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Episode 6 – Your DNA is Not Your Destiny with Sharon Hausman-Cohen, MD, FAAFP, ABOIHM – IntellxxDNA and Dr. Craig Tanio, MD, FACP, IFMCP

Podcast The Rezilir Way

Hosted By:

Show Notes

In this episode of The Rezilir Way hosted by Jacob Gordon, Dr. Sharon Hausman-Cohen joins Dr. Craig Tanio to discuss using genomics testing to merge science and practicing medicine to help patients battle cognitive decline. Promoting the understanding of how various genes and pathways can affect every part of the body, especially the brain, has led to personalized medicine and targeted protocols that can impact and improve patient care and assist patients in achieving optimized health and wellness.

(1:07) Background of the beginning and development of an interest in genomics. Building a company that can help physicians untangle diseases on a genomic level. Collaboration with other integrative functional clinicians to get a broader understanding of genomics to help more individuals.

(3:53) DNA Snips and what they are and how they can change how genes work.

(5:00) Genetics, genomics, and the difference between the two.

(6:27) What Intellxx DNA looks for, and how those things make differences in various health situations. The importance of focusing on clinically significant and evidence-based science and combining the art of practicing medicine with science.

(8:20) A passion for genomics, especially related to the brain. Typical Intellxx Reports and the Snips that are available.

(10:39) How physicians who are trying to practice precision medicine should think about genomics. DNA is not destiny. Knowing a patient’s genomics to help create precision medical and nutritional recommendations that can streamline a patient’s care.

(17:28) Using genomics testing as a tool that can give clues to a patient’s health. Genes that provide insights that biomarkers cannot. The blood-brain and blood-gut barrier. DNA expression.

(22:17) The most important genes for cognition. APOE4 – the Alzheimer’s gene, and the difference between APOE and APOE4.

(29:33) Hippocampal sclerosis and atrophy. How genomics can help distinguish between Alzheimer’s and other cognitive disorders or issues that can impact your brain’s overall health.

(33:55) Toxin and infection exposures at a young age and pathways that are involved in cognitive issues that are not related to Alzheimer’s. Detoxification pathways and the effects on the body.

(39:58) Vascular issues that drive cognitive impairment.

(46:14) How genomics can help unpack what’s happening in the mitochondria and figure out how to treat it better.

(50:04) Inflammatory pathways and using genes to be precise about the types of inflammation that is occurring to understand what is happening.

(55:40) Using genomics to create an encyclopedia of the body and managing the new evidence that comes in.

(1:00:15) The social responsibility of understanding how to use genomics, and the Mental Wellness report and the focus on supporting the brain.

(1:02:15) Where to learn more about Intellxx DNA testing, and how to contact Intellxx.

Transcript

Sharon Hausman-Cohen:

Even if the person’s coming to them for brain, they’re still going to look at heart, and blood sugar, and all these other things, iron storage. It affects your body, and your brain’s part of your body. When we gave her mitochondrial supplements, it was like a little over a month later, came back walking in our office with a cane instead of a wheelchair.

Jacob Gordon:

Hey guys, welcome to The Rezilir Way with Jacob Gordon. I’m your host, Jacob, and I’m so excited for you to be here today. In today’s episode, we have a very special guest. We have Dr. Sharon Hausman-Cohen of IntellxxDNA. She’s been using genomics for over a decade to deliver personalized medicine and help her patients achieve optimal health and wellness. In today’s episode, we’ll be talking about the basics of genomics, and overall, the pathways in your genes that could lead to decreased cognitive performance. What genomics can tell us that biomarkers can not provide and much, much more. I hope you guys stick around until the end of the episode, because you’re not going to want to miss this. Without further ado let’s get started. All right, Sharon, thank you for coming on the show.

Sharon Hausman-Cohen:

Thank you so much for having me

Jacob Gordon:

Now we want to know a little bit more about you and how you got into genomics. What is your background and what got you started on this path of genomics?

Sharon Hausman-Cohen:

I would actually say that I got started on genomics without even knowing it when I was in high school and was an exchange student to Japan. I was living with a family where the mother was a nutritionist, and it got me interested in things like, how does green tea work? Because she would take me to the market and say, “Oh, this has really good benefits for inflammation, and this is really good for your health.” Then when I was a college student, I was interested in how things worked, and so I ended up doing research in genetics.

Sharon Hausman-Cohen:

At that time, it was cancer genetics that was what the lab I worked with was looking at. Then when I became a physician, I was interested in genetics because we had the revolution where we were sequencing, not me personally, but people were sequencing the human genome, and people, ultimately, once genomics became available and more popular, would come to me and say, “Can you use my genes in order to help me to figure out why there’s Alzheimer’s in my family, or why there’s heart disease?” I thought about it and I started digging into it. My personal interest had been the mechanisms of how different supplements worked. What I realized is we really could use genomics if we went down to the level of, how do genes work and how we can modify them? We could really use genomics to help untangle some of these diseases, but then there wasn’t anything for physicians to use that gave them that knowledge, so I started to build it.

Jacob Gordon:

How did that company grow into what it is today?

Sharon Hausman-Cohen:

Well, initially, I was building this genomics tool for my patients. I have, at this point in my life, a small practice, whereas part of my practice, I do research for my patients. When I realized it would take me sometimes dozens of hours for one little snip, one little piece of a gene, and hundreds and hundreds of hours just to do something like figure out heart disease, I realized that this did not make sense for me to do on my own and so I decided that I needed to do it as a collaborative and do it as a product, or something that I could share with my fellow integrative and functional medicine-trained clinicians.

Sharon Hausman-Cohen:

Because again, to do it for one patient, doesn’t make sense. That’s why we eventually worked with other people and decided to make it into a company of something that other people could access, not just my practice.

Jacob Gordon:

That’s great. You mentioned the term, a snip. Could you explain what that is so our listeners know?

Sharon Hausman-Cohen:

Absolutely. A snip sounds like it should be a little piece of cloth.

Jacob Gordon:

Right, yeah.

Sharon Hausman-Cohen:

But it actually stands for a single nucleotide polymorphism. DNA is made up of what are called base pairs, but they’re symbolized by letters, so A, and T, and C, and G. A snip is when you get a tiny little change in your DNA, so it’s like changing an A to a C, or a G, to a T, or whatever. These little changes in your DNA can have subtle changes in how a gene works, or sometimes bigger changes.

Jacob Gordon:

What are some examples of little changes, like eye color, or the way that you would make a protein?

Sharon Hausman-Cohen:

Right, exactly. Whether you have blue eyes or brown eyes would be something simple, but it also, on a medical level might be, are you able to carry B12 efficiently into your brain, or are you able to make vitamin D from the sun, or does that reaction not work very efficiently for your skin?

