We recently discussed Mast Cell Activation Syndrome with Dr. Lawrence Afrin. Today we dive into part 2 of this discussion and tackle mostly audience questions in the diagnosis, treatment and troubleshooting of MCAS.
Dr. Michael Ruscio, DC: Hey, everyone. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio. Today, I am here with Dr. Lawrence Afrin (of Armonk Integrative Medicine) who was on the show a few months ago. We talked about mast cell activation syndrome, and today he is back to do predominantly a listener question/answer session. And, Larry, thanks for coming back on the show.
Dr. Lawrence Afrin: My pleasure, Michael. Appreciate the opportunity.
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Dr. R’s Fast Facts Summary
When mast cells release, can it feel similar to a hot flash?
- Yes, a flare can feel like a hot flash.
Can MCAS in the GI Tract cause symptoms such as anxiety, brain fog & extreme hunger immediately after eating?
- Yes, however, MCAS is a systemic condition it is not just limited to the gut. Mast cells anywhere in the body can cause symptoms anywhere in the body.
Should someone do a biopsy or test the suite of markers noted in the previous episode?
- Biopsy – can be used, but may not fully identify the issue.
- Increased mast cell density does not necessarily imply over activation.
- We don’t yet understand the correlation between how many mast cells and their state of activation.
- Additionally, it is helpful to perform a blood and urine test.
Can MCAS cause IBS? And is there any link between estrogen and MCAS, in the gut?
- There have not been any studies that show MCAS has caused IBS. There is certainly some suspicion but more research is needed.
What is the difference between the classification of Primary and Secondary MCAS?
- Primary MCAS – The Mast Cells themselves are fundamentally abnormal.
- There is currently no clinical testing available for this.
- Secondary MCAS – Totally normal Mast Cells that are being activated in response to something else like an infection, autoimmune disease, malignancy.
- There is no testing available that can definitively distinguish the two.
- There is a third classification.
- Idiopathic MCAS is the most prominent, basically if you can’t prove that it’s either primary or secondary, it’s classified as idiopathic.
**Keep in mind this is a VERY broad division of classifications
How do we test this? Can we test it in Australia?
- It is recommended that you go through H1 and H2 antihistamine treatment trials while waiting on test results, see previous podcast for protocol.
- One could fail OTC (over the counter) antihistamines, but respond to other drugs. This is why testing is important.
- Most MCAS patients will experience noticeable improvements on OTC antihistamines alone, but the majority will need the addition of an Rx to achieve full resolution.
- Initial adverse events to H1 or H2 blockers could still indicate that patients need treatment – it could be an excipient that is causing a reaction. Trying to identify the excipient can be important. (Excipient – inactive substance that serves as the vehicle or medium for a drug or other active substance)
- Unsure about the testing availability in Australia.
Questionnaire – a validated questionnaire can be obtained from this study.
Can cold induced urticaria be due to MCAS? And if so, is it due to an underlying gut issue like SIBO?
- Yes urticaria could be due to MCAS.
- There is not enough research or evidence to explain if it could or could not be induced by gut health issues like SIBO.
- Gut health issues, like SIBO, can present with symptoms like urticaria, working to clean up the gut can resolve these issues in some cases. More research is needed to determine if MCAS plays a role here.
Can you discuss the new research into the benefits of LDN regarding Mast Cell Activation?
- Some patients are seeing nice responses to LDN (low dose Naltrexone)
- We’re still a long way away from any research or evidence
Could you give a rough estimation of how many patients would achieve some degree of notable improvement on over-the-counter antihistamines compared to how many would have to go on to a prescription drug level therapy?
- Most MCAS patients do experience some meaningful degree of improvement on just H1 and H2 blockers.
- A lucky few experience what they consider to be a satisfactory level of symptom improvement. A great majority of patients do go on to try additional medications beyond antihistamines in order to get them to that goal.
Can A Flare Feel Like A Hot Flash
DrMR: Absolutely. So we had a number of questions. I thought we could kind of go through some of these and use this as fodder for discussion. I’ll start off with one from—I believe this is Anita Hill, and it may have been a typo. She wrote her name is Alita Hill. So either Alita or Anita. She asks, “When mast cells release, can it feel similar to a hot flash?”
DrLA: Absolutely. Many patients describe just that sort of a sensation. Of course, it can also feel like many other things too. But, yeah, a hot flash is well within the range of what a flare can feel like.
Can MCAS Cause Anxiety & Brain Fog
DrMR: Ok. And Karen Binks asks, “Can MCAS in the gut cause symptoms such as anxiety, brain fog, and extreme hunger immediately after eating?”
DrLA: The short answer is yes. The longer answer is MCAS is a systemic condition. So to say that MCAS in the gut is causing a certain set of symptoms, it’s not just going to be MCAS limited to the gut. But certainly, mast cells… Well, mast cells anywhere have the potential to cause symptoms not only in the local surrounding tissues but the mediators that get released from mast cells can wind up causing a huge variety of issues at very distant sites too and through a whole variety of mechanisms.
Mediators could get into circulation. There can be distant actions through hormonal or neural mechanisms, and I quite commonly see patients who have just what the questioner described, where mast cells getting triggered in the gut wind up causing a wide variety of neuropsychiatric issues, other issues in many other sites in the body.
I still remember being flabbergasted. A patient I saw fairly early on, who—I’ll spare you the long story, but the bottom line is it became apparent that the inappropriate activation of the mast cells in her GI tract was causing intensive suppression of red blood cell manufacturing, erythropoiesis, in the bone marrow. And she had actually presented with severe anemia that had been labeled as an idiopathic pure red cell aplasia.
But finally, once we got specifically the GI tract mast cells under control, that’s when the bone marrow just snapped right back into action. And her previously completely refractory pure red cell aplasia just completely reversed itself. And the hemoglobin returned from 6.0 to 13.0 within a month.
DrMR: So the far-reaching impact, I guess, you could maybe loosely determine it as the immune system?
DrLA: Yeah, I think it’s some complex assortment of mediators. Obviously, a different package of mediators is going to be directly and/or indirectly driving different effects in different parts of the body. But, sure, neuropsychiatric effects from GI tract mast cell activation, I see it all the time.
Case Study for Autistic Patient
One of the most interesting patients I’ve seen in that regard was an unfortunate young man who in his first year of life had been perfectly normal and then, within hours of his first DPT vaccine at age one, devolved into just a terrible multi-system inflammatory mess, including essentially acute onset of autism. And then19 years later, a smart gastroenterologist began to realize that the multitude of issues the young man was having probably were all a mast cell issue. He did the umpteenth EGD on the patient and obtained biopsies, and this time sent the biopsies for special staining for mast cells.
