Welcome. To another edition of “Mycotoxins and Chronic Illness.” Today, it’s just exciting and a pleasure to be interviewing Sharon Houseman-Cohen, who has many attributes. So right now, She is the Medical Director and Co-founder of IntellxxDNA. Her background is, she has a Master’s in Cell and Cell Development and Developmental Biology, and she’s a M.D., a graduate from Harvard Medical School. And as I think I mentioned the other day, one of the hallmarks of most of the doctors that I’ve interviewed is that they had training in usually a master’s level in an element of science before they went to medical school. So, they learned to think scientifically because unfortunately, many doctors start off they desire to be a scientist, but we were trained after a while to just be expert at pattern recognition, and that’s good.
But if you don’t think, and you just recognize patterns and you only have five minutes to interview the patient, those of you with chronic illness have seen the results. You’re constantly frustrated, okay. ‘Cause people aren’t listening to your whole story and they’re not finding the parts that don’t fit. And what Sharon has done for us, is created a tool that allows physicians and patients to begin to see where they fit in the world. To find out their own special individual characteristics and why, and often not just why, but what we can do about why, that they are and you are in the position of having a chronic illness. So, but she’s done this to the use of genetics. And first of all, I’m gonna start off and just give us a little overview of how genomics has come to play such a big role in your career.
Well, I am an integrative trained physician and like you deal with a lot of patients and deal with a lot of patients with chronic disease, whether it be Alzheimer’s, or mycotoxin, or mold related illness, or whether it’s just relating to chronic illnesses, like heart disease and diabetes. And I had patients that were coming to me as everybody knows in the last decade or so, everybody’s gotten their genome, their M.D. 23andMe, or whatever direct to consumer product. And I had all these patients bringing me their genomics and saying, “Can you use this to prevent my Alzheimer’s that runs in my family?” “Can you use this to help figure out why I am so sick from mold, but my husband who is in the same house is not sick?”
And when I started looking into options for physicians to really make genomics useful in clinical medicine, there was no tool that was evidence-based told us, what does that gene function do? Which of the snips, which are the little changes, are clinically significant? And most importantly, what can we do about them to modulate? So being the X-research type, it’s still the ongoing research type. I have a really strong background in genetics. I’d been working in genetics research back even before I went to grad school. I set out with my colleagues and we built this tool. So, it’s now being used by hundreds of clinicians across the country in the world to help people with different kinds of chronic diseases. Dr. Bredesen has used it in his most recent study for the “Reversal of Cognitive Decline.” It’s being used in autism work across the country and in Australia, and in people with chronic illnesses from environmental illnesses. So, it’s really a great tool.
And it’s, so what is… Just go back and talk a little bit about genetics. I mean, how we think about it, how we use it, because so many people get confused with snips and they’re especially people who’ve done some of the multiple labs that, I mean, been going on for the last 10 years looking at methogenetics, I mean, or like that pathway. And I think people erroneously run after individual snips that are sometimes more or less common. So, give us a little background on how we should think about this ’cause I’ve found your course is very helpful.
That’s a great question, Eric. So, genetics versus genomics. Genetics tends to refer to the study of inherited illnesses. Things like tastes acts things like cystic fibrosis, where you can have one gene that has it’s called pathogenic. You have changed to that one gene. Sometimes it’s a little single letter change. Sometimes it’s a big insertion, or deletion, or a duplication of things. And that, if you have two copies of it, if you have one copy of it, you’re going to get that illness. But genomics is the study of small changes in an individual’s DNA that by themselves are not disease causing, but when combined with environmental exposures, differences in nutrition, like, do you have enough zinc or copper, Coleen in your diet and when combined also with each other can make really significant differences in a person’s health and well-being.
Their physical health, their mental health, their cognition, and genomics can give us insight into things like; who gets a really big inflammatory response in their brain to the mold? Who needs more or less of specific nutrients? Who has problems removing pesticides, mercury, mycotoxins? and you brought up the methylation pathway. Well, the MTHFR gene was one of the first genes that was clinically significant that was identified. And of course we look at that in our genomics, but that gene 47% of the population have at least one copy. So while it’s important, what I find more useful is when I have a patient with, again, mold is one of the topics today, mold related illness, looking at some of the genes that they have they are only found in five or 10% of the population that had been shown to be clinically significant.
Methylation and MTHFR were studied ’cause it was easy to find people with that gene, it does have important information and implications. It can increase your risk of things like depression. It can increase your risk of hearing loss. It can increase your risk of high homocysteine, but it’s one of many, many, many hundreds of thousands of genetic or genomic snips that are significant, and I would say it’s important but that there’s many, many more, we can talk about some of those today that I think are more important in the study of people who have mold related illness.
