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Dr. Julie Greenberg speaks about an Integrative Approach to Eczema with Dr. Ben Weitz at the Functional Medicine Discussion Group meeting on April 22, 2021.

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Podcast Highlights

2:03  Like Hippocrates said, all disease begins in the gut.

2:22  The goal of Naturopathic and Functional Medicine is to look beyond the symptoms and the triggers to treat the root cause(s).  For dermatological conditions we can use topical steroids to treat their rash, but that’s not the goal of Functional Medicine.  We also don’t want to get stuck on triggers.  A trigger is something that can make the skin condition worse, like diet.  There are too many practitioners, esp. in the Functional Medicine world, get stuck on diet to treat dermatological disease.  While there may be a few conditions where diet is the root cause, like pediatric eczema, but for most derm conditions, such as adults with rashes, the root cause is very unlikely to be food.  Food is more likely to be a trigger and just eliminating those foods will be unlikely to clear up the condition.  Dr. Greenberg believes that Functional Medicine testing, esp. stool testing, organic acid tests (OAT), and urinary mycotoxin testing can be helpful in discovering some of the root causes of many derm conditions. 

4:54  Stool testing, like the GI Map, helps us to see both commensal (normal), opportunistic, and pathogenic bacteria in our microbiome. It also tests for fungi and yeast.  But it is not that reliable for candida, which is why Dr. Greenberg likes the OAT, which is better for identifying candida overgrowth.  A stool test will also look for parasites, like worms and protozoa, and for viruses. It will also give information about digestive markers, short chain fatty acids, inflammation, and intestinal permeability.

5:57  The organic acid test (OAT) is more complicated than the stool test and the one Dr. Greenberg orders from Great Plains Lab includes 74 metabolites from urine.  It includes yeast and fungal markers, and markers for bacteria, clostridia, and oxalates. It also looks at mitochondrial function and neurotransmitter metabolites. It takes more work and training to learn how to use the OAT test.

6:35  Mycotoxin testing.  Mycotoxins are toxic secondary metabolites of mold and can be found in urine.  The mycotoxins found most frequently are aspergillus, penicillium, fusarium, stachybotrys (the black mold), and chaetomium.

8:38  Up to 80% of our immune system comes from our gut.  If the gut isn’t healthy, the skin is not going to be healthy.  When you see someone with a skin problem, you should be thinking that’s somebody with a gut problem.

9:07  Immunology.  Eczema is a Th2 mediated pathway. Th22 is also involved in skin inflammation. Also, Th17 primes out immune system and it is also involved.

10:09  The gut affects the immune system.  Gram negative bacteria often produce endotoxins like lipopolysaccharides (LPS), which trigger an acute inflammatory response.  LPS also inhibits the liver’s ability to do its job and detoxify.  It can even cross the blood-brain barrier and promote neuroinflammation.  Gram positive bacteria can also stir up the immune system and create inflammation.  They contain a peptidoglycan layer and teichoic acid and lipoteichoic acid in their outer cell walls.  Staph aureus, which is a gram positive bacteria, is a major player in eczema.  Candida is also present in so many derm patients and it produces extracellular proteinase that breaks down collagen and keratin in the skin.  It can also break down the IgA complement and decreases IgA production.  Candida also increases vascular permeability and leaky gut.  Candida also weakens our immune system and makes it more difficult for our immune system to kill staph aureus and E. coli.

13:33  Leaky gut.  The bloodstream is right below this one layer of intestinal epithelial cells, which should have tight junctions that prevent large food molecules from getting into the blood.  There is a thick mucosal layer that helps protect the epithelial layer and secretory IgA is in this mucosal layer and it provides immune protection and it grabs onto pathogens and endotoxins like LPS.  When this mucosal layer is eroded, we will have a loss of the tight junctions and leaky gut.  There are two keystone species of bacteria that help protect against leaky gut and these are faecalibacterium prausnitzii and akkermansia muciniphila.  Akkermansia is mucin loving and while it eats a bit of this mucus layer it stimulates the goblet cells in our gut to produce more mucus.  Faecalibacterium is a butyrate producer, which is the main food for our intestinal epithelial cells, which turn over every 24 hours.  Butyrate also calms our immune system and enforces the tight junctionsl of the epithelial cells and helps to prevent leaky gut. We need to feed the Faecalibacterium with prebiotics or fiber.  Unfortunately, antibiotics can kill off good bacteria like faecalibacterium and akkermansia while it’s killing off the bad bacteria. Alcohol, NSAIDs, and a lack of fiber can also kill these two keystone species of good bacteria.

21:22  Eczema, aka, atopic dermatitis, is a disease of skin barrier dysfunction and inflammation.  While we see the inflammation in the skin, there is inflammation in the gut and the system.  We think of eczema as a Th2 mediated disease with its related cytokines, IL-4, 5, and 13.  But there is also a chronic phase of eczema where there’s increased levels of Th1, Th17, Th22, and related cytokines.  By treating the gut, we can treat all these types of inflammation.  Patients with eczema tend to have lower levels of beneficial gut bacteria like bifido and bacteroidetes and higher levels of pathogenic bacteria like C. diff, E. coli, and staph aureus.  Staph is often found in patients with eczema, including in the skin, the gut, and the nasal passages.  The staph suppresses IgA and IgG production in peripheral blood lymphocytes and increases IgE and histamine synthesis.  IgE is the Th2 pathway.  Many eczema patients also have candida overgrowth and when you treat the candida, the eczema will improve.

27:07  It can be helpful to use butyrate supplements, for adults one capsule three times per day with meals and for infants, one scoop mixed into milk or apple sauce once per day.

28:44  The first case study is Sam, who is an 11-month-old male with eczema.  His eczema started 2 months prior and 2 months after receiving pasteurized donor milk.  His mom has been using triple therapy cream on him, which contains triamcinolone, which is a steroid, nystatin, which is an antifungal, and mupirocin, which is an antibiotic. The triple cream worked at first and then it stopped working. This is typically what happens when they go to a conventional dermatologist. Then they will need a stronger and stronger steroid. Dr. Greenberg then ran a stool and an OAT test on him. When you look at the stool test, you might see C. Diff, which might be alarming in an adult, but is fairly common in infants.  Sam was low in certain healthy bacteria, including lactobacillus and two keystone species, akkermansia and faecalibacterium prausnitzii.  Akkermansia helps the goblet cells in our gut produce the mucus layer, and faecalibacterium is the main butyrate producer.  He has high enterococcus, which in adults causes a lot of UTIs.  He is high pseudomonas, which is a gram negative bacteria and a huge LPS producer.  Both staph and strep are also overgrown.  Eczema patients often have candida, but it often is present in the upper GI tract rather than the colon, so it may not show up on the stool test, which is why the OAT test is better for picking up candida.  Both citrobacter and klebsiella are present and these are bad actors, so we want to clear them out. Also, his secretory IgA is very low, so we want to support this.  When we look at the OAT we need to look at 7. Arabinose, which is the marker for candida, we see that Sam’s is very high.  So he has high candida, high staph, and high strep, which is often seen in eczema. But he also has high aspergillus, which is mold. He also has high oxalates, which you don’t need to treat, since it will come down if you treat the candida and the mold. When there is candida and mold you want to look at B2 riboflavin, which they will also often need, and she will give in drops for infants.  Dr. Greenberg will treat the bacterial overgrowth with antibacterial herbs and antifungal herbs that are safe for infants and a lactobacillus-bifido blend probiotic. She does not like using spore based probiotics for infants, since she has found that spore-based probiotics don’t play well in the guts of infants.  She also uses a new akkermansia probiotic that is available from Pendulum Probiotics and a prebiotic, Mega Pre from Microbiome Labs that helps to bring up levels of faecalibacterium prausnitzii and akkermansia.  She will also give butyrate supplements.  To bring up the IgA, Dr. Greenberg will use Mega IgG2000 or SBI Protect. 

Dr. Greenberg may use a botanical topical on the skin of patients with eczema, but this works best if it is acidic rather than alkaline.  The skin pH is supposed to be acidic but it is often alkaline in patients with eczema. If the skin becomes more alkaline, staph will really proliferate, so using things that are both antibacterial and acidic will be the most effective.  She may use things like colloidal silver spray or a mix of apple cider vinegar and water, but if the skin is really compromised, then apple cider vinegar will likely burn too much.  Rosemary hydrosol works well and is both antifungal and antibacterial.  She likes to use a neem oil that has a bit of peppermint and lavender essential oils. Sometimes she will make a salve with essential oils.

50:37  Sam’s parents agreed to run the mycotoxin test and it showed a lot of mycotoxins, including ochratoxin A from aspergillus and sterigmatocystin that’s specific to penicillium. Dr. Greenberg treated the mycotoxins with binders and glutathione and she adds fish oil, because mycotoxins are lipophilic. Then we have to have the family investigate the home to find out the source of the mold and remove it.

53:10  The second case study: Alice, a 39 year old with eczema.  She had eczema as a child and on and off as an adult, but the eczema on her neck got severe during her pregnancy nine months ago and she cannot sleep at night. A dermatologist prescribed tacrolimus, which is a topical calcineurin inhibitor, and crisaborole, aka, Eucrisa, which is a topical PDE4 inhibitor. These drugs are like steroids trying to suppress inflammation, but they are not working now. The fact that the skin is oozing indicates that there’s a staph infection. You should either refer them to a dermatologist or swab it and send it out for testing.  Dr. Greenberg ordered a stool test, which showed high H. pylori, which indicates that there is low stomach acid. Not only should we treat the H. pylori, but we also need to give HCL.  Low HCL can lead to overgrowth of dysbiotic bacteria like enterococcus and prevotella, and even SIBO.  Akkermansia is not found, which means no mucosal lining, which means leaky gut.  She also has overgrowth of methanobacteriaceae, which can cause constipation and methane SIBO.  There are two large groups of bacteria, the bacteroidetes and the firmicutes, and most of the inflammatory bacteria are in the firmicutes, which in this patient is overgrown.  Her pancreatic elastase is low and in Functional Medicine we want to see this level above 500, which means that she needs enzymes, so she will recommend digestive enzymes that also contain HCL and bile.  The stool test did not show candida, but we need to also look at the OAT test for this. She did show another type of fungus, geotrichum. When you have this much dysbiosis, it allows yeast and fungus to get a foothold.

1:00:25  Dr. Greenberg will not usually use enzymes with infants, but she may use the chewable enzymes with kids. There is no way to get bile into them, since you have to swallow a capsule and if you open the capsule, the taste is really bad.

1:02:11  Beta-glucuronidase.  This is an enzyme that is part of how the liver removes estrogens and certain toxins, in this case by attaching glucuronic acid onto the estrogen, so then it will be excreted through the stool.  Beta-glucuronidase is the enzyme that will cleave the glucuronic acid from the estrogen and this can lead to reabsorption of the estrogen back into the body, so this is a bad thing.  It can make women more estrogen dominant, so you might want to supplement with calcium d-glucorate, though since this patient is breast feeding, Dr. Greenberg will not give it.  Also she had a really low secretory IgA. 

                                                On her OAT test, we see that her aspergillus is not an issue. This is all nice and low, but she has candida overgrowth as I would expect with eczema. So, we have to treat the candida. The fusarium is undeterminate. It’s elevated, but it’s not frank high. So, I’ll think about whether or not she needs a mycotoxin test.  We talked about candida and oxalates. So, hers are elevated. She’s not high yet, but she’s going that direction. Again, this is due to the candida throwing off oxalates. Her vitamin B2 actually was not deficient because she’s still on prenatal vitamins. So, she’s getting a whole pop of B2 and it’s helping her, but I think if she wasn’t on the prenatal vitamins, she would be deficient in this vitamin B2 as we talked about.

                                                So, for her, I have to treat the staph infection on her skin. She’s bleeding and oozing. She cannot sleep at night. I am okay with topical antibiotics. Mupirocin ointment for a few days is a really good way to quickly get a staph infection down, and it’s a topical. It’s not an oral, but then I created an antibacterial essential oil salve for her to use. So, we just used the mupirocin for a few days, but it does a pretty good job of whacking it down, and then we’re going to work on all the underlying factors.    For her H. pylori, I have to give her altered protocol because she’s breastfeeding. So, she didn’t get my normal H. pylori, but there’s a different protocol, of course, safer for baby. It’s mastic gum and all this stuff that I think most of us treat H. pylori with. Her low elastase, this is where I give her that and the H. Pylori, the digestive enzymes, the hydrochloric acid, and the bile supplement.

Dr. Weitz:                         Which is your favorite digestive enzymes?

Dr. Greenberg:                 I really like DuoZyme by Karuna. They have all three of these. Integrative Therapeutics actually has a very good one, too, Panplex Phase 2, and I use that one a lot as well. So, those are my two favorites because it’s hard to find the digestive enzymes, the hydrochloric acid, and the bile together. So, one of those two.   For the bacterial overgrowth, again, I’m going to treat with herbs, but a modified protocol, safe for breastfeeding mom knowing her infant is going to get exposure to these herbs, and same with the candida. She doesn’t have akkermansia, so I’m going to give her the probiotics with akkermansia, the Pendulum, and give her the IgA supplement while I’m treating all these dysbiosis.

                                                Again, I would have given her calcium D-glucarate for this high normal beta-glucuronidase, but she’s breastfeeding and this has not been proven safe for breastfeeding, so she did not get it. Then, of course, addressing the skin barrier disruption with topical protocols to support.

                                                This was Alice on her first visit. Three weeks later, we can see it’s actually in a better state. This is really common for staph infections. They start off really concentrated, and thick like that, and oozing, and crusting, and bleeding, and creating all sorts of havoc, and as we start to treat it, it does spread out, and I think this is just partially as they’re putting the topicals. It’s spreading it around a bit, but it’s okay. You can see that. It’s a much better state actually than where it was and she’s not being tortured at this point.   Then a few weeks later, it’s gone. You can see that the skin is still not completely normal because it’s been traumatized like this for nine months. It’s going to take some time for the skin to repair itself, but there’s no more eczema. There’s no more staph infection. She’s completely normal. Then, actually, the baby had eczema. So, once we cleaned her up. I started treating the baby for eczema.

Dr. Weitz:                         What are your favorite candida formulas for adults and infants?

Dr. Greenberg:                 Well, so for infants, it’s different. For infants, I really like Biocidin Liquid. It’s broad spectrum, and it addresses a lot of things, clostridia, candida, bacteria, and it’s safe for most infants. It just have walnut hull and leaf, so make sure that there’s not a walnut problem in any patient. There’s also formulas by another … Obviously, infants cannot swallow capsules. Infants, we’re not going to give alcohol. So, I give them glycerides, and Biocidin is a glyceride.  There’s also a company, Beyond Balance, that makes glyceride formulas. So, I use some of their formulas in infants as well to treat the dysbiosis because, again, it’s not alcohol-based, and it’s proven safe for infants, and we can get it down easily.    For adults, I use a lot of different things. I actually like Candida Support now. I like grapefruit seed extract, caprylic acid, neem. It just depends. I do different protocols for different people, and it depends on the full spectrum of what I see as well, but those are some of my favorite internal candida protocols.

Dr. Julie Greenberg is a Naturopathic Doctor who specializes in Integrative Dermatology. She is the founder of the Center for Integrative Dermatology in Santa Monica, California, a holistic clinic that approaches skin problems by finding and treating the root cause. Dr. Greenberg holds degrees from Northwestern University, Stanford University, and Bastyr University. She lectures at naturopathic medical schools and speaks at conferences across the US on dermatology. Her website is IntegrativeDermatologyCenter.com.

Dr. Ben Weitz is available for nutrition consultations specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss and athletic performance, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111. Dr. Weitz is also available for video or phone consultations.

Podcast Transcript

Dr. Weitz:                            Hey. This is Dr. Ben Weitz, host of The Rational Wellness Podcast. I talk to leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to The Rational Wellness Podcast for weekly updates, and to learn more, check out my website, drweitz.com. Thanks for joining me, and let’s jump into the podcast.

                                                I’d like to introduce our speaker for tonight, Dr. Julie Greenberg. Dr. Greenberg is a licensed naturopathic doctor, who specializes in integrative dermatology. She’s the founder of the Center of Integrative Dermatology in Santa Monica, a holistic clinic that approaches skin problems by finding and treating the root cause, but Dr. Greenberg sees patients now mostly virtually in various parts of the United States. Dr. Greenberg holds degrees from Western University, Stanford University, and Bastyr University. Dr. Greenberg, you have the floor.

Dr. Greenberg:                 All right. I’m going to screen share with you guys. Can you enable screen sharing for me?

Dr. Weitz:                         Oh, yes. There you go.

Dr. Greenberg:                 Okay. There we go. Okay. All right. So, thank you guys for joining today. I appreciate your time and I’m going to try to make the most of it. I know all of our time is very precious. So, this is functional medicine test for treating dermatology, and we’re going to focus on stool test and OATs or organic acid urine tests. You just heard a little bit about me, but I’m licensed naturopathic physician in California, Oregon, and Washington. I’m also a registered herbalist, and, yeah, my clinic, the Center for Integrative Dermatology is on Wilshire. I’m still there. Just right now for COVID practicing mostly virtually.   So, this guy may look familiar. He’s our old friend Hippocrates, and he said, “All disease begins in the gut.” If we were old school and still at the Santa Monica Library, I’d ask everyone who agrees with this statement raise your hand, and I’m sure all of our hands would shoot up because this is the functional medicine group and we know how important the gut is.  So, the goal of naturopathic or functional medicine, as we know, is we want to treat the root cause. There are triggers and symptoms. So, symptoms, we know especially in derm, somebody walks in, they got a rash, that’s their symptom, and we can do things like put topical steroids on it, but that’s not the goal of functional medicine.    At the same time, we want to treat root causes. We don’t want to get stuck on triggers. What a trigger is is something that can make it worse, but even if you eliminate it, it’s not going to fix the problem. I bring up triggers versus root causes because when we get to dermatology, particularly in the functional medicine and naturopathic world, people focus a lot on diet, and I have too many people who are really exclusive focused on diet to try to treat their derm disease.

                                                So, I’m going to pose a question, is diet the root cause of dermatological disease or a trigger?  Really, it’s usually a trigger.  There are some exceptions to this, pediatric, infant eczema that’s moderate to severe. There really can be food root causes, but in adults who breaks out on a rash, it is very unlikely to be food and people get stuck on it.  Can changes in diet affect dermatological disease? Absolutely 100%. I’m not saying diet doesn’t matter, but I’m saying it’s a trigger, and even if you eliminate those flares, if the skin condition doesn’t clear up, it was a trigger and not a root cause.

                                                So, why are we talking about functional medicine testing?  Why aren’t we just using conventional testing?  Again, I think everyone here knows the answer. We can run CBCs and CMPs, but we’re just not always going to get the answer.  A lot of times, they’re going to come back normal.  Your patient’s hair is falling out, there’s rashes all over the place.  That’s not normal.  So, these aren’t particularly helpful most of the time.  We definitely want to get to the root cause, so we aren’t just suppressing symptoms.  So, really, we have to run these tests to get there.

                                                I know there’s differing levels of knowledge of functional medicine, so I’ll just really briefly review it so that we’re all at a baseline. What are functional medicine tests?  There are so many and we can use all sorts of substances, urine, stool, blood, saliva, breath, DNA. Here’s just a sampling list of different types of functional medicine tests.  Again, there are just so many.  I know many of us here use a variety of these.  Today, we’re going to focus on stool testing and OAT or organic acid testing, and then we’re going to do a dash on mycotoxin testing.

                                                So, stool testing, again, in case you’ve never run one and you’re wondering what you get out of it, it’s testing for both pathogens and commensals. Three to five pounds of our gut bacteria lives in the colon. It makes it really convenient. We test the stool. That’s where it’s coming from. We see the bacteria. So, I like to see H. pylori. We want the normal, the opportunistic, and the pathogenic bacteria. It also tests for fungi and yeast. I have found it is not super reliable for testing for candida, which is very important in dermatological disease. That’s one of the reasons why I run the OAT is I find it a lot more reliable for testing candida and then other types of molds.  Stool tests will look for parasites, protozoa, and worms, viruses, and then a host of other things, digestive markers, short-chain fatty acids, which we are going to be talking about butyrate quite a bit, inflammatory markers, and intestinal permeability. You can test for zonulin. It is one marker of leaky gut.

                                                The OAT, organic acid test, is a little more complicated. There’s about, I think, 74 metabolites of the urine testing in the OAT that I use. It does do the yeast and fungal elements, some bacterial and particularly pathogenic clostridia, which we’ll look at, and then lots of other information that you can get.  In terms of being a practitioner using these tests, I think it’s much harder to learn how to analyze and use the OAT, but it is a very useful test. The stool test is much more straightforward because you’re looking at strains of bacteria or lists of protozoa, but this requires more training.

                                                So, mycotoxins, I mentioned that we’re going to touch on mycotoxin testing. Some of you may be wondering what’s a mycotoxin. Other of you may be mold and mycotoxin certified. Again, just to make sure we’re on the same page, mycotoxins are defined as toxic secondary metabolites produced by organisms of the fungus kingdom. In simple terms, what that means is that when certain molds feel threatened, that other mold or bacteria is encroaching on its face and it’s going to come and kill it. It has to fight back and it produces chemical warfare, and it creates these things called mycotoxins and shoots them into the air.   They are quite toxic and they can cause disease in both humans and animals. So, this is a big deal in livestock. They eat moldy grain and the whole herd can die, but it’s an issue for humans as well. Some of the molds that we look at in terms of mycotoxin production are aspergillus, penicillium, fusarium, stachybotrys or the black mold, and chaetomium. So, we’re going to look at little bit at some mycotoxin tests.

                                                Just to make sure, again, I know everyone knows a lot of gastro, but just to make sure we’re on the same page and so that the significance when we go do the case studies because we’re going to look at a pediatric and an adult eczema case, we’re going to look at their labs, before and after pictures, and how they were treated, I want you guys to understand what I’m assessing.  So, why are we doing a gastro review for a derm talk?  Well, we know that gut dysbiosis leads to systemic inflammation. No doubt about that. Systemic inflammation leads to chronic disease, and chronic dermatological disease.  For some reason, derm has been left out of the functional medicine world and even the naturopathic world. I’m one of the only specialists I know in the naturopathic world who specializes in derm, and it is so important and so tied to the gut.  So, I hope to prove that point out to you guys so that you think about derm problems in a different way after this talk.  So, we’re going to test and treat the gut to treat derm.  I won’t go into all the ways that our gut basically primes our immune system and all the crosstalk that goes. I think you guys know this, and we’ll be touching on some of these points, but there’s estimates saying 80% of our immune system comes from our gut, and it’s very real.  If the gut isn’t healthy, the skin is not going to be healthy.  Basically, when you see someone with a skin problem, I want you to be thinking that’s somebody with a gut problem.

                                                So, a little bit of a microbiome, actually, I guess this is an immunology review. So, we have T cells and cytokines that influence the immune system. When we look at T cells, when we first develop them, they’re called naïve because they don’t know what they’re going to be when they grow up. The body has to tell them, “Here’s the problem and this is what you need to become.”    So, I talk to patients and I say it’s like Army, Navy, Air Force, Marines. Where is the threat coming from and what kind of T cells do we need to attack that invader? So, when we look at different T cells, we typically think of eczema as a Th2 mediated pathway, and that is true, but we’re going to see that it is much more than that. Th22 is involved in tissue inflammation. So, any derm disease, any skin inflammation is going to be Th22. Basically, this is what’s priming our immune system, and Th17 is often involved. That’s mucocutaneous sites. That’s the gut. So, we’ll look at some of these pathways.

                                                So, I think we know that there’s some of the major influencers of our immune system from the gut would be bacteria, gram negative and positive, candida and molds, whether we have leaky gut, and even short-chain fatty acids. So, here’s a microbiome review. Just real fast, I think we focus a lot on gram negative bacteria and endotoxins. So, there are similarities, right? We have a peptidoglycan outer layer wall in gram positive bacteria, things like staph, strep, and clostridia.  We do have a peptidoglycan layer in gram negative bacteria, but what we really see is this outer cell wall of lipopolysaccharides, LPS. We refer to them as endotoxins. We focus a lot on these LPS endotoxins in this world, but I want to give a little screen time to the gram positives because they can get the immune system flared up, too.  In addition to the peptidoglycans, there’s teichoic acid and lipoteichoic acid in their outer cell walls. Staph aureus is a big player in eczema. So, I called this out particularly for today’s talk because if you have a patient with eczema, you do have a patient with staph problems and it’s a gram positive problem.

                                                So, all of these things fire up our immune system, great, and that ultimately leads to an uptick in complement and cytokines, AKA inflammation. So, if we dive a little bit deeper, we’d look at the LPS, lipopolysaccharides or endotoxins. We know that they trigger an acute inflammatory response in the body. It increases leaky gut. It inhibits the liver’s ability to do its job and detoxify. It can even cross the blood-brain barrier and promote neuroinflammation.  The gram positives cause problems as well. This teichoic and lipoteichoic acid in the cell walls, they cause a lot of issues in our immune system. They trigger neutrophils and macrophages and, basically, that leads to a cascade of inflammation as well.  The peptidoglycan layer fires up the innate immune system. We know that there’s relation to various autoimmune diseases, and it can even produce toxins. Usually, that’s a toxic shock syndrome. That happens less frequently, but the gram positives are not good players in our immune system just as much as the gram negative, even though I think we focus on LPS a lot more.

                                                Candida, we can’t forget about candida. It’s present in so many of my derm patients. It produces extracellular proteinase that breaks down collagen and keratin in skin. It also breaks down IgA complement, and we’re going to talk about secretory IgA in the gut. We’re going to see how deficient it is in some of my patients, and candida can be a cause of that. It erodes the mucosal layer in the stomach and, therefore, decreases the IgA production.  It also increases vascular permeability. Think leaky gut. We know that it compromises the immune system. So, there are studies that show a reduced ability of the body, of our leukocytes to kill staph aureus and E. coli in the presence of candida. So, I know that any of patient who has candida overgrowth, their immune system has been compromised and that’s part of why I’m going to be seeing all this other overgrowth and dysbiosis.

                                                Again, I know this crew talks about leaky gut and knows leaky gut, but just to make sure we’re on the same page, again, when we go to the case studies, I’ll take just a few seconds to talk about this. I think the easiest way of talking about a leaky gut is looking at a healthy gut. So, what we’re looking at here is a cross-section of the gut. These, of course, are the intestinal epithelial cells, and they’re stuck together with tight junctions so things don’t get through. Our bloodstream is right below our entire digestive tract because the whole point from mouth to anus of this GI tract is to digest food, break it down into very small pieces like amino acids, vitamins, minerals, get that into the bloodstream and send those nutrients out to every cell in the body.   So, of course, the entire GI tract has the bloodstream underneath it, and we have an immune system just at the ready in case something goes wrong. What’s happening up top here, it’s the hole. So, if you swallowed a plastic ball, we’re like a pinball machine. It’s just going to go through and you’re going to poop it out the other side. We have a hole, and three to five pounds of gut bacteria live up in this zone. Undigested food is up here. Then the critical part, of course, is this blue zone or strong mucosal barrier, whose job it is to separate the contents of our gut from these intestinal cells. These really need protection. They’re not too robust, and they can’t be in contact with all this.

