Today we speak with researcher and gastroenterologist Dr. Leonard Weinstock. We cover how SIBO can be the underlying cause of non-digestive issues like skin conditions, pain, and others. We also cover his research and recommendations regarding low dose naltrexone for autoimmune conditions.
Dr. R’s Fast Facts
- Extra-intestinal manifestations of SIBO include:
- Restless leg syndrome – which is associated with hypertension and stroke
- Rosacea – which illustrates the gut skin connection
- Chronic pelvic pain syndrome – which can look like frequent urination, painful intercourse, prostatitis, pelvic pain, difficulty urinating
- LDN (low dose naltrexone) is an anti-narcotic drug that can increase endorphin levels and aid with certain autoimmune conditions and the immune system.
- LDN May cause insomnia in 10-15%. 40% with GI conditions may have side effects; insomnia, vivid dreams, muscle aches, diarrhea.
- Morning dosing may help with insomnia.
- How long to evaluate if LDN is working?
- It takes about 2 months.
- When starting LDN, ramp up dose over 10-14 days from 1mg to 4.5mg.
- How long do you use LDN for?
- Partially depends on the condition. Dr. Weinstock usually uses long term.
- Dr. Ruscio’s conservative recommendation:
- Permanent conditions = lifelong dosing. Conditions that go into remission = shorter term use.
- Certain probiotics can be helpful for SIBO; they may be best administered after SIBO is cleared. Or for those with SIBO negative IBS.
- IBS check is a test for intestinal autoimmunity that may suggest someone needs to be treated with prokinetic agents after SIBO treatment.
If you need help with SIBO, click here.
Episode Intro … 0:42
Extra-Intestinal Manifestations … 3:25
LDN: Low-Dose Naltrexone … 21:26
Evaluating if LDN is Working … 31:45
How Long Should One Take LDN? … 35:02
Probiotics and SIBO … 42:17
IBSchek … 51:02
Episode Wrap-up … 57:40
Download Episode (Right click on link and ‘Save As’)
LDN, Autoimmunity, and How SIBO Causes Symptoms Outside of the Gut with Dr. Leonard Weinstock
Dr. Michael Ruscio: Hey everyone, welcome to Dr. Ruscio Radio. This is Dr. Ruscio. I am here with Dr. Leonard Weinstock, and we’re going to be talking about some extra-intestinal or outside of the intestinal tract manifestations of SIBO, which I think is going to be a fascinating topic. So, Leonard, welcome to the show, and thanks for being on!
Dr. Leonard Weinstock: Thank you so much!
DrMR: Absolutely! Absolutely! I think we first met at the SIBO Symposium. I know we run in some of the same circles. And I’ve always been really impressed with the information that you’ve presented so I’m really excited to be having this discussion. But before we jump into that, tell people a little bit about your training and experience with SIBO before we launch in.
DrLW: Okay. Well, I can jump into this as pre-and-post SIBO. So half my career was basically the routine, standard, conservative GI practice. Was trained at Washington University, a very traditional, conservative training program. And yet, I’ve always thought outside the box in general, no matter what I did. So that was 1987.
And then, I had an interest in irritable bowel syndrome. In fact, I was on an Internet panel that helped the IBS support group through with questions on pharmacology. And one of the questions came out to me on the Internet on, about 2000—I think it was October 2000—and said, “Well, what’s going on with antibiotic treatment of irritable bowel syndrome?”
And that was funny because the journal, the American Journal of Gastroenterology, was sitting on my desk and the Red Journal. I picked it up, and lo and behold, there was the article by Lin and Pimentel on treatment of bacterial overgrowth in irritable bowel syndrome. And how neomycin, when it reversed the breath test abnormality, resulted in improvement in the IBS.
And so that started my Y2K, so to speak, and made my life change in the way I viewed irritable bowel syndrome, thinking of it in a different way. So that’s the pre-and-post SIBO era. And then, I changed even further midway through the decade in 2005 when Xifaxan or rifaximin was released in the U.S. market.
DrMR: Got you. And I know you’ve spoken quite a bit about some of the extra-intestinal manifestations. And this is something that we’ve discussed in the Podcast, where I’m not certainly on the cutting-edge of all the research that speaks to the non-digestive manifestations of SIBO, but it’s certainly something that I see in the clinic. And I think many people understand that the gut connects to many other systems of the body. So it’s not too much of a jump to think that if we correct a problem in the gut that may manifest as improved skin or improved sleep or what have you.
But I know you’ve been involved in some of the published research in this regard, so there’s definitely a few things I’d love for us to expand upon. And one of the things I know that you’ve published regarding, or speak a lot about also is restless leg syndrome. So can you tell people what that syndrome is and more about the SIBO connection to that?
