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In this episode, you will learn about the role of genomics in complex, chronic conditions.

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About My Guest

My guest for this episode is Dr. Sharon Hausman-Cohen.  Sharon Hausman-Cohen, MD is the co-founder, Chief Science Officer, and Medical Director of IntellxxDNA™.   Dr. Hausman-Choen has been using genomics for over a decade to deliver personalized medicine and help her patients achieve optimal health and wellness.   As a researcher and clinician advocate, she recognized that information inaccuracies and complexity were previously barriers to entry for many.   She saw the need for an easy-to-use, accurate, science-based genomics interpretation tool for clinicians, and she began to develop what is now IntellxxDNA™.   In addition to being a well-regarded doctor and researcher, Dr. Hausman-Cohen is a sought after speaker and educator on genomics, personalized medicine, and integrative medicine.   Dr. Hausman-Cohen received both her master’s and medical degrees from Harvard Medical School.   She is board-certified in Family Medicine, a Fellow of the American Board of Integrative and Holistic Medicine, and possesses additional board certification in Integrative Medicine through the American Board of Physician Specialties.  She has been practicing full-spectrum Family Medicine and Integrative Medicine for more than 20 years.

Key Takeaways

  • What is a gene?  What is a SNP?  What is genetics vs. genomics?
  • Can modern diseases be the results of genetics?
  • Are genes our destiny?
  • Can supplements be used by bypass every potentially probelmatic SNP?
  •  What are the contributors to brain fog?  What can be done to improve mental clarity?
  • What is the role of ApoE in Alzheimer's disease?
  • How similar or different is autism to conditions like Lyme disease or MS or Alzheimer's?
  • What role do genes play in our ability to detoxify environmental toxicants?
  • What SNPs may play a role in biotoxin illness such as CIRS from Lyme disease or mold?
  • Can the Lyme spirochete itself be an epigenetic influencer of gene expression?
  • What role does the HLA-DR gene play in mold illness?
  • Do genes play a role in immune modulation and autoimmunity?
  • What is the connection between genes and MCAS?
  • When is nitric oxide a good things vs. potentially a bad one?
  • Are genes involved in hypermobility syndromes such as Ehlers-Danlos Syndrome?
  • Are some more likely than others to have adverse reactions to anesthesia?

Connect With My Guest


Interview Date

January 20, 2023


Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast.  They are not a full replacement for the discussion.  Timestamps are provided to facilitate finding portions of the conversation.  Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed.  Please Contact Me with any corrections.  


[00:00:01] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now, here's Scott, your Better Health Guy.

The content of this show is for informational purposes only and is not intended to diagnose, treat or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health related decisions with your own personal medical authority.

[00:00:35] SCOTT: Hello, everyone, and welcome to episode number 179 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Sharon Hausman-Cohen. And the topic of the show is Genomics.

Dr. Sharon Hausman-Cohen is the Co-Founder, Chief Science Officer, and Medical Director of IntellxxDNA. Dr. Hausman-Cohen has been using genomics for over a decade to deliver personalized medicine and help her patients achieve optimal health and wellness.

As a researcher and clinician advocate, she recognized that information inaccuracies and complexity were previously barriers to entry for many. She saw the need for an easy-to-use, accurate, science-based genomics interpretation tool for clinicians and she began to develop what is now IntellxxDNA.

In addition to being a well-regarded doctor and researcher Dr. Hausman-Cohen is a sought-after speaker and educator on genomics, personalized medicine, and integrative medicine.

Dr. Hausman-Cohen received both her masters and medical degrees from Harvard Medical School. She is board-certified in family medicine, a fellow of the American Board of Integrative and Holistic Medicine, and possesses additional board certification in integrative medicine through the American Board of Physician Specialties. She has been practicing full spectrum family medicine and integrative medicine for more than 20 years.

And now, my interview with Dr. Sharon Hausman-Cohen.


[00:02:08] SCOTT: A mutual colleague connected Dr. Sharon and I and asked us to do a podcast. And many will know that, historically, I haven't really felt that the solution to complex chronic illnesses was found in the genes. That it's much more epigenetically driven. But when the opportunity arose to interview Dr. Sharon, who is an expert in the genomics realm, I really could not resist the chance to learn from her and to have a conversation around where genetics fits into the broader landscape of healing. And so, thank you so much for being here, Dr. Sharon.

[00:02:42] DR. HAUSMAN-COHEN: Thank you for having me. I'm looking forward to it.

[00:02:44] SCOTT: What was your personal journey that led you to having a focus on genetics and genomics and working with patients with really complex chronic conditions?

[00:02:55] DR. HAUSMAN-COHEN: My journey with genomics started back when I was doing genetic research in 1986, which makes me feel a little bit old. But I was looking at what were then called restriction fragment length polymorphisms, which are basically now SNPs, that were relating to cancer.

I started out as a researcher doing a PhD in medicine, and then later I switched to becoming a family physician, which a lot of people thought was kind of a funny switch. You go from studying one thing in great detail to studying people from birth to death. But it was really because of that that I switched because I didn't want to spend my whole career on one or two topics.

But I was that detective sort of personality. I wanted to untangle science. Figure out what underlying factors were. And I eventually decided I want to do that with humans, with patients and figuring out their symptoms or their diseases.

When genomics became widely available in the last decade, I started out to do personalized research for my patients using their genomics and then focused my research on could that explain what was going on? But then I found that there wasn't a tool out there that was really geared at helping physicians and clinicians make better medical decisions. And so, that kind of led to what became IntellxxDNA and my journey of having a genomics platform that I helped to develop. Because genomics is really the ultimate tool for helping to untangle medical mysteries because it allows you to kind of look at the root causes of one individual's chronic diseases.

Regarding my journey with complex illness, I know a lot of people get into a field because of their own health journeys. But for me, it was due to a patient that I wanted to help. It was a patient that came to me and really had a story where she and her family had huge health challenges related to mold and the mold related illness. And she told me that she was traveling to Arizona for care because there were no mold literate doctors at that time in Central Texas.

She asked me if I would learn more about the topic. And then the next thing I knew I and my friend who was actually became the co-founder of IntellxxDNA started to develop a whole program for mold related illness.

And as you know, once you start on the mold path, then by necessity you learn about mitochondria, and toxins, intoxicants, and POTS, and tick-borne illness, and all of those things. But I do want to stress that genomics is not just for people with complex illness because it can help people understand everything from why you have brain fog and memory problems, to why heart disease runs in your family and can help untangle medical mysteries.

[00:05:45] SCOTT: Beautiful. Beautiful. And for people listening, the two “x”s in IntellxxDNA are the two women who created IntellxxDNA as I understand.

[00:05:54] DR. HAUSMAN-COHEN: Yes. Yes. My co-founder, Carol Bilich, and I, we were sitting around trying to come up with a name. And as she will say, there were margaritas involved. But she was kind of joking to dumb chick's DNA. And I really didn't like that name, but we took it from intelligent approach to DNA because it's a very evidence-based approach. And the two “x”s are for the two co-founders.

[00:06:21] SCOTT: Let's set the stage with some terminologies. For people who aren't familiar with this arena, what is a gene? How many of these do we have? What are they really doing in the body? And then let's talk about SNPs. You mentioned the term SNPs. What is a SNP? Why are some clinically relevant and maybe others have no functional impact at all? And then building on that – I like to throw lots of questions out and then just let you kind of run with it. Building on that, is there a difference between genetics and genomics?

[00:06:50] DR. HAUSMAN-COHEN: Your genes are ultimately the cellular information that provide a blueprint or detailed instructions for how to make you. That's how come they can clone. Because from any tissue, you can isolate the genetic code for that individual. On a science level, genes give the recipe for how to make every single protein, enzyme, receptor, tissue in your body.

Now, it's really kind of amazing because we only have 25,000 genes or so. So, you go, "Well, we see more complex than that." And absolutely, we are. And that is one of the things that makes genomics complex because each gene does more than one thing.

That leads into the study of SNPs, because you can't just look at a list of genes and go, "Oh, I've got a bunch of variants in MTHFR." Or, "I've got a bunch of variants in VDR," or any one gene. Because each gene, the different parts of the gene interact differently with other genes in the genome.

Each gene is made up of anywhere from a few hundred to over a million base pairs. And you could have kind of like an elephant. The head of an elephant and a trunk is going to have a different function than the tail. You have to be able to look at a particular location in a gene. And that is where SNP comes in. SNP stands for single nucleotide polymorphism.

Going back a step, you might remember from high school, or nowadays they're talking about it in middle school, that your DNA is made up of these little letters which are building blocks. And there's four of them. A, T, C, and G. And there's about three billion of these letters in your human genome. And then SNPs stands for single nucleotide polymorphism, which is a one letter change in your DNA.

And then, depending on where that change occurs within the gene will affect whether or not it's clinically relevant and how it's clinically relevant. Again, you can have five different SNPs in the vitamin D receptor gene and one might relate to turning off excessive bone growth and that can relate to osteoporosis. Another one might relate to being able to turn off mast cells and that can cause mast cell disease. Now you can see why it's like really, really specific. Does that make sense?

[00:09:14] SCOTT: Absolutely. I kind of think of SNPs as a typo. And depending on where the typo is in a word or sentence or how many typos there are, then that can impact your ability to understand the meaning of what's written on the page. Is that a reasonable –

[00:09:29] DR. HAUSMAN-COHEN: Exactly.

[00:09:29] SCOTT: Okay. Perfect.

[00:09:30] DR. HAUSMAN-COHEN: Yes. Yes. And then, some SNPs cause visible changes from the outside. There's a SNP that increases pigmentation in the skin. When you have a person who has darker skin, they're likely to have one or two of those SNPs, which by the way is not necessarily a bad SNP. It's a good SNP and that it cuts the risk of melanoma in half. But then there's other SNPs that you can't see or measure from the blood. There's a SNP that codes the transporter of B12 into the brain. And then there's other SNPs that have no consequences at all.

The SNPs that we use in our work at IntellxxDNA are not pathogenic. Meaning they are not mutations. They do not generally cause diseases by themselves. The way they contribute to disease is because SNPs can interact with each other. They can interact with diet. They can interact with lifestyle and environment.

If you have genes that affect your detox pathways or oxidative stress pathways, and I think we'll talk more about that as we have our conversations, and you're living out in a rural area where there's no pollution and no pesticides in the water. That might not have as big of an effect as if you're living in India, or Houston, or a place that has – or New York or anywhere with more pollution, or more pesticides, or all those kinds of things.

