The Dr. Hyman Show - Dr. Sharon Hausman-Cohen: How to Address Dementia, Autism, and Other Chronic Diseases with Genomic Testing

Episode Date: February 21, 2024

View the Show Notes For This Episode Get Free Weekly Health Tips from Dr. Hyman Sign Up for Dr. Hyman’s Weekly Longevity Journal Get Ad-free Episodes & Dr. Hyman+ Audio Exclusives Dr. Sharon Hausman-Cohen is the Chief Medical Officer and co-founder of IntellxxDNA and has been in the field of integrative medicine for over 25 years. She is the co-author of many publications and a textbook chapter on using genomics to improve outcomes in cognitive decline and autism. This episode is brought to you by Rupa Health, Fatty15, BiOptimizers, and ARMRA. Streamline your lab orders with Rupa Health. Access more than 3,000 specialty lab tests and register for a FREE live demo at RupaHealth.com. Fatty15 contains pure, award-winning C15:0 in a bioavailable form. Get an exclusive 10% off a 90-day starter kit subscription. Just visit Fatty15.com and use code DRHYMAN10 to get started. Tackle an overlooked root cause of stress with Magnesium Breakthrough. Visit bioptimizers.com/hyman and use code HYMAN10 to save 10% and receive free gifts with your purchase. Save 15% on your first order of ARMRA Colostrum and unlock the power of 400+ functional nutrients. Just visit TryARMRA.com/Mark or use code MARK. In this episode we discuss (audio version / Apple Subscriber version): What are genes and what do they do? (6:37 / 4:33) Genetic predisposition does not mean predestined (9:22 / 7:18) The difference between genetics vs genomics (13:10 / 11:06) Polygenic risk scoring for chronic disease (18:18 / 16:14) Dementia risk and treatment (33:59 / 29:24) Mental and cognitive health issues in children (46:00 / 41:25) The similarities between Autism and Alzheimer’s patients (49:49 / 45:14) My genomic test results, specifically related to detoxification and osteoporosis (52:21 / 47:45) Genetic vs genomic testing (1:06:29 / 1:01:54) Learn more at IntellxxDNA.com.

Coming up on this week's episode of The Doctor's Pharmacy. Diabetes, heart disease, cognitive decline, depression, anxiety, autism, they're not caused by any one gene variant. There is no diabetes gene. There are actually over a thousand genes that contribute to diabetes and many hundred that contribute to heart disease, but there's probably about 20 or 30 that are the main contributors, and those are the ones that my research is focused on. Hey everyone, it's Dr. Mark. They say knowledge is power, and that's definitely the case for those of us who are functional medicine doctors or practitioners. We need the right data to determine

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I'm Dr. Mark Hyman, and this is a place for conversations that matter. Now we're in an incredibly exciting time in medicine and our ability to look at our unique biology and genetic makeup is available in ways that we have never had before and allows us to personalize interventions and optimize our health, which is exactly what my conversation today with Dr. Sharon Hausman-Cohn is all about. How do we use your genome and your genetic variations and learning about them to optimize your biology,

to prevent disease, and to optimize health. It's very cool stuff. Now, Dr. Sharon Hausman-Cohn is the chief medical officer and co-founder of IntellX DNA. Dr. Hausman-Cohn has been in the field of integrative medicine for over 25 years. She is a co-author of many publications and a textbook chapter relating to the use of genomics to improve outcomes in cognitive decline like dementia and autism. She's proud that IntellX DNA is being used in studies being done by Dr. Bredesen and his team and other groups studying complex illnesses, as well as by well-respected functional medicine-trained physicians across the country.

She and her co-founder developed IntellX DNA as an answer to an unmet need in the medical community, the need for accurate, evidence-based genomics tools geared at helping physicians practice true root cause medicine, whether the patient has cardiometabolic disease, brain concerns, or other medical mysteries. Dr. Hausman-Cohn received both her master's degree and medical degree from Harvard Medical School. In addition to supervising the research for Intellix DNA, she practices at Resilient Health in Austin. Now, there's a common misconception out there that many of the diseases we're experiencing are due to our genetics. I begin our conversation by explaining

what genes actually do and explain why being predisposed to certain health issues is not the same thing as being predestined. Dr. Hausman-Cohn then talks about the difference between genetics and genomics, a field that didn't even exist when I went to medical school. And we explore how advances in genomics

can offer a greater personalized understanding of how to prevent and manage disease. Dementia and cognitive disease is on the rise. Dr. Hausman-Cohn and I share patient cases that illustrate the potential for reversing cognitive decline. She explains why it's not always about what genes you have, but what genes you don't. We also discuss similar health profiles that we've observed in children with autism and adults with Alzheimer's disease. Think about that. The genetic profiles of those with autism and Alzheimer's are often very similar. And we talk about that in the podcast. Dr. Hausman-Cohn sheds light on how helpful the genomic revolution can be in addressing our mental health crisis as well. So we've got a whole mental health crisis. How do we look at genetics and genomics to

understand that better and treat people in a more personalized way? Now, before our conversation, and out of my own curiosity, I did the Intellix DNA genomic testing, and then Dr. Hausman-Cohn talks about what my own test revealed. Dr. Hausman-Cohn talks about what my own test revealed and how I personally can apply its finding to support my long-term health. Personalized information about our own biology is the future of medicine, which is why I'm so excited to share my conversation with Dr. Sharon Hausman-Cohn with you today. Now let's dive in. Well, Sharon, welcome to the Doctors Pharmacy Podcast. It's so great to have you here and to talk about something that most of us have no clue about. It doesn't make much sense, which is genetics, genomics, the omics revolution, our individual variations, what we can do about it. We're going to get all into the deep story of what we need to know in this new era of genomic medicine. So welcome. Thank you. Thank you for having me.

So yeah, before we get started, I want to kind of just set the table because I think most people don't have a clue about DNA. I certainly didn't. And even after medical school, I don't think I really understood it despite having studied genetics in medical school. And what's happened over the last 30 years is just nothing short of a revolution. I mean, I remember that the human genome wasn't even decoded till about 15 years or more after I was in medical school. So it wasn't even when I was in medical school and I'm, you know, I guess I'm old now, not that old. Uh, I, I was, I was completely clueless about this because it, there wasn't even the science about it. So let me just set the table for everybody and help you understand what is DNA? What does it do? Why is it important? Why are we having this conversation with Sharon about, uh, the work she's doing to help us understand

how to personalize and individualize our lifestyle, our diet, our habits, our exercise, how to optimize our genes? How do we think about this? So what are genes? What are genes? Well, you've got chromosomes, which are essentially inherited from your mom and your dad. You get 23 pairs from your mom, 23, I'm sorry, 20 chromosomes from your mom, 23 from your dad. That's 46 chromosomes, 23 pairs of chromosomes. The chromosomes contain genes. You have about 20,000 genes or so. You can correct me if I'm wrong. The number keeps changing, which is not that much different than an earthworm, but clearly we're different than an earthworm. What makes it so different is this incredible variety in our genetic code. So we may have

variations in the code we call SNPs or single nucleotide polymorphism. So basically you're thinking about your genes as a software or maybe hardware, depending on how you think about it. But your genes are pretty fixed according to this code that is made up of four letters. So your computer is a one and zero. It's a two-letter code, a binary code. Your DNA is a quaternary code. It's like four letters

that combine into different genes. And usually a gene is a three-letter combination. And it's like A, C, T, G. They stand for, they're different nucleotides. We're not getting into the names, doesn't matter. But anyway, the point is that there are a lot of variations of these genes in humans. So while there may be 20,000 genes, there may be five to seven million variations in these genes that affect the function of those genes. So what do genes do? Genes make proteins.

