Episode 68: What’s the deal with Lectins and Autoimmunity? with Dr. Datis Kharrazian

If you’re practicing functional medicine, you’re aware of (and likely prescribing) the autoimmune paleo diet. You’re pulling folks off of many foods, lowering carbs, reducing or eliminating lectins (including nightshades).

In my conversation with Dr. Datis Kharrazian, we talk about his impressive PhD research (under the guidance of Aristo Vojdani, PhD) in stratifying who’s at risk for lectin intolerance. Dr. K suspects that roughly 30% of his autoimmune patients are truly lectin sensitive – they tend to be those with arthritic musculoskeletal autoimmunity – most classically rheumatoid arthritis.

However, lectin/nightshade elimination may not be required for, say, Hashimoto’s; although he’s identified a collection of potential cross-reactive foods that could play a role in promoting antibody production (and likewise, removing will reduce antibody production). But the flipside of this coin is that Datis also encounters patients who’ve been following these restrictive diets for so long, they’ve greatly compromised their microbiomes, inadvertently furthering disease pathogenesis.

What’s the solution? Join us for an illuminating drill-down conversation into Dr K’s research, and individualized approach to the lectin/AI connection, and be sure to like, rate, comment wherever you listen to New Frontiers! I so appreciate your feedback! ~DrKF

Dr. Datis Kharrazian has a long list of letters after his name — PhD, DHSc, DC, MS, MMSc, FACN — and wears a variety of hats.

He is a clinical research scientist, academic professor, and a functional medicine health care provider.

He specializes in developing evidence-based models to treat autoimmune, neurological, and unidentified chronic diseases using non-pharmaceutical applications such as diet, nutrition, and lifestyle medicine.

He is an Associate Clinical Professor at Loma Linda University School of Medicine and a faculty member for the Institute for Functional Medicine. In this podcast, he talks with Dr. Fitzgerald about understanding, testing, and treating patients with autoimmune and neurological conditions with diet and lifestyle.

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• Kharrazian Institute
• Dr. K News
• Islet Cell Cross-Reactivity
• Thyroid Cross-Reactivity and Dietary Proteins
• BPA and Autoimmunity
• BPA and Alpha-Synuclein Antibodies

Dr. Kara Fitzgerald: Hi everybody. Welcome to New Frontiers in Functional Medicine, where we are interviewing the best minds in functional medicine, and today is no exception. If you like what you’ve been hearing over our years of broadcasting this podcast, please, please, please consider shooting over to iTunes and leaving a review. I would be most grateful.

Today, we’re talking with just really one of the fabulous luminaries of the functional medicine field, Dr. Datis Kharrazian. I know you know who he is, and hopefully we’ll touch upon the many, many, many different areas that he’s working on, and you get to hear about your particular favorite Datis area.

But, his background. He has a Doctorate in Chiropractic, which he obtained from Southern California University of Health Sciences. He’s also got an MS in Human Nutrition from the University of Bridgeport, and a PhD and Doctor of Health Science from Nova Southeastern University. His PhD was in Health Science, with concentrations in immunology and toxicology. 

He completed post-doctorate training at Harvard Medical School and Mass. General Hospital. At the same time, he completed a Master’s of Medical Science degree in Clinical Investigation, also from Harvard. He’s now a professor, a research scientist, a functional medicine healthcare provider, and actually an educator beyond.

In healthcare, he develops evidence-based models using diet, nutrition, lifestyle and neurological exercises for various chronic diseases. 

He’s an Associate Clinical Professor at Loma Linda University School of Medicine, and a research fellow at Harvard Medical School, and a research fellow at the Department of Neurology at Mass. General Hospital. Dr. Kharrazian, welcome to New Frontiers.

Dr. Datis Kharrazian: Thank you.

Dr. Kara Fitzgerald: So when I was reading this bio, which incidentally is the abridged bio, my first thought was what’s a day in your life these days, Datis?

Dr. Datis Kharrazian: So I have a unique schedule. I do research and writing one week and I see patients the other week, and it alternates month to month. So I usually just wake up, try to get a quick workout in, and then I just start hitting papers, reading papers, or hitting a patient case file I need to go through before I see patients.

So it alternates between reading research papers, writing, and doing data analysis to getting ready to evaluate a patient and figure out a strategy to manage their case. 

Those are my two main hats, either doing research writing for education and manuscripts, or for seeing patients.

Dr. Kara Fitzgerald: Yeah. Right, interesting. So then, your practice is in California?

Dr. Datis Kharrazian: Yes, I practice in San Diego.

Dr. Kara Fitzgerald: You’re in San Diego still, okay. And are you with other clinicians, or are you on your own?

Dr. Datis Kharrazian: No, I have just a solo practice. I’ve always just wanted the peace of having a quiet environment just with me and a patient, so I don’t have anyone else there. It’s really basically a small office with a bunch of examination equipment and everything everywhere, and like a living room environment. 

Patients come in and we sit down. I usually spend the full day with a new patient, and figure out everything. My exam usually takes about four hours. It’s very thorough. And then we send them out for labs and imaging and anything else we need to do, and then we put together a treatment plan. It takes me a few days to organize the treatment plan, to really think through it. 

I only see a small handful of new patients a month, no more than six, and most months mostly just four, complicated cases. I spend quite a bit of time in each one.

Dr. Kara Fitzgerald: Okay. Yeah, I know you do. And are you accepting referrals? I mean, I’m assuming your waiting list is probably huge.

Dr. Datis Kharrazian: Yeah, I mean we’re always working with new patients. We require a lot for our new patients. We require them to get all their past medical records, send us detailed narratives, do long paperwork, so we get a lot of them that don’t filter through because they’re not willing to give us all the information that I need to know their case.

Dr. Kara Fitzgerald: Okay.

Dr. Datis Kharrazian: So, even though we do get a lot of referrals, by the time people go through the process of getting all the material in to us, we kind of narrow it down to the amount of people we can handle, so it works out great.

Dr. Kara Fitzgerald: Okay, all right. Well that’s perfect, that sounds a unique model in a profession where we’re already spending a lot of time with folks, but we will link to your appropriate contacts as you’d like us to have on our show notes.

So, talk to me a little bit about how you got into the field. You’ve got a lot of initials after your name. You’ve continually pursued really deep education. 

I’ve been following you in your PhD trajectory and some of the cool post-docs you’ve been doing with Martha Herbert, and I know Aristo Vojdani was, I think, your PhD advisor, and just layers of cool work that I’d love to drill down on. So just kind of walk me through how you got into functional medicine, bring us to current and then we’ll talk about some of that.

