A Radical & New Approach To Eliminating Disease & Cognitive Decline | Sharon Hausman-Cohen

While we may have predispositions, we're not predestined to most of the things we see.

Diabetes, heart disease, chronic disease, there is no one gene. There are thousands.

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, 20 chromosomes 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 us so different is this incredible variety in our genetic code. So we may have variations in the code we call SNPs or single nucleotide polymorphisms. So basically you're think about your genes as a software. Or maybe hardware, I don't know 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 fitter combination. And it's like A C T G. They stand for their different nucleotides. We're not getting into the names, doesn't matter. But anyway, the point is that there are a lot of variations in 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 can be structural proteins, they can be immune proteins, they can be regulatory proteins, they can basically do everything. Information, 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 or 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 a 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 100 years ago or 150 years ago, I had no diabetes, no obesity, no heart disease. They lived their traditional lifestyle, but they were highly predisposed when given a high starch 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 genes. 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 learned a lot about this as a practicing physician. I've used this with my patients for decades. I, I keep learning more and more as we understand genetics more and more. So, you know, it used to be I was like, I think $3 billion for the first decoding of the human genome. Maybe one guy did it for 100 million. I mean, there's a lot of money. Now you can get it done for under $1,000 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 we didn't even know about, 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 revolutionary medicine where 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. But when you get your genes done, then I say forget about your microbiome. There's probably 100 times as much DNA material in our microbiome as our own DNA. So there's like a whole another level of meta information that is regulating our biology. If we understand our own unique genetic variations, we're going to 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, you know, everything. Medication is really here. And, Sharon, you're at the forefront of this and, you know, there's full transparency, everybody. I have no relationship with business like 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 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 or 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 flush 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, because 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 100 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 InkRitin. And not to get too technical, but InkRitin is what yeah. 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 in which 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 is 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 what you just said, Karen, that chronic disease and inherited genetic diseases are quite different. 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 50s, heart attacks in their 50s. 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 didn'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 well 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. and I've been following my numbers. And actually, I do have an inherited 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 is 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 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 of which are tested by other companies, but they 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, that SNP can put you at particularly risk. So can you explain this whole idea of like polygenic risk and, and what that is and, 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 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 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 micro clots 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 co-factors. 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 right patient and physician know, make sure you optimize these co-factors, make sure you optimize this, make sure you, if you have high TNF alpha, you can use lion's mane, you can use aloe polymanos. So we give specific from the literature what you can do for each gene variant. And I think that's what makes intelligence DNA unique.

I think that's right. I think it's to sort of back up a little bit, you know, the, the ability to kind of personalize is so important. But in, in, 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, yeah. Sickle cell.

Right.

That's almost.

Right.

Right. I think it was approved or just about to be approved.

Yeah. The studies going on and the family already had some people that have had their sickle cell genes edited out, which is. A couple things from Mendel's work.

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 or recessive disorders. This is like Mendel's peas, right? This is not 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 much stress you have or how you manage it. where you live, your social connections, your microbiome, environmental toxins, everything influences the expression of those genes. Like playing the score of your music. That's the song of you in 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 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 Apima Indians 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 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. And so 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 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 with my blood sugar.

Yeah.

So I, I want to dive into the, the, the work you're doing around dementia because this is such a big issue. And I, I've personally seen some fascinating things about this. You're working with Del Bredesen to look at, at the DNA of patients with complex illnesses and dementia. They know there's 7 million people in America who have dementia. There's, they're 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 is that 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 the set of genes that affects your, your methylation process because you need certain types or more B vitamins. You can actually have a high level of a marker called homocysteine 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 downhill fast. And I'm like, listen, I don't know if I can help you. This is like, you know, 15, 16, maybe seven, I don't know, 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, 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 when he had ApoE4/4, 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 effects methylation. He had two copies of this MTHFR polymorphism. He had an impaired glutathione genes, GSTM1, which is a gene that regulates glutathione, the main detoxifier in the body. And he also had a gene, a CYP gene, which is cholesterol ester transfer protein, which affects your cholesterol and lipid metabolism. Now, I, I never saw this collection before in a dementia patient. I was sort of seeing it for the first time. And 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, you know, 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 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 pre-diabetes 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 said, begin to sort of treat. So I didn't treat his dementia. All I did was helping 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?

So, 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 Swede, he talked about the 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 ApoE4-4. So that, you know, and even with an ApoE4, it can triple their risk. So being able to kind of get the 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 triple the risk of vascular dementia. So this gentleman that you had talked about that had high cholesterol and MTHFR, 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, we're the genomics that's being used in his current study, the AvenThia trial, but 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 Intellec's 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 4 individuals. You want to, you know, 4 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 a as close to it as you can, a very 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 choline 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 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 is this?