                                                Secretory IgA, we’ll talk about a lot. I call it the Y guys to my patients. We see it grabbing on to LPS or endotoxin. It’s secreted by the mucosal barrier of the gut, and it helps us deal with the pathogens in the gut. So, we do want a good amount of secretory IgA.

                                                Well, leaky gut is what happens when the mucosal barrier is eroded, of course. Two specific bacteria we’re going to be talking about when we get to stool test are faecalibacterium prausnitzii and akkermansia muciniphila. Akkermansia, it’s in his name, mucin-loving. So, he actually eats a little bit of that mucus layer, but he stimulates these special cells in our gut, goblet cells, to produce more mucous. So, we want good levels of akkermansia to not have a leaky gut. We’ll talk about faecalibacterium in a minute, but he’s a butyrate producer. He does a lot of good for us. So, these are two keystone species I look for on every stool test.  So, over here when we get the leaky gut situation, how do we get in this situation? Antibiotics, it’s going to kill off good bacteria like faecalibacterium and akkermansia while it’s killing off the bad guys of the UTI or mastitis or whatever you’re taking the antibiotic. Also, we can get candida blooms when we take antibiotics and candida will erode that mucosal layer. Alcohol will do it, pathogenic bacteria-producing toxins, NSAIDs like Advil, and just a general lack of fiber, where we’re not feeding the good guys and they’re not there in the right amounts.

Dr. Weitz:                            How do we know if our patients have leaky gut? Is zonulin a good test for leaky gut or should we almost assume that most of our patients with dysbiosis probably have leaky gut?

Dr. Greenberg:                 That’s a great question. I used to run the zonulin test, but I’ve found that it’s just one marker of intestinal permeability. If it came up as not high, then my patients will be lulled into this false sense of security like, “Oh, I don’t have leaky gut,” which is not true.   So, I do assume that almost all my patients have leaky gut, but I’ll show you when I look at the stool test, I’m looking for that akkermansia muciniphila. Is it present in good numbers? Faecalibacterium prausnitzii, is it present in good numbers, and the secretory IgA.  When those three things are off, you can pretty much assume that your patient has leaky gut, whether or not it’s zonulin. So, I don’t even test the zonulin anymore, unless a patient specifically asks for it.

Dr. Weitz:                         Are there any other tests for leaky gut that are valid?

Dr. Greenberg:                 There are other gut permeability tests that-

Dr. Weitz:                         We used to do the lactulose mannitol permeability test.

Dr. Greenberg:                 Exactly, but, for me, I can get what I need out of the stool test and so I don’t have patients go do that.  Sometimes I’ll do a SIBO breath test in particular patients, but a lot of times I don’t have to.  Sometimes if it’s really bad, I need to determine is it hydrogen or methane or both, but I can also usually tell from the stool test whether or not they SIBO and potentially SIFO.

Dr. Weitz:                         Okay.

Dr. Greenberg:                 So, we were looking at a cartoon of the gut and, of course, that’s really easy to draw. This is a stain of an actual gut. We can see the importance of the mucosal layer. So, this is the three to five pounds of bacteria. These are those intestinal epithelial cells stuck together with tight junctions. This is the mucosal barrier separating the two, creating a calm immune system.  If we start erasing the mucosa, and this bacteria floods the cells, that’s basically leaky gut, and now our immune system has to deal with this stuff. So, I really love the stain. Just to drive the point home, this is a rat gut, but it was a study that showed this very thick mucosal layer from the stomach all the way to the backend. We have a very robust mucosal layer in all mammals, and it serves a real function and without it, we’re in trouble.

                                                I mentioned faecalibacterium prausnitzii. He’s such a keystone species and so important to intestinal health because he produces butyrate. Butyrate is the main food source of our intestinal epithelial cells, and they turn over every 24 hours. We have so many cells that need food.   So, what we see here is that process of we feed the faecalibacterium prausnitzii with prebiotics or fiber. Faecalibacterium is the probiotic and it produces postbiotics for us or beneficial things like butyrate. Butyrate has benefits all over the body, but we do focus on it in the gut. So, it’s that preferred fuel of enterocytes. It calms the immune system, and it creates a calming effect. It enforces tight junctions and also helps to prevent leaky gut. So, this is a keystone species I look for.

                                                Then when I’m assessing GI function of my patients, I think about it in two buckets. One bucket is their digestive function. How is their stomach acid? Are they producing enough bile? Are there enough digestive enzymes? We can get this a lot from the stool test.   Then, of course, what is the microbiome? Is there H. pylori in the stomach that’s affecting the stomach acid? The stool test I use has H. pylori on every test because I need to see it particularly for derm. I’m assessing if there’s SIBO and just what kind of growth and dysbiosis is in there.   Of course, as a functional medicine and naturopathic provider, we treat the whole person. So, I’m really thinking about the microbial distribution on the whole body. We certainly talked about the GI tract, how important that is, but I’m also looking at, I’m checking their oral mucosa. Do they have root canals? Do they have bleeding gums? We swallow a liter and a half of saliva a day. That’s going into our gut. That’s going to impact our GI health.  Of course, the skin microbiome. We’re talking about eczema today, and I don’t really have time to go into it, but staph aureus is a huge player. It’s on the skin. It’s overgrown in the gut, and it’s in the airways. It colonizes the nasal passages. Even urogenital, so many of my female patients with candida overgrowth in the gut get vaginal yeast infections. So, we always are treating the whole person and thinking about the microbiome everywhere.

                                                So, let’s talk a little bit about eczema, and then we’ll get into the good stuff and dive in to case studies.   So, what is eczema or atopic dermatitis? Fundamentally, it’s a disease of skin barrier dysfunction and inflammation. We can see the skin barrier dysfunction and we see the inflammation on the skin, but it really is inflammation in the gut and in the bloodstream and the system as well.  When we think of eczema, we think of it as a Th2 mediated disease with these Th2 cells that we looked at and related cytokines, IL-4, 5, and 13, but we now know that there’s a chronic phase of eczema where there’s actually increased levels of Th1, Th17, Th22, and all those related cytokines, and anytime you get any sort of skin barrier disruption, you’re going to get additional cytokines that are released. So, you can see that when it comes to eczema, there’s just a whole world of inflammation going on.

                                                There’s a fascinating study that was done because eczema tends to be this catch all bucket. If you have a rash, they call it eczema, and everybody’s in the same group, but dermatologists and people who specialize in derm, we know that they’re actually different, and there are actually subtypes of eczema.   This brilliant study done in 2019 divided up groups of people eczema. There was three adult groups, a pediatric, and then they were comparing it to psoriasis as showing. Psoriasis is a completely different disease. Too often, I have people come in, “I don’t know if I have eczema or psoriasis.” It matters which you have. They are two totally different diseases with totally different pathophysiologies. Even in eczema, we need to know who our patient is.   So, we can see that they took European-Americans, Asian-Americans, African-Americans, and then pediatric groups. What we see is quite fascinating. When we look at these immune pathways, they’re all Th2 for eczema, right? We know that. That’s the classic pathway we associate with eczema. In contrast, we can see psoriasis not a Th2 mediated pathway, none whatsoever.   There’s really interesting part and Th22 we said is in barrier disruption. So, any derm disease count Th22, and you can check that box. When it comes to Th17 and Th1, psoriasis is a very heavy Th17 mediated disease, but the interesting thing is it’s really present in pediatric eczema and it’s present in Asian-American eczema, but it seems to be absent in African-American eczema. So, it really does matter who you’re treating, and there are endotypes.

                                                Now, the good news is by treating the gut, we’re going to treat all of these types of inflammation, but we do want to keep in mind underlying pathophysiology. When we look at published research, so I gut test all of my patients and I can attest to this, but you don’t have to take my word for it. There’s lots of published research that shows that when you have a patient with eczema, they tend to have lower levels of the beneficial gut bacteria, bifida bacteria, bacteroidetes, bacteroidetes and higher levels of pathogenic bacteria, C. diff, E. coli, staph aureus. We’re going to keep saying staph aureus in eczema, and they have GI diseases in higher amounts than normal healthy controls.  I briefly touched on this, but staph is going to be all over your eczema patients. It’s going to be in the nose, on the skin, and in the gut. It colonizes the nasal passages, and so you have to treat them. We talked a little about this teichoic acid from the gram positive bacteria. It’s sticking out of that peptidoglycan layer. It suppresses staph. It’s gram positive, and this teichoic acid suppress IgA and IgG production in peripheral blood lymphocyte from eczema patients. Exposure to the staph aureus cell wall containing the teichoic acid or peptidoglycans led to increased IgE and histamine synthesis, two very big problems in eczema, IgE is elevated, that’s the Th2 pathway and histamine. So, again, I never want to ignore my gram positive bacteria because they can wreak havoc even in addition to the gram negative LPS ones.

                                                Candida is definitely a huge problem in eczema patients. They have statistically significant higher levels of antibodies to candida albicans. They’re pretty much colonized with it. When you treat the candida in your eczema patients, the skin will improve.

                                                Leaky gut, again, you don’t have to just take my word for it. It’s in the published literature that patients with eczema appear to have increased intestinal permeability, and there is an association between the level of increased permeability and the severity of the eczema. The worse your gut, the worse your eczema is going to be. This is absolutely true.

                                                We mentioned short-chain fatty acids like butyrate. Do they matter? They do. This whole study is called severity of atopic disease inversely correlates with intestinal microbiota diversity and butyrate-producing bacteria. So, we talked about faecalibacterium prausnitzii is one of the main butyrate producers. The study found infants who are healthy or have mild eczema have higher levels of this butyrate-producing bacteria compared to those with severe eczema. Remember, butyrate, these are intestinal cells, enhances tight junctions, and decreases inflammation. It decreases leaky gut.

Dr. Weitz:                            So, since there’s no supplements of prausnitzii faecalibacterium, I butchered that name, sorry, but is it best to try to increase butyrate production by using the appropriate prebiotics or is it more helpful to use butyrate supplements?

Dr. Greenberg:                 Yeah, and we’ll get to this once we get to my treatment plans. I do start off supplementing with butyrate because I want to come in and make a big impact immediately, and I find that it really, really helps my derm patients, their gut, and the skin issues. So, I give them the butyrate, but definitely, obviously-

Dr. Weitz:                         What’s an appropriate dosage for butyrate?

Dr. Greenberg:                 Well, so the products I use I do one cap. For adults, I do one cap three times a day with meals, and for infants, there’s a little scoop of powder that they’ll put in to milk or mix it into apple sauce, depending on the age of the kid. So, actually, I don’t know the micrograms or the actual numbers. I just know what I dose.

Dr. Weitz:                         Okay. Thanks.

Dr. Greenberg:                 Yeah, but then to your point, we don’t want to keep somebody on a butyrate supplement forever. That’s not treating the root cause. So, we treat the gut dysbiosis, and I do then go use the prebiotics that are going to try to increase the akkermansia and faecalibacterium, and we’ll talk about akkermansia because there is a probiotic on the market now for akkermansia, but, yeah, I’m not aware of the faecalibacterium prausnitzii probiotic at this time.

                                                So, okay. So, let’s hop in to the interesting stuff, the cases, now that we’re all on the same page. So, our first case study is Sam. Sam is an 11-month-old male with eczema who came to see me. I think you can see the eczema. It was on other parts of the body as well, but the face was the worst. His eczema started two months ago when he was nine months old. He’s always had dry skin.  It was interesting. It started a few months after receiving pasteurized donor milk. I do hear this story not infrequently, and it begs the question, was it really pasteurized? What happened? Is it other things in the milk? We don’t know the answers, but this is not an infrequent story that I hear.  Mom has been using triple cream on him. This is a prescription given by a dermatologist including triamcinolone, which is a steroid, nystatin, which is an antifungal, and mupirocin, which is an antibiotic.  It’s not working anymore.  If any of you guys see eczema patients, you will hear this story over and over again.  If they go to a dermatologist first, they’re going to get a steroid or a triple cream. It is going to work at first, and then they’re going to need more and more and more and stronger steroid, and stronger steroid, and it’s going to stop working eventually, and then people will often try to come to people like us in functional medicine to offer them something that’s not just a tube of steroid cream.   So, my next steps are going to be I got to test his stool and his urine.  I’m going to run a stool test and an OAT.  So, we’re going to go through some of Sam’s results.  So, we see, first of all-

Dr. Weitz:                         Let me just ask you real quick. Somebody asked, “What’s the minimum age that you could do a stool test?”

Dr. Greenberg:                 I don’t know that there is a minimum age. I treat infants as young as four months with eczema and we do test them, but I am going to discuss here that the microbiome of infants is different than the microbiome of adults. You have to assess them in different ways. So, if I got this on an adult, this would be a lot more alarming than on a kid because we see it’s C. diff, C. diff that’s capable of producing toxin A and B. This doesn’t mean that it is producing that. If it was, your patient would be having bloody diarrhea. So, this would be a lot more alarming in adults.  We often see, for example, C. diff in infant microbiomes. We’re not sure how it gets there or why it’s there, if the microbiome is just trying to sample everything. So, this isn’t super alarming. I mean, I’m still going to treat the C. diff, but it’s not like, “Oh, my God! This baby has C. diff. How did it happen?” A lot of the infant stool test will come up with C. diff. So, you do need to get used to assessing infant microbiome and understand that it’s different than the adult microbiome, but I’ll do it on the four-month olds.   Okay. So, we just talked a little bit about C. diff. Yeah, I’m going to treat it, but it’s not as alarming as it would be as if Sam was an adult because it’s just often there.

                                                So, when we look at the normal flora, there’s a couple of things. First of all, this stool test puts clostridia in the normal flora. We already know there’s clostridium difficile. That’s a pathogen. So, we take these normal flora with a grain of salt, right? There’s good and bad within a lot of these different groups. So, that’s the first thing. It came out here that there’s C. diff, but the OAT test for pathogenic clostridia. So, I always look at the OAT to see what levels of pathogenic clostridia are part of this number.

                                                What we can see here is a mix of things. So, Sam is overgrown on certain types of bacteria. He’s low on lactobacillus, which is not rare for eczema patients. We can see when I go those keystone species for akkermansia and faecalibacterium, a lot of times I will see none for either. This symbol means below detectable limits. They didn’t find it. That’s good for the pathogens like campylobacter. It’s not good for faecalibacterium or akkermansia. We want to see good levels. How we read these values are this is 1.28 times 10 to the second power. So, we read this as 128, and the range of akkermansia is one times 10 to the first power or 10 ranging to five times 10 to the fourth power or 50,000.  So, he’s got 128, but the range goes up to 50,000. This is way too low akkermansia. We need akkermansia to be higher and we certainly need faecalibacterium prausnitzii to be higher. Again, akkermansia helps our gut, our goblet cells produce the mucus layer, and faecalibacterium is that main butyrate producer.

                                                Then when I get to the section for his dysbiotic bacteria, we can see a lot of stuff, enterococcus faecalis and faecium. So, in adult females, this causes a lot of UTIs. Pseudomonas is a gram negative. This is a huge LPS or endotoxin producer. So, when we are talking about endotoxins flooding the system with a leaky gut, pseudomonas is not one that we want to see.

                                                I will tell you that for my different types of dermatological disease, I see different patterns of these results. So, when it comes to my eczema patients, there’s three things that I expect to see. I expect to see staph aureus is high, and we’ve talked about staph aureus a lot. You saw it in the published literature that staph aureus is overgrown in the gut. You see it on this patient. I know it’s on his skin, and I know it’s in his nose, and strep. So, staph and strep are usually overgrown and candida is usually overgrown.

                                                Sam’s stool test did not show high candida, and this is as I talked about part of the reason why I used the OAT. Candida often will grow up in the small intestine. It doesn’t always show up on the stool test because, again, the stool test is from the backend, the colon. So, just because the stool test doesn’t have a high candida reading, that’s meaningless to me. I have to go look at the OAT.   So, right now, he’s two for three. He’s high on staph and high on strep, and that’s typical of my eczema patients, but they’ve also got other stuff, which is why I need to test them, and we can see he’s got a lot of pseudomonas and other overgrowth that needs to be addressed.  He’s got growth of citrobacter freundii and klebsiella pneumoniae. These are not good guys. These are in the potential autoimmune triggers. This does not mean that Sam has or will develop autoimmune disease, but these bacteria are associated with certain autoimmune diseases like klebsiella is associated with ankylosing spondylitis, for example. So, we don’t want them around. We want them to be less than detectable limits, and I want to clean all of this stuff up in him.

                                                His secretory IgA is low. If you remember, I said that was the Y guy on that picture. The Y guy was grabbing onto the LPS. So, you see we got tons of pseudomonas. That’s LPS and other ones. We need a good level of secretory IgA to help him cope with this, and he’s low. This is one of those markers. So, the three things I said I’m looking for leaky gut, two little akkermansia, two little faecalibacterium, and low secretory IgA. I can absolutely, even though I was suspicious that Sam had leaky gut, he absolutely has leaky gut now and there’s no doubt about it. So, his secretory IgA is 54. That’s a 10th of the lower limit of the scale. We want 500 to 2,000, really, to be healthy.

                                                So, now, I got to his OAT test. Now, we see a whole other world, which is the fungal world. If you just pay attention to the bacteria, you’re really doing your patients a disservice. I think this is what happens in SIBO a lot is that they’re testing and treating for bacteria and not paying attention to the fungal world. It’s huge.  So, what we see on his OAT test, the first marker I go to is seven arabinose. That’s the marker for candida. We can see his absolutely high. He has three times over the upper limit of what we want to see in candida. So, he’s just fulfilled the trifecta in my eczema patients, high candida, high staph, high strep, and other things.   What’s concerning on this OAT is these aspergillus because this is mold. Candida is yeast. It’s a single-cell fungal organism. Aspergillus is a mold. We don’t want to see mold overgrowing in him. The question is where is this coming from because candida is actually commensal. We all have candida. We just don’t want it overgrown, but we shouldn’t have aspergillus. So, there’s exposure coming from somewhere. So, we’re going to have to detangle that. Now, my hackles go up for mycotoxins. Am I worried about mycotoxins in this infant? We’ll see how I assess that and what we do with it.

Dr. Weitz:                            I just wanted to comment that I’ve seen a lot of times with patients who end up having mycotoxins and they also are dealing with fungal overgrowth.  What exactly is the relationship between those and how do they interact?

Dr. Greenberg:                 Yeah. It’s intimately connected. So, at the beginning, when I talked about those mycotoxins, mycotoxins are produced by mold. So, you’re not going to have mycotoxins without mold. Mold is two problems. One, is the mold growing in the system? This test is showing yes. He has actual aspergillus, fuzzy mold growing in his system. Then the second question is, is that mold producing mycotoxins? We can be affected by mycotoxins either by mold growing in our gut or mold growing in the environment.   So, I think people look around their house and say, “Well, I don’t see mold. I don’t live in a moldy environment.” You don’t actually really know that unless you come in and have full inspectors or rip up the walls because you’re doing construction. Mold hides behind the wall. It eats paper. It eats wood. That is what we build our homes out of, and all it needs is just a little bit of water, and it’s off to the races, and there can easily be tons of mold growing behind walls. If that mold is feeling threatened, it’s going to start pumping out mycotoxins. So, they are intimately related. You don’t have mycotoxins without mold.

Dr. Weitz:                         Thank you.

Dr. Greenberg:                 Then when we look down here, we see the bacteria markers from the OAT. They’re all overgrown, but we already knew this from the stool test and from the stool test, we know the specific strains of overgrowth that are driving these numbers, but these are two different labs. One is urine, one is stool, and they usually do back each other up, which is nice to us providers to feel like the labs are valid.

                                                So, I want to point out that there are patterns that you learn to recognize on the OAT. So, for candida, once I see that there’s candida overgrowth, I’m specifically looking at two other markers, the oxalates and the vitamin B12. So, let’s look at his. Sam’s oxalates are high. This is because candida and mold kicks off oxalic acid or oxalates. So, when I have patients who have candida overgrowth and high oxalic acid, I don’t do anything to treat the high oxalates. I treat the candida and the oxalic acid will come down.   I mean, there are foods that are high in oxalates, but they’re healthy. It’s spinach and Swiss chard. So, unless someone is really going crazy like eating massive amounts of spinach, I never take away the high oxalate foods. I just treat the candida and mold, and this will come down naturally, but expect to see it and know where it’s coming from.

                                                Then the second is vitamin B2 or riboflavin. Candida and mold create acetaldehyde. If you have ever had too much alcohol one night and the next morning you woke up and had a hangover and felt terrible, you know what acetaldehyde is because that’s what pretty much poisoned you the next morning. So, candida and mold produce this and we use up our vitamin B2 trying to deal with it. So, I do supplement patients with additional B2 while I’m treating the candida and mold because I want to help them out. Again, they don’t need to be on B2 forever. We’re going to clean up the candida and mold and then they’re not going to need vitamin B2 supplementation. So, look for those two when you see candida.

                                                Then I need to look at the indicators of detoxification. I know he has mold growing in his gut, and now I need to try to figure out, do I think mycotoxins are a problem for this kid? Two of the ones that I look at are glutathione and this methylation toxic exposure.   So, his glutathione needs are not elevated yet, but he’s 11 months old. So, we may not have just depleted it yet, but if we keep going with all this overgrowth, he is going to be deficient in glutathione, but this toxic exposure methylation, this 2-hydroxybutyric marker is elevated, and that really worries me when it comes to somebody who’s got aspergillus overgrowth because my number one suspect for the toxic exposure is mycotoxins. So, in this case, I would recommend to the parents that they do a separate mycotoxin urine test to make sure either this is a problem or it’s not a problem, and we need to fix it or we don’t have to worry about it.

                                                So, we look at all of these issues for Sam, and we’re going to have to deal with all of them. Again, this is to treat the eczema. So, he’s got massive bacterial overgrowth of both commensals and dysbiotic bacteria. So, I need to treat with antibacterial herbs that are safe for infants. So, we’ll talk about it or if you’re an MD and you want to prescribe pharmaceuticals, then that’s your path. I really rely on herbs much more. There are occasions where I’ll prescribe antibiotics, but 95%-99% of the time I’m using herbs.

                                                I do give probiotics. I’m a huge fan of spore-based probiotics, but not in infants or breastfeeding moms. So, this infant would be getting a lactobacillus-bifida bacteria blend. I just find the spore-based, they just don’t play well in the guts of infants and even through the breast milk. I just get complaints from mom that the poop is this and it’s that. It just doesn’t happen with the lactobacillus and bifida probiotic. So, those are the type of probiotics I give infants.

                                                Then he had massive fungal overgrowth. He’s got candida and aspergillus and elevated markers of detoxification. So, we have to start investigating the source of the mold. Where did he get this aspergillus overgrowth in his gut? Is it coming from his home? I had one parent, not this infant, but another one who opened up the bottles and there was hidden pockets in the bottles and she found this black disgusting mold in there, and the infant was overloaded with molds. So, we have to figure out where it’s coming from.  This is related to testing the environment. So, you can do mold plates, which are agar plates, ERMIs, which are dust collections or call in mold inspectors, which are the best, but certainly the most expensive.  Then we need to treat with antifungal herbs safe for infants. So, a different protocol, and I don’t have an eczema protocol because I’m treating on the dysbiosis that I see in the gut.  Then I recommended the mycotoxin testing, and we’ll take a look in a minute, and an anti-candida diet. Now, he’s 11 months old. He’s not eating that much stuff, but we’re going to limit fruit and sugars and things like that because we don’t want to be feeding the candida while we’re trying to address it with herbal protocols.

                                                So, there’s no faecalibacterium prausnitzii, we discussed it, I am going to give a butyrate supplement. There’s a powder for infants and capsules for adults, and then eventually work on feeding prebiotics that will help the faecalibacterium come back. The akkermansia, there are probiotics that are available that now contain akkermansia. They came out last year. So, the good news is akkermansia is available. The bad news, it’s $200 a bottle, and they’ve been back ordered, so it takes a few months to come.  I called the company and asked if it works for infants or children to open the capsules if the akkermansia will survive, they’ve never tested it. They don’t know for sure. So, I do tell the parents that because it is $200 a bottle, but the company feels like it’s worth a shot as long as they eat it right away. So, I will give the infants this akkermansia.

Dr. Weitz:                         What’s the name of the company that sells this?

Dr. Greenberg:                 It’s called Pendulum Probiotics. It’s marketed as a diabetic, a glucose control one because as it turns out, diabetics have no akkermansia muciniphila, and leaky gut, and chronic inflammation. I think that’s why they priced it at $200 a bottle, but, yeah, it’s a glucose control, but it’s akkermansia and beneficial clostridia.

Dr. Weitz:                         Are there certain prebiotics that would stimulate the growth of akkermansia?

Dr. Greenberg:                 Yeah. I mean, I know MegaSpore has been on here and people use it. They have a Mega Prebiotic that they claim helps enhance the growth of faecalibacterium prausnitzii and akkermansia muciniphila. So, I haven’t looked at their studies, but I do use the Mega Prebiotic because they made those claims and I do find it’s a nice prebiotic.

Dr. Weitz:                         Okay.

Dr. Greenberg:                 So, for the low secretory IgA, of course, this is due to the leaky gut, but, again, while we’re waiting, I’m going to give a supplement that has IgG, IgA, and IgM because we’re not going to fix the gut overnight, and there’s so much dysbiosis, and especially as we start to kill off this dysbiosis, we need that secretory IgA to be there to capture the LPS and gram positive and all of this stuff. So, I just give it as a supplement when I start.  We talked about his need for-

Dr. Weitz:                         Is there a particular product for IgA, IgG, IgM that you like?

Dr. Greenberg:                 So, again, I do use Mega IgG2000 in adults, and in infants, we just open up the cap. That’s the one I tend to use, but there’s others. There’s SBI Protect and some other ones as well.

Dr. Weitz:                         Okay.

Dr. Greenberg:                 Then we talked about this need for vitamin B2 or riboflavin. He is deficient in it because of the candida and mold. So, I’m going to go ahead and give him, for infants I do drops of vitamin B2. For adults, I just do one cap a day of a vitamin B2 supplement while we’re treating the overgrowth.  Then, again, we don’t have time to get into it in this lecture, but I’m obviously addressing the skin barrier disruption, the staph aureus on the skin. I use natural botanical topicals, no steroids, no antibiotics, nothing like that.