And SNPs differ from genetic illnesses, which are inherited with what we call a pathogenic genetic event. Genetics is the science of heritability or inherited traits. And you can have a genetic disease caused by a SNP. So, Tay-Sachs is one SNP that can cause it. But most genetic diseases are caused by bigger genetic events. Like, Huntington's has a big repeat of a bunch of genes or deletions of big pieces of a chromosome. A genetic disease, you can inherit from mom or dad. A genomic disease is an interaction with a number of different little genetic changes.

[00:11:37] SCOTT: The pathogenic SNPs are much rarer. Those are not what you're looking at with IntellxxDNA. And as I understand, also the much more common ones that maybe happen in 50% or more of the population, those also are not really the target of what we're looking at when we're trying to unravel some of these contributors to chronic illness. Correct?

[00:11:58] DR. HAUSMAN-COHEN: Right. And so, pathogenic genes are what you're going to find out if somebody does whole genomic sequencing. Whole genomic sequencing has the better name, but it's not what you think it is. Because whole genomic sequencing is to look at all those three billion base pairs and go, "Let's make a list for the doctor of anything that could be a carrier for a pathogenic gene." Because a lot of diseases, you have to get one from mom and dad. And those tend to be found in less than one out of a thousand in most cases and sometimes even more rare.

The genes that we look at, the variants are generally in anywhere from 1% of the population, up to 15%, 20%. And while we will report on some that are in 30% or 40%, that's because if someone has one copy of a gene that is clinically significant when you have two copies, you're still going to see it pop up. You have to be able to look at it.

But I think that another factor is not just the frequency. It's not just about only looking at the genes that are in 5% or 10%, but it's sorting through the literature and having a way to use genomics to be able to look at the genes that are clinically significant. Because if you're a clinician and someone brings you a report and you go, "Wow! That's lovely. There's a lot of reds, and yellows, and greens." And I have no idea which of these genes might relate to your cognition issues or your family history of heart disease. And so, it's about being able to use genomics in a way that allows the clinician to know what's clinically significant and what you can do about it.

[00:13:39] SCOTT: Well, I think that's really important because part of my hesitation about using genes and SNPs over the last many years has been that you get this really complex report. And then some practitioners will look at all of the SNPs that maybe are red or maybe yellow and then it'll say, "Oh, there's a supplement for this one, and a supplement for that one, a supplement for this one." And suddenly the person is on 20 different supplements for genetic potential. But that's not actually always an indication of how they're functioning. And so, I'm wondering does that approach work looking at all of these SNPs? Giving a bunch of supplements? And then when will things evolve to us being able to look more at gene expression or transcriptomics as I understand rather than genetic potential?

[00:14:28] DR. HAUSMAN-COHEN: Good questions. With regards to the first part of your question, you absolutely should not try to address every gene variant an individual has. It's impossible. It would lead to taking a huge pile of supplements and pills and is just not relevant. You have to use genomics in combination with the medical history. Things like a patient's age, their diet, and their symptoms have to be taken into consideration. Because genomics is just a map to help you kind of do that detective work and make decisions.

As we kind of talked about before, there are genes that contribute to your ability to remove pesticides and mercury. But natural foods can also act as epigenetic, which means on top of genetic forces that make you transcribe or print more or less of a gene product or a protein.

One person might have plenty of Brazil nuts in their diet. And so, their glutathione peroxidase gene might be working just fine. And another person might need extra selenium. Regarding some of the other genes, one person might have more or less of the cruciferous vegetables and the things that make you have better glutathione production in their diet. And again, another person might not. Some people have more exposure to pesticides, and mercury, and environmental things.

The idea of optimizing overall genes expression and going, "Well, let's take one supplement for each gene that we think you have potential," would really create a system that doesn't work for most individuals.

There's another piece of that, is you have to understand regulating different genes is going to be specific for that gene. And again, gene transcription, gene health, your body's health can change as you, again, get older. Somebody who's having a gene that can relate to things that contribute to brain fog, certain kinds of inflammation, that may not become an issue until they're older.

With regards to the idea of can we look at transcriptomics? There's a problem with that. And this is a really great question because there's a lot of people saying, "Oh, we need to look at metabolomics, transcriptomics. But the problem with that is the idea of differential tissue expression. And what I mean by that is if you had every gene expressing in your blood, that would be a mess.

Our blood cells only have a certain number of genes expressing in them that relate to blood cells. And actually, your blood is only going to have a certain number of nutrients. And so, your brain has its own tissue expression. Your gut has its own tissue expression. Your kidneys.

Right now, we're trying to do further evaluation with a blood biopsy or a urine biopsy because that's the tissue. But if you're looking at things that affect the gut lining, or you're looking at a gene that's in the promoter of TNF alpha, and there's one that relates to brain inflammation both with autism and with cognition, how are you going to be able to look to if that gene is expressing in the brain?

Most parents or people aren't going to want to have a brain biopsy or a spinal tap to look at that blood-brain barrier. That's why genetics becomes important, because if you know that somebody has a gene that makes them have a promoter, which is an on-off switch for the TNF alpha, the inflammatory pathway that one of the pathways that's important in the brain, and that it's four to five times more active. In other words, when they're on, they make four to five times more than the person who doesn't have that SNP. Then you have to just use that knowledge and go, "Okay, they're having symptoms of autism. They're having symptoms of cognitive decline. They're having symptoms of just anything that you think could relate to that TNF alpha in the brain. Let's try lowering TNF alpha with something that crosses the blood-brain barrier and see if they get better." I don't think we're going to have true proteomics, metabolomics for brain disease, for kidney disease, for liver disease. It's just not all possible from the blood.

[00:18:52] SCOTT: When we have a SNP that represents a potential for something to be functioning in a less than optimal way, is it always the case that changing your nutrition, or adding a supplement, or removing an environmental toxicant, or mitigating an infection, is it always the case that there is a bypass so to speak? Or can we have specific SNPs that there isn't necessarily an action item that you can do to improve that genetic expression?

[00:19:24] DR. HAUSMAN-COHEN: Yeah, I think we wish there was always a bypass for the SNPs and for the gene. But there, again, are 25,000 genes. One million SNPs. And I would say that we know what to do about less than 10% or 20% of them. And in fact, again, that has been my area of research of saying what can we do to look at what does this gene do? What is the gene SNP cause in terms of a problem? And what can we do based on the literature with diet, lifestyle, supplements to make this gene either work better or be a bypass?

In our genomics, in IntellxxDNA's genomics, we only put in genes that we believe research supports that you can kind of address. Because to list a bunch of genes, there's some genes that are known to contribute to frontal temporal of dementia. But nobody knows what to do about them. And I couldn't find any literature that made me feel like anybody has a hack for them. It doesn't make sense to report them to patients.

In our genomics tool, we only give clinicians and, thus, patients the empowerment of things that that they can address. Because otherwise, again, it's just going to make someone worried. There are some genes where the only tool for it is going to be CRISPR or gene editing. And again, that's a young science as well.

But if we start with the things that we know how to address, you can still make a lot of improvement. Things relating to inflammation, detox. Sometimes even the neurotransmitters. And just there's so many that we can't address. I mean, hundreds and hundreds.

[00:21:08] SCOTT: My understanding is that it takes a long time for a gene itself to actually change. I've heard some people say over 2,000 years. That the genes themselves may not explain the epidemic of modern diseases that so many people are facing. That maybe there's more epigenetic influences.

When we have a specific SNP that's present, how much of that SNPs potential to lead to a change in function is epigenetic? What are some of the top epigenetic influencers of gene expression in your opinion? And then, lastly, is our DNA our destiny? Or do we have significant influence over how our genes express?

[00:21:46] DR. HAUSMAN-COHEN: Again, some really good questions there. In terms of the changing of the human genome, absolutely, evolution is a slow process. When you talk about changing the human genome, we're talking about the process of evolution. And we know that chronic illnesses are becoming more common. There are many more children with autism now than there were a hundred years ago. Autism used to be a pretty rare thing. And now, it's up to one out of – On the CDC website, they say it's one out of every 44 children. Another paper recently said one out of every 60. It doesn't matter which is correct because it probably depends on the population. But it absolutely used to be something that was one out of many hundreds of children. Not one out of 50. You go, "What's going on?"

And it has to do with these genes that our bodies have. Things that relate to gut permeability. Things that relate to detox. Things that relate to inflammation being triggered by the exposure. Some people call it the exposome in our environment. And so, those influences are important.

The diet in America has changed tremendously. For example, there is one gene that's very involved in pervasive developmental disorder and also autism. So, like, five times the risk of autism. 12 times the risk of a developmental disorder. That has to do with how the brain develops, how what's called the glutamatergic synapses kind of put together like a scaffold before you build a building. You can imagine, scaffolding of the brain is very important in development. And this gene has been around a long time.

But if you have enough zinc, and enough of exposure to sunlight during the day, and many other things, this gene will not have as big of an effect. We have children that have autism where their parents have this gene and don't have autism even though an odds ratio of five times. That's 400% increase. That's huge. And you go, "Well, what's different?"

Well, one generation ago, the parents may have gotten been served liver and onions. And so, liver is really high in zinc. The children were playing outside. Not on their computers. Again, we can go on and on and on. But these are all super important things to the evolution of chronic disease. And we know that it's the same that's true for heart disease, for cognitive decline, for diabetes. So much of our environment interacts with the genes. And by our environment, I kind of mean environment, what we eat, pollutants, all of that, and lifestyle.

I'm 100% sure that DNA is not our destiny. And I think that you know. Because we've talked, Scott, that my work actually began with adult cognition work. I was interested in improving outcomes in people who had cognitive decline. I actually taught very early on at the first conference at the Buck Institute that Dr. Bredesen had about environmental illness. But that's why, during the time, we were building our cognition-related genomics. And we have seen, not only in my office but in many, many, many, dozens and dozens of offices across the country, people using genomics to help people understand where their kind of pitfalls are and their genomic, I'm going to say, weaknesses. And then addressing them and having people, not everyone, but many people, stabilize their cognitive decline or improve it. And to the point where we have in a paper.

And we do have some papers on the topics about cognitive decline and autism. But one of the case reports in our cognitive decline paper that was one of my partner's patients, she'd already been accepted into a study for Alzheimer's. She's an ApoE 4/4. Had cognitive decline, and amyloid pet scan positive, and was already mild dementia. And she got back to being within the normal. Now, she still has a few memory challenges but very, very different than having the diagnosis of dementia.