Came back highly positive, and we started treating. Antihistamines helped a little bit; a little bit of low-dose Ativan helped a little bit more. But then, when adding oral cromolyn, which, as you know, is not absorbed. So it’s only going to impact the GI tract mast cells when you take cromolyn orally. And the improvement at that point in his previously very challenging, behaviorally challenging autistic behavior was just remarkable, the improvement with the oral cromolyn.
And then I got to thinking, well, autism is a brain on inflammatory fire in many patients. Where’s the inflammation coming from? Well, MCAS is a disease of chronic, multisystem inflammation. And I also got to thinking that feeding into the brain inflammation might be signals coming from the… I mean, where are the mast cells in the body? They’re at the environmental interfaces, dominantly speaking.
So I began wondering if mast cells in the sino-nasal tract might be coming to impact the olfactory nerve which interfaces with a lot of different brain centers. And so, I added nasal cromolyn at that point, and the young man came back at the next visit even further remarkably improved. That’s nasal cromolyn which, again, does not get absorbed, on top of oral cromolyn. So, yeah, mast cells in one part of the body can have very substantial distant effects and that absolutely can include neuropsychiatric things.
Sorry for the long answer to a short question.
DrMR: No, it’s a great answer. I know last time that we discussed this there was a number of biomarkers that you found helpful: tryptase in the serum, chromogranin-A, prostaglandin D2, plasma histamine, plasma heparin. You went through the whole panel. And for the audience, the whole suite of markers is in the notes for the last podcast.
Biopsy and Testing Markers
But what about the biopsy? Is that something that you feel… Is that a standalone tool that could be used as a diagnostic measure or would you rather someone do the full suite of markers that you ran through in your last discussion?
DrLA: Actually, the way the diagnostic criteria that I prefer to abide by published in 2011 in the Journal of Hematology and Oncology. And the way those diagnostic criteria are structured, yes, a biopsy finding, an extracutaneous biopsy, showing an increased number of mast cells in that tissue can be used as a point of laboratory evidence. Actually, finding an increased number of mast cells in an extracutaneous biopsy is considered one of the major criteria for the diagnosis of MCAS in that proposed set of diagnostic criteria.
But I’ll tell you, Michael, my own style in doing this is I don’t think it’s called a mast cell activation syndrome for nothing. And although an increased number of mast cells is admittedly suggestive that there’s also improper activation of those mast cells. To my way of thinking, there’s nothing that asserts activation as definitively as finding an increased level of some mediator relatively specific to the mast cell in the blood or urine.
So even in patients who come to me already having found increased mast cells in a biopsy, typically a GI tract biopsy, I still feel more comfortable in going ahead with blood and urine testing. It is just non-invasive testing. I’m not asking them to do another invasive endoscopy. But I do ask them to consider going ahead with blood and urine testing to look for some mediator elevations.
DrMR: Gotcha. And that’s what I’ve seen in some of the reading that I’ve done. And again, please correct me if you disagree with this. But the increased mast cell density, if you will, doesn’t necessarily mean there’s going to be overactivation.
DrLA: I don’t think we understand yet just what the nature is of the correlation between how many mast cells there are in a given tissue and what their state of activation is. There are different processes going on in the mast cell and, more particularly, the mast cell precursors because the mast cells themselves don’t reproduce. But the precursors…
There are certain molecular pathways in the precursor that drive proliferation, and there are other pathways that drive production and release of various mediators, the so-called activation of the mast cell. I can well imagine there might be pathways that drive both proliferation and activation. But I think we’ve still got—there are a whole lot more unanswered questions about the biology of the cell than there are answered questions.
DrLA: Unfortunately, a long answer to a simple question. I will see an occasional patient where we’ve got good evidence on biopsies for the diagnosis and I try to get mediator evidence. And I just sometimes can’t do it. And it’s not like I’m going to reject the diagnosis in that patient because, again, the way those criteria from 2011 are structured, if you have symptoms that are consistent with chronic inappropriate mediator release and you have increased mast cells in a biopsy, then those are the two major criteria in that diagnostic proposal. So, fine, you technically meet criteria and I’ll accept that and go forward with it.
We’re talking about a diagnosis you’re going to carry forward for the rest of your life. It’s a life-changing diagnosis in my opinion. And I just think it’s helpful to have at least one positive elevated mediator level on file as you go forward.
DrMR: Sure. I think that makes sense. It certainly, I don’t think, is unreasonable to be in a situation where no one test will tell you everything. And even if you could do all the tests, you may not have a perfect picture emerge. You have to kind of do the best with the findings that you have and make the best educated guess—not guess, but the most well-informed decision that you can.
DrLA: I think it’s important too to keep in mind just how small a slice of the total activity of these cells we are surveying when we do the testing for mast cell activation. Yes, from one perspective, it looks like a lot of tests. All of the mediators that you mentioned and a few more. But at the same time, we have to understand that these cells are already known to produce more than 200 mediators.
And yet, we’re only measuring roughly 10 of them because those are the ones which are relatively specific to the mast cell and which are measurable in the clinical laboratory at present. Most of the mast cell mediators, we really can’t even test for them in the clinical laboratory at present. They’re testable in the research laboratory, but not the clinical laboratory. And of the minority of the total repertoire of mast cell mediators that we can test in the clinical laboratory, the majority of those are not particularly specific to the mast cells.
So, yeah, you can measure in the clinical lab an interleukin-6 level, a potent inflammatory molecule absolutely produced by the mast cell. But it’s also produced by a lot of other cells, so if you find an elevated IL-6 level, you have no idea where it’s coming from. And that doesn’t necessarily pin down that it’s a mast cell activation syndrome. So in the end, we may have started with 200+ mediators, but we’re left with about 10 that are specific to the mast cell and clinically measurable at present.
Well, that’s what we measure. But anybody who thinks that the symptoms that a patient with this disease is having, that those symptoms are necessarily coming from the very few mediators we’re measuring, heck, if you play the odds, measuring 10 out of more than 200, the odds are overwhelming that the symptoms a patient is having are probably coming about from mediators other than what we’re measuring. But this is the best we can measure, so that’s what we make do with.
Can MCAS Cause IBS
DrMR: Coming back to the gut for a second. Hector asks, “Can MCAS cause IBS?” And I think we already know the answer to that. And then he also continues, “Is there any link between estrogens and MCAS in the gut?”