                                         Okay. So, let’s look at what happens. So, this was baby Sam when he first came to see me and three weeks later. We can see. So, he’s not totally cured of his eczema, but it’s a lot better even three weeks later. He’s not itching as much. Your eczema parents are suffering as well the children. They’re watching their children suffer, and they’re kept up all night because the child is up all night scratching and itching.   So, he’s gone from a situation where he wasn’t able to sleep. The kids will scratch themselves until they bleed, and then they risk infection because the pain of scratching themselves until they bleed feels better than the itch. They’re this tortured by the itch of eczema. So, already, I mean, he’s not looking perfect, but he’s no longer awake and itching and on all of that stuff.

Dr. Weitz:                         Can you name a topical botanical cream that you like?

Dr. Greenberg:                 Yeah. It’s not like one thing, unfortunately. With naturopathic medicine, there’s no tube of magic cream like the steroid. It’s a whole thing, and I lecture on this at conferences and other situations, but you have to address the staph aureus on the skin. The staph is high pretty because the skin pH is off. The skin pH is supposed to be acidic, and when it raises and it becomes more alkaline or neutral, staph aureus will grow out of control. So, I’m doing things that are naturally antibacterial, and also will create an acidic pH on the skin. So, things like colloidal silver spray, antibacterial, a mix of apple cider vinegar and water, it is so acidic. Staph hates it. The problem is when the skin is really compromised, you’re not going to be able to use the apple cider vinegar because it’s going to be too stingy, but as the skin starts to heal up, then you can get in there with the apple cider vinegar and whack the staph down.

                                                I use hydrosols, which are water-based plant extracts. I love rosemary hydrosol. It’s antifungal and antibacterial. Depending on what’s going on, we’ll use different topicals. There’s a neem oil I like that has a little bit of peppermint and lavender essential oil. Peppermint essential oil is good for soothing the itch. So, we get a two for one, but there’s lot of things. Sometimes I’ll make a salve with essential oils or instruct the parents how to do it. So, it really depends, but a combination of topicals that are going to be antimicrobial, and pull that skin pH back down again to acidic.

Dr. Weitz:                         Is there a benefit to use some phototherapy for eczema?

Dr. Greenberg:                 I mean, people do find some benefit from red light therapy. At a certain place when people are suffering, anything you can do to ease the suffering, but I don’t find that I need it. They’re expensive machines. It’s time-consuming. It’s hard to get an infant to sit still in front of a red light machine. I find that I don’t need it most of the time. So, again, it is controlling symptoms, but it’s not actually getting to the root cause. So, I’m much more focused on let’s just clean this thing up.

Dr. Weitz:                         Okay.

Dr. Greenberg:                 Okay. So, the parents agreed to run the mycotoxin test on Sam, and what we see is he’s got a lot of mycotoxins. So, there’s two things going on here. We already knew that he had aspergillus overgrowth in his gut, and ochratoxin A is going to be your most common mycotoxin that you see on any test because aspergillus is the most common mold. He’s got a massive amount of ochratoxin A. It’s seven, eight times the limit. So, there’s a green zone because we live on the planet, we eat food, food can have mold and mycotoxins. The only totally clean mycotoxins I see are the infants. So, just having a little bit in the green zone is not concerning, but these are concerning levels. His aspergillus is producing mycotoxins, and we need to get rid of the aspergillus in his gut at the source and deal with the mycotoxins.   There’s something else. So, penicillium is another kind of mold that produces mycotoxins. The OAT, unfortunately, only tests for aspergillus and fusarium molds. It doesn’t test for penicillium. So, we didn’t know that he had penicillium overgrowth or was being exposed to penicillium in the home, but, indeed, he has mycotoxin sterigmatocystin that’s specific to penicillium. So, there’s two molds, two mycotoxins, and this is absolutely creating immune suppression and exacerbating his condition.

                                                So, we have to treat the mycotoxins. We treat with binders. I add glutathione. I add fish oil because mycotoxins are lipophilic. So, the skin and the organs are lipophilic, but we want to give some fish oil like those mycotoxins find in the fish oil. Then we definitely have to do that home investigation and figure out where is the aspergillus and penicillium that he got exposed to because this is an 11-month-old infant. It narrows it down. It’s COVID, he’s not going to daycare. He doesn’t get up and go to work every day. He’s not sitting in a car for hours in traffic. It’s a home environment, and that’s what we need to figure out.  So, I think it’s important for people to get mold and mycotoxin training to become mold and mycotoxin literate before you try to treat patients. We’ll talk a little bit about that, but these are some foundations of treating mycotoxins.  So, at the initial visit, we see Sam. Three weeks later, much better, and then two months after that, the eczema has basically cleared up and everyone was happy. Okay.

                                                So, now, we’re going to look at the second case study. This is an adult with eczema. So, we looked at our pediatric eczema. We going to now look at adult eczema. This is Alice. Alice is 39 years old. She had eczema as a child. She’s had occasional eczema on and off as an adult, but her neck went really crazy during her pregnancy about nine months ago. She cannot sleep at night. This thing is itching and oozing. It’s just torturing her all day and all night.  Her baby is now four months old. She’s a breastfeeding mom. A dermatologist prescribed tacrolimus and crisaborole. Tacrolimus is a calcineurin inhibitor. It’s a topical cream. Crisaborole is also known as Eucrisa. It’s also a topical cream, a PDE4 inhibitor. So, both of these things are like steroids trying to suppress the inflammation, just shove it back down into the skin, which is clearly not working.

                                                So, my next steps are I’m going to give her a stool test and an OAT test, but I want you to note, this eczema has a secondary staph infection, and this happens a lot in eczema patients. You’re not just treating eczema. They’re staph way overcolonized and actually infecting. The keyword here that should clue you in that there’s a staph infection that needs to be addressed is the oozing. Once you get to the point when something is oozing, you could pretty much figure you got an infection.   You can send them to a dermatologist or if you can, swab it yourself. You need a wet sample. I don’t even do it. I just assume it’s staph and it needs to be treated stronger like a staph infection instead of just the colonization that we see in typical eczema.   So, let’s look at Alice’s stool test. So, she actually has high H. pylori, and once I see H. pylori, now my red light is flashing. Is this impacting the stomach acid? Is she having hypochlorhydria or too low stomach acid.  Is she not digesting her food properly?  Is this leading to overgrowth of commensal and dysbiotic bacteria and potentially SIBO? So, we have to go on.  When we look at her normal bacteria, we do see overgrowth of enterobacter, which in high amounts can be inflammatory. That akkermansia, not found.  No akkermansia, no mucosal lining.  I’m already basically diagnosing her with leaky gut. Her faecalibacterium prausnitzii was actually in the range, so not too bad. So, the bacteroidetes and the firmicutes are the big groups of bacteria. Together, they’re about 80% of the gut bacteria, and she’s high on this whole group firmicutes. So, there’s a lot of overgrowth of normal bacteria in there.  Usually, this is the more inflammatory class.  So, if one of them is going to be overgrown, usually it’s going to be the firmicutes like hers is.  When we look at her dysbiotic bacteria, we also see a lot of overgrowth. Again, we see strep is overgrown and staph is present in her. She’s also got this enterococcus, and prevotella, and methanobrevibacter, which can cause constipation. We definitely don’t want constipation in these patients. We want them moving out all the stuff on a daily basis, but these produce methane and it paralyzes the gut.

                                                Then, again, her candida stool test did not show that she had a candida problem, but I got to wait and look at the OAT. There was this other type of fungi or yeast, the geotrichum. I will see this on the stool test. There’s another one, rhodotorula, that can show up. Basically, when you’ve got this onslaught of dysbiosis, it allows these yeasts and fungi which we should normally be able to clear to get a little foothold. So, it’s not unusual to see other little yeasts pop up as well like this and the rhodotorula.   Then when we look at her digestive health, so her elastase is low. In functional medicine, we actually want to see this over 500. She’s definitely low. One of my number one reasons why I see elastase low is that there’s high H. pylori. The stomach acid is now hypochlorhydric, and the pancreas is not getting the strong enough signal to produce the pancreatic enzymes. So, this tells me that she is hypochlorhydric, and I need to be worried about not just treating the H. pylori but also dealing with the enzymes.   Her beta-glucuronidase is high normal.

Dr. Weitz:                         By the way, how do you deal with the enzymes?

Dr. Greenberg:                 I will talk about it, but there’s an enzyme that contains HCL because I want to raise that stomach acid, and that’s hydrochloric acid, enzymes, and ox bile. I like the ox bile. Even though her steatocrit was not elevated, so she is digesting her fats. Bile is antibacterial and antimicrobial. So, it’s actually really beneficial to give that extra bile when they’re eating because that’s when they’re going to get the flood of LPS and endotoxins is when we eat, and those tight junctions have to open up so we absorb food. So, I like an enzyme that has HCL, enzymes, and bile.

Dr. Weitz:                         You just showed on previous test how the methane producer was high, and that’s one way that you could potentially diagnose SIBO. What are the other ways you can potentially diagnose SIBO through a stool test?

Dr. Greenberg:                 So, obviously, we want symptoms in SIBO, right? So, we’re going to start with, is there the gas and bloating? Are they having the GI symptoms? Because I think, and it will be interesting to see if Mark Pimentel talks about this when you have him back on. There was another talk I listened to where basically, now, whatever the SIBO breath test show, if they don’t have symptoms, it seems like now we don’t diagnose them with SIBO, that they have to be symptomatic.

                                                So, I take that to heart. Are they having any any GI symptoms? If they’re not, I’m not going to diagnose them with SIBO, but if they have the gas and bloating and all the rest of it, then the H. pylori is going to be your first clue because we know H. pylori is related to SIBO because of this hypochlorhydria and we swallow a liter and a half of bacteria a day, we eat food with bacteria and mold, and if the stomach acid is not acidic enough to kill off most of those bacteria and fungal elements, first stop is the small intestine. What a great place to set up shop, right? There’s no competition. You’re already here. So, we know that H. pylori and SIBO are related.

                                                So, if I see H. pylori, and then I see, is there overgrowth of commensals, especially down here in the phyla group, and is there a lot of overgrowth of dysbiotic bacteria, and particularly, is there constipation? Is the methanobrevibacter high? There has to be symptoms for me. They have to be constipated. They’d had to have all of the SIBO-type presentations, but that’s how I use it.

Dr. Weitz:                         Good. Thank you. Somebody asked, “Can you use pancreatic enzymes in infants?”

Dr. Greenberg:                 I tend not to do it because a lot of times they’re on milk and other things, and I feel like it will work itself out. So, I tend not to give them. I mean, in kids, there’s the chewable enzymes, so depending on the age. I tend not to give it in the really tiny infants, but in the ones that can chew, I might give them the chewable enzymes. There’s no way to get the bile into kids because you have to swallow a capsule. I’ve tried opening up capsules and tasting bile to see, is there anything we could hide the bile in? It is so revolting. I almost vomited.

                                                As a naturopath, we’re pretty immune to most of these tastes. I can take almost anything. The ox bile was too much for me. No one is going to be able to take ox bile if it’s not in a capsule that they’re swallowing. So, there’s no opportunity for that, but I will give chewable enzymes to kids, but in infants, they’re usually doing a lot of milk. I mean, we might need to talk about their supplement if they’re not on breast milk and get them off of the dairy supplement. I tend not to give enzymes until they start getting to the chewable phase.

Dr. Weitz:                         Can you use bitters to stimulate enzymes?

Dr. Greenberg:                 Absolutely. So, a lot of times, I’ll start off with the stronger HCL, enzymes, and bile, and then as the gut is improving, switch to bitters because the bitters are a lower forced intervention. It stimulates the system to get going instead of just giving it to them. So, yeah, we love bitters in naturopathic medicine.

Dr. Weitz:                         Cool.

Dr. Greenberg:                 So, I was talking about the beta-glucuronidase. Just in case you guys do stool tests and wonder what this is, beta-glucuronidase, it tells us ASE. It’s an enzyme, and just a little biochem lesson, it has to do with the liver. So, the liver in phase two detoxification, phase one is how do we change the molecule into something and then phase two is how do we get it out of the body. So, one way that the liver can make a substance water-soluble is to do something called glucuronidation. It takes the glucuronic acid and sticks it on the molecule.   Estrogens are taken out of the body this way through glucuronidation as are some toxins.  So, the liver puts this glucuronic acid on, and now it can be put into the poop, and you poop it out, and we get rid of that excess estrogen and the excess toxins.  Well, this enzymes, beta-glucuronidase, can be produced in high amounts by a bacteria and it does something not good.  So, now we’ve got the substance the body was trying to get rid of, estrogen or toxins, the liver has put a glucuronic acid on it.  Well, at the last minute, beta-glucuronidase comes in and goes, “Hiya!”  It releases that glucuronic acid.  Now, this substance is like, “I’m free,” and it goes back into circulation in the body.  So, if you have estrogen-dominant females and they have high beta-glucuronidase, this might be why they’re estrogen-dominant. They’re not getting the estrogen out, but it can also impact other toxins and things the body is trying to get out.  Normally, you treat down the overgrowth and it will rectify this, but there is a supplement called calcium D-glucarate that you can give to block the beta-glucuronidase. She’s breastfeeding, so she’s not going to get the calcium D-glucarate, but if she wasn’t, I might give it to her, and that’s a pretty classic supplement that we give in naturopathic medicine. It’s a symptomatic treatment, but to deal with the high beta-glucuronidase while we treat down the gut.  Then her last thing, her secretory IgA is really, really low. Again, leaky gut, no akkermansia, low secretory IgA. She’s got leaky gut, and so we’ll have to deal with that.

                                                On her OAT test, we see that her aspergillus is not an issue. This is all nice and low, but she has candida overgrowth as I would expect with eczema. So, we have to treat the candida. The fusarium is undeterminate. It’s elevated, but it’s not frank high. So, I’ll think about whether or not she needs a mycotoxin test.  We talked about candida and oxalates. So, hers are elevated. She’s not high yet, but she’s going that direction. Again, this is due to the candida throwing off oxalates. Her vitamin B2 actually was not deficient because she’s still on prenatal vitamins. So, she’s getting a whole pop of B2 and it’s helping her, but I think if she wasn’t on the prenatal vitamins, she would be deficient in this vitamin B2 as we talked about.

                                                So, for her, I have to treat the staph infection on her skin. She’s bleeding and oozing. She cannot sleep at night. I am okay with topical antibiotics. Mupirocin ointment for a few days is a really good way to quickly get a staph infection down, and it’s a topical. It’s not an oral, but then I created an antibacterial essential oil salve for her to use. So, we just used the mupirocin for a few days, but it does a pretty good job of whacking it down, and then we’re going to work on all the underlying factors.    For her H. pylori, I have to give her altered protocol because she’s breastfeeding. So, she didn’t get my normal H. pylori, but there’s a different protocol, of course, safer for baby. It’s mastic gum and all this stuff that I think most of us treat H. pylori with. Her low elastase, this is where I give her that and the H. Pylori, the digestive enzymes, the hydrochloric acid, and the bile supplement.

Dr. Weitz:                         Which is your favorite digestive enzymes?

Dr. Greenberg:                 I really like DuoZyme by Karuna. They have all three of these. Integrative Therapeutics actually has a very good one, too, Panplex Phase 2, and I use that one a lot as well. So, those are my two favorites because it’s hard to find the digestive enzymes, the hydrochloric acid, and the bile together. So, one of those two.   For the bacterial overgrowth, again, I’m going to treat with herbs, but a modified protocol, safe for breastfeeding mom knowing her infant is going to get exposure to these herbs, and same with the candida. She doesn’t have akkermansia, so I’m going to give her the probiotics with akkermansia, the Pendulum, and give her the IgA supplement while I’m treating all these dysbiosis.

                                                Again, I would have given her calcium D-glucarate for this high normal beta-glucuronidase, but she’s breastfeeding and this has not been proven safe for breastfeeding, so she did not get it. Then, of course, addressing the skin barrier disruption with topical protocols to support.

                                                This was Alice on her first visit. Three weeks later, we can see it’s actually in a better state. This is really common for staph infections. They start off really concentrated, and thick like that, and oozing, and crusting, and bleeding, and creating all sorts of havoc, and as we start to treat it, it does spread out, and I think this is just partially as they’re putting the topicals. It’s spreading it around a bit, but it’s okay. You can see that. It’s a much better state actually than where it was and she’s not being tortured at this point.   Then a few weeks later, it’s gone. You can see that the skin is still not completely normal because it’s been traumatized like this for nine months. It’s going to take some time for the skin to repair itself, but there’s no more eczema. There’s no more staph infection. She’s completely normal. Then, actually, the baby had eczema. So, once we cleaned her up. I started treating the baby for eczema.

Dr. Weitz:                         What are your favorite candida formulas for adults and infants?

Dr. Greenberg:                 Well, so for infants, it’s different. For infants, I really like Biocidin Liquid. It’s broad spectrum, and it addresses a lot of things, clostridia, candida, bacteria, and it’s safe for most infants. It just have walnut hull and leaf, so make sure that there’s not a walnut problem in any patient. There’s also formulas by another … Obviously, infants cannot swallow capsules. Infants, we’re not going to give alcohol. So, I give them glycerides, and Biocidin is a glyceride.  There’s also a company, Beyond Balance, that makes glyceride formulas. So, I use some of their formulas in infants as well to treat the dysbiosis because, again, it’s not alcohol-based, and it’s proven safe for infants, and we can get it down easily.    For adults, I use a lot of different things. I actually like Candida Support now. I like grapefruit seed extract, caprylic acid, neem. It just depends. I do different protocols for different people, and it depends on the full spectrum of what I see as well, but those are some of my favorite internal candida protocols.

Dr. Weitz:                            Somebody asked about Saccharomyces boulardii to increase sigA.

Dr. Greenberg:                 Yeah. I know a lot of people use sac boulardii. The problem is it’s a yeast, and I would say most of my patients have candida overgrowth, and I just don’t like to give more yeast when yeast is a problem. So, I know a lot of people do sac B. I just don’t really use it because almost all of my patients have candida overgrowth, and I just don’t want to be plowing them with more yeasts. So, I think it works for some practitioners. I just personally don’t use it.

                                                So, you guys just saw two case examples on eczema, and you may be thinking, “Well, that’s great, but does it work for other dermatological disease?” I’ll just show you some quick before and after photos. So, this was an acne patient, 20-year-old, complaining of back and chest acne. Test, treat the gut. One month later, pretty significant improvement in the acne, and this was the chest. Same patient.

                                                This is a patient with actually fungal acne. So, we see those little white spots. That’s malassezia yeast in there. It’s different than acne vulgaris, which is bacterial. This is in the first visit, and in three months, we can see clear skin.

                                                This was another patient with classic acne vulgaris on the cheeks, another teenage female. Two months later, we see it’s clear and the other cheek.

                                                This is a patient who’s an adult who came to me with a full body rash. A lot of her body looked like this. It was pretty brutal. She thought it was, again, she was really focused on food, and it’s a food reaction and a food allergy and I had to be like, “We’re leaving this food discussion behind. It’s not food. It’s pathogens.” Test and treat the gut. Two months later, gone, done, cleared up. That was her arm. This was her stomach.

Dr. Weitz:                            What kind of rash is this?

Dr. Greenberg:                 This, she had a lot of candida. I mean, again, it was a lot of different types of dysbiosis, but there was a big fungal element to this one. Candida will just wreak havoc on your gut and havoc on the skin. Clean up the gut, you’re going to clean up the skin. Of course, I had a whole topical protocol for her as well, but it was pretty uncomfortable.

                                                This is a rare condition called palmoplantar pustulosis. It’s in the family of what we call papulosquamous disorders, so psoriasis. It’s also called pustular psoriasis. Although the interesting thing about it is these pustules are sterile. So, if you sample them, there’s not going to be anything in there, and it’s really considered a mysterious disease. We don’t know why it’s happening. This patient, her dermatologist was trying to put her on Otezla. She’s a medical professional, needs to use her hands. It was a huge problem. So, at the first visit, five months later, she’s got a big improvement. She’s able to use her hands for her job.    Two months after that, we’re starting to see some good clearance, and then one and a half months later. So, these kind of autoimmune diseases take much longer to treat than a simple eczema, but this is considered an untreatable disease, and you can see from the first visit to now huge, huge difference, almost normal, and the dermatologist say it’s untreatable mostly. You have to go on biologics for it.

                                                This is another patient with a psoriatic type disorder. If you look down at his ankles, you’ll see red, oozing, crusting, bleeding. I said oozing, I hope you all are already thinking that’s a staph infection or an infection. You’d be right. We get these staph infections on top of other skin diseases, even psoriasis. So, he’s been living like this for two years. You can see it’s going up his legs. He’s not able to wear shoes and socks. Total disaster for him. He’s not able to participate in his family.   Seven months after treating him, he’s totally cleared up from this and also, he’d seen many dermatologists over the two years and nobody could help him. This was the front at month zero and seven months later. His feet are also clear. He just took it in the shoes.

                                                This is an infant with alopecia areata. You lose hair. It’s not just from the scalp. You can lose your eyebrows, your eyelashes or full body hair. This infant actually lost all his eyelashes and we were able to treat the gut and have them come back. This is a progression of it. It was also on his head, but I just got the eyelash pictures in here.  So, does this method work for other dermatological disease? It does. It really does.

                                                Some things that you may want to consider as a practitioner using these methods. You’re going to have to analyze all of the problems that you’ll need to address on both labs. So, I look at everything as these are all my problems, and then I have to decide what order I want to treat them in. You can’t treat everything all at once. There’s going to be probably too many issues to address.

                                                I pretty much start with mold and candida and/or H. pylori because the H. pylori is upstream in the stomach, but it does depend on what I’m seeing and what the symptoms are.

                                                You want to learn the best protocols to treat each issue, both topical and internal. Then, of course, you’re going to adjust your protocols based on your patient, infant, toddler, breastfeeding mom, what allergies do they have. I move through different protocols every one to three months depending on the patient and how things are going.   So, there is no one protocol. Everyone’s like, “What’s the eczema protocol?” I don’t have an eczema protocol. It changes and it’s different for every patient. This really is individualized medicine, and that’s how you get good results for people.

Dr. Weitz:                            Have you ever treated lichen sclerosus?

Dr. Greenberg:                 I haven’t. I have a new patient who I think I’m going to be seeing soon. I’m planning on treating it the same way. It’s an autoimmune attack. Depending on how far the scarring is, it’s very hard to bring back skin that is already sclerosed. I think the goal would be to reduce the further sclerosus. I haven’t treated it, but I certainly plan on applying the same methods to it.

                                                So, if you’re wondering like, “Well, how can I learn how to analyze stool test and OATs and mycotoxin test?” The labs who you can run these with, they usually have a lot of free educational videos available, and you’re going to need to invest a significant time doing it. Some of the labs has been on weekend training courses. I think it’s vital for the OAT. It’s so complicated. When you first look at it, it’s like, “What is happening on this test? I don’t understand this. How could I ever understand it?” Do the weekend training course if you want to understand OATs.  There’s paid courses offered by a lot of functional medicine and naturopathic doctors and professionals. I think they’re a couple of thousand dollars. I’ve never taken them, so I can’t say whether or not they’re worth it, but I think you can do it on your own if you can put in the time.

                                                The labs offer free consults on each lab that you run. I would suggest that you take those free consults at least on the first 20 tests that you run that’s a new test for you. You’d schedule a half hour visit, and that professional at the lab is going to take you through it and help you understand what are you looking at, how do you put these pieces together. It’s really useful.   I always say start by running the test on yourself first. Be your own guinea pig. Schedule a consult and see what’s going on in your own gut and try to treat yourself. Then you can start using it on patients.

                                                How do you learn to use herbs? I really think people need formal education and training. I know it’s not like pharmaceuticals where you need to be licensed. Anyone can prescribe herbs, but I think you really need, in order to be responsible, to get formal training, and not just an online course.      There are a lot of courses and ways to become trained as a registered herbalist or a lot of professional degrees with herbs built in like naturopathic doctor. We have four years of herbal training and it’s part of our board exams to pass an herbal medicine section. Otherwise, you won’t be a licensed naturopath. Same for traditional Chinese medicine in Ayurvedic doctors. The herbs are built in and they’re tested and formally trained on it.

                                                In terms of getting mold and mycotoxin literate, I also think you should get some formal education and training. This one can be online. There’s a lot of doctors who offer courses on it. Like there’s SIBO training courses, there’s mold and mycotoxin training courses as well, but they’re going to assume that you either have formal herbal or pharmaceutical training because, again, this is mold. So, you’re going to be treating it with prescription antifungals or herbal antifungals, and you need to know what you’re doing and have proper licensing.

                                                If you guys like skin and find it interesting, I am the Program Chair of the Naturopathic and Integrative Dermatology Series on LearnSkin. This is free. There are 20 courses. They’re CE accredited. So, you can earn up to 10 free credits, either AMA PRA Category 1 if you’re an MD. There’s naturopathic credits if you’re an ND and CBRN for nursing. It’s a lot of the stuff that I talked about. So, there’s naturopathic approach to atopic dermatitis, gut dysbiosis and its role on skin disease. So, you can check out. There’s SIBO testing for dermatological disease conditions. You can head on over the LearnSkin and take any of these courses. Again, they’re totally free.  This is my contact information. I’m at the Center for Integrative Dermatology. If you want to contact me, it’s drgreenberg@integrativedermatologycenter.com. Yeah. That’s it. Well, we’re at 8:00, but I can stay and take questions if people are interested.

Dr. Weitz:                         A couple more questions. Somebody asked about seborrheic keratoses.

Dr. Greenberg:                 Seborrheic keratoses and not dermatitis? So, seb keratoses is, yeah, it’s a disease of keratinocytes, and it can look pretty fungi on the skin. They can be removed. They are never going to turn into anything carcinogenic as opposed to actinic keratoses. AK, actinic keratoses can and will turn into basal cell carcinoma or squamous cell carcinoma. Those are the non-melanoma skin cancers, but seborrheic keratoses is never going to turn into a malignancy. It’s just unsightly, and a lot of people, it can be genetic, it can be due to sun exposure, but it’s nothing to be concerned about medically, but you can have them removed. They’ll burn them off or cut them off. Yeah, but they can never turn into something carcinogenic.

Dr. Weitz:                         Somebody asked, “Which mycotoxin course do you recommend?”

Dr. Greenberg:                 So, Dr. Shoemaker is probably the most famous protocol. I, personally, Dr. Jill Crista is a naturopathic doctor. So, I did Jill Crista’s course for mold and mycotoxin certification. I really enjoyed her course, and find it very usable. I also just signed up. I think it’s AAEM, just had a mold and mycotoxin course that I’m still working through, but I found it helpful. I like both of them because … So, Dr. Jill Crista is a naturopathic doctor, so she does talk about some prescription pharmaceuticals, but she’s a lot heavier on the supplement and herbal treatments.   The AAEM course that I’m doing right now is MDs. So, they’re pretty heavy on the pharmaceutical stuff, but I like learning about both and getting both perspectives. So, even do more than one, but I can personally recommend Dr. Jill Crista, C-R-I-S-T-A.