Dr. Datis Kharrazian: Sure, I mean I got into functional medicine because I had a sick family member and they were helped by someone who did nutrition at the time, where functional medicine still wasn’t developed as a concept and as an institution. And I started going to a lot of IFM meetings and going, “Okay, this totally makes sense.” This whole model of doing laboratory analysis, not guessing, and doing a systems biology approach seemed to be the most logical, and I just resonated with it right away. My mom was helped by the chiropractor and the nutrition, so that’s what I ended up doing. I didn’t even think of any other route. And then, when I finished with that, I realized I needed to learn more about nutrition, so I went and got my Master’s in Nutrition, and then as I was going through the cross-link, I really need to understand research, and I was working with Dr. Vojdani. He was like, “You really need to own your data analysis,” and I’m like, “Okay.”

So then I went to finish that Clinical Investigation course at Harvard Medical School, just on data analysis and statistics, and research methodology, and then I got a chance to do my post-doc there, just around some of the best researchers and really learning how to do good medical research and how to do proper data analysis and study designs and it’s been a great journey. It’s been fun all the way along, and now I feel like I’ve been able to finally put stuff together like I never have before, now that I have this background in research, and I’ve always practiced with chronic patients. 

It’s been a fun journey, it’s been enjoyable.

Dr. Kara Fitzgerald: Yeah, it’s been fascinating to watch you, and I think you’re just bringing a lot of richness to the field. Listen, I just want to jump back to a day-in-the-life of Datis. 

I just want to point this out to our listeners. I’m reading a pretty cool interview that you gave to Dr. Bob Rountree and I’ll link to this in our shownotes. So folks, if you have access to alternative and complimentary therapies, if you have access to that journal, or if you want to actually pay for this it is behind a pay wall, you can download a great conversation that Dr. Rountree and Dr. Kharrazian had.

As I’m reading your background, Datis, just over the years that our paths have crossed, I know you’re a busy guy and you’re doing a lot of stuff. I’m like, is he actually walking the walk, and applying what you’re teaching your patients and lecturing on?

And we were talking about it, you mentioned that you take the whole summer off with your family. Like you really just kind of check out and get into some, what sounds like, is probably really grounding nourishment. 

Let me just ask you, why don’t you speak to that rather than me making a comment? How you actually manage this and engage in some degree of self-care as well?

Dr. Datis Kharrazian: Yes, I do take the summer off. I’ve just kind of always been fascinated with how Europeans live, and my wife and I, years ago, decided we need to just take time off as a family, and just disconnect from the world. So we work very, very hard throughout the year and then we plan for two months off in the summer, and we just kind of disconnect from the world.

I still have to stay in touch with some patients, because they need constant communication, but it’s just a matter of having time to find out who you are, be with your family and not getting stuck in the rat race, which I’ve done. I also do take one day off a week where I don’t do anything, and that seems to really make things work, where I’m excited.

So just one day off a week, don’t plan anything, not even a phone call or a meeting or anything, can really help you revive and function and stay at peak performance. 

I know all this because I’ve completely burnt out, like most of us have, and I’m sure you have. Just really been really excited about what they do.

 Dr. Kara Fitzgerald: Well, you’re at Loma Linda, and they’re a Blue Zone. That’s where you’re teaching and I think that’s kind of the Seventh-day Adventist way, isn’t it? They really actually take a day of rest on Sunday, unlike most of us.

Dr. Datis Kharrazian: Yes, it’s interesting. I don’t know much about the Seventh-day Adventists, even though I teach at Loma Linda. I know that they’re a very close group, and they do have a huge family and community together and they do take the day off and they’re very much interested in diet and nutrition, which is great for medical school. But yeah, it is true, it is a Blue Zone and people there have been found to have less cardiovascular disease and live longer. I think a large part of that is just the great sense of community they have and trying to do things like take a day off and balance things out.

Dr. Kara Fitzgerald: Yeah. So, talk to me about your PhD work, and that was one of the reasons I wanted to have a conversation with you.

You’re looking at sort of neo-antigens, so chemical protein antigens and I think you were doing some research in that with Dr. Vojdani, and you’re looking at cross-reactions and so forth, so kind of talk about your PHD work and maybe some of the research out of that.

Dr. Datis Kharrazian: Sure, so my PhD mentor was Dr. Aristo Vojdani, and I was very fortunate to have him as a mentor in my life. My actual PhD thesis was the association between tetrabromobisphenol A and neurological target sites, and basically the premise of what we were able to prove was that chemicals circulate in the body, but they bind to proteins. When they bind to proteins, they change the structure of the protein, and the protein becomes a new antigen. Then that antigen now can trigger inflammatory reactions, and then that new protein antigen may have the potential to have cross-reactivity, or molecular mimicry with soft tissue proteins. 

So we were able to show a very strong relationship between fire retardants and the development of neurological autoimmunity in my PhD, and it’s just a different model. It’s a new model, where we always think of chemicals as being toxic and they destroy the mitochondria, and they cause oxidative stress. My PhD work was showing that it was a completely different mechanism, which really involves… chemicals aren’t just toxic, but they can change proteins and when they change the proteins that becomes the new antigen. It was a completely different model of autoimmunity.

Dr. Kara Fitzgerald: Right. How did you do that? How did you figure out that, so BPA is damaging a particular protein structure and then that compound becomes antigenic, and there’s a molecular mimicry with actual tissue? 

Dr. Datis Kharrazian: So I was very fortunate to have Dr. Vojdani as a great mentor, number one, and it was really through his guidance and his conversations and his help that led to my thesis. But basically, for the most part, you can look at every amino acid sequence in the data. So we can print it out and then you can match and see if they are linked together. And if they are linked together, then you can use monoclonal antibodies and look for specific cross-reactivity with [inaudible 00:13:01]. And there’s a lot of trial and error, and there’s a lot of time where you think something’s going to work and it doesn’t.

But it was just a matter of having a really experienced mentor to help me in discussions that made the difference. And I was very fortunate to have great mentors in my career, and I think my PhD work was really based on having a great mentor. That really helped me.

Dr. Kara Fitzgerald: Yeah. 

Dr. Datis Kharrazian: So I can’t take really any credit for it myself. It was him.

Dr. Kara Fitzgerald: It sounds like you asked the right compelling questions.

Dr. Datis Kharrazian: The only thing I knew was to find who the right mentors were so far. That’s the only credit I can give myself.

Dr. Kara Fitzgerald: So, we’re all exposed to BPA, unfortunately a lot of it unless we’re wearing gloves when we go to any store, or turn down a receipt. I mean, it’s just, BPA is horribly ubiquitous and there’s a ton of good research, thinking about Randy Jirtle and the agouti mouse model, and BPA causing the expression of the agouti gene and turning on cardiovascular disease and obesity and all of that, and then there’s of course the BPA research as an endocrine disrupter. 