DrLW: Absolutely. Well, the SIBO connection to that was a lightbulb moment for me, if you will. In 2005, Mark Pimentel was talking about Xifaxan in treatment of irritable bowel syndrome and the breath test abnormalities in IBS and in fibromyalgia. And at that time, I was treating—something you shouldn’t do—but I was treating a relative who had post infectious irritable bowel syndrome and suffered primarily from restless leg syndrome.
And so when I got back from the meeting, I asked him did his symptoms of restless leg syndrome start alongside the IBS and was it in reference to an infectious phenomenon. And indeed, 14 years earlier, he had acquired an infection, a diarrheal infection. And then sometime later, he wound up getting a terrible bout of restless leg syndrome and a mild condition of irritable bowel syndrome. And so I offered him rifaximin and treated him. And he got dramatically better. And then, I starting thinking, “Well, why would that be?” And then, I looked at fibromyalgia, and it turns out 20% of people with fibromyalgia have restless leg syndrome. So it’s highly associated with it.
So jumping from that, I thought, “Well, okay, we can jump over fibromyalgia and say that IBS and restless leg syndrome are linked with a common mechanism,” namely small intestinal bacterial overgrowth. And I’ve learned a few things since then that I can embellish upon the relationship and other factors that go into it because it’s not just SIBO that’s the major factor for restless leg syndrome.
DrMR: And for the people listening, restless leg, of course, manifests as the inability to keep one’s leg still, I guess you could say. But are there other factors of this also associated with, for example, I believe it can be associated with insomnia or a hard time sleeping? So what are some other things that can affect people as a secondary byproduct of the restless leg?
DrLW: Okay. So basically, there’s four basic criteria: the compelling urge to move, often with discomfort. And it can be a creepy, crawly feeling. It can be a tingling, a numbness, or just the urge to move. It can drive people crazy. It generally starts when they’re at rest, and generally at night. And it worsens at bedtime. And then, when you get up and walk around, those symptoms go away. And then, there’s a fifth component, which is to exclude other or less-like conditions like sciatica or back pain that could reproduce the same set of symptoms or nerve pain in the back from a disc. But it’s always that compelling urge to move. And some people, it starts earlier. It can be on a car ride, a plane ride. And that just prevents the people from going to bed.
Now, it’s a lot more than just that. If people are fatigued, they don’t get good sleep. That’s one phenomenon. There is an association with periodic motor limb disturbance, where there’s kicking that’s unconscious kicking and jerking, which can drive the bed partner out of the bed. But it also is associated with more severe phenomenon, namely hypertension and stroke. So we don’t know exactly why, but it probably is related to the sympathetic tone that’s increased.
DrMR: Do you think there’s a tie in with how that affects sleep? Because I know certainly, things that interfere with sleep have been pretty tightly linked to different cardiovascular mortalities and morbidities. Do you think there’s a tie-in there?
DrLW: It certainly could be. That has not been definitively worked out. Just the association, an increased risk have been.
DrMR: Got you. Got you. And what about rosacea? I know this is something else that you’ve spoken about. And certainly, there’s the old philosophy in naturopathic medicine where the skin is a reflection of the gut. And I think this is why it’s probably not uncommon for that provider to see in a patient that if they clear up dysbiosis or SIBO or get a patient off of a food that they’re intolerant to like dairy, for example, if they have a dairy intolerance, they see the skin improve.
So tell us a little bit more about the connection between SIBO and…And for the audience, rosacea—and, Leonard, if you want to give a better definition than I do, please go ahead—but rosacea is essentially this rosiness of the cheeks that many people find unpleasant cause it is fairly pronounced. So tell us a little bit more about this, Leonard.
DrLW: Okay. So rosacea, there are several different stages and classifications. But one is the rosiness and flushing, so the redness and flushing. And that gets worse with changes in temperature or heat. Then, one can develop pustules and papules, which can be normally uncomfortable because of stinging and discomfort, but very bothersome with a poor quality of life because it’s embarrassing. They have this terrible look. Thickening of the skin is another phenomenon. So they can get thickening of the cheek, skin, or the nose—phimosis—so that a W.C. Fields’ nose can develop.
And then there’s ocular rosacea, which is mainly dryness, crusting around the eyelids, decreased tears, so dry eye, a foreign body sensation in the eye. And that’s one of the research projects that I just published on in terms of the incidence of SIBO and ocular rosacea and what the outcome was with rifaximin.
But, Michael, the gut and rosacea’s been tied together since the 13th Century. Alcoholism and obesity in pictures in Chaucer’s books have suggested a relationship. And then, I looked this up in our rare book collection, going back to the textbooks in 1895 on rosacea. And it was associated with dyspepsia. And then, going through the literature, in the 20s through the 60s, people were interested in food allergies, and the relationship, then achlorhydria, which probably was due to Helicobacter. And celiac-type conditions in the late 60s have been associated with chronic pancreatitis, which probably is related to either small intestinal bacterial overgrowth or possibly alcoholism, too, which is associated with it. Then a number of studies with H. pylori in the 1990s, and then even relationship to Crohn’s disease and ulcerative colitis.