Dr. Weitz:                         Somebody asked, “What stool test do you recommend?” I know you like to use the GI map, right?

Dr. Greenberg:                 Yup, and I know that they’ve been on here. I really love the GI map. I find it price-wise is great for patients. I love that it includes H. pylori. I find it really easy to read, very usable and actionable. When I treat on the basis of my results, I usually get very good results for my patients. I’m doing, if any of you guys are members of IFM, the Institute for Functional Medicine, they have an upcoming conference. There’ll be an international conference in June, and I was selected to present a poster, and I’m presenting the OAT and stool test for about 35 acne patients showing what dysbiosis I see in acne patients. So, if any of you guys are at that conference, you could check it out, but it’s based on 35 GI maps and 35 great plain OATs. Those are the two tests that I used.

Dr. Weitz:                         Let’s do one more question. Can you answer, how do you treat hair loss, in 30 seconds or less?

Dr. Greenberg:                 Well, it depends. There’s two types of hair loss. There’s alopecia areata, which is an autoimmune problem, where you’re attacking the hair follicle and there’s androgenic alopecia. It is very complicated. If any of you guys are interested, through the CNDA or California Naturopathic Doctors Association, I’m going to be doing a two and a half hour presentation webinar on hair loss through the CNDA in August. So, there’s no 30-second description for hair loss. It’s pretty complicated, but if you want to attend the two and a half hour webinar, go over to the CDNA and the California Naturopathic Association, and I’ll be giving that webinar in August.

Dr. Weitz:                         That’s great. If you could post that on the Facebook page also, that would probably be helpful. Thank you so much, Dr. Greenberg. So many of the practitioners said it was an amazing presentation, which it was. So, thank you so much.

Dr. Greenberg:                 Thank you all for your time. I really appreciate you spending Thursday evening with me.

Dr. Weitz:                         Thank you. Bye, everybody. See you next time.

                                                Thank you listeners for making it all the way through this episode of The Rational Wellness Podcast. Please take a few minutes and go to Apple Podcast and give us a five-star ratings and review. That would really help us so more people can find us in their listing of health podcasts.

                                                I’d also like to let everybody know that I now have a few openings for new clients for nutritional consultations. If you’re interested, please call my office in Santa Monica at 310-395-3111. That’s 310-395-3111, and take one of the few openings we have now for a individual consultation for nutrition with Dr. Ben Weitz. Thank you and see you next week.

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Dr. Mark Houston discusses HDL Cholesterol with Dr. Ben Weitz.

[If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.] 

Podcast Highlights

4:28  What are LDL and HDL?  These are apolipoproteins that transport fats through the body and serve many functions, including immunological function. They help protect us against infections and parasites and they are part of our metabolic system for making steroids and vitamin D and sex hormones.  Today, the biggest threats to us are no longer infections, but more from environmental toxins, nutritional imbalances, obesity, and other risk factors that result in chronic diseases like heart disease and diabetes that kill us.  In order to protect us from environmental insults the LDL particle number may become elevated, which is the driving risk for heart disease and myocardial infarction.  LDL is considered the bad cholesterol and HDL is considered the good cholesterol.

7:24  The main job of HDL is to produce Reverse Cholesterol Transport (RCT), also termed Cholesterol Efflux Capacity (CEC), which are the primary functions of HDL that go into the cell and the artery walls and pick up the LDL like a garbage truck and take it back to the liver where it will be excreted with bile. HDL if it is functional can reduce atherosclerotic plaques and reduce rupture and it can improve plaque stability.  There is soft plaque that is composed of a very aggressive core of lipids and smooth muscle cells and inflammatory cells, and it’s surrounded by a sort of a firm top that is very thin. This protective top can rupture, resulting in the contents of the plaque spewing out into the artery and this can cause thrombosis and an acute myocardial infarction.  Such patients may present with an acute MI while doing intense training, such as interval training or a marathon, though they may not have much obstructive disease.  The other type is calcified plaque, which is more stable and less likely to rupture, but this type of plaque tends to become obstructive.  It may not result in any symptoms until you get to 95% stenosis.  Calcified plaques can be picked up by coronary calcium scans or by an exercise echo or by nuclear medicine scans, while soft plaques will often not be seen by such scans or tests. But soft plaques can often be seen on MRI imaging with contrast or by a PET scan or a CT angiogram.

12:36  HDL has a number of positive functions, including RCT, anti-inflammatory, antioxidant, and it reduces vascular immunologic damage in the arteries.  HDL is composed of over 100 different molecules, proteins, lipids, and other components and there are at least 25 different beneficial effects of HDL on atherosclerosis prevention.  We used to think that the HDL level and the HDL size determined the true risk, but the only thing that really gives you the true risk is the functionality of the HDL.

15:37  There are two labs that can measure HDL functionality, including Cleveland Heart Lab, which is owned by Quest Diagnostics, which offers the HDL Function Test.

18:35  There are some who feel that APOA is a better marker for assessing heart disease risk than HDL.  APOA, which is the carrier for HDL, may be a little better marker than HDL, but it still does not correlate as well with cardiovascular disease risk as HDL function does.  One study found that in a male if the HDL is over 50 or 55, and in a female if it is over 75 or 80, most of it is likely to be dysfunctional. 

20:28  Oxidized LDL and Myeloperoxidase (MPO). LDL is not atherogenic (will not cause vascular damage and create arterial plaque) until its oxidized or otherwise modified. MPO is a compound that is made by white blood cells and while it is antibacterial, it is a bad actor.  MPO increases coronary calcium and it can cause high blood pressure, coronary heart disease, atherosclerosis, and even plaque rupture. When you have high levels of oxidative stress and high MPO, it damages the HDL and makes it dysfunctional.

22:15  Dr. Houston has developed a nutraceutical that improves HDL functionality called CardioLux with Metagenics that contains quercetin, pomegranate, lycopene, and vitamin E.  These components reduce oxidative stress and inflammation, making the HDL more functional.

25:31  A lot of HDL functionality is related to the proteins in HDL. Essentially the reason why we have LDL and HDL particles is that fats don’t move readily through the bloodstream, which is water soluble, so they are surrounded with various proteins that coat the lipids.  One of the important proteins in HDL is PON1, peroxidase, which is very important for HDL function.  These nutritional compounds (quercetin, pomegranate, lycopene) protect and raise PON1 levels.

27:30  CoQ10 is a very important nutrient for heart health, but there is an issue with getting CoQ10 not only into the cell but into the mitochondria. There is a new form of CoQ10 that’s a thousand times more effective than regular CoQ10 at penetrating the mitochondrial membrane, called MitoQ.  Dr. Houston has a series of 10 patients who were on the cardiac transplant list who had end stage coronary heart disease. They couldn’t put stents in and they couldn’t do bypass surgery. He put them all on MitoQ and every one is now asymptomatic with no chest pain and their ejection fractions have gone up significantly and they’re off the transplant list.  Dr. Houston noted that he still uses the metabolic cardiology program, so he uses regular CoQ10 for the vasculature, MitoQ for the heart, and he also uses d-ribose, taurine, L-carnitine, magnesium and a few other supplements that improve the myocardial contractility and mitochondrial function.

29:44  The best diet for improving HDL functionality is a low refined carbohydrate intake and sugar intake should be less than 25 gms per day.  You should have at least 8 servings of organic multi-colored vegetables per day, which are rich in phytonutrients.  Wild game, a variety of berries, and pomegranates should be part of that diet.  Pomegranate raises HDL functionality through raising PON and it has been shown to reverse carotid atherosclerosis in one year.

31:07  Dr. Houston has developed the Coronary Heart Disease Plaque Regression and Coronary Artery Calcium Regression Program, which includes about 15 different nutritional products, including Neo40 (a nitric oxide booster), Arterosil (which protects the glycocalyx), vitamin K2 MK-7 (a dosage of at least 360 mcg per day and K2 does not promote blood clotting or interfere with the blood thinner coumadin), omega 3 fatty acids (EFA-Sirt Supreme), VasculoSirt, curcumin, and quercetin.  Quercetin has anti-inflammatory, antioxidant, and anti-immune effects and it’s the only compound that reduces SASPs, which are senescent proteins.

35:30  Exercise.  Both resistance and aerobic exercise improve HDL functionality.  In Dr. Houston’s book, What Your Doctor May Not Tell You About Heart Disease, there’s 2 chapters on the best form of exercise that Dr. Houston wrote with Charles Poliquin, a great trainer who undortunately died about a year ago with a heart attack.  Dr. Houston and Charles also wrote an exercise program that combines aerobics and resistance training with interval training to get the best cardiovascular benefits, which is published in a book titled, ABCT, Aerobics, Build, Contour, and Tone.

38:03  Most of the medications that have been developed to raise HDL levels have not been effective.  The exception is niacin, which actually improves total HDL, HDL particle number, HDL size, and HDL functionality.  There was an older lipid drug used in the VA-HIT trial, which raised HDL, but we don’t know if it improved functionality.

Dr. Mark Houston is an internal Medical Doctor and a hypertension and cardiovascular specialist. He is the director of the Hypertension Institute in Nashville, Tennessee. Dr. Houston is triple board certified in hypertension as an American Society of Hypertension specialist and Fellow of the American Society of Hypertension, Internal Medicine, and Anti-aging Medicine.  Dr. Houston teaches at the Institute of Functional Medicine and the A4M programs. He is a prolific writer and has written What Your Doctor May Not Tell You About Hypertension, What Your Doctor May Not Tell You About Heart Disease, Nutritional and Integrative Strategies in Cardiovascular Medicine, Nutritional and Integrative Strategies in Cardiovascular Medicine, and his two latest books, Vascular Biology for the Clinician, and Precision and Personalized Integrative Cardiovascular Medicine. You can contact Dr. Houston through The Hypertension Institute web site HypertensionInstitute.com.

Dr. Ben Weitz is available for nutrition consultations specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss and also athletic performance, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111. Dr. Weitz is also available for video or phone consultations.

Podcast Transcript

Dr. Weitz:                            Hey, hey this is Dr. Ben Weitz, host of the Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting-edge health information. Subscribe to the Rational Wellness Podcast for weekly updates. And to learn more, check out my website drweitz.com. Thanks for joining me, and let’s jump into the podcast.

                                                Hello, Rational Wellness Podcasters. Today, our topic is HDL cholesterol, and we’ll be speaking with Dr. Mark Houston. The focus of HDL cholesterol which has been called the so-called good cholesterol is that this molecule could potentially help to prevent and reverse cardiovascular disease. Much of the research about heart disease has really been focused on the so-called bad cholesterol, the LDL, which is now generally seen as a significant player in the formation of atherosclerotic plaques in the artery walls that can lead to heart attacks, strokes, and heart failure over time.  of the cardiovascular medications are designed to lower LDL levels including statins, niacin, Zetia, bempedoic acid and the new PCSK9 inhibitors. And there are a number of nutraceuticals that are also effective at lowering LDL particles, including red yeast rice, fish oil, plant sterols, niacin, berberine among others.  We also know that the proper diet and exercise can also be very effective in reducing LDL cholesterol in our bodies especially the more atherogenic small dense LDL particles. But today, we’re going to be focused on the so-called good cholesterol, HDL. We’re going to go into how to understand it, how it works, and how we can improve HDL to improve our cardiovascular health.

                                                We first learned about the potential benefits of HDL cholesterol about 70 years ago. And in 1977, we learned through the Framingham Heart Study that low levels of HDL are generally associated with increased risk of coronary artery disease. And we thought at one time that simply the more HDL, the higher the levels, the better off we are.   But our thinking about this has changed as we have learned that the HDL story is much more complex than we thought it was. And drugs that were developed to raise HDL have really failed to be effective in reducing heart attacks or death. In fact, some people with very high levels of HDL may actually be more at risk for heart disease. And so, this is why we’ve asked the expert, Dr. Mark Houston, to join us to explain what current knowledge about HDL cholesterol is and how we can use this to prevent a reverse heart disease.

                                                Dr. Mark Houston is a internal medical doctor and hypertension and cardiovascular specialist. He’s a go-to expert on cardiovascular disease in the functional medicine world. He’s the director of the Hypertension Institute in Nashville, Tennessee Dr. Houston is triple board certified in hypertension as an American Society of Hypertension Specialist and fellow of the American Society of Hypertension, Internal Medicine and Anti-Aging Medicine.  He also has a master’s degree in human nutrition and a master’s of science degree in functional and metabolic medicine from the University of South Florida. Dr. Houston teaches doctors around the world about cardiovascular medicine as part of the A4m programs. Dr. Houston is also a very prolific author, having written what your doctor may not tell you about hypertension, what your doctor may not tell you about heart disease, nutritional and integrative strategies, and cardiovascular medicine, nutritional and integrative strategies in cardiovascular medicine.  And his two latest books which are Vascular Biology for the Clinician And Precision and Personalized Integrative Cardiovascular Medicine. Dr. Houston, thank you so much for joining me.

Dr. Houston:                      Thank you, Ben. It’s a pleasure to be with you as always.

Dr. Weitz:                           So, maybe you can give us a little bit of a explanation in general what is HDL. In fact, what is LDL? Why do these molecules exist at all?

Dr. Houston:                      Well, let’s start with the LDL story first because I think people are most familiar with that one, explain why it exists and then we’ll merge into the HDL story a bit. These molecules are termed apolipoproteins in the medical world. And apolipoproteins exist for good reasons we have to have them for a lot of health benefits.   For example, one of the major benefits of all the types of cholesterol whether the LDL or HDL is immunological function. It actually protects you from any type of infection, whether it’s viral, bacterial, parasitic, fungal, or TB, and it’s also part of our metabolic system for making steroids and vitamin D and sex hormones. So, there’s a teleological explanation for why these lipids were important in the early time to protect people from getting serious infections and dying from them.   And so, over time, what has happened is the functionality, the levels of HDL and LDL, have changed because in our modern society, people don’t die so much of infections anymore. But they’re dying from other types of environmental toxins, nutritional problems, obesity, and a myriad of other risk factors like diabetes. And so, what has happened to our cholesterol levels, particularly LDL, and to a lesser extent HDL, they’re going in the wrong direction in an attempt perhaps to protect us from these various types of environmental insults.  So, LDL for example, if it’s protecting us from something, it tends to go to very high levels. The LDL level’s elevated. And then, what’s called LDL particle number becomes elevated which is the driving risk recording heart disease and MI. There’s also genetic forms of dyslipidemia. But most people who have dyslipidemia in this country, it’s environmental. It’s not genetic.  So, LDL has been considered, as you said, the bad cholesterol. And HDL is considered the good cholesterol. But it’s much more complicated obviously than that, and that’s what we’ll get into today. So, that’s sort of an introduction, and we can kind of banter back and forth with questions as you wish.

Dr. Weitz:                           So, we generally think of HDL, its main function is to produce reverse cholesterol transport, right?

Dr. Houston:                      Right.

Dr. Weitz:                           And so, what exactly happens during that process?

Dr. Houston:                      So, reverse cholesterol transport or RCT, also termed cholesterol efflux capacity or CEC, are the primary functions of HDL that go into the cell, attach to the cell wall through various receptors that pick up the LDL just like a garbage truck and then take it to the liver where it dumps the LDL and is excreted into the bile. That’s the normal process. However, if HDL, RCT and CEC are not working, our HDL becomes we say less functional, then that process does not occur.  LDL accumulates in the cell. And then, that starts the LDL process of particle size going up, LDL levels going up, LDL size being smaller. And then, you get atherosclerosis, coronary heart disease.

Dr. Weitz:                           And so, HDL can actually take the cholesterol from the artery walls, right?  And so, it can reduce plaques potentially.

Dr. Houston:                      That’s right. It can literally take them out of the cell. But also take them from the cholesterol wall itself, and it’s very important in reducing plaque rupture, and improving plaque stability in coronary heart disease.

Dr. Weitz:                           And what’s the significance of plaque stability?

Dr. Houston:                      So, there’s at least two, maybe three, major forms of plaque. There’s the vulnerable plaque which has a very aggressive core in the middle composed of lipids and smooth muscle cells and inflammatory cells, and it’s surrounded by a sort of a firm top that is very thin, and that protective top can rupture.  So, what happens is all this activity inside the plaque can eat through this protective coating or cap and rupture into the arterial wall once that spews out into the artery.  It causes acute thrombosis which is an acute myocardial infarction.  That’s the really bad type of plaque. It’s considered soft plaque. It’s usually not calcified as vulnerable.   The other plaque is one that has a much thicker cap and has less of a activity in the center with less lipids and inflammatory cells.  And because it’s more stable, it’s not as likely to rupture. But over time, it can become very obstructive and impede the blood flow through the artery.  The problem we have is those people who have stable plaque may not have any symptoms whatsoever until they get to a 95%-plus stenosis.  But the ones who have unstable plaque, the ones that have the really thin cap, those can be only a 50% blockage, but they tend to rupture.  And those are the ones that typically present with intense training, like they run a marathon, interval training, whatever, and the plaque ruptures, and they have an acute MI even without much obstructive disease.

Dr. Weitz:                           And those soft plaques wouldn’t be picked up, for example, by a coronary artery scan.

Dr. Houston:                      Those can be completely missed because they’re not necessarily calcified, and they can be missed by exercise echo and nuclear medicine scans and other non-invasive ways of looking at plaque because it’s only maybe 50%. So, it doesn’t obstruct the flow.

Dr. Weitz:                           So, what’s the best way to get a clue as to whether those exist or not?

Dr. Houston:                      You can do other testing. For example, the MRI imaging with contrast of the heart, which can pick up any kind of plaque, soft or hard. And there’s other types of metabolic testing called a PET scan which picks up activity of plaque in the arteries. You can do a CTA, CT angiogram, looking at plaque. And, of course, the gold standard is a coronary arteriogram where you actually inject dye into the coronary arteries.

Dr. Weitz:                           Is the MRI being used regularly?  I haven’t heard of it being used that often.

Dr. Houston:                      We use it routinely in the institute.  We have an MRI scanner, and it’s incredibly accurate for plaque but also for valve function, cardiac contractility, diastolic dysfunction.  It’s expensive.  But if you have a patient that needs it and get it pre-approved by the insurance, it’s extremely valuable when you don’t want to do an arteriogram.  But also, there’s no radiation exposure, usually not much and with a contrast or some.  But you can’t do it in people who have metal.  So, pacemakers and artificial joints, you can’t put them in an MRI.

Dr. Weitz:                           Right. So, we have a number of positive functions of HDL making plaques more stable, helping to reverse cholesterol transport. And in recent years, we’ve learned about the antioxidant and anti-inflammatory properties as well.

Dr. Houston:                      Right. HDL is composed of probably over 100 different molecules, proteins, lipids, and other components. And with that degree of composition being so complex, it has a very complex anti-atherosclerotic effect. You mentioned a few, anti-inflammatory, antioxidant, anti-immunologic which means it reduces vascular immunologic damage in the arteries, reverse cholesterol transport. I mean there’s probably 25 or 30 different beneficial effects of HDL on atherosclerosis prevention.   But the key point here is that no matter what your HDL level is and no matter what the size of HDL is, those used to be thought to be protective or good things.  But now, it turns out that those don’t actually tell you the true risk in an individual. The only thing that really gives you the true risk is the functionality of the HDL.   Now, in a population, if you look at statistically, is your HDL level this or is your HDL size this, there’s a correlation in a population.  But if you take an individual, and you measure their HDL total, you measure their HDL size, whether it’s big or small, and you measure the HDL map, and there’s five forms of HDL from pre-beta all the way up, those may look great on paper.  But that patient may still be at risk for coronary heart disease because you didn’t measure the true value and true risk which is functionality of the HDL.  Does it do all the things it’s supposed to do to protect you?

Dr. Weitz:                           Now, why is it that drugs that have been developed to raise HDL have all failed so far?

Dr. Houston:                      There’s a lot of reasons. Some of the studies were just bad studies. They didn’t have the right population. Another is they had other adverse effects, like one of the drugs raised blood pressure, and that counter balanced the effects of HDL. But what happened is all of the studies were done prior to the understanding really of what HDL function was all about. So, they may have raised HDL. But it wasn’t functional HDL. So, the HDL maybe went up 30 to 50%. But it didn’t work. So, there was no reduction, as you said, in MI or total mortality with it.

Dr. Weitz:                           Right. So, what is the best way to measure HDL and HDL functionality?

Dr. Houston:                      There are two labs that are presently available clinically to measure functionality of HDL, and that’s really the key to getting at the risk for a patient in their coronary heart disease and MI risk.  As I mentioned to you earlier, Ben, we’re in the process of completing a large clinical trial on HDL functionality looking at a nutraceutical compound that not only improves HDL function, but also can improve HDL size and also HDL particle number which is another thing I neglected to mention earlier.   And let me just maybe comment on that while we’re talking about it. HDL function is the most important thing to measure. So, we can do that now clinically. HDL particle number, how many particles of HDL do you have, is also very high correlated with HDL functionality. And you can measure this in traditional labs to do advanced lipid testing. So, when you look at those two, there’s a 90% correlation between HDL particle number and HDL functionality.  But what we’re trying to do is see which of those has the best overall predictability in a population and see if we can actually improve both of those numbers.

Dr. Weitz:                           And then, when it comes to particle size, you want larger HDL particles.

Dr. Houston:                      That’s what we used to think. But that now has not turned out to be correct either because there’s labs that do HDL mapping, and there’s five HDLs: pre-beta and alpha one, alpha two, and others that range from very small to the large ones. For example, the pre-beta which is a really small one is the one that actually picks up the HDL, excuse me, that picks up the LDL out of the cell.   So, if your pre-beta is not working well, you can’t do good transport out of the cell. But then as the HDL matures, it goes to different sizes, and that progress across there involves a lot of different enzymes, a lot of different complexities, but eventually gets to the form of HDL which takes it and dumps it into the liver through what’s called scavenger receptor SR1 receptor in the liver. So, you’ve got to have all five of these.   And we used to think, “Well, the big one’s like a big dump truck, and it can carry more LDL with it.” It turns out, the size turns out to be not a great predictor nor does the actual total HDL level for heart disease.

Dr. Weitz:                           Now, I’ve heard one prominent functional medicine doctor talk about measuring apoA, and that being maybe a better marker than HDL. What’s the relationship between apoA and HDL? And is there a value in measuring the apoA?

Dr. Houston:                      There’s apoA1 and apoA2, and those are the carriers for HDL. So, that’s the apolipoprotein we mentioned earlier, and they are probably a little bit better than HDL total. But even those do not correlate well with risk because neither of those are functional tests. You’re again just measuring apolipoprotein as a carrier for HDL, and it can be again dysfunctional. So, for example, if you measured total HDL in a population, you could say, “Well, if it’s between…we’ll just throw out some numbers here, 30 to 100.  If you’re below 30, you’re probably in trouble, and if you’re over 100, you’re probably in trouble because those tend to be people who have more dysfunctional HDL. There’s actually a study that was done in men and women, and it suggested that if a male was over around 50 or 55 of their total HDL, most of it was likely to be dysfunctional.  And a female, if it was over 75 to 80, was more likely to be dysfunctional, and that’s because these tend to build up in the blood because they’re trying to cancel the bad effects of the LDL. So, you make more and more of it. But as you make more of it, it’s more dysfunctional. So, the levels keep going up. But less of it’s actually working.

Dr. Weitz:                           And what is the relationship between oxidized LDL and myeloperoxidase and HDL functionality?

Dr. Houston:                      So, all of those are inflammatory and oxidative stress measurements. Oxidized LDL is the form that is atherogenic. So, LDL and its circulating in the regular serum is not at atherogenic until it’s modified into a oxidized or some other form. There’s different forms of LDL that are called modified LDL, and that’s the one that go across the vascular endothelium and actually cause damage or plaque formation.  Myeloperoxidase or MPO is a compound that’s actually made by the white blood cell, and MPO causes all kinds of havoc. Well, it’s good that it kills bacteria. But if you keep making MPO due to other reasons, it causes high blood pressure, coronary heart disease, atherosclerosis, and even plaque rupture. It’s a bad actor and increases coronary calcium.  So, MPO has both inflammatory and oxidative stress implications. Now, once you develop those, they are the cause for atherosclerosis and myocardial infarction. So, your HDL has to be around to clean that up. What happens when you have a high oxidative stress and MPO level, it damages HDL, and it makes it dysfunctional. So, when your MPO is high, you can say, “Well, chances are, my HDL is not functioning well.”

Dr. Weitz:                           So, what’s the best way to improve HDL functionality?

Dr. Houston:                      What we’ve developed is a nutraceutical product that underwent initial study with 10 patients just to see if we could demonstrate effects, and that’s actually published as a white paper through… Can I mention the name of the company? Is that okay?

Dr. Weitz:                           Sure. Yeah.

Dr. Houston:                      Okay. So, the initial study with 10 patients with Metagenics. And then, they asked us to do a double blind placebo control trial which is really the way to get the true data. The initial trial showed that the nutraceutical proprietary compound that we’ve developed is called CardioLux, CardioLux, and it’s got pomegranate. It’s got quercetin, curcumin, vitamin E and few other things in it, looked positive in the initial pilot trial of 10 patients.    So, we’re in the process of finishing the double blind control trial now. We’ll be then done April 15th. I don’t know the results because I’m blinded, and we’ll do the statistical analysis. We will then publish the trial in a journal, and we’ll know the true efficacy of CardioLux in these patients.

Dr. Weitz:                           Now, why did you pick those particular nutritional compounds?

Dr. Houston:                      It’s based on all the scientific trials that are in the literature. Plus, what we’ve done in patients over the years trying to figure out which works the best. And when you take each one of those, it improves HDL function. Each one of those also has other good effects on reducing oxidative stress, inflammation, and immune dysfunction and although they actually had an effect on raising total HDL and improving the HDL mapping and the HDL particle number.  So, the only missing piece was can we put all this together into one product and take the best of each and make the entire picture better but specifically concentrating HDL functionality.

Dr. Weitz:                           Yeah. The interesting thing is those particular compounds, we generally think of a lot of them more as antioxidants than as cardiovascular-related compounds.

Dr. Houston:                      Yeah. And that’s exactly correct because it may be that what we’re doing when we reduce oxidative stress and inflammation is we’re making the HDL compound which has all these proteins and lipids in it work better. So, the functionality actually gets improvement. And the other thing we’ve seen then is when HDL becomes dysfunctional, it’s not all or none.  And so, think of it… We’ll just pick a number. Let’s say you’ve got 100 different components in HDL, and let’s say 20 of them become damaged, but the other 80 work well. So, that HDL still functions but just not at 100% whereas you can go all the way down to zero, everything gets wiped out. And you have no function whatsoever.   So, the two tests that we use actually give you the ability to measure the functionality of HDL with a number. So, you can see where you are on the scale from that 100% great to zero which is terrible.