But in terms of this cross-reactivity potential, is there any particular population who’s vulnerable to this, or are we all vulnerable with this chronic BPA exposure?

Dr. Datis Kharrazian: So, if you look at the studies published, one study published found that if they test any random human, 90 percent of the population they test will have very high levels of BPA. So we know most people have them. We’ve published a study in the Journal of Applied Toxicology a couple years ago, when we checked to see how many people in the population have antibodies to BPA-bound to albumin, the protein, in their blood. It was about 13 percent. 

One of the key things we learned was that, even though most people have very high levels of BPA, there’s only a subset that actually make antigens against them. So the question is why? Why does that happen? So one of the groups we studied was Parkinson’s disease patients, because patients with Parkinson’s have been shown to have impaired pathways to clear BPA. If you can’t clear BPA out of your body through your biotransformation pathways, Phase I, phase II in the liver, then the BPA sits around in your blood. 

The most abundant protein in the blood is albumin, to help with our osmotic pressure and so forth. So then we looked at BPA binding to albumin, and then we found that, yeah, people have antibodies against this protein. Then what we did is we looked at associations and risk ratios between these new proteins with BPA and alpha-synuclein and other autoimmune target proteins, and we found really, really significant associations. 

I think it’s a combination of why people react and build antibodies to chemicals, not a protein, is personal. They probably can’t clear them, they can’t biotransform them, which is a key concept in functional medicine. Then also they lose what’s called an intolerance, so we don’t react to everything. You only react to some things. People that start to react to everything lose their Treg function. Their genetics are overactive, or they have intestinal permeability or things like that. It’s a combination of all the things we treat in functional medicine, biotransformation issues, loss of tolerance, permeability, Treg dysfunction, that really lead to that expression.

Dr. Kara Fitzgerald: Awesome. It’s great, I mean it’s disheartening that 90 percent of us have a BPA burden, and that some of us just can’t clear it over time, but understanding the pathophysiology as you’ve just outlined in functional medicine also provides the map to back out of it. Ideally, we’re doing prevention. In fact, I know you have a neuro-inflammation conference coming up, and we’ll link to it on the show notes, and Dr. Kharrazian will tell us about it as well.

So basically, we need to have our biotransformation pathways humming along. What’s interesting, one of the things I was taught back in the lab, when I was working under Richard Lord, is that you spend, unlike using glutathione as a redox compound, when you’re actually using it as a detox molecule, you spend a mole, mole per mole of whatever you’re moving out. So if somebody’s got an endless burden, they need to be replenishing those biotransformation compounds. So if somebody’s inundated with BPA, they’re going to need glycine and glutathione and whatever biotransformation pathways, they’re going to need those nutrients replenished over time. 

Certainly, if we’re inundated with toxicity, and we’re not adequately nourished, the levels could accumulate and we’re not clearing them. And then you talked about gut and the loss of tolerance, the microbiome disturbance, intestinal permeability. In your mind, what would be the first imbalance to happen, or is it just kind of concurrent exposures through life? Gut imbalance, liver imbalance, how might you think through the peeling away the onion?

Dr. Datis Kharrazian: That’s a good question. I think, so for me if I see someone who is, if we do for example, a food immune reactivity profile and they react to every single food, then we know they’ve lost their oral tolerance, so we focus on their Treg function in their gut and dendritic cells more, and then maybe start the biotransformation pathways.

I like to do Cyrex Array 11 to check for chemical immune reactivity, and I like to do Cyrex Array 10 to check for food reactivity. So if I see a lot of chemical antibody reactions with Cyrex Array 11, then I may start with biotransformation pathways, and if I see a lot of loss of tolerance to food proteins and reactions to the food protein, I may start with gut. 

A lot of times, those two work together, and it’s not that hard to support someone’s tolerance by things like Vitamin A and Vitamin D and short-chain fatty acids like butyrate and then start working with let’s say a detox biotransformation product to help the phase I and phase II pathways together as they’re making some lifestyle and dietary changes to kind of break the vicious cycle. At the end of the day, it’s a vicious cycle, so it’s kind of, how do you approach pulling on the web with as many different factors that can unwind it. 

It’s typically a combination approach, I think, how most people in functional medicine practice. It’s kind of how I usually do it. I don’t think it’s much different from other practitioners.

Dr. Kara Fitzgerald: Yeah. Okay, got it. What about, just out of curiosity, your thoughts on using sublingual immunotherapy and building tolerance that way?

Dr. Datis Kharrazian: Well, I think it’s hit or miss. I think when we look at the different antigens, like low-dose antigens to see an effect, for me clinically, I don’t know what the other variables are that make it work or not work, so it’s not a first line of therapy. But if we do get desperate at times, we’ll have patients go that route, if we’re just running out of options to support them. 

There’s obviously some clear literature that shows that it has a very re-modulating effect, in isolated research studies, but in real practice there’s too many variables that don’t make that as clear as we’d like it to be, so it’s not an area that I have a lot of expertise in and it’s not my first line of treatment because I simply don’t know what the variables are that make the change that some of these studies show.

Dr. Kara Fitzgerald: Right. Well, I would imagine that it has to do with some of what you’ve already outlined, intestinal permeability, Vitamin D, Vitamin A, you mentioned butyrate. 

What kind of diets are you prescribing?

Dr. Datis Kharrazian: Well, I work with a lot of autoimmune patients and I work with a lot of patients with head traumas and neurological diseases. So, I mean at the very baseline, I’m doing a gluten/dairy-free diet with most of these patients, but most patients are already on a gluten/dairy-free diet by the time I get to see them. I guess the next level up would be a paleo diet, and then the next level from that would be an autoimmune paleo diet. Then maybe the next level from that would be maybe a ketogenic diet, and then the next level above that would be a microbiome-diverse diet combination with the ketogenic diet. 

The other thing that we’ve been doing…

Dr. Kara Fitzgerald: Let me just stop you. What do you mean a microbiome-diverse diet?

Dr. Datis Kharrazian: So I think one of the problems we have in functional medicine is our patients have the same thing. They get off gluten and dairy and they feel great, so then they keep looking for more foods to take out of their diet. Then they eventually take so many foods out of their diet that they’re not eating much. When they stop eating a diverse form of foods, their microbiome diversity goes away. Then when they lose their microbiome diversity, their tolerance becomes disrupted, so now they start to react to everything.

One of the key things of a microbiome-diverse diet is really making sure that they have as many different vegetable fiber proteins as possible. In studies when things show up on lab tests, as long as they’re not nightshades or lectins, they seem to really support a diverse vegetable intake to get that microbiome as diverse as possible.

We have a lot of patients that come in that have an autoimmune disease and they’re on gluten-free, dairy-free, they’re only eating a few things. They have the same salad every day, or the same lunch every day, and then when you look at their bacterial diversity in their gut, it’s gone. They don’t have any. So with those patients, it’s kind of like an opposite approach, we want them to start eating all these different things to get their diversity back.