Jacob Gordon:

Oh, wow. I know those are a few things that we’ll get into a little bit later in this episode. I want to talk a little bit about and ask you what the difference between the term genetics and the term genomics is. We hear genetics all the time, and sometimes interchangeably used as genomics. I know that could be incorrect.

Sharon Hausman-Cohen:

I think that’s a great question, but genetics is technically the science of how we inherit traits, so things that … You get genes and people think of, you get, okay, I got this from my mom. I got this from my dad. When people talk about genetic diseases, they’re generally talking about diseases that can be mapped to one gene, something that can go wrong, and if your mother had it, you get it. It’s things like Tay-Sachs, cystic fibrosis. That one’s recessive, meaning, if both parents had a gene for it, then the child can have it. Things like down syndrome is a genetic disease, a big chunk of DNA, or a whole chromosome that gets duplicated so you have three copies of it.

Sharon Hausman-Cohen:

Genetic diseases tend to refer to inherited diseases. Genomics, because we’re talking mostly about the science of those little one letter changes refers to components of diseases. There’s not one gene that causes heart disease, or Alzheimer’s, or diabetes, or obesity. It’s the combination of lots of these little teeny changes along with environment, lifestyle, what you eat.

Jacob Gordon:

With IntellxxDNA, you’re looking at those little differences along the chromosomes?

Sharon Hausman-Cohen:

Absolutely. One of the things is, not only we’re looking at the little differences, we’re looking at the little differences that in the published medical literature have been shown to make differences in various health situations, or various disease risks, because there’s lots of changes that don’t matter at all. If you think about your DNA as a big, long recipe, a recipe for a protein, that’s going to, again, carry that B12, or carry a hormone, or create certain reactions, and there’s lots of words in that recipe, if you change a recipe from blend to stir, no difference. You’re just not going to notice anything about the end product.

Sharon Hausman-Cohen:

But if you change a recipe from bake to broil, that’s a big difference. IntellxxDNA looks at snips, but only ones that are clinically significant with published literature supporting them as being important.

Jacob Gordon:

Great. I love that you’re using published literature, and so it’s science-based there.

Sharon Hausman-Cohen:

Yeah. I didn’t really say it at the beginning, but I initially was going to do a PhD in medicine, and I went to Harvard to do a PhD and I was studying the neurodevelopment of the brain. For me, having something that’s evidence-based was really important because I was a scientist first and then became a physician. I think that most of us as physicians really want to wed the art of practicing medicine with the science. I felt that genomics had been really left to consumers that didn’t have always the science to filter through everything, so that’s been really important in IntellxxDNA, that it’s a clinical decision support tool. It’s meant to be clinically relevant with science backing every sentence.

Jacob Gordon:

That’s great. Is your passion in this more towards the brain health side of things, or the cardiovascular side of things, or is it all genetics and genomics?

Sharon Hausman-Cohen:

I have a lot of passions. That’s why I left graduate school and went to medical school because I was not a one type of topic person, but my strongest passion has really been things relating to the brain. So, we do a lot with cognition, with mental wellness, children with neurodevelopmental issues is another topic that we’re working on now. But what we realized is how your heart functions, how your blood sugar is, whether or not you’re obese. Do you store too much iron, all of those things, all of the different nutrients that you can absorb and carry, they all affect your brain because your brain is part of your body. I kind of do it all. I’m a family medicine physician by board certification, along with integrative medicine, and so those of us in family medicine, we’re kind of, oh, we take care of people birth to death. It’s a big specialty.

Jacob Gordon:

Yeah. It’s a lot to cover there. In terms of snips, how many is IntellxxDNA looking at?

Sharon Hausman-Cohen:

That’s a really hard question to answer because we have the ability to look at thousands and thousands and thousands, but when somebody purchases or works with their doctor on an IntellxxDNA report, they’re not going to see 10,000 snips. That would overwhelm both the patient and the physician.

Jacob Gordon:

Yeah, absolutely.

Sharon Hausman-Cohen:

Yeah. It would overwhelm me, and I wouldn’t have time to go over it with them, even if I spent all day with the patient. A typical report, like our report that is memory and cognition, it’s going to focus on 500 or 600 different snips. That gives you the ability to look at the things that are most important. We don’t need to tell the physician every snip that’s been associated with a 5% increased risk of memory impairment, but if we look at the things that are associated with two times the risk, or three times the risk, or even a 50% increase of risk, that is really where we, as the physicians, want to start. A typical report will have, depending on what report you’re looking at, 300 to 700 snips.

Craig Tanio:

Sharon, how should physicians who are trying to practice precision medicine, how should they think about genomics? Because as certainly in medical school, or really most of us, everybody has been pretty well-trained in how to think about biomarkers and how there’s something in the blood or other type of tissue, elevations or reductions associated with pathologies, and then we can kind of track that. Genomics is a lot more complicated because it ultimately gets into risks and systems, and whether they’re being expressed or not. Have you developed a good mental model for how to think about that?

Sharon Hausman-Cohen:

Absolutely. I think that Dr. Bredesen really gave us a framework for thinking about the brain. He talked about let’s think about inflammation, let’s think about mitochondria, let’s think about nutrients, let’s think about all these different pathways, and we use a lot of those same principles. In our report, we have one report that really focuses on the genes that are known to have significant increased risk with memory and dementia in particular, but they’re not causative. Your DNA is not your destiny.

Sharon Hausman-Cohen:

Everything in our report is just a clue, a clue as to what’s important for the doctor to address, and they’re all modifiable. There’s no gene that gives you, if you have two copies of this gene, you will get memory problems, or you will get heart disease, etc, but the way that genomics forms a framework is you can have someone and you can say, let me look and see which of the different snips, which of the different genes are affected for this person, especially the ones that are less common or have been associated more highly with whatever I’m worried about in this person and then address it.

Sharon Hausman-Cohen:

For one person who’s having memory problems, they may actually be gluten intolerant and also have problems with removing mercury from their system, or other detox, and we think of detox sounds like this fluffy word that only integrative doctors use. But detox is, how do we remove things that get into our body that shouldn’t be there, things like mercury, things like pesticides, and just molecules that aren’t good for us? That might be one person. Another person, it might be that they don’t transport B12 well into their brain, or they need more zinc. Then for a third person, it might be something like ApoE4, which we can talk about more, but affects a lot of genes, including inflammation and mitochondria. If you, as a physician, know what is the main, or what are some of the more important underlying contributing factors for that person, it really lets us design a personalized kind of more precision medical type plan, where you can say, rather than just saying, well, let’s try this and let’s try that, let’s start with the things that it looks like you really would benefit from an often we can get people well using less supplements or more precision dietary recommendations and nutritional recommendations.