Now, you mentioned different forms of cromolyn that can be used, and there have been a few studies showing that effective in IBS. So I think we have that connection pretty well established. At least some of the interventional trials have shown benefit from treating histamine and MCAS in the gut for IBS. But curious. I think that’s an easy yes for you. But maybe more so the link between estrogens and MCAS in the gut.
DrLA: Well, I don’t know that it is such an easy answer. IBS is a very complex condition. It’s a highly variable condition. And although there certainly is emerging literature suggesting that mast cells play an integral role of some sort in at least some portion of the IBS population, I want to be very cautious before making a blunt statement that mast cell disease causes IBS.
Yeah, I have my suspicions that mast cell disease, that the primary mast cell activation syndrome can cause IBS in some fraction of the IBS population. But I don’t know what fraction of the IBS population it is that has mast cell disease at the root.
DrMR: Sure. And just to clarify—and I totally agree. It’s better to be discerning and cautious in the language, absolutely. His question was, “Can it cause IBS?” Not “is it the only cause of IBS”.
DrLA: Well, again, I don’t know that anybody has done a study yet that shows that primary MCAS has ever been proven to cause a single case of IBS. It’s not that people have tried and failed to do that research; it’s just that nobody has even tried yet.
DrMR: Well, I’m assuming you’ve seen some of the studies that have used various antihistamines and shown improvements in IBS symptoms, right?
DrLA: Yeah. Absolutely. But that doesn’t necessarily prove that primary MCAS is the root of what’s going on there. It’s always possible that there’s a secondary MCAS in those patients that, of course, is causing symptoms. And because there are H1 and H2 receptors on the surface of the mast cell, then you give antihistamines to those people, it’ll simmer down that mast cell activation to some degree, lead to some symptom improvement, but that doesn’t necessarily prove that MCAS is the cause there.
Again, I’m with you. We all have our suspicions. Mast cell activation syndrome, if it is nothing else, it is a disease of chronic, multi-system inflammation. And obviously, IBS is a chronic inflammatory disease. And so, it could easily be the case that MCAS is the root cause of IBS in at least some IBS patients.
There’s just an extraordinary amount of research that needs to be done, not only with respect to the relationship between mast cell disease and IBS but between mast cell disease and pretty much every other idiopathic, chronic, inflammatory disease out there to tease out exactly what the relationships are. So time will tell. The research has just got to be done.
Link Between Estrogen and MCAS in the Gut
With regard to estrogen, there are receptors for all the major sex hormones on the surface of the mast cell. I very commonly hear from my female MCAS patients, my premenopausal MCAS patients, that they see flarings in their symptoms which are likely attributable to mast cell activation. And we see flarings of those symptoms in concert with their menstrual cycles.
DrMR: Right. Yep.
DrLA: And for many of these women, use of oral contraceptives can be very helpful to tame at least that portion of their MCAS.
DrMR: I’ll second that, Larry. We use more so things like dong quai and Vitex that can herbally help to balance female hormones. It’s remarkable some of what I would more so term histamine intolerance-type symptoms, because that’s where I have a little bit more familiarity with. But I think there’s, as you said in your last episode, kind of this continuum between histamine intolerance and mast cell activation syndrome.
But however exactly we’re going to label it, those types of inflammatory/immune-mediated symptoms seem to improve quite a bit in women once getting their hormones to a more balanced state. So I see that same thing.
Primary and Secondary MCAS
Coming back a moment, can you clarify between primary and secondary MCAS?
DrLA: Sure. The notion as it presently stands of how best to classify MCAS—I mean, to be clear, it virtually certainly is a humongous spectrum of conditions rooted in inappropriate activation of the mast cell. But if you try to divide it into some very broad classifications, you have, first of all, the notion of primary MCAS in that the mast cells themselves are the root of the problem.
They are fundamentally abnormal mast cells. And what appears from the preliminary available research to be driving such intrinsic abnormality are mutations in KIT and likely quite a variety of other mast cell regulatory elements. So if we can find evidence of mutations in the mast cells in a given patient with MCAS, then you can make a statement “that patient has primary MCAS.”
It’s just that the testing that is needed to demonstrate those mutations is essentially not available in any clinical laboratory anywhere at present. It can be done in the research laboratory but not in any clinical laboratories. In time, we’ll get there. The testing will advance.
But for right now, about the only way you can prove that somebody has a primary MCAS is in a couple of rare situations. Number one, you could do flow cytometry on most commonly a bone marrow aspirate sample where you would look for co-expression of CD117 which is the extra-cellular domain of KIT, the transmembrane tyrosine kinase receptor that is the dominant mast cell regulatory element.
So you do flow cytometry looking for co-expression of CD117 which brightly studs the surface of the mast cell together with co-expression of CD25 and/or CD2. Those are T cell antigens that should ordinarily never be co-expressed on the surface of the same cell as CD117 is being expressed. But roughly 20 years ago, it was first discovered that there is that abnormal co-expression pattern that is seen actually quite commonly in mastocytosis, quite rarely in MCAS. But when you do see it, it’s fundamentally abnormal and it represents a clonal mast cell disorder.
So in MCAS, we would then say, “Oh, you have a monoclonal mast cell activation syndrome.” So that is a primary MCAS. And the only other way to define primary MCAS would be again in the very rare situation of finding a KIT mutation or some other mast cell regulatory gene mutation.
But you look at the testing for mast cell gene mutations that are presently available in the clinical laboratory and the vast majority of the labs that have such capacity, the only mutational test they can do is for the KIT D816V mutation analysis by PCR, looking for that one mutation that we find very commonly in mastocytosis and almost never find in MCAS.
So if those are the only two tests presently available in the clinical laboratory for looking for the mutations which the research has shown are—there’s just a huge menagerie of mutations in KIT and other mast cell regulatory genes that have been found in the research lab. We just can’t do the clinical testing for it yet.
So our ability at present to find primary MCAS is extremely limited, even though, again, the research strongly suggests that when MCAS is found it appears to be primary in the vast majority of people who have it. It’s just a matter of whether you can prove it at present in a clinical laboratory or not.
So then that leaves you with secondary MCAS which is a situation where you have totally normal mast cells. It’s jus that they’re being activated in response as a reaction to something else that is the primary problem, whether that is, oh, perhaps an infection or an autoimmune disease or a malignancy, so on and so forth. If you can pin that down, ok, you can call it a secondary MCAS.