That’s a common thing also, with diets in my practice. We’ll see a lot of patients who have suffered from an autoimmune disease, and they limited everything, and we have to get them to eat foods again and try to get their microbiome back to functional diversity so that we may do that in combination with putting them in a ketosis state because we can do ketogenic diet with vegetables, no problem. So I think, for the patients that I see that are, like most of your patients I see have brain dysfunction to the point they have neurological autoimmunity and be autoimmune to other target sites. They maybe have six or seven autoimmune reactions and then their brain’s in trouble, and then they have neurological deficits and they can’t function. 

With those types of patients, we’ll probably put them on a ketogenic diet to get ketosis, because ketones have actually been shown to reduce brain inflammation. They’re not just fuel sources for the brain. There’s two studies now that showed that ketones can help heal MS plaques, so it’s this weird anti-inflammatory effect. Then we’ll do that in combination with a numerous list of vegetables to really get their microbiomes as diverse as possible, and see if we can get their Treg functions to improve, and their tolerance to improve. That’s kind of what I end up with. 

Some of my more chronic patients, when we’re doing a combination of very diverse plant diet in combination with getting into a ketogenic state, really bring down their systemic inflammation and their brain inflammation.

Dr. Kara Fitzgerald: So, we are seeing more and more sort of, quote, orthorexic patients coming to us. People who’ve really limited their diet, and there tends to be a lot of anxiety with expanding it. I’m curious what are some of the vegetables that you’re talking about? What are some of the outliers?

Dr. Datis Kharrazian: So we’ll basically just tell patients, “Hey, go to the health food store, grocery store, get as many vegetables as you can. Just avoid the nightshades,” so no tomatoes, no eggplants, “and the lectins,” no nuts, seeds. I have them get those all, break them up, put them in a blender, like a Vitamix. I don’t want to juice it because I want the fiber. I have them put it in a Vitamix, and I have them drink that once a day. Then we tend to see their microbiome change pretty quickly when they start doing that. It’s really as many as they can possibly put together, as far as vegetable sources, the better. 

We know lectins are an issue. I just did a data analysis, a study I didn’t publish yet. But we got 400 subjects and we found if you have lectins, your risk of autoimmune reactivity goes up like 400 percent, for whatever autoimmunity marker you check.

Dr. Kara Fitzgerald: I was going to ping you later on lectins. Talk to me about that. That’s been a controversial topic in our space, at IFM where we both come from. But yeah, talk to me about what you’ve found.

Dr. Datis Kharrazian: So, I can tell you from doing some data analysis where we looked at 400 samples, where we looked at 20 different tissue antibodies, we found that if a person did have immune reactivity to lectins, not everyone has immune reactivity to lectins, so to say everyone needs to be off them is a little bit too much of an issue. I think it’s just not correct. But there are people that definitely do have reactions to lectins and that’s a big issue. And if they do have antibodies to lectins, we know without a doubt that the risk for autoimmunity goes up dramatically. 

The key thing with lectins is also this process called agglutination, where you get proteins that stick together. People look at rheumatoid factors, IgG, IgA, agglutinating together. So whenever you see positive rheumatoid factor, for example, you know they have agglutination issues, and you know they are very prone to lectin issues. Patients like that we definitely want them off lectins. When we’re dealing with autoimmunity, trying to get diversity, I do like to have them off lectins. 

And then the other things that I like to use if people do have reactions to lectins, or the antibodies, I use compounds that decrease agglutination. I use [inaudible 00:27:15] bromelain, ginger extract combined together and that helps with reducing agglutination. I’ll do that with patients that have rheumatoid factor issues, or people that are very sensitive to lectins. 

Dr. Kara Fitzgerald: Will you actually see antibody levels drop when you use those interventions?

Dr. Datis Kharrazian: We don’t actually see antibodies drop, but we’ll see things like rheumatoid factor change.

Dr. Kara Fitzgerald: You’ll see that drop? You’ll see the concentration of rheumatoid factors reduced?

Dr. Datis Kharrazian: Yeah.

Dr. Kara Fitzgerald: What about TPO or some of the other anti-nuclear antibodies? I suppose those aren’t necessarily agglutination products?

Dr. Datis Kharrazian: Could you repeat that? I kind of lost the question.

Dr. Kara Fitzgerald: Sorry. So, you’ll actually see rheumatoid factor drop?

Dr. Datis Kharrazian: Yeah.

Dr. Kara Fitzgerald: Are there any other markers associated with agglutination that you might see change, using this combination?

Dr. Datis Kharrazian: No, that’s the only one we’ve been able to see so far. We don’t have a really good marker for that yet. But we do check lectin foods that have high antibodies. The reason I like the Cyrex Array 10 so much is they actually check for the agglutinant part of the vegetable, which is the lectin portion of the vegetable. So if you do a Cyrex food sensitivity panel, which is I think the best one out there. I work with them, so I do have bias and conflict of interest, but with them they actually do check the specific agglutinant for each of the different key vegetables.

Some patients only have strong reactions to all the agglutinates, you know they’re going to have significant reactions to lectin exposure.

Dr. Kara Fitzgerald: What percentage of your autoimmune patients are lectin-intolerant, would you say?

Dr. Datis Kharrazian: About 30 to 40 percent, I see lectin reactions with.

Dr. Kara Fitzgerald: Okay.

Dr. Datis Kharrazian: It could be more, I mean that’s just the for sure obvious ones.

Dr. Kara Fitzgerald: That’s pretty interesting, yeah. What else do I want to ask you on this topic?

Here’s my other question. Now, again, you’re living in a Blue Zone over there, or at least you’re nearby Loma Linda University in the heart of one of the main Blue Zones. When you look at Blue Zone data, all of those folks are eating loads of lectins. They’re eating wheat, they’re eating things that we’re commonly pulling our patients off of. So clearly, one can live a very long life eating things that, for others, are toxic. There are some underlying variables differentiating the 100-year-old centenarian in Loma Linda, versus the folks coming to your practice. 

Tease that apart for me.

Dr. Datis Kharrazian: Well I think there’s all those different variables, and when we look at the Blue Zone data, it’s very general. I think if you were to stratify the data and you were to look at lifestyle factors, then you would see it. 

Association with other studies that really show the fact that they do have social groups, that they do have live interaction that way. It may have much more of an effect on the lectin exposure, that’s causing their illness. I don’t think it’s conflicting data, I just think the data in the Blue Zone is too general and not stratified enough, so we can’t see a clear signal, so we have to kind of look at the other studies that were published on lifestyle, and risk factors and cardiovascular disease and that.