What infection?

Yeah. And is it, is it lime? 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 ethanoloamide that's in about 8% of the population.

There's, it's in chocolate, right?

No, is that chocolate? Well, it's, it's, it's, so endocannabinoid inflammation. which, and you do get some anandamide, you get some endocannabinoids, but there's, yeah, it works on a couple pathways, but you're right, it does work on the endocannabinoid pathways, which is where chocolate works some. 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 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, it 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 nattokinase or lumbrokinase, 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 with a doctor using Intellux DNA that have early memory loss, Mild cognitive impairment, early dementia, we are having very significant percent of the people get dramatically better or 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, 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 the big plus. It's kind of a miracle, right? You just take a little Q-tip, roll around your cheek, get all this information. It really is amazing. It's amazing. pretty miraculous. We have come so far. I, you know, I think, I think what you're saying is just so critically important is that, is that, you know, these conditions that we label in the medicine as Alzheimer's or diabetes or this or that autoimmune disease, whatever the date disease is, are very heterogeneous, meaning they're very different. There's, 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. we can't when you and what you're saying, just, you know, I don't want, I don't want to sort of skip over because, you know, it's one thing to say, well, if you have diabetes and you don't eat sugar and starch and exercise, your diabetes is going to get better or go away. Okay, I get that. You lose 100 pounds, whatever, it'll get all get better. But you're talking about a condition where we've spent 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 AiraSAP 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, you know, tens of thousands of dollars a year on, which is just, to me, insane. And, and we're looking up the wrong tree or barking up the wrong tree or digging in the wrong hole or whatever we're doing to find the answers. And the answers really lie in, in, 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, like this guy I met, I tested, and it was one case. I don't think everybody I see with dementia has high mercury or has the same gut issues he has or, say, has the same levels of metabolic dysfunction that he had, but there are commonalities. And so we, 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, mostly dismissed by traditional medicine and neurology. But we're starting to kind of collect data 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 slow but 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 or the 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 the 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 gene, right? But that doesn't mean he's going to get it. and so I wish someone would tell, I wish someone would tell them, 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, we need to do a toxin screen, look at your gut, we need to look at your metabolic health, we need to look at your nutrient status, we need to look at all your snips, 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, that's what's so beautiful about this. I agree. I mean, I have an APOE 44 patient who is 81 years old, who's in the 89th percentile for cognition for her age. And I have, I have a couple of APOE 44s that are doing really great, but again, in their 70s and 80s. And I also think we don't want to just focus on the, on people who are seniors.

Yeah. Sorry. Sorry to interrupt. It just reminded me of this patient I had who's like 93 years old. She used to come see Canyon Ranch. She was a dentist. She was still working. She was APOE double four. 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. It's also about what genes. So, two things. One, it's also about what genes you don't have. It's not just the diet and lifestyle. There are some APOE 44s 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 in 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.

Kids, it's like 20 some percent of children or more, depending on the age group that are on medicines or have diagnoses of of ADHD, of anxiety, of neurodivergence. And 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, 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 cofactor 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 a number of times, but you've talked about how our nutrients in our soil have changed and in our food supply. And like, there's one of the genes that's highest risk for 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, Jing, 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 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 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, it's so important because they're setting the stage for their whole life. And I had the privilege of taking care of people from all ages, 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, fluoride problems, inflammatory genes. I was like, wow, this is really interesting. And I, you know, I, I didn't, this is not something I saw in literature 20 years ago, just stuff that I started noticing. And I was like, well, this is some, there's something here. And I think now we're having much more data, much more science around what's going on 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. You know, 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, and how those influence our genes. But also, also there are interesting genes that you see pop up. For example, there's genes that look at dopamine receptors and, and appetite regulation that, that make it clear, like, why does this person, like, binge on this stuff? Or why does this person can't control their behavior? Why, why are they so addictive? You know what? 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 they have different genes and it's just fascinating to see this. And it actually maps out when I take their story as a doctor, I take their medical history and then I see their gene, I'm like, oh, this makes sense. It's so interesting. I had somebody actually yesterday that was just like that. I was like, wow, this so makes sense.

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, because 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 different behaviors. And I was like, do you by any chance think you might have a food addiction? And we found that she was at night watching a movie and eating a whole bag of whatever snack it was. And when we gave her a snack and made her aware of kind of the food addiction, she was able to lose weight again. So it's fun.

Yeah, it's amazing.

Do you want to talk a little bit about some of the things we learned from your genetic-- Me? Just nothing.