They assemble amino acids into strings that form proteins. And those proteins could be structural proteins. They can be immune proteins. They can be regulatory proteins. They can basically do everything. The information superhighway is essentially proteins in your body. They're controlling everything. And that's why your DNA is so important. And what we do is come into life with a certain set of fixed letters or code. But what we don't often realize is that we can influence the expression of that code. Just like, let's say you have a software program on your computer, like Microsoft Word. Well, you probably don't have a clue about most of the stuff it does. You can type, you can do

spell check, you can do word count, you can do all that, font colors. But there's like a million functions that we don't even know, most of us, how to operate. I certainly don't. I've been using Microsoft Word for 20 years. So the influence of our lifestyle, our diet, exercise, stress, environmental toxins, what we call the exposome, regulates our gene expression and turns on or off different genes or it turns them up or down and regulates what they do and affects our health. And so while we may have predispositions, we're not predestined to most of the things we see, you know, oh, I have my family history of diabetes or cancer or heart disease or dementia. You don't necessarily have to get them. You know, the great example I use of this is the Pima Indians who a hundred years ago, or 150 years ago, had no diabetes, no obesity, no heart disease. They'd lived their traditional lifestyle, but they were highly predisposed when given a

high-star sugar diet to get diabetes. So now they're the most obese population outside of Samoa in the world. 80% get diabetes by the time they're 30. Their life expectancy is 46. So do they have the diabetes gene? Well, kind of, but not really. They have the predisposition gene. So we're going to talk about how today, how we can understand what our predispositions are, how we can understand

our unique genetic code and how we can use that to optimize our health at every level. And I've learned a lot about this as a practicing physician. I've used this with my patients for decades. I keep learning more and more as we understand genetics more and more. So, you know, it used to be, you know, I was like, I think $3 billion for the first decoding of the human genome. Maybe one guy did it for a hundred million. I mean, there's a lot of money. Now you can get it done for under a thousand dollars for your entire genome sequencing. And we can also more specifically look at not just your whole genome sequence, because there's a lot of stuff that just we don't even know about. It doesn't make sense, is specific genes that we know are

common in the population that we can influence by how we live and what we do that are relevant for different conditions and that are modifiable. And so that's what we're going to talk about today. And that's what Sharon has sort of spent her life focusing on, which is this entire field of genomics and genetics and how we begin to kind of unpack that in a way that is usable. And by the way, everybody, we're just on the verge of a revolution in medicine where the enormous amounts of data that we're going to be able to collect on us. You know, I mean, think about it.

When you go to the doctor, you don't get 7 million blood tests, right? But when you get your genes done, let's just forget about your microbiome. There's, you know, there's probably 100 times as much DNA material in our microbiome as our own DNA, right? So there's like a whole nother level of meta information that is regulating our biology. If we understand our own unique genetic variations, we're gonna be able to actually map this out with machine learning and AI that's coming and have insights into what's going on about how to personalize our approach.

And this whole area of personalized medicine, personalized nutrition, personalized supplements, personalized microbiome support, personalized everything, medication is really here. And Sharon, you're at the forefront of this. And just full transparency, everybody. I have no relationship with Business for Life with Sharon. I did the test that our company provides.

It's Intellix DNA. I was fascinated by it. It was far more in-depth than most of the genetic tests that I've done before. And we had a chance to go through, we're going to unpack some of my own problems, let's say, or predispositions and explain some of my own health challenges that I've had and kind of go into all that. So I hope I set the stage right, Sharon. You can add in here, jump in if anything I didn't get right, or if you want to amplify anything I said, please do. But I think I just wanted to kind of give people a level set of what's going on here

with our genes. Yeah, I think you gave a lot of great information. I do want to kind of flesh out two things. One, genetics and genomics. When you and I were in medical school, because we're pretty much the same generation, there was no genomics, only genetics. And genetics is the study of inherited diseases. That's why you didn't get genomics, is it wasn't invented yet. But genetics is things like sickle

cell disease, cystic fibrosis, Huntington's. It's a disease that if your mom and dad, each are either carriers, or you get one copy or two copies of the affected gene, depending on the particular disease, you're going to get the disease. But that's not how chronic disease works. So you mentioned diabetes, things like diabetes, heart disease, cognitive decline, depression, anxiety, autism, they're not caused by any one gene variant. There is no diabetes gene. There are actually over a thousand genes that contribute to diabetes and many hundred that contribute to heart disease, but there's probably about 20 or 30 that are the main contributors that increase the risk or decrease the risk more than 20%. And those are the ones that my research is focused on. So you take that group of the Pima Indians and maybe they have a gene like FTO,

which is a pretty well-known gene that is kind of your metabolic switch. It turns on a hundred other genes that relate to your metabolism and exercise and fat have big interactions on that, particularly exercise. But maybe there's another population that has a gene that's called TCF7L2, which codes for incretin and not to get too technical, but incretin is what it is. Yeah, but it's basically a hormone released from your gut that tells your pancreas there's incoming carbohydrates, release insulin. Well, if you can't make insulin, then your blood sugar is high because it can't get from the blood into the cells and you can't handle carbohydrates. And there's dozens and dozens of other gene variants that contribute to diabetes. So the same thing, again, is true for heart disease, cognition. And what the study of genomics is and what our

research has been is figuring out what do those gene variants do and then how we can modulate them. And you talked about expression. Sometimes you can up or down regulate expression with your diet, sometimes with supplements, and sometimes you might not be able to affect the expression of that gene, but you can address downstream pathways. So if you know that somebody's really bad at transporting B12 to their brain, we can flood the system with B12. So we really have had great success at precision medicine and improving outcomes in chronic disease by understanding what are the root causes. I think it's so important when you said, Sharon, that, you know, chronic disease and

inherited genetic diseases are quite different. You know, I have deafness in my family. My grandmother was deaf and she had three other deaf siblings. So that was a recessive gene. So the mother and the father, my great grandmother and great grandfather had each had somewhere in their genetics, a copy of this, and they had nine kids and four of them were deaf. That's an inherited genetic disorder. Thank God I don't have any deaf kids. But things like diabetes or heart disease are different. And for example, my grandfather was a great example of that.

Everybody in his family had heart disease, like all these nine brothers and sisters, and they all had bypasses and angioplasties in their like fifties, heart attacks in their fifties. And he was great. And why? Because he was a laborer and he walked every night after dinner and he was deaf and he couldn't, he wasn't that educated. So he didn't have a desk job. He had to use his body all the time. And so he was alone in his 80s before it really affected him. And then I was like, well, I'm pretty healthy. I'm just going to check my

stuff. And I've been following my numbers. And actually, I do have an inherent lipid disorder. And I do have a higher absorption of cholesterol from my gut after it's secreted by my bile. I have certain genes related to triglycerides that affect my risk for heart disease. I have certain genes that increase my risk of heart disease that I wasn't even aware of that I can see by looking at these. And what's really interesting is it's not just one gene we're looking at. It's patterns of genes, right? It's clusters of genes that put you at risk. And you might have three or four genes that put you at high risk, but you might have three or four others that actually really reduce your risk. So it kind of levels out or you at risk. And you might have three or four genes that put you at high risk, but you might have three or four others that actually really reduce your risk. So it kind

of levels out or you might not. So it's really interesting to see the whole pattern of your genes. And that's why your work is so important because, you know, a lot of people are in this space of genomics and genomic testing. But you really done some really interesting things by creating a map with your company of a wide variety of genes, some which are tested by other companies, but actually have a much deeper look and also a much deeper look at what the things we know about what influence each of these genes. So, you know, these gene variants are called SNPs, right?