Yeah. Yeah, that’s what we wanted. I’m excited to get you. And, I just really wanted to get this on the table cause too many… I mean, I think the, yeah, just the way we think about things really helps us understand and not panic, but also know when we really should be careful. And, I just like to emphasize, and maybe you can talk a little bit more about how important it is to think about how common a gene is, because sometimes if a gene is very common it may be serving a purpose as well as creating a risk.
Yeah, I think that frequency of genes goes back to Darwin, “Survival of the Fittest.” And so, in our genomic report in IntellxxDNA, if someone were looking at it for brain health or environmental illness, they’d be looking at a bunch of panels, inflammation, and vitamin levels and detox pathways and all these different things. And you would have a total of about six, 700 different snips that you’re looking at. So one of the things that clinicians always say is, well, how do I get started? There’s so much information.
And I say, start with the rare things because chances are, if you can identify in patients the things that they have that are only found, and again, 5%, 10%, 1% kind of that less than 15, 20% of the population, you’re gonna get your biggest improvement by addressing those gene variants. Just like we always had that 80-20% rule, 20% of your effort is going to get you 80% of the results, the same thing I think is true with genomics. You look for those that are less common but you can’t just look at any old report, and look at frequency because you also have to know if the snip is clinically significant, has it ever been shown to be associated with diseases? Otherwise we would be dealing with way, way, way too much information to sort, you have to have some kind of a tool to help you kinda look through that.
Yeah, no, I think that’s what I’ve found so helpful with the Intellex DNA reports is because you’ve done that work. I mean, what people don’t understand, I think, oh, people, especially patients don’t understand because they’re the ones who are using our services, is how time consuming it is for doctors to learn new things. Okay. And learning new complicated things is especially difficult. I mean, so most of us, most of the profession unfortunately relies on the expert, the advice of the expert. And so that’s why you can have like five experts drive the train and we don’t always get the best results. And, with genetics there’s so much information that without someone funneling it and helping curate it, the average physician isn’t gonna be much ahead of the patient. So we really, we know, I think it’s really important to have a report that helps us. It’ll put a lot of people, I think, too much focus either on genetics or too much focus on blood tests. And, so tell me about how you like to look at the balance between like, where you find the genetics is more helpful than the blood tests are many times?
Yeah. So, I think if we think about what blood and urine and those kinds of tests are, we realize that, that is one tissue of the body. So, as functional and integrative physicians and clinicians were introduced to all these different evaluations and a lot of them over the past 20 years, which is kind of the lifespan of functional medicine used blood and urine. But the big limitation is that your genes are expressed differently in different tissues. So, you can have things going on in your bones, going on in your brain, going on in your gut, that you’re not gonna be able to measure from the blood and the urine.
The other thing is blood and urine will measure the level of metabolites and products that you excrete, but a huge, huge number of regulatory genes are receptors. So, there’s vitamin D but then there’s the vitamin D receptor. Well, the vitamin D receptor binds to the vitamin D goes into the nucleus and then turns on a thousand other genes, same things with the estrogen receptors. So you might be measuring someone’s vitamin D levels or someone’s estrogen levels, but if you can also know how their estrogen receptors work. There’s estrogen receptors that are responsible for dampening inflammation. If you know that those ones are underactive or you know that you don’t have enough vitamin D receptors or receptors for calming neurotransmitters, they’re actually interventions we can do to up regulate the receptors. So the limitation of blood and urine is it’s one tissue of the body.
Genomics is kind of because it’s the code to you, in the cells, from your spit, from the inside of your cheek, you have the genomics for your whole body for every single tissue. The problem with that, is that the science is relatively young at knowing which snips are systematically have effects. So, for those of the snip, for example, NQO1 and when you have, and we’ll talk about it with one of the patients who had two copies of it. When you’ve got two copies of it, it doesn’t matter about it being turned on or off. You have 98% less ability to recycle your cocuten.
Well, that would be really useful to know about yourself. There’s carriers kinda think of like the little shuttles that shuttle the vitamins into the cell. And if you have a mismatched carrier, it’s not about a gene being turned on or off, you’re gonna have less ability to transport that B12 into your brain or into your tissues. So the rate-limiting step on genomics is there are 3 million snips that have been identified. Yeah, I know. Not all of them do anything that we know of so far, but in terms of how many we know what they do, we’re still only at a couple hundred thousand where we even know the complete function. So that’s the big rate limiting step but a lot of the really important ones, a lot of ones we’ve discovered have very important clinical significance and that’s the problem.