Again, we don’t have available yet in the clinical laboratory the testing that could definitively distinguish between primary MCAS versus secondary MCAS. So this is clinical judgment to some degree. And then, finally, the last category which, to my way of thinking actually, is the dominant category at present, again, because of limitations in available testing is the idiopathic MCAS category.
If you can’t prove that it’s primary and you can’t identify some other disease which is just obviously the primary driver of reactive mast cell activation, and so you can’t call it secondary mast cell activation, then what you’re left with is idiopathic. You can define that the patient does have mast cell activation; you just can’t sort out whether it’s primary or secondary. So you’re left to call it idiopathic.
And all of this, to my way of thinking, is largely academic at this point because it’s all going to get treated pretty much the same. Down the road, as we get better at defining assorted variants of primary mast cell activation, we’ll probably be better able to pin down which treatments are more likely to help which variants of this disease. But for right now, it’s such a devilish problem distinguishing the different variants of this that the approach to treatment remains quite largely empiric and just trial and error and working your way through. Patiently, persistently, methodically working your way through trials of fortunately the large assortment of medications which have been shown helpful in various mast cell patients.
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Primary and Secondary MCAS Cont.
And is it correct to say that if you were to find objective lab evidence on the panel that you outlined in your last discussion with us, that would be suggestive of secondary MCAS? And if someone was just one who responded to empiric treatment without the laboratory evidence, that would be idiopathic? Or is there another way you’re distinguishing?
DrLA: No, no, no, no. I don’t think we have any way at all at present of distinguishing based on elevated mediator levels. You can’t use that to distinguish primary versus secondary versus idiopathic. So it’s a clinical determination. Primary, that’s not a clinical determination; that’s objective laboratory evidence. If you can find a KIT mutation or you can find that particular flow cytometry pattern I described, that’s it. You have primary clonal disease.
But otherwise, you’re left to decide between secondary versus idiopathic. If you can find a disease and that all of the mast cell activation obviously stemmed from the development of that infectious or malignant or autoimmune disease, then fine, it’s a secondary MCAS.
But the thing is, Michael, you take a careful history in these patients. And what you almost always find is that even in the mast cell patients in whom somebody has defined a particular infection, let’s say Lyme disease, for example, or a particular autoimmune disease like, oh, say, scleroderma or a particular, let’s say, a lymphoma.
If you take a careful history, then what you often find, almost always find, is that the symptoms of mast cell activation actually extend far back earlier than the other defined disease, the scleroderma, the Lyme disease, whatever became apparent. So you get this strong suggestion from the history that the patient has actually had aberrant mast cell activation going on a long time, most of their lives.
And then, at some point in their lives, another incident may have developed, another disease may well have developed, and that disease could easily have kicked up a notch, so to speak, the misbehavior of the patient’s already dysfunctional mast cells.
So what do you call it in that situation? Do you say it’s secondary on top of primary MCAS? Do you just say, “Well, the heck with it. It’s too complicated. We’re just going to call it idiopathic MCAS because it’s still going to get treated the same way”? I’m telling you, Michael, there’s just terrible terminological challenges in this area.
And I think, ultimately, it’s going to come down to just getting much better testing to distinguish the different variants of this disease at the molecular and genetic level. Then we’ll just get a much better handle on what’s going on in the individual patient.
DrMR: Sure. Ok. So for right now, we’re not overly wrapped up in the particulars of the diagnosis but more so just focusing on clinical endpoints, response to treatment, what have you?
DrMR: That’s a nice actually segue into Jane Elizabeth’s question which is, “How do we test this and can we test this in Australia?” And I’m going to add something to this question that I think will help contextualize for her. I know that the healthcare system is a bit more regulated in Australia. So I’m assuming that they probably have a decent amount of the markers that you discussed on your last interview.
But I’m wondering if there’s a lot of hurdles to testing in Australia if you might recommend doing an empiric trial with the over-the-counter treatments to at least get an initial suggestion if going through the hurdles and the labors of doing further testing would be justifiable or not. Or would you recommend a different path?
DrLA: No, I think there is nothing wrong with trying at least a little bit of treatment, particularly the antihistamines. Let’s be honest, with appropriate dosing, it’s really hard to hurt somebody with H1 and H2 blockers. You can’t hurt them medically; you can’t hurt them financially. The problem with making a decision as to whether the patient is or is not likely to have MCAS based on therapeutic response is that, again, the disease behaves so heterogeneously not only in its clinical presentation but also in its patterns of therapeutic response.
If a patient fails to respond to, oh, say, the first one, the first two, even the first three things that you empirically try, that doesn’t even begin to say whether the patient does or does not have a mast cell activation syndrome.
DrMR: I’m glad you say that because that ties back into something from your last episode that I was wondering about which is if these over-the-counter antihistamines are essentially safe and inexpensive, then what would be the argument against starting with an empiric trial rather than going through the testing?
But it sounds like what you’re saying is because someone may not respond to the first or the second or even the third protocol that they try, it’s more efficient overall to first identify if MCAS is present and then use that as kind of your principle that you’ve established. Ok, now we want to make sure to keep going through the available treatments until we find one that works, even if you have failed out of the first, the second, and the third protocol that you’ve tried.
DrLA: Right. And actually, it’s probably worth pointing out that when I’m doing an evaluation on one of these patients, I tell them, look, we’re going to send off all of these blood and urine samples. It typically takes about a month to get back results on the complete set of tests on any one round of testing. And I invite the patient to go ahead and go through some rotations of trials of the different H1 blockers and H2 blockers while we’re trying to gather the diagnostic evidence, the laboratory evidence of disease.
I’m not aware of any papers that have demonstrated that taking antihistamines, actively being on antihistamines, actually confounds any of the particular tests that we run in trying to diagnose this disease. So I invite the patients to go ahead and empirically try the antihistamines while we’re trying to nail down the diagnosis.
But just because they don’t respond to antihistamines does not at all necessarily say that they don’t have this disease. I’m a big believer in listening to the patient and what the patient’s body is trying to tell us. If the history is more consistent with mast cell activation than any other disease I know of, then it’s most likely the case that the patient has mast cell activation syndrome.
There are a lot of challenges to getting the tests done properly, even here in the United States. So sometimes we have to repeat tests and do repeating testing. We keep working at it to a reasonable point. But I’m perfectly ok with going ahead and empirically trying antihistamines. You just don’t want to make any premature conclusions from a failure to respond to antihistamines.