And I published a relationship in terms of my patients with Crohn’s disease, how when they were treated the rosacea got better. Their GI symptoms went away. Their Crohn’s went into remission. Their rosacea got better, which was a pretty cool thing.
And then finally just to wrap up, the diagnosis of small intestinal bacterial overgrowth, in the setting of rosacea, was evaluated by Italians, a research group. And they found a definite relationship in treating the group with bacterial overgrowth—with either placebo versus rifaximin—showed a dramatic improvement. And then, when the placebo patients were treated, they responded very well to the rifaximin, as well. So they cleared—just clearing up the SIBO and the breath test led to 85% resolution of all rosacea findings in the patients.
DrMR: That’s a great point that you’re making. And I’m so glad that you made that point. And it’s something that we’ve discussed on the Podcast many times, which is, just because two things are associated doesn’t mean treating the one is going to have a positive impact on the other. So it’s great that we have the treatment data and we can actually show by treating the SIBO, we can see improvements in the rosacea.
DrLW: Right. So in the Italian article, they found that 47% of 133 patients had abnormal breath tests. And I tried to duplicate their study. And I looked at 57 patients. And 51% had an abnormal breath test. And in my study, 65% had a marked to moderate response in their condition. So I was, of course, very happy with that. The patients were happy. And I gave some…It was an open-label study. But it was helpful in terms of confirming what the investigators in Italy found.
DrMR: Right. Yeah, and it’s important I think that we continue to publish this research just to keep moving forward the position that there might be a gut component to a lot of these non-gut diseases. And certainly, this is something I think many people, from our audience, are familiar with. And it’s just nice to start seeing the published literature reflect that. So this is not some airy-fairy, left-winged concept, but it’s actually something we have some published clinical science to support. So a hat tip to you for verifying or trying to verify their study’s results as best you can.
Something else, Leonard, that I know you talk about—and I’d be curious to get some elaboration on is chronic pelvic pain syndrome. So can you tell people, for people who might not be familiar with what chronic pelvic pain syndrome manifests as, what this typically looks like? And what the SIBO tie-in to this is?
DrLW: Okay. Well, basically, when I got home from that meeting and I made the connection of RLS, I started looking at everything listed as a syndrome and what other syndromes could be going on. Little did I know that at UCLA Cedars-Sinai, where they were getting their patent on rifaximin, they looked at every disease and syndrome known to man and had a patent for the—a use patent for treating those conditions. But nobody had actually published anything. So I looked at interstitial cystitis syndrome. And some of my patients had it. And it was actually well known in irritable bowel syndrome, that up to 5% to 10% have increased urinary frequency and discomfort.
And so looking at interstitial cystitis, I realized, okay, reading about it. As a gastroenterologist, we’re not really included in that research or in that patient phenomenon. They go directly to the urologist. But they’re basically syndrome patients who have severe symptoms, that frequent urination, urgency, get up. I have patients get up 20 times at night to urinate little bits. And they have pelvic pain and pain with intercourse. And nobody knows what’s going on. It’s thought to be visceral hypersensitivity, which is the watch-word for irritable bowel syndrome, as well. And they can have inflammatory markers in their urine, but patients really suffer.
So I thought, “This is one group to study.” And so I actually got a very good urologist to collaborate who sent a number of patients. And with that, it seemed like, with an open-label study, that people had a good response. I’ll go over that later.
The other main chronic pelvic pain disorder is in men, which is chronic prostatitis type III. So even though they “have prostatitis inflammation,” it can be hard to detect. When the urologist massages the prostate, they may or may not have white cells. But they don’t have bacteria. And then, when you look at inflammatory markers, there are a number of prostaglandin abnormalities that can be seen in the urine. And yet, again it starts to be a visceral hypersensitivity. And the symptoms are pain in the pelvic area, pain in the testicle, pain in the perineal area, urinary discomfort, and pain with intercourse.
So they’re very similar, men and women. And yet, it’s another big unknown. And so I did studies on both sets of patients, open-label for the IC looked very promising. And the problem, and I was told this years ago when I was studying it in 2008, he said, which was, “If you have a positive study in interstitial cystitis, report it because there’s a chance that it’s going to backfire. And it’s not going to work.”
Well, indeed, I did a double-blind study in 30 patients. And it was shown not to work, namely treatment of bacterial overgrowth was shown not to be effective in interstitial cystitis. In the chronic prostatitis study, it did show a positive, significant value, P-value in treatment using rifaximin.