They're single nucleotide polymorphisms. And what that means is one of the nucleotides, the ACTG, is different. So think about it like a spelling kind of variation. If you're from Britain or, you know, I went to med school in Canada, like color is spelled C-L-O-U-R. Here it's spelled C-O-L-O-R. Sort of the same, but a little different. And it's not a mutation. It's just a variation, but that SNP can put you at particularly a risk. So can you explain this whole idea of like polygenic risk and what that is and why we need to be thinking about not just one gene or one risk factor, but looking at these collectively? Absolutely. So a polygenic risk is just another

way of saying that chronic disease, there is no one gene. You get the risk from so many things. And there's a problem though with polygenic risk scores. So we'll talk about polygenic risk, but then we'll talk about the problem with the system when people get a polygenic risk score. So if you take the topic of cognition, for example, if you're going to look at a polygenic risk score. So if you take the topic of cognition, for example, if you're going to look at a polygenic risk score for Alzheimer's, it's going to include APOE4. It's going to include some genes that affect amyloid processing and some other specific genes that affect mitochondria and on and on. And a polygenic risk score might actually include over a hundred different gene variants, but it's only gene variants associated with Alzheimer's and it doesn't tell you what to do

about it. So we don't include everything that's in the polygenic risk score. We include the most important and the ones that the gene function is known and modifiable because to tell someone that you have this gene that's called LOC17 blah, blah, blah, and we don't know what it does, but we know it increases the risk of Alzheimer's, that's not useful information. So we take the genes that we know what they do, or that in the literature it's been shown, and we figure out how to modify them. But there's another really important factor. If you look at a polygenic risk score for Alzheimer's, it's not going to include the detox's, it's not going to include

the detox genes. It's not going to include the genes that affect brain ischemia that can contribute to stroke risk, either because they increase the risk of AFib or they make you have atrial fibrillation. It makes little clots go to the brain or that affect the clotting in your brain, which is a big factor after COVID. People who are more prone to microclots are getting brain fog, or it's not going to include all the inflammatory pathways. And you and I both know that inflammation is involved in everything, in heart disease, in diabetes, in cognition, in autism. And so we took a different approach. We do look at a multitude of different gene variants, but we look at the nutrients, we look at detox, we look at inflammation, we look at gut with every single patient. And then

depending on what they and their doctor are working on, we look at the genes related to chronic disease or the genes related to autism or the genes related to brain health. And even with an autism, you also have to look at the genes that are related to things like pandas and pans. And so we've had a really great success with the, especially combined with the functional and integrative knowledge of our, that we have so many doctors now being trained on at not only untangling people who come in with cognitive decline and been told there's Alzheimer's, there's nothing you can do about it, but also people who have mystery type illnesses, the person who's having pain that you can't understand. And then what our research team has done is we have spent the time figuring out what can you do to modify that gene. So if it's a TNF alpha gene, there's a TNF alpha,

which is a bad kind of inflammation that crosses the blood-brain barrier and also affects autoimmune. There's a gene that's in the promoter, which is the on-off switch. Makes you get four to five times more TNF alpha in your brain whenever it's triggered. Well, you can do things to turn off the promoter and turn off TNF alpha, but you can also do things that affect the master inflammatory switch. So you can look at genomics and epigenetics more broadly and look at cofactors. If you have a detox pathway that relies on selenium and it's not working well, well, you don't want to be short on selenium. So we let the patient and physician know, make sure you optimize these cofactors, make sure you optimize this, make sure if you have high TNF-alpha, you can use lion's mane,

you can use allopolymanos. So we give specific from the literature what you can do for each gene variant. And I think that's what makes IntelliX DNA unique. I think that's right. I think it's to sort of back up a little bit, you know, the ability to kind of personalize is so important. But in the thinking about this, I want people to understand that your genes are fixed. You can't really change your genetic code. You might do gene editing in the future. There may be ways we can hack our genes. Yeah, unless you're a sickle cell, but we're getting there. Yeah, yeah. Sickle cell, right. That's almost right. Right. Right. I think it was approved or just about to be approved. Yeah.

They have studies going on and the Fowler had some people that have had their sickle cell genes edited out, which is amazing. A couple of things. Yeah. It's incredible. Imagine editing out the cystic fibrosis gene. I mean, this is really huge advances, but this affects, you know, these are less than 1% of diseases.

These inherited genetic autosomal dominant recessive disorders. This is like Mendel's peas, right? This is not the stuff that we're really digging into now. But what's important to understand is that while your code is fixed, you know, it's like the keys on a piano, maybe 88 keys. But think about what that piano can do. It can play Mozart, it can play jazz, it can play reggae. It can play rock. It can play classical, every kind of potential music just from 88 keys. So think about your life washing over your jeans as the piano player. Everything you do, every bite of food you take, how you exercise, how stressed you have, or how you manage it, where you live, your social connections, your microbiome, environmental toxins, everything,

everything influences the expression of those genes. Like playing the score of your music. That's the song of you and your life. And that is changeable. And that is called the exposome. And essentially, Sharon, I think that's what Intellix DNA is focused on, is how can we modify the exposome to change the regulation expression of these genes to reduce their impact and adverse impact, or to optimize their function in ways that protect us. This is really an important concept. And I think we're going to get into the weeds a little bit, but I want to set the stage here because I think most people don't understand

the power we have to modify and regulate our gene expression and change our trajectory. Even if we have predispositions, even if you're a Pima Indian and you're at risk for type 2 diabetes at a rate far greater than most populations on the planet, you never have risk for type 2 diabetes at a rate far greater than most populations on the planet, you never have to get type 2 diabetes if you follow the right approach to regulating your gene expression, which they did naturally through their evolution and living in the desert in

Arizona. So I think this is such a key point. Right. And I think that if I had access to a Pima Indian's genomics, I would be able to say, okay, well, this is what's going on because it's not all about medicine. It's not all about diet. It's not all about supplements. It's not all about lifestyle. It's all of the above, trying to avoid medicine if we get things early. So there's one gene that I'd mentioned, FTO. Well, they've actually shown that the best thing to upregulate that when you have low expression of that is intense exercise. It does better than any supplement. That's one group of people, but then there are other genes that whey protein can upregulate.

There are other genes that berberine can affect and that cold plunges can affect. And so again, the cool thing about genomics is we can, everybody wants to get their diabetes under control if they're starting to pre-diabetes or get their heart to risk down or get their cognition optimized. But we can say for this particular person, if you're only going to do six things or four things, here's the top for you that would help. So that cold plunge I did this morning, maybe it will help me prevent problems in my blood sugar. Hey everyone, it's Dr. Mark. Supplements are one of those things that I'm always being asked about. Is it worth spending the money on them? Do we need them if we really eat well? And can your body even absorb them? The answer to most of these questions is, it depends. One important one is

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dementia. There's 7 million people in America who have dementia. There's probably going up to 15, 16 million in the not too long future. There's 55 million people worldwide America who have dementia. There's probably going up to 15, 16 million, not too long future. There's 55 million people worldwide. It's the most expensive condition that we have more than cancer or heart disease to deal with in America. And it's a terrifying disease. And I see it increasing. And, you know, I just kind of want to share a story that I think I want to kind of set the stage. Because I think this story, I did not really know about all these

sort of relationships, but I was just sort of hunting for why my patient had dementia. In functional medicine, it's always about the why. And so we did deep dive into so many different aspects of his biology. We also measured a bunch of SNPs. Now, what's really interesting to me is that if you pay close attention, when you look at people's genetic predispositions, and then you follow it up with their life history, medical history, and biomarker testing, basically lab testing, you can see the expression of those genes and you can change the expression of those genes and see the changes in the lab results, which is quite interesting to me. Like the most obvious one is if you have a methylation problem, which is you can't regulate this particular gene well, which are a set of genes that affect your methylation process because you need certain types or more B vitamins. You can actually have a high level of a marker called thym cysteine in your blood. You can take the vitamins. It reduces that. And you normalize the expression or you mitigate the risk from that gene. Now, this patient was 70 years old and he had pretty significant dementia.