You can't repair everybody's brain. It depends on what's going on. But the earlier that you start to identify problems in somebody and address things like inflammation, and detox, and all those other factors, the better the chances are of getting improvement.

[00:26:27] SCOTT: Maybe another myth that I kind of want to talk about is whether or not all SNPs are bad. Or are they two sides of a coin? For example, COMT. Do we also potentially get some beneficial traits, or characteristics, or functional abilities along with some potentially less than optimal ones?

[00:26:48] DR. HAUSMAN-COHEN: Yeah. It's fun to talk about the pop genes that a lot of your listeners will have heard of. And COMT or COMT is one of them. And that's one of those genes that they will give people extra energy. Because COMT relates to your ability to break down adrenaline. And it is a slower breakdown of adrenaline so that you break it down three or four times. It takes you three or four times longer to break it down.

What does that mean? Well, you get this high adrenaline state. And that can be good for some things. It's actually been shown to be associated with overachievers. I was at a conference, and after the conference a bunch of just went out to dinner. And virtually, every single one of the speakers there knew they were a double COMT. Because they were just kind of like that go-getter type personality.

But there's negatives to that gene as well because that high adrenaline means when you get stressed, it kind of can trigger that cortisol adrenaline cycle and it can be associated with increased risk of sudden heart disease. There's definitely pluses and minuses of genes.

[00:27:55] SCOTT: What are some of the things that we can glean, or learn, or insights from looking at genetics that clinically would otherwise be difficult or maybe even impossible to determine? What is it about looking at the genetics that brings us something beyond traditional lab tests, and history, and those types of tools that are more commonly used?

[00:28:16] DR. HAUSMAN-COHEN: Yeah, and I think that that is what we were talking about with the differential tissue expression. Genomics sort of started in the realm of nutrigenomics where people were going, "Yeah, this person has low B12. I wonder if I can see it in their genetics." It's kind of more of a, "This is kind of fun."

And as it moved into the topics that were diseases. And, again, it doesn't matter whether it's obesity, or heart disease, or diabetes, or autism, or PANDAS, or Lyme, or can be anything, ADHD, depression, it allows you to see things that there's absolutely no way you can test foreign blood.

If we take the topic of depression, everybody knows that not everyone responds to serotonin medicines. And I don't think that any of your listeners believe that depression is caused by the absence of Prozac, or Paxil, or Zoloft. And so, then you go, "Well, what causes depression?"

And the thing about chronic disease is there is no one cause. That's why there's not one drug that works for any chronic disease, even high blood pressure. And so, what genomics adds is it helps you look at the root causes. There are people who have more depression because of relationship with some of the serotonin receptors and serotonin reuptake. But there's also genes that relate to cortisol. There are genes that relate to not being able to make the serotonin to start with, with methylation, like MTHFR. But also, with TPH, tryptophan hydroxylase.

There're genes that relate to an enzyme that helps you make norepinephrine, and serotonin, and dopamine, tetrahydrobiopterin related gene. And then there's genes that relate to things that you would kind of like be totally like, "Wow! Why does that relate to depression?" But EMFs, which I know is an area of interest of yours.

And so, there're so many different genes. And if you have a map of what might be involved in this person's depression, or this person's anxiety, or ADHD, or cognitive decline, you can then really address it in a more personalized way. And there just are no blood tests for most of those things. The blood tests for brain science are really just not there because of the blood-brain barrier. That's why I love doing genomics with brain science. I still do it for chronic disease because it helps there, too. But with the brain, there's just nothing else like it.

[00:30:51] SCOTT: You mentioned MTHFR, and this kind of brings me to one of the other hesitations I've had about looking at genetics, genomics. And I think this is largely when there's not the clinical support to paint a more accurate picture. Someone gets their MTHFR results. They immediately feel they're broken, they're hopeless, they're fearful, they're not going to get better.

And I actually would argue that there's probably many backup genes even in the methylation realm. MTHFR is only a small part of the story. And that that feeling broken or feeling hopeless because of your genetic results, that itself I would speculate becomes an epigenetic influencer of gene expression that maybe even more significant than the MTHFR itself might be. What are your thoughts on that?

[00:31:45] DR. HAUSMAN-COHEN: Well, you're correct in that. They've shown that adverse events in life definitely do a gene transcription and gene expression. You're right, that we don't want to create anxiety or depression for someone by scaring them. Because when you get that high cortisol, that has effects on your transcription and on your epigenetics and such.

And the thing I would say about MTHFRs, MTHFR, COMT, some of these pop genes, they're popular genes because they are so common they were able to be studied a long time ago. And so, we have a fair amount of research on them. But MTHFR, it is an important gene. It can relate to depression and anxiety. When you have two copies of it, it can contribute to hearing loss. It can contribute to spina bifida risk. It can contribute to a lot of things. But one copy of it is found in 45% of the population. This is not the answer to most issues.

And so, I think that the thing to realize is, as you said, the human body is very redundant. MTHFR is one of the ways that we recycle homocysteine back to methionine. And again, I don't want to get too sciency. But methionine is really the ultimate methylator. Methionine goes to the SAMe pathway. And that's where you get methylation.

And our genomics, our body, is really amazing because we have three or four different ways of getting methionine repleted in addition to food. It's more that if somebody has MTHFR and then they have depression, you go, "Gosh! Maybe giving a little more methylfolate might be beneficial."

And just from a kind of fun aside, one of the things that may have contributed to more depression is we started putting folic acid into our flour and into our bread. And that's good because, for most people, they can go from folic acid to methylfolate and have no problem. But people with MTHFR, they're not good at making that. They're not good at turning the folic acid into the methylfolate that can cross the blood-brain barrier. And the folic acid almost gunks up the transporter into the brain so then they can't get the methylfolate in.

It's really about the beauty of science. And when you understand you, then you go, "Okay, either I want to also decrease the folic acid and increase the methylfolate. Or what other hacks can I do?" And so, that's really – the benefit of genomics is it lets you understand, or your doctor, or your clinician understand you a little better so that you can have guidance for how to best kind of care and water yourself.

[00:34:33] SCOTT: Your specialty is the brain. I want to talk about some conditions that involve the brain. Let's start first with brain fog. It seems like so many people talk about brain fog, not being mentally clear, having some cognitive challenges, executive functioning. What do you see is the bigger contributors to brain fog? And what are some of the things we can do to improve mental clarity and brain function?

[00:34:58] DR. HAUSMAN-COHEN: Yeah, I love talking about brain fog. And I don't love having it, but I would love talking about it. And I think we've seen a lot more brain fog in the era of COVID. I think that's a good starting topic.

Brain fog, or cognitive decline, or memory, a lot of people kind of did the same thing that they did with MTHFR. They go, "Oh, I must have ApoE 4." Well, ApoE 4 is 20%, almost 25% of the population depending on your ethnicity. And so, ApoE 4 was made part of the pop literature and well known by all the work of Dr. Bredesen because it is one of the main Alzheimer's genes.

And ApoE 4 turns on 1700 other genes. And that's why it's such a big deal. It interacts with the promoters of 7 – it turns on or off 1700 different genes that relate to growth hormones, and inflammation, and all kinds of other things. But that is not the only source or even necessarily right now during COVID, the most common source of brain fog.

With regards to ApoE 4, it's really good to know that ApoE 4 alone is not necessarily the cause of brain fog. And if somebody has brain fog, they should not, just because they're ApoE 4, go, "O, it must be that." Because there are people who have ApoE 4 who don't have it with mitochondrial genes, don't have it with some of the other important genes that might go, "Oh, gosh! It's the ApoE 4." And it might be something completely different.

Some of the categories of other causes of brain fog, one is things that relate to detox pathways. Those have been associated with brain fog. Things that relate to what I'm going to call growth factors, BDNF. That can be important. And just so you know, if you guys know that you happen to have some of those BDNF pathways associated with cognitive decline, exercise is super important.

But another group that we found when looking at participants in a study that Dr. Bredesen, Dr. Kat Toups, Ann Hathaway, the recode group we're doing, is genes that relate to brain ischemia. And so, what I mean by that is if your brain can't get enough oxygen for a variety of reasons, that's going to cause brain fog. And that's where COVID comes into play. Because some of these genes cause you to have higher levels of these fibers in your blood called fibrinogen. And there's some gene SNPs that contribute to that as well.

And if you already were genetically prone to making a little thicker blood or more fibrinogen, now you get COVID, which pushes it up further. That can be a cause of brain fog. And that one has been super important to realize. Because in our practice, we don't have anyone with long-haul COVID because we have been addressing the brain fog in a genomically targeted way. But the most common thing that we're seeing again is the fibrinogen. And we're using Pycnogenol, which is from pine bark, which has studies for people for like long-haul flights for DVT prophylaxis. We're using lumbrokinase, which is from earthworms. I know that sounds a little funny. But earthworms move really slow. So, they have to have something to keep their blood from getting too thick. And we're getting really great results. Yeah, there's a lot. I could go on and on but I don't want to take off too much time on one question.

[00:38:24] SCOTT: No. I love that. And I totally agree. I think with COVID, the coagulopathies, the hyperviscous blood, I think the vascular health, the endothelial health, I actually think that's probably the most significant thing that COVID is doing that's leading to heart attacks, and strokes, and all kinds of other long COVID type symptoms. And yes, I've had my lumbrokinase this morning before our conversation. Hopefully my brain will not be foggy.

Depression and anxiety are very common as well. You talked about that a little bit earlier. Some of it can be situational, life related. But are there certain genetic wirings that lead people to being more depressed or anxious? How do you break that cycle? I know we could have a whole podcast on it. But I know with IntellxxDNA, you have an anxiety panel, for example. When we're talking about depression and anxiety, what are maybe some of the genetic predispositions that your testing can reveal?

[00:39:21] DR. HAUSMAN-COHEN: Yeah, I think that's a great question. And we have separate panels for doing anxiety, depression, OCD. But anxiety is one of my favorites to talk about. Because when we worked on that and went into the literature, I found a lot of really interesting things.

As we talked about, of course there's some genes that relate to serotonin. And then there's some genes that relate to adrenaline, which makes a ton of sense. Because if you think about it, adrenaline is that fight or flight hormone. The person who's running from a tiger. And if you have an adrenaline receptor that's 30 times more active, then it makes sense that when you start to be worried about something, it's just going to be accelerated.