Dr. Weitz:                          So, a lot of this functionality has to do with the proteins, and it’s my understanding that basically the reason why you have these LDL HDL particles is because fats don’t move readily through the bloodstream because that’s more water soluble. So, we surround them with these protein structures. So, you have all these various proteins that are coating the lipids and the HDL. And one of these proteins is PON1, I understand, which is an important one.

Dr. Houston:                      Yeah. What you said is exactly right, Ben. You have to package the lipids into a water-soluble form which is apolipoprotein. And so, one of the proteins you mentioned is called PON, peroxidase, and peroxidase is incredibly important to make HDL function. And if it’s damaged, HDL does not work well. And what we found in all the different compounds we were looking at, most of these raised PON, which helps to improve the functionality.

Dr. Weitz:                           It’s kind of interesting how in the body, if you want to get something into the bloodstream that’s a fat, you have to make it water soluble. And then in a lot of other areas, we’re taking things that are water soluble and surrounding them with lipids, so we can get them into the cell membranes.

Dr. Houston:                      Right. Yeah. It’s a conundrum of how to get it into the blood. But also get sure into the cell.

Dr. Weitz:                          Right. Even a couple of the new vaccines for COVI actually take the RNA instructions and surround them with a lipophilic surrounding to get them into the cells.

Dr. Houston:                      Yeah. Exactly.

Dr. Weitz:                          And we do the same thing with glutathione and other ingredients that we’re trying to get incorporated into our cells.

Dr. Houston:                      Yeah. And actually, another compound that we use that everybody is familiar with is Coenzyme Q10. Well, the problem is it’s got to get into the mitochondria. So, it’s not only got to get into the cell, it’s got to get into the mitochondria to be affected. And a lot of the CoQ10s, they get in the serum fine. But they don’t even get into the cell. But if they get to the cell, they don’t penetrate the mitochondrial membrane.  So, there’s new forms of CoQ10 developed now, that get into the mitochondria in a concentration that’s like a thousand times greater than regular CoQ10. So we’ve able been able to reduce congestive heart failure, improve ejection fractions, reduce diastolic dysfunction using a very highly potent CoQ10 that gets into the mitochondria.

Dr. Weitz:                          Is that like the ubiquinol versus a ubiquinone?

Dr. Houston:                      No. It’s actually called MitoQ. MitoQ.

Dr. Weitz:                          Right, right, right.

Dr. Houston:                      It’s from New Zealand.

Dr. Weitz:                          I heard about that. I saw a study where it reversed… What was it? Like aortic stenosis or something like that.

Dr. Houston:                      Yeah. It’s amazing. Actually, I’ve got a series now of about 10 patients who were on the transplant list, a cardiac transplant list, and also a couple that were at end stage coronary heart disease. They couldn’t put stents in. They couldn’t do bypass. Every one of them that we put on CoQ10, has become asymptomatic with no chest pain for their coronary heart disease or their ejection fractions gone up significantly, and they’re off the transplant list. This stuff is a breakthrough, I think, in cardiology.

Dr. Weitz:                          Oh, interesting. Are you still using the combination of the CoQ10 and the ribose and the L-carnitine for the-

Dr. Houston:                      Yes, we still use the metabolic cardiology program. So, we use regular CoQ10 for the vasculature, CoQ10 MitoQ for the heart, and we use d-ribose, taurine, carnitine, magnesium and all these other wonderful supplements that improve the myocardial contractility and mitochondrial function.

Dr. Weitz:                          Interesting. So, what diet and lifestyle factors outside of these specific supplements?  What type of diet is beneficial for improving HDL functionality?

Dr. Houston:                      Well, you want to use a low refined carbohydrate intake. Sugar intake should be less than 25… excuse me 25 grams a day which is pretty strict, a lot of vegetables, at least probably eight servings of multi-colored vegetables per day. That’s got all your phytonutrients, high-quality protein that has no pesticides, organicized hormones in it.  So, you got to kind of go to wild game for that, and then a wide variety of berries particularly that are low glycemic index, blueberries, blackberry, strawberries, and always pomegranates.   So, pomegranate seeds, if you’re not prone to dysglycemia. You can use the juice. But any pomegranate whether it’s the seeds, the plant, or the juice has benefit in atherosclerosis and raising HDL in raising PON.

Dr. Weitz:                          Interesting. A pomegranate’s kind of an amazing compound seems to have a lot of efficacy and prostate issues as well.

Dr. Houston:                      Yeah, and it’s been shown to actually reverse carotid atherosclerosis in one year.

Dr. Weitz:                          Really?

Dr. Houston:                      Yeah.

Dr. Weitz:                          Wow. What’s your current protocol for patients who come in who have plaque who want to reverse it?

Dr. Houston:                      We have a very specific protocol. It’s called the Coronary Heart Disease Plaque Regression and Coronary Artery Calcium Regression Program. We’ve actually been able not only to stabilize plaque but actually to reverse it in patients. So, we use a whole host of things. It’s probably about 15 things we use. I’ll give you the name of some of them. We use Neo40 which is a nitric oxide booster. We use Arterosil which protects the glycocalyx, vitamins-

Dr. Weitz:                          Like a seaweed moss or something like that, sea moss.

Dr. Houston:                      Well, yeah. Sort of like that. It’s a glycocalyx with all kinds of glycoproteins in it. And you can get that from a company called Calroy. So, Arterosil. We use a vitamin K2 MK-7, omega-3 fatty acids.

Dr. Weitz:                          What’s the dosage of MK-7?

Dr. Houston:                      K2 MK-7 is a minimum of 360 micrograms minimum per day.

Dr. Weitz:                          So, how high might you go?

Dr. Houston:                      K2 MK-7 probably is very safe even up to 1000, 2000 micrograms. It’s really good for reducing coronary calcification and plaque formation.

Dr. Weitz:                          And unlike K1, there’s not a significant effect on blood thinning.

Dr. Houston:                      We’ve never seen any issues with Coumadin or warfarin with K2 MK-7. Now, if you got really high doses, it might. But at 360, there’s no issues like there is with K1 because that can interfere with the clotting. But it has no issues with the new antithrombotics, the factor X inhibitors like Eliquis. Those are not affected whatsoever by any form of vitamin K. So, they’re okay.   The other things we use are omega-3 fatty acids in high dose. We use one from biotics research called EFA-Sirt Supreme. Then, we have a compound called VasculoSirt which I developed about five years ago with Biotics, and it’s really good. It’s got 25 or 30 different compounds in it that improve endothelial function, reduce inflammation oxidative stress and so forth.   And then, we’ve got curcumin, use a very highly absorbable curcumin, quercetin, and then there’s a few other things you’re throwing. That’s the primary things that we use for plaque regression.

Dr. Weitz:                          Right. How does quercetin have activity in this regard?

Dr. Houston:                      Quercetin is an amazing nutraceutical. It has anti-inflammatory effects, antioxidant effects, anti-immune effects, and it’s the only compound I know that actually reduces SASPS. SASPS were like the garbage in the cells. If a cell gets sick, for example, it starts to die, and it makes saps. So, it’s senescence proteins.

Dr. Weitz:                          Oh okay.

Dr. Houston:                      Senescence proteins. And so, these senescent proteins leak out, and they kill all the cells around it. So, you start to get a fast aging process in the blood vessel or you get a fast aging process in general. So, quercetin reduces SASP formation. So, it actually can slow down vascular aging and aging in general.

Dr. Weitz:                          Interesting. interesting. So, you’re talking about cleaning out the garbage from cells.  Do you think intermittent fasting or fasting can play a role as well?

Dr. Houston:                      Absolutely.  Intermittent fasting of any type, we’ve used the prolonged trial.  We published it.  It’s going to be published pretty soon, we hope. But the initial data with fasting, in general, is you can slow down aging.  You can actually reduce some of the SASPS.  You can improve stem cell production, increase nitric oxide, and actually maybe even stabilize reverse type 2 diabetics.

Dr. Weitz:                            Really? Wow. Cool. And what about the benefits of exercise? Can exercise play a role in HDL functionality and then reversing cardiovascular disease?

Dr. Houston:                      Absolutely. HDL is generally improved in all the parameters we’ve talked about with resistance and aerobic exercise. In one of the books you mentioned, what your doctor may not tell you about heart disease, there’s two chapters in there on the best form of exercise that we developed with one of the great strength trainers, Charles Poliquin, who unfortunately died about a year ago with a heart attack. But Charles and I did some clinical trials.   And then, we wrote together an exercise program which is published in this book called ABCT, Aerobics, Build, Contour and Tone. And it’s combining aerobics and resistance training with interval training to get the best cardiovascular benefits, protection for coronary heart disease but also improve your lipid profile and your blood pressure.

Dr. Weitz:                          Interesting. What about hormones? I know some of the men that I’ve seen who had the lowest HDL levels were guys who were taking testosterone.

Dr. Houston:                      Yeah. That’s a really tricky topic. In my practice, I have really not done hormones. I’m not trained in hormones, and I’m really probably not qualified to even prescribe them and really talk intelligently about them, and then source in. So, I would just say this. When I review the data hormones and heart disease and hormones and lipids, it’s very confusing. It’s very controversial and you can kind of find whatever you want to out there to support your opinion. So, I’ll leave it at that and let the hormone specialist get into the intricacies of that topic.

Dr. Weitz:                          Yeah. Did you see that paper, that Felish Gersh published recently on the benefits of estrogen for reversing cardiovascular disease?

Dr. Houston:                      Yeah.  There’s a lot of good articles out there that you can read.  Absolutely.

Dr. Weitz:                          Yeah.  I mean you know it makes some sense since we know women have much lower rates of heart disease than men until menopause. So, it makes sense that estrogen has somewhat of a protective role.

Dr. Houston:                      Right.  Exactly.

Dr. Weitz:                          Cool.  And what about any of the medications for HDL?

Dr. Houston:                      None of them work. There’s a whole list of things out there. Probably niacin’s been sort of the primary nutraceutical that’s been looked at. And niacin actually does work. But it’s not really a medication per se. I mean, obviously, you can get it as a prescription. You consider it that way. But we don’t think [crosstalk 00:38:29]. Niacin improves total HDL, HDL particle number, HDL size, and HDL functionality. They’re one of the few supplement/drugs that does that.   Most of the other drugs that have been attempted really don’t work well. There was an older lipid drug that was used in the VA-HIT trial, and it raised HDL. But they didn’t even measure the functionality in that study. So, we don’t really know whether that change in HDL had anything to do with the outcomes.

Dr. Weitz:                          I mean when you look at all the benefits of niacin, it’s pretty amazing. It’s one of the few compounds that will increase LDL particle size. It’s one of the few compounds that can have measurable effect on Lp(a). It’s one of the few things that can improve HDL, and yet it’s not generally considered something that should be recommended by most cardiologists today.

Dr. Houston:                      Yeah, and that’s a shame, Ben, because it’s based on three clinical trials that came out that said that niacin didn’t work to reduce coronary heart disease and all these other things. But if you go back and look at all those studies as you’ve read them as I have. They’re flawed. They have an incredibly bad methodology. I mean you can take them apart literally, just massacre those trials if you really know about what they looked at.   And I’ve written several editorials with a lot of folks that that tear up the studies and say, “Look. Niacin is still a good supplement. It’s a good drug, [inaudible 00:40:13] you want to classify it.” You should use it. But you have to know how to use it. You’ve got to know what dose to give. You got to know what side effects it has, and what to monitor.   If you know how to do that, you can be a very wise clinician and use niacin to improve your lipidology and your coronary heart disease risk and a lot of other factors.

Dr. Weitz:                          Yeah. I think if you use niacin as part of the package rather than just rely on a super high dosage of niacin, you can avoid some of the blood sugar, liver stress that can occur.

Dr. Houston:                      Yeah. And you’re exactly. If you keep it in kind of a low dose and you use it as a combination agent, I mean I don’t usually go much over 500 milligrams of niacin in one day with one exception in Lp(a), that’s about the only time, and that’s about the only thing that really works. You’ve got to go to higher doses to get Lp(a)down. But for the other things we’ve talked about, 500 milligrams used with other compounds is very effective, and you don’t get the hyperhomocysteinemia, the hyperglycemia, the liver dysfunction, the itching, the pruritus, all that stuff is not very, very bad.

Dr. Weitz:                          Yeah. Lp(a) is a tough one. Anything new on the horizon for that?

Dr. Houston:                      Well, it’s interesting you should ask me that because our next clinical trial product development will be with Lp(a), and we’ll be working again with Metagenics on that one. [crosstalk 00:41:40] the HDL trial. I hope that we’ll be starting the Lp(a) study.

Dr. Weitz:                          Let me guess.

Dr. Houston:                      There is a drug being developed in fast track as you know that could be out within one to two years if everything goes well.

Dr. Weitz:                          Right. Then, all of a sudden, all the conventional MDs will want to measure Lp(a). But right now, you try to get it measured [inaudible 00:42:06] What are you doing that for? It’s a [crosstalk 00:42:07].

Dr. Houston:                      Once you get the drug for, people will start measuring kind of backwards thinking.

Dr. Weitz:                          Well, let me guess. Niacin, L-carnitine, let’s see, vitamin C, lysine.

Dr. Houston:                      But what we’ve got right now, we’ve got niacin [inaudible 00:42:29] aronia berry which is chokeberry. Yeah.  It doesn’t work all the time. It works pretty good. And you mentioned the others. There’s a Linus Pauling Protocol, vitamin C, lysine, proline, carnitine, CoQ… I mean there’s a lot of things that may work. The number consistent is the problem.

Dr. Weitz:                          All right. Okay. Cool. Okay. I think that’s the things I really wanted to talk about here. Any final thoughts you want to leave our listeners and viewers?

Dr. Houston:                      I think you’ve covered the topic incredibly well, Ben. You’ve asked all the pertinent questions, and I think that’s kind of the state of the art right now. Now, you and I both know it could change in a month. But at least after today, we’re up to date.

Dr. Weitz:                          So, are there any conferences that are going to occur this year or is that going to be-

Dr. Houston:                      Yeah. We’re getting back online. We’re going to probably have A4M in Las Vegas in December.

Dr. Weitz:                          Oh really?

Dr. Houston:                      I think that’s going to happen. They actually have something even in the fall if this pandemic ends. But I think the virtual meetings are going to phase out, and we’re finally get back to live ones pretty soon.

Dr. Weitz:                          By the way, I don’t say we’re going to wrap this up. But have you had any long COVID patients with cardiovascular issues, and do you have any insights on that?

Dr. Houston:                      I will give you my insight. I have had not very many patients in Tennessee. I live in Nashville. So, at least in my practice. I haven’t had a lot of patients who’ve had COVID. I’ve had a few. But just give me just a second. I think the reason I haven’t had a lot of people in my practice with it is because we had a lot of patients on high dose vitamin D plus a lot of nutraceuticals. They were healthy people in that respect.   And so, that was a protective thing. But the ones who did get COVID, none of them got very stick with it. Very few of them even ended up having more than like a seven-day period. They quarantined, but they stayed at home. Almost none of them ended up in the hospital. But I’ve had a few that have ended up in the hospital.

Dr. Weitz:                          Have you had any that had the long-term-

Dr. Houston:                      We’ve had a few people had had, I would say, more short-term stuff with shorts of breath. But I haven’t really seen any long-term in my practice like long-term effects with cardiac dysfunction or pulmonary dysfunction.

Dr. Weitz:                          Okay. Cool. What’s the best way to get a hold of you?

Dr. Houston:                      Oh, probably go to my website. We’ve got everything on there. It’s hypertensioninstitute.com. Our website’s very user-friendly. You can find our emails, phone numbers, all our protocols, books and so forth thrown there.

Dr. Weitz:                          And once again, the product from Metagenics for HDL is-

Dr. Houston:                      CardioLux, C-A-R-D-I-O-L-U-X, CardioLux.

Dr. Weitz:                          And that’s currently available.

Dr. Houston:                      Available through Metagenics presently.

Dr. Weitz:                          And the dosage that you recommend for that.

Dr. Houston:                      It’s two twice a day with food.

Dr. Weitz:                          Okay. Excellent thank you so much, Mark.

Dr. Houston:                      My pleasure, Ben.

Dr. Weitz:                            Well, thank you, listeners, for making it all the way through this episode of the Rational Wellness Podcast. Please, take a few minutes and go to Apple Podcast and give us a five star ratings and review. That would really help us, so, more people can find us in their listing of Health Podcast.  I’d also like to let everybody know that I now have a few openings for new clients for nutritional consultations. If you’re interested, please, call my office in Santa Monica at 310-395-3111. That’s 310-395-3111, and take one of the few openings we have now for a individual consultation for nutrition with Dr. Ben Weitz. Thank you and see you next week.

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Shivan Sarna discusses a personal perspective on SIBO with Dr. Ben Weitz.

[If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.]

Podcast Highlights

2:30  Shivan recalls having food poisoning when she was five and then again when she was eight.  She spent a lot of time in the bathroom growing up due to constipation and she was called “Buddha belly” due to abdominal bloating. Then after college she found herself working in a moldy building and she was getting really sick. She went to a Gastroenterologist who told her that she had IBS and prescribed an antidepressant.  Shivan did a SIBO breath test and she was told that the results were negative, but it was actually positive but someone had written positive and then crossed it out and wrote negative.  She finally saw another doctor she calls the digestion detective, who showed her that it was clearly a positive test result.  She became an ideal patient and she sought various treatments, including seeing Dr. Allison Siebecker and going for Ayurevedic, rolfing, steroid shots for firbromyalgia, acupuncture, etc. and she took notes and became knowledgeable about SIBO and IBS.  Then Shivan started the SIBO SOS Summit One and then did SIBO SOS Summit Two and the IBS and SIBO Summit. Shivan also did the documentary Digestion SOS: Rescue and Relief for IBS, SIBO, and Leaky Gut. She also did the Microbiome Rescue Summit and then her book, Healing SIBO: Fix the Real Cause of IBS, Bloating, and Weight Issues in 21 Days, came out.

8:40  Shivan has post-infectious IBS that she learned through taking Dr. Pimentel’s IBS Smart test, which is a blood test that measure antibodies to Cytolethal Distending Toxin and to Vinculin.  The concept that Dr. Pimentel discovered is that after a bout of food poisoning, the bacteria secrete an endotoxin called Cytolethal Distending Toxin. The immune system reacts and creates antibodies to the Cytolethal Distending Toxin and then these antibodies cross react with a structural protein in the intestinal wall called Vinculin, which then damages the motility of the digestive tract. This is the autoimmune component of IBS and SIBO, aka, post-infectious IBS.

11:12  Essentially the IBS Smart Test tells us that IBS is an autoimmune disease.  There is a new breath test from Gemelli Labs called the Trio Smart test that can diagnose SIBO and the type of SIBO based on which gas is found, whether it be hydrogen, hydrogen sulfide, or methane.  Treatments include pharmaceuticals, herbals, or the elemental diet. For hydrogen and hydrogen sulfide the preferred pharmaceutical would be rifaximin, while for methane rifaximin would be combined with Neomycin.  The advantage of rifaximin is that it acts locally in the small intestine and it is not systemic, so it will not devastate your microbiome, which can happen with broad spectrum antibiotics.

13:40  Shivan took rifaximin but had to do multiple two week rounds of it.  She kept relapsing because her migrating motor complex was not working properly, so a key for her recovery was to take a prokinetic drug.  Shivan described the migrating motor complex (MMC) as the sweeping motion of the small intestine, which is like the crumb clearing that occurs when the waiter at a restaurant clears your tablecloth. If you have scleroderma or diverticulitis or endometriosis, these can all inhibit the migrating motor complex.  The collagen condition, Ehlers-Danlos, also negatively affects the MMC.  If the MMC doesn’t clear out the small intestine, then bacteria can overgrow and then the bacteria eat fermentable carbohydrates and it becomes like a microbrewery. It causes bloating, and can lead to nutritional deficiencies, anemia, rosacea, and restless leg syndrome.

16:05  SIBO breath test preparation.  This test requires a 12 hour prep diet followed by a 12 hour fast.  For the diet, there are no veggies. You can have white rice, eggs, chicken without the skin, and black coffee. You don’t want to eat anything that will take a long time to digest and that can cause fermentation. Shivan also suggests for the 12 hour fast to sleep as much of that time as possible.  She suggests to do the test at home instead of at the doctor’s office. It is best to pre-label all of the tubes ahead of time and so you don’t mess it up, it is best not to plan to do anything else during those 3 hours.  It is also helpful to have two timers, like two phones or a timer and a clock.  But this test is important to find out what your levels are and what type of gas you have.

18:43  SIBO can cause brain fog, which Shivan suffered both from doing the breath test and from SIBO.  Dr. Satish Rao has done an interesting study about brain fog and gut issues. (S. Rao, A. Rehman, S. Yu, N.M. de Andino.  Brain fogginess, gas and bloating: a link between SIBO, probiotics and metabolic acidosis. Clinical and Translational Gastroenterology: June 2018 – Volume 9 – Issue 6 – p e162.)

19:52   Does taking probiotics help with SIBO?  Do probiotics, which are bacteria, contribute to the bacterial load in bacterial overgrowth and make the condition worse?  Some practitioners find that prescribing probiotics can be very helpful for patients with gut problems like SIBO/IBS, while other practitioner find that they often cause their patient’s symptoms to flare and get worse.

21:50   Quick Symptom Relief Strategies, which includes strategies for relieving bloating, pain, constipation, diarrhea, acid reflux, etc., including applying castor oil packs by getting good, organic castor oil and apply it to a piece of flannel or an old T-shirt and then place it over your stomach with a piece of parchment paper and a hot water bottle on top. It will stain your sheets and make your night clothes sticky, but it really helps with pain, inflammation, and motility.  It works best if you do it consistently for a while, like five nights in a row.  Activated charcoal can help with diarrhea, but you should take it apart from food and supplements.  There is a form of butyrate–tributyrate–that helps with diarrhea.  Iberogast is a good natural prokinetic, though it is hard to find.  For constipation, you want to drink a lot of water and magnesium can be really helpful.  Abdominal pain can be related to visceral hypersensitivity and curcumin can be helpful.  For abdominal bloating, Atrantil can be helpful, and it helps irradicate SIBO, esp. the methane form.  Peppermint oil and peppermint tea are helpful for pain. Gas-X and Pepto-Bismol can also help with pain.  Also IB Gard is a form of peppermint oil capsules that is sold in drugstores.

32:16  SIBO diet.  Shivan used the SIBO specific food guide developed by Dr. Allison Siebecker, which is her version of the low FODMAP diet. You want to eat in a manner that will reduce your fermentable load.  You have to understand that while diet can help to avoid feeding the bacteria and this can make you feel better, diet alone cannot cure SIBO.  To this day, even though she feels much better with her SIBO, she still cannot tolerate garlic or onions and she eats gluten free.  You can get green onions and just eat the green part, so it is like eating an onion without eating an onion.

37:30  Shivan used antimicrobial herbs, including oil of oregano, allicin in the form of Allimax or Allimed. She used CandiBactin-AR and BR from Metagenics. She also tried the Elemental diet and she tried both Integrative’s and Dr. Ruscio’s version of it. Shivan continues to take a prokinetic and she cannot really tolerate most of the natural ones because most of them contain ginger and she gets reflux from eating ginger. She takes Motegrity, which used to be called Resolor.  You also have to make sure to space your meals out so you have 4 or 5 hours between meals to stimulate your migrating motor complex to work.  Shivan also found it helpful to use the biofilm busting agent that was developed by Dr. Paul Anderson at Priority One.

Shivan Sarna, who was originally a patient, but Shivan has now become an expert at IBS and SIBO as a result of her experiences as a patient and due to her being the creator and the primary interviewer for the docuseries Digestion SOS: Rescue and Relief for IBS, SIBO, and Leaky Gut, as well as the SIBO SOS Summits. Shivan has now just published a book, Healing SIBO: Fix the Real Cause of IBS, Bloating, and Weight Issues in 21 Days.  

Dr. Ben Weitz is available for nutrition consultations specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111. Dr. Weitz is also available for video or phone consultations.

Podcast Transcript

Dr. Weitz:            Hey, this is Dr. Ben Weitz, host of the Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to the Rational Wellness Podcast for weekly updates. And to learn more, check out my website, drweitz.com. Thanks for joining me, and let’s jump into the podcast.  Hello, Rational Wellness Podcasters.

                            Today our topic is SIBO, small intestinal bacterial overgrowth, with Shivan Sarna. Now, we’ve certainly discussed SIBO quite a number of times. However, there’s always different perspectives, and today we’re going to get a little bit of a patient’s perspective, along with additional scientific information that she’s gleaned both from her own experiences, as well as being the primary interviewer and creator for the docuseries Digestion SOS: Rescue and Relief for IBS, SIBO, and Leaky Gut, as well as the SIBO SOS Summit.  And now Shivan has published a book, Healing SIBO. It’s a very readable, helpful book for anybody dealing with SIBO. And so, what is SIBO? SIBO is small intestinal bacterial overgrowth, and it is the most common cause of irritable bowel syndrome, IBS, which is the most common digestive disorder.  IBS is characterized by one or more of the following symptoms: abdominal pain, gas, bloating, diarrhea, constipation, sometimes alternating, nausea, and the urgent need to defecate, as well as a whole bunch of other symptoms. Sometimes skin issues, sometimes brain fog, et cetera. And so, Shivan Sarna, thank you so much for joining us today.

Shivan:                 Oh my gosh, thank you so much. I’m a long time listener and a huge fan. I appreciate it. I got to get the word out, man, so thank you for letting me talk about constipation, diarrhea, and bloating on your show.

Dr. Weitz:            Yeah. Hopefully, we won’t have constipation of the mouth. Maybe you can tell us about your personal journey with digestive disorders and SIBO.

Shivan:                 Before I tell my story, I always say I’m going to tell the story in a way that hopefully will help someone else. Not just like, “Ooh, what’s my story?” Because I usually … As an interviewer, I’m like, “Oh, is anyone going to listen to the story? What’s in it for you? I’m going to tell you.”  I had food poisoning when I was five. Then I had food poisoning when I was eight. Trip to India. Trip to a farm. And I was never the same afterwards. And the reason I know that, it’s not that I have these overly vivid memories of that time in my life, although I do remember the episodes. My father’s from India. My mom’s from Upstate New York.   And my dad, familiar with Ayurvedic basics, was like, “I don’t think Shivan’s going to the bathroom enough,” to my mom. And my mom made inquiries to me, the five-year-old. And that was the first time ever experienced shame. Like, “Really, am I doing something wrong? Get out of my beeswax. I’m five.”    But that was a big, like, “Is something wrong with me?” And they had a poster in the bathroom with this long quote on it and it’s the first thing I ever memorized, because I spent so much time in the bathroom. So, that’s the beginning. I grew up and we called it “Buddha belly,” with all respect to Buddha. And I’m skinny everywhere else, but I have this bloated belly, and-

Dr. Weitz:            So we’re going to talk about the spiritual aspect of SIBO.