Craig Tanio:

So, sometimes looking at the genomics can actually help if a clinician’s following up a ReCODE protocol and just doing the … And looking at the labs knowing that genomics might actually lead to a more targeted efficient protocol.

Sharon Hausman-Cohen:

Absolutely. Dr. Bredesen, in fact, in his current study, and he has said this publicly, so I feel comfortable sharing it, is using our genomics because there are things that you can’t get at with just blood work, but also, for that very reason, it does allow you to kind of prioritize. In my practice, I find that there’s some people, they’re like, I’m already having some cognitive impairment. If you want me to take 30 things, I’ll take 30 things, but there’s other people that come to me and say, “I’m noticing a little bit of mild cognitive impairment, but I’m the kind of person, I really don’t think I can take, at most, more than eight things.” They’re just being honest with themselves. If I can prioritize and say, “Let’s dig into your genomics and see if we can figure out what’s going to give you the biggest bang for your buck.”

Sharon Hausman-Cohen:

Then, if they’re not getting to where they need to get cognitively, but they’ve seen improvement, then they also have the trust in the genomics, and I can say, okay, well, you’ve got from a mild cognitive impairment score of 21 up to 20 … Well, 21 is actually technically dementia, but you’ve got from 21 up to 25, but we really would like to see if we can go a little more. You want to try going back towards the genomics and going back and looking and seeing if we can look for some more clues and add the next layer? When people get benefit with kind of a serial approach, I also think it makes them feel confident and have trust, but it also helps them to prioritize.

Craig Tanio:

Prioritization just is really happening because you get a better understanding of where the risks really are.

Sharon Hausman-Cohen:

Yeah, and I think a good example of that is gluten. We might … About carbohydrates in general if you have certain kinds of brain inflammation, many of the kinds that contribute to dementia are not great for the brain. The issue is, do I need to avoid gluten? Well, it really depends. There are about six different genes that really cover more than 98% of gluten intolerance. If someone has none of those six genes, or gene variants that increase the risk of gluten tolerance, and there’s one that increases the risk more than seven times so it’s at the top of the list, but if you have none of those, then why make the person’s life harder? Not that we’re going to have them go eat tons of carbs, but at least they don’t have to avoid it.

Sharon Hausman-Cohen:

But also, let’s take a person who they’re not ApoE4 to before, and we probably we’ll have to go back and talk about what ApoE4 is for people who aren’t, but somebody who their risk for cognitive impairment turns out to be related to blood vessel issues, that they tend to do a little more clotting of their blood, which makes them get low oxygen to the brain. Well, then, they don’t need to get rid of carbs in their diet. They need to get more blood flow to the brain. Sometimes you unearth really major clues that will allow you to really change what you’re going to do for that person. We’ve had that happen both in patients in various studies and in practices across the country. I don’t know if you’ve had similar experiences.

Craig Tanio:

No, absolutely. I think that there’s … Using the tool I think is quite complimentary to biomarkers, and as you said, just gives you some additional clues. I think one of the areas that I could see the biggest value from right up front was, you had mentioned it before, the things you can’t get at when you do the blood work. There are some insights that you’re getting with genomics that, given testing today, that you can’t figure out with the biomarkers. Do you want to highlight a couple of those genes that you see in cognition?

Sharon Hausman-Cohen:

I would love to. First, just so our listeners understand, there’s something called the blood-brain barrier, and we also have a blood gut barrier, and that’s to protect bad things from going into the brain. But because of that, you have things going on in your brain that you can’t measure in your blood, and DNA is expressed differently. Expressed means where the recipe is being made, your little factory in different places throughout the body.

Sharon Hausman-Cohen:

Everybody has heard of endocannabinoids because right now, CBD and THC, and the legalization of marijuana has made the endocannabinoids in the media. The endocannabinoid receptors, there’s very, very little expression in the blood, and there’s different expressions. Some of them express in the gut, and then other ones express in the brain. Well, if I was trying to see if someone was having brain inflammation that’s relating to that pathway, there’s nothing I could check in their blood that’s going to give me that information, because it’s just not in the blood. It’s kind of like if you’re looking for information about the kidneys, or the heart, or the brain, or the bones.

Sharon Hausman-Cohen:

You can’t go do a bone biopsy, a brain biopsy, a cardiac biopsy, but if you go and look at genes that are known to be associated with different things, calcification, inflammation, mitochondrial function of those tissues, we just get a whole different picture because not everything’s in the blood the same as the brain, but there’s another factor. You can have normal B12 levels in the blood because most of the B12 in the blood is carried by this transporter called TCN1. But if you have two copies of TCN2, which is the carrier that goes to the brain, your levels in the brain can still be low and you might eat extra. That you can only get it with DNA. Even the same is true for thyroid hormone. You can have normal levels of free thyroid hormone in your blood, but low levels in your brain, and symptoms of low levels in the brain can be mood symptoms, depression, anxiety, and a little bit cognition. Again, your blood levels might be okay, but when you know that as a physician that a patient has that, you might give them a little extra of the three T3 if you know that their brain’s not converting that well.

Craig Tanio:

On the B12, I’ve certainly seen a number of patients who have come in with, not even just sort of low normal B12, but B12s of 500 or 600, just looking quite good, and then when they have the TCN2 double variant and we put them on iron shots of B12 for one or two months, the changes have been quite profound, and so it’s definitely something that you wouldn’t pick up unless you knew to look for it with the genomic test.

Sharon Hausman-Cohen:

Absolutely. Now that we even have sublinguals, I mean, sometimes after you get people built up, it’s so easy to maintain. I don’t hesitate to admit, I ended up having two copies of that, and that was one of the most reassuring things. As I was building this, of course I was looking at my own genomics, and I had figured out that I felt better when I took higher B12, and my levels were almost 2,000, but I was like, I knew if I stopped taking the B12, I didn’t feel well and didn’t feel as clear in my head, and as much energy, or anything, and so there’s like, oh, wait, this makes sense now. I think that, of course, the other wonderful thing about genomics, it’s kind of your user manual to you.

Sharon Hausman-Cohen:

I’ve had a lot of patients that are doing it, whether they do it for memory, or they do it more for anxiety or other things that relate to mood. They’re like, oh my gosh, this makes sense now, that why, I kind of, when I get panicky, it just feels so big to me, and so I think that it’s really helpful to understand yourself. Your DNA doesn’t change, so you do your DNA once, and we’re always adding new information, but you do the DNA and you kind of go, okay, this is me, now I know how I have to care for me.

