Hi friends, I’m very happy to be speaking with Dr. Sharon Hausman-Cohen today. She’s been using genomics for over a decade to deliver personalized medicine to help her patients achieve optimal health and wellness.
As a researcher and clinician advocate, she recognized that information inaccuracies and complexity were barriers to entry for many trying to use genetic information. She saw the need for an easy to use, accurate science based genomics interpretation tool for clinicians and began to develop what is now IntellxxDNA. In addition to being a well respected doctor and researcher, Dr. Hausman-Cohen is a sought after speaker and educator on genomics, personalized medicine, and integrative medicine.
Dr. Hausman Cohen received both her masters and medical degrees from Harvard Medical School. She’s board certified in family medicine and is a fellow of the American Board of Integrative and Holistic Medicine, possessing additional board certification in integrative medicine through the American Board of Physician Specialties. She’s been practicing full spectrum family medicine and integrative medicine for more than 20 years. She’s also the co-founder, chief science officer and medical director of IntellxxDNA that we’ll be talking about today.
Welcome, Dr. Sharon! Tell me a little bit more about your personal background. What ultimately brought you from practicing family medicine to create IntellxxDNA?
So in order to explain that, I think I’m going to go back one step before I went into medical school when I was in college. I was very involved in research and after college went to grad school, I was doing drug design making drugs more specific for the receptors. I did genetic research, and then I went to Harvard Medical School not to do a medical degree, but to do a PhD in medicine.
And what happened is when I was there, I discovered that I was interested in too many things. I didn’t want to dedicate my life to just studying one pathway in the brain or one receptor. Really as a PhD you go deep deep deep into one topic, and I realized I like so many things that after I finished my masters I left Harvard Graduate School – it was a PhD program at the medical school – and then applied to the medical school, and because I liked everything, I chose family medicine because what is that but specializing in people birth to death? So that’s pretty broad. You get to learn everything, but then through my career I always was interested in evidence based medicine.
I was always interested still in genetics and I was also interested in supplements and how they work because I had been an exchange student to Japan when I was younger.
So over time I got involved in integrative and functional medicine and then people would be bringing me their 23andMe and saying, hey, can you tell me how to prevent heart disease, how to prevent Alzheimer’s? And when I would look at the different tools out there for clinicians for interpreting DNA there wasn’t one that was evidence science based for doctors and other healthcare professionals that not only told you what the different genes do, but how you can modulate them. And why would you order a test if you don’t know what to do with it?
So for my patients I started setting out to kind of say OK, let me see if I can use your genomics to help you, and that led to the realization that every little SNP, the research of it, and figuring out how it works and how to modulate it took many, many, many dozens of hours, sometimes 100s of hours, and that I couldn’t do this just for myself. So my co-founder and I of the practice that we had – which was that we had moved to a practice that gave more private attention to patients – we said, let’s just build this tool. And so we did, and that became the groundwork for IntellxxDNA.
That is amazing. Having met you at one of Dr. Bredesen’s trainings, I know you are a dynamo and your interests are varied and you are so well versed on so many topics. At that particular training you were presenting on his Type 3, and I know that’s one of your areas of focus.
You know, it seems to me that your product would be so helpful for people that are having complex chronic issues. Allopathic medicine works beautifully for acute things like pneumonia, but it’s you know so many people in our community are having these complex chronic issues, and it seems like your product would just work beautifully in those cases.
It really does. I mean, I think that the way to think about it is … ApoE4 for example, which is obviously of great interest to your listeners. It’s one gene, but there are about 25,000, 30,000 genes in the genome, and ApoE4 interacts with, you know 1700 of them to start with, because it turns on and off a bunch of other ones, and so when somebody has an issue like an ApoE4 individual has a problem with mold or an ApoE4 gets long haul COVID, we’ve had the genomics really help us figure out how to get them well, because then we can kind of say oh this particular person some of their Achilles’ heels are, for example, that they make too much of a specific kind of inflammation, or that they really have more mitochondrial problems, so then we might give them more of those kinds of support …
Whereas we had another guy and he’s an APOE 4/4 and he got really scared after he got COVID because his cognition just dropped. I mean we had him at, you know, essentially a perfect MOCA, really doing great. He’s only in his 50s, but he’s worried ’cause he’s APOE 4/4 and he does a lot to protect himself. And then his MOCA suddenly dropped down to like 22-23 and he was really, really stressed. As you can imagine because he uses his brain for a living. He’s in the world of finance, and that’s pretty important, and so we went into his genomics ’cause we have genomics on the vast majority of our patients, and he has something called Factor 5 Leiden, which makes you have thicker blood and make more fibrinogen. He also has other genes that relate to the brain not getting enough oxygen. So what we immediately did is we put him on lumbrokinase, which kind of helps with dissolving that extra fibrinogen. And we put him on a lot of pycnogenol. Because again COVID makes that fibrin that extra clotting problem worse.