They always say, if you’re gonna build something, what’s the problem you’re trying to solve. The problem we are trying to solve is how do we make genomics clinically useful in an evidence-based way that physicians and other clinicians, natural paths, physicians, PAs, nurse practitioners, people who are practicing medicine can use knowing that they’re using evidence-based medicine. And that means knowing what the gene snip is doing, how it affects the body, and what can you potentially do about it to modulate it, and that’s what we did.
And it is amazing because we’ve always been confronted. I mean, what I have found is that basically I always have to explain to people that I do clinical medicine, meaning I look at you and I figure out if the test applies to you, because and you mentioned the B12, is it many people committed, “Oh my God, my B12 level was sky high.” But if you don’t take enough B12 to give you that very high level, you don’t feel well. So, no, you don’t have cancer cause that’s some very high B12 levels can be a marker, but you just have, and until you’re tested, I didn’t really understand what was going on. It was one of those black, many unknowns that we face, is that the same thing with the thyroid. How many people have difficulties with thyroid receptors and the estrogens? Again, because the levels, if we’re looking at blood, I mean, you can drive a truck through those levels of normal, they’re just ridiculous.
But only when we look at the patient, we can sometimes make sense. But when you add the genetics through your filter, through the Intellex DNA report, we can then get another level of preciseness and hopefully not, and one of the things we’re gonna I’m looking forward to asking you some more questions about because what excites me is I always hated what I call the shopping bag. I especially cause you said 21, I’ve been doing this stuff for 30, 35 years. So this is, I used to call it the alternative medicine before we had functional medicine, but the shopping bags, people even 30 years ago, they’d come in with shop literally, one or two shopping bags full of supplements. And that always seemed a little much, I mean, in my mind. And, but on the other hand, sometimes it was hard to sort through ’cause they were all good.
Right. And it’s ideas like knowing what’s right for what person. And is–
And that. Yes, run with that because that is what I’m loving is that at least when I’m looking at some of the people who are dealing with memory and early concerns about their brain function, is to be able to filter and reduce those supplements the ones that they really need to keep taking for the next rest of their lives rather than get tired and stop everything.
Absolutely. And you know, that’s where a lot of my interests started in genomics. In that, I was doing a lot of what we were calling CIRS at the time. And I met Dr. Bredesen at the first conference that he ever presented his cognitive impairment and reversal of cognitive impairment work at, which was an AIHM conference in San Diego a number of years ago. And he was talking about all the different causes of brain fog and dementia and cognitive impairment, and he mentioned mold. And I had never heard a doctor talk about like a standard neurologist ’cause at the time he was just had previously been known in the neurology world talk about this. And I had had a whole program that myself and my co-founder, Carol Bilich had developed for mold illness here in Austin and also had a strong interest in Alzheimer’s.
And I went up to him and I said, “Hey, I’d be happy to help you learn more or do more teaching about the mold.” And so at the first conference at the Buck Institute, I helped to teach the clinicians a little bit about some of the mechanisms that mold caused brain fog. But at the same time I was working on this genomics tool Intellex DNA was in its infant stages. And I said, the same way that you’re taking the different 36 holes, now it’s 50 holes or however many. And you’re saying, is it mitochondria? Is it Coleen? Is it estrogen? Is it vitamin D? Is it homocysteine? I can build that into our genomics as a clinical decision support tool and help you hone in on what is important.
And so that’s been a lot of our work and we have a whole product on brain optimization that allows you to kind of go, gosh, this person has problems where they’re really a lot of problems in the detox pathways, and they’re not able to recycle their cocuten and not able to carry B12, but this person here, they’re having too thicker of blood and that’s not getting enough oxygen to their blood vessels. So it’s more in an ischemic form, contributing factors, or they have MTHFR with some interleukin-6, which is another inflammation pathway. That combination gives you 2.5 times the risk of Alzheimer’s and 3.7 times the risk of vascular dementia. Then you get ideas as to, okay, here’s how we can then address it. But that’s exactly why we built it because none of my patients in Austin wanted to… They would be like, I’m willing to take some things, doc, but I want it to fit into like a small pill container. I don’t want 30 things three times a day–
Especially for a prevention patient. That’s really important for having a regimen that they feel is tailored right to them and that they will stick with.
Yes, no. I mean that and for prevention, because again, what you’re talking about, many of these illnesses it’s gonna require a lifetime of supplementation. If they really do have, that young lady you mentioned, if you’re not recycling your CoQ10, you better know about that. I mean, God forbid you get put on a , I mean.
Yeah, it was a really interesting case ’cause she is a mold case. Do you want me tell you–
Well, yeah. Let’s just run through, like you say, what do you, when you… I didn’t even realize that you had studied in this world of mold and this serious world, okay. So, we can come back a little bit and tell me a little bit about that and tell me about this patient.
