take a 50 plus ingredient blend of whatever.

It'S too little of everything.

It's too little of everything or maybe it's a couple scoops of it. The problem is like oh, you don't handle that supplement at all or this one is not enough for you. So what I find is most of the time people are getting not the results they expected because at least one ingredient wasn't right for them. The personalization is important. You could do it with genetics, which is your approach. You could also do it with metabolomics. What's the difference between genetics and metabolomics? How do you know what to use?

That's a great question. So one of the issues with metabolomics is what it is is the idea that we're looking at some genetic expression. So what in your metabolism. The reason that the area of weakness for metabolomics is brain health. And again, I started out at doing my PhD in neuroscience, so I always am thinking about the brain because the blood brain barrier, I don't think metabolomics helps as much with things that are cognitive because you can have like in. They've shown this in autism studies. You can have a child that has 45 times the normal amount of TNF alpha in their cerebral spinal fluid, but their blood levels might only be minimally high because something got into their brain and is inflaming their brain. So I think that metabolomics has its place and a lot of people say, oh, it's better than genomics. Things aren't better or worse. They have different purposes. But even for something like osteoporosis. And I consider bone health part of longevity. You can't get at everything going on in your bones with your blood. So anything that's from a blood draw is kind of a blood biopsy. And there's limits to what it can help. So it has its place. I don't use it a lot in my practice, to be honest, because I find genomics more useful.

I'm a huge fan of more data is better and let the computer sort it out. And I've had great learnings from metabolomics, especially in combination with my gut bacteria. Bacteria like the vitamin stuff.

Gut bacteria is definitely one where you definitely need not genomics because you're not talking about your DNA, although there are genes that make you more prone to getting more colonized with yeast and getting more. And having a worse immune system and your first kind of gut exposure. So I agree that there are definitely areas that you need other data.

Yeah. So just if you're listening to this and like, I have lots of money and I really want to live a long time and you know, I'm into this, this longevity thing, you probably need to know what's going on in your gut. Right. That's important. You need to have, I believe, a metabolomics report, like a viome sort of thing to, to know, like, what, what's actually going on in there. And then also you need a full genomic analysis so that like, okay, these are things my genes are capable of and these are the things that they're doing. And if you have all of that data now, you're as fully equipped as you possibly could be. And, you know, if there's a weird plant virus in your gut or something that's tweaking a gene, gene that you know you have. And it, it's more than any brain even yours is going to be able to do. But you have all the tools that support your brain.

Right. And I think that using different tools together. So when somebody so, for example, In Intellix's Intellix DNA's mental health report, which we use a lot on our young adults, the genes that relate to ocd, some of them also relate to your ability to fight infections because that. And that makes complete sense because infections can. If you can't accurately fight an infection and you hit. Then get your gut microbiome off, that creates inflammation and that can. Because the blood gut barrier affect the brain. And so you said you need your, you know, you need your. Your genome. I say we need an informed genomic tool.

Yeah, you need an analysis of your genome. Just a bunch of numbers won't do anything.

Right. We need something like, you know, and. Yeah, and one of the things with intelligence DNA that I think helps our patients and doctors get better outcomes is you were talking about, like, the person who gets the supplement. They're like, oh, I need alpha lipoic acid. This has it. And it has 20 milligrams. We actually have information about what doses were used in the different studies. So that if you're looking at a brain report or a blood sugar report, what dose of berberine was used to improve blood sugars? Because again, you can't. You can't just take a little bit of something and think it's going to have the same effect as two grams.

Totally true. It's funny you mentioned OCD and infection. When I was a kid, I had tons of strep throat and sinus infections because I lived in a basin with toxic mold, and that's a symptom of toxic mold. But then when you have a lot of strep, it makes proteins that create antibodies, and antibodies to those proteins also go after parts of the brain, which causes OCD and odd, which I had. And if you guys don't know what ODD is, think of the Rage against the Machine song. F you. I won't do what you told me. It just makes it normal to do that. And, yeah, I was able to turn off the inflammation. I, like, unpacked all that, but, my God, there's a lot of. A lot of. Dave was a bad child in my seventh grade report. And thank God my brain worked well enough to get good enough grades, because otherwise I'd probably be in prison or something.

And. And what you're talking about is pans, which is when you get psychiatric symptoms from neuroinflammation from different infections. And we used to think it was just strep Pandas.

Yeah.

But now we know that it's both things, like mold, yeast, lime, strep all.

Kinds of infections and environmental bacteria from water damaged buildings, Right?

Absolutely. But one of the fun things about that people who get kind of the OCD from infections is they tend to either make too much TNF alpha, which affects the blood brain barrier and the blood gut barrier, or they have problems with a pathway that's called their Manno spinding Lexin pathway, which is the first line of defense against. They might have a normal level if you were to check their blood, but it might be that the gene protein is misformed and doesn't work. And that's your first line of defense against yeast and lots of bacteria and mold. And so the people who get the kind of OCD from mold, they often have problems with their immune system. So this is kind of why I get. You know, I was a physician, a family physician, integrated physician for 30 years, and now I love training physicians across the world and leading the research team because it's so much fun for me to go hear these different cases and go, oh, this makes complete sense. This makes complete sense. Let's publish this. Let's talk about this, because we're making sense of why did this woman have such severe pmdd? Why did this person have such severe depression, even starting as a little kid? Or this person have ADHD that didn't respond to stimulants well, because their ADHD wasn't caused by low norepinephrine. It was caused by more of a connective pathway.