And then I saw him back literally 2 weeks later. And he’s like Doc, my brain is completely back to normal. Thank you so much. I was so scared and we wouldn’t have been able to kind of figure out what might have happened that quickly had I not known his genomics.
Wow, that’s a beautiful example of how your product could help members of our community.
Before we dive into a couple of case studies, let’s take a step backwards and cover a few basics. What is genomics? What is a SNP? Can you kind of go over some of those things?
Absolutely, and sometimes we’re so excited to talk about all these things that we forget that some people are listening that are new to this field.
So a SNP sounds like it should be like a little piece of cloth, but it actually stands for single nucleotide polymorphism.
And if you remember from science and for some people we didn’t get this until high school, kids are now learning this in 7th grade, but your DNA is that double helix and it’s made up of all these letters or base pairs, that we call nucleotides, and there’s only four. There’s A, G, T, and C, and it’s kind of like computer code with just 4 letters.
You can do a lot by switching up the order and encoding for what your DNA makes, what proteins. Well if you switch out a letter in your DNA, so a single nucleotide polymorphism is switching out one letter, it might not do anything, but it might change from whether or not you’re going to have dark hair that’s curly or straight hair that’s blonde, and in the medical world, it might make it so that you make 10 times more of an inflammatory product like TNF alpha because it might be on the on switch or it may make it so that you don’t transport B12 well into your brain.
So these little teeny changes can have significant changes on proteins, on hormones, on nutrient carriers. By themselves they don’t cause disease just like ApoE4 by itself is not causative for Alzheimer’s. Thank goodness. I mean 20% of the population has this, but it has an effect that can be modulated.
So a SNP is a single change in the DNA that can have an effect. How big the effect is depends where that little change in the DNA is, so that’s that’s kind of that piece.
Most genetic diseases are bigger events. There are some that are SNPs, but when you think of most genetic diseases there, they tend to be big deletions or big insertions, or sometimes it’s a SNP, but not the ones that we’re looking at, so our genomics looks at little changes in the DNA that by themselves don’t cause disease.
But when you add them up with the interactions with the environment can have a profound effect in an additive way, so that’s the that.
The other question you asked was what is genomics as opposed to genetics? Oh, I should have done that first, but genetics is kind of the study of heritability so there’s diseases that if your mom had, you have a 50% chance of getting, so that’s a genetic disease. But genomics is kind of more microscopic changes and so it’s genetic diseases again tend to be bigger events.
OK, as you can imagine epigenetics is huge in our community. As most in our community know, epigenetics is the study of how specific behaviors and environment can cause changes that affect the way your genes work. Does your product take epigenetics into account?
Well, one of the things that makes our product unique is we only list genes that we know how they work and that we have potential ways of addressing them of modifications.
And the vast majority of our modifications would be considered working on epigenetics, so the classic medical definition of epigenetics has to do with methylation. Methyl groups can turn off genes.
But we also know that food and environment and different things you know, exercise, can also have effects on the genome, so that definition of epigenetics has been expanded and, absolutely, every single one of the SNPs we look at. We give three, four, five, sometimes seven or eight different potential interventions. And some of them might be supplements. Some might be vitamins. Some might be foods to eat. Some might be things like exercise.
So there’s a gene BDNF, and I think a lot of your community have heard of BDNF. So BDNF is the growth factor. That’s kind of like fertilizer for the brain. And there are about 4% of the population that are really, really bad at converting Pro-BDNF. the kind of storage form, into the active form. Well, if you’re in that 4%, if you really, really exercise more intensely, you can bring your levels of BDNF almost to the norm. If you eat a higher butyrate diet. So a keto diet is a higher butyrate diet. If you take certain things like green coffee bean extract or other supplements. Milk thistle can affect BDNF.
All these different things and so we use the epigenetics in that broader sense is to say, OK, our DNA is not our destiny. What can we do about each of these genes?