Well, I’m mostly gonna tell you about the patient. In terms of the mold world, I’ll tell you that anybody who does the mold world as part of their practice, doesn’t usually want to advertise it unless they want it to be their whole practice ’cause there’s not that many of us that do it.
We did it because in Austin there’s a lot of air conditioners which creates a lot of mold with leakage from air conditioners and stuff. And one of my patients asked me, she was flying to Tucson to see Mary Ackerley who’s wonderful in the field of And she was the one who asked me if I would spend the time to learn it, and so we did.
That’s perfect. No, that just fits you. I said we just spoke to Mary the other day. Yes, ’cause people wanna listen ’cause, yeah. She’s been working at this a long time.
And so in terms of the patient, so, this woman got significant mold damage, water damage. We’re gonna call her Naomi. And she presented with brain fog, but also a lot of anxiety and low blood pressure. She had a very strong pots like picture, which was huge. And so we looked at her genomics and a lot of the classic times you’ll find the problem with the genomics, for people who have mold related to their glutathione pathways. And think of glutathione as kind of the paper towel. I call it the ultimate quicker, picker upper, it’s taking all those different toxins out of the brain and kind of helping you to eliminate them. But for her, she had different things going on. Now, we’re gonna circle back to the glutathione and maybe I’ll do a divergence. Everybody with mold has glutathione problems. The reason for that has to do, not with the individual’s genetics, but with how mold works. And so I think I’m gonna, is it okay if I take a divergence?
Please, please do. I mean, glutathione is a part of our favorites.
Okay. So one of the things that happens is mold species like Ochratoxins, or mold toxins like Ochratoxins, which is from the penicillium and aspergillus, which grow on water damaged buildings. They literally turn off the master detox pathway switch, which is called NRF2. So for all mold patients, they’re gonna need to have their glutathione pathways pushed, whether you use something like Ag local, which is the sulforaphane with from three-day old broccoli sprout extracts is activated with Marissa NACE or whether you give them intranasal glutathione, or whether you can glutathione lozenges.
So, you always need that because the mold, Ochratoxins I’m sure, is one that you see a huge amount of. It’s the one I see the most. So the Ochratoxins will turn off glutathione. So we always have to address glutathione, but then there’s a lot of additional pathways. There’s people who need a ton of glutathione support because they have problems with their glutathione related genes. There’s some people that have complete NOLs, meaning the complete one of the glutathione transfers is completely missing in their genetics.
We can get at that. There are people who don’t, who have problems with the glutathione pathways that affect mitochondria and oxidative stress, and we kinda circle back to that as well. But for this woman, the glutathione pathways, weren’t the real issue. And it really, it took us when we first started with her We didn’t have genomics because it was years ago. Now we have it and everything makes sense because she really, really had things that we were able to go, wow, this kind of lightheadedness and a lot of allergy type symptoms, but brain fog anxiety. We know that sometimes that’s mass cell and she had high-ish IgE levels. But when we finally got her genomics, we were able to see that she had a gene.
So there’s a whole bunch of inflammatory genes. Inflammatory genes are interleukins and cytokine genes, and chemokines, and there’s all bunch of names. But she had one that specifically, and it’s only in less than 10% of the population that is associated with releasing more IgE and causing degranulation of mass cells. And so, yeah, it’s a receptor and so interacts. So that, and it’s about 5% of the population that had this particular one that she had. So, ultimately what we found once we knew that was we could use things like , quail egg protein, apigenin, luteolin to kinda help stabilize those mass cells and they made a big difference for her, but the story went even deeper because she also had some problems with her nitric oxide pathways. And I’m sure a lot of your audience has heard of nitric oxide, but I think nitric oxide is a vasodilator.
It kinda opens up blood flow, which is good. Except if you have a lot of mass cells that may not be good because it relaxes the blood pressure, the blood vessels and you get even lower blood pressure, but kind of to add fuel to the fire, nitric oxide normally inhibits a number of mass cell dependentory inflammatory processes. And if you can’t and she had the problem where she couldn’t make enough nitric oxide. So then she was not able to inhibit the mass cells. So, you need nitric oxide for blood flow, but kinda how to address it where we wouldn’t make her mass cell issues worse, was difficult, but super important because it was adding to the whole histamine issue.
Which is, I’m just gonna start with that is what makes this tool so exciting is because what you were just describing is something that without the IntellxxDNA,, we wouldn’t know what we were doing. We would find out maybe by hit or miss, but we would probably have exacerbated her symptoms until we figured out to back off.