So I would say not pre-dementia, but sort of mild to moderate dementia and was sort of going down hell fast. And I'm like, listen, I don't know if I can help you. This is like, you know, 15, 16, maybe 17, 18 years ago. So it was quite a while ago, maybe longer. No, it was probably like 20 years ago, actually, now I think about it. And I was saying, let's check your genes. Let's check all the risk factors. And we found he had a collection of genes that I think were high risk. So one, he had APOE44, which is an Alzheimer's risk gene.

And that's one we can measure now, test pretty easily. And it's important because it dramatically increases your risk. It doesn't mean you're going to get it. It just means you're much higher risk in the average population, like maybe 10 times. He also had methylation genes, MTHFR, which is a gene that affects methylation. He had two copies of this MTHFR, which is a gene that affects methylation. He had two copies of this MTHFR polymorphism. He had impaired glutathione genes, GSTM1, which is a gene that regulates glutathione, the main detoxifier in the body. And he also had a CTP gene, which is cholesterol

ester transfer protein, which affects your cholesterol and lipid metabolism. Now, I never saw this collection before in a dementia patient. I was sort of seeing it for the first time. I was like, well, this makes sense because he's got the risk for genes. He's non-methylating. We know homocysteine is high in dementia patients. We know that toxins can have an impact. He's not good at detoxifying. And we know that metabolic and lipid problems can also contribute

to risk. And when we looked at his biomarkers, yeah, he had extremely high levels of mercury because he couldn't detoxify it, methylate and sulfate. He had really high levels of, of, of problems with, oh, sorry, what was I thinking? Blanked out. Yeah. He had really abnormal lipids. He had severe insulin resistance, dyslipidemia. So he had prediabetes. He had a terrible microbiome on top of that. He had, like I said, really low glutathione, high load of heavy metals. And so all these things I began to sort of treat. So I didn't treat his dementia. All I did was help him get rid of the heavy metals. I optimized his gut. I improved his methylation patterns.

I helped regulate his metabolic health with prediabetes. And his cognitive function dramatically improved. He kind of lost the diagnosis of dementia. I mean, you know, you see cancer survivors, but you don't see dementia survivors, right? Well, we're starting to see a lot more of them. We're definitely seeing more. What this taught me was that by understanding someone's genomics and their SNPs and their expression, that we can modify their biology in such a way to reverse the course of some really serious illnesses.

And I want you to now dive into what you're learning with Dale Bredesen and the work you're doing with his dementia patients, what you're seeing, what you're learning through the extensive testing you're doing? So what we're learning is there's a lot of gene-gene interactions and that people initially, when Dale came up with the different hypotheses of dementia, he talked about the sweet, he talked about the toxic, the different combinations. But really when you get it down to the gene level, it's more like 400 different combinations. And so the person that you were talking about, that GSTT1 gene is missing in 20% of the population. It's just completely gone. So that really affects their ability to get rid of

a lot of the mercury and some of the other toxins. Half the population could be missing a GSTM1. And when you have that combined with APOE4, it can make the risk five times higher for dementia when you have it combined with an APOE4. So that, you know, even with an APOE4, it can triple the risk. So being able to kind of get rid of the toxins is important. When you talk about MTHFR, MTHFR doesn't increase the risk of dementia that much, just about 14%. But when you combine it with problems with certain inflammatory pathways like IL-6, it can more than he probably had a vascular dementia component. And by getting rid of his detox risk, his vascular risks, you get dramatic improvement. With the work with Dr. Bredesen, where the genomics that's being used in his current study, the EVAN-THEA trial, but he also in the publication that was in the Journal of Alzheimer's last year, where they're taking patients, they're using a variety of modalities of testing,

but using Intellix DNA genomics to help get a deeper understanding. And what they're finding is, again, if you optimize, there's certain things you can do for APOE4 individuals. You want to, you know, APOE4 individuals don't use sugar well in the absence of estrogen. And so that's really important to get them on a keto diet or at least as close to it as you can, a very low, low glycemic index diet. But when you also understand what else is going on with their detox, with their inflammation, with their different nutrients, you can then kind of prioritize rather than saying, take these 30 different supplements. You can say, oh, okay, you don't make choline well. So we need citicholine for you because choline is really important for insulating the nerves. So they fire well, and you make too much of this particular kind of

inflammation. And it's not that one supplement would work for inflammation for, for cognition, because some people make too much interleukin-1 and interleukin-1 alpha and beta inflammation, and that dramatically affects Alzheimer's risks. Other people make TNF alpha inflammation. Other people make this other type. And it's kind of like if I were to say to you as a physician, hey, I want you to go treat my patient with an infection in room three. And you would say, well, what kind of infection?

What infection? Yeah. And is it Lyme? Is it a virus? Is it bacteria? And if it's a bacteria, which kind? Well, we're getting that kind of granularity with inflammation because there's this inflammation that responds to palmitoyl ethanolamide.

That's in about 8% of the population. There's chocolate, right? No, is that chocolate? Well, it's endocannabinoids. So endocannabinoid inflammation, which, and you do get some anandamide, you get some endocannabinoids, but there's, yeah, it works on a couple of pathways, but you're right. It does work on the endocannabinoid pathways, which is where chocolate works. But there's also, you know, inflammation like interleukin-1-alpha and beta, that's more sulforaphane and quercetin and curcumin. And again, like I saidukin-1-alpha and beta, that's more sulforaphane and quercetin

and curcumin. And again, like I said, TNF-alpha is different things and I don't want to make it alphabet soup, but the idea is we can take it to a much more granular level. And there were people that were coming into the study. They had read Dr. Bredesen's book. They had done, you know, started on the protocol of 20, 30 things. And then when their genomics were back, it was clear that their risk for dementia was more about hypercoagulability. So then you're going to use, which is a fancy word for your blood getting thick and making clots too easily. So they were switched to things like pycnogenol, which comes from pine bark and has been used

in studies to help prevent DVTs, things like natto kinase or lumbro kinase, and their cognition got dramatically better because you were addressing the root cause. So the exciting thing about dementia is if you look at dementia publications, they've shown that even a very experienced neurologist is going to mislabel people as Alzheimer's more than 30% of the time. And the reason for that is because Alzheimer's is more of a after you die diagnosis based on what the brain looks like. And you can have more than one thing going on. So by knowing what's

going on with inflammation, detox, nutrients, cardiovascular risk, clotting, you can really help a lot. We never would promise that we're going to get everyone with cognitive decline well, but when people come to us, to a doctor using Intellix DNA that have early memory loss, mild cognitive impairment, early dementia, we are having very significant percent of the people get dramatically better or mild, anywhere from mildly better to dramatically better. There, of course, are some people that don't get better. It depends on what's going on.

But the fact that we're making progress is really exciting. And brain disease in general, it's because you talked about being able to measure the blood and see what's going on. And that works pretty well for cardiometabolic. But because of the blood-brain barrier, it doesn't really work as well for depression, for anxiety, for autism, for cognitive decline. So genomics can give you a window into what's going on with the brain with just a cheek swab. And that's a big plus. It's kind of a miracle, right?