Wow. One of the things that is just as a patient that's coolest about this is that if you're listening to the show, like, something's wrong with me. No, you just have a hardware problem. And it's so validating to see your pathways and to see, oh, it's not that I'm not trying hard enough. And this was my thing. Like, I'm failing out of Wharton Business School. And like, no matter what I do, I can't lose weight and all these things. And I remember when I got Dr. Daniel Amen's brain scan, he's like, you have holes in your brain. Not actual holes, but areas of zero metabolic activity as a result of chemical exposure from mold. I'm like, oh, God, I have a hardware problem. And if there's things that have tormented you in your life and then you get your genomics report, you're like, oh, my God, I just needed this one supplement. And like you said, in four days. Some people are like, I got my life back.

Absolutely. And not everybody do. We get well in four days. Just want to Put that disclaimer. But actually our co founder and CEO, one of the reasons that she was so dedicated to building Intellix DNA was so many people, including she had been told, you know, she's more of an Ehlers Danlos type person. And people get labeled. Oh, you're just complaining about pain, you're just complaining about this. You've got fibromyalgia. And she was like, we have to stop the labeling in medicine when people go to a physician and they get labeled or the person who's depressed will just get over it. Well, if we can instead look at the root cause or blaming a child or a parent because the child has adhd, let's instead look at the root cause and stop blaming people and labeling. And instead say we now are in a time when we can have the technology to understand and address what's going on.

And there's an epidemic of physicians who don't have enough time to deal with patients. So they just make a really quick assessment. I remember very well when I went into a psychiatrist when I went failing out of school. And he looks me, it looks at me. You can tell with this skeptical thing. I'm like, I'm on these supplements, things don't work. I'm failing out of class, it's just not working. And he's like, tech bro wants Adderall, classical Palo Alto thing. And like, I didn't even want Adderall. I wanted Modafinil because I'd done my research and it was an off label use for ADHD back then. And it's one of the most potent pharmaceuticals for cognitive enhancement that isn't addictive like Adderall is. And when I came back and he saw my data, which wasn't even genomics back then, we didn't have the ability to do that. He was like, inside your brain is total chaos. I don't know how you're standing here in front of me. You have the best camouflage I've ever seen. And I was like, I just relaxed. I thank God someone believes me for like the first time. And with a genomics report like this, it's like, oh, you're not crazy. There's nothing wrong with you. It's just you're riding around in a meat suit with, with dysfunctions. You have a flat tire in your car. Well, if you change your oil, it's not going to fix it. But you put air in the tire, you might like it. And like, we're almost there for humans, aren't we?

Yeah, I think we've made great strides. And so I think that what precision medicine looks like now is leaps and bounds beyond what it was 10 years ago. And I think it's going to continue to improve. And it's a really exciting time to be a human because you can, you know, I don't, I don't yet believe that we're going to get to, for most people, to 130, 140. But I think what we can do is make our years on this planet much healthier so that we are having a brain that works. We're having the energy to exercise and enjoy life and feel vital and so, you know, feel calm. And so I think that it's a really exciting time to be a human.

It is. And you said one important thing for most people, and if we can take one person and we can do 10 years better than our current best, we've meaningfully extended human life. And if everyone else is working towards the goal of extending their life as a side effect, they just have a great health span. Like, that's great.

Right.

It kind of makes me sad, though, when people say our goal is health span. I'm like, I want health span for twice as long, thank you very much. And I'll just take whatever I can get.

Right, right.

So it's just a difference of framing of the longevity movement. Are you on the health span until you die at the average age, or are you on the health span for extended time?

Right. And I think that you're absolutely right. I think that if we get the average lifespan extended 5 years, 7 years, 10 years, that's huge. Long as we take care of our world along with it so that we have a healthy world to live.

The side effect of, of believing you're going to live longer than you're supposed to, like, you're not going to throw the plastic in the ocean because you know you'll eat it.

And you're not going to drink things with plastic because they're, you know, hormone disruptors and you understand how they affect your. They're, they're big effects on epigenetics.

If I am successful living to at least 180 and I ate unlimited microplastics, I would be made out of Tupperware by the time I'm 150. I don't want that. Sharon, it's been a great pleasure. Thanks for your just incredibly complex and interesting work, both as a clinician and as a researcher. I'm, I'm really excited to see how genetics went from, you know, almost useless at the very beginning of this to something that's has meaningful predictive power for what you can do today. So thank you.

Thanks for having me. And if there are any of your listeners that want an Intellix DNA report, they can go to our website and you can actually we put in a special thing for you guys where they can click that. What they're looking for is a Human Upgrade consult, a longevity consult, and that way they will find clinicians that feel comfortable working with biohackers on the topic of longevity and doing an initial one hour consult to get them going and then giving you the report and the tools you need to continue to explore. And if you want to do more, you can. But the one thing is it does two Ls and two Xs I n t e l l xx DNA because it's an intelligent approach to DNA. And my co founder and myself are both women, so that's the two X's.

Awesome.

Thanks for having me.

See you next time on the Human Upgrade Podcast.

A Human Upgrade, formerly Bulletproof Radio, was created and is hosted by Dave Asprey. The information contained in this podcast is provided for informational purposes only and is not intended for the for the purposes of diagnosing, treating, curing or preventing any disease. Before using any products referenced on the podcast, consult with your healthcare provider carefully read all labels and heed all directions and cautions that accompany the products. Information found or received through the podcast should not be used in place of a consultation or advice from a healthcare provider. If you suspect you have a medical problem or should you have any healthcare questions, please promptly call or see your healthcare provider. This podcast, including Dave Asprey and the producers, disclaim responsibility for any possible adverse effects from the use of information contained herein. Opinions of guests are their own and this podcast does not endorse or accept responsibility for statements made by guests. This podcast does not make any representations or warranties about guest qualifications or credibility. This podcast may contain paid endorsements and advertisements for products or services. Individuals on this podcast may have a direct or indirect financial interest in products or services referred to herein. This podcast is open, owned by Bulletproof Media.