Yeah. And we did do a lot of hit and miss before we got it, but you’re absolutely right, it helps so much. And then we were also better able, we tried before we got her genomics, she was having anxiety and we were like, oh, you’re stressed, you’re anxious because you’re living in a trailer now because your home is maybe a mess but she’s like, “No, I’m not an anxious person. I really just started with the mold and I’m okay with it. We’ve got a nice trailer. We’re doing okay as a family.” And she saw a psychiatrist, they put her on serotonin medicines, didn’t help at all. She felt worse on it. And then again, once we got her genomics, we actually found that she had, again, some genes that make her have an exaggerated response to stress that make her in response to stress release more of something called Orexin, which just think of it as the wakefulness hormone.
So it’s the opposite of this, of like we have ghrelin to help us go to sleep or Rex that helps us feel awake in the morning. And it makes us have more histamine. So she was getting histamine from all fronts and that was what was causing her anxiety, her stress, her tachycardia. I mean, she had other contributing things that… There’s a lot of genes oversimplification to say that there were four genes that were causing it, but still each of these four genes that she had were in four to 10% of the population, the two copies of it, they explained a lot.
Yes, that’s just actually, can we just digress for one second?
Yeah, just a quick for our audience about the difference between heterozygous and homozygous having one or two copies, just a quick minute.
Sure, so everybody gets DNA from their mom and their dad so that we get 23 pairs of chromosomes. So you get 23 chromosomes from mom, 23 chromosomes from dad. And if you have a gene variant that little one letter change in the DNA on just one of them, moms or dads, that’s called heterozygous or one copy. But if you have that same little change from both parents that’s homozygous and that can often have a bigger effect. So, that NQO1 that she also had and we can circle back to that as well. NQO1 lets her recycle CoQ10. A lot of people have one copy of it, about 30% of the people that decrease your ability to recycle CoQ10 by about 60%. So it’s still really important, but when you have two copies, which is only 4%, it decreases your ability to recycle CoQ10 98%. So that was another huge problem for her because of mycotoxins, so mycotoxins is the fancy word for mold related toxins. They produce an oxygen type toxicity and you need certain antioxidants and CoQ10 is one of the most important antioxidants to deal with that stress. And so she also couldn’t, her body couldn’t deal with the stress from the mycotoxins. It couldn’t repair it properly from it.
Oh, okay. Thank you. Just ’cause and one of the things that I’ve noticed. I mean, you’re doing great today, but sometimes I can wind up going into either acronym hell or jargon.
Yeah. Sometimes we do podcasts with myself and Carol, our co-founder, because then she just kind of interrupts and goes, “Okay, now in English, that means.”
Always a good thing. So, I mean, this is… I think what I emphasize is that how important it is for these individuals snips and especially in coordination with each other. Very often you might find someone might have one of these, and if all they had was one, might not be so bad, but they’re additive.
Right, absolutely. So– And,
Yeah, no. So for example, if you don’t make enough glutathione and that’s another snip we often see in mold related patients is the ability to synthesize glutathione. There’s a whole set of genes involved in that, if you have decreased ability to synthesize glutathione, and then you have decreased ability to have the glutathione pathways work, that’s gonna have an additive problem.
Yeah, and what’s so interesting. We all have our stories to explain things and one of the things that I’ve always, my internal story if you will, and sometimes the patient gets it too, is that why certain people become sensitive to mold and mycotoxins. Sometimes the allergy and, but more likely just the inability to clear the mycotoxins where before they were, because most of us have been exposed to high mycotoxin levels at one time or the other and we tend to like do just fine. I always blamed it predominantly on a prior infection. Something like Lyme, which try to change how your immune system, if you have it, if you don’t deal with it quickly enough. Deals with its anti-inflammatory pathway. Sometimes you increase IO10, but it’s just so interesting to see of course how simplistic one story is and how the multiplicity of things because probably I wouldn’t be surprised if chronic infections happen easier in people with some of these snips.
That kinda is a good lead into a different case because what we know about chronic infections is a lot of times chronic infections will increase the level of TNF-alpha in the brain and just think of like alpha dog, you know, alpha is an important thing, but TNF-alpha is one of the big brain inflammation factors, anything the interleukin one alpha, the TNF-alpha, they all cross the blood brain barrier and TNF-alpha has become a really big factor, become clear to be a really big factor in things like PANDAS and PANS, and for people who don’t know what PANDAS and PANS are, it’s people who mostly children it gets identified in, who get infections. They might get a strep throat infection and that’s PANDAS. And then PANS is any kind of infection. It could be mold, it could be a virus, it could be another bacteria. And then all of a sudden they get that kinda “Brain on Fire” autoimmune brain disease, where they get OCD and they get all kinds of symptoms.