My assumption is, I think most people we underestimate how impactful social interaction and community are, and one of the key things in the Blue Zone is that. Not so much foods.

Dr. Kara Fitzgerald: The other thing that I thought about, because I’m compelled with the fact that it does seem, and I think you’re right, I think that they could drill down into the data a little bit more, but the fact that they do drink, they’re eating loads of wheat and so forth, and they’re living these really long lovely lives. They do have strong community. They’ve cultivated a lot of these really important habits that you outlined. They’re also not living in the midst of high stress, kind of sedentary, perhaps toxin-laden exposures that those of us in the west are in. Even in Loma Linda I think their lives might be structured a little bit differently, adhering to some of the Seventh-day Adventist ideas.

So perhaps intestinal permeability and disruption of the microbiome, some of these impacts of the western lifestyle are bypassed. Does that make sense, in addition to the community?

Dr. Datis Kharrazian: Yeah. And I think Loma Linda as a region of changing too. I used to remember hearing that there was a huge issue when McDonald’s was first moving into Loma Linda. At the end of the day, I think if they were to reevaluate the Blue Zone, it may have different data now. But we don’t know, someone’s gotta do it. It’d be interesting to find out.

Dr. Kara Fitzgerald: What is the mechanism prompting nightshade reactivity? Well first of all, let me ask you two questions. What’s the percentage of nightshade reactive folks you see in your practice? And we could talk about autoimmune specifically. And then what’s the mechanism, or mechanisms?

Dr. Datis Kharrazian: Well, pretty much all nightshades have lectins, so there’s a lectin agglutination connection with them, which I think is the main one. And I think it varies for different autoimmune diseases. 

When you look at autoimmunity and you have antibodies, and the antibody structure in the protein, we know that certain autoimmunities have more sensitivity and proneness to agglutination, and this is where lectins come in. For sure, the rheumatoid and joint autoimmune diseases, where you have collagen antibodies and arthritic peptides and situating antibodies, lectins play a huge role. But they don’t necessarily play a role with even some things you would suspect, like myelin antibodies. We see a lot of patients have myelin antibodies, and no reactions to lectins.

So I don’t have clear data analysis on that yet, but I can tell you just from the observation as a clinician, I can tell you that lectins are definitely a key factor in some autoimmune diseases more than others. For sure, in joint autoimmunity we see that association. Some of the data that we just analyzed with 400 subjects showed very high reactions with arthritic peptide and collagen antibodies with lectins. 

I think it also has to do with your autoimmune target proteins. So, some people have systemic autoimmunity, like Hashimoto’s, some people just have RA, some people have just MS, some people have a combination of them. But I don’t think lectins play a role in every autoimmune disease. I think it’s specific to autoimmune disease very prone to agglutination.

Dr. Kara Fitzgerald: Right, okay. And then that again, you think the musculoskeletal autoimmune diseases seem to be most prone to agglutination?

Dr. Datis Kharrazian: Well for sure the arthritic ones. We do see risk for all autoimmunity to some degree, but most dramatically, joint, just from some preliminary data analysis. 

We’re actually writing a manuscript right now. Hopefully we can get that published.

Dr. Kara Fitzgerald: That was my next question. When will this be published?

In your experience clinically, if you put someone on a full autoimmune paleo, which is a lectin/nightshade-free diet, along with all of the other “frees,” do you see turnaround relatively quickly? And then does the introduction, if they go out and have some refried beans or something, are they going to be feeling pain pretty quickly?

Dr. Datis Kharrazian: I think it varies, as you know, from patient to patient. But I think we see all types of responses. There are some patients with autoimmunity, they have such severe blood sugar instability they have to eat some nut butter to get through the day and that’s what makes them work. They don’t have any reactions when you check them to those proteins.

We’re not 100 percent on using a lectin-free diet with all.

Dr. Kara Fitzgerald: No, I get it. I’m just wondering if it prompts agglutination, would it actually exacerbate symptoms pretty quickly? That’s my question.

Dr. Datis Kharrazian: Oh I would think it’s immediate. I think as soon as you expose, it’s immediate. It’s not a delayed reaction or anything. Because once those proteins come in and they agglutinate, the immune response is immediate just to the complement proteins. You can see complement proteins, like C3/C4a go up really quickly with people that have agglutination, when they have an acute response.

The other key thing is, this is also why we did some of our cross-reactive work with food proteins. We purified 200 foods to see which cross-react with autoimmune target sites, and those with people that have Type I diabetes, by looking at the target proteins for those autoimmune diseases. 

The reason we did that is because when you see patients come in that have autoimmune disease, they have pretty much lost their tolerance to food proteins, so they react to almost every food protein you test. Then the question is, well, you don’t want them to go off everything because then they’re not going to have much to eat, and if they limit their food so much they’re going to lose their diversity in their gut, and that’s going to cause more problems. So which food proteins really matter most? 

This is why we did some cross-reactive research and published it, where we looked at, for example, people that have Type I diabetes who had a cross-reactivity with GAD65, and we found certain food proteins directly cross-react with GAD65.

Dr. Kara Fitzgerald: Which ones?

Dr. Datis Kharrazian: I don’t have the list in front of me, but I would say a third of them were, because we checked six different target proteins. So we had different ones for each one. Usually what I do is when we have a patient that has Type I diabetes, we’ll do a Cyrex Array 10, see which foods they react to and then compare that with their Type I diabetes autoimmune target protein, whether it is eyelet cell or GAD65, for example. Then we’ll see RA2 or ZN28, then see which ones are the ones that they had results positive with the foods and their specific tissue autoimmune target protein antibody are on that list, then we get them off those foods. That allows us to be a little bit more versatile, when we look at the food proteins that they need to avoid for sure. 

So I think that we need to break down all the different autoimmune diseases with their specific cross-reactive food proteins. That will make the practice of autoimmune disease much more clear. That’s really what we’ve been trying to do, to some degree. We’ve been trying to pick out the autoimmune disease and go, “Which chemicals make my anti-proteins cross-react? Which foods cross-react? So when they react against everything, which ones do you really need to do?”

Dr. Kara Fitzgerald: Right, right, right.

Dr. Datis Kharrazian: We started with the Hashimoto’s one, we published that paper in the Journal of Thyroid Research, where we purified 200 foods, and checked for cross-reactivity with TS8, TPO, thyroglobulin, T3, T4, thyroid binding globulin, and we found a list of foods. So if I have a patient with Hashimoto’s, I’ll check them against this food and see what they react for.

We then, just recently, submitted a paper that’s in submission right now, where we looked at many chemicals that can bind to proteins and then cross-react with the thyroid. So we’re trying to map out the foods and chemicals that cross-react with each autoimmune disease, specifically. We’re starting with Type I diabetes and Hashimoto’s first, because they’re the most prevalent. That’s what I’m doing in my practice, with some of my autoimmune disease patients, because we have the data for it. I wish we had more research done, it’s just hard and expensive to do.