And where I’m heading now with these patients, and really just waiting for the right patients to be referred, is treating them with low-dose naltrexone to reduce the neuroinflammatory pain that may be present. So everything can’t be viewed as just one problem. And so you really have to think out of the box and think, “Well, how else could this be going? What else could be going on? And how can you deal with it?” And that’s actually where things have led in restless leg syndrome, too.
LDN: Low-Dose Naltrexone
DrMR: Mmm hmm, I’m glad you brought up low-dose naltrexone because that was one of the next questions I wanted to ask knowing that you use rifaximin quite often for SIBO. But you’ve been using LDN or low-dose naltrexone in conjunction with that. So I wanted to segue us next into the treatment with rifaximin and LDN, and how you’re using those. And just for people listening, low-dose naltrexone…Well, actually, doc, why don’t you give the layperson definition of low-dose naltrexone just for people who haven’t heard of it. And then, we can go into the treatment using both rifaximin and LDN.
DrLW: Absolutely. Well, naltrexone is in the anti-opiate. And used in the normal FDA-approved doses for this drug that came out in 1984, it’s used to prevent alcohol abuse and narcotic abuse in people who
have weaned off of them, especially for narcotics. So once a narcotic abuser is off, then you can start this drug, given enough time, so they don’t have a withdrawal. And then, while they’re taking it, it basically decreases their interest in taking narcotics. And if they take narcotics, they don’t get an effect because they’re taking basically an anti-narcotic. And somehow, the same kind of phenomenon occurs in alcoholism. Although, it can be started while somebody abusing alcohol. And it decreases the effectiveness and desire to drink.
Now, what was found by Dr. Bellary in 1984 was that using this drug in a very, very low dose increased endorphin levels. So basically, although it’s an anti-narcotic, it binds to opioid-producing cells or endorphin-producing cells, and blocks it temporarily. And then, while it’s hanging on to the receptors for four hours or so, the cells and the body say, “Okay, we’re deficient in endorphins. Let’s make more receptors and gear up.” And basically, there’s a rebound phenomenon that occurs. And more endorphins are produced. Fifteen-fold more endorphins are produced when you’re giving somebody low-dose naltrexone. So basically, in doses of 0.5 to 4.5 milligrams, you get a very short-acting drug that tricks the body into producing more endorphins. And endorphins play a very important role. Did I elaborate, Mike?
DrMR: Yeah, let’s go more into the role of endorphins because I’m sure people are curious as to what kind of health benefits can be garnered by that.
DrLW: Okay. So basically, what they do is they regulate T and B cells, which are lymphocytes. And many of our diseases that we deal with, such as autoimmune diseases, Crohn’s disease, multiple sclerosis, there’s upregulation of these cells. And also LDN triggers the production of Tregs, so T-cells’ regulating cells. And so with that, the consequence of hyper T-cells is reduced so there’s less interleukin and cytokine production that causes inflammation and damage to the body. There’s less TNF-alpha production, which causes damage to the intestinal lining, chronic fatigue. It can also be responsible for central fatigue and depression.
And then finally, as it plays a role in complex regional pain syndrome and central pain phenomenon, such as fibromyalgia, the naltrexone, it basically—it goes to the inflammatory cells, the macrophages that are sitting on top of the sensory nerves, and it diminishes the activity of those inflammatory cells, which then in turn would decrease the sensory nerve function. And so it has this toll receptor blockade that’s so important in regulating neuroinflammatory pain.
DrMR: And I know that LDN’s been studied in, gosh, a plethora of conditions. Is that correct? Has there been quite a number of conditions where this has been evaluated?
DrLW: Yes. So 176 conditions, if you will. On the LDNResearchTrust.org website, I helped go from a list to more of groupings of disorders and diseases by system’s approach, ranging from the brain to the heart to the gut, and so forth, and went through all the lists that they had. And it was 176 conditions, pretty, pretty remarkable.
DrMR: Yeah. Wow! And so I think that if people have heard of this, or when they hear of it, and how many conditions this has been studied in, it’s not unreasonable for someone to include, “Well, irrespective of the condition, why don’t I just give this a try, and see if it benefits?” So would you say that people need to be more discerning? Or is a short-term and peered trial of this something that you think is generally safe?
DrLW: I think it’s one of the safest drugs we’ve got around. And in terms of side effects, I actually published a study on this. You can look at the double-blind studies that have been done. And generally, it’s a 10% to 15% incidence of insomnia and vivid dreams. I looked at my patients with gastrointestinal illnesses. And actually, the number of side effects were in the 40% range, just a whole variety of things. Many of them were temporary. But I had about a 15% dropout rate because people couldn’t tolerate the insomnia, the vivid dreams, headaches, rare muscle aches, rare diarrhea, very rare depression.