Shivan:                 Oh, absolutely. Oh, honey. There is no doubt about it. It has taken me there. Lot of praying. Praying, expressing gratitude. It all blends together in my world.

Dr. Weitz:            There you go.

Shivan:                 So, I went to college and my girlfriends in the sorority house, they clearly didn’t have the same patterns that I had. I had been drawn into health food starting at age 15 with food combining, if you remember that. And just, I was different, which I’m used to. It’s fine, but there was something going on.  And then fast forward, I have this big career. I work in a moldy building that I didn’t know was moldy for 20 years, and I’m getting really, really sick. And people are asking me if I’m pregnant on Facebook, which I am not.  And that’s devastating for somebody who’s supposed to be an aspirational TV host. But I’m also really not feeling well. So, I finally go to a gastroenterologist, and the gastroenterologist is like, “Well, you probably have IBS. Run three miles. Here’s an antidepressant.”   And I thought, “Are you trying to tell me it’s all in my head? And I don’t have the energy to run a block, much less three miles.” So, I had this other girlfriend at work, and she was another weirdo, because we were gluten free, and we were weird. Fine. That’s fine.  And she told me … I saw her randomly and she’s like, “Oh my gosh. I’m doing this really crazy antibiotic, and I had to do this test where I breathe into this test tube. Got to go. Talk to you later. Bye.” And I was like, “What? Wait a minute.”   So, I got the information. She was not … She was wonderful, but did not know what the heck she was talking about. She was just doing what her doctor said. I did a SIBO breath test. Same thing, didn’t know what I was talking about. I was just like, “Whatever. Maybe it’ll help me. I don’t know. I’m desperate.”   And I got the wrong information, in that someone said it was negative, when actually, it was positive, and I lost 18 months. And when you’re chronically uncomfortable and you’re trying to figure out your diagnoses, you’re like, “Oh, don’t have that. Great.”   I begged for a colonoscopy on the last appointment before Christmas break. They were closing the outpatient clinic down, basically, as I was recovering. “Oh. No, I don’t have cancer.” Which is great, thank you. But, “Oh, don’t have cancer. What is it? What is it? What is it?”  So, it was difficult because I actually did have SIBO, but for 18 months of intense questing, didn’t know that was it. Finally went to a doctor who I call “the digestive detective,” and he’s like, “I want to see the results. I want to see that graph.”

Dr. Weitz:            Yeah, there’s a lot of differences in interpretation.

Shivan:                 Well, there it was. Someone had written “positive,” crossed it out, and wrote “negative.” And when you look at the graph, if you’re even mildly familiar with this, it’s so blazingly obvious that it was a positive result. So, that made me really mad and sad.   And my husband was getting his CPA as a grown-up, and so he was studying a lot. And I became, for the first time since the ’80s, someone who had a little bit of time on her hands. So I sat there in front of my computer and did Dr. Google, and took all my notes, and the typical chronic condition patient journey.  And I would go to all my doctor’s appointment. Ayurvedic, Rolfing, steroid shots for fibromyalgia, acupuncture, you name it. And every time I’d sit down, I’m like, “Here are all my notes.” I was super like, nerd patient. And they’d look at me and they’d be like, “You know, you really need to write a book.”   My spiritual teacher: “You know, you really need to write a book.” So I’m sitting there and I’m like, “Listen, God. I really need to tell the world about what I’m discovering, and if I figure it out, I will tell the world.”   What happened was, I was trying to write the book. It’s not that easy. I’m a TV person. I can definitely do an online summit. I can do video. I can do interviews. So, I started with the SIBO SOS Summit One, which Dr. Allison Siebecker was so pivotal in, because she introduced me to all of her colleagues.   And then, I did SIBO SOS Summit Two. I did the IBS and SIBO SOS Summit. I did the documentary you referred to, Digestion SOS: Rescue and Relief for IBS, SIBO, and Leaky Gut. Looks better on paper than mouthed. And then I’ve done the Microbiome Rescue Summit, and then the book came out, because I took everything I learned from these summits as well, and put it into the book.    So, that’s how I got here. I do have post-infectious IBS. I learned that from Dr. Pimentel’s blood test, which I know your listeners … Go back and listen to Dr. Mark Pimentel’s session, if you haven’t listened to it. So I know I have the antibodies, which we’ll explain, and therefore I’m very religious with the prokinetic, which we’ll also explain. And so, another message is, if you have a chronic condition that goes untreated, you can feel horrible. If you have a chronic condition that is treated, you can feel 100% better. And that’s what I do.

Dr. Weitz:            Right. So, for those listening who don’t understand about the autoimmune component, how you could take a blood test and tell you that you have SIBO, is that Dr. Pimentel discovered that one of the most common causes of SIBO is that somebody gets food poisoning, and the bacteria that causes the food poisoning causes an immune reaction.  And the immune system reacts against a toxin that that bacteria secretes, called “cytolethal distending toxin,” and then those antibodies, again, cytolethal distending toxin, then also react against a structural protein in the intestinal wall called “vinculin.”  And so, there’s a blood test that Dr. Pimentel developed, that measures antibodies to cytolethal distending toxin and vinculin. And so, when this test is positive, it shows … and then what happens as a result of the immune system, the antibodies attacking the vinculin, it affects the migrating motor complex and the motility of the small intestine, and that allows the bacteria to build up. And so, this blood test will tell you that you have these antibodies, and that’s how your SIBO developed.

Shivan:                 So, officially, if you have post-infectious IBS, like if you talk to the guys at the lab, they will not say that it’s a SIBO test, right?  Because the SIBO breath test, which Gemelli Labs, also from Dr. Pimentel, does. But it tells you have post-infectious IBS, which is SIBO, which is … but it’s not a SIBO, officially, according to all the medical people. It’s not.

Dr. Weitz:            Right. [crosstalk 00:11:07]

Shivan:                 Yeah. But I’m really glad I did it, because now I know my underlying cause.

Dr. Weitz:            Yeah. And one of the most fascinating things about that test is, it tells us that IBS, which is the most common digestive condition, is actually an autoimmune condition. So, how should patients think, who have IBS and they go to a conventional gastrointestinal doctor, and they’re told to just take some drug to treat the symptoms, like you were told to take a antidepressant?  Or maybe they have diarrhea and they’re given a drug to control the diarrhea, or maybe they even got diagnosed with SIBO and were given two weeks of an antibiotic known as rifaximin, and then they’re still not better? What should SIBO patients think about that situation?

Shivan:                 Well, first of all, there is a breath test for SIBO that you can take, that will tell you what kind of SIBO you have. Do you have hydrogen-dominant? Do you have methane-dominant? “IMO” for short. Or do you have hydrogen sulfide? And that’s called “Trio Smart” from Gemelli Labs, and also Aerodiagnostics does a beautiful job with breath testing.   So, you find out what your levels are, right? And what kind of gas you have: hydrogen, hydrogen sulfide, or methane. Then that will dictate the treatment, and there are three major treatments. One is pharmaceuticals. One is herbals, and one is the elemental diet. And that rifaximin that you were just talking about is the antibiotic that Dr. Pimentel discovered works in the small intestine, stays in the small intestine.  It’s actually the one given for traveler’s diarrhea. So, since e. Coli is the cause of much of the SIBO out there, that makes sense. And then if you have the methane-dominant, it’s combined with Neomycin, and then if you want to do … and there’s some other variations, but those are the main ones.   And you need to realize that, after you do that round, it’s not like normal antibiotics, where like, “I was sick. I took the antibiotic. I’m well.” You may have to do multiple rounds, but the studies show that to rifaximin, the resistance … I would say the clinical experience, at the very least, the resistance is not like with other antibiotics. It also stays in the small intestine, so it’s not like a nuclear bomb goes off in your microbiome, whereas Neomycin, it is bigger.

Dr. Weitz:            You took rifaximin, right?

Shivan:                 Oh, yeah. Oh, yeah. I’ve done it all.

Dr. Weitz:            What was your experience with it?

Shivan:                 Well, so to your point, I was not told that I would have to do multiple rounds. So I took it and wasn’t better, and I was like, “What the hey?” Like, “Wait a minute. This isn’t normal.” So I took it and then re-tested, and saw that it helped, so then I did a couple multiple rounds.  This whole time, though, I was not told to do a prokinetic.  So, I was relapsing because I wasn’t still moving my migrating motor complex.  So, in a prokinetic-

Dr. Weitz:            Maybe you can explain what the migrating motor complex is?

Shivan:                Yeah. Sure. You know… 

Dr. Weitz:            I know, I know.

Shivan:                 You [crosstalk 00:14:22]. The migrating motor complex is that sweeping motion of the small intestine. They call it the “crumb-clearing” … like, think of a waiter in a white tablecloth restaurant who comes around with that little crumb clearer. Fancy, fancy. That’s not my analogy, but I do love that one.  And it sweeps out the debris from the small intestine, and if you have adhesions, if you have scleroderma, if you have endometriosis, diverticulitis, those all can impact the migrating motor complex, along with the antibodies that you were just talking about.  And if it’s adhesions or endometriosis, it’s because literally, it can be pulling the small intestine out of a particular place in the body. Ehlers-Danlos, the collagen condition as well. So, your migrating motor complex actually might work from a mechanical, chemical perspective. But the physicality of the placement of the intestines could be inhibiting that motion.

                                Or if you’re like me and you have post-infectious IBS, then you have that mechanical chemical thing going on. So, when you don’t sweep the debris out, the food in the small intestine can overgrow, thus small intestinal bacterial overgrowth, because … not the food. The bacteria eats the food in the small intestine, and that is what overgrows, and become like a micro brewery.   And it ferments your food, all that bacteria overgrowing, and that’s why the bloating comes, and it can rob you of your nutrition. It can lead to imbalances of anemia, rosacea, restless leg syndrome. I’ve spoken to some of these doctors and they theorize, some of them, that it may even impact fertility, which I found fascinating.

Dr. Weitz:            Interesting. So, do you have any suggestions, you mentioned a breath test, for patients who are getting ready to take the SIBO breath test, from a patient’s perspectives?

Shivan:                 Yeah. No, I’m a vegetarian, so it’s even more intense because you have to do a 12-hour prep diet, followed by a 12-hour fast. And so, they suggest that, for the 12-hour fast, you sleep-

Dr. Weitz:            You don’t have any vegetables?

Shivan:                 Oh. Well, during the diet, it’s no veggies … Well, it’s rice. You could do white rice. You can do eggs. You can do chicken without the skin. You can do black coffee. It’s super, super limited. And the reason is, is because they’re trying to get you to not ferment your food.   And even though rice is a carbohydrate, it stays higher up in the intestine and gets digested fairly quickly, so it doesn’t really get a chance to ferment in the low intestine. So, I suggest doing the prep diet, being very strict on it.

                                Then I suggest sleeping for as long as possible the next day for that 12 hours. I’m not saying sleep for 12 hours, but if you can sleep for eight hours, then you only have a four-hour window until it’s time to take the breath test.   And you could take it in the office of a doctor who gives them, but you can also do it at home. And I prefer that, because I can … especially now, do it at home. But I tend to not do well with lactulose, which is the sugar that you drink prior to breathing into the test tubes. The body doesn’t digest it, but the bacteria love it.   And then, you breathe into these test tubes every 20 minutes for two or three hours. It depends on whichever test you’re doing, by the manufacturer and the lab. But I tend to get a lot of brain fog when I drink lactulose, so I have messed the test up, simply by going, “Did I just breathe into this test tube? Is this test tube eight or is this test tube nine?”   So, pre-label everything. Have two timers, like two phones or a timer and a clock, and try not to get too distracted, because keeping track after a while … and it looks … not nothing, but it looks like, “Oh, I can handle this.”    Now, Dr. Siebecker will run an errand, go to the grocery store and do a SIBO breath test no problem. I’m like, “Okay. I’m locked and loaded. For the next three hours, no one bother me.” So, everybody’s different. But it is a little bit of a project but it’s totally worth it to find out what your levels are and what type of gas you have.

Dr. Weitz:            Right. And so, you have some issues with brain fog from lactulose. Do you get that from your SIBO as well?

Shivan:                 I do. I did have really bad brain fog from … I do believe it was my SIBO, combined with my mold. At one point, I couldn’t … It was one day, I should say. I mean, it’s been fluctuating, but the worst brain fog I ever had was, I couldn’t speak. And that was extremely scary since I talk for a living.   And it was on a weekend, so I was able to actually recover. But I couldn’t speak. And it’s fine to lose a word every now and then, but I literally could not find a couple of words. Not to mention the mechanical, putting my lips together and breathing, speaking. It was bad. It was bad.  So, that was the worst case scenario. But brain fog is real. And Dr. Satish Rao has done a very interesting study about brain fog and these gut issues, which was not without controversy, but I think was quite compelling.

Dr. Weitz:            Are taking probiotics good or bad for SIBOs? Some practitioners say if you take any bacteria, it’ll only add to the bacteria you’re trying to eliminate. There are some practitioners, like Dr. Ruscio, who feels that probiotics, after you institute a diet, should be your first intervention, and that alone can take care of the SIBO. What do you think about probiotics and SIBO?

Shivan:                 So, I’m definitely a big fan of Dr. Ruscio’s, and I’ve heard his … I’ve interviewed him about this topic, about the rotation and the different types of probiotics. I think it’s fantastic. I mean, if you’re sitting there going, “I’ve tried everything.” First of all, Dr. Siebecker always says, “Have you really tried everything?”    But anyway, if you feel like you’ve tried everything, I would definitely read Dr. Ruscio’s book and go to his website for his blog posts about it, about the rotation of these three types of probiotics, to see if it helps. He has incredible clinical results with it.   Classically, people are very split down the middle. Why would you take a probiotic and add more bacteria when you already have an overgrowth of bacteria? But if you sit and think about it, is that bacteria making it to the small intestine from the probiotic? Is that probiotic full of a gatekeeper-style probiotic that will actually help to balance the diversity, and actually help to get rid of the bad guys in an overgrowth?  So, I think it’s very personal as the microbiome is, and I think if you feel like you’ve tried everything, it’s worth a try. But so, I don’t have an answer for you that’s clear-cut and like, “Yes, this always works,” because it doesn’t. It’s very personal. I know people that it has been like a miracle for, and I know people that it’s been really uncomfortable for.

Dr. Weitz:            You have a chapter in your book on quick symptom relief strategies, and I thought some of those were really interesting. Maybe you can talk about some of these quick symptom relief strategies for … You have ones for bloating, pain, constipation, diarrhea, acid reflux.

Shivan:                 So, remember, I’m the patient, right? And I’ve interviewed all these experts, and so this is based on Dr. Allison Siebecker’s symptomatic relief guide. And-

Dr. Weitz:            Right. Now, one of them that you talked about was applying castor oil, and you put that directly over your stomach. Tell me about that.

Shivan:                 Love it. Love it.

Dr. Weitz:            Okay, so how do you do it, exactly?

Shivan:                 Okay, so there are a couple of techniques. So, you get the organic, good castor oil that’s in a dark glass bottle, and you take a … This is an old school naturopathic technique, right? You take a piece of flannel. I know some people who only do organic flannel, whatever. I have seen people use a T-shirt before.  This is before you go to bed, right? And you put the castor oil on, and you put the flannel on. Maybe you put a piece of parchment or wax paper on, and then you put a hot water bottle. Some people put heating pads. They’re going, “Oh, the EMFs,” whatever. So you have to decide.  But then you just keep it on for as long as possible. It will stain your sheets. It will make your night clothes sticky, so I put on a … To be very personal, I take my husband’s boxer briefs. I wear them that night, and I take an old T-shirt of his, and I put it on underneath and kind of tuck it in and around, and it works great. This is not something to wear with your pretty nighties.  And basically, the castor oil, which is, in my opinion, not a great idea to consume, it’s an old school, very, very strong laxative. There are so many other options.

Dr. Weitz:            Yeah. Remember, castor beans are where the poison ricin comes from.

Shivan:                 Exactly. Let’s not go crazy here, people. There are too many other options. But it reduces inflammation. It helps with motility. It helps balance things. So I know people with diarrhea that have done really well with them. I know people with constipation. Just even the bloating. It’s very soothing.  I also … I have a Facebook group with 18,000 people in it. So when I’m talking about, “I’ve seen people do this and I’ve seen people do that,” the SIBO SOS Facebook community is what I’m referring to. Not to mention all the emails I get.   But I’ve heard people say like, “I tried it for two nights and didn’t notice it.” Give it like five nights in a row, and I mean, chances are you’re really going to notice something good. It’s pretty magic from that perspective. So, that’s very soothing. Very, very soothing. And I think we need to be soothed. I think we need to be comforted.

Dr. Weitz:            Yeah. What are some of the other relief strategies?

Shivan:                 Some of the other relief strategies include, if you have diarrhea, activated charcoal which is sold everywhere. If you feel like you ate something that was, “Did I just get food poisoning?” That’s really handy, and it does tend to constipate, so Dr. Siebecker suggests that you take it with magnesium if you’re worried about that. Although it does also absorb nutrients, so maybe wait a little bit, then take the magnesium. You don’t want to take it with food.  We see charcoal showing up as an odor remover, as a teeth whitener, which I don’t suggest. I’m doing a dental summit, so I know, don’t do that. I mean, it can be totally life-changing for people. So charcoal if you have diarrhea. I also just talked to Steve Wright, I don’t know if you know him, from SCD Lifestyles?

Dr. Weitz:            Oh, I’ve heard him. I’ve never met him. Yup.

Shivan:                 Lovely guy. Really smart guy. And he just talked to me about Tributyrin-X, basically tributyrate, for diarrhea, and that works like a champ as well, so I thought that was really interesting, that particular-

Dr. Weitz:            Tributyrate? Is that similar to butyrate?

Shivan:                 Yes. Yes, but they’re different forms of butyrate, so this is the tri. But yeah. He’s had great success with that. Some of the other things are Iberogast, which is hard to find with American English writing on the box. You can get it on Amazon, and it looks like it might be an Eastern European language. I don’t know if it’s Russian or what.  But that is a natural prokinetic, and interestingly enough, will help people if they’re nauseous, help people if you have diarrhea, constipation. It’s really interesting. It is not to be taken if you are on opioids, so that’s just a little disclaimer.  But that’s been also pretty miraculous for a lot of people, and you can play with how many drops that you take. I personally don’t like the taste of it. I’m a super taster, so I was doing our course, the SIBO Recovery Road Map with Dr. Siebecker, that we created together. And we were taping that day and I was like … I’d just come back from work. I’d just been in the mold. I didn’t really feel well.  And we had all these products out in front of us, and I’m like … She’s talking to me about Iberogast and I’m like, “You know I hate the taste.” She’s like, “Yeah, but you don’t feel well to begin with.” I’m like, “I know. It’s terrible. I feel terrible.” So, we caught me on tape taking it, and then how I reacted within an hour, and it did the trick. It really did the trick, so that’s my personal testimonial for that.

Dr. Weitz:            What about for constipation?

Shivan:                 So, that does work for constipation too, but certainly, making sure you’re drinking enough water. I’m not going to say, “Do fiber,” because if you have SIBO, the bacteria feeds on fibers. So that’s why, in my book, it’s a vegetarian set of recipes, because you can always add any kind of protein you want.  But when you are doing recipes and eating for SIBO, it’s hard if you want vegetables. Of course, we all want veggies. And so, if you are constipated, I’m not going to say, “Do fiber.” I am going to say that Dr. Siebecker talks about … Let’s see. I’m going to try to remember here.

Dr. Weitz:            Well, magnesium, of course.

Shivan:                 Oh my gosh. Magnesium, of course. Magnesium is her go-to. Most people, she says, don’t do enough. Right? So we think, “Gosh, I’m doing 600 milligrams. That seems like a lot.” And for somebody, it is. But maybe for you, it’s not. So, she likes the Vitamin Shoppe’s magnesium. I like it, but my husband has it around the house, so I usually just take that, but magnesium is like magic for a lot of people with constipation.

Dr. Weitz:            And what about any other hints for pain? You had a couple of interesting ones in there.

Shivan:                 For pain, it’s definitely something that … So, I just want to talk about pain for a second, from the perspective of people with IBS. You may have visceral hypersensitivity. And visceral hypersensitivity is pretty much what it sounds: visceral, the belly/abdominal area, and hypersensitivity. What hurts you might not hurt somebody else.  It could feel over the top for you. Like, “Oh my gosh, I feel like I’ve got a knife in my belly.” Other people could eat the same thing or have the same experience and they’re like, “Oh, I’m fine. It’s no big deal.” So, in your practice, how do you handle visceral hypersensitivity?

Dr. Weitz:            Curcumin is an interesting nutrient that’s been shown to be beneficial.

Shivan:                Oh, we love. Love. Okay, do you do the pepper or no pepper?

Dr. Weitz:            No pepper. I don’t like the pepper.

Shivan:                I don’t like the pepper either!

Dr. Weitz:            Patients hate it, especially if you want to do a high dosage. The pepper’ll just irritate their gut, so we use the one blended with phosphatidylcholine, the Meriva form.

Shivan:                Oh, yeah. Nice. Nice.

Dr. Weitz:            Yeah.

Shivan:                So just real quick, this is the section on the symptoms, like you were talking about. There’s a section on bloating. Oh, Atrantil, I have to give a shout-out to. If you have methane-dominant, methanogen overgrowth, Atrantil is worth looking at.

Dr. Weitz:            Yeah, we use that. Dr. Ken Brown, yeah.

Shivan:                He’s awesome. Awesome. So, peppermint oil and peppermint tea is also great for pain. It helps things move, but not in a laxative way. Also, some of the pain, I think is … depends, obviously, but from gas. And Gas-X helps to break the big gas bubbles into smaller bubbles, so it doesn’t feel as much pressure.  And also, Pepto-Bismol is around for a reason, for a really long time. There is a brand from Target. I can’t remember the name of it right now. I think it’s in here, but it’s the in-house brand of Target. They have the safest for SIBO-

Dr. Weitz:            We just can’t do that. I just can’t … Artificial sweeteners and artificial colors, and …

Shivan:                Yeah. Oh, the color. Oh, yeah. The nature pink. What? I’m not saying it’s natural. I’m not saying it’s natural.

Dr. Weitz:            I know, I know.

Shivan:                I’m saying, in desperate times, sometimes, desperate measures.  This is full of natural [crosstalk 00:31:35]

Dr. Weitz:            I notice in your book, you talked about, if they’re having abdominal pain, that if they use … If the pain is in the upper part of the abdominal cavity, that peppermint tea might be better, whereas if it’s lower down, enteric coated peppermint capsules might be better.

Shivan:                Because of the enteric coating, it’s going to make it further down.

Dr. Weitz:            Right. Yup, yup.

Shivan:                The IB Gard, I think is what it’s called. And that’s been studied, and you can get it at all your local drugstores, so that’s a Godsend too. And it’s something like … It’s not going to hurt. It might help, right? So, very low risk. Very low risk.

Dr. Weitz:            So, let’s go to diet. Which version of the SIBO … There’s multiple SIBO diets out there. The one that’s talked about today the most is the low FODMAP diet. And you mentioned the specific carbohydrate diet. There’s one diet where you actually count up the points for the amount of fermentability.

Shivan:                Fast tract diet, Dr. Norm Robillard. Yeah.

Dr. Weitz:            Exactly, so there’s that one, and then there’s Nirala Jacobi’s got her version in phases, and …

Shivan:                Bi-phasic diet, which is based on …

Dr. Weitz:            Bi-phasic diet.

Shivan:                Which is based on Dr. Allison Siebecker’s SIBO specific food guide, which is kind of all of them combined.

Dr. Weitz:            Right. And Pimentel likes the Cedars-Sinai white bread, white rice diet, of low fiber diet.

Shivan:                Diet Coke.

Dr. Weitz:            And then, Allison Siebecker has her version of it. So, what did you find best for you?

Shivan:                For me, I did the SIBO specific food guide, and that’s in the book. Allison very graciously let me use her work in the book, and it’s based on all of those things combined, to way oversimplify it. And it’s very portion-specific, so you have to be careful not to get too focused on the portions, or I think we can go a little bit overboard.  And also, on the one hand, it’s careful. Like, “Oh, I can only have this many grams of this, or half a cup of this.” And then we get really, really uptight about it. On the other hand, this is what happened to me in the beginning. Like, “Oh my gosh, I can eat zucchini.” And I would eat five zucchinis in a day.  That’s the other end of the spectrum, so you have to be aware of those portions. But you’re trying to reduce your fermentable load, so that the bacteria doesn’t go crazy on these carbohydrates that are more easily fermented than others.    So, this is so important. The diet does not cure SIBO. The diet controls the symptoms. That’s really important. There is a lot of mythology around that the diet is going to cure SIBO, and it doesn’t. It will make you feel better. It definitely controls the symptoms.    You could feel better in a couple of days by fixing your diet, by being on the SIBO specific food guide, or some of these other carefully calibrated, low fermentation carbohydrate diets. So, that is a huge point in the book. But also, I have 40 recipes, vegetarian. Again, if you’re a vegetarian, it’s much harder if you have SIBO. And so, I wasn’t going to make it like, for the easiest common denominator. I was going to make it for the most difficult common denominator. And then you can always add whatever protein you want.

Dr. Weitz:            So, how long do you have to stay on this kind of diet? And do you still have restrictions in your diet?

Shivan:                So, do not give me garlic. It’s not going to work. It’s not happening. I stopped liking it. It doesn’t work for me. It makes me sick. I hate it. I love the smell and I’ll put it in some garlic-infused oil. That’s fine, and it’s occasional.   So, how long should you be on the diet? So ideally, you’re on the diet while you’re trying to get your treatment under control. This is not a long-term fix, because the biodiversity of the microbiome will be impacted. It’s not going to be devastated.  If you’re doing it for eight weeks, you can rebuild it. Your microbiome is changing all the time. Ideally, you’re trying to do, even within these foods … In the back of the book, there’s this chart. There’s a lot of diverse foods in there. It’s not like you’re eating three foods. You can do bok choy and all kinds of fruits and vegetables and cabbage and green beans.  I mean, it’s not like you’re going hungry, and it’s not like you couldn’t even really, maybe eat some foods you didn’t usually eat to diversify your microbiome. But it shouldn’t be forever. I know people who’ve been on it for five years. That’s too long. It’s really too long. You need to diversify.

Dr. Weitz:            So, other than garlic, where are you in terms of food restriction?

Shivan:                 I’m, by choice, gluten free. I don’t do onions. Really, it’s onions and garlics. I used to not be able to do apples, which are notoriously high in FODMAPs, and something I literally said to myself, “I’ll eat an apple. It’s good for me. It’ll keep the doctor away, right?” And then was like, more bloated. This was way back. So, I can eat almost anything now. I just don’t do garlic and onions. That’s me. Everybody’s different.