And I should point out too that sometimes what patients will interpret as a failure of an antihistamine is they start taking a given drug, let’s say loratadine or cetirizine or famotidine or ranitidine, and they actually have an adverse reaction of some sort right out of the starting gate. And they interpret that as a failure, that the drug’s not going to help them.
And I say, “Wait a second.” It’s largely the case that all of the non-sedating H1 blockers and all of the H2 blockers are extraordinarily well-tolerated drugs at appropriate doses. So I’ve learned the hard way with this disease that if a patient takes a medication product—if a mast cell patient takes a medication product that contains a drug that is ordinarily a well-tolerated drug and right out of the starting gate that patient is having a problem with that product, it’s far less likely that the problem they’re having from it is due to reactivity by the patient’s dysfunctional mast cells directed against the drug.
It’s not the drug that’s provoking the activation of the mast cells to produce whatever the symptoms, whatever the “side effects” are. Instead, it’s far more likely an excipient issue: fillers, binders, dyes, preservatives that are riding along with the drug. I get very suspicious any time a patient tells me they’re taking antihistamines and tell me, “Oh, it’s actually making me sicker.” No, it’s very unlikely that it’s the drug doing it. It’s probably an excipient, and actually that’s a huge opportunity to investigate the full ingredient list for that particular formulation of that drug and try to identify what the excipient is that’s provoking the reaction.
I’m telling you, Michael, I’ve seen so often these patients will go from looking and feeling virtually the picture of health to looking and feeling like death warmed over within minutes of exposure to even a trace amount of whatever agent happens to be a trigger for them.
So finally, the other part of that question, Australia, I honestly don’t have any idea what testing for mast cell disease is available in Australia. It’s a big country, and they’ve got a number of very fine academic medical centers there. I would be kind of surprised if the full range of testing or most of it is not available. But it’s just that I don’t have any direct experience with that and don’t know what’s available and what’s not available there.
DrMR: How are you getting around an excipient issue? Are there other drugs that are cleaner than others? How are you grappling with that?
DrLA: It’s not an issue of what’s cleaner than the other. It just depends on what the individual patient’s dysfunctional mast cells are going to react to and what they’re not going to react to. Many patients, they’re afraid to take commercially-available formulations of a drug because they have various excipients in them. And they say, “Oh, well, I’m just going to start with a compounded formulation.” And I say, “Well, don’t go assuming that a compounded formulation is necessarily going to serve you any better.”
Just because a drug is obtained from a compounding pharmacy doesn’t mean it’s excipient-free. The drug, the pure drug is still going to be mixed with other things in some fashion through the compounding pharmacy. So I’ve had a few patients who, out of their fears, they actually start with a compounded formulation of some drug, and right away they have some adverse reaction. And I say, “Well, wait a second now. That drug is really not expected to cause that type of a reaction. So it’s probably some excipient in the compounded formulation that’s causing this trouble, so why don’t we switch to some commercial formulation?” And sometimes patients do quite well in that fashion.
And then, at the same time, plenty of patients, they take commercial formulations and they have troubles with those formulations. So you switch either to alternative commercial formulations or you sometimes have no choice but to go to the compounding pharmacist and have a new formulation custom-made for you.
So I advise all my patients who are taking medication products—they’re newly trying medication product and right out of the starting gate they’re having a problem with that product—that they’ve got to think about the potential for excipient reactivity. You stop taking the product since it’s causing you a problem. And you go back to the pharmacist and you say, “Look, I’m a mast cell patient. I’m reacting to this thing you just gave me. And it’s much more likely to be an excipient issue than a drug issue, and I need your help. I need you to pull the full ingredient list for exactly what you gave me.”
You don’t go looking at the ingredient list for a different dosage strength of the product. You don’t go looking at the ingredient list for a different formulation, like gel cap instead of the tablet you were actually given. You don’t go looking at the ingredient list for a different manufacturer’s version of the product, because all those different formulations could easily have different excipient packages. They’ll all have the same drug, but they could easily have different excipient packages.
So you look at the ingredient list for exactly what you were given, and you try to figure out what it is in there that you’re reacting to. And I understand that’s hard to do when you’ve adversely reacted to one medication product that has a dozen excipients in it. But most mast cell patients who have adversely reacted to one medication product have actually adversely reacted to multiple medication products. And therein lies a golden opportunity to pull the full ingredient list for the multiple products and line them up and say, “What the heck do these things have in common?”
And when you finally get to the point of suspecting that the common element to all of these intolerable products is—I don’t know. I’m going to just make up an example here—red dye number 40. Then the pharmacist has another job to do, to help the patient find an alternative formulation of that drug that just doesn’t have red dye number 40 in it, whether it’s a commercially-available formulation or, worst case, off to the compounder you go to get a new formulation custom-made without red dye number 40. And you try the alternative formulation, and if you have a better experience with that, you’ve just proved it’s not the drug you’re reacting to. It’s the excipient.
And at that point, by God, it’s the excipient that goes on the allergy list, not the drug. And then at that point, frankly, the pharmacist has got another job to do, to look through the full ingredient list for all of the rest of the patient’s products to make sure they don’t contain trace amounts of that excipient.
DrMR: Right. Ok. All right. Now, you mentioned also a thorough history can be helpful. I’m wondering, has anyone put together a questionnaire that can be helpful for identifying or at least suggesting MCAS?
DrLA: Oh, you must be setting me up, you straight man. Actually, yes. One of the world’s leading researchers in this area, Gerhard Molderings over at the University of Bonn and his team actually were first to publish a questionnaire of the sort you’re describing. I think the original was published in German, gosh, perhaps as far back as ’06 or so. And then, it got republished in English in another article in, I think, 2009, and it has since been republished in other articles.
So, yes, that is validated. It’s a whole set of questions about symptoms and findings in the patient. And I think the threshold score on that questionnaire, if you hit like a 14 or higher, if I’m remembering correctly, then it’s an awfully good bet that you’ve got a mast cell mediator release syndrome.
DrMR: Now, is there a certain term one can search for? Or if I were to shoot you an email, could you send me a link to that so I could include that in the notes? Because I know our audience would benefit a lot from that.
DrLA: Yeah, actually I recall that one of the papers in which that was republished actually is an open-access article. So by definition, anything included in that article is open-access. So, sure, I’d be happy to send you that paper. It was a paper on actually the diagnostic approach to MCAS. And it was something that Dr. Molderings and I published in the World Journal of Hematology back in 2014, I think it was. So, happy to send you that paper.