In fact, studies have been done, which just came out as double-blind studies showing actually improvement in depression in patients taking LDN. And so, and yet, none of these things are permanent. They go away. Some people get over it. Some of the insomnia problems go away if you change from the night time dosing to the morning dosing. And you can get a reasonable effectiveness. The business of the nighttime versus morning is that most endorphins are made in the two and four a.m. time. And so theoretically, if you take your LDN at 9 or 10, you block it. And then, you get a rebound when there’s the normal circadian rhythm. So that’s one thing can be done.
And let me just check if the ambient noise is too much, hold on one second.
DrLW: Okay. So most people who prescribe will recommend nightly dosing. For a long time, I was getting tired of the emails saying, “You know, I can’t sleep, so I went to all morning.” But it’s funny. I had a patient with restless leg syndrome who was taking herbal therapy for SIBO. And the herbal therapies, as you know are for usually three to four herbs and numerous pills. And she was getting so confused that she got confused and took her LDN at night and had her best sleep ever and had no urge to move. And so she wrote back saying, “Should she take it at night?” And I’m saying to myself, “Oh, maybe I should have given more in my publication nighttime LDN.” So I’m back to that phase. And then, I’ll just change it if they complain.
Evaluating if LDN is Working
DrMR: So something else that I think a lot of people are wondering is what is a reasonable window to be on LDN, in which to evaluate if it’s going to work for them or not?
DrLW: I think you’ll know by two months.
DrMR: Two months.
DrLW: Yeah. First of all, in general, you should ramp up over one to two weeks, 10 to 14 days to gradually increase the dose. Some people will also say if you have an autoimmune disease like thyrotoxicosis, Hashimoto’s, that you should only go to three milligrams. And more is not better. The anti-inflammatory dose though is thought to be 4.5 milligrams. And then, it can take definitely two months to get a full benefit. And if you don’t have it by then, I don’t think you will.
DrMR: And what’s a typical dose that you like to see people start at?
DrLW: I’m doing one milligram. But I do a little bit by body weight. So if they’re heavier, I will start off with a half of three milligrams, so it’s 1.5, then three to seven days, go up to three, then three to seven days later go up to 4.5.
DrMR: Okay. And I know that you’re using—at least, as I understand it, and if I’m wrong in this please correct me—but you’re pairing rifaximin with LDN. Rifaximin for treating the SIBO, LDN as a prokinetic to prevent SIBO reoccurrence. I guess first question is it is correct for me to say that that’s a typical pairing that you use when it’s appropriate?
DrLW: It’s a common pairing. So if patients have extra intestinal manifestations with their SIBO and their IBS—so they have restless leg syndrome. They have rosacea with it. They have severe chronic fatigue—I will definitely give LDN with it. So there are just a few studies, mostly in animals and one in humans, looking at endorphins and the effect on the migrating motor complex. And it appeared to be effective. And accordingly, I’ve given it to patients with idiopathic constipation who have failed other therapies. And it’s helped, not everybody. But it’s helped about 40%. And so I definitely will give it for prokinetic therapy. The typical prokinetics are the low-dose erythromycin, which mimics motilin, and then low doses of prucalopride available in Canada, which is a serotonin agent.
A probiotic for milder cases of IBS/SIBO would be bifidobacter species because those have been shown in animal models to increase the migrating motor complex. So I’ll give those at night, as well.
How Long Should One Take LDN?
DrMR: Got you. Now, coming back to LDN for a moment, the other thing I think people wonder about is, if they do respond, is it something they should be taking in perpetuity? Should they take it for a certain amount of time and then wean off, take a drug holiday so to speak, and see if they maintain the improvement or what have you? So do you have guidelines for the longer term application if someone does respond to LDN?
DrLW: Yes. So restless leg syndrome is a permanent condition. The only ones where it’s not is where they’re iron deficient for a particular reason, and treatment with iron gets them better. Otherwise, there’s an abnormality. And my research partner, Art Walters, discovered the endorphin deficiency associated with restless leg syndrome. So he actually did dissections on autopsy brain material in RLS patients, and found that there was decreased number of endorphin-producing cells.
And then, other research looked at, in animal models, iron depleted mouse model and giving endorphin, by giving endorphins to those mice improved the dopamine function. And it’s also shown in humans with a PET scan study. So if you don’t have enough endorphin-producing cells, then under the situation of iron deficiency, central iron deficiency or a genetic reason for getting RLS, you’re going to have troubles. So I think it’s long term, and once again, don’t do this at home.
But the second patient I treated with restless leg syndrome was my wife who had constipation disorder and restless leg syndrome, and had it badly for three years. And she got a breath test, and was a methane producer. I treated her with dual-antibiotic therapy. And I gave her LDN, in part, because she was taking a statin cholesterol medicine. And this is how I just by luck tripped into this because there was no report at that time of endorphin deficiency. And she had a dramatic response. And so she stayed on the naltrexone at night. And I was using it as “a prokinetic agent.” But actually, it may well have augmented the response, and has done a great job.