And just so you know that the BDNF one, the reason I brought that up is, BDNF, even if you don’t have ApoE4, if you have a combination of three BDNF genes, it gives you 2.7 times the risk of Alzheimer’s, so it’s almost as much as an ApoE4, so it’s a really important gene, so knowing how to modify it is important.
Wow, so on top of fine tuning our protocols it seems as though your product will help us also better understand our risk.
Absolutely! So one of the things that I always say is that knowing your ApoE4 is either too much information or not enough information. And the reason I say that, the too much information is because if you know the classic is you give for Christmas or for Hanukkah your relative a kit for a direct to consumer ancestry type, you know, genomics tool. They go online, they find out they’re an ApoE4, that’s all they know. Well, they’re going to get panicked and go, oh my gosh, I’m gonna get Alzheimer’s. So that’s not enough information, because they’re then not knowing, well, what are some of the other things that interact, and there’s a lot of genes that if you don’t have certain genes, your risk as an ApoE4 gets cut in half.
I love that!
And then there’s other genes that make your risk higher, and so it’s not enough information to know just your ApoE4, because otherwise, what is your choice? Do you want to?
Do you know 60 different things or 30 different things without knowing if you need to, and if you’re young and you don’t have any cognitive decline, that can be very onerous and kind of really heavy, whereas if you can go oh, I’m a lucky ApoE4, not that I’m going to ignore it and, you know, eat a bunch of sugar and things like that, but if you don’t have some of the other genes that interact with ApoE4 and you know for me, my risks are really mitochondria or my wrists are really choline or my risks are really my detox pathways. Then you can come up with an empowering specific treatment plan to help you stay well, that feels very specific to you.
Oh I love that. I hope you brought some ApoE4 case studies that we can talk about.
I did and do you want to start with one of somebody who was having cognitive decline and we got better or you want to start with somebody who’s an APOE 4/4 in their 70s and is still doing great? Which do you prefer?
You could go ahead and pick because I think we have almost everyone represented in our community, so any ApoE4 case studies would be great.
So I’m going to start with a woman who is an engineer, and we’re going to call her Sandy. And for our clinicians, ’cause I know some of the clinicians who watch our party or community may be listening, this is one of the cases we used during the ReCODE Apollo training when we’re teaching on genomics, ’cause it’s such an interesting and, really, a great illustration of why it’s important not to immediately go to somebody who starts having cognitive decline in their 50s, oh my gosh, you might have, you know, APP or Presenilin-1 because a lot of times it’s just a belief or with some other things that kind of happened, and so she came to us because she was 52, an engineer, and was starting to have problems with math. And that is difficult for engineers, and was thinking that she needed to switch careers or retire and was really scared. She is an ApoE4. But again, most people with ApoE4 don’t start having problems until they are in at least their 60s and many times 70s or later.
So what we did is we did her genomics because that allows us to kind of dig deeper and say well what is going on. And she had some things that we would not have known about. She had a particular mitochondrial pathway. So ApoE4s in general have a lot of mitochondrial issues. It’s a common and one of the reasons is one of the big mitochondrial membrane genes that is important for the health of the mitochondria is right next door to ApoE4, and 75% of the time it’s co-inherited. Meaning, 75% of ApoE4s get this problem with their mitochondria just because of the way the genes are inherited and then ApoE4 can affect mitochondria, but she didn’t have that.
But instead she had a different mitochondrial problem, and the reason that that’s important is different problems take different solutions, so for people who have mitochondrial membrane issues, things like phosphatidyl choline, phosphatidyl serine, the different membrane lipids like NT lipid factor or ATP fuel can be really helpful as well as giving all the different things mitochondria need, like a K-PAX or a MitoCore or I know that there’s some LifeSeasons products as well that have the acetyl L carnitine and have the alpha lipoic acid and the CoQ10 and all those things.
But that wasn’t her issue. Her issue was in the ability to make mitochondrial DNA to make the purines. Well if you can’t keep your mitochondrial DNA alive, your mitochondria don’t stay alive and the treatment for that is different because it’s not CoQ10, it’s actually folinic acid and betaine and citicoline that kind of helped push that pathway. So that was we wouldn’t have known that otherwise.