Yeah, yeah, yeah. Yeah, I was going to get there. I was going to get there. So, you know, this is all set up. And I think now hopefully you understand a little bit about 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, you know, it was only just nutrition helping wellness, 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 lead levels just from being in China. I was like, I never seen anything like it. You don't see high blood levels in adults unless they're eating pain chips or, you know, I don't know what they're doing. So she had extremely high levels. And, and I, and I've, I actually learned about my own genetics back then. I learned some of my own variations, but we did a deeper panel, and you helped me kind of understand some of the things that put me at risk and why I ended up with chronic fatigue and wind up with mitochondrial dysfunction and, and why I, I struggled so much and how, I mean, the, the silver lining 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 not 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. Of course, I think mercury is a part of it. 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. 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 SNP, it must make it so the gene doesn't work.

Yeah, no.

But having overactive genes is a problem as well. And it's called CYP1B1, and it's a particular variant. We can't just look for for a gene name, you have to know where, what location. And for CYP1B1, you can make it less active with resveratrol, with terastil beans. Terastil beans from red grapes, terastil beans 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 vacations for you.

Yeah, I think I'm good with that.

Yeah.

And then you also- so you're saying this 1B1 basically sort of metabolizes these toxins, but then it kind of creates oxidative pathways, radicals from them, and it makes me more sick. Is that what you're saying?

Right. And so it makes them so that you, 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 get 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 in my family.

Exactly.

So again, for you, resveratrol would be one of the things that I would say should be in your daily kind of pathway.

So 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's not so great for metabolizing. You're also not good at your anti-inflammatory pathways. We have genes that make you have more inflammation, and we have gene products that make you have less. 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%. I would also tell you you're going to get more of it.

IL-10 is one of the cytokines that's actually helps reduce inflammation.

Right.

So it's not like a break on the inflammation. All cytokines aren't inflammatory. We learned that through 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 things, not, you know, for everything from widespread, 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, individuals with this SNP are prone to 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 lactobacillus strains increase IL-10. Sesame oil, garlic, cinnamon, they all increase IL-10. Yeah. 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. Animals do that.

They, when they, when they actually graze these wild animals, they find that this is the main food crops, but they find all these medicinal plants that they use to regulate their biology sort of intuitively. So 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. And 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 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 in ApoE2, which is great. That gives you more longevity and it gives you better memory.

I call that the jackpot gene.

Yeah, that's a great team. I get mad at my friends that are APOE2s because they remember things. Remember 10 years ago when you said such and such? It actually can increase the risk of PTSD though because they have such good memories. But so for you, 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-1 alpha and Interleukin-1 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 just. yeah.

So kind of a mess, right?

You know, let's say you've got some really great genes. You just have. And again, it's you really. And 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 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, 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 pre-existing inflammation, so I've got to be clear about avoiding things that are triggering inflammation. And there's certain compounds and phytochemicals that will help me regulate that and also have On the positive side, like APOE2, what we call the jackpot genes, 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. So I'm already taking a lot of things 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. So, 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 in.

I was like, I think in my late, like early fifties or I was like, I checked my bone density and body comes. 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 IntelleX 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 IntelleX 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 aldehyde dehydrogenase doesn't really matter exactly, but this gene regulates your bone building when you're younger. People who have this, they don't have enough of these cells called osteoblasts growing up, so they never get as much bone. 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 actually stimulate. Yeah, it's amazing that you figured that. So again, and even NAD and NMM. 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. Yeah, If you ever were to 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 teriparatide with Forteo or Tymlos 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 gonna 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 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 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 gonna 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, and actually, I talked to Anne Wojcicki, who co-founded it, and I, 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, half siblings, you know, which is kind of interesting. I have a friend who has, like, seven siblings. She didn't know she had that. They're 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 snip testing. Initially, it was just a few steps we checked, and now there's 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 we did. Well, if I take, you know, 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. my detox path is way better. And that's all really fairly 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 this or should I take, you know, 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 National Library Medicine database that is sort of almost impenetrable to most people and, and, 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 more 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, 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 I'll think 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 Intellux 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 consult 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 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 IntelleX 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 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 IntelleX DNA in their state. It's a simple buccal swab which 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 kind 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 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 hot spots? So we we help you, we have a, 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 found out 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 genes interact, There's APOE4s that have only 1.7 times the risk, and there's APOE forms 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 even growth factors and inflammation and homocysteine. So there's about 20 different kind of panels in each report so that 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 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 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 another layer of depth. And I think, you know, we've talked about in 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, you know, sounds scary to some people, but medicine, I think is one of the use cases where this is, you know, going to be best applied to help create, you know, 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, you know, potholes. Like maybe there's a few little, you know, 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's 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 want to 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.

If you love that last video, you're gonna love the next one. Check it out here. Just as everyone should get a colonoscopy when they turn 50, everyone should get a Cognoscopy when they turn 45 or over. If you're 55, 60, whatever, check out where you stand and see you can do this.