And I’ve seen it, where if patients don’t have SIBO, they still can improve. And so I published that data in the LDN book—a book that just came out–with Linda Elsegood, is the editor. And so in those patients where the lactulose breath test was normal…Let’s see, there were seven patients. Two were markedly better. Two were moderately better. And three had no change. So they were what I term 57% responders.
And then, I looked at some data recently of patients since that 2014 data. And I’ve had a dramatic response, in particular, by a woman who couldn’t go on the plane without just being distressed and having to walk around the airplane when she could. Couldn’t go to sleep, would have to sleep with the full body pillow so her legs wouldn’t be near each other and rub. And literally, and this is the crazy part, one day after LDN, she was dramatically better, a dramatic response, and has maintained it for nine months, and so far.
So I’m giving LDN long term in these individuals. And if you think of yourself as being an endorphin-deficient person for whatever reason, or endorphins is a good healthy thing, as good as a multivitamin, then I don’t see the harm.
DrMR: So do you notice a certain presentation that may lend itself to more improvement? For example, two people come in. One person is extroverted, happy-go-lucky. They seem like that more endorphin-rich person, compared to someone else who maybe is a bit more introverted, mellow, melancholy. Is it fair to say that you’ve observed any way that the people that may present like their more endorphin-deficient respond better?
DrLW: Interesting. I don’t know I can state that one way or another. I know there are chiropractors that will say somebody’s more sympathetic high tone or low tone, which they can tell by their examination. I can’t. But I can say that I see patients with IBS who have systemic manifestations of something going on. Their skin is ashen. They have fatigue. They’re depressed. And these patients do better when treated aggressively, whether it’s additional therapy for increase in intestinal permeability, or adding LDN early on in their protocol.
DrMR: Mmm hmm. Mmm hmm. And so for conditions that have more of a relapsing, remitting prognosis or manifestation, do you also participate in long-term dose? Like, if someone has IBD, and it doesn’t seem to be a very severe case of IBD, so it has pretty long periods of being in remission, do you use it until they’ve been in remission for a few months, and then curtail them off and maybe have them go back on in the future if symptoms start to reoccur? Or are you doing long term across the board?
DrLW: Oh, long term. So I’ve had patients on LDN, with IBD, for eight, nine years now. And I don’t stop it. You think about all the drugs that we use for inflammatory bowel disease. And every single one has serious complications and problems.
Probiotics and SIBO
DrMR: Right. Right. No, it totally makes sense to me because the stronger you go with the IBD drug classes, the more the side effects tend to go up, almost exponentially. So I totally agree with you there.
I quickly wanted to ask you your take on probiotics. And my thinking here is it’s great at some of these conferences like the SIBO Symposium. And there’s also, I think we’re both going to be speaking at the Integrative SIBO Symposium. And I’ll see if we can fish out a link for that, which I believe is in Chicago in March of next year. It’s great—
DrLW: March 25th.
DrMR: Twenty-fifth. Okay. Good. And it is entitled the Integrative SIBO Symposium, right?
DrMR: Okay. Thank you. So it’s great at these conferences where we have different types of allied health care providers and conventional providers coming together. And all giving their take on how we can help patients experience better outcomes. One of the things that I found—I don’t want to say a bit odd.
Maybe that’s not the most tactful term—but it struck me is that, even though it seems that there’s a fair amount of high-quality data like systematic reviews and systematic reviews of meta-analyses, and certainly, of course, you can’t have those without a number of randomized-controlled trials that show that probiotics seem to have overall benefit in a very, very small amount of adverse events for IBS, so if probiotics help IBS, I’m at a bit of a loss why some gastroenterologists are pretty resistant to the use of probiotics for SIBO.
But I think that’s starting to change. And it seems like you have a little bit more of a maybe a middle of the road in this, where you don’t take a hard stance at either end of the spectrum. But that’s how I look at this. And so that’s why I’m curious to hear what your take is regarding probiotics and SIBO.
DrLW: Okay. Well, I think they have a healing role. But if somebody’s loaded up with bacteria, I don’t give the probiotics while I’m giving antibiotic or herbal antibiotic therapy. I give it as a second step, as a healing role. If I get a patient, whose breath test negative, and yet they’re bloating, then I’ll give a line Bifidobacterium infantis because it’s been shown in double-blind placebo-controlled study to be effective in improving bloating. If somebody’s more along the line of diarrhea, then Florastor, S. boulardii, or VSL3 will be my drugs of choice.
DrMR: Got you. Okay, I think that’s reasonable.
DrLW: And then, the problem is there’s so many probiotics out there. How do we judge what’s better than another? And it’s hard. There have been studies using culturelle and helping kids get over antibiotic-associated diarrhea, but not C. diff., sooner than not. So that’s something that I’ll apply to my practice. But the problem is what really works and how. It’s tough.