Craig Tanio:

On the whole issue of cognition, what are the most important genes that our readers and listeners should know about cognition?

Sharon Hausman-Cohen:

Well, I think that the most famous and most important one that people hear about is ApoE4. I would love to talk a little bit about ApoE4 with you, because it’s really, really important, but I always say that knowing your ApoE4 status is either not enough or too much, depending on how you look at it. Because if you only know ApoE4, you might get super worried. The best way to think of ApoE4 and why it got labeled the Alzheimer’s gene, is ApoE4, it carries fats, it carries lipids and helps to clear them, but it doesn’t do just that, and Dr. Bredesen was one of the original researchers in the ApoE4 world. What he and his lab found out is that ApoE4 is what is called a modifier. It binds to promoters. It’s a transcription factor, so it’s kind of like a regulator, and it binds to 1700 different genes throughout your body and your brain. That can affect whether they’re turned on or off. The reason that it is so important for Alzheimer’s and cognition and memory, is it can turn on and off genes that relate to inflammation, genes that relate to growth factors, to mitochondria, to things called sirtuins, which are anti-aging proteins.

Sharon Hausman-Cohen:

ApoE4, if you look at the whole population, one copy of ApoE4 gives you about three times the risk of Alzheimer’s, and two copies of it can give you anywhere from 10 to 14 times the risk, depending on the study. That sounds super scary. But the reason that I say that it’s not enough to know just that alone is because there’s a bunch of other genes that can lower that risk. There are some ApoE4s that have much lower risk than that, and then there’s other ones that are at high risk and really need to be very proactive about keeping their inflammation down and kind of keeping all those factors under good control.

Jacob Gordon:

From my understanding, reading through Dr. Bredesen’s information, or research, showing that how ApoE4 is actually a protective mechanism.

Sharon Hausman-Cohen:

Okay. You said ApoE4 is a protective mechanism. ApoE, so let me kind of clarify the ApoE versus ApoE4, and I think that will really help our listeners. Apolipoprotein E is the name of the gene. ApoE two, three, and four are the different gene variants, because if you were really talking about the gene variants, to kind of call it ApoE RS429358, that’s kind of a lot big mouthful, so they gave numbers to these different little one letter changes in the ApoE gene. If you have none of the well-known changes, that’s called an ApoE3, that’s a normal. I don’t know why they put three as the normal. Then there’s no ApoE1. We’ll just say there’s none. It’s extremely, extremely rare. ApoE2 make sure you have more of the apolipoprotein.

Sharon Hausman-Cohen:

So, it’s a protectant because it helps to remove amyloid, and it makes a lot of those genes work better. With ApoE4 variants, they have less of the ApoE protein and it’s folded differently. If you think of ApoE as this wide-open kind of an angle that’s maybe 160 degree angle normally, ApoE4 individuals, it’s locked down and it’s at a 50 degree, angle and it changes the shape of ApoE and there’s less of it. So, it’s less efficient at removing amyloid from the brain, it’s less efficient at interacting with genes, and effects all of these other genes.

Sharon Hausman-Cohen:

Having the ApoE variant puts you at increased risk, not because of just ApoE, but because then you make less growth factors, something called BDNF for the brain. You make more of something called alpha, which creates inflammation and your mitochondria don’t work.

Craig Tanio:

Sharon, I guess you’re making the point though, that ApoE, there is a risk, but there are genes that both increase the risk and genes that decrease the risk. So, when you’re kind of looking at the whole pathway through your tool, you’re able to get a good sense of the overall risk that somebody is going to face if they have one or two or no variants of ApoE4, is that right?

Sharon Hausman-Cohen:

Yes, and no. The part that I do want to clarify, because it’s important from a situation of understanding what a clinical decision support tool is legally, it’s different than a risk calculator. There’s risk calculators, and they take into account a thousand different snips, very, very different things, and they’re FDA approved to give you a number. They go through an algorithm and say, this is your risk. That’s not what IntellxxDNA is, because we are instead giving clinicians modifiable genes, and so we don’t say that we include every single gene out there, but we’re giving them the most common modifiable genes, and so it’s not so that the doctor can go, “This is your X risk.”

Sharon Hausman-Cohen:

It so that the doctor can say, “Okay, you’ve got ApoE4, but did you know that there was a study of this other gene that when people had no copies of it,” and this has to do with butyrylcholinesterase is what I was thinking of, and don’t worry about the name, but if you don’t have this gene with ApoE4, then instead of having a 3.4 times the risk, you only have 1.7. Well, that would be really important to me as a patient to know that I have lower risks than average so I wouldn’t be as worried. It would make me feel somewhat of relief. But then there’s other genes, and there’s one that relates to inflammation and oxidative stress and estrogen.

Sharon Hausman-Cohen:

It’s one of the many CYPs, there’s a lot of CYPs. When ApoE4 individuals had two copies of that gene, there was a study that was published that showed that it decreased their risk of getting Alzheimer’s by 65%. I think it’s really important for somebody not to live their life in fear, but to live it realistically. If they do their genomics and they’re like, okay, I’ve got ApoE4 and I’ve got it combined with things that further increased my risk because of inflammation and mitochondria, then yeah, I’m going to want to be really careful, to make sure I really lower aggressively that inflammation and the mitochondria, and do everything possible.

Sharon Hausman-Cohen:

But if I have somebody who has more benefits, it’s not that I’m going to tell them to be flippant about their ApoE4, but we might start with a Mediterranean diet, not a ketonic diet, and just a few supplements if their cognition is doing great that are targeted to them, and then just monitor and only add things if we need it.

Craig Tanio:

In terms of other clinical situations, I’d love to talk about the whole notion of hippocampus sclerosis and atrophy and kind of situations where sometimes a clinician will see a smaller hippocampus, but it may not necessarily be Alzheimer’s.

Sharon Hausman-Cohen:

Sure. Just so people know what the hippocampus is, the hippocampus comes from the Latin word for seahorse, and that’s because it’s a little part of the brain that looks like a little seahorse, and it’s the memory center. The thing about the hippocampus is some parts of our brain, you can form them when you’re 20. You don’t need to do a lot of remodeling to them. The muscle control, you’ve got it. You don’t need to constantly be remodeling your ability to move your right arm. But your memory, and your mood, so your frontal cortex and your memory, can you imagine if we couldn’t remodel? We wouldn’t be able to learn.