She also had some pretty significant B12 issues. Being able to carry B12 into your brain is really important. If we measure in the blood B12, you’re going to get different levels, but the carrier for B12 in the blood is different than the carrier in the brain. So 80% of your B12 is this carrier TCN-1, which is in your blood but the brain carrier is TCN-2. So if you have two copies of TCN-2, you need a much higher level of B12 than someone who doesn’t have that because you have to kind of flood the receptors.
She also had problems with vitamin D, which is relatively common, and then had some different problems with detox pathways. And again, depending on what detox pathways are affected, we have different ways of modulating them with glutathione, with N-acetyl cysteine, with even rosemary up regulates certain of the detox pathways.
And so we kind of just went through all of her DNA. We did also – she was new. She was not a member of your community. She didn’t understand that diet has a huge effect on ApoE4, so we helped her change her diet to a mild ketotic diet, and she responded great. Literally, within three months she was feeling so much better and able to feel comfortable that she’d be able to stay at work.
And so, but really some of those key pieces were ones we wouldn’t have been able to measure in the blood. Oh, the other one that she had that we wouldn’t have been able to measure in the blood is the ability for the brain to convert thyroid hormone to its active form. Thyroid T3 in the blood does not relate to T3 in the brain, and I think that’s a really important fact here is that you can measure something in the blood, but because of the blood brain barrier, it’s not the same. And every tissue – your bones, your heart, your kidneys, your brain – they all have different expression of DNA.
And then the last one she had, which was I would say that the mitochondrial thing and then this are probably the most important was she had something called a TNF alpha promoter SNP, and, have you heard of a promoter, Julie?
Yeah, but explain what that is for our listeners.
Yeah, so genes, we don’t want our genes on all the time. It’s kind of like you wouldn’t want everything electric in your house on at once. It would create chaos or in the world, so we have these things called promoters which are basically on off switches in front of our genes and her TNF alpha promoter was way too active. So it’s kind of like always having the light switch on. Well high TNF alpha will cause not only inflammation in the brain, but it leads to almost destruction of tissue if you get too much inflammation.
And lion’s mane, for example, is really good at turning off TNF alpha expression, lowering it. And there was a study done in Japan using lion’s mane in people who had mild cognitive impairment and at the end of this study, just giving lion’s mane, and they didn’t have the genomics, but in this study they showed that 72% of the people who got two grams of lion’s mane a day had an increase in their score – it was kind of like a MOCA but a Japanese equivalent, so, memory test – of three points or more and 27% had an increase of two points or more and in the placebo group it was the opposite. 70% of the people in the placebo group had no improvement or zero to one, and only 7% had an increase of three points or more during the course of the study.
So you know, we think about the drugs that were recently approved for Alzheimer’s that showed 20% less worsening of cognition. Can you imagine if a drug showed that 70% of the people got three points improvement on a 30 point test?
They went from an average of 23 to an average of 26, which is a huge difference, and so for her, that was another really important one, adding the lion’s mane. And so again, we were able to get her feeling comfortable. She was one of our first patients, so that was three or four years ago, and she’s still doing great. She barely needs us anymore because she now knows what to do for her body.
I love that! That is such a hopeful example. You mentioned you have another example of somebody who’s using this for prevention.
Well, I have a woman who came to me – and I have quite a few APOE 4/4s all doing great. So first of all, that’s really helpful. And one of them is about 67. The other woman is 79 and she’s still doing perfect. I mean, her cognition is probably as good as mine. I mean, she is amazing and very, very with it. And so when you get these people and you go, well, she’s APOE 4/4 and she didn’t even know she was an ApoE4.
So this woman came to us, and her main complaint was fatigue. She’s 77 years old when she came to us and now I think she’s 79. And she came because she wanted to optimize her health. She mostly was feeling tired and she was having trouble losing weight, had a little bit high blood sugar, had high blood pressure that was hard to control, so some just kind of normal things that people worry about in their 70s as they get older and we did her genomics because it can help also with optimizing blood sugar, understanding why your blood sugar goes high, understanding your cardiac risk, and so we were really surprised when it came back, and it showed that she was an APOE 4/4 because she wasn’t complaining about cognition. And so I asked her, are you having any cognitive impairment? She said, well, you know, I mostly just feel tired, I wouldn’t really describe it as brain fog. And at that point we’d already given her vitamin D because I had some blood work back and I had given her mitochondrial supplements because what she was describing with that kind of fatigue and she also had a little bit of just sensations in her legs, which is common in people who have mitochondrial things. Their nerves just don’t feel right.