DrMR: I agree. And just for the healthcare consumer who might be listening to or reading this, you do have to be careful with probiotics because it seems every few weeks there’s a new probiotic out there. And I think that’s great from one perspective of, “Let’s try to research more and have a broader array of probiotics that might be able to help people.”
But you also have to be careful because, just because there’s a new probiotic, doesn’t mean it’s any better than the probiotics we currently have. And certainly, until we have some research to show if these things are actually going to be beneficial or not, we should be a little careful about the use of a probiotic.
And I say that because at least once a week, I get a patient asking about a new probiotic that has almost no research to support it, but they have a really good marketing campaign. And people get sucked in. So let’s be progressive. But also, let’s be a little bit cautious in how we look at probiotics. And I totally share some of your concerns, Leonard.
Something else I wanted to get your take on. And I know you aren’t an expert in SIFO. But I’m curious. We had Dr. Satish Rao on a while ago. He’s the SIBO guy, or SIFO guy, excuse me. And he’s been using, in conjunction with SIBO treatment, 100 milligrams of fluconazole. So is this something that you have any experience with? And if so, what’s your thoughts on that?
DrLW: And I think they can co-exist, certainly. The same reasons why we’ve got a bacteria in a stagnant loop, your fungus can be stagnant, too. I’ve addressed this question to Henry Lin who I respect as a microbiologist and gastroenterologist. And many people, most people are black and white. They say there is no role of fungus in the gut below the esophagus and above the rectum.
So it’s something that we’re not trained in. We don’t have good diagnostic tools for it. There’s no good breath test for it. And examining with a microscope the stool to see fungus, we all have fungus in our stools. So it’s a problem. And yet, this whole bit of candida is widespread. And the whole idea of low-sugar diets making people better. Well, you give a SIBO patient a low-sugar diet, they get better.
And there are ancillary tests that frankly I’m not trained in. Chemical tests and so forth, which may well have merit. Now, that said, when I’ve got a SIBO patient who is not responding or gets a 70% response, but still has bad bloating, I will treat them for possible fungus. And I have one patient who’s very smart. A nurse who runs a home nursing agency. And I just kept on treating her. I’ve treated her probably three times for SIBO.
And we’re both, “Look, well, what else could it be?” Treated her for fungus, and a dramatic response. Could not believe how much she got better. Although, I’m sure, I’m the outsider giving you that rendition saying, “You know, I didn’t believe it. I didn’t believe it. Now, I do believe it.” But I would love to be able to be turned on to a truly good diagnostic test to know when to treat with antifungal medicine.
DrMR: Well, Dr. Rao made me aware of something that I thought was fascinating—and hopefully, it will be available in the somewhat near future—is like a smart pill that can take samples in the small intestine. And then, I suppose, do a culture from the pill or maybe there would even be sensors inside the pill, itself, that would be able to give you a read. But essentially, capsules that have timers on them that would be able to duodenal and degeneral, what have you samples to give an idea of the fungal environment in the gut. So that’s something that seems pretty exciting.
DrLW: Interesting. How about there’s, oh, chemical changes that can be measured—
DrMR: The organic acids?
DrLW: Yeah, the organic acids. So what…
DrMR: Well, that’s a good question. And that’s something that we’re making some preparations to do a comprehensive review on the literature for what the organic acid show in terms of fungus and if, more so, if there’s any treatment data showing that a certain organic acid finding that may “suggest fungus,” if then treated, correlates with some beneficial outcome.
So I’m open to organic acids. I’m a little bit suspicious at the same time. And so we’re going to perform that review of the literature. And hopefully, sometime in the next few months, we’ll report back with a podcast or an article on that. So I share the same question that you do, Leonard. And hopefully, we’ll have a decent answer for that sometime soon.
DrMR: One final question for you. And if it’s quick, maybe a quick follow-up second to that. But IBSchek seems like a great test for screening or trying to differentiate between diarrheal IBS versus IBD. But there are others who are maybe trying to use it to predict response to prokinetics or maybe even monitor excessive therapy. And I’ve heard varying things about some clinicians finding it helpful. Others finding the correlation doesn’t seem to really be there. And they were left scratching their heads after running this test for a few months. What’s your experience, if any, with IBSchek?
And I’m sorry. For the audience, IBSchek is a test that you can use to quantify or detect autoimmunity to the motility apparatus in the gut that may underlie SIBO so that when food doesn’t move through the intestines at the appropriate pace, when there’s not healthy motility, that can be one of the factors leading to SIBO. And so this test can identify if the underlying autoimmunity that can drive this motility impairment is present. And that test is known as IBSchek.