Sharon Hausman-Cohen:

If you have a smaller hippocampus, or you start to get other changes in the hippocampus, that’s a different cause of memory problems and it’s not technically Alzheimer’s, but you still want to be able to address it. One of the things that we have done with genomics is a lot of stuff gets lumped into Alzheimer’s. I know people who they come to me and they say, “My dad had Alzheimer’s or my grandmother had Alzheimer’s,” and as we get to know their genomics, and oftentimes they bring in family members, so we actually get to see dad, it’s like, no, dad’s got vascular dementia, or dad has something called white matter changes, liquorice, or hippocampal atrophy.

Sharon Hausman-Cohen:

It’s a combination of the different studies, things like MRIs or SPECT scans or PET scans, or all kinds of different advanced testing that we can use to look at the hippocampus, but genomically, it’s different genes. Some of the genes that contribute to hippocampal atrophy are, for example, there’s a gene that’s in the TMEM, family, which again, don’t worry about the gene names, but think about it as a gene that helps to remove garbage.

Sharon Hausman-Cohen:

If you’re what’s called lysosomes, or where we kind of as signified the garbage to dissolve it and then remove it, if your lysosomes aren’t working well and you can’t kind of get rid of your garbage, then you’re going to have more brain aging because that garbage hangs around. Well, that’s a completely different issue and ways that you can improve lysosomal and function and acidification of them, and just improving the garbage might be completely different. Things like NAD, things like vitamin C, things like, even perhaps hyperbaric oxygen. There’s a lot of studies going on as to what you can do in both humans and animal models. Quite a few genes, again, that can relate to hippocampal atrophy, but I think that’s a good example.

Craig Tanio:

The important distinction here is that a lot of people might just, if a clinician sees a small hippocampus, they might just sort of jump to the conclusion, there’s amyloid involved and we kind of need to go down how to fix amyloid, how to address the root causes under amyloid. But in fact, what you’re saying is that there’s a whole different pathway that can drive smaller hippocampus, and that needs to be treated actually in a quite different way.

Sharon Hausman-Cohen:

Right. It’s not even just one gene. If you know that the person has the lysosomal dysfunction, that may make you as a clinician, make one set of choices if they have a different gene, and I call it WIFI, it stands for Wnt inhibitory factor, but I call it WIFI. That one’s also associated with hippocampal volume, but it’s a completely different set of interventions. So, if you felt like that was your patient’s main risk, they had two copies of that, estrogen, for example, can help work on that pathway.

Sharon Hausman-Cohen:

Sometimes certain mushrooms, sometimes low dose lithium. For me, as a clinician, and I know you use this in your practice as well, Craig, the more information I have, the better conversation I can have with the patient regarding what they can do in terms of diet, lifestyle, supplements, to address issues that are particular to them, and then I see better results and then the patient’s happier, and then they’re willing to go to the next level if we need to.

Craig Tanio:

That makes sense. Let me bring up another sort of clinical scenario that we see with cognition, which is, in our practice, we see a lot of patients, who unfortunately have been exposed to a lot of toxins or infections at an early age and just have a lot of general atrophy in the whole brain, and so that the, in particular what’s called the gray matter, the cerebral gray matter tends to be lower and sometimes in the single percentiles and somebody who’s 30, are pretty young age. Are you seeing particular pathways sort of involved in those type of situations where it may be younger and they’re having cognitive issues and it might not be classic Alzheimer’s?

Sharon Hausman-Cohen:

Absolutely. We had a professor who came to us. He was a physics professor, smart guy. I am sure since he was a professor of both physics and engineering, and when he came to us, he had a score of 19. For people who don’t know the scoring system on these different cognition tests, it goes from zero to 30, and less than 21 is dementia. He came to us and he’s like, I think I’m getting Alzheimer’s. The fact that he could realize that was good, that he was able to drive himself in and he was willing to do whatever, and he had already started to do some things with diet, but when we looked at his genomics, he was an ApoE3.3. Then we’re like, okay, let’s go on this treasure hunt here and figure out what’s going on.

Sharon Hausman-Cohen:

He had really, really bad detox pathways that made it … Detox pathways can affect not only your ability to clear mercury and your ability to clear pesticides, but it can cause what’s called oxidative stress, the ability to clear the natural waste products that your mitochondria makes. I think the mitochondria as kind of a nuclear power plant. They’re taking oxygen and making all this good stuff out of it, but just like a nuclear power plant develops nuclear waste, your mitochondria develop oxidative waste. His detox pathways made him really bad at getting rid of oxidative waste, which is damaging to the mitochondria, and then his mitochondrial pathways made him at much higher risk for cognitive impairment because of getting the pores of the mitochondria gunked up so you couldn’t get all the nutrients in, the CoQ10 and alpha-lipoic acid and carnitine and all the things mitochondria need to be happy.

Sharon Hausman-Cohen:

Those were really two things we’re just glaring. It’s like 1% of the population, the mitochondrial issue that he had, or 4%, I can’t remember exactly. But by addressing just that glutathione and oxidative stress and the mitochondrial pathways, so we gave him really about three or four supplements. One of them was a nose spray to help with the glutathione getting higher levels in his brain. He went from a 19 to a 26 in four months. That’s a very big deal. Again, without his genomics, I wouldn’t have been able to guess as to what made sense to … He did have some other risk factors of vascular. I don’t mind to make it sound like people have only one thing contributing.

Sharon Hausman-Cohen:

Even with that, it’s actually an interesting story. For vascular dementia, statins are really pretty important for plaque stabilization, but he had been tried on statins. His LDL was completely out of control, and he just got muscle aches on statins. Well, we were able to use this genomics to figure out why he was getting muscle aches on the status and make it so he could tolerate a statin. So, we also lowered his cardiovascular risk, and I’m sure that helps his cognition as well.

Jacob Gordon:

Wow. So, you were looking originally at something that was cognitive and ended up fixing something that was overall his systemic profile.

Sharon Hausman-Cohen:

Right.

Jacob Gordon:

Pretty amazing.

Sharon Hausman-Cohen:

That’s why we don’t just have one, we call them panels. You don’t have just one panel. Most of our physicians, even if the person’s coming to them for brain, they’re still going to look at heart and blood sugar and all these other things, iron storage, that can affect … It affects your body and your brain’s part of your body

Jacob Gordon:

So, these multi-system parts are also affecting cognition.

Sharon Hausman-Cohen:

Yeah. I think that we’ve learned that, like I said, so many things. When Dr. Bredesen started and I heard him speak many, many years ago, the first time he spoke publicly at an integrative medicine conference, he said, oh, there were 36 holes that he was trying to patch. I think that a few years later, it was up to 50, and I think if we were to ask him now to count, he would be like, there’s a lot of holes. I think it’s just looking for clues as to where are those holes so that we can patch with a priority system.