Dr. Kara Fitzgerald: God, that’s really pretty interesting. And so then when you put them on that specific diet, and you’re not pulling them off of everything, they respond and that’s sufficient?

Dr. Datis Kharrazian: Yeah, we’ll see sometimes they’ll just go off a certain food like seaweed in Hashimoto’s, and then you’ll see a huge change in how they feel and how they function. That’s a cross-reactive one that’s very specific.

Dr. Kara Fitzgerald: Seaweed?

Dr. Datis Kharrazian: That was just an example. I have three case studies, one I just submitted to a journal, about how we looked at cross-reactivity and we removed those cross-reactive foods and we saw some changes in the lab markers and how they function. I’m hoping to publish the other two as well, at least get them submitted.

That’s really the focus of our clinical model with autoimmune disease and its cross-reactivity in specific foods, instead of just the whole list.

So lectins, for example, are getting a lot of attention, because I think agglutination takes place in a lot of people that have arthritic autoimmunity, in agglutination with their autoimmunity. That’s not the case for everyone, but when people aren’t looking at specific auto-antibody markers and evaluating them, they just kind of catch up with that theory, then it’s a little too aggressive. 

But when you actually look at people’s immune responses, for example, if we do a Cyrex Array 5 and see 24 tissue antibodies, and then we compare that with their food cross-reactivity, and the chemical cross-reactivity, and Cyrex Array 11 and 10, and then we can see the big picture. Not everyone reacts to lectins, and not everyone reacts to chemicals, and not every autoimmune target protein shows up with everyone, not everyone is systemic, and then there’s specific cross-reactivity for each form of autoimmune antibody reactions. 

Each of those patients are totally unique. I think one of the things that happens with autoimmunity is people just classify that as a group, practitioners go, “Oh, it’s an autoimmune disease. Just fix your gut, and just take them off lectins,” and you’re like, that’s too general. They still need an individual and personalized approach to them.

I think functional medicine does a really good job of that. But I think also, it can be done with greater depth where each autoimmune disease is personalized, and each target protein is personalized, and each cross-reactive reaction is personalized. So that’s what I’m trying to do in my clinical practice, and that’s what I’m trying to do with the research we’re publishing, is to try to dig deeper there that way.

Dr. Kara Fitzgerald: So I have a couple of questions around that. It does make a lot of sense, and then of course we would steer people away from kind of this orthorexia thing. I think that’s what’s happened. Everybody who has autoimmune disease adopts an autoimmune paleo, and then they’re sort of on the journey towards fasting their microbiome unless they’re really careful, developing micronutrient insufficiency, and maybe losing tolerance beyond where they were.

If you stratify, as you’re doing, that’s really pretty cool. So in theory, you might be able to pull an autoimmune patient off of just a very select handful of foods using your approach?

Dr. Datis Kharrazian: Right, exactly. That’s the point. We’re trying to keep the diet as diverse as possible.

Dr. Kara Fitzgerald: And you’re actually finding that to be true? In your clinic practice? That you’re able to really…

 

Dr. Datis Kharrazian: Yes, but I’m going in biased too, so I have to be careful how I’m looking at my information, because I want it to be so true.

Dr. Kara Fitzgerald: Well one of the interesting things, I understand certainly having worked with elimination diets for my entire career, and looking at a lot of laboratory data. You can tell by the intensity of the response, the antibody level, what might be the primary sensitizer, and then you can tell by the strength what’s probably cross-reaction, so that’s one thing. But if somebody’s got long-time intestinal permeability, or immune dysregulation, those cross-reactions become clinically very relevant. So therefore, you can’t for everyone, put them on that nice abridged elimination. You actually have to do something pretty broad while you’re rebuilding. Would you say that’s true?

Dr. Datis Kharrazian: That’s very true. And I think, also, that when we look at, as functional medicine practitioners, we have different groups of patients come in. Some come in and, the most appropriate thing to do is just put them on an anti-inflammatory diet, and just put them on a [inaudible 00:44:00] diet, and see them get their inflammation down. 

But then we have a whole different group of patients that come in that have already been on a leaky gut diet, or they’re taking 30 different supplements, have worked with six different practitioners. They come in with their list. They’re a complete different clinical scenario. With those patients, there’s nothing left to remove. There’s nothing left to do there. 

Also, a lot of the research we publish on cross-reactivity, let’s say with the thyroid and Type I diabetes, many of those foods were on the autoimmune paleo diet. Even though they’re on the autoimmune paleo diet, they still reacted to various food proteins that drew out the cross-react with the target proteins. 

Dr. Kara Fitzgerald: Yeah, I get that. Things that we would think are pretty hypoallergenic.

Dr. Datis Kharrazian: Yeah. I think it depends on the kind of practice each functional medicine practitioner has. If they’re new doing functional medicine, and in the community somewhere, just getting a patient on some fish oils and cutting out fried foods, and maybe supporting their gut is going to have a huge impact with them.

Dr. Kara Fitzgerald: Yep, that’s right.

Dr. Datis Kharrazian: And for other functional medicine practitioners, they’re seeing people who have already been in the functional community, and then maybe the sixth person on their list, and they’ve already done a lot of things and now you’re trying to just get them to eat more food. 

So there’s just these populations of patients, and I think that’s why functional medicine is so cool.

Dr. Kara Fitzgerald: Yeah, I know. We can enter into the conversation and really effect great change at any level. Those of us who have been doing this for a while are starting to see more of these people who have self-prescribed a lot of other stuff, or have been to a lot of other clinicians. 

There is careful expansion with diet and rebuilding the microbiome, and making sure micronutrients are at adequate levels. So what you’re proposing, and I’m saying this to all the clinicians out there encountering this, you know what Datis is really talking about here is sort of this precision investigation around what are the primary problem proteins that cross-react with the tissues in the body, and this is something that you’re flushing out.

What if, if a clinician wants to actually understand this and practice this, how are they going to learn what you’re doing? Has this been published? Are you teaching these concepts?

Dr. Datis Kharrazian: I mean, I put together the Kharrazian Institute, that’s an education resource for people. We’re starting with neuro-inflammation, and going to some of these concepts, but yeah we have published this information. 

Dr. Kara Fitzgerald: Can you send me, if I have my staff ping you, I’d really like to list as many citations as possible. Because you’ve mentioned a lot today, and I think people are going to be extraordinarily interested in them.

Dr. Datis Kharrazian: Sure, and the papers we publish, we only pick journals where the journal will give us an open access option once it gets approved. We try to make all of our publications open-access. We feel like everything put together a budget for a research project, we have to budget in the fee to make it public access. The information just doesn’t get out there when people have to spend 60 dollars to get a copy of the journal. 