DrLW: Correct. So the anti-vinculin is a critical antibody in that, which binds to nerves and damages nerves, the interstitial cells of the Cajal that are responsible for that important migrating motor complex. And there’s evidence that if you take away insults to the migrating motor complex, one way or another, they can regenerate. So there’s some hope that if we can treat the autoimmune phenomenon possibly with naltrexone, or who knows if there’s something more specific for anti-vinculin that you might be able to get your motility back.
But basically, the exciting thing about the anti-vinculin phenomenon is that post-infectious irritable bowel syndrome may well count for 60% of irritable bowel syndrome, as opposed to what was thought of before just by history of 20% to 30%. So again, it gives us an explanation. It takes the syndrome away from IBS, if you will, and puts it more as irritable bowel disease and more of a phenomenon of an autoimmune condition that allows for bacterial overgrowth. And yes, if the levels are high, there’s some suggestion in preliminary work that their symptoms are worse.
When a patient comes to me and has multiple relapses, I will get an IBSchek at that time. And if it’s negative, then I have to really start thinking a lot harder, A) how to treat them, B) what’s causing their bacterial overgrowth, because there are many, many causes for IBS with small intestinal bacterial overgrowth. And it could be adhesions, as we saw at the last SIBO conference. In fact, I just in the last month, opened a branch of Clear Passage, which deals with adhesions, lice’s treatments manually from the outside. And so I’m excited about that, adding that modality to my treatment protocol. And also, it gives patients some feeling of validity that they have a disease. And it’s not psychological.
DrMR: So do you not give a prokinetic if someone has IBSchek negative? Or are you only ordering it in non-responsive patients? Is that how you’re using it?
DrLW: No, I’ll do it in both. Both in conjunction with LBT with a new patient and with non-responders or rapid relapsers, because especially if they’ve had a history of surgery and adhesions or surgery, let’s say in endometriosis, I want to dissect that away. So if their IBSchek is positive, then I’m less apt to worry about adhesions as being the main phenomenon.
Although, I do have a patient whose problems all started after surgery, complicated surgery. And she is IBSchek-test positive. So it can be maddening at times. So a range, a wide range, they kept the range of what’s normal and what’s abnormal a little bit wide so they’d capture enough patients in those ranges to be “diagnostic,” but to separate it from celiac and inflammatory bowel disease.
And yet, you look at the papers. And a number of the patients with IBS, I’m sorry, IBD and celiac have an anti-vinculin. But then again, that’s where I think of phenomenon like ANAs. ANAs’ common in women, antinuclear antibodies. And yet, if the levels are low, we don’t worry about it. We just chalk it up to some minor autoimmune condition.
DrMR: Mmm hmm. And I’m glad you make that last point because sometimes I think people see an autoimmune marker positive. And they can freak out. And I think it’s our job, as clinicians, to educate people on what dictates risk and what may not really have any huge clinical meaning or prognostic weight. And, Leonard, are you finding that the IBSchek status is somewhat predictive to someone’s response to a prokinetic?
DrLW: I haven’t studied it to be able to say that.
Episode Wrap Up
DrMR: Okay. Fair enough. All right, my friend, well, I’ll let you go. I know this has been a longer call. But it’s been a great conversation. Is there anything else you would like to mention in close? And then, would you also please tell people where they can connect with you, whether it be a website or a blog or what have you.
DrLW: Okay. Well, basically if you’re suffering from IBS, it’s not in your head. It’s an organic condition convinced in most patients. And if you don’t have a doctor that only does a colonoscopy and basically hands you a Bentyl pill, you got to find somebody else who’s a little more compassionate. There are many things that we can do with, both FDA-approved medications and non-FDA-approved techniques, in terms of improving your health.
And with respect to syndromes, once again, I have to say that it’s unfortunate that medical doctors often blame the syndrome on the patient, dealing with POTS patients-Postural Orthostatic Tachycardia Syndrome patients. And they look normal on the inside. But they have 50 different symptoms that they can have from autonomic dysfunction. And it’s terrible because they are left out in the cold, as far as medical caregivers, so look for that.
As far as information, I’ve got quite a bit of information on my website, GIDoctor.net. And LDN, there’s some very good resources, LDNScience.org, LDNResearchTrust.org. And then my papers, research papers are on the website. And then, as far as LDN on the Research Trust, there’s a list of prescribers in the 50 states and across the world. And many doctors don’t want to prescribe off-label, which is when you’re dealing with a very safe medication at a much, much lower dose of medication is really unfortunate. And yet, the people can find providers.
DrMR: Well, I think that’s very well said. And, Leonard, thank you again for your time. And if I don’t speak with you before then, then I guess I’ll at the very least see you at the Integrative SIBO Symposium in Chicago in March.
DrLW: My pleasure. Thank you for the interview.
DrMR: Absolutely, Leonard, take care.
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