Jacob Gordon:

Yeah. We spoke to him a few weeks ago. I think he said the number is now around 150.

Sharon Hausman-Cohen:

That makes sense.

Jacob Gordon:

It’s constantly going.

Craig Tanio:

Then we were talking with him around vascular, maybe you could expand a little bit around vascular and it being a driver of cognitive problems.

Sharon Hausman-Cohen:

Absolutely. An example of a vascular patient where we uncovered that their dementia, really not dementia, mild cognitive impairment was vascular, was a gentleman who was having kind of fluctuating cognitive impairment. If he went on a long airplane ride, he felt like his brain fog got worse. He also tended to get a little bit of ankle swelling, and he was doing everything. He had read Dr. Bredesen’s book, and he was taking acetylcholine, and he was taking mitochondrial support, and he was eating ketonic diet and exercising, and doing everything he could.

Sharon Hausman-Cohen:

When we got his genomics back, he was ApoE3.3, his cognition panel, as we call it, was beautiful. I think anyone would be happy to go, “I’ll take that cognition panel. It looks great.” He even had some benefits. Then you kind of go, well, why is he having this fluctuating mild cognitive impairment? Well, he was having snips that affected his ability to break up fibrin clots. We have in our body, we don’t want to bleed to death, that’s really important, so we have the system and platelets kind of the stop the bleeding initially, but then there’s something called fibrin, which is exactly what it sounds like.

Sharon Hausman-Cohen:

It weaves fibers together to stop bleeding. But if you have an inability to break up fibrin or you make way too much fibrin clotting or fibrinogen, then that’s not good because your blood’s too thick, and then when you go up and fly internationally, he was flying a lot internationally, that was in before COVID days, when we could fly internationally, he was getting hypoxia. He was getting low oxygen. Well, once we understood that one of his major risk factors, that really his most major risk factor was a combination of three genes, that all independently affected the clotting pathways, but together had an additive effect. We were able to change what he did and really focused on things that helped to lower his vascular inflammation and vascular clotting risk, and then he stopped getting that kind of symptom. So, it was great. It’s much easier than what he had been doing.

Craig Tanio:

Wow. In him, did it show as vascular problems in the larger vessels, or was it more sort of microvascular on the MRIs?

Sharon Hausman-Cohen:

This is not my patient, so I don’t know what the MRI showed. This was a patient that a clinician told me about, and so I’m very familiar with their genomics and their history overall, but I don’t know the specifics of the MRI. But I do know that commonly with patients like this, what we’ll see is they tend to be the people who, when they go on airplanes, their ankles swell, or they just swell more easily, because it’s more that the blood vessels, when they get more fibrin, they can’t bring back all the fluid well.

Craig Tanio:

I think, in terms of smaller blood vessels, we see a lot in MRI reports, a lot of microvasculations. Radiologists will read those all the time. A lot of times in conventional medicine, they’ll just get bleeped over and not really paid attention to. What’s your thought on, on how microvascular problems contribute to cognitive issues?

Sharon Hausman-Cohen:

They absolutely contribute, and I have … Absolutely had my own patients, so I can tell you what the MRI showed, and had a young man, I consider 40s young. I think you would too, who once in a while, he would get not all the time, but he would start to get this kind of brain fog, almost even sometimes a little dizziness symptoms. When we did his genomics he … Well, because he is having those, he got an MRI done because it’s not normal to have fluctuating cognition in your 40s, and they showed all the white matter changes, is what they call them, that were disproportionate for his age. White matter changes are relating to damage to these small blood vessels and it damages the kind of outer coating, which is myelin, and then you get these white matter changes.

Sharon Hausman-Cohen:

The good thing about white matter changes is there’s very specific, different reasons, and so it doesn’t usually take doing six different things or 10 different things. It’s more about figuring out, is it a gene that’s relating to oxidative stress that’s causing the white matter changes? Or is it because they don’t make enough nitric oxide? So, there’s a number of genes and nitric oxide pathways. I think of nitric oxide as what opens up the blood vessels. If you can’t open up your blood vessels well, then at the end of the line, so think of like a river, how it gets into smaller streams, our blood vessels do that.

Sharon Hausman-Cohen:

There’s these areas in the brain called watershed areas, which is where the blood vessels are small. You just don’t get enough oxygen if you don’t open up the blood vessels and you get these white matter changes. Then there’s also different genes that affect how strong the collagen is of the blood vessels. Well, if you know which of those things are contributing, and each of these different things will have three or four times the risk of getting these white matter changes, then you can address it, because for nitric oxide, we use things like from beet powder, or citrulline, but if it’s from the oxidative stress, we use things that affect oxidative stress, which food-wise is things like pomegranate and green tea, or quercetin.

Sharon Hausman-Cohen:

It really lets you target. In terms of, does this affect cognition? Absolutely. There was a study showing that the grading, how bad, or how many of these white matter changes you have correlates to your mini-mental status exam, which is what one of the exams that’s used to determine when people are dementia. The more of these white matter changes you have, the more likelihood you are to have a lower cognition, lower mini-mental status exam, and more urinary frequency at night, which is something we see in our seniors.

Jacob Gordon:

That’s interesting that you say found how the vascular component contributes to the edema or the swelling, and also the nocturia that these people are having. Is that nitric oxide or the microvasculature relating to antidiuretic hormone?

Sharon Hausman-Cohen:

No. I think that when you get little damage to areas of the brain, it just can affect your control of your bladder is one of the areas, and the watershed is my suspicion. But think of nitric oxide, so of increasing blood flow, one of the things that, that same nitric oxide snip can cause is like four times the risk of erectile dysfunction. That’s why they say that men that have problems in the bedroom need to be thinking about how are their blood vessels doing elsewhere because you have blood vessels throughout the body. That’s the kind of how nitric oxide works. It just opens up blood vessels.

Craig Tanio:

You mentioned the mitochondria a fair amount. I’ve certainly heard that a lot of neurodegenerative disease is, at its core, is a mitochondrial issue. Can you just help us understand how genomics can kind of unpack what’s happening in the mitochondria and how to treat it better?

Sharon Hausman-Cohen:

Well, genomics is still evolving, and I will say that, can we understand a lot of what’s going on in mitochondria? Sure. Is there a lot more to yet uncover? Absolutely. But I think that one of the risk factors for, not just Alzheimer’s, but just cognitive impairment in general is again, if there are mitochondrial issues, but there’s different issues that can contribute to mitochondria. There’s genes that again, affect oxidative stress, but then there’s another gene that affects the outer membrane of the mitochondria. So, our mitochondria are kind of encased in these fatty membranes, and they have basically little secret doors that we’re going to call pores, or channels that allow you to get all of your mitochondrial nutrients inside the mitochondria.