But there were a couple of other really interesting pathways. There's a pathway that relates to orexin. I'm not sure if you've heard of orexin. But for your listeners that haven't, orexin is the wakefulness hormone. And so, if you have one cup of coffee, it might make you feel a little bit awake. But if you have 10 cups of coffee, you know how that can be like too much. Well, the same thing's true with orexin. If you have a gene that makes you have 10 times the response to your orexin, then you're going to have an easier time feeling overly panicked because it's supposed to make you feel awake. But too much awake can feel like panic.

There are genes that relate to blood sugar. And I have a fun story relating to a young woman with anxiety that we did her genomics and she definitely had some adrenaline related SNPs. But she also had two copies of this gene that made it that when she had high carb foods, she couldn't lower it quickly. It relates to incretin, which is the signal to lower your blood sugar.

And so, literally, all we did for her was we gave her one ashwagandha to kind of help keep her cortisol down and the adrenaline down. And then as she was walking to class, she was drinking a huge, huge Coke because she wanted the caffeine in it and the energy to – And she was a college student. We switched her to tea. We let her keep her caffeine. You can't do too many changes at once. But we got rid of the sugar. And her anxiety was dramatically better with two small hacks.

And there's many other things that contribute to anxiety as well. There're SNPs that relate to your thyroid metabolism of your brain, the ability to convert T4 to T3. There're SNPs that relate to your hormones, which makes sense. Estrogen related SNPs and such. Lots of fun things with anxiety.

[00:41:52] SCOTT: Let's talk a little bit more about Alzheimer's. And you touched on the ApoE 4. But I want to talk a little bit about what's the functional impact of having one copy versus two copies of ApoE 4? And is that the full picture? I know there's other genes that are involved as well. There was a TV show out recently with the famous actor who they told him he had ApoE 4 and apparently it was a big thing that he had to stop acting and really dive into this thing. And there seemed to be a lot of fear and kind of hype around it. And I realize it's important. But is it really by itself the full picture in being deterministic around your potential for the development of Alzheimer's?

[00:42:34] DR. HAUSMAN-COHEN: Absolutely not. And I sort of alluded to that. And on our website, there are some videos, there's an excerpt with Dr. Bredesen. There's also a video I did a long time ago with Dr. Perlmutter. And both of them have – when we've had conversations that anybody who can do the more detailed genomics with ApoE 4, they should.

Because, first of all, you can be in a state of fear with ApoE 4 unnecessarily because it may not have as big of risk. But second of all, ApoE 4 interacts with so many other genes. And again, this is where our research shines where we can kind of help give you a map of some of the things that are important.

And we have, again, in our practice just in the past month, I've seen two of my ApoE 4/4 seniors. One who is in her 70s and the other one who's in her 80s. And both of them are above the 80th percentile for memory. And my 81-year-old patient, even though she's in ApoE 4/4, she is in the 90th percentile using CNS vitals on her composite memory score. And I'm like, "That's amazing." And so, you don't want to go, "Oh, have this defeatist attitude." You want to go, "What else is going on?"

ApoE 4 interacts with a lot of things. But then, all the other things – Dr. Bredesen will divide people into categories. He'll say there's the sweet category, and the trophic, and all these different categories. But the reality is genes are like shuffling a deck of cards. You get some from mom, some from dad. And you can get a little of each. You might get a nice neat full house, but you might get a hand that has just a lot of everything in it. You can have problems with your growth factors, BDNF. You can have – there's a wide variety of different kinds of inflammatory pathways that can affect brain. There're things that really need specific nutrients, more zinc, more folinic acid, more B6. There're so many things that can contribute to cognition.

As we said, detox. People not making enough nitric oxide and not opening up those blood vessels wide enough. That's an easy one to fix. There're so many different options that more information, as long as it is actionable, is going to allow you to optimize your brain health.

And the reality is you can see if things are helping. You can do tests like CNS vitals. You can do things – like, there's ones called MoCA and SLUMS. But they're not quite as detailed. And you can do it before with your doctor or your clinician. And then you can kind of say, "Let me try three or four things, and some lifestyle, and some diet, and let me recheck six months later." So, you don't have to guess. We have the ability to go, "Am I getting benefit from my genomics?"

And while we are not – we do not yet have a prospective large trial, we are working on getting funding and getting that going, we have a lot of published case reports and case series from across the country showing that we can get improvement for many individuals.

I do tell people, if you know you have ApoE 4 in your family or any kind of dementia, once the brain gets too much amyloid, too much tau, some of the more neurodegeneration, you're not going to get as good results. When you are 50 or 60 and you're saying, "Gosh! I'm just having a harder time recalling names. I'm having to go back. And I was looking at that number and I was typing it and I had to re-put it in." That's the time to go and get help and learn your genomics and optimize. Because the earlier you catch symptoms, the better results you get.

[00:46:20] SCOTT: In Dr. Bredesen's pre-code and recode program and his work with Apollo Health, they will run a number of lab tests blood tests, other types of tests. And using that data, come up with some determination about which of the six subtypes. And you can be more than one of them. But which of the six subtypes? You mentioned earlier some of them. Blood sugar related, inflammatory, toxicity, those types of things, vascular.

And so, if we look at how those tests are then used to determine what area to focus on, I'm wondering if you could take your genetic testing and look just at their genes and almost paint the picture of which of those subtypes they might need support in in order to improve their cognitive health?

[00:47:11] DR. HAUSMAN-COHEN: I first want to say that I am very, very appreciative to Dr. Bredesen because he has been the father of this work.

[00:47:18] SCOTT: Yeah.

[00:47:18] DR. HAUSMAN-COHEN: But I do think that the genomics can give insight in a similar way and even in many areas in more depth in the testing. But really what you want to do is use the combination. Sometimes – homocysteine, for example. It can relate so much to not only your genes but how much protein and what kinds of protein you eat. You would want to use the homocysteine blood levels along with the genomics. But the advantage to the genomics over just using blood tests, like we said, is his prediction of vascular dementia is based on cholesterol, homocysteine, some of the kind of common markers, CRP. But he's not going to be able to get at all of the SNPs that affect endothelial nitric oxide production because of the blood-brain barrier. All the things that can affect the hypercoagulability in the brain. The carotid intimal thickness. The amount of – some of the other things.

I do believe that genomics can take it a step further. And that's why Dr. Bred – And I think that Dr. Bredesen would agree. Because in their most recent study that was published in the Journal of Alzheimer's just this past year in 2022, which by the way is the number one read reference of the Journal of Alzheimer's for the past year. Very proud of Dr. Bredesen and his team for that work. But they used our genomics to help improve outcomes. And they're doing another study right now that's larger, again, where they're using the genomics along with all these other tools.

And I think that's how most clinicians use genomics. It's not the only tool. But it's a really great backbone tool. And then if the genomics show that you have horrible detox pathways, then you might want to do further things to go well. What's this person's mercury level? De does this person have evidence to a lot of pesticides? Or give it further history regarding roundup exposure.

And I had a patient in my practice where he was having significant cognitive decline. Getting lost – Well, I wouldn't call it cognitive decline because it was reversible. He was having significant memory problems even sometimes kind of getting lost in the grocery store, not talking as much. His wife thought he was getting frontal temporal lobe dementia. And it ended up being very heavy pesticide exposure because he had a ranch and was spraying pesticide on the weekends along with horrible detox pathways. And he's back working and doing great. But needs a little extra maintenance and had to stop being around pesticides.

[00:49:51] SCOTT: I want to talk a little bit more about autism. You touched on it earlier in our conversation. I've generally been of the opinion that conditions like autism, maybe in a child they get certain environmental toxicant exposures or they get certain infections. And because of their state of neurodevelopment, that may lead to autism. And maybe an adult that gets similar exposures might have chronic Lyme disease or MS. Maybe an older person with similar exposures maybe gets Alzheimer's. I'm wondering, from your perspective, how similar or different are the underlying root causes in these conditions? What has your work in the genetic realm showing you that might make autism more unique as compared to those other conditions that I mentioned?

[00:50:37] DR. HAUSMAN-COHEN: With autism, I think it's a lot of the same story as we see with Dr. Bredesen's work and the work of cognition. It's not one cause. It's multiple causes. Common causes again include inflammation, problems with some of the scaffolding during neurodevelopment, problems with how they respond to infections and their gut microbiome. And so many more. Oxytocin receptors. There're just lots and lots of different things.

But in terms of circling to that question of the role of infections in some of these complex chronic illnesses, it does relate to genomics. But from what I'm seeing, slightly different genomics and slightly different infections may relate to some of these different topics. And then there is some overlap.

For example, MS. A lot has come out in the literature in the past few years that inability to fight off Epstein-Barr virus and having a chronic Epstein-Barr infection might contribute to MS. But it may be some of those genes that relate to your immune system because there's things that relate to the initial ability to fight off infection, which is the complement pathway and things that relate to more specific ability to fight off infections like the toll receptors. But it may be that plus one of the big autoimmune genes like TNF alpha.

But then you might have Lyme disease is obviously caused by Lyme spirochaetes. But then you might have with autism, Lyme might contribute but you also might have bartonella contributing. For OCD, you can have strep causing it. That's what PANDAS and PANS is. And so, it's a mixture of genes and infections.

And I think that, again, genomics is still at the beginning of helping us untangle it. But we do know that, for example, specific toll receptors. And toll receptors help you fight different infections. Some fight viruses. Some fight bacteria. Have been associated with cognitive decline. And some of the toll receptors associated with cognitive decline relate to the herpes viruses. Other ones that are of genes related to cognitive decline relate to your ability to kick out Lyme disease from intracellular space. It's not the only cause. I think that infection would probably be in my neighborhood a smaller cause of cognitive decline than many other factors. But it's definitely one to consider especially if you see that someone has problems with some of those infection fighting pathways. Then you're going to want to dig deeper.

[00:53:11] SCOTT: Let's come back to the environmental toxicity conversation. We agree that it plays a major role. Maybe the most important role in many of our modern-day conditions. When we look at someone's ability to detoxify, you've mentioned that genetics plays a role there. I believe the PON genes, for example, can play a role in your ability to excrete pesticides.

And so, when we're looking beyond methylation and into some of these other detox pathways, what are some of the commonalities that you see in terms of genetic SNPs that might impair detoxification capacity but also some of the common optimizers or nutrients that can help to better optimize one's detoxification potential?