You just take a little Q-tip, roll it around your cheek, get all this information about your genes. It really is amazing. It's pretty miraculous we have come so far. I think what you're saying is just so critically important is that these conditions that we label in the medicine as Alzheimer's or diabetes or this or that autoimmune disease, whatever the disease is, are very heterogeneous, meaning they're very different. There's no such thing as dementia or Alzheimer's. They're highly variable within any diagnostic group. And we label people in medicine according to their symptoms. That's how you get a diagnosis in medicine, not according to the causes or the

unique genetics. And we're moving away from that. And this is what you call it, network medicine, systems medicine, root cause medicine, functional medicine, I don't care what you call it. This is where we're all going. And I think that the work that you're doing is sort of highlighting how we can't ignore this anymore. And what you're saying, I don't want to sort of skip over know, it's one thing to say, well, if you have diabetes and you don't eat sugar and starch and you exercise, your diabetes is going to get better, go away. Okay, I get that. You lose 100 pounds, whatever. It'll all get better. as a nation, over $2 billion, probably more by now, over 400 plus studies with really zero, I would say zero benefit. There are a few drugs here and there that are approved and they

essentially, they either don't work like Aricept or they might slightly delay the admission to nursing home by a few months. That's considered a wildly successful drug that we're willing to spend tens of thousands of dollars a year on, which is just, to me, insane. And we're looking up the wrong tree or barking up the wrong tree or digging in the wrong hole, whatever we're doing, to find the answers. And the answers really lie in understanding the heterogeneity or the variations in these problems, partly informed by the genomics and the SNP testing and metabolic testing and all the things like this guy I tested in one case. I don't think everybody I see with dementia has high mercury or has the same gut issues he has or has the same levels of metabolic dysfunction that he had. But there

are commonalities. And so we begin to see patterns and we begin to see these connections. And so what you're saying is you're taking people using this methodology and you're helping them not only slow, but even reverse and significantly reverse cognitive decline, which is something that we just don't see in medicine, right? It's like, it just doesn't exist and and yet it's happening and i think it's happening on the margins it's mostly dismissed by traditional medicine and neurology but uh we're starting to kind of collect data and and show the evidence people like richard isaacson from cornell has done you know studies looking at multimodal

interventions that are personalized to each person's cognitive decline and using this to show not only slope and improvement, there are finger trials, large scale lifestyle intervention trials and risk factor management trials where they optimize risk factors and they improve lifestyle and they see not just slowing but actually reversal of cognitive decline. There's no drug that can do this. So we're not going to find the answer by finding the single pathway

or the single drug or the single nutrient of a single intervention that works. It's going to be understanding the complexity and being able to work with that complexity. And that's what I think you're bringing to light, Sharon, is this incredible complexity that we now can see into and use to modify our own behavior, lifestyle, and well-being and prevent things. For example, I was just watching the news. I don't watch news, but I was reading something. And it was about Chris Helmsworth. And he has an APOE double four. And, you know, he's a young guy, an actor, super fit,

but he's got the highest risk Alzheimer's disease, right? But that doesn't mean he's going to get it. And so I wish someone would tell, I wish someone would tell him, Hey, you know, here's, here's what you need to really look at. Here's all the other genes that play a role. Here's all the other factors that we need to look at with your health. Here's when you do a toxin screen, look at your gut. We need to look at your metabolic health and look at your nutrient status. We'll get all your steps. And then we need to modify what you're doing based on that to regulate and optimize your biology so that you don't end up with having a problem. That's what's so beautiful about this.

I agree. I mean, I have an APOE 4-4 patient who is 81 years old, who's in the 89th percentile for cognition for her age. And I have a couple of APOE 4-4s that are doing really great, but again, in their 70s and 80s. And I also think we don't want to just focus on people who are seniors. Yeah. Sorry, sorry. It just reminded me of this patient I had. She was like 93 years old. She used to come see me at Canyon Ranch. She was a dentist. She was still working. She was APOE 4-4. She was sharp as a tack. Now, I'm not sure I want her drilling in my mouth in 93, but, you know, she was going and she was focused on her health her whole life. She exercised. She ate well. She took her vitamins and she was fine. There are some APOE4-4s that are at a lot lower risk than others because of genes that they have that relate, that are beneficial genes.

So just like there's negative genes, there's some like Clue and some that relate to other pathways that help you clear amyloid more that are benefits. Sometimes if you have an APOE4 and you don't have certain other things with it, like certain mitochondrial genes with it or certain genes that relate to detox, that can have an effect. So I think it's both. But we've been talking a lot about cognition and brain science and people who are in, you know, 50s and 60s start to get very worried about memory, 70s, 80s. But I think that the other area that genomics can be really helpful with is we're facing a mental health epidemic in the United States. Yeah.

It's like 20 some percent of children or more, depending on the age group that are on medicines or have diagnoses of ADHD, of anxiety, of neurodivergence. And those when you have any kind of a disease where it's kind of gone like this to this, which is what we've seen, we've had escalation and doubling and tripling and even more increased risk in autism, but also again, in anxiety, depression, ADHD, that's not a gene. That is a multitude of, it's not one gene, it's a multitude of genes interacting with environment, diet, lifestyle. So we've had kids that they're diagnosed with ADHD, but really it's that they need more magnesium. They need more vitamin C because they can't recycle vitamin C. And vitamin

C is the co-factor for making the main brain chemical that you use for focus, norepinephrine, which is for focus and motivation. Or maybe they have a genetic pathway that relates to auditory processing that makes it harder for them to learn with auditory processing. Well, what do we do in our classrooms? We put them and make them listen all day. So for those kids, if they know they have problems with auditory processing, there are things that can help that gene. Oxytocin helps, GABA helps. But you can also educate the child and say, okay, you need to take notes. I've had eight-year-olds instructed to take notes. Basically, they're drawing pictures and writing words, listening to the teacher just so they

can get other pathways involved. And with anxiety, we've had kids that the main missing piece was, for example, they didn't make their brain chemicals well because they didn't make something called tetrahydrobiopterin, which you need for serotonin, you need for everything. So I feel like if we can switch to a precision medicine approach to each child, we can also overcome some of this label the kids and this sickness epidemic and let children be healthy. You have talked, I've heard you speak because a number of times, but you've talked about how our nutrients in our soil have changed and in our food supply. developmental disorders and autism that's in 5% of the population that the difference between you being a cardiologist or a PhD versus having intellectual disability and being floppy and not speaking well is how much zinc you got when you were younger. And we have, yeah, it's crazy. And we actually have a whole paper on that gene and how we figured out how to modulate it, but it's called SHANK3. But the way we figured out that it had to be modulated is we were doing the genomics and we had kids with two copies of this gene or one copy of this gene that had pretty significant autism. It's in the literature with autism and supposedly intellectual disability, but it's because it affects their ability to speak. So it's how do

we measure intellect? And yet the mother or the father was a professional with 20 some years of education. And we're like, wait a second, they have the gene as well. There have to be things we can do about it. So my goal is that we start to not label kids. Don't give them the label of ADHD. Don't give them the label of ADHD. Don't give them the label of anxiety or autism. Let's figure out what's going on and see if we can't improve their foundation. With gut, of course, as well, detox, and all the contributing factors

and kind of help them live a healthy life. And again, I care about adults as well, obviously, but I think we need to- No, it's true. It's true. The kids are so important because they're setting the stage for their whole life and i you know i i had the privilege of taking care of you know people from all ages uh from autism to alzheimer's and what was often striking to me was that they were very similar the profiles the genetic profiles of those with alzheimer's and autism were actually very similar they had a lot of the same methylation problems with theutein problems, inflammatory genes. I was like, wow, this is