The paper said we talked, we did a cross-reactivity in the Journal of Thyroid Research and Diabetes Research, we did opt for the open access so everyone can access the paper without having to pay for it.

Dr. Kara Fitzgerald: Perfect, that’s fabulous. Listen, I just wanted to circle back to this comment you made about Hashimoto thyroiditis and seaweed. I mean, we tend to pull people who’ve got autoimmune thyroid disease off of seaweed, because we want to kind of be in control of the iodine exposure, so that’s usually something most of us are careful around. But you’re actually saying that there is a cross-reactive protein within seaweed that promotes autoimmune thyroid disease?

Dr. Datis Kharrazian: I believe it was cross-reactivity with T3. Remember, the cross-reactivity only matters if you actually make antibodies against that food protein. If somebody’s eating, let’s say a food protein but didn’t have an antibody against it, then there’s no concern for cross-reactivity. But if they do make the antibody, and the antibody has structural similarity to the target protein, like TP anti-bodies or TP trigger proteins, then you can have the interaction take place. 

We met at 8 different target sites for the thyroid, so I think seaweed was on specifically the T3, but it’s all on the paper. I actually still look it up myself, I don’t have them all memorized. I just look at the food reaction list I have, and look at the data we have, and then we try to have those patients not eat those foods.

Dr. Kara Fitzgerald: Okay, well we’ll link to it for sure, and I completely understand needing to look up your work. I completely understand that. Oh my gosh, just having worked on the laboratory evaluations in Integrated Functional Medicine, and I published a collection of case studies, I have to refer back if I want to remember.

Dr. Datis Kharrazian: Yeah, especially if you’re doing one study and another study’s similar to another study, similar to another study, similar to another study, and then you’re manuscript writing for one, the analysis another, it’s too easy to, well I know for me I need to look at the actual document again.

Dr. Kara Fitzgerald: Fair enough. Let me just ask you, for clinicians, so you’re using the Cyrex Arrays, and you’re looking at the foods, you’re looking at the various, I think you’re doing the predictive auto-antibody panel, and then you’re doing the chemicals?

Dr. Datis Kharrazian: Yes.

Dr. Kara Fitzgerald: What kind of stool testing are you doing?

Dr. Datis Kharrazian: I just do the basic one through Genova.

Dr. Kara Fitzgerald: You do?

Dr. Datis Kharrazian: Yeah.

Dr. Kara Fitzgerald: Okay. The culture one, the CDSA?

Dr. Datis Kharrazian: Yes.

Dr. Kara Fitzgerald: Okay. And then, what else are you doing for tests? Oh, you actually mentioned about looking at T-cell function. What kind of panels, what are you doing there?

Dr. Datis Kharrazian: Most of my testing I do is actually mostly from LabCorp. It’s not really from the functional medicine labs.

Dr. Kara Fitzgerald: Yeah, I got it.

Dr. Datis Kharrazian: I mean, I think that’s such an undervalued thing with functional medicine practitioners. They’re so into all these designer labs, and it’s like there’s so much data to get from just routine lab work. 

I do a lot of just routine lab work, T and B-cell profiles, Comp. with proteins, Chem 24, CBC. I would rather do a complete blood chemistry profile than any functional medicine test any day, because I get so much more information from it. I do do a lot of routine lab work, in combination with a lot of the Cyrex testing, and I’ll use some profiles from Genova. 

That’s kind of the fundamental basis, then you can diverge out to other specialty labs based on the patient’s complaint. But for the most part, those are the three fundamental types of testing I do.

Dr. Kara Fitzgerald: Good, okay. And again, we’ll link to your Institute. I’m assuming that you’re doing some teaching over there about the labs that you’re using and how to interpret them?

Dr. Datis Kharrazian: Yes.

Dr. Kara Fitzgerald: Okay, good. Because I know if you’re doing a chem screen and a CBC and gleaning more information off of it, as you say, than some of our specialty tests, people are going to want to know what you’re doing.

Dr. Datis Kharrazian: Yeah, absolutely. I’m trying to teach people step by step the clinical model that, for me I rewrite my exam every few months, and I rewrite my intake forms, rewrite everything I do, because I’m always trying to fine tune my clinical model. So I’m just trying to teach the clinical model, after many, many revisions. Like for the first one is neuro-inflammation. The second course I’m teaching is gastrointestinal. The third course I’m teaching is autoimmune. 

I spent countless hours refining how I go through a step-by-step approach, to not miss anything, so that’s what I’m teaching at the Kharrazian Institute, is the clinical approach that I have been working on and I hope it’s useful for clinicians. I think that many times, we all go to seminars and we get a lot of good research information, but not really a step-by-step clinical approach. We usually get that at the breaks, talking to each other. 

The whole purpose of me developing my Institute was to just get to that information and share it with people.

Dr. Kara Fitzgerald: Perfect. Yeah, what is actually going to change the way that we practice and deliver patient care, and helpfully walk our patients towards health.

I’ve got so many other questions for you. You’ve just done a lot of really interesting work over the years. So again, I was reading this pretty nice interview that you had with Bob Rountree, and you talked about being at Harvard and Harvard a) being remarkably open-minded, much to your surprise. Like really kind of embracing who you are and what your area of interests are, and what you’re bringing to science, or you representing sort of, quote, alternative medicine. So a) they were way more open-minded. And b) they’re recognizing the limitations of the clinical research model as it exists today. 

Just in summary, I wanted to kind of leap from this idea to sort of where you see us heading in clinical research. What kind of model is viable and is actually going to be able to capture what it is we do as functional medicine clinicians?

Dr. Datis Kharrazian: I think with functional medicine, we definitely cannot do the clinical trial model. And that’s unfortunate, because the double-blinded, placebo-controlled clinical trial is really where the highest level of evidence is, because you can knock out all the different variables that can skew your data. But the problem with the clinical trial is you have a short period of time where you collect data, and you look at one endpoint, maybe a risk factor. You do one intervention, and then you compare that with the control group and you see an outcome and that’s not really how we practice in functional medicine, and that type of clinical trial model, the whole purpose of that is to have what they call generalizability, where that data applies to the general population and the goal of the clinical trial is to make it as generalizable as possible, because when they do drug intervention that they can have it apply to as many people as possible.