[00:53:53] DR. HAUSMAN-COHEN: Yeah. There are a lot of detox pathways. Again, when you think that we only have 25,000 genes, and I would be able to list for you 15 or 20 things relating to detox, that's actually a pretty – and there's many, hundreds, if I really were to go into everything peripherally. Detox is an important part of our body. And you go, "How come evolutionarily?"

And it's because even if you're living in a clean world of a thousand years ago, even plants have toxins in them. You have to be able to remove. Like, even in basil. There's parts of basil and parts of plants that are good and parts that we want to excrete and get rid of. We have all these natural pathways.

And then, also, the detox pathways do other things. For example, PON1, which is how we respond a lot to the organic pesticides, it also keeps our LDL from being oxidized. And so, it's also related to heart disease and even macular degeneration. But I think that the more specific – and then we'll go to the oversimplification. The more specific thing is the more you know about which detox pathways, it's kind of like the inflammation story, the more specific you can be in your interventions.

PON1, you can upregulate PON1 transcription. Upregulate that activity about 80% with two ounces of pomegranate juice. But that's not going to help your glutathione pathways or your CYP, your conjugation pathways of those sorts. And so, if you were to say what is the most specific one? That you have to kind of look at each gene. For glutathione peroxidase, selenium is really an important cofactor that's been able to upregulate.

For certain genes, the ability to make glutathione, for example, GCLC and acetylcysteine is good. But sulforaphane, which comes from three-day-old broccoli sprouts, can also work on that. I don't think there's any one master detox supplement that covers everything. But the one that covers the most would be, in my opinion, sulforaphane. And that's because sulforaphane affects the nerve II pathway and some of the overall inflammatory pathways, and overall detox pathways. But it also upregulates the synthesis of glutathione.

If you're like, "I just have bad detox." A lot of people go to milk thistle, which kind of helps the liver with some of that kind of phase one CYP sometimes. But I would say if you're only going to do one and you think you have bad detox, probably sulforaphane is the broadest. It comes from three-day-old broccoli sprouts. Adult broccoli is not going to have the same benefit. It has like a thousand times less. And you do want to make sure you have a product that's been used in studies that has myrosinase in it that has good activity.

[00:56:47] SCOTT: Something like Avmacol? Is that one that you –

[00:56:49] DR. HAUSMAN-COHEN: Yeah, Avmacol. And then Designs for Health has one that has myrosinase. You just want to be careful because some products have been studied and they did know better. They did worse than giving the people a little bit of young broccoli. That was not – you want to make sure you get it at a standardized product.

[00:57:07] SCOTT: Well, and that glutathione piece is so important for detox as well. I know in past conversations you've called it the master paper towel of the brain. That sounds pretty important to me what we're talking about. Yeah.

[00:57:17] DR. HAUSMAN-COHEN: It is. Yeah, it is. And people kind of joke. They're like, "Oh, you can just give that to almost anyone coming in with something brain-wise." And it's true because it affects interleukins, some of the inflammatory pathways, some of the detox. It affects nerve repair. Yeah, if you don't have access to genomics and you're having something brain neurodegenerative, autism, cognitive decline, that's always a good one to start with.

[00:57:41] SCOTT: Detoxification and inflammation are two ends of the seesaw. When inflammation goes up, detoxification goes down. When detoxification is optimized, inflammation goes down. What are some of your observations in those that are more prone to chronic pathogenic inflammation? What are some of the tools that can quench the fire of inflammation? And are these tools working directly? Or are they working through optimization of specific genes that inhibit normal inflammatory responses?

[00:58:13] DR. HAUSMAN-COHEN: A little bit of each. In the past, I don't know exactly what year, I think it's now probably 15, 20 years ago, there was work that came out of a lab at Harvard, Dr. Charles Serhan, showing that our interleukin-1 beta – So, anything that's labeled alpha or one, that's always an important one. Interleukin-1s are important inflammation. That part of how the whole inflammatory cascade works is it turns on the inflammasome pathway.

And so, if you are kind of trying to turn – A lot of times they all kind of tunnel into that inflam – not everything, but many inflammatory pathways tunnel into that NLRP3 inflammasome pathway. And so, resolvins, they're sold as either specialized pro-resolving mediators or pro-resolving – or resolvins. They can turn off some of that master inflammasome pathway. And that's a a good anti-inflammatory for some of the pathways. But it's also looking like a lot of brain inflammation is relating to chemokine tissue destruction. It's not just about the inflammation. It's about the inability to stop the inflammation and having genes that relate to over destroying tissue in response to inflammation.

That particular pathway has been important in COVID related lung inflammation. And again, resolvins are one approach to it. But it's been really interesting because many of the things that you guys will recognize from COVID, andrographis, astragalus, sambucus also turn off that chemokine tissue destruction. And then palmitoyl –  actually turns that off. And you can look and see PEA has evidence in autism. It has evidence in cognitive decline.

But again, I could list a hundred different things that you address for inflammation. So, you can start with some of these broad things. But that's why if you truly are having cognitive decline, neurodevelopmental disorders, any kind of brain thing, getting the actual map of your brain with more specific genomics is going to allow you to kind of hone in. Because the idea is if you can pick two or three supplements that are going to give you the biggest bang for your buck that are more specific to your issues, that's going to be more helpful. Lion's Mane is fantastic for TNF alpha. But it's not so great for interleukin-6. You have to kind of know. Ideally, you want to know what's going on.

[01:00:51] SCOTT: Chronic Lyme disease and mold illness are known as biotoxin illnesses or CIRS, chronic inflammatory response syndrome. So, they tie into this whole inflammation conversation as well. And I'm really excited about what we talked about previously and getting ready for this conversation. I think this was an aha for me. And so, that is can the Lyme spirochete itself be an epigenetic influencer of gene expression? Particularly in some of those genes you mentioned earlier that allow us to manage infections? And if so, how can we mitigate that potential issue specific to the Lyme spirochete? What are some of the top tools or approaches that you find helpful for your patients in dealing with chronic Lyme, chronic vector-borne infections?

[01:01:35] DR. HAUSMAN-COHEN: Yeah. And I think the most helpful thing for people with chronic vector-borne infections is to understand that they tend to hide in their inactive forms. Like, Lyme will hide intracellularly. We do have a panel that looks at Lyme response and it looks at there are some genes that have been identified in the literature that have been associated with persistent neuroborreliosis, which means Lyme in the brain. And that was my aha moment for Lyme, in that the gene that is most associated with it has to do with inability to kick Lyme disease out of the intracellular brain space. And that it's an efflux transporter.

Allow and then amyloid, we think of as relating to Alzheimer's. But amyloid, just think it was kind of like this protective gunk. Well, gram-negative bacteria, but also Lyme disease and spirochetes, they secrete it. And so, that's that whole biofilm thing. If you're hiding intracellularly in, you're making amyloid, that's going to be harder to fight.

And so, you have to, when you're thinking about Lyme disease – and you, with your experience with some of the nutraceuticals. Probably have even more experience in this than me. But you have to be thinking about what can get into the blood-brain barrier and also has an effect on these inactive forms? Things like cryptolepis. Things like resveratrol from Japanese knotweed. Knotweed. All these different kinds of things.

And again, genomics, the beauty of it for me is that it helps me kind of go, "Now this makes sense as why we have a problem." I do also always tell people that be careful. Again, as you said, Lyme can affect hundreds of genes but so can mold. And mold will trigger molecular mimicry, which means it will make people make a whole bunch of different IgMs, which are the early antibodies to things.

And so, if you have somebody that has on these different tests a lot of IgM, IgM is only supposed to be there for the first 10 days after an infection. If you're seeing that kind of non-specific pattern, think could it also be molecular mimicry from mold? And test for molds. Because they're pretty common with air conditioners.

[01:04:02] SCOTT: If I understood from our last conversation, I just want to dial this one in a little bit, that there are some genes that lead to us not being able to manage the Lyme spirochete as well as if we didn't have specific SNPs. And that resveratrol can actually help so that our genetic expression is supporting our immune response to borrelia in a more efficient manner. Is that a reasonable statement?

[01:04:29] DR. HAUSMAN-COHEN: Yeah, resveratrol does have some specific effects not only on killing some of the forms but also on the whole immune system itself. Some of the mannose-binding lectin pathways and some of the other pathways.

[01:04:44] SCOTT: Talking then about mold illness, there's a lot of focus on HLA-DR genes. I would say they don't seem to have held up as strongly over time in being predictors of treatment outcome even though they might be good predictors of one's predisposition to developing mold illness if they have an exposure. I'm wondering what your patterns of observation have been relative to mold and mycotoxin illnesses. I know there's a concept of bouncer genes. I'm not clear whether that's similar or different from the HLA-DR genes that are often discussed. And then might mold and mycotoxins themselves be broad influencers of our genetic expression?

[01:05:24] DR. HAUSMAN-COHEN: Yeah. Those are a lot of good questions. In terms of the HLA-DR and what type of people get mold, that is a little bit more hypothesis than fact. One of the things I started out at – So I started out doing a PhD. That I was doing my PhD at Harvard. And so, it got drilled into me, you've got to do evidence-based medicine. You have to use the research and really be careful about your science.

Of course, we have to create hypotheses but then we have to prove them. And in the literature, I have not found anything that says that one specific HLA type has higher risk of mold related illness. I do think we have to be careful about that. It could be true. But somebody's got to do a study showing it before we say it's true. And it was thrown out there as a hypothesis that has been treated like fact when it really has not held up in the literature.

I think that there's a lot of research ongoing. But the bouncer genes, there have been some. Bouncers are like the ABCs. There's like ABCC. They're the things that cause drug resistance. There's one of those genes that is normally thought it was a drug-resistant gene that has been shown to be related to having higher risk of aflatoxin illness. Not necessarily every single kind of mold illness.

There are genes that are associated with mast cells that can be contributed to mold related illness. And of course, when you have mast cell activation, you get more barrier permeability. That makes sense. Because if you have mycotoxins are really tiny, mold should not be able to enter the bloodstream. But the more barrier issues you have, the more that you can then release more histamine, which can cause more kind of, I mean, barrier issues, blood-brain barrier permeability, blood gut barrier. That causes all kinds of symptoms of joint pain, and muscle pain, and brain fog.