Sharon Hausman-Cohen:

If you have variants that affect how these mitochondrial pores are affected, and then amyloid can kind of gunk them up and make it even worse, and then you have to really do extra things to protect the mitochondria. There was some work that got nominated for a Nobel Prize by Dr. Garth Nicolson, that showed that if you give them mitochondria everything they need, extra of the particular lipid support that they need, extra the CoQ10, extra of all the different factors, mitochondria can repair themselves with fission and fusion.

Sharon Hausman-Cohen:

But again, there’s so many supplements out there to choose from. There’s so many foods out there to choose from, that if you can know that someone’s Achilles heel, their area of weakness is their mitochondria, then you can guide them as to what things will help their mitochondria, because you might give them higher levels of CoQ10, more acetylcarnitine, more alpha-lipoic acid, more of certain B vitamins, and even more of the lipid membrane components to help those mitochondria repair. Because every time you have surgery and have anesthesia, every time you get a decade older, and that one we can’t prevent, you lose quite a bit of mitochondrial function, and it can make profound changes, not just to your brain.

Sharon Hausman-Cohen:

I have a patient where she has just some mitochondrial issues. She was literally getting to the point that she was using a wheelchair 80% of the time, not 100%, but she was getting progressive neuropathy and weakness. When we gave her mitochondrial supplements, and that’s kind of a classic mitochondrial pattern with neurons getting worse, she, within a month, which was actually crazy quick. It was a little over a month later, came back walking in our office with a cane instead of a wheelchair, and now it’s years later. Yeah, it’s crazy.  Sometimes just uncovering clues can be really, really helpful to the patients. I’m not going to say we’re going to get everyone from having weakness to walking by giving mitochondrial supplements, but the point of a clinical decision support tool is not to make the decisions for the doctors, but it’s to bring different things into the awareness of the doctors so that they can make better clinical decisions along with lab tests, along with blood tests and biomarkers, imaging, so that they can kind of say, let me treat not just a disease state, but let me treat a person.

Jacob Gordon:

I love the way that you just described that, how it’s now another tool that we are fortunate to use to help treat a patient.

Sharon Hausman-Cohen:

Thank you. I’m glad you like it.

Craig Tanio:

So, we have a lot of patients who come in and they’ll just … They’ll come in with some predisposed ideas around inflammation. That word gets used a lot as a root cause of most chronic conditions, but I believe in your work. You’ve really been able to outline some different inflammatory pathways and how to use genes to really get a little bit more precise about which type of inflammation is actually occurring.

Sharon Hausman-Cohen:

Absolutely. So, everyone uses inflammation as if it’s all the same. Inflammation, well, that’s what ibuprofen works on, and there’s so many different types. We have a very extensive inflammation pathway. When you again know the kind of inflammation, it can help you understand what’s going on. For example, there are certain inflammatory mediators, certain of the interleukins and TNF alpha, that they cross the blood-brain barrier, and so they can have bigger effects on things like depression, things like autism, things like cognition, things like auto-immune brain disease.

Sharon Hausman-Cohen:

There’s other gene variants that affect tissue destruction more. Right now, again, as we’re recording this, COVID is a hot topic, and they’ve shown that some of the tissue destruction, people who get more inflammation in their lungs in the presence of a virus, that cytokine storm, they may have higher levels of CCL2, which is … Basically, it’s a call in the guards. It’s what’s called a chemokine or chemoattractant, but it calls in inflammation to a site of injury, meaning to repair that injury. But if you have too much of it, it can cause too much inflammation and too much tissue destruction or scarring.

Sharon Hausman-Cohen:

When you know that somebody has specific gene variants, you can address it, so CCL2 is lowered, not only with things that classically lower inflammation, so classic one for it is resolvins, the pro-resolving mediators, but it’s also specifically lowered by things like andrographis, or astragalus. It’s lowered by PEA. So, if you know, again, that somebody is at high risk for this kind of inflammation, then whenever they get sick, they can take those things. Interestingly, many of the things that lower CCL2 conveniently also have good antiviral properties. I think they can be a double help to them.

Sharon Hausman-Cohen:

We all have these patients that have the weird reactions. I had a patient who had horrible, horrible fibrotic reaction to breast implants, ended up getting other inflammatory reactions, including an inflammatory reaction in her sinuses that was causing … Went to her brain and caused her to have visual losses. Again, this is the kind of thing that in 30 years of practice, you see one case of, and she has really, really overactive inflammatory pathways, and probably why she got such a big inflammatory reaction to her breast implants is because she had more of such high levels of this CCL2, is one of the contributing factors, not the only.

Sharon Hausman-Cohen:

We also have people who tend to get kind of gouty arthritis. They have a different pathway that particularly relates to tissue destruction of the joints. We can also see that in people with Lyme disease, people who get the bigger swelling of their joints may have more of some specific genes of inflammation that affects joint swelling, and then the people who have the horrible allergies, may have higher levels of like interleukin 4 receptors, where they get more of that mass cell activation and they get more IgE because of specific genes.

Sharon Hausman-Cohen:

I love inflammation. In fact, usually, when I start with a patient who has any complaints that of brain, of joints, of achiness, I’ll start, even if it’s a young child with neurodevelopmental issues, I’ll start with the inflammation pathway because that’s where we get some of our biggest bang for our buck. TNF alpha is all over the medical world. People just don’t realize it. Every time you hear that commercial, ask your doctor about blah, blah, blah, all those injectable medicines for autoimmune disease, it’s because auto-immune disease is triggered by higher TNF alpha. If you know that you have a family history of auto-immune disease, and then you know that you have genes that increase that risk because they make you have high TNF alpha, then there are things you can do, like lion’s mane mushroom, which is an inexpensive powder, or capsule that has been shown to lower some of those auto-immune risks, lower risks of the improved cognition. There’s big study out of Japan where it improved cognition pretty quickly, and you can be preventive. Part of what I, as a family physician, I’m dedicated to, and I know you are as well, Craig, is I want people to better understand how to care for themselves so they can keep themselves healthier.

Sharon Hausman-Cohen:

That’s why I was dedicated to developing this genomics tool. I had the science background, I had the medical background, and I was like, wow, if we can help people have a book of you, a book that helps them understand themselves and prevent things before they happen, as a family physician, that’s really a big part of what we’re doing. If we can reverse things that are starting to happen, that’s great, too, of course.