DrMR: Great. That would be great. I want to be respectful of your time. I know we are going a little bit longer than we initially thought. Do you have a few more minutes?
Can MCAS Induce Urticaria
DrMR: Ok. From Kelly, “Can cold-induced urticaria be due to MCAS? And if so, is it due to an underlying gut issue like SIBO?”
DrLA: Yeah, again, urticaria, if you just look at that process in general, it’s almost certain that what’s at the root of most instances of urticaria is abnormal mast cell activation. So in a sense, you’re talking about a semantic issue here. Do you want to call it mast cell activation syndrome in which one of the clinical features is cold urticaria? Or do you just want to call it cold urticaria? I have absolutely no problem with keeping it simple and just calling it urticaria or just calling it angioedema or just calling it, oh, say, idiopathic anaphylaxis if the only thing that’s going on in the patient is urticaria or angioedema or anaphylaxis.
It just strikes me though that if the patient starts having such a rafter of problems that they have not only those problems but they come to acquire a problem list of 57 other issues, most of which are inflammatory of some sort or an allergic nature of some sort, then what’s more likely? We’ve talked about this before.
Is the patient really so uniquely unlucky that they’ve coincidentally acquired so many different problems, all of them developing independently of one another? Or is it more likely there’s just one thing going on that is biologically capable of driving, directly or indirectly, everything that’s been seen in the patient?
Well, obviously, it’s more likely there’s one thing going on, and mast cell activation disease is a disease of chronic, multi-system inflammation, plus/minus allergic phenomena, plus/minus aberrancies in growth and development and potentially any tissue. And I know that’s a nebulous description, but it’s a direct biological consequence of the known vast array of effects of the vast menagerie of mast cell mediators.
So it just strikes me that in patients who have a multitude of problems that probably are due to aberrant mast cell activation it’s easier just to call it mast cell activation syndrome.
Impact of Underlying Gut Issue
DrMR: I follow you. Let me ask one question that’s also embedded in that which is the impact of an underlying gut issue. And just a few things that are always at the forefront of my mind are trying to reduce as many symptoms as we can through optimizing one’s gut health because there, at least in my experience and what I’ve seen in the published literature, does seem to be many symptoms that one could potentially attribute to MCAS that could be remedied by improving one’s gut health.
We have some evidence showing that, for example, things like atopic dermatitis can improve when people restrict gluten who have non-celiac gluten sensitivity. One study showed improvement in fibromyalgia after going on a low FODMAP diet. We see restless leg syndrome and rosacea improve after one treats SIBO. So there’s certainly a number of things we’re seeing emerge in the published literature, showing that some of this reactivity can be due to something imbalanced in the gut.
And I think it’s a decent approach to start there and then reevaluate. And then, if there are still a number of symptoms present, consider continuing on to something like MCAS. That general structure, would you agree with that or would you modify that somehow?
DrLA: I think this is such a complex, multi, multi, multi-dimensional puzzle that it’s almost inconceivable that you could attack it in just one angle and just resolve all the patient’s problems. So, yeah, it’s going to be a matter of hacking away at it piece by piece until the patient gets to the point of being satisfied. It’s virtually impossible to control this disease so well the patient feels perfect.
You can’t even get them to the point where they’re going to feel significantly improved all the time. You’re looking to get them to the point where they can feel significantly better than the pre-treatment baseline the majority of the time. And fortunately, at least in my experience, the majority of patients who have this actually can get to that goal. But you’re right; it’s just hacking away at it a piece at a time until you find the particular cocktail that works best for the individual patient.
But the good news is as best as we can tell, at least on a preliminary basis, the average patient who has this is going to have a lifespan that’s equivalent to that of the general population. It’s not a cancer that’s going to cut their lives short. So they’ve got the time to work through this in a patient, persistent, methodical fashion. And fortunately, there are a lot of things to be tried.
I understand that everybody who is unwell wants to get as much better as possible, as quick as possible. But if you start making multiple changes in the regimen around the same time and the patient gets either better or worse, you’ll have no idea what’s making them better or worse and it’s a whole big mess to sort it out at that point.
As challenging as it is sometimes to just be patient, nevertheless you’ve got to be patient and work through it a piece at a time. Make one intervention. Observe for a few weeks to see what the results are going to be. And then either retain that intervention because it obviously made a significant difference or ditch that intervention and move on to the next.
DrMR: I want to second that because this is a conversation I have in the clinic probably one or two times per week where a patient will come in who doesn’t feel well, and I’m totally empathetic with being in that position. But they’re also reading stuff on the internet incessantly. And I have to explain to them that it’s very important that they understand if we set the mini-experiment of X and our goal is to run that experiment for three weeks and reevaluate and then either go one way or the other.
If they read something a week in and they jump ship and change gears and they keep reading new stuff and deciding to change the experiment parameters every week or so, it’s very difficult to collect any data and learn anything, because before we can even run one short experiment of two to three weeks, they’re jumping out of that experiment and going to something else. And they’re doing that because they want to feel better quickly, like you said, and we totally are empathetic to.
But it’s important to try to stay the course because you want to be able to ask the body a question, note the body’s response, and whether that was a success or failure, you’re still taking steps toward the endpoint of feeling better. Because even if it is a failure, that information can help you get one step closer to the ultimate endpoint.
DrLA: And I just want to be careful. We’re not placing all the blame for the rush, rush, rush on the patients because not uncommonly where I see the problem is with the providers. Many times, the patient is quite willing to be patient and to do this in a very methodical fashion. But the physician, for various reasons, just isn’t as willing to take that much time and to invest that many visits and checkups with the patient.
So the physician sometimes just writes prescriptions or gives instructions to the patient for a large number of interventions. Says, “Here, just start these five things.” And I kid you not. Sometimes that’s how many things are simultaneously prescribed. And then they say, “Come back to me in four months, and we’ll just try to sort through it all, what happened.” It’s just utter chaos to try to figure out what’s going on in that situation.
DrMR: Which that’s a top-down kind of approach, which is treat with everything, and then if someone’s better, you can then try to wean off therapies to determine what’s working. And I see the rationale in that approach. But one of the things I’ve been doing more so is layering.
So let’s say we’re going to give someone three therapies to start because let’s say we’re not able to see them for six weeks. So we say, “Ok, we’re going to run three mini experiments, each two weeks in duration.” Instead of starting them—and this is just for clinicians in case you’re trying to grapple with maybe someone doesn’t have the money to be seen every two to three weeks, and you’re trying to find that happy middle ground. What I have found to be helpful is giving them a few experiments to run in succession.