That’s completely opposite of our research model, and our treatment model in functional medicine, because it’s not a generalizable model, it’s a personalized model. We really can’t do an effective clinical trial in a functional medicine model doing real functional medicine. In real functional medicine we’re coming in and we’re not just giving them like alpha-lipoic acid for the next six weeks or six months, and then seeing the endpoint change. We’re changing diet, we’re changing lifestyle, we’re changing sleep, we’re giving supplements, we’re modifying, we’re changing all the way through the treatment, depending on how they respond and not respond. So we can’t do an effective clinical trial. Not to say we can’t take evidence from clinical trials about various things and use them in our clinical model, which we can, and we do in functional medicine, but we have to do what they call an n-of-1 trial. N-of-1 trial is when you look at a patient and you look at their data, and you see how their data changes with different interventions. For example, COP or homocysteine, or TPO antibodies, and you can then see which variables combine together, make the biggest change.

I was actually speaking with some of the people at IFM, and they were talking about, because I research, and the only chance we have is the n-of-1 clinical trials to really show this personalized lifestyle medicine model, and that was something that I learned from Martha Herbert, as my mentor at Harvard Medical School. She is working with children that suffer from autism, and they have to do n-of-1 trials, or they can’t get accurate data because there’s too many variables, and one child with autism is going to be different than another child, and there’s different things that aggravate and flare them up from one to another, and they respond to different things. 

I think the problem we have is we have a lot of physicians that just go, “If it’s not a double-blind clinical trial, then it’s no use to me,” but they don’t understand research models, and that’s a generalizable model, and that’s completely different than a personalized lifestyle medicine model. At the end of the day, we can look and say, they want a personalized model.

Dr. Kara Fitzgerald: It seems like they’re sort of getting that at Harvard. Would you say that science is going in that direction?

Dr. Datis Kharrazian: My experience, being at Harvard Medical School for a while in such a small, great community, they’re frustrated with everything and they’re open to everything. Basically, everything I learned, and I talked about this before as a researcher, not a medical student, so it might be a different experience as a medical student there. But as part of the research community there, as a research fellow and then getting my Masters in Medical Clinical Investigation, there’s different subsets. I could tell you that they see everything they do has limitations, and everything has a bias. And then they look at their healthcare system that way, and data that way. When you do it that way, it’s really hard to have a prejudice. 

Let’s say alternative medicine versus conventional, because each one of them have their own biases and their own limitations, right? It’s just data. It was really surprising to see such a pure evaluation of information because they’re highly trained researchers and they understand these things, and I think clinicians tend to have really significant bias, because if they haven’t learned it, it can’t be real. They don’t really understand research methodologies, so they tend to just listen to whatever their peers do and what they’re told to do, and they’re not critically analyzing anything, but Harvard is completely open to alternative medicine. 

What’s the study with leaky gut, Mass General – lot of brain-gut access research there. You’ve got the Osher alternative medicine clinic there right at the Brigham Young hospital. There is a lot of women’s health studies, they’re dealing with diet and lifestyle changes done over many years.  I mean there is so much functional medicine research done at Harvard Medical School that it’s completely shocking, and at the same time very refreshing. And then there’s a whole division at the Harvard School of Public Health, which is just doing chemical research on things like BPA and they totally get it. There are also those that are doing the large drug trials, but it was really fascinating to see, Harvard medical students ranked number one medical research for 80 years in a row.

Dr. Kara Fitzgerald: That’s a pretty good track record.

Dr. Datis Kharrazian: They have 12,000 active research labs there.

Dr. Kara Fitzgerald: Really? That’s pretty extreme.

Dr. Datis Kharrazian: Yes. It’s huge. It’s a small community, but there’s lots of research labs all over. I think what they’re doing there is just supporting everything we do in functional medicine. Not by intent, but just because they’re looking for ways to help chronic diseases. And they’re doing some major breakthrough research right now with the blood-brain barrier, they discovered a model where they can really evaluate the blood brain barrier in connection with celiac and gluten and the whole Beijing study

The microbiome research on the heart and on the brain, it’s amazing.

Dr. Kara Fitzgerald: Well, we could just keep going. I would love to continue to talk to you about this and how you evaluate blood brain-barrier, for example. 

Dr. Datis Kharrazian: I do use Cyrex Array 20 is a good test. And then that’ll be more stable, if you’re looking for an acute reaction just with lab work you can order S100B, and I like to order both, so if it’s very acute, I’ll see S100B protein elevations with just routine lab tests, and then I’m looking to see a more stable blood-brain barrier marker on the Cyrex Array 20, which is blood-brain barrier protein antibodies. And if those are breached, the patient’s at serious risk for significant brain inflammation and developing neurological autoimmunity. I mean, it’s a really big deal if there’s blood-brain barrier permeability.

This is one of the things that I spend two-and-a-half hours on on the neural information course that I’m teaching, listing all the mechanisms that break down the blood-brain barrier, things we can do to try to heal it, and what are the effects when the blood-brain breaks down, and research studies now, and what do we know about it.

I mean really, if you’re a clinician and you see blood-brain barrier protein bodies positive, you should be very worried about your patient.

Dr. Kara Fitzgerald: Have you used the Cunningham panel at all? Have you explored that?

Dr. Datis Kharrazian: I mean, just the dopamine receptors. I think that’s a great way to look at infection related to autoimmunities, the different dopamine receptors, and it’s a great test.

Dr. Kara Fitzgerald: And folks, the S100B test that you can get at LabCorp that Datis just mentioned is S100 calcium-binding protein B. And it looks like it’s, I have never ordered it before, but this is something we can get, this is a standard auto-antibody protein that we can measure.

Dr. Datis Kharrazian: Yeah, it’s not as stable and reliable as blood-brain barrier protein antibody, because it’s an acute phase breakdown, that usually goes up with it, meaning if someone had a head injury you’ll see the S100B elevated for a while, but then the blood brain barrier could still be breached, and you would only catch that with antibody Array 20. 

But if you saw, for example, high S100B, and high blood-brain barrier protein, you know there’s an acute inflammatory breakdown of the blood-brain barrier. If the S100B level’s normal, the blood-brain barrier protein antibody is positive, you know it’s not an acute breakdown anymore, it’s just permeable, and that’s still an issue.

Dr. Kara Fitzgerald: Okay. Well Dr. Kharrazian, it’s been really great to talk to you, and hopefully I’ll see you actually, at AIC. Are you going to be at the annual conference?

Dr. Datis Kharrazian: Yes. See you there. Great.

Dr. Kara Fitzgerald: Good, good. All right well thanks for coming in New Frontiers. Thanks, everybody.

Dr. Datis Kharrazian: Thank you so much. Thank you.

Dr. Kara Fitzgerald: And that wraps up another amazing conversation with a great mind in functional medicine. I am so glad that you could join me. None of this would be possible, through the years, without our generous, wonderful sponsors, including Integrative Therapeutics, Metagenics, and Biotics. These are companies that I trust, and I use with my patients, every single day. Visit them at IntegativePro.com, BioticsResearch.com, and Metagenics.com. Please tell them that I sent you and thank them for making New Frontiers in Functional Medicine possible.

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