But her MOCA was perfect and, well, I think she had a 29, but that’s still very good, obviously. And so then I dug into her DNA to go, this is really interesting – let’s look at why you’re doing so well, and there’s quite a few genes that work in combination, so MTHFR works in combination with certain inflammatory genes and that TNF alpha works in combination so TNF alpha and ApoE4 can have a huge additive effect in some people, dramatically increasing the risk. Again, there’s a gene in a cholinesterase pathway, so – you guys heard of acetylcholinesterase – well, there’s other cholinesterases that relate to how these brain chemicals are treated, and she had really none of the ones other than one copy of 1 mitochondrial one that interact with the ApoE4 to cause additive risk, so that made her actual risk much lower than a typical APOE 4/4.
So I have patients who came to me really terrified in their 50s, or whenever, because their cardiologists or their regular doctor did a Boston Heart or a Cleveland Clinic, and they go oh, and by the way, you’re in APOE 4/4 without giving him more information. And they look it up and they go. oh my gosh, I’m gonna, you know, get Alzheimer’s.
But we were able to kind of say hey look, let’s make sure we do things to protect your brain, but you’re doing really well. Let’s understand why you’re doing well, and then let’s say, what do we need to do to ensure that that’s going to continue? And it’s not that taking 20 or 30 or 40 supplements is necessarily bad for you, but number one, it’s expensive. And if you don’t need to, if some of those aren’t necessary for you, because you’re really good at making choline or because you are great at transporting B12, or you don’t have the mitochondrial issues as much as someone else, you might not need as much mitochondrial support. It’s just nice to be able to kind of be more selective and there’s a lot of other pathways that contribute as well that we haven’t even talked about like hormone pathways. And you know, different inflammatory ones.
Absolutely. I mean, you’re taking precision medicine to a whole new level.
There’s a case that I’m following where they just ordered an IntellxxDNA report. It’s a woman with mild cognitive impairment who’s several decades post menopause, and her practitioner put her on estradiol. And she’s having hot flashes in response, and they can’t quite figure it out. So somebody thought, let’s order IntellxxDNA, so I’ll be very curious to see how that plays out.
You, you’ve totally convinced me and I’m going to go ahead and run my own genomics. And if you’re willing, let’s go ahead and make a Part 2 of this discussion, and maybe you can share some highlights from my report so that our listeners can see in real time how my protocol might change or how I might be able to fine tune it based upon my results.
Absolutely, and one of the things Julie that you and I had talked about that I think we do want the audience and your listeners to understand is IntellxxDNA has so much information in it. It has things not only about supplements, but things about medications. It gives dosing of supplements. It links to thousands of studies. It talks about things like brain ischemia, which is kind of like the stroke risk with different coagulation factors of blood clotting risks.
So it falls under a little bit different FDA category than any of the direct to consumer genomic tools.
It’s what’s called a clinical decision support tool, which means IntellxxDNA can only be sold to a licensed healthcare professional – an MD a DO, a naturopath, a nurse practitioner, a PA. So we understand that there are lots of people who want this information, but know that what your listeners will have to do is either reach out to IntellxxDNA and we can let them know people trained already in their state or we are happy as kind of a special for your listeners if they have a doctor that’s been working with them on their brain protocol or a naturopath or a licensed healthcare professional … if they let us know that they’re part of your ApoE4 community and that they refer their doctor, we will give their doctor online access to training. We will waive the training fees. We don’t want people to have to switch their doctors or switch their healthcare provider. So we will give them free access to our online training and we also help train our clinicians. We actually walk them through their first three reports so that they can feel 100% comfortable that they’re giving as good of a consult with the first report as they are with their 100th report.
So don’t be afraid to reach out to your clinician. Most of them will have heard of it, and maybe be kind of waiting and going, I don’t know, do I want to do this? Do I not? ‘Cause it does take a little bit of time on the clinician’s part to learn. I can pretty much guarantee that once they start using it, they’ll be like, oh my gosh, this is getting outcomes is so much easier and that they will love it, but know that they’ll get a chance to work directly with me and with our research team so that we will help make sure that your community patients all get great responses and understanding.
Thank you so much. That is very generous.
So you’ve covered some really important stuff – we can’t order a report ourselves. We have to go through our practitioners or identify one of your providers and many of them do telemedicine, so geography shouldn’t be a limiting factor.