And I’m also seeing that’s another pattern that I’m seeing in mold patients, is patients who have genes that make very, very high levels of TNF-alpha, where they have a change in what’s called the promoter, which is the on, off switch of the gene, where they naturally in response to whenever that gene gets activated. And so you talked about like an infection can be activated, they’re gonna get two to three times the response compared to somebody who doesn’t have those gene variants. And in the other case that I was thinking that we could talk about the patient, we’ll call her Julie, and of course, all of these patient’s names have been changed. Seriously ill after being in a house that had serious mold damage, including some black mold, but she got out of that house. But over the last 10 years, she’s had to move three times. Yeah, it’s been really–
Yeah, oh that’s.
If her house gets any water damage, any mold, she starts getting super sick again with brain fog and aching and with her genomics that TNF-alpha, which is again the ones there’s a lot of there’s… You could go look at 23andMe or again, I don’t mean to pick on 23andMe any of those things, ancestry, Genetic Genie, you can see there’s like a 100 TNF-alpha snips. Some of them might be more related to autoimmune gut issues. Some more to the brain inflammation. Some might do absolutely nothing, but she had some variants in the TNF-alpha that are known to relate to brain inflammation.
They’re associated with almost three times the risk of OCD, for example. And so as soon as she gets exposed to mold, she gets brain fog back. And she also gets joint pains because she had some TNF-alpha snips that are in the low side and in the location that relates to TNF-alpha going up in the joints. Ones related to rheumatoid arthritis and psoriatic arthritis. So all, and then gets you a double snips in both these pathways. Well, so once we know that we can use things that lower TNF-alpha, which include the sulforaphane, but even more strong, we can low more potent. We can lower TNF-alpha with things like Lion’s Mane Mushroom, and then she had a whole different set of mitochondrial issues, which we can talk about in a little while if you want.
Yeah, no, I just want to emphasize that the other… One of my big points to patients is that if you develop severe anxiety, severe depression, OCD, when you’re 40 or even 30, and you never had a hint of that stuff before you have an infection, you have chronic inflammation, you have ’cause that doesn’t happen in general. Most psychiatric illnesses, there’s a flavor of them when we’re young. I mean, we all have a little OCD or a little this or a little that, but it’s usually a pretty mild flavor and if it suddenly becomes overwhelmingly big at 30 or 40, it might be losing the job or the divorce, but think of infection or inflammation or exposure to something triggering your system.
I think that’s a great point, Eric. I think it’s also really important because some of these same inflammatory compounds that can cross the blood-brain barrier, like interleukin one alpha and interleukin one beta and TNF-alpha, it’s not only that they can contribute to psychiatric symptoms. IO-6 is another one. They can also contribute to cognitive decline if you leave them unchecked, they can contribute to OCD, so they can contribute to a lot of things, and so I agree. I think that not just assuming that, oh gosh, all of a sudden I’ve become stressed and that made me anxious or depressed or OCD, but saying, “Hey doc, what’s going on? Can we dig into this?” And so we actually have a whole product of looking at depression and anxiety and OCD as well, because, and as part of that, we give the same functional medicine basics of the gut panels, the inflammation panels, all the nutrients, because if you are low in certain nutrients, like let’s say you genetically overly throw out your magnesium or you don’t absorb magnesium well. Well, you can get magnesium depleted because you took some omeprazole, like some Nexium, the purple pill or whatever over the counter and it depleted your magnesium. And then all of a sudden you can become anxious because you need magnesium to make GABA which is the common thing. So, it’s really fascinating when you dig into the–
Yes, yes, yes, yes, yes. I mean that is, I mean these tools are what most of us who’ve been doing functional alternative medicine have always been looking for. And we have chased them, believe me. I mean, all the testing that I do over the years and I have, it’s like I call them the flavor of the month. Searching–
I’ve been in the field for awhile too.
Yeah, right. I mean, the beauty is you created one that actually, because I think that’s the thing of being a clinician. So many times people develop clinical tools because they read an article and they were a scientist and they figured out, oh, we can do this, We can test that. But I think what’s made this, what makes IntellxxDNA special is that you’ve been a clinician before and continuing. And so you’re in there with us and you’re making sure that these things actually supply us with the information. But I, so… Going back from it, ’cause you mentioned something that I’m very interested in, is how do you use looking at some of the things that affect mitochondrial function.
Yeah, so that’s great, that same patient I started to tell you about Julie. We can circle back to her as an example.