really interesting. And I, and I didn't, this is not something I saw in the literature 20 years ago, just stuff that I started noticing. And I was like, well, this is something, there's something here. And I think now we're having much more data, much more science around what's going on. And, and we're going to keep learning more and more and more. And there's stuff that we don't even know we don't know yet. So I think we're going to just keep improving and expanding what we're doing. I think the whole mental health issue is such a big factor because it's the biggest burden economically in society. It's the biggest source of disability, depression, anxiety, and the whole spectrum of mental health disorders, the disease of despair. And partly it's related to our diet and lifestyle environmental toxins

and how those influence our genes. But also, there are interesting genes that you see pop up. For example, there's genes that look at dopamine receptors and appetite regulation that make it clear like, well, why does this person like binge on this stuff? Or why does this person can't control their behavior? Why are they so addictive you know why and i'm like well i i just i could never eat a whole sheet cake but there's some people that can eat a whole sheet cake you know i just just it wouldn't happen to me and i and they have different genes and it's just fascinating to see this when i and it actually maps out when i take their story as a doctor i take their medical history and then i see their gene genome, like, oh, this makes sense. You know, it's so interesting. I had somebody actually yesterday

that was just like that. I was like, wow, this so makes sense. You know, it's, it is, it's fascinating. I had a patient and she was struggling with her weight. She had gained like 40 pounds and her obesity panel, cause we divide things into panels. So there's cardiac disease, diabetes, obesity, her obesity panel wasn't that bad. And so then we opened up more of her mental health report and she had tons of genes relating to addiction and high glutamate and high dopamine. And that will create, you know, different behaviors. And I was like, do you by any chance think you might have a food addiction? And we found that she was like at night watching a movie and eating a whole bag of whatever snack it was and when we gave her knack and made her aware of kind of the food addiction she was able to lose weight again so it's it's fun yeah it's amazing i do you want to talk a

little bit about um some of the things we learned from your genomics? Just nothing to reveal. Yeah, I was going to get there. I was going to get there. So, so, you know, this is all set up and I, I think now hopefully you understand a little bit about, you know, our DNA, the idea of variations in our DNA, why it's important to measure them, how they can be modified, how your risks are not predetermined, but you have a, I mean, you might have a predisposition, but you're not predestined to various problems that even in things like Alzheimer's or autism, they can be modified. This is really exciting stuff.

And I came into this field because I was always just a nutrition help among this, but I ended up getting chronic fatigue syndrome after living in China. And I lived in China and I lived there through the winter for over a year. And I don't know if you've ever been to China, but you could look out your window on a sunny, bright day and literally could not see the building across the street because the air is thick with pollution. And it's petrochemicals, it's mercury, it's lead.

I literally had a patient yesterday who had really high blood levels just from being in China. Uh, I was like, I never seen anything like it. You don't see high blood levels in adults unless they're eating paint chips or, you know, what they're doing. Uh, so, uh, she had extremely high levels and, uh, and I, and I, I actually learned about my own genetics back then. I learned some of my own variations, but we did a deeper panel. You helped me understand some of the things that put me at risk and why I ended up with chronic fatigue and why I ended up with mitochondrial dysfunction and why I struggled so much.

The silver lining in that is it made me figure out functional medicine and heal myself and help a lot of people. It was a painful process. I wish I'd kind of met you almost 30 years ago when all this happened. So can you talk about what you found in my, in my tests and, and what my genes showed and, and kind of the things that were insights that you had that could help me optimize my own genetic expression and reduce my risk of having more problems? I think that two of the interesting topics were the detox and also the osteoporosis. And I think

those would be fun to talk about. So the detox, you obviously made it known that you got the chronic fatigue and felt horrible with China and thought that a lot of it was mercury. And obviously there is a lot of mercury there. And of course, I think mercury is a part of it. But then when we looked at your pathway that related to the glutathione related detox with the mercury related pathways, they really weren't so bad. You've got a few SNPs that affected that. But when we opened up your pathway that related to more air pollution, it was horrible. You had, we're in the 7% of the population

that really converts air pollution into a more toxic chemicals and can't eliminate it. And so how that's going to change if you were my patient, how I would kind of tell you to maintain yourself as you're traveling, because that particular gene is actually an overactive gene, not an underactive. People get an idea that if you have a snip, it must make it so the gene doesn't work. But having overactive genes is a problem as well. And it's called CYP1B1. And that is a particular variant. You can't just look for a gene name. You have to know where, what location. And for CYP1B1, you can make it less active with resveratrol, with terastilbene. So resveratrol is from red grapes, terastilbene is from blueberries, hesperidin, certain flavonoids. It also, though, makes it much harder for you to get rid of alcohol and smoke exposure.

So, you know, India and China might not be like the best places to vacation. Yeah, I think I'm good with that. So you're saying this 1v1 basically sort of metabolizes these toxins, but then it kind of creates oxidative pathways, radicals from them, and that makes me more sick. Is that what you're saying? Right. And so it makes them so that people who have this are known to have increased sensitivity to the aromatic hydrocarbons, which is a fancy word for air pollution and smoke. And it's also more carcinogenic for them. And I think you and I talked a little bit about you have this and you also have a SNP called PON1 that affects the ability to clear pesticides. But because of some of the detox genes that you have, if you do kind of ignore it, it gives you a higher risk for lymphoma.

So it's not just a, oh, I don't want to feel tired. Yeah, I remember. I wasn't going to say that. That would be, you know, I feel comfortable, but I remember we were going through it and I said, okay, this gene pattern that you have in the literature is associated with like, you know, more than three times the risk, more than a 200% increased risk of lymphoma. And you said, well, what type? And I said, B cell. And that's when you said, yeah, that runs. So again, for you, resveratrol would be one of the things that I would say should be in your daily

kind of pathway. Drink a bottle of wine a day. Is that what you're saying? Probably be better off using a long acting resveratrol supplement because it you're also not good at your anti-inflammatory pathway so that we have genes that make you have more inflammation and we have gene products that make you have less. And the main one that makes you have less is called IL-10. Well, 7% of the population don't make enough IL-10 and you're in that 7%. So I would also tell you, you're going to get more. So IL-10 is one of the cytokines that's actually helped reduce inflammation, right?

Correct. It's like a break on the inflammation. All cytokines aren't inflammatory. We learned that from sort of COVID about cytokines, but they're not all bad. They actually modulate your immune system. So this is a good one that helps reduce inflammation. Right. And that checks and balance is really important for everything from widespread pain, so what we call fibromyalgia. That is actually, if you look in our report under the key point, I'll actually read it to you. lower levels of the anti-inflammatory molecule interleukin-10. Decreased IL-10 correlates with reduced ability to turn off inflammation and is associated with numerous conditions such as chronic widespread pain, rheumatoid arthritis, asthma, and inflammatory bowel disease. And so it's kind of like you go, wow. And then if you were to look at the things that help you to

have more IL-10, CBD, quercetin, they have been used in some of those same things, arthritis, pain, asthma, and even certain bacteria, bifidobacteria and certain lactobacilli strains increase IL-10. Sesame oil, garlic, cinnamon, they all increase IL-10. Yeah. All my favorite stuff. Yeah. You know, that's really common that people, I'll tell someone, these are the foods that help.