We do on our website have a little sheet you can download and take to your doctors. Saying, here’s some information about it, because sometimes if they haven’t heard about it, they’re like, oh, you know, I tried some of those genomic tools. It didn’t really give me any information.
Well, they weren’t legally even allowed to give information because if you sell to the consumer, but also we took many years and many millions of dollars to build a tool useful for functional and integrative trained providers and particularly ReCODE providers because I was in the middle of building it, I’d just built heart disease and macular degeneration, when I was presenting about the CIRS as it was called at that time, the mold issues, at the conference at the Buck Institute where you and I met, and I went up to Dale and I said, hey, I’m thinking of adding all the cognition into our genomics. Can I make it kind of match to be supportive of the ReCODE providers because I can include the BDNF and the choline and the hormones and the mitochondria and the CoQ10 and all those things. And he was like, of course!
You know, he always says if somebody is going to do something that’s gonna help, I’m agnostic. We’re all here to try to help people, and so this was built to help clinicians. And of course it helps patients. But we want to work as a team, but there is a sheet you can take to your clinicians.
On our website there’s some podcasts and webinars if you want to listen, like Dr. Crag Tanio who is one of the ReCODE providers. He did an interview specifically about how he’s using it. We have ones that you can watch that are video, so please feel free to to link.
Definitely, yeah, we’re going to go ahead and link to your website so people can go ahead and look through all of your information. And you are so right that the practitioners who do become trained with IntellxxDNA are hooked. I’ve heard very very positive things. And Dr. Bredesen is more than agnostic. He’s actually used your tool in his most recent clinical trial, which he’s still writing up, so that’s very exciting.
And we have we have a link to that preprint on our website as well, because that preprint is available. And yes, we were of course honored to be the genomics tool that he chose to use as part of the study.
And one of the things that Dr. Bredesen will tell you is, in the study, there were just some really interesting cases where, like a gentleman who was flying from California to Asia – this was before COVID – on a regular basis and he would get worse cognition every time he would fly. Well, we were able to identify what was going on with him that was causing that, and again, it was something that was more related to brain ischemia, and then we were able to reverse it.
So we’re not at the end of genomics by any means. We’re still the beginning of our understanding of how we can use personalized medicine, but we do address many, many hundreds of SNPs that allow you still to have a much more personalized plan of understanding.
Are you someone that has horrible detox pathways, but it’s not just one detox pathway? There’s some that are modulated by vitamin C, some that are modulated by glutathione, some that are modulated by NAD, and NAC, and sulphurophane. So it really helps personalize even within a subset of being a Type 3, well. which kind of toxins do I build up and why?
Right, I’m very excited to have my own genomics done, and I love that you mentioned we’re really at the infancy of understanding how this affects health, so I assume that your research team is always reading new papers and updating your reports.
We are, so there’s two different ways our reports get updated. So for example, I was working reading and there is a transporter of amyloid that we didn’t have in our report, but we have it on our array. We have it on our backbone. We have a few hundred thousand things we could talk about. Can you imagine if we gave a report that had 200,000 pieces of data? No one would want it, but this one was important because it turns out that it’s involved in removal of amyloid from the brain, and it’s associated with increased cognitive impairment in Alzheimer’s, but also persistent Lyme. Well, that’s like a really important SNP and it gives you three times the chances of having ongoing symptoms after having had Lyme disease, because it kind of traps stuff in the amyloid biofilm. Amyloid can be part of a biofilm itself, and so we just added that this week, and so we’re constantly adding new things.
And then we also for people who have different things going on will have additional kind of add-on reports, so not so much in the ApoE4 world but for example we have a mental wellness report that is more geared at psychiatric things like OCD and anxiety and depression and stress and ADHD, which of course we all have those as well and then we have an add-on report for children with neurodevelopmental disorders like autism.
And so we’re in a lot of different topics and constantly ongoing research right now further into Lyme and mold and chemical sensitivity. And there’s so much that we can study. We’ve got hundreds of things to study. It’s all a matter of time and energy and funding and all that.
All of the things you mentioned, the Lyme, the Lyme coinfections, the mold, affects so many members of our community, so I can’t thank you enough.
I encourage everyone to check out our show notes. We’re going to have a transcript. We’ll have more information. And we will have a link to Dr. Sharon’s site.
So thank you and goodbye until our next podcast.
Thanks, Julie. Thank you so much for having me.
Yeah bye bye.