So, she had major mitochondrial issues, but it wasn’t in the same pathway. It wasn’t that NQO1, which is just a mitochondrial resettles to 10, which is a mitochondrial co-factor. She had instead a problem with her mitochondrial membrane. So mitochondria has this kind of like coating, like a capsule around it. And in the capsule there’s channels to bring in all the nutrients. She had a problem with that mitochondrial membrane, and that I think had a big, big factor for her, with her cognition and how she felt when she got exposed to mold, because mold again causes damage to your mitochondria. So she already had problems keeping her mitochondria alive and healthy. But there was some studies, some work by a physician. Actually, I think he’s an M.D.-PhD Garth Nicholson–
Oh, yeah, Garth. Who was nominated…
Yeah, he was nominated for a Nobel prize. So he is now retired, but he was at M.D. Anderson and chemotherapy from cancer patients would damage the mitochondrial membrane and make them feel tired. So, he showed that if you give mitochondrial membrane lipids and other mitochondrial cofactors back to patients who’ve had damage, you could really help their fatigue because you’re helping their mitochondria. And it sounds like a physics experiment, but it’s called vision and fusion. You take one damaged mitochondria and another damaged mitochondria, you give them all the new things they need to survive and they kinda share their broken parts and make a new one. And I think that’s pretty cool.
Yeah. I think that’s also assigned to mitochondria. When mitochondria are in a, what we call anti-inflammatory state, they actually hang together in like filmids and when they’re stressed, they break apart into more like into globules or into frown forms. And it’s interesting with the right nutrients that they would then form this more anti-inflammatory format of mitochondria. Yeah, so which are the particular genes that you, I mean, like one or two off the top of your head that you really look at for the pores for that trend?
Yeah. So there’s a bunch of, it’s mostly mitochondrial membrane genes. And again, like Tom40 is one of them they’re against other mitochondrial ones, but again, you have to know which variants and then you have to, and the interesting thing is then you have to kinda decide how are you gonna address it? Because it may depend on what’s going on with them. With her, she had mold damage and so the mold can actually damage that mitochondria. So not everyone with mold responds really well to mitochondrial lipids. In fact, I would say it’s only about 10%, which kind of fits with again, the genomics, but for her ATP fuel, which was a mixture of kind of those lipids and some other mitochondrial things worked really, really well along with like CAPEX or mitochon, she kind of alternates between.
But I think that the thing is, just so you know, mitochondrial there’s other mitochondrial pathways, all of that COX1, COX2, there’s tons of mitochondrial pathways. Mitochondrial genomics is really confusing because there’s two parts. There’s the mother or the fathers, there’s the DNA of the person that you get from both mom and dad. And then there’s also specific mitochondrial genes that you’ll only get from mom. So, we still are at the very beginning of mitochondrial genomics, but it does help in terms of, again, what I do is I kinda say, the genomics of mold. So, people have been asking me, from people like you, have been saying, “Hey Sharon, can you make a panel on mycotoxins and mold genomics?” And I’m really, I’m getting close.
I think that we will be able to this year. I couldn’t initially, because there was so little in the literature about how mold works on your genes, but then how your genomic variants interact with the mold. We’re now getting enough literature that I think we’ll be able to do that. And so right now, I think the biggest thing is to just kind of, you just go through the person’s report and say, “Let me just look at those things that are in less than 20% of the population and use my science brain and say, “Could this relate?” And when you come to one that says it relates to mitochondria, you go, “Oh, wow. She’s having brain fog, it relates to mitochondria.” This mitochondria are turned off by mold. Yes, let’s make sure we put that on the priority list to address.
Yeah, I think that is what people always, when I ask them to spend money on a test, that’s one of the things is, is what it’s gonna do. What is it gonna do for me? And, I like to be honest there are people who… I just say, we’re gonna treat because based on your story, I’m fairly sure you’ve got ABC and if finances are an issue, we can test only if I’m wrong or actually, I often do that with things like mass cell testing because I think it’s just easier to see if somebody responds, than to do a test that is just because of the technical issues around things being frozen and cold and transport, it’s gonna screw up. So, but what you’re offering us is one that we now have a reason, because we’re gonna save you a lot of time and money if we can figure it out correctly.
Yeah. And one of the things is, the tools are always being developed. So, I’m constantly, along with my research team, reading the research. Literally last night, as I was preparing to talk with you today, I was reading more about another gene pathway that I’m seeing a lot of in my mold related patients and it has to do with the response. So, chemokines are kind of chemical signals that call in colon inflammation to specific tissues. And so think of them as the guy at the parking lot, when we used to be able to go to concerts and different sporting events with the kind of going over here, over here, over here, that’s the chemokine. So, she had a chemokine pathway and it’s pretty common. It’s in about 25 to 28% of the population, but it causes more immune cell activation and more injury, more tissue damage ’cause it’s over-activation.