I think that the story is still being untangled. But I would say that from what I have seen in my patients looking at genomics and from some research that we are currently working on relating to some of the mast cell issues and the mold issues that its inability to kick the mycotoxins out of the brain is going to become important. As well as some of the things that relate to bigger inflammatory responses, bigger mitochondrial – well, poorer mitochondrial function. As well as some of the mast cell issues.

[01:07:56] SCOTT: With the mast cell issues, some of that, some of the predisposition to having mast cell activation syndrome or the severity can be associated to specific genetic SNPs. In a patient that you might be working with that has mast cell activation, is the approach to treatment then considering these genes and how to optimize them? Or is it the more functional medicine approach of reducing histamine intake and adding mast cell stabilizers and antihistamines? Or is it a combination of both of those things?

[01:08:28] DR. HAUSMAN-COHEN: A little bit of a combination. But I do want – there's a lot of urban legend out there again regarding mast cell, all of these different pathways. Because, again, there's people in the genomics realm that have these theories or that they've compared databases that don't make sense. They'll compare a group of people that have had genomics that have Lyme or mast cell to using 23andMe, which is a non-standardized database and not know if the genes are even clinically significant or even accurate. And then compare it to 10,000 genomes, which is a completely different population and go, "Oh, this must be significant."

But I think in terms of the other urban legend with histamine, is that the histamine intake genes that the genes that relate to histamine intolerance in the gut and the histamine to mast cell, that they're highly related. And they're really different pathways. People who have gut histamine intolerance, that's completely different than mast cell activation pathways. And the solution for them is make sure your gut barrier is good. Make sure you use glutamine so you're not having diarrhea. Try to lower the high histamine foods. Maybe take the enzyme, the DAO, diamine oxidase, when eating high histamine foods.

And then with the mast cells in the blood and in the brain, because, again, the gut is different than the blood, which is different than the brain, there are other genes. And there's some that relate to certain vitamin D receptors that can activate mast cells. And there's some that are different interleukins. And so, it depends on what the underlying etiology is.

For vitamin D receptors, we can go back to that sulforaphane. There's a particular vitamin D receptor that relates to mast cell activation. Not all of them. That's a vitamin D receptor variant. And sulforaphane and resveratrol upregulate, so you transcribe more vitamin D receptors. But if you're having more interleukin-4 and other – there's a whole bunch of interleukins that relate to mast cell. Then it might be something more like quercetin. Or drug-wise, you might benefit from something like a ketotifen. It just depends on the etiology.

But again, if you feel like you're having mast cell activation, general basics, if you don't have your genomics, make sure your gut is good. If after you're eating certain foods you're getting diarrhea, you get this kind of intermittent diarrhea, that's kind of a potential that you might have histamine intolerance. If your gut gets bad and you have histamine intolerance, then you can start to have the lower blood pressure, or the flushing, or other symptoms.

If you're having other kinds of mast cell issues, quercetin is good. It's also good for gut because it's a direct inhibitor of histamine release or isoquercetin. For food sensitivities, quail egg protein. There's a lot of things we can do. And I think that if you don't know what your etiology is, I would probably say your number one thing for stabilizing mast cells is quercetin plus or minus the quail like protein.

[01:11:24] SCOTT: And for people listening, the quail egg protein I'm assuming is the Integrative Therapeutics AllQlear product?

[01:11:30] DR. HAUSMAN-COHEN: Correct. That's the one that we use.

[01:11:31] SCOTT: Great. In both chronic Lyme disease and mold illness, there's often an immune dysregulation, a lack of immune tolerance where the immune system or immune response is overactive, hyper-vigilant, autoimmune. How much of a role do genetic SNPs play in one's potential to develop autoimmunity?

[01:11:51] DR. HAUSMAN-COHEN: Quite a lot. And one of the fun things to talk about is – everybody knows that celiac is a big risk for autoimmune and that gluten. And that's partially because gluten directly increases zonulin levels. And so, again, for any listeners who aren't familiar with zonulin, your gut cells are kind of like your hands. And if you were to put your hands, fold your thumbs in, put your hands together the gut cells kind of look – Like, you should do it that way. Like, your hands stuck together. And the fingers would be the villi. And they're supposed to be this triple filtration system so that you break down your protein to amino acids. You break down your carbohydrates to carbonic acids. And you only put these very basic building blocks into your blood.

But if your gut permeability gets messed up and if you don't – if you make too much zonulin or you damage your gut, then it's kind of like you have your triple filtration system. So, you've got a screen door but the window is open. You have space between the cells and all the junk can go into your bloodstream. And that just starts triggering all kinds of antibodies.

And so, autoimmune disease, one of the biggest factors is gut permeability. Again, histamine can contribute to that. But even more so, gluten contributes to it. But TNF alpha, which is one of the particular kinds of inflammation, is another – and again, it's not every TNF alpha SNP. But some of the TNF alpha SNPs, the ones that regulate gut stuff, can also affect autoimmune disease.

And if you think about late night TV, ask your doctor about this drug. Tons of those drugs that are autoimmune disease drugs. That's why we're having so much more rheumatoid arthritis, and psoriatic arthritis, and MS because we're triggering – our guts are not in good shape partially because of exposure to glyphosates. That's a very big factor for gut permeability. Partially because of other things in our diet. And the TNF alpha particular snip that has been associated with more autoimmune disease is right in the middle of the HLA 2.5 gene. Right in the middle of the big main celiac gene. That's kind of interesting to me.

Yeah, if you have all autoimmune disease, you really want to do everything you can to control gut permeability because I think that's probably one of the number one factors for autoimmune disease. And then, I also think that mold is another factor that you've got to control.

[01:14:23] SCOTT: I agree. And I would even say that mold is also a factor that impacts intestinal hyperpermeability as well, mold mycotoxins, that whole piece. I know Dr. Ann Corson says that mycotoxins in the gut are like throwing sparks on a silk scarf.

[01:14:39] DR. HAUSMAN-COHEN: Yeah, yeah. I think that, absolutely, that mycotoxins, it's another issue. And again, why do we have more mold related illness? Because people have air conditionings now. And air conditioning condensers, if they're not watched carefully, they can kind of condense moisture. And in the air conditioning closet, people can get mold. You get this drywall, that if it gets wet because you have a flood, because something – floods because of a roof leak or any kind of a leak that grows mold in it. And people used to have houses where it was different materials and then the windows were open and they just weren't as prone to growing mold.

[01:15:17] SCOTT: And my mentor, Dr. Klinghardt, is going to argue that the EMF exposures we have now in our homes actually make the mold problem worse as well, which probably is also another factor that's new to our modern times.

I want to come back to the vascular conversation just for a moment. Looking at how genetics might impact vascular health, the production of nitric oxide. And then the question that I've always kind of had in the nitric oxide conversation is how do we know when increasing nitric oxide, there's lots of supplements and other things that suggest they can help there? How do we know when that might be health-promoting versus it starts to lead to the production of peroxynitrite, which then becomes health-negating?

[01:16:02] DR. HAUSMAN-COHEN: I think that there's three different kinds of nitric oxide production. And this is really an important factor. What we want is, inside the lining of the blood vessels, we want the production of endothelial nitric oxide. because when you have too little nitric oxide in the lining inside of blood vessels, the blood vessels get too tight. And so, if you increase endothelial nitric oxide, that tends to generally be health-promoting. And low endothelial nitric oxide is associated with things like brain ischemia, heart disease, erectile dysfunction. That one's good.

Now, the one that's not so good is iNOS, inducible nitric oxide. That's in response to – like, in response to a traumatic brain injury, you're going to have more problems with getting inducible nitric oxide. And that can be a negative factor because it can lead to more peroxynitrite. It can relate to more inflammation. Again, it's about we want to promote endothelial. Not inducible.

[01:17:10] SCOTT: Or some other tools then that are available. You know, Neo40 and others. There's a lot of them coming on the market that are talking about increasing nitric oxide. Are those then more focused on the health-promoting endothelial nitric oxide? Or do they still –

[01:17:25] DR. HAUSMAN-COHEN: Absolutely. Yeah, absolutely.

[01:17:26] SCOTT: So, they don't have the same potential to create the peroxynitrite.

[01:17:30] DR. HAUSMAN-COHEN: Correct. And that's an important piece of science. The resveratrol. And there's a new resveratrol that's a piceid resveratrol that lasts 12 hours. That's great. It induces nitric oxide 70%. That's called VINIA. There's Neo40, which is a beet – Yes. Yeah. Yeah.

[01:17:50] SCOTT: You told me about that one in our last conversation. I just got a bottle.

[01:17:53] DR. HAUSMAN-COHEN: Yeah, I loved it because the company's doing real research. They're showing that you actually increase the nitric oxide production. And whenever we have companies that are – and there's a lot of great companies, the supplements out there that are putting the money into the research. And you want to use things that have evidence-based because we don't have regulation of our supplements.

Neo40 is another good nitric oxide producing product. It's made here in Austin. I met the owners at a conference once. But it is made from beets. Eating beets is great. So, I teach my patients that have poor endothelial nitric oxide production how to make soups with beets and all kinds of things. Use the Trader Joe already peeled beets. There's also Pycnogenol, is another great inducer of endothelial nitric oxide. Again, you have to just know which ones help which kind of nitric oxide.

[01:18:45] SCOTT: Hypermobility syndromes, Ehlers-Danlos Syndrome, they seem to be becoming more and more common. There can be this more genetic form of EDS. But then there can also be these secondary EDSs where things like Bartonella, or glyphosate, or maybe mold exposure, other factors are playing a role. And maybe those secondary triggers are then epigenetic influencers of some of the gene expressions. I'm wondering what your thoughts are on hypermobility syndromes, Ehlers-Danlos and the potential role of genetic expression in those conditions?

[01:19:22] DR. HAUSMAN-COHEN: Yeah. There are some genes that are pathogenic genes for a form of Ehlers-Danlos, very, very rare. I have never had a patient that has one of the pathogenic ones that affects the heart blood vessels come up on any testing I've done. You have to do that kind of testing through a lab like Invitae, where it's looking for the pathogenic genes.

And you're absolutely right. The number of people with hypermobility syndrome has increased. I don't think we fully understand all the causes. But the one that I do think that you mentioned that's worth highlighting is Bartonella. Dr. Bob Mozayeni, who was previously the president of ILADS, the International Lyme and Associated Disease Society. He did a paper years ago, he was a rheumatologist for the NIH, showing that Bartonella can be a great mimicker for rheumatological disease and cause hypermobility.