So ok, for two to three weeks you’ll do one and then you’ll do two and then you’ll do three and then we’ll follow up.
DrLA: Absolutely. I agree. To do it in succession, in series, that’s perfectly sensible. It’s just that to do it all in parallel and then sort out the results, it’s just chaos.
DrMR: Right. Yep.
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Long Term Use of Antihistamines
So Randy asked what I thought was a good question which is, “Could you explain any potential downsides to using antihistamines for an extended period of time? I am particularly interested in what effect, if any, they could have on gut health.”
DrLA: I’ve not seen any data to demonstrate that long-term use of antihistamines causes any particular problems. I’m aware of the relatively recent studies noting associations between long-term use of certain H1 or H2 blockers in other significant health issues. For example, there was that study, oh, I don’t know, two or three years ago that showed that there was a correlation, an association, between long-term use of H1 blockers and development of dementia. But that doesn’t even begin to say whether the H1 blockers are actually causing dementia.
And you ask yourself, well, who are the people who would feel benefit from long-term H1 blocker use? And you pretty quickly arrive at the notion that it’s probably patients who have chronic mast cell activation are the patients who are going to be most likely to chronically use H1 blockers.
Well, what are the effects that chronic mast cell activation can drive? Well, included in that huge range of effects, there’s a huge range of neuropsychiatric effects, including dementia.
DrMR: The chicken or the egg kind of quandary.
DrLA: Yeah, so I’m not concerned. I’ve seen no data to say that long-term H1 blocker use causes dementia. And if the choice is between going the next 40 years of your life with unrelieved symptoms of histamine docking with your H1 receptors to an excessive degree versus enjoying the benefits of a blocker, most people, I think, would probably say, “Give me the blocker.”
DrMR: I’m glad you mentioned that one study. And that study did get a bit of press which essentially suggested that there could be some tie between antihistamine use and cognitive impairment. And the real thing that was left out of that study… Actually, that study I thought made a simple conclusion. It’s people’s interpretation of that study that I think got a little bit…
DrMR: Exaggerated. We don’t know from that study if it was people who had more inflammatory and immune issues were using more, let’s say, Benadryl and that’s why they had more cognitive impairment. We really can’t answer that question based upon that study. So I’m cautious in how much we derive from that study’s conclusions.
DrLA: Yes. I tell my patients that with the available data I am comfortable with recommending long-term use of H1 and H2 blockers. Who knows what data will emerge in the future? Recommendations may change. But for now, this is the best I can figure out to recommend.
New Research About LDN
DrMR: We had another question come in from… Ok, this is on Instagram. Sorry. We went from names to, I guess, usernames. This is @downwithpsychiatry. “Discussions of new research into the benefits of LDN, regarding mast cell activation.” And that’s actually an interesting question. Do you have any information there?
DrLA: Yeah. Not a whole lot. I have been increasingly hearing from colleagues who are finding that some of their patients are seeing nice responses in certain aspects of their mast cell activation to LDN. I myself have not yet seen—I’ve not had quite as much luck, if you will, with that drug. I think I’ve seen perhaps a couple of patients who’ve had nice responses to LDN.
I’ve seen far more patients who have tried the drug and not seen any response to it. But other colleagues are having a little bit more luck with it than I am. As far as the science as to why that drug might help certain patients, I think we’re a long way away from understanding that. From what I’ve seen of the patients who do respond to that drug, I couldn’t describe to you the manner in which those patients clinically appear similar to one another. What is the particular clinical feature that would mark for likelihood to respond to LDN? I can’t tell you that. I think it’s just going to take a lot more time, a lot more research to tease apart the molecular mechanisms of this disease.
Advice for Working with a Conventional Medicine Doctor
DrMR: Gotcha. So one or two other ones and then I’ll let you get on to the rest of your evening here. And thank you again for taking the time. Kelsey asks, “Could you provide advice for a patient that is stuck with a conventional medical practitioner who”—I’m assuming she means in the sense that may not be very open-minded to this area of work and with an insurance company. And she’s trying to get tested properly within that context of, I’m guessing, just her regular insurance plan and a doctor that doesn’t have a lot of familiarity with this area. Anything that you would advise there?
DrLA: Yeah. Always a challenge. Doctors are human and every human is different. Different people are going to respond in different ways. There are plenty of doctors who are, for various reasons, probably pretty legitimate reasons, just not going to be willing to investigate this. So fine. You move on and find another doctor who’s more willing to learn and more willing to try.
But if you want to try to win over, so to speak, a doctor, the best that I know to do is to try to provide education. None of us, not you, not I, not any doctor on the planet has been trained on this. It was first recognized just too recently for this to have been incorporated into any training programs.
So it’s a matter of continuing medical education and you can try to provide the doctor and the insurance company reviewer articles from the literature. This is peer-reviewed literature that explains how this disease works and the range of symptoms it can produce, and here’s how you diagnose it, and it is treatable.
And the good news is, at least from the insurance company’s perspective, that if you can diagnose it, for most of these patients, you can find significantly helpful treatments. So instead of continuing to waste unbelievable amounts of money on unproductive diagnostics and therapeutics in these patients, you can finally get these patients on the right track and get them doing significantly better and in the long run significantly reduce expenditures.
And if there’s any carrot I’ve been able to find for the practitioner, it’s that—my experience has been that most of the providers who I’ve helped come to recognize this disease in their first one or two patients, many of them follow up with me six, 12, 24 months later and tell me, gosh, now that they understand this exists and now that they understand what its overarching patterns are—the inflammation, the allergy, the growth issues—they realize they’ve actually been seeing this disease their entire career. They’ve actually been seeing it relatively frequently; it’s just they couldn’t previously recognize it for what it is because they had never been trained on anything like this.
But once they can recognize it, now they know how to diagnose it and then they can treat it. And they’re all just delighted that these patients who previously were the diagnosable, unimprovable, often psychosomatic patients, the chronically mysteriously multi-systemically inflammatorily ill patients suddenly they’re getting better by finally applying the right treatments to the right diagnosis.
And they’re just tickled that they’re finally seeing so much improvement in all these patients that they just were so frustrated by in the past because they couldn’t effectively treat them. And of course, they couldn’t effectively treat them because they didn’t have the right diagnosis. So the carrot to the practitioner is if you figure this disease out in me, then along the way you’re going to learn a lot of useful stuff that’ll probably help you figure this out in a lot of other patients, because it’s turning out to be a pretty prevalent disease.