And I started noticing that it was in both of the two patients that I was telling you about. So then I went into some other mold patients and I’m like, this is a very common one. And so I was like, “Hm, I wanna kinda look and see it just can relate to mold.” And it turns out that mycotoxins already, one of the mycotoxins made by some of the trichothecenes, like just Trichothecium and you know, don’t worry about the names of them if you are not a mold expert, it’s just one of the ones that we see. It makes even more of this chemokine-8. So if you’re already making a lot of it–
That’s problematic. Well, what do we see in some of the mycotoxin people, some gut issues. So some of the people will have snips that make them highly intolerant to gluten. TNF-alpha can also affect that, there’s a whole bunch, but this chemokine-8, it turns out there’s a new intervention that I found. Have you heard of GOs like B-GOS as opposed to FOS, GOS?
No, tell me, tell me.
It’s in the family of the prebiotics–
I think it’s related to Acacia fiber and guar gum, and they showed that it was able to protect the intestinal bacteria against some of the mycotoxins. There’s a mycotoxins made by these fusarium called DON. I’m not gonna even try it–
Yeah, yeah, DON Yeah, Deoxynivaleno. It’s also a vomitoxin.
Yeah, it’s a Deoxynivaleno
So it turns out that GOS protects the intestinal barrier against that. So, now what? And it also improves your tight junctions. It helps block the inflammatory response, and you can get it in different. You could just like search there’s probiotics. There’s one from like True Health Nutrition, so it has it. There’s one called, I think it’s called . You just look for GOS or B-GOs. And then, so now I go back and I’m gonna add that to the chemokine-8 to the pathways. So our doctors that use Intellex DNA, they get the benefit of when I’m constantly doing reading. But then we also, I get emails constantly from all of our users and we have some wonderful users that used to be at the Mayo Clinic that had been at the NIH and the complementary medicine section from all over the world, they’ll send me different things. So the tool constantly builds. So that’s the other thing I love about it, is we can all share our knowledge and then have a place to kinda put it so we can all get better interventions over time and better response.
Yeah, no, it is the thing. I mean, I’m very impressed. I remember years ago we tried to build a Wiki to try and remember, what we did for what, when, because I mean, Dr. Anderson and I would laugh ’cause we’ve been working at this for so long, we would just forget about stuff because it worked for three to five patients. And then you hit a period when it just stopped working for the next bunch, because we didn’t know who we were treating.
And we would forget about these things. And the beauty of your tool is that you keep a nice current list of why, where, and how these things work.
Right. And I tell doctors, don’t try to learn the genomics. You have better things to put in your brain than 600 snips and their function, how to intervene. That’s why we have it in the tool right there for you. So when you get a patient’s genomics back, just kinda go through it and look at the ones that are most unique for that patient. Start there, and again, oftentimes we see great response and there can be really esoteric things. Like one of my mold patients, she had an inability to make vitamin C. Now mammals, humans, and all mammals, they can’t, I’m sorry to recycle vitamin C.
Make vitamin C, but if you have less ability to recycle it, you’re gonna need more. And vitamin C is also really important for clearing ochratoxins and for some of the glutathione pathways. So, I’m working in conjunction like the glutathione pathways. So, it’s fun because you don’t have to memorize. I actually say that I built it because I was never good at memorization. I was good at science, but I was not good at just, like to just sit there in anatomy and memorize something that was not my favorite. So, this helps me to keep my things organized.
Yeah, and it’s a beautiful thing. So, I mean, this has been so interesting and more important and so clinically relevant, you know? I mean like that is what’s exciting because I mean you’ve gone so far past what we started with list of snips, that we had no idea if they were up regulating snips down regulating snips–
Going into nucleus and affecting 20 other snips or a hundred other.
Yeah, we just did. We couldn’t tell, we just got lists of them. Oh, you have 20 snips in this pathway, maybe, does that mean as good or bad? Anyway, so it’s just really nice to have something that is taking the promise ’cause I mean genetics, I think promised a lot more than it could deliver for the last 30 years. We’ve been, I mean, everybody expected after 2000, when they had the genome, that life was gonna be easy to cure all disease was around the corner. And as we can see that hasn’t quite happened but understanding chronic illness, I think you’re really helping us move in that direction, and that’s very big and thank you.
If anybody has… So, one thing that people have to realize they cannot, a patient can’t order an Intellex DNA report. It is what’s called a clinical decision report tool, which means it has to be used by licensed healthcare professionals that are qualified to treat that kind of illness or chronic disease. But we do have something they can download on our website to let the doctor that they’re working with and we are happy to train their doctors. We even will walk physicians, again, I use physicians in a generic word. We’re happy to walk clinicians through their first three reports. We have training things. So we just, there… We definitely can give patients a list of doctors in their state that are licensed to, that are using Intellex DNA, but we’re also really happy to train new physicians. And there’s again lots of other information about it, it’s not just about mold and Lyme and brain–
Lots of other information, and we can always talk again more another time.
Looking forward to it. Again, thank you so much for your time.
Thank you, Eric.
Jeffrey Wood – Mechanical Causes of Chronic Illness