Anyone out there who has hypermobility that maybe has some funny stretch marks or remembers maybe they got some swollen lymph nodes one time. Maybe they got scratched by a cat, but it also could be from tick bites. There are also other animals that can carry it. They need to think about bartonella. The problem with bartonella is it's super hard to identify. It's not always in the blood. So, it's hard to test for sometimes. That's a whole other story.

The story is still young with the genomics of Ehlers-Danlos. What is the role of mold on connective tissue? There are so many things that affect connective tissue tone, even vitamin C. It is something that people ask me all the time. They say, "Sharon, when is IntellxxDNA going to have a hypermobility pathway?" And I'm like, "We first have to finish our traumatic brain injury, and our mast cell, and all those others."

And every single one, every time we take on a SNP or a topic, it takes hundreds of hours of research to not only go what SNPs are clinically significant. But figure out how do they work? Is there anything in the literature that we can modulate? No time soon.

[01:21:23] SCOTT: Yeah, there could be some very interesting things you could unravel though. Because unfortunately those conditions I find that they are – that the Ehlers-Danlos syndrome, I find that it is a challenging condition for people and there isn't always there – there're things that can improve it but it isn't always fully resolved. And so, it would be interesting to see what other insights you arrive at when you do start digging into it.

[01:21:47] DR. HAUSMAN-COHEN: Yes. And I encourage other people, other scientists, if they have any breakthroughs or insights. I think one of the things is, with IntellxxDNA, we have a user community and we try to share insights. Because I have some really well-known, great doctors across the country that have been working on these problems that are Lyme specialists, or mold specialists, or brain specialists. And it's great because we all kind of share our insights. And that makes the work stronger. If anyone ever finds good breakthroughs that they think are helpful of understanding some of the more, I would say, acquired hypermobility, I would love to hear about it.

[01:22:27] SCOTT: I wanted to get a few of your thoughts on the role of genes in iron and copper regulation. I would say most people tend to think of iron deficiency and copper toxicity. But there are voices in the community that think more about iron toxicity and copper deficiency. And so, what are your thoughts on that iron-copper regulation? Do genetics play a role? And I know in some cases people even explore things like therapeutic phlebotomy in order to bring down their iron. What are your thoughts on iron and copper?

[01:23:01] DR. HAUSMAN-COHEN: Iron, absolutely, can be iron toxicity. And hemochromatosis, HFE carriers, that is a well-known gene. People who overstore iron, it can get stored in their pancreas, in their joints. And that's something that most – I mean, even 23andMe has that gene, that gene variant.

And so, if you have a gene variant that is the main gene variant for hemochromatosis carrier and you are a man, one copy of it won't necessarily cause hemochromatosis in terms of fulminant disease. But it will help make you store iron if you have an iron-rich diet.

And so, if you're having joint pains, if you're having diabetes, if you have low hypogonadism and low testosterone, and again, you don't have access to your genetics to be able to see if you might be a carrier for that gene, it is worth checking. Because too high of iron stores is bad. With women, it tends to not be a problem until they're post-menopausal.

Now, there are other genes that relate to autism that have to do with iron going in the wrong places. Iron metabolism is a little bit complex. And that's a little more difficult because again you'd have to look at genomics for that.

With regards to copper metabolism, the things I tell people to be aware of is you hang onto your copper a lot longer. Children can have problems with low copper sometimes. And adults have more problems with high copper, particularly women on birth control pills. Because birth control pills will make along with – and it also has of course to do with SNPs. But birth control pills interact with certain SNPs.

And I had one patient where her copper – you want copper usually to be about less than 1200 or less than 120 from a cognition standpoint depending on what scale you're using. And hers was like 1600, 1800. We could not get it under control until we ultimately had to switch her to a different form of birth control.

Low copper is a little more tricky in adult because it may be that they have a problem with their copper-carrying protein ceruloplasmin. Can't teach all the medicine here. But those are just things to think about if you're having problems with that.

[01:25:17] SCOTT: I mentioned EMFs earlier. There are many people that are dealing with sensitivity to EMFs. But then the more extreme electromagnetic hypersensitivity syndrome in some cases. How much do you find that one's reaction to EMF and the environment correlates to specific genes or gene SNPs?

[01:25:37] DR. HAUSMAN-COHEN: Yeah. There have been studies showing that there are some specific gene SNPs, some specific calcium channel SNPs, that make people more prone to EMFs. And the most exciting thing for me regarding EMFs was that I was at a conference, an Age Management Medicine Conference, and they had a physician from I think the University of Washington, completely classically-trained physician, talking about his research with EMFs. And that was just amazing that it's gotten into the regular university setting and is not just those of us in the functional integrative world.

The EMF understanding is still again at the infant stages. But there are people – if you think of calcium regulation, as calcium is excitatory. Calcium can make people get more glutamate. Calcium can make things – think about calcium and high blood pressure. Some of the medicines we use for high blood pressure are calcium channel blockers. If you have too much calcium flying around, EMFs can affect how we electrically send signals via calcium in our body. And that is amazing.

And I have had many patients who realized that they need to turn off their router at night. They needed to move the cellphones farther from them. And it's not everybody. But I think that Jason Mraz had a song about the EMF towers and how the landscape is changing. And he's a big environmentalist. And I think we need to be kind of thoughtful about do we put all these cellphone farm towers right next to preschools and right next to where anybody is? And so, we're just going to have to be a little more open-minded as we move forward in the world if we want this world to be a safe place for our children and grandchildren about being open to studying the consequences of our actions.

[01:27:35] SCOTT: Yeah, sadly, I just moved to Denver a few months ago and was walking near a park. And there was a school with the playground. And literally right next to the playground was the new 5G cell tower. And I thought, "Of all the places you could put it, that probably isn't the best."

I want to come back to the long COVID conversation and wonder – you mentioned some of the vascular issues, some of the oxygen issues. But are there any genetic patterns or fingerprints that you identify in those people that don't seem to recover from COVID infection and go on to have long COVID? And then do you anticipate that COVID will increase the prevalence of cognitive decline in the future?

[01:28:16] DR. HAUSMAN-COHEN: So, we have seen – if you look in the literature and you just kind of Google cognitive decline incidents in the last few years and since COVID, absolutely, the incidence has increased. And as I kind of alluded to before. To me, it appears that one of the biggest factors from what I'm seeing not just from genetics, but from blood work, is that we know that both COVID and the COVID vaccine increase fibrinogen levels in people that are particularly susceptible.

One of the things, I actually had this hypothesis couple years ago because of genetics. Somebody who came to me and got horrible brain fog after COVID. I looked at his genetics. He happened to have something in the factor five pathway, which is a known hypercoagulable gene. And I started to go, "Hmm, I wonder if part of the brain fog in COVID is due to the hypercoagulability?"

I gave him lumbrokinase and pycnogenol. I kind of upped the doses of that. And within days – I mean, we did a CNS vitals before and a CNS vitals afterwards. We kind of knew that we were on the right track with addressing this. Within days, his kind of brain fog was better. We just started empirically doing this because you don't have time to get genetics when someone calls you and they have brain fog after COVID. There's no harm in trying.

And so, we then started measuring. And we had been watching fibrinogen. Watching some of the genomics. I don't think there's any one gene SNP that I have correlated to these are the people who have the most significant long-haul COVID. I think there's a couple of different categories. And I think it's people who are genetically prone to making more fibrinogen. That's a big factor. It also can be a factor towards pain, people with chronic pain.

And then there's another kind of fact of long-haul COVID with more of the inflammatory pathways. And for people who have some of that more aggressive inflammation will tend to use more resolvins. But I think that there's a lot of work out there. And of course, there are different tools for evaluating long-haul COVID. And they'll look at like interleukin-8 has been one that's been popular in the discussion. But IL-8 will trigger more fibrinogen. That's why there's not any one gene because there's a lot of genes that then can lead to different pathways.

[01:30:42] SCOTT: I want to talk a little bit about oxidative stress, about reactive oxygen species. We know with infections that sometimes we need that oxidative burst. We also know that we can have too much oxidative stress. And sometimes we then need antioxidants. However, antioxidants in some cases, if you take too many of them, also have some negative implications. How do we support a balanced redox response in the body? And how much of that is tied to genetics?

[01:31:12] DR. HAUSMAN-COHEN: Again, this is again an exposure thing, an exposome versus a genetics. And it's a combination. Oxidative stress, if you think about what we use for energy, we're using oxygen for energy. The mitochondria in our bodies take oxygen. They turn it into ATP. Think of oxidative stress like nuclear waste. If you are going to make nuclear power, you're going to have nuclear waste. If you're going to make oxygen-supplied power, like ATP, you're going to have oxidative waste.

And the question is how do we get appropriately rid of it? And is there too much of a good thing? Can we over get rid of oxidative waste? And the answer would be, yes, I do think we have to be a little bit cautious regarding that. Because oxidation and oxidative stress is also part of how we use things like myeloperoxidase, it's involved in how neutrophils kill bacteria. It's involved in how we fight off cancer cells.

There're a lot of different pieces of the puzzle. But if you have somebody that you know genetically has problems with some of the oxidative stress pathways, supporting them can be very important. CoQ10 – We really have a number of antioxidants, but CoQ10 is one of the master antioxidants.

If you genetically see that somebody's bad at synthesizing or recycling CoQ10, they're going to need a little extra support. You're not going to overdo it in someone like that because you're not getting rid of all their oxidative stress. You're just giving them one of the natural factors that can fight oxidative stress that they don't make enough of.

Other ones that are antioxidants are vitamin E, vitamin C. Glutathione is an antioxidant. And so, I think that that's where genomics comes in handy because you don't want to – glutathione peroxidase is another one that is kind of glutathione, but kind of other pathways. You don't want to just take vitamin E, take Vitamin C, take this, take that.

In fact, we've seen some studies that too much of certain antioxidants can be a negative. Using genomics to kind of go, "Okay, this person doesn't naturally recycle their vitamin C. So, I'm going to have them get a little bit more from diet or from the supplements. This person doesn't naturally recycle their CoQ10 or make it. We're going to give them more." And then you pair that with what's going on people.

With heart failure, for example, there's a lot of evidence for CoQ10 in the literature. People with autism, there's evidence. People with cognitive decline. If you see that they're also not good at making it, of course it makes sense to support it.

I like being a family physician because I don't need a lot of certainty in life. I like using hypothesis and then combining what I'm seeing going on in the human along with the genetics. But I would tell anyone entering the field of genetics, if you're dealing with humans, you have to just kind of be able to use as much factual information as you can get. But there's also a little bit of an art still to being a clinician and going, "Well, what's going on with that patient?"