OTC Antihistamines Plus Prescriptions
DrMR: Good point. Last question for you. If you had to give a rough estimation of how many patients would achieve at least some degree of notable improvement on over-the-counter antihistamines compared to how many would have to go on to a prescription drug level therapy, do you have any rough estimation there?
DrLA: Well, let me answer it in a slightly different way. I think actually most mast cell activation patients actually do experience some meaningful degree of improvement on just H1, H2 blockers. But to be honest, it is the lucky few who attain what they consider to be completely satisfactory improvement, maybe not perfect improvement, but completely satisfactory improvement on just antihistamines.
The great majority of these patients usually do go on to try and find additional medications beyond antihistamines that are needed to get them to that goal.
DrMR: Gotcha. Ok. Well, that makes sense, and that’s actually very good to know because especially for a clinician who is new to this knowing what’s normal in the grand scheme of things. If someone sees a 50% reduction on an H1, H2 OTC antihistamine combination, knowing is that the best response that we may be hopeful to achieve or is that a good indication but we want to keep working from there.
DrLA: Well, the way I explain it to my patients is, look, at present I don’t have a single test I can run that’s going to tell me when you’re at the goal. So fundamentally, when you get to the point in working through this series of medication trials, when you get to the point where you are feeling well enough, whatever that means to you, for enough of the time, whatever that means to you—again, with the understanding you can’t control the disease so well that they’re feeling significantly improved all the time. They’re still going to have some ups and downs with it.
So when they get to feeling well enough for enough of the time that it’s just no longer worth it to them to keep trying more medications for this, then congratulations. You’re at the goal. And you’ll likely sit with that regimen, enjoying that degree of control over the disease for a long time to come. There’s always going to be the risk downstream from that point that at some random point you might suddenly suffer a substantial escalation, sort of a step-wise escalation in the baseline misbehavior of these cells.
But when those escalations happen, they tend to shortly follow major stressors, either physical or psychological stressors. This is not to say that every stressor will provoke an escalation of the disease. It’s just that major stressors create potential for the disease to significantly escalate. And if that happens at any point and you want to resume at that point trying more medications to get the disease back under better control, that’s perfectly fine.
But that’s the fashion, sort of the long-term strategy in managing this disease. And let’s face it. When it comes to stressors, at least major stressors, very few of us are so fortunate as to be able to predict or control the major stressors…
DrLA: To which we are experienced in our lives. Most of the time, they just hit us out of the blue. Well, you just have to deal with that.
DrMR: I’m very happy you said that because one of the things that I see both patients and practitioners struggling with alike is looking for this highly definitive point for which they are to stop therapies or to know when they have achieved the perfect response. Is it a specific lab marker or is it a very specific resolution of symptoms? Oftentimes, in clinical practice, the lines between these things are grayed, but I think you made a very practical recommendation which is when you get to a point where you’re feeling well enough where you don’t want to be inconvenienced with trying another medication, that means you probably don’t have enough symptoms motivating you.
DrMR: And at that point, you’re probably at a good space. I think that’s absolutely very practical advice.
DrLA: Right. And besides, again, just the biology of this cell and of the disease, the fact that it’s putting out more than 200 mediators under normal circumstances, honestly, what are the odds that we’re going to find one lab that’s going to be the marker of satisfactory control of mast cell activation. I think that’s kind of a naïve impression of this. And to date, the fact is that the few studies that have been run, trying to identify correlations between changes in certain mediator levels resulting from certain medication, we’ve seen no such correlations in activation symptoms.
There is some data that if you apply neoplastic treatments, chemotherapy and whatnot, to mastocytosis, then you will see a decline in the tryptase level. But then again, we now understand the tryptase dominantly reflects simply the number of mast cells you have in you, not their activation state.
So, yeah, if you give some chemotherapy and you cut down on the number of cells in mastocytosis, then, sure, the tryptase level ought to come down. But beyond that, when you talk about activation rather than proliferation, my god, this is so complex I can’t envision identifying a single marker that’s going to say, “That’s it! You’re at the goal. It really doesn’t matter how you’re feeling, but I can show you by this number you’re at the goal.”
DrMR: I get it. I totally get it. All right. Well, Lawrence, thank you so much for taking the time. I think this is going to be really helpful for our audience. And I know you have a book, and I’m not sure if you’re doing much on the web these days. But if there’s anything that you want to refer people to if they wanted to learn more, please go ahead.
DrLA: Not really. I’ve recently transitioned out to my new practice here in New York, joining up with my partner Dr. Tania Dempsey who understands this disease just as well as I do. And we’re laying the groundwork to establish a new institute, an independent institute for advancing the care and the research and the education in this area and still going through a whole lot of set-up for that.
Obviously, there will be new websites and all sorts of other communications on that matter in times to come. And you’ve already mentioned the book, and hopefully some point in the next year or two I’ll somehow—ha, ha, ha—find the time to write a sequel, so to speak.
DrMR: It was entitled Never Bet Against Occam.
DrLA: Singular. Never Bet Against Occam. It’s a reference to Occam’s razor. All things being equal, the simplest explanation is the most likely. It has a long subtitle to it. I don’t even remember what it is anymore. But, yeah, Never Bet Against Occam. O-c-c-a-m. Available at all the usual outlets.
DrMR: And with the clinic you’re setting up, will you be able to accommodate any kind of telemedicine or distance visits?
DrLA: We are already, in my new practice, accommodating telemedicine to a degree. Initial evaluations need to be done in person. But visits beyond that point, we’re willing to consider telemedicine type visits beyond that. But I think it’s important to… It’s such a complex disease. There are so many facets to it. I think it’s important to establish that initial relationship face-to-face, in person. Others may disagree, but that’s just the approach we take.
DrMR: Gotcha. All right, my friend. Well, thank you again, and I guess until our paths cross again, keep doing what you’re doing because I think it’s fantastic and you’re helping a lot of people.
DrLA: All right. Thank you very much, Michael. Appreciate the opportunity.
DrLA: You have a good evening. All right. Bye.
What do you think? I would like to hear your thoughts or experience with this.
Dr. Ruscio is your leading functional and integrative doctor specializing in gut related disorders such as SIBO, leaky gut, Celiac, IBS and in thyroid disorders such as hypothyroid and hyperthyroid. For more information on how to become a patient, please contact our office. Serving the San Francisco bay area and distance patients via phone and Skype.