Dr. Weitz:            I noticed in one of your recipes, you were talking about taking a green onion and just not eating the white part. So, it’s kind of a way of sort of getting an onion without getting an onion.

Shivan:                 Exactly. So, the green part of scallions is-

Dr. Weitz:            “How to get an onion without getting an onion.”

Shivan:                 Yeah, that’s the way to do it. That’s the way to do it.

Dr. Weitz:            So, let’s see. What else do we want to talk about? Did you do antimicrobial herbs? And which ones did you find helpful for you?

Shivan:                 So, I did the pharmaceuticals. Then I did the antimicrobial herbs. I did oil of oregano. I did the allicin, like Allimed, or Allimax. And Allimed is stronger, even though “Allimax” makes it seem like it’s stronger. And I also … This was on a rotational basis. I did CandiBactin-AR and BR, which is what was studied compared to the rifaximin, and was found to be a little bit more effective, but you have to do it for a month versus two weeks.  I’ve pretty much done it all. I’ve done the elemental diet as well, and that was okay for me. I didn’t last the whole time, which is supposed to be anywhere between 14 and 17 days. My lifestyle at the time … You have to really be prepared mentally, because it’s only liquid diet for that time, and-

Dr. Weitz:            Really hard.

Shivan:                 It is hard, and a lot of people say, “Oh, I wish I had this to begin with,” because it’s so effective. It is the most effective treatment, but it is hard. And I couldn’t take 17 days off to do it. And if you do the high performance job that I have, of doing live television, you can’t mess around. You have to feel good when you go out there. There is no messing around.  So, I played with it. I also have used it as a meal replacement on occasion, and it’s a great gut reset. This is a diet that is originally a liquid diet that was for feeding tubes, and it’s made up of amino acids that are quickly absorbed into your body, almost like instantly digested, and it feeds you but it doesn’t feed the bacteria, so you’re starving the bacteria instead of killing it through a killing agent like an antibiotic.  They used to taste disgusting. Disgusting. And people, speaking of desperate times, were so desperate to change the flavor that it became sort of famous that people put Crystal Lite to fix the flavor, and it still didn’t fix it.  But Dr. Ruscio and Integrative Therapeutics, they’ve made a much, much better-tasting set of elemental diets that you can pick from, like chocolate and vanilla, and they taste like really sweet milkshakes, like really sweet. But I mean, it’s so much better by comparison.

Dr. Weitz:            I think that’s Ruscio’s version, not Integrative’s. Theirs is just one flavor.

Shivan:                Yeah, it’s vanilla. Right. He’s got more variety. I like his taste better, but maybe you’ll like the Integrative Therapeutics better. Who knows? But you have to make you’re doing enough calories so you don’t lose weight.

Dr. Weitz:            Right. Prokinetics. Do you continue to use a prokinetic? Is it a natural one or a prescription one? Have you tried the natural ones?

Shivan:                I can’t do ginger, because I tend to have a little reflux with my lower esophageal sphincter, so I get the ginger burn. Or you get it once and you never even want to try it again. But other people love ginger. It is a natural prokinetic which is what we talked about earlier, of moving the migrating motor complex so that it sweeps the bacteria out of the small intestine so it doesn’t overgrow.  It’s what helps prevent relapse. There are prescriptions that are … like Motegrity, which was called “Resolor,” which was usually only available in Canada, and now it is available in the States. There’s MotilPro, which is also natural. It has a lot of ginger in it.  There’s one called … It used to be called “Zelnorm,” and it was taken off the market, and it’s back on the market. And I cannot remember the name of it to save my life right now.

Dr. Weitz:            I think it’s called “Prucalopride.” No?

Shivan:                Yup. Well, Prucalopride is the Resolor, which is now Motegrity.

Dr. Weitz:            Oh, okay. Okay.

Shivan:                Tegaserod. I think it’s called “tegaserod,” or something similar to that. That is another prokinetic. You could literally type in “Zelnorm” and you’ll find the new name for the prokinetic. These are IBS medications sometimes.

Dr. Weitz:            Right. So, do you continue to take a prokinetic?

Shivan:                I do. Oh, yeah. I definitely do.

Dr. Weitz:            Which one do you take?

Shivan:                I still have those antibodies, so I definitely still take it, and that’s-

Dr. Weitz:            Which one do you take?

Shivan:                I take Motegrity, which was Resolor in Canada.

Dr. Weitz:            Okay.

Shivan:                Love the stuff. Love it. I never thought I’d say that about a prescription medication, but I’m like, “I love it.” Does the trick. And it doesn’t necessarily cause a laxative type reaction, so prokinetics are not laxatives. You may have a laxative experience, but it’s not the goal. The goal is to keep the migrating motor complex going.

Dr. Weitz:            Right. So, you have the motility that occurs when you’re eating, that pushes the food down, and then you have these cleansing waves that happen in between eating when you haven’t eaten for three or four hours, and that’s what you’re really trying to stimulate.

Shivan:                Yeah, and I’m glad you just said that. Meal spacing is super important. You want to not eat small meals throughout the day, unless your doctor’s advised that because of your blood sugar scenario. But to get the migrating motor complex moving, you need to not consume calories for about four to five hours, because the migrating motor complex will not work when you have that full mode of the body and calories indicate that, so you need to have, like … A lot of people take their prokinetic at night. I do, because you’re not taking calories in at night.

Dr. Weitz:            Right. You mentioned biofilms, and that being an issue with trying to get rid of the bacteria. Did you find anything that was effective in breaking up biofilms on your journey?

Shivan:                So, I’ve had the pleasure of interviewing Dr. Paul Anderson multiple times, and his combination, he’s got a formula at Priority One, and then he has a prescription biofilm buster. That has proven to be really helpful for me, and if anybody doesn’t know what a bio-

Dr. Weitz:            Do you use the Priority One one, or the prescription one?

Shivan:                I’ve used them both. I’ve used them both. They were both great for me. If people have long-term SIBO and they have not been able to reduce the bacterial load, I do suggest reading up on how a biofilm buster can help you, because maybe that biofilm is keeping that bacteria overgrown in a lockdown position … not to be medical, because that’s not a medical term, but in a state where it isn’t breaking up and releasing, so it’s not behaving as it normally would, if a biofilm wasn’t there.   And we have biofilms everywhere, right? The skin, the mouth, the genital area. Yeah, the intestines. So, it’s like … I call it “mucus” in my head. I just think of that as a biofilm, and it keeps pathogens trapped in it, and it’s very elaborate in the way that it likes to survive. It’s quite interesting.

Dr. Weitz:            Right. Yeah, I think we’re all aware of the fact that bacteria often have biofilms, and that could be a problem in getting rid of them. The problem is, is a lot of the strategies we try, the products on the market all seem to be somewhat disappointing, so maybe we’ll have to look into the Paul Anderson formulas a little more.

Shivan:                Oh, yeah. I think people have a lot of success with those. A lot of success. And if you have been trying for a long time to get rid of SIBO and you just can’t beat it, and you haven’t done a biofilm buster, I would definitely suggest doing that in conjunction, very carefully timed with your treatment.

Dr. Weitz:            Right. So, how can our listeners and viewers get ahold of your book? Where is it available?

Shivan:                Well, I’m so glad you asked, darling. Thank you. It’s on Amazon and …

Dr. Weitz:            Barnes and Noble.

Shivan:                Barnes and Noble, and where all books are sold. We’ve just gotten it into the UK, and a couple of other overseas markets, at the very least, in Kindle. And yeah. I mean, this is what I wish I had known five years ago when I started my figuring out about SIBO. It is loaded with information.   Some of the feedback, which I so appreciate, has been like, “It’s an easy read.” It’s something that they’re highlighting. On page 111, there is a map. We call it the “SIBO recovery road map.” It is the algorithm that Dr. Pimentel originally created, that then Dr. Allison Siebecker and Dr. Steven Sandberg-Lewis added to.   And it literally takes you step by step through what to do. Like, “Test, symptom relief, diet. Then do your three-hour lactulose breath test. Choose a treatment: elemental, herbal or antibiotics. Afterwards, test again. And if you’re well, manage. If you’re not well, treat again.” And it just takes you through the whole cycle so you don’t have to keep memorizing everything I was just talking about.   So, that’s in there, and that’s also what the core SIBO recovery road map is based on as well, is that algorithm. So, sibosos.com is my website. And our SIBO SOS Facebook community, we’d love to have everybody there. And that’s how you can get ahold of me.

Dr. Weitz:            Awesome. Thank you.

Shivan:                Thank you so much. Keep up the great work. We love your work, and getting us all educated. Appreciate you.

Dr. Weitz:            Excellent, excellent. Thank you so much.

Dr. Weitz:            Well, thank you, listeners for making it all the way through this episode of the Rational Wellness Podcast. Please take a few minutes and go to Apple Podcasts and give us a five star ratings and review. That would really help us, so more people can find us in their listing of health podcasts.

                                I’d also like to let everybody know that I now have a few openings for new clients for nutritional consultations. If you’re interested, please call my office in Santa Monica at 310-395-3111. That’s 310-395-3111. And take one of the few openings we have now for a individual consultation for nutrition with Dr. Ben Weitz. Thank you, and see you next week.

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Dr. Yael Joffe discusses Nutrigenomics with Dr. Ben Weitz.

[If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.]

Podcast Highlights

1:40  Nutrigenomics has to do with the relationship between genetics and diet and lifestyle, including exercise, stress management, meditation, trauma, and anything that impacts our health.

3:06  Weight control.  We are all 99.9% identical genetically, but we can still have millions of places in our DNA where our code sequence is different. 1. One thing to consider is what drives us to eat?  We experience hunger differently and this is driven by our genes.

8:24  Epigenetics is how the choices we make in our environment change the way our genes express. When you switch on a gene it makes a protein and proteins are often enzymes that drive our metabolism. Let’s say we find out that we have a gene that means that we are not efficient at detoxifying. We can then encourage them to eat cruciferous vegetables like broccoli sprouts and brussel sprouts, which contain sulforaphane, which can switch on your detoxification genes once it is activated by an enzyme called myrosinase, which is also in the vegetable.

Dr. Yael Joffe has a PhD in genetics and the nutrition of obesity from the University of Cape Town in South Africa. She is part of the team that created the first nutrigenomic genetic test in 2000 and she cofounded 3X4 genetic testing and she is the Chief Scientific Officer and the website is 3X4genetics.com.

Dr. Ben Weitz is available for nutrition consultations specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111 or go to www.drweitz.com.

Podcast Transcript

Hey, this is Dr. Ben Weitz, host of The Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to The Rational Wellness Podcast for weekly updates. And to learn more, check out my website, drweitz.com. Thanks for joining me, and let’s jump into the podcast.

Hello Rational Wellness podcasters, today our topic is nutrigenomics with Dr. Yael Joffe. To give us some idea of what nutrient genomics is, I looked at an article in Nature Magazine and here’s the quote, nutrigenomics is a study of the effects of food and food constituents on gene expression and how genetic variations affect a nutritional environment. It focuses on understanding the interaction between nutrients and other dietary bioactives with the genome at the molecular level, to understand how specific nutrients or dietary regimens may affect human health.

Dr. Yael Joffe has a PhD in genetics and the nutrition of obesity from the University of Cape Town in South Africa. She’s part of the team that created the first nutrigenomic genetic test in 2000, and she co-founded 3×4 Genetic testing. Dr. Joffe, thank you so much for joining me.

Dr. Joffe:   Hey, Ben. Thanks for having me join, thank you.

Dr. Weitz:  Absolutely. I do think that we really need some more detail and nuance about this whole concept of genomics and nutrigenomics and epigenetics. How how do you… I gave a definition of nutrigenomics from Nature Magazine, but how do you define nutrigenomics?

Dr. Joffe:   I actually thought that was a excellent definition, but I think you could probably break it down a little bit more and maybe just make it a little easier. So it was great for me, I’m not sure it was great for everyone else. So maybe we can start by just coming down to some really basic concepts of what is this story of the relationship between genetics and nutrition. And when I say nutrition, I’m always talking about diet but I’m also talking about lifestyle, exercise, stress management, meditation, trauma, anything that impacts our health. So-

Dr. Weitz:  By the way, I would think it would be great if in this next 50 or 60 minutes we have, if we could get some help on, is can we get some idea from genetics, what type of diet different people might do well with as well as a little more detail about some of these genetic SNPs and how to handle it?

Dr. Joffe:   All right. We can focus on one topic. So if you want to do weight, we can do weight or we can do exercise because we haven’t got enough time to cover them all, but I’m going to use weight as an example which is a great example. I think everyone can relate to it. Let’s start off with the idea that we are 99.9% identical genetically. And what I mean by that is we have a code, we have a blueprint in our body. Everyone’s heard of the word sequence, that’s our DNA blueprint. But at 0.1%, we’re different from each other.   And that means that at millions of places in our DNA, our sequence code is different. We call this genetic variation. Now, why is this important? It’s because these differences determine how we respond to the world around us. So we know that we’re different in the foods we respond to and the way we respond to exercise, training, how injured we get or how well we recover from training, but we’re going to talk a little bit about weight because we chose one topic. So why is it that we respond differently in terms of weight gain and weight loss? When I studied dietetics which was my first degree, I was taught calories in calories out. If you reduce the calories and increase the expenditure of calories, you would lose weight. And I soon found out this was absolutely not the truth, that patients would come to me and they would say, “But I did what you told me to do,” and yet they didn’t lose weight?  And because it was 20, 30 years ago, I’d be like, “Well, you must be lying to me and you must be cheating.” So what has genetics taught us? Genetics has taught us that actually there is an amazing amount of variability in how all of us respond to the food we eat, the way we eat, the behavior about eating, the way we store energy in our bodies, store fat and how we burn up fat. And this is around the concept of genetic variation. So I’m just going to touch on why that is because it used to be, my mother used to say like, “Oh, she’s got such a high metabolic rate, she just looks at food and burns it up.” But the reality is it’s much, much more complex than that.

So when we think about weight, I like to think about genetics in three different ways. One is what drives us to eat? So when we see food, some of us are snacking, some of us are binge eating, some of us are hungry. So what are the drivers? Well, we experience hunger in a different way. I always used to think that everyone was the same hungry as me, but actually we experience hunger completely differently. And the same way that if we all eat a cheeseburger with fries, we experience fullness of the word satiety in a different way. So I might need two or three burgers to feel full and you might be okay on one burger. These differences in how I feel hunger and satiety are actually driven by our genes.  Now we walk into a buffet and we see this beautiful spread of food and we’re all kind of hungry and some of us will go and have a plate of food, we’ll load it up, we’ll come and we’ll eat and we’ll go, “Yeah, that was a great meal, I feel full,” but the others will just take a look at that buffet table and even if they have a sense of fullness, they’ll still go back again and again. So even our eating behavior when we see food is driven by genes, and that’s just the beginning of the story.  Because once that food is in our body, we manage those calories in different ways. Some of us are really efficient at storing and we hold on to it, it’s very evolutionary, it’s from when we were hunter gatherers from the plains of Africa, others of us are very good at burning that up. So how do we burn up energy? Two ways, through exercise and through what we call basal metabolic rate, which is sitting at our desk working, you’re burning up. And yet we are so different in our ability to burn it up.

Now suddenly I’ve just mentioned like six things that would change how you, Ben and I respond to the world of calories around us. So when a patient walks into your practice and says, “I’ve been battling my whole life, I’ve been tried every single diet, I just can’t lose weight,” what we really want to do is we want to use genetics to try and discern why. What is your story, your journey that is driving these calorie interesting conversations in a different way? That’s the first part of the story. Any questions on that part?

Dr. Weitz:  Well, I’ll wait a few minutes to let you drill down but I do want to drill down and come out with some practical ways of dealing with these things.

Dr. Joffe:   Okay. It’s like that’s where I was going. So when you did the definition from Nature, they spoke about two things. They spoke about genetic variation which is what I’ve just spoken about. It’s what gives us our insight about ourselves, it’s self knowledge. How do I react to the world about us? But there’s a second part, the other 50% of the equation, which is how do I change gene expression? And I call this the action part. So insight, I find out about myself or you find out about your patients, action, what are we going to do now? So what? So I find out all the stuff about you, now what difference does it make? I’m sure you’re all familiar with the word called epigenetics.

Dr. Weitz:  Yeah, yeah, yeah.

Dr. Joffe:   Epigenetics, that’s what we’re talking about now. Epigenetics is when choices we make in our environment change the way our genes express, or I like to say the way our genes behave or even better, think of genes as being light switches. When you switch on a gene, it makes a protein, when you switch it off, it stops making the protein. Proteins are enzymes, they drive our body. So I have found out something about myself, I have found out that… let’s talk about detoxification. Everyone understands detox, right?  We have exposure to toxins, we have exposure to internal metabolites that are made by body that we want to make sure that it’s clearing whether it’s through over-training exercise, whether through its exposure. Now I can have a genetic test done and understand how optimally my body is detoxifying toxins or hormones. Now I know that, and I’ve discovered that I am not so brilliant at detoxifying, I want to take action. And the best way to take action is to be able to switch on the genes that are responsible for detoxification in the body.  Because if I can get the genes to make enzymes that detoxify, that is way more powerful than anything I can do. So I’m not just going to take a supplement and plug a hole, I want to switch on enzymes that are going to do stuff that it’s going to heal my buddy and my body is much better at heating itself than me plugging it with another 25 supplements, right? Here’s an example. So you know the… because we want to be practical. So cruciferous vegetables, cauliflower, cabbage-

Dr. Weitz:  Brussel sprouts, yeah.

Dr. Joffe:   Brussel sprouts, and my favorite broccoli sprouts, the little sprouts. So they contain this extraordinary compound where you spoke in again, a fantastic Nature definition, bioactives, plant practice, but actually all they are, are molecules of compounds that we find in plants. But they’re very magical, they’re very powerful. And there is one called glucoraphanin, and this really amazing compound when it is acted on by an enzyme called myrosinase which is also in your vegetable, you bite into your cauliflower, when you bite, you actually break open that enzyme, it changes accurately and you land up with this very magical plant molecule called sulforaphane. Now this is what is so magical about sulforaphane, it can switch on genes. So sulforaphane, once it’s activated in your body, switches on your detoxification genes.  So you walk into the house and everything’s dark, you switch it on and suddenly you have light, sulforaphane’s doing the same thing in your body with detoxification. And your body is now able to clear those toxins from your system. And we could talk about sulforaphane for hours, but it is probably one of the most potent ability of a plant molecule to switch on genes. So we used to think vegetables were good for us, vegetables is still good for us but we never understood why are vegetables so incredibly good for us? It’s because they are more powerful than anything at switching on genes, epigenetic mechanism. But epigenetics can work the other way as well.

Epigenetics can be environmental toxins, pesticides and herbicides and fertilizers which are getting into our body, and those toxins also switch genes on. They just switch on the genes we don’t want, which is inflammation oxidative stress. Does that make sense? So insight is I want to understand myself, I do a genetic test to understand myself, action is I use what I have, be it exercise, meditation, cold water immersion or nutrition to change the way genes get switched on or switched off.

Dr. Weitz:  Let’s drill down on the weight loss thing. What are a couple of genes that affect whether or not we feel full and whether or not we feel full, is it related to other factors?  In other words if I’m constantly eating large meals, does my stomach get stretched out?  So maybe I don’t get full as quick, maybe I eat quick, so I haven’t even gotten to the point where my body’s getting a signal that it’s full because the food hasn’t even gotten to my stomach yet and I’m still eating. Maybe there’s psychological factors on eating because I feel stressed, I’m tired of this raging pandemic and I just want to eat myself into oblivion. How much do these other factors and then talk about somebody’s genes, maybe one or two of these genetic snips, and then what can we do about these genetic snips?

Dr. Joffe:   Yes, yes and yes, absolutely. There are many factors that contribute to how we experience fullness and you’ve actually named some really well. But here’s the interesting thing, they did a lot of the research on children, little children. Now we as grownups are really complicated and messed up when it comes to food, so it’s about overeating. It’s about watching TV and eating, it’s about comfort eating, it’s about soccer social dynamic of connection and loneliness and isolation, so complicated. And then it becomes really hard to say what is genetic, what is this? But I did a lot of the research in children and in twins, which is the best genetic research. And when they did them in kids, they found that there were certain children who would be very, very hungry. And when they were given the same amount of food as the other kids, they would just have no sense of being full.

And this was before they had enough time to develop company eating or eating disorders or TV watching, this is when they were still really small. So they started looking at what are the genes in the body that are really driving them? So there’s a very famous gene called FTO, which is actually bizarrely named fat mass and obesity gene, barely you’ll find it in the media, it’s all over the place. What’s really interesting is it has been related to fullness. But what I find fascinating about FTO is that if you have the genetic variant, so the alternative version not a Deepak design mutation, it’s just a different version. You have less locus of control around food. So when I walk into that buffet and I see the food, I am likely to have less control in how many times I’m filling up my plate than if I had a different genetic variation that didn’t have the AA gene. There are other ones that drive taste. So we taste food-

Dr. Weitz:  Hang on a second. So if I have that AA variant of the FTO gene, what’s the solution?  Don’t go to buffets?  What else?

Dr. Joffe:   Don’t go to buffet. Two things I want to say, is you cannot make recommendations on a single gene. So I just did that with you, but actually I don’t believe man, you can never say, oh one gene and they’re like… and one gene, don’t ever do this. We look at all your genes that impact your weight, all of them and then we build schools around them and say, you know what? Your issue actually, because you only one gene that impacted fullness, but the other 10 genes that impacted fullness didn’t, so let’s not overreact. So I just want to say that. So we group genes together to understand that we don’t create recommendations phase one.

Now, what do we do? Where I’ve had patients who’ve come to me, I’ve said, “You know what? I’ve been dieting my whole life, and we do the genetics.” And the genetics do come back to say, “You know what? You hit the tough road. Your genes are not helping you. What are we going to do about it?” So the first thing is… And this has led to many patients crying in front of me, [inaudible 00:15:56] is saying, “I’ve been told my whole life, I’m a failure, I have no self control and no willpower. You’re the first person who’s seen me through who I am.” That’s the first thing, is we start dealing with self-acceptance. This is my inheritance, this is what I got. Once we can get positive and say, okay, now let’s think about realistic goal setting.

We’re not going to use the BMI which is based on population, let’s talk about you and your genes and say, you know what? If we can get to a BMI of 27, if we can get like… that is all, even like 20 or 30, that is not bad if we can make sure you’re healthy. So let’s focus on your health parameters. Let’s look at your insulin, your glucose, your lipids, let’s look at your apple versus pear. So we want to focus on what will make them overweight healthy, which is a real thing. You know that it’s that absolute real thing.

That we can keep people a little bit overweight or even completely overweight, but actually still have them extremely healthy by using exercise and making sure that the quality of the diet is right. The third thing I do is a lot of behavioral work. I work with psychologists and psychiatrists who do a lot of behavioral work. In the same way that they work with addiction, they work with eating. In the same way that I’m driven to drink or to gamble, how do I manage those triggers? With a buffet? Be at a bowl of pasta? Be at a party? How do I manage my triggers because my genes are pushing me to the table, but I want to use my mind and my brain to override those triggers?

Dr. Weitz:  Okay. Are there any secret sauces for influencing the FTO and the other genes?

Dr. Joffe:   Well, FTO responds really well to protein, and I don’t say like, everything was one’s protein, I’m not like everyone’s got to be on like a [crosstalk 00:17:48]-

Dr. Weitz:  We certainly heard they’re proteins, one of the foods that’s associated with society.

Dr. Joffe:   It definitely is. And that’s why FTO probably does respond well to protein, is because entirely protein works really well at driving society. So if I have a patient who’s got FTO-

Dr. Weitz:  By the way, does that drive satiety as well, or almost as well as protein?

Dr. Joffe:   It depends on the individual. So fat is much more complicated in terms of responsiveness on how people respond to fat, which is why we would see things like the ketogenic diet works extremely well in some people and really badly and others. That people’s response at part of that is that genetically, we learn about how you break down fat and which pathway fat goes on. And depending on where that pathway fat is, will determine your response to fat and that’ll determine lots of things, not just satiety, and what’s the ability to store and burn fat? Some people are super fat-burning efficient, and others are super fat-storing efficient. That’s also driven by genes.

Dr. Weitz:  Wait. I want to know that.

Dr. Joffe:   Which part?

Dr. Weitz:  How do we know if somebody doesn’t process that well? You’re talking about looking at their lipids and seeing if their LDL or… what-

Dr. Joffe:   No, no, no. We can look at your genes, so genes are going to give us some of that insight and to tell us about how efficient you are at metabolizing and storing fat. So those of us again who are really, they could have the refugee and apotheosis, that when we consume calories, particularly fat calories, we store that, we hold onto that fat, it’s actually a protection against the old evolutionary thing. We can see in your genes when we look at that, whether you’ve got more of these kind of fat storage hold onto energy genes, or whether you’re actually quite good at burning it up.

Dr. Weitz:  Can you name a couple of those?

Dr. Joffe:   The main ones would be ADRB2, the adrenergic receptor genes. We always think of ADRBs, there’s ADRB twos and threes as the burning up versus the storing. I don’t know how long we’ve got, but I’ve got a really great story I can tell you about a Japanese trial where they… Can I quickly tell it?

Dr. Weitz:  Yeah, sure.

Dr. Joffe:   So they did this amazing research study in Japan and they took 127 Japanese men who were overweight. Not obese, overweight. They were like BMI 27. And they put them on a program for two years, 24 months, where they decreased their calories to about 1,200 calories a day and they increased the energy expenditure to 20,000 steps a day, which is a lot of training because we normally base on 10,000, it’s a lot of training. And they tracked them for 24 months. They tracked them to make sure that they were staying on the program, the calories and the expenditure, and they tracked them to see how they lost weight. Now being Japanese, and not American-

Dr. Weitz:  By the way, just for clarification. I believe that somewhere’s around two hours a day of same walking, right?

Dr. Joffe:   Correct, exactly. So they did, I think it was mostly cycling. So they managed to get it in a little bit less at a higher rate, but it was roughly an hour, hour and a half of training a day.

Dr. Weitz:  Okay. [crosstalk 00:21:08]-

Dr. Joffe:   You’re 100% right. I was saying that because they were Japanese and not American or South African, they listened and they did exactly what they were told. Non drops of the study. They all decreased their calories to 1,200 for 24 months and managed to train for 24 months. And at the end of the program, what they did was they took them and they put them into weight loss groups, and they observed that there were four different ways that they lost weight. So in group A, in the first six months, they lost the weight they needed to, they went from like BMI 27 to BMI 22. And after six months, they maintained their weight loss for another 18 months. Brilliant, that’s what we call very successful weight loss.