And they go, you know what? I love those. And I think that we innately as humans, we do. We figure out some of that. Yeah. I think, you know, animals do that. When they actually graze these wild animals, they find not just the main food crops, but they find all these medicinal plants that they use to regulate their biology sort of intuitively. I think I wonder if we do the same thing. And I actually, you know, I did have, you mentioned the fibromyalgia. I did have,

when I was really sick, I had severe fibromyalgia. Like my muscles were aching all the time. I was so sore. And I also developed after C. diff infection, I developed inflammatory bowel disease, which I've cured, but it's like, wow, you know, like it's kind of makes sense when you see what your, what your potholes are. Yeah. You have these genes that you have a few other inflammatory genes that increased your risk for getting that inflammatory bowel disease. But you, when you treated it, instead of using anti-TNF alpha, because it because it wasn't TNF-alpha for you that increased the risk, when you used all those great plant substances, the polyphenols, and decreased the inflammation, fixed your gut bacteria, you were able to fix your risk. And even from a brain standpoint,

so you're an APOE2, which is great. That gives you more longevity and it gives you better cognition, better memory. I memory i actually jackpot gene yeah that's a great gene i get mad at my friends that are apoe2s because they remember things remember 10 years ago when you said such and such um it actually can increase the risk of ptsd though because they have such good memories but um but so for you if you were get when you get older if you were feeling like your brain was having any brain fog i would look at your genomics and i would go you, if you were get it, when you get older, if you were feeling like your brain was having any brain fog, I would look at your genomics and I would go, you know what? You have more issues with interleukin one alpha and interleukin one beta. Like for you, the inflammation was just like,

I call it bright red because you know, that's kind of the big flame for you. So you have, again, I think have figured that out. And that probably, if I were to ask you what things work for you, a lot of the things, curcumin, sulforaphane, cat's claw, resveratrol that work on your genes, you probably have already figured out you feel better on because it, it lacks that inflammation, keeps your brain feeling clear. That's just, yeah. So kind of, I'm a mess, right? No, let's say you've got some really great genes. You just have, and again, it's, you really, in your mercury detox, your glutathione detox pathways, which are important for a lot of things, they were very good. You just had some things where, you know, magnesium, you need more magnesium. You don't absorb it well. You need to keep your inflammation at check.

And then those environmental check. And then those environmental toxins. And then osteoporosis. That's so helpful. That's so helpful. So this is just to slow down for a minute. And what you're saying is so important. So by knowing my genes, I know I'm not good at detoxifying environmental toxins. So I need to make sure I reduce my exposure and upregulate all the pathways that help me clean them out. I know I have a predisposition to inflammation. So I've got to be clear about avoiding things that are triggering inflammation and there are certain compounds and phytochemicals that help me regulate that. And I also have on the positive side, like ApoE2, what we call the jackpot gene,

it's like longevity gene. That's good. So I have a mixture. It's not all good and bad. It's really about how to personalize what I'm doing. And so I'm already taking a lot of things that you mentioned just intuitively. I think I know my body needs that. I know based on my biomarkers that I can measure. So, right, your genes are your genes, but then what you can measure in your blood as a result of those genes is how those genes are expressed, right? So I might have a risk for high IL-1 beta, which is an inflammatory cytokine, but it might not be high in my blood if I do all the right things. Right, right. And some of them you can measure in blood, but again, the benefit of genomics is some things are only expressed in the heart or in the bones or in the kidneys. So when we were starting to open your genomics, I said, well, we can just

skip the top gene because you're a guy and it's probably not of concern to you right now but you have much higher risk than typical of osteoporosis and you said wait stop and you said that you actually do not have a good bone density and so we would have never been i was like i think in my uh late like early 50s or i was like i checked my bone density, body count. I was like, I'll just check it. And I was like, wow, it's kind of on the lowish side. And it doesn't make sense because I've been a runner my whole life, biker.

I mean, I didn't lift weights by yoga. I mean, I really shouldn't have had low levels, right? Right. And that's one of the differences between what my area of research and what Intellix DNA does and a lot of the nutrigenomic products is we also look at the genes that contribute to chronic diseases. And osteoporosis runs in my family. So of course, in the Intellix DNA report, I included a pathway of osteoporosis because I wanted to learn more about that.

And you are in the 1.1% of the population that has the number one gene that contributes to osteoporosis called ALDH7A1 and aldehydrogenase doesn't really matter exactly, but this gene regulates your bone building when you're younger. So people who have this, they don't have enough of these cells called osteoblasts growing up. So they never get as much bone. So if you had known this when you were younger and you can still, as a man, because you keep your testosterone good, you can still have benefits. Things like alpha lipoic acid, things like ashwagandha, things like sulforaphane will actually stimulate. Yeah. It's amazing that you said that. So again, and even NAD and NNM. So I think the thing is, genomics just gives us this map.

And so now you know you're at higher risk. So you're going to keep your testosterone under control. You're going to do things. And if you ever were to kind of be really at high, high risk, you could then know, okay, not that I want to use a medication, but a bone building medication like teraparotide with Forteo or Timlos would really help you stimulate those osteoblasts. So I think that the difference in medicine in the year 2025, 2026, 2030, 2035, is we're going to have the ability to take somebody of any age and give them their instruction manual because that's really what our genome is. It's our book of

ourselves and having a doctor that's trained in integrative and functional medicine right now is really where people are going to get this kind of work because we're being trained with the institute that you helped to create to think about what are the root causes. But I'm hopeful that within the next decade, every cardiologist, every endocrinologist, every family physician will be thinking this way about why does this child have ADHD? Why does this person have cognitive decline or osteoporosis? Or why did they get sick when they went to China and get, you know, chronic fatigue? I mean, listen, I think what you're doing is so remarkable. And I think people are aware of genetic testing. There's now, you know, over the counter genetic testing, like 23andMe, I've had that done and it's kind of fun. It's like,

oh yeah, well, my urine's going to smell funny if I eat asparagus. Great, thanks. Or, you know, it's kind of like not really news to use most of the time. It's sort of more entertainment value. And actually, I talked to Anne Wojcicki, who co-founded it. And when she was doing that, I said, you really have an opportunity here to actually help people understand, you know, how to modify these gene expression patterns and not just tell them what they have or find out that they have, you know, 25 siblings from their, you know, firm donor dad or something. They're half siblings, which is kind of interesting.

I have a friend who has like seven siblings. She didn't know she had their half siblings. That's all cool. But it's really not a useful tool in medicine. And, you know, since I've been doing this, I've been doing genetic testing for over 20 plus years through SNP testing. Initially, there was just a few steps we checked. And now there's a whole suite of SNPs that we have now learned about that are things that we understand their role in different diseases.

We also understand how to modify those SNPs so that we can change the trajectory just like you did. Well, if I take alpha lipoic acid or resveratrol, I'm going to modify this or that pathway so it will work better. It won't be as much inflamed or my bones will be better or my detox pathways will be better. And that's all really, really helpful information for me as an individual who wants to optimize my health. And it's also important for me as a physician to be able to use that information to guide my therapy with my patients. So, you know, there's a lot of over-the-counter tests for, you know, nutrigenetics and nutrigenomics and pharmacogenomics, and they're all interesting. And there are some doctors who are using

genetic testing and SNP testing to look at what we call pharmacogenomics, which is how we respond to different drugs. Should I take a statin? Should I take this blood thinner? Or should I take the aspirin or not? And there's really the increasing use of this in traditional medicine, but it's still limited. And it doesn't include all the things we're talking about today. It doesn't include the wealth of science that's sitting in a kind of a National Library of Medicine database that is sort of almost impenetrable to most people and even most physicians don't have a clue, to be honest with you, about this. But you're making this for the first time accessible, and you're making this really usable by practitioners. Now, this is not a consumer-facing company that you have. It's really for practitioners, right,

to learn how to understand SNP testing, how to learn what the data is behind each SNP, how to learn the data that informs what to do with each SNP, you know, so what's the evidence base for this? Is it good? Is it not? And you can start to customize that. So you're telling me to take, you know, alpha lipoic acid.