But in general, if you're using targeted antioxidants that affect specific pathways, I don't think at the normal doses that you would give supplements. You're going to be overdoing it with the one exception. If you have a patient that's fighting cancer, you need to be very, very thoughtful and generally not give extra antioxidants because you can impair how chemotherapy works.

[01:34:47] SCOTT: You mentioned ATP. You mentioned mitochondria. I'm wondering how much of a role genes play in our ability to produce that energy currency, that ATP, and in the health of the mitochondria, the mitophagy, the recycling janitorial process, autophagy? How much of that arena is impacted by our genetic SNPs or gene SNPs?

[01:35:10] DR. HAUSMAN-COHEN: Yes, it is genetic SNPs. But there are again – this is a field where there's a quite a bit of conjecture. I won't necessarily say urban legend, but conjecture. There, again, are people out there saying, "Okay, the mTOR pathways are super important. And you've got to look at someone's mTOR SNPs." And mTOR is one of the autophagy pathways.

But then when you look at the SNPs in mTOR that are not pathogenic, because mTOR is so important. It's an autophagy gene. Generally, if somebody has a significant variant in it, they've got problems at birth. They'll have seizures, or failure to thrive, or bad things happened at birth. And so, you can't just go, "Well, this is an important pathway," so that somebody has variants when I pull up 23andMe or when I pull up this DNA report. That must be that there are problems with autophagy. You still have to use the literature.

And fortunately, most of these most important pathways, so far, there's very few people that have clinically significant SNPs because they're so important. But on the other hand, where we do see a lot of problems is mitochondrial repair. Mitochondrial membrane genes. And so, I think that the other thing to realize about mitochondria is they have their own set of genes. And that science is even more in its infancy than human genomics because they've got about 25 of their own genes and we don't know how to address them all.

What I would say when you're addressing mitochondria, partially think about mitochondrial factors in somebody who is fatigued, somebody who's got unexplained neuropathic type symptoms, somebody, again, with neurodevelopmental issues. But sometimes, for mitochondria, you really want to pair. Or most of the time, if you're trying to evaluate mitochondria, you're going to want to consider doing urine organic acid testing because that's a good way to get some of the mitochondrial by-products. You're going to want to think about nutrient pathways that support mitochondria, like carnitine. You're going to want to think about the outer membrane, which you can get at with genetics.

And just again, I like to – again, because I'm a scientist. I like to encourage people to go to ask. If you're thinking of doing something, whether it's thinking of using a supplement, whether you're thinking of using a genomics product, ask and say, "Tell me. Show me the literature."

And I know you've been involved in a lot of areas of research with supplements and different things. And you know that there is good literature out there. If someone's going, "I think that this person has mitochondrial problems," and maybe they wanted to try to prove it. And then maybe they showed that they're having it because of their urine organic acid testing. Know that there's good mitochondrial research for anti-lipid factor, for things like ATP Fuel. There're so many products that have evidence that to just go, "Oh, I'm going to address mTOR with rapamycin." There are some longevity studies that are looking at that pathway but it's not necessarily SNP specific. Does that make sense?

[01:38:24] SCOTT: Absolutely. NT Factor Energy, ATP Fuel, for people listening, those are from Research Nutritionals I believe is who you're referring to?

[01:38:31] DR. HAUSMAN-COHEN: Yeah. NT lipid factor, the work was developed by Garth Nicolson in trying to help people after they had chemotherapy. He was at MD Anderson. And NT lipid factors also in some products by Allergy Research. ATP Fuel has it in it. And then there's an ATP 360. And that's Research Nutritionals. And that's specific – yeah, those are kind of specific products where they put stuff for the outer membrane and mitochondrial factors in the same pill.

[01:38:59] SCOTT: And Dr. Nicolson, I was fortunate to have him as a prior podcast guest as well. We primarily talked about his work with mycoplasma, but certainly has contributed a lot.

My last question before we get into a couple of short wrap-up questions is are there certain people that are more genetically prone to have bad reactions to anesthesia? And in those cases, can we optimize their gene expression to create better tolerance? Or is avoidance the solution? And then how does anesthesia potentially impact our mitochondrial function?

[01:39:30] DR. HAUSMAN-COHEN: Yeah, the answer to that is, yes, there are absolutely genes involved in how you tolerate anesthesia. The main hack for that is to know about it so that you can let your anesthesiologist know. Because if you have problems tolerating the deep anesthesia, the succinylcholine and things like that, and you get it anyway, which would be a major surgery like a heart surgery, or an abdominal surgery, even a hysterectomy, it's going to take you anywhere from an hour and a half, to four hours, or six hours longer before you can be extubated. And nobody wants to be under anesthesia thinking they're going for a 90-minute surgery and then be there for five hours intubated. Knowing your genomics is most powerful.

With things that relate to the genomics of propofol, which is what they use for colonoscopies, it's really, again, just tell them to use less and let them – because if you take less or take longer to metabolize it. But those pathways also can relate to how you affect pesticides. Pesticides are also cholinesterase inhibitors. If you're the kind of person and you're like, "Gosh! I'm around ant spray or pesticides and I feel like my throat's funny and I feel off." You might have a problem with your anesthesia pathways.

The tie-in with mitochondrion anesthesia is also the same time as mold. Molds can have a negative effect on mitochondria. Anesthesia can have a negative effect on mitochondria. But the things that affect your mitochondria are the three As; anesthesia, aging, and antibiotics. And one of them, aging, there's not a lot to do about. Well, there are things. We're both trying to do things for healthy aging.

It's possible that somebody was like, "Well, why did I start having this problem? I don't have diabetes. Why am I starting to have kind of numbness and tingling and neuropathy type symptoms?" That's a common presentation of mild mitochondrial issues. "And I am in my 40s or 50s. How come I didn't have it when I was 15?" Well, you have a lot more mitochondria when you're younger. Even if they're not perfect, you have four times more than when you're older.

[01:41:38] SCOTT: Yeah. And unfortunately, the antibiotic piece, that's been a big challenge in the Lyme disease arena. I know back when I was diagnosed with Lyme in 2005, we didn't have any of these tools beyond antibiotics. And so, while I'm not completely against them, I was on them for three and a half years, all different kinds, IV, oral. I would not personally use that exact same path again given that we have lots of new tools and new understandings. But the impact to the mitochondria is probably one thing that we don't often consider.

[01:42:09] DR. HAUSMAN-COHEN: Yeah.

[01:42:10] SCOTT: Talk to us about IntellxxDNA. What you offer? How people can learn more about potentially working with their practitioner to incorporate the work that you do into their health program?

[01:42:21] DR. HAUSMAN-COHEN: Yeah. IntellxxDNA, the best place to get more information about it, if you're interested as a patient and having it done, is to go to the website. And it is a little bit tricky of the spelling. It's I-N-T-E-L-L. Like, from intelligent. And then two “x”s. And then DNA. So, IntellxxDNA.com. Or if you Google “Sharon Hausman-Cohen genomics”, that might come up as well.

[01:42:45] SCOTT: I'll put it in the show notes.

[01:42:47] DR. HAUSMAN-COHEN: Yeah, and we'll have it – but IntellxxDNA, because it gives so much information, is considered a clinical decision support tool. It's not available to people who are not licensed healthcare professionals. You do need to work with your nurse practitioner, your naturopath, your physician. Somebody who has training both in medicine and in IntellxxDNA. If you have an integrative or functional medicine provider and they're not trained, we are happy to get them trained. Tell them to reach out to us and we will walk them through their first three reports. We have great online training. And we will get them trained so that they get the best results they can even on their first report.

But if you also just want a list of physicians and clinicians that are already trained, we can get that for patients. They can put in on our website their city or town and we can get the people licensed in their state.

I also, people wanting to learn more, encourage them to look at our publications, webinars, podcasts and reach out. But we are a smaller company. Have been around since 2016. But a lot of people haven't heard of us. But we're a powerful tool that we know we're getting results. And we would love to help people untangle not only their medical Mysteries. But just kind of get themselves a road map for better health.

[01:44:10] SCOTT: Beautiful. My last question is the same for every guest, and that is what are some of the key things that you do on a daily basis in support of your own health?

[01:44:18] DR. HAUSMAN-COHEN: I am somebody who has to exercise. I definitely, just like everybody else in our office and every clinician that's using IntellxxDNA, I have changed what I do based on my own genomics because I wish we got a free pass for being physicians on perfect health. But there's things in my family history that I want to avoid.

And so, for me, I do try to make sure that I give myself that exercise prescription meaning. Meaning I'd go into work later a couple days a week and on weekends so I get my intense exercise, because BDNF is important for me. That growth factor. And it's really important for brain health, but it also is important for mood.

I do take some supplements. I take some that are anti-inflammatory. I take some that – things like vitamin D with vitamin K2 that have cardiac and other benefits. But I think that the other thing that we can't underestimate is the power of food. And if you look at how I ate when I was a resident in medical school and how I eat now, it's different.

And I spent a lot of time in my practice teaching patients how to cook for their DNA. And in our IntellxxDNA reports, we actually have a whole set of handouts. Not just supplements that can work for different genes, but foods. And so, I use my genomics in kind of planning my meals.

And for most people, again, if you don't have access to genomics, lots of plants are going to be beneficial. Because in general, your protein and fats, those are kind of the animals. But your micronutrients that support your genome, most of those come from plants. I do try to eat mostly plant-based. I still absolutely eat animals. But I still have well more than 50% of my diet come from plants. I think that's quite helpful.

[01:46:10] SCOTT: Beautiful. This has been such a fun conversation. I love the path that you're leading for all of us that are dealing with complex chronic conditions. I'm excited to see where this continues to lead, and evolve, and other connections that you make. I know you've already made a number of connections in conditions like Alzheimer's. But as you continue to explore this, I think a lot of exciting insights will emerge. So, thank you so much for being here, for being generous with your time, sharing your wisdom, and just incredible knowledge that you have brought to the table today. And I just want to honor you and thank you so much, Dr. Sharon. So, thanks for being here.

[01:46:44] DR. HAUSMAN-COHEN: Thank you for having me. I appreciate it.


[01:46:47] SCOTT: To learn more about today's guest, visit IntellxxDNA.com. That's IntellxxDNA.com. IntellxxDNA.com.

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