Craig Tanio:

Beautiful, a book of you. I like that. What I tell patients when they’re using the tool is this is like an encyclopedia. Most people don’t read the encyclopedia from first page to last, but it’s going to have a lot of useful information. You go after what’s most important first, and then you can always go back and look further, and that it’s also an encyclopedia that’s updated on an ongoing basis. One of the, I think things that must be challenging for you and your company is the amount of new evidence that’s sort of coming in here.

Craig Tanio:

How are you managing sort of the new evidence that comes in? Then, what’s been the most compelling new evidence that you’ve seen this last year or two?

Sharon Hausman-Cohen:

That’s a good question. So, how do we manage new evidence? We have to prioritize, we have a hundred topics that we want to do, and so part of what we do is we go to our users, meaning our users are physicians, just so your listeners know. This tool, it really does require medical knowledge to use, so this is something that’s ordered by a physician for a patient. We talk to physicians about what problems are they having trouble solving. That helps us to guide where we go next. So, do they want us to have the things that come out next to be related to fibromyalgia, or chemical sensitivity, or what kinds of problems they’re solving, and then we prioritize.

Sharon Hausman-Cohen:

But we are dedicated to maintaining the products we have by adding new information when it comes available about the different genes, about the … When you’re talking about cognition, new information comes out, and because it’s an online tool, we can add it. Now, sometimes we have to go back for … If people want to have the cognition report and they want to now add the mental wellness report, well, the mental wellness report was designed in 2019, and so not all of the genes that were there in 2017 or ’16 when we did their cognition were available. Sometimes we do have to kind of go back and re-pull their DNA, which we store under a barcode, so it’s completely secure and kind of rerun the DNA.

Sharon Hausman-Cohen:

It’s a challenge between what we design to do, decide to do design-wise and how we update. There’s some updating that comes with once you’ve purchased it, it’s going to be updated for free, and there’s other updates that you would have to go and buy a whole new report as new reports design. In terms of some of the exciting, I’d call it like a spoiler alerts of things that we’re working on for the future. I did give you a couple of them. The other issue, as I said, my passion with inflammation is looking at some of the interactions between the viruses and cognition as well. It’s going to be a hot topic in the next couple of years, and there’s more information and more research coming out, and so there’s constantly new inflammation research coming out, but there’s constantly new research coming out on every single thing.

Sharon Hausman-Cohen:

We just kind of pick our topics and know that there’s lots and lots of snips out there. There was a cartoon was done because every human being has about 3 million snips and 3 billion base pairs. It’s a cartoon of a bunch of scientists working around the genome and saying, I think I found a corner piece, and that’s a puzzle, and the box says puzzle 3 million snips. That’s where we feel like we’re at. There’s 3 million snips to choose from, and which ones do we want to highlight? But we’re trying to find the most important pieces first that are issues that aren’t as easy to uncover with blood. Cognition has not been something that we have had good success with based on just blood tests because of that blood-brain barrier.

Sharon Hausman-Cohen:

A lot of what we do focuses on helping our physicians better understand things that aren’t clearly understood by blood tests alone.

Jacob Gordon:

True. Is there a difference between age groups in terms of that they should be looking at their genomics versus someone who’s young and healthy, versus someone who is just diagnosed with dementia?

Sharon Hausman-Cohen:

Absolutely. I think there’s a social responsibility issue of understanding how to use genomics, and our physicians are really good about that. I would not order a cognition report on somebody in their twenties because their grandmother has cognitive impairment because they may not be emotionally … What if they find out they are an ApoE4.4? They may not be emotionally ready to fully understand it or handle it. When I have somebody young, usually, if a doctor has a patient coming to them with somebody young, they have some issue going on, so we have other reports.

Sharon Hausman-Cohen:

For younger patients, we usually would order what we call our mental wellness report. The mental wellness report, and it just got launched in late 2019, so it’s a little newer, it focuses still on all the things that are really supportive of our brain, all the B6 and the B vitamins, and the vitamins and minerals that help you make things that make you feel calm and make your brain chemicals. It focuses things like OCD, and we call it attention and focus, because ADHD isn’t one specific disease. It still focuses on gut. It still focuses on detox. It focuses on inflammation.

Sharon Hausman-Cohen:

But that allows us to set up a young person, a child, or a young person with a lot of things they need to know about themselves, but it doesn’t necessarily benefit them to know that they have these genes that have been highly associated with Alzheimer’s. They’re not ready to accept that information, but also, because they’re modifiable, we’re going to get more knowledge. We already made so much progress in the last five years as to how to prevent cognitive decline. Let’s not have them worry about that at 25. Let’s have them worry about optimizing their nutrition and their brain health that will benefit them feeling well and energetic.

Jacob Gordon:

Where can people learn more?

Sharon Hausman-Cohen:

They can, if they’re a patient of Dr. Tanio’s, they can ask Dr. Tanio about it. If your listeners who are listening to this or not, they can go to the IntellxxDNA website. It is currently being revamped to have more information, so we hopefully will have some more videos and information. They can also ask for, if they’re not in Florida, they can ask for a list of practitioners that are licensed in their state that they could consult with about IntellxxDNA.

Jacob Gordon:

Great, and how can people contact you?

Sharon Hausman-Cohen:

I think the best way would be to just go through the IntellxxDNA website. IntellxxDNA is an unusual spelling, it’s two Ls and two Xs, and that’s because it comes from an intelligent way to approach DNA, and the two Xs is kind of a double entendre. There’s two X chromosomes, and it sounds good with intel, Intellxx, but the co-founder of IntellxxDNA is also a woman. So, since both the co-founders of IntellxxDNA were women, we thought the double Xs at the end of the intelligent approach was a good kind of fun way of having a name for a company. So, it’s www.intell, I-N-T-E-L-L, XXDNA.

Jacob Gordon:

Great. I love how you came up with that name. You can add XY, if you had a different co-founder.

Sharon Hausman-Cohen:

Then it would be IntellxyDNA.

Jacob Gordon:

All right. Thank you so much, Sharon, for coming on the show. You have a phenomenal tool. I’m so happy that you were able to come on.

Sharon Hausman-Cohen:

Thank you so much for having me. It was really fun to talk with you guys,

Craig Tanio:

Thanks, Sharon.

Jacob Gordon:

Thanks guys for listening, and if you want to learn more information about IntellxxDNA, I recommend heading over to their website, Intellxxdna.com, or if you want to know more about epigenetics in general, I have a whole website dedicated to epigenetics at mybiohack.com. I recommend reading it. You’ll learn some really cool stuff. Now, let’s talk about Rezilir Health. Rezilir Health has access to all of IntellxxDNA’s tools. So, if you’re a patient in Florida and want to get your genomics evaluated, head over to rezilirhealth.com and schedule an appointment. Thanks guys for listening, and I’ll catch you in the next episode.

 

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