There's really no downside, right? And there's a lot of upside, right? If you're saying, well, take this drug, well, maybe I'll take twice or I'll be more careful. But it's really an incredible moment in medicine where the future is going to look very, very different. And I think Intellix DNA is looking at many, many things. So, you know, why don't you take us through, you know, what this panel of tests you have are and what's being measured and sort of just sort of how people can access it and what to do with it. Absolutely.

So as you mentioned, it's not that we don't want to be able to help consumers directly. If we were to be having a consumer product, we couldn't give as much information. We're what's called a clinical decision support tool, which under the FDA, you can only sell to licensed healthcare clinicians. And so by doing that, we're able to give, we're a tool that helps doctors, whether they're naturopaths, DOs, MDs, PAs, we can sell to anyone who's a licensed healthcare clinician, help them kind of take that genomic science that's in the literature and make it applicable. Because as you mentioned, I have a strong, I started out doing a PhD in medicine. I quit after my master's, but I,

so I have my research background, my genetics background, my molecular biology background, and my functional integrative medicine and family practice background. So with my background, I was able to lead a team of researchers to develop this, but it would take an individual physician many hundreds of hours to kind of just hand start to look through someone's genome. So what we did is we went through the literature, figured out for all these really important clinically significant genes. We don't want ones that aren't important because, you know, again, we would be looking, there are over a million SNPs in the human genome, and that's a lot of data to go through. So let's start with the most important things. And then we figured out

based on the literature, how does the little change, that one letter change affect the gene? And then based on the literature, what can we do to help address it if somebody has that with diet and lifestyle? So the way the process works is a patient who wants this, they can, if they already have an integrative or functional medicine doctor, they can ask them if they have been trained on Intellix DNA. If they haven't, we are happy to train doctors for free. My goal is in my lifetime is to improve the field of medicine. You had your way of doing it by establishing IFM. And this is my way of doing it is let's help get more precision to the foundation that you and so many have built. So they can ask their

doctor, not only do we train them when they order their first report at no charge, but we mentor them. So we, they will get great success even on their first report. We have a mentoring program. We have all kinds of things, but then, if they don't have a doctor, they can also go to our website and find out who is trained on Intellix DNA in their state. It's a simple buckle swab, which is means inside of your cheek takes about three weeks to come back. We have three different basic reports. Some people get all of them,

but we have one that's focused on chronic illness, kind of the heart disease, diabetes, thyroid, statin response, osteoporosis, macular degeneration, all those kinds of chronic things. We have one that's focused on the brain and it's not just about, as we said, genes associated with Alzheimer's risk or classic dementia, but also low oxygen to the brain. Hormone receptors can affect the brain. We didn't talk about that coagulation. And then we have one that's more focused on mental health, which is also used as our pediatric backbone. But then we add on autism and some other things. All of them are going to have what I call the foundations, which is things that relate

to gut, things that relate to inflammation, nutrition, detox. Really the brain ones have much more extensive of that, but they all have a certain amount of that. And so then they just order the report and it takes about three weeks to come back. We, again, help the physicians learn, how do you take that data and make it so you can kind of go, what is the most important thing? We kind of call it, how do you find the hotspots? So we help you. It comes up with a little hotspot report. And we do have a patient version, but the physician needs to get access to it first and then release it because

you really we never want to arm and harm. And, you know, the companies, when you have that, somebody is an APOE4, and if that's all they know, that's harmful because if they don't know what they can do, what other that's all they know, that's harmful because if they don't know what they can do, what other genes interact, you know, there's APOE4s that have only 1.7 times the risk, and there's APOE4s that have 12 times the risk of cognitive decline, but all of these genes are modifiable. And then there's people who are APOE3-3, and they're not off the hook. They can have high risk for things that create vascular

dementia and, you know, growth factors and inflammation and homocysteine. So there's about 20 different kinds of panels in each report. So the typical report will look to 400 to 600 SNPs, but it's all organized. So it sounds a little, you know, like drinking from a fire hose, but we, we organized it. You saw when we went through it, it's like, we get this hot spot of here for this person, pay attention to these 15 or 20 genes first. So. Yeah. Yeah. So it's, it's, it's a lot of information. And I think, you know, as someone who's been doing this for 20 plus years, 25 years, it's still, uh, like, I feel like a newborn babe, just kind of figuring it all out. So I, I think while I do have a pretty deep understanding and I've used this clinically

for a long time, this just provides a whole nother layer of depth. And I think, you know, we've, we've talked about, you know, the future what's coming and even, even for you, you know, who's deeply steeped in this, who understands so many of these pathways deeply, who understands all the science behind it. It's still hard to kind of put all that together. And I think using the power of machine learning and artificial intelligence, which sounds scary to some people, but medicine, I think, is one of the use cases where this is going to be best applied to help create a predictive model of the hierarchy of priorities, what you should be doing, what you should be looking at, and what are the most important potholes. Maybe there's a few little tiny divots here in the road, but then there's this giant pothole in front of you. So you want to make sure you pay attention to that one. So

I think we're going to be able to sift through that in a much more robust way. And I think your work is going to just be the foundation for so much of that. Yeah. The machine learning we can't use yet, not because we couldn't, but the FDA doesn't let us use artificial intelligence machine learning. The doctor is going to have to make the final decisions right now. Really? Why does the FDA not let you do that? Because, so we, if people want to join with us in studies, we will get there.

But that would make it so that you become a medical device. And there is a brand new category of the FDA for these kinds of low risk medical devices. But we are in the process of doing studies. But we will need more studies before we can layer that on. And again, if any of your listeners, if your friend that you interviewed that was the head of 23andMe, people wanna collaborate on doing a big study

where we do this, reach out. And eventually I absolutely do think that being able to do those kinds of decision trees and machine learnings, of course, that makes sense. But we're not, again, right now, that's the other reason it takes a physician is, or a trained healthcare licensed clinician, is because you do have to use a lot of your own medical knowledge. We can give you the references, everything is referenced. We can give you information on the supplements. So if you've

never used a particular one, you can learn about dosing and what it was done in the studies. But it still takes the human brain, which gives us job security for a little while. Well, this is exciting. Thanks so much for what you've done as an open of the field and provide help for so many people through their practitioners. And I hope more and more doctors will start to use this in their practice. It's been game-changing for me as I guide my patients on how to best optimize their health or treat complex chronic conditions. And I think this will just become part of medicine. So thanks for what you do. And Sharon, lastly, where can people go to learn more about the test? So they can go to intellixdna.com. It's a little bit of a tricky spelling, but if I tell you where the name came from, you'll remember it. It's from an intelligent approach to DNA. So it's I N T E L L. And then

the two X's are because myself and our co-founder are both women and then DNA. Oh, I wonder what the XX works. I mean like XX. Okay. It should be capital X though. Yeah. You can capitalize it. It'll still work. And there's a lot of, there's some publications and podcasts, but there's also a find a practitioner link so that you can find someone in your area. Oh, Shannon, thanks so much for what you do. And we're just going to keep learning more when we head back on to talk more about things that I learned so much from doing the test myself and appreciate all your support and help. Thank you for having me. And we'll have to circle back in a year or two

because we have more things coming down the pipe. Thanks for listening today. If you love this podcast, please share it with your friends and family. Leave a comment on your own best practices on how you upgrade your health and subscribe wherever you get your podcasts. And follow me on all social media channels

at Dr. Mark Hyman. And we'll see you next time on The Doctor's Pharmacy. Hey everybody, it's Dr. Hyman. you next time on The Doctor's Pharmacy. Hey everybody, it's Dr. Hyman. Thanks for tuning into The Doctor's Pharmacy. I hope you're loving this podcast. It's one of my favorite things to do and introducing you all the experts that I know and I love and that I've learned so much from.

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