In the second group, at the six month, they hadn’t lost much weight, very slow to weight loss. But by 24 months, they had got to almost the same place as the first group. So they lost weight but it was extraordinarily. So think of all the programs are blues, 10 kilograms and 10 days. In this group, they lost very slowly but they got there. In the third group, they called the rebound group. At six months, they lost all the way to that the first group lost but by 24 months, all of the weight came back again, plus a little bit of extra.  Remember they never changed their intake or expenditure. So it’s not like six months they lost the weight then they started eating again and it bounced back. It didn’t change their calories, it bounced back. And the fourth group never lost any weight. They decreased their calories to 1,200, they did 20,000 steps a month for two years and they never shifted any weight. Now, why I love this study more than anything is it makes us understand that when we sit in with a patient or a client in front of us, we must always remember those four different groups, that we all react differently and we cannot start off with an assumption of what our expectation is of patients.

Now what they did was they then did their genetics. And I said, “Can we try understand why this group didn’t lose weight? This group lost weight?” And some of the genes that came up as being the most insightful were these ADRB2 genes and the ADRB3 genes. ADRB2 is around how do I store energy and store fat versus burning it up? And ADRB3 is really interested in how responsive am I to exercise training? Because some people will only use exercise to lose weight not successfully, and actually they really to manage their intake to be able to lose weight.

Other people can use exercise and it’s quite efficient. So the ADRB3 is really informative about understanding that nuance between them. And they came up exactly, they could divide them into four groups and see where the genetics were in the four groups. So really, really fantastic study. There are other genes, the FTO gene, the awesome MC4R, TCN2, that also are how do we store fat? How do we… and PPAR gamma. So you put up PPAR gamma, a very, very well-researched gene has been around for 20 years and it’s very much around insulin and glucose, which of course relates a lot to how we store fat. Our insulin levels driving fat storage, and and so PPAR gamma is always a gene that we look at when we’re interested in that.

Dr. Weitz:  So what do we do with the group that wasn’t able to lose weight based on these genes?

Dr. Joffe:   We make them believe that having a BMI of 27 is what is going to be their BMI. What we really want to do with those, that fourth group is we want to make sure they’re healthy. So we’re going to check all their parameters because 27 BMI is okay. If they-

Dr. Weitz:  But you’re saying they can’t lose weight, no matter what.

Dr. Joffe:   They can’t… So we could have tried some different stuff, right? Which of course wasn’t done in this study. So we can manipulate the macronutrients, we can have a look whether we can change around into kind of a different macronutrient distribution because remember they got the same macronutrient distribution. It was not low carbohydrate, it was very moderate carbohydrate. We could try that, that could shift things. We could also change the way they exercise. So there’s a lot of research that says in some people, that kind of aerobic endurance type exercise does not drive it but if we get them into gym and we do high intensity weight training, we might be able to change it. That’s when we start playing around and we can get some of those insights because remember, genetics is not about weight. We have a whole part of our panel which is about exercise potential. How should we be training? How do we respond to training?

Dr. Weitz:  But can you take a set of genes and say based on these genes, this person should do weight training, not cardio, this person needs a low fat diet, this person needs a low carb diet? And there are programs out there that we can send our patients for and they’ll give you this detailed panel that will tell you, this person should eat in this kind of way and this person should do this kind of exercise. What do you think about that?

Dr. Joffe:   In my genetic test, I do a lot of-

Dr. Weitz:  What is your genetic test?

Dr. Joffe:   My genetic test which is 3×4 Genetics, it looks at a whole lot of different stuff from what we call action, which is detox inflammation oxidative stress. So what’s the stuff that’s most caught your body?

Dr. Weitz:  Is it using more… I’m sorry to keep interrupting you, but-

Dr. Joffe:   No, no, it’s fine. Exactly.

Dr. Weitz:  Does it have more genes than I could get from a 23andMe or Ancestry or is it just organizing those genes and give me an explanation? In other words if I did a 23andMe or an Ancestry, and got the raw data, would I have what I need, or?

Dr. Joffe:   Great answer. So I have way less. I have like 134 genes in my report and you are going to get thousands from 23andMe, thousands and thousands and thousands.

Dr. Weitz:  So all the genes in your report, are they included in 23andMe if they were just analyzed the right way?

Dr. Joffe:   Not all of them.

Dr. Weitz:  Okay.

Dr. Joffe:   That’s one that comes to 23. But here’s the thing. I actually can test 600,000 of your genes, 600,000 of your snip genes, because we only have 25,000. But actually of that 600,000 snips of test, I believe and my science team believe that only 134 of them are well-researched enough to give me as a practitioner insight in what to do with you. So one of the problems we’ve had in genetics is everyone kept on coming out of the test and going, “I’ve got 500 genes, I’ve got 1,000 genes, I’ve got 6,000 genes for 29 99.” But actually there’s no value in that because what you need to make sure is, so what?

So you can get raw data of 600,000 snips and you can know nothing about yourself. What do you need to make sure that whatever company you choose to work with genetically is what can I do with this information? Will it be useful to me with my clients and practitioners? How would it change my decision-making? Will it help me decide, should I go to the gym? Should they do endurance? How many days a week should they train? What kind of active recovery should we build in? What about collagen and bone and joints? What are the susceptibilities to ACL injuries? So you need to make sure that we’re answering very specific questions. So the problem is by-

Dr. Weitz:  So if we order your panel, we’re going to get a specific report telling us how this person should eat, how they should exercise, what they should do for bone density?

Dr. Joffe:   Yes. All of that, except a test does not come to you directly. So 23andMe, you can order get at home or send you an answer. We do not do that, we only work with practitioners. Chiropractors, nutritionists, doctors, naturopath. Here’s the reason why. Genetics does not exist in isolation. All the answers to your problems are not just in your genes. You raised this earlier on, right? So when someone comes to me, “Tell me about yourself.” Like, why did you come here? What are you trying to look for? What’s worrying you? What are you looking to get out of it? Tell me what happened when you were growing up. What has your training been? What’s your diet like? What’s your connection like? Do you have friends? How are you feeling? What’s your stress levels?

So I want to take some black tests, I want to understand who you are but I also want to know your genes because if I can know your genes, remember insights of knowledge and know who you are sitting across me and know what you want to get out of this consultation with me, now as a practitioner, I’m super powerful to be able to personalize what you need.

But if I just produce… So there are many companies that you can buy genetic tests from and it’ll say to you, “You’ll do really well on a low fat, high carb diet or a high carb, low fat diet.” I don’t believe that’s true. So for me, the science cannot determine that. We can give you many insights about fat storage and fatty acids and protein and FTO, but you as a practitioner need to take the information and the insights we give you and put it together with everything you know because you’re a practitioner and give the advice. So I, that’s why I like practitioners and that’s why we train our practitioners. We teach them, we mentor them so that they’re able to integrate genetics, but you should never only do a genetic test and believe that they know who you are.

Dr. Weitz:  Now, of course you know in the functional medicine world that there’s a tendency to have the patient get one or several gene tests and then on a result and the basis of that, claim to know the answer to why they’re having this problem that nobody else has solved because we just measured your MTHFR and in case you’re heterozygous or one of the variants, that proves that you need methylated B vitamins which you weren’t taking, or you weren’t taking the right amount and now all your problems will be solved because you have MTHFR. And by the way, you should walk around with a sign that says I have MTHFR.

Dr. Joffe:   And what your sign says, you can have a tattoo and it says MTHFR defect, which is my favorite. So thank you for raising the MTHFR-

Dr. Weitz:  I have the disease of MTHFR.

Dr. Joffe:   I’m going to join the 6,000 MTHFR forums that I can find on the web. So you’re 100% right that one of the worst things [crosstalk 00:32:16]-

Dr. Weitz:  We should not let MTHFRs cross the border. No, I’m kidding.

Dr. Joffe:   Oh, we should board the wall and [inaudible 00:32:22] MTHFR. We’ve got to stop. Stop, stop, stop.

Dr. Weitz:  Okay.

Dr. Joffe:   But MTHFR is a problem because the genetic testing, and MTHFR is one of the first genes that was ever researched and it’s beautifully researched-

Dr. Weitz:  And we couldn’t have a discussion without mentioning MTHFR.

Dr. Joffe:   Right. But here’s the thing. 15, 20 years ago, everyone got so excited at MTHFR, they stuck MTHFR’s really big pedestal and they said, “Oh my God, I can make so much money from this gene because what I can do is I can say, if you have MTHFR which is just a snip,” it’s just a single snip, it’s just one of 600,000. But if you have it, I can sell you lots and lots and lots of supplements, I can sell your diet plan, you’re going to come to my forum because if you have MTHFR, you’re going to have 6,000 diseases. Well, this MTHFR has been the absolute worst thing that happened to the genetic testing industry. It made some individuals very, very wealthy, I will not name them, but it made them very, very wealthy. But what it did was it actually undermined the true value of genetics for the individual.

And so if you study one of my courses I teach, you get a whole module on what we’re drawing with MTHFR and why it is so damaging and why it is wrong. So when you hear people say I have MTHFR mutation or defect and I’m going to take 20 supplements and I’m going to get these diseases because I have it, this should be the biggest red flag and fireworks going on. It’s like, no, no, no, these genes are not that powerful. They’re informative, they’re interesting, they give us some information about the biochemistry of our body, but by themselves and that’s what I said early on, we never make a recommendation on a single gene or a single snap, whether it’s FTO, APOE, MTHFR, I don’t care. We group genes together that are interesting to us in methylation, in cognitive, in detox, in fat storage, we group them all together and we evaluate what did you inherit altogether? And we get a sense whether we should address that issue.

And one of the things that happen in MTHFR is that the supplement industry made so much money that they took people who had MTHFR and made them more sick because they gave him so many methylated B vitamins. And I think people are starting to wake up. So you’ve got to be really careful about what genetic… Genetics is awesome, it gives us self knowledge and insight but you’ve got to be very careful. It is [crosstalk 00:34:56]-

Dr. Weitz:  I have gone down the MTHFR rabbit hole a little bit. It’s been that much time with it. And then I ran a couple of these detailed methylation panels that look at say 15 or 20 different genes and then correlate it with various factors like homocysteine and still after all that, it seemed to me almost every one of these genes said check vitamin B2 and B3, check folly, check B12. And we ended up with the same thing. So I couldn’t help but think, okay, if I just give everybody methylated B vitamins, I guess that pretty much takes care of.

Dr. Joffe:   Yeah. That is a problem. So the companies have [crosstalk 00:35:48]-

Dr. Weitz:  And maybe a slight variation like this one, [crosstalk 00:35:51] a lot of it just is around these B vitamins, right?

Dr. Joffe:   Well, not in my test.

Dr. Weitz:  Okay.

Dr. Joffe:   Not in my test. So methylation is a single pathway, right?

Dr. Weitz:  Right.

Dr. Joffe:   I have six pathways that we analyze and each pathway has 10, 15, 20 snips it. But methylation isn’t an important pathway but a single pathway. So we never say that one pathway [inaudible 00:36:17]. And so what happened to many of the companies that were testing MTHFR, when they got into trouble for only testing MTHFR, they’re like, “Well, let’s just test methylation because if MTHFR is awesome, methylation must be more awesome and we can make a million decisions just of methylation. Wrong, right? Because there are multiple biochemical processes happening in our body and they all interrelate with each other.

So we can’t understand what’s going on in methylation and not understand oxidative stress, what’s happening with our mitochondrial stuff, glucose, insulin, hormone metabolism? Methylation is important but the same way that you cannot make a recommendation based on a single gene, you should never make a recommendation based on a single pathway. Because otherwise we’ll land up where we started, which is too many methylated B vitamins, which actually, excuse me for saying, you don’t actually need because methylated B vitamins bypass MTHFR. So the amount and the dose you need is actually really low.

Dr. Weitz:  And on his methylation pathway, methylation is a way to actually get a sense for anti-aging now as we look at these methylation time clocks. However, it’s not just whether all the genes are methylated, but it’s whether some of the genes are demethylated, and you mentioned the FTO gene, and this is actually a gene that demethylates. And so you don’t necessarily want all your genes methylated, some of the genes should not be methylated with health, right?

Dr. Joffe:   Yeah. And so there’s a huge confusion here which is a great place to address it. Huge confusion about methylation. You actually spoke about methylation and there’s two different kinds of methylation, is what I’m trying to say, right?

Dr. Weitz:  Okay.

Dr. Joffe:   Two different kinds, and this is where everyone gets completely confused. There is genetic variation methylation. That means… We know that there’s the methylation pathways. And if you have a whole lot of genes, MTR, MTRR, CBS, MTHFR, and they have snips in them. So they have speeding changes in the sequence that change how efficient they are. We get a sense for how efficient or inefficient or optimal or suboptimal our methylation pathways are working. And those methylation pathways are involved in DNA repair and making new DNA. So they’re like the basic engine. Now the other methylation you spoke about is actually epigenetics, which is attaching a methyl group onto a gene which either switches it on switches it off, which is what you spoke about. Demethylated or methylated.

And this goes back to our previous conversation where we switch on genes and then we switch off. And there’s some choices we make in our life that will either switch on and switch of genes. So methylation is so complicated and [crosstalk 00:39:07]

Dr. Weitz:  So there’s two methylation processes in the body, are they related, directly related, somewhat related or totally separate?

Dr. Joffe:   They are related in the sense that those first ones I told you about, the ones that have gene variants and they’re producing methyl groups. And they need to produce enough methyl groups to be able to switch on and switch of genes. So that’s how they’re related, but they’re actually doing two different things. One is we’re looking at genetic variation and how optimal we are at producing those methyl groups. I mean, looking at epigenetic methylation, I call it epigenetic methylation, it makes more sense of how efficient are we at switching on and switching off genes without methyl groups? Now, the problem is there’s a couple of tests in the marketplace that are being sold to consumers of epigenetics. They say that they can measure how your genes are being switched on and switched off. There’s about three companies out in the marketplace at the moment.

Dr. Weitz:  Yes.

Dr. Joffe:   Here’s the thing, is I think they all, genetics was 30 years ago, where they can measure something, it doesn’t mean they’re able to understand what they’re measuring and here’s why. If you wake up in the morning and you go to the coffee shop and you have a double kotato, double shot espresso caffeinated thing, that’s not just the caffeine, but the other compounds in the coffee are going to switch on a whole lot of genes, either through methylation or demethylation. Anyway, they’re going to switch on a whole lot of genes. So if I measure your epigenetic profile, your methylation profile, after your double espresso, I’m going to get a reading. Then you’re going to go home and you’re going to do your 30 minutes meditation and then I’m going to test your epigenetic prevalence. Guess what, I switched on and I switched off a whole lot of different genes.

Dr. Joffe:   So when I test you, what actually am I testing? And that is the problem. If we just… I’m going to say one more thing and then you can bug in there. Every single decision we make, sorry, you and I be like, every decision we make every minute of the day changes the way our genes express themselves. When I wake up in the morning and I choose what coffee, if I wake up in the morning and grab my phone to look at as opposed to going to do 20 minutes of meditation, changing the way my genes behave. So health is not something that we decide of a month or year, it’s a decision we make every minute of every day.

Dr. Weitz:  So you’re saying that all this research being done by Steve Horvath at UCLA and these other folks and they described this as epigenetic methylation clocks, that it’s not an accurate way to assess our biological aging because minor things that you do switch on and switch off before you get the test.

Dr. Joffe:   I think his research is brilliant and I definitely think he’s leading the charge, but just because we can measure it in a research which came out of research doesn’t mean we understand how to translate it yet. And I think he is at the forefront and I think he will lead the forefront but personally, I don’t think we’re close to understanding how we’re measuring it, what it means because we haven’t been able to figure out what is the influence of the decision I made two minutes before I took your test even more? So I’m waiting.  I’m waiting and I’m watching, we’re definitely going to be doing in the future. We can definitely do it in clinical trials, but there’s a difference remember between insights measuring and then actually what do we do? And so I’m going to stay on the fence for a little bit longer.

Dr. Weitz:  My methylation epigenetic measurement test, it should be arriving today.

Dr. Joffe:   Well, let me know. With the true age. Did you do true age?

Dr. Weitz:  True age, yeah.

Dr. Joffe:   So let me know how that goes, I’d be fascinated to… It’s cutting edge but I’m not happy yet that the science is ready, but that’s how it works, that’s how science works. You get… When we built the first nutrigenomic test in 2000, it was three years before the human genome was developed and everyone said to me, “It’s too soon, you don’t have enough,” and they were right right?

Dr. Weitz:  Right.

Dr. Joffe:   So someone’s got to start it.

Dr. Weitz:  I know this is a huge topic in every one of the categories we’ve talked about you could spend a week with and I know I’m taking you down another topic that could take a week to discuss, but it’s on my mind and I had to ask you about the APOE gene. So maybe we can just talk about that for the last 10 minutes or so. For those of us who aren’t aware, if you have the APOE 34 or 44 snap, that increases your risk for heart disease and Alzheimer’s disease. And I know in practice, it’s not unusual to put somebody on what seems to be a healthy program or maybe get somebody who comes in the office who’s on what seems like a healthy program, and then you find out they have a 34, 44, and a lot of times they don’t respond in the same way.

But we’re still debating in the literature what that means. Do you have any insights? I know we haven’t had enough long-term large-scale prospective randomized clinical trials, but we know on patients who have APOE 34 or 44 if they’re going to do better on a ketogenic diet or a vegetarian diet, or do we have any idea?

Dr. Joffe:   I have a deep fascination with this gene, it’s an amazing gene. Do you know that it’s called the God gene?

Dr. Weitz:  Oh, is that right? I hadn’t heard that.

Dr. Joffe:   It’s referred to as the God gene. And I’ll tell you something even more interesting is that if you look at evolutionary biology, because of course genetics is evolutionary and then we got this really bad, dark messed everything up. The original version of APOE was E4.

Dr. Weitz:  I thought it was E2.

Dr. Joffe:   No, it was E4.

Dr. Weitz:  Okay.

Dr. Joffe:   So when we were hunter gatherers on the plains of Africa, E4 was the common variant, not E2.

Dr. Weitz:  That’s right, that’s right, that’s right, that’s right.

Dr. Joffe:   E2 came later. So why would we have this E4 variant to help us survive on the plains of Africa? And then suddenly we’ve got E2, E3 and everyone’s terrified of E4, right? It’s because it’s such an interesting gene, it’s an inflammatory gene. And when we were attacked by the tiger and we needed to heal quickly, you actually want to be able to get a very quick acute inflammatory response to be able to heal. But the problem is we don’t get attacked by tigers anymore and we have these very bad diets and all the various entry and everything. So suddenly the inflammatory aspect of APOE became harmful instead of helpful.

Dr. Weitz:  And the biggest risk to survival was starvation, not getting some chronic inflammatory disease. So having a lot of inflammation was beneficial, whereas now the predominant cause of disease are chronic inflammatory conditions like diabetes or heart disease and cancer.

Dr. Joffe:   [inaudible 00:46:55] Cancer, they’re all inflammatory diseases, right. So it’s fascinating how the gene itself has evolved because the problem of health is the problem of the disconnection between our genetics which is ancient and evolutionary and our diet, which is very modern and very quickly changing and very bad. And it’s this clash between the two that we’re seeing is causing so much disease. Anyway, back to APOE. APOE when you start studying is actually not this great body that actually everyone thinks, but one thing it is, is hyper responsive. So we talk about the E4, whether E 44 makes you hyper responsive, which means when I change your diet plan to a health diet plan, you are unlikely to be very responsive to those changes, which is a really good thing, it’s a really good thing.  So if I have a patient with hot stuff happening, particularly like lipids, lipid metabolism, and I see they have a three, four or a four, four, before I go in yet any start on, I’m going to do everything in my data and lifestyle, because they’re more likely to respond to a healthy data and lifestyle intervention than to resend to medication. Let’s talk about Alzheimer’s and cognitive decline. There is absolutely-

Dr. Weitz:  By the way… I’m sorry. When you say they’re more likely to respond to healthy diet, what type of healthy diet?

Dr. Joffe:   Well, that depends on what impact [crosstalk 00:48:23]-

Dr. Weitz:  It depends on the person still?

Dr. Joffe:   Yeah, it depends on the person, depends on the other genes. It depends on… there’s so many things I don’t want to say, but we know that we’re going to move them towards a healthier diet. It’s going to have less sugar and it’s going to have more plant foods and it’s going to have great diversity and it’s going to be safer and not have… et cetera, et cetera.

Dr. Weitz:  But just on APOE, there’s no way we could say better to be on a vegetarian diet or better to be on a ketogenic diet?

Dr. Joffe:   No, not just on APOE. First, I’m going to send you an article that they did about APOE and ketogenic that is absolutely fascinating. I’m going to send it to you, you’re going to find it very interesting. But there isn’t a single definitive job. Here’s what’s interesting. So I’ve got a family history [crosstalk 00:49:07]-

Dr. Weitz:  I guess one thing we could say is whatever diet they’re on, if they come to us and they have heart disease, then we know that’s not the right one.

Dr. Joffe:   Probably not the right one. You need to make some change, that’s always a good start. Most people don’t come to us with the perfect diet. So there is interesting stuff around APOE 34 and the ketogenic and I’m going to send it to you.

Dr. Weitz:  Thank you.

Dr. Joffe:   I don’t want to talk about it now because I actually contract with the detail and I’m part of making this of it.

Dr. Weitz:  Okay, sounds good.

Dr. Joffe:   But what makes… I come from family of Alzheimer’s. My father had two sisters, they both got Alzheimer’s young in life, so young Alzheimer’s [crosstalk 00:49:40] and I’ve known since I first started in genetics that I had E 34, so I’m carrying one of the E4s, right? Someone has got a family history like I do, and he’s having that E 34, I was convinced, but convinced that Alzheimer’s was going to be my burden to carry. That it was going to happen to me and it was going to be my life.  When I started learning more about genetics and became a bit more experienced in it, I started understanding again, this idea that a single gene, a single snip cannot determine a disease, not even Breca which is the breast cancer gene, not even Breca which is 10 times more powerful than APOE. And when we both, these what we call polygenic risk scores, where we look at a pathway, so the pathway is cognitive decline dementia, that’s the pathway.

We get more plugs, we lose connection, the neurotransmitters. So we looked at all the genes that would impact that. APOE is definitely one of them, it’s definitely significant but it’s one of them. And when we built these polygenic risk scores, so a score based on all my genes and cognitive decline, I actually landed up with a no risk. I was like, come on, I’ve spend my whole life believing I’m going to get Alzheimer’s, how’s that possible?   And the reason was I only had the E 34. But actually all the other genes that are driving cognitive, I was actually doing well. So I embrace APOE because it’s the one thing that gives us so much we can do. If you look at Dale Brisbane’s protocols now, there is so much we can do and that includes with APOE. It is not a sentence, it is not a disease, it is none of that. What it does do, and in fact they’ve done research to show that people who knew the APOE results, particularly if there was E4 made better and more lifestyle changes than those who didn’t know the APOE result.  So we teach our practitioners not to be fearful of APOE but rather to embrace it because the patients are responsive. If they understand how powerful their diet and lifestyle choices are, and especially because since Brisbane came into our lives and many other great scientists, we understand that there are so many ways we can reverse cognitive decline and APOE being a responsive gene, APO, really helps with that. So actually there’s some Alzheimer’s with E2 is more of a problem because it’s not a non-responsive one.

Dr. Weitz:  Interesting, interesting. I think it’s probably time to wrap.

Dr. Joffe:   Yeah, we can talk about APOE also for hours. I’m going to send you a link to a webinar I did on APOE [crosstalk 00:52:26]-

Dr. Weitz:  Peter T I just had like a two hour some researcher talking about APOE. So that was an interesting one. So how can, which scenarios practitioners find out about your genetic test? And by the way is there one version of it or multiple versions?

Dr. Joffe:   Single version, only one. So I don’t want you to have to figure out whether you want to buy energy, which is we don’t talk about weight, energy, exercise, everything is important to you. So it’s a single test, you can come to a 3x4genetics.com or email info@3x4genetics.com-

Dr. Weitz:  Saliva, [crosstalk 00:53:13]-

Dr. Joffe:   Saliva, Cheek Swab, easy peasy, [crosstalk 00:53:15].

Dr. Weitz:  Okay.

Dr. Joffe:   We’re drug shop, so we send it to your house, you send it back to us, goes to our lab, but remember we will always do it through a practitioner. So if you contact us, you tell us what you’re looking for, we’ll find you the best practitioner that suits what you’ve come looking for. And they are trained, they’re mentored, they’re nurtured, they’re looked after, they’re really what we call expert practitioners.

Dr. Weitz:  So what does that say for somebody like me? Let’s say if I want my patient to get that.

Dr. Joffe:   If you want to, you’d have to come. So we do a basic three-hour training. You’re not allowed to go near our product until you’ve done the basic training, which is… I’m sorry. And we want to make sure you know what you’re doing. I can hear you understand what you’re doing, right?

Dr. Weitz:  Right.

Dr. Joffe:   It’s going to be easy for you, you’re already deeply into genetics. But we want to make sure you understand polygenic risk scores. We want you to understand scientific and clinical utilities. A couple of things we want to make sure you understand before you represent our tests to your patients. When you do that, you get an amazing portal which has got an incredible back end clinical guide, everything you need to research is there. And then you go, you have access to a mentorship program.  So we have these amazing mentors that’ve been working with me for 10, 15 years that you can access in every way. We have webinars, we have a next level education program for practitioners. If you want to take your expertise to a higher level and become more specialists, we’ve got layers of education, layers of mentorship and we have an incredible community of practitioners in the U.S. totally multidisciplinary.  So chiropractors, dentists, psychiatrists, psychologists, nutritionists, doctors, natural paths who are working with our tests and are also teaching and learning from each other. We have amazing, I can see you’re in a very sports space, we have amazing sports dietician, sports people who… And I haven’t even touched on sports unfortunately, because one of our absolute areas of expertise is sports and genetics. And I have three scientists whose only job is sports genetics. So maybe another time you’ll invite me back.  And in fact not even me, you can invite them back. And they’re actually world-class to athletes as well and they’re geneticists. So they’re really, really great to talk to and it’s another whole fantastic conversation.

Dr. Weitz:  Cool. So what’s the website again?

Dr. Joffe:   3×4 Genetics. Three and then the little X, four genetics.com.

Dr. Weitz:  Excellent, excellent. Thank you so much, Dr. Joffe.

Well, thank you listeners for making it all the way through this episode of The Rational Wellness Podcast. Please take a few minutes and go to Apple podcasts and give us a five-star ratings and review. That would really help us so more people can find us in their listing of health podcasts.

I’d also like to let everybody know that I now have a few openings for new clients for nutritional consultations. If you’re interested, please call my office in Santa Monica at 310-395-3111. That’s 310-395-3111 and take one of the few openings we have now for a individual consultation for nutrition, with Dr. Ben Weitz. Thank you and see you next week.