Psoriasis is a challenging condition for both patients and practitioners. With multiple clinical presentations and a laundry list of triggers and exacerbating factors, what's clear, is that there is no one-size-fits-all when it comes to treatment.
Today we are joined by integrative dermatologist Prof Michael Tirant who has a passion for sharing the knowledge he's amassed over three decades as a clinician and a researcher. Prof Tirant takes us through the many aetiological factors underlaying psoriasis and what guidance he gives to his patients about diet, lifestyle, nutritional and herbal considerations as part of a personalised, integrative approach to treatment.
Covered in this episode
[00:30] Introducing Prof Michael Tirant
[04:41] What is psoriasis?
[06:20] What are the drivers of psoriasis?
[10:40] How many types of psoriasis are there?
[14:02] What are the triggers for psoriasis?
[16:32] The role of the microbiome
[20:34] The rise of antibiotic resistance
[25:16] The role of super-antigens
[31:07] Dietary and Nutritional considerations for psoriasis
[39:03] Herbal medicines for psoriasis
[44:53] Long term vs. short term results
Andrew: This is FX Medicine, I'm Andrew Whitfield-Cook. Joining us on the line today is Professor Michael Tirant. He's the founder and principal consultant specialising in integrative dermatology at the Psoriasis Eczema Clinic in Melbourne, Australia.
Professor Tirant is a full professor of the dermatology and venereology at the University of Rome "G. Marconi" in Rome, Italy. His special interests are the pathogenesis and integrated treatment approach for psoriasis, eczema, vitiligo, and other auto-immune disorders.
Welcome to FX Medicine, Michael. How are you going?
Michael: Yes, good morning, Andrew. How are you?
Andrew: I'm well, thanks. I understand you're a little bit jet-lagged. You've just flown in from overseas?
Michael: Yes, I've just attended a conference in Vietnam and in Malaysia and just flew in yesterday morning. The voice is a bit croaky, so bear with me, please.
Michael: That is correct, yes. We did one yesterday, and we'll be doing another one on the 18th of June.
Andrew: What topic is that going to be covering?
Michael: The one yesterday was on super-antigens and the way super-antigens act in dermatological conditions, and our treatment approach, and the innovative approach of how to now treat a lot of these very severe dermatological conditions, where bacterial, viral, or microbial infections are involved. Especially in psoriasis. The treatment in June will be primarily with psoriasis.
Andrew: Well, that's what we're talking about today. So I guess let's start off, right at the beginning, a little bit about you, because you've been in dermatology research for over 30 years, right?
Michael: Yes, I have. My research in dermatology actually started in the early '80s. A friend of mine had a severe dermatological condition, and the condition was...had a waxing and waning pattern. Obviously, went to see GP, got improvement, but one week, two weeks later, was back to square one. So, that's when I started thinking surely there must be something else involved, that we must be meeting the causative factors or the main issues driving the condition, and that's what got me started.
Andrew: I mean, this seems to be...it's almost like the perfect drug, isn't it? The perfect drug is something that never heals the condition but treats the symptoms of the condition, the expression of the disease, very well. Hence, the need for the medication continues.
Michael: Right. And it's been going on in the majority of the diseases that we treat. I mean, patients want quick results, so they want that quick drug. But then, when you tell them the reasons why they've got their condition and the approach that they should take to get a better long-term solution, most of them would like to do it, but they are a bit reluctant because they want the quick results.
Michael: So, the whole basis of integrative dermatology is to teach the patients how to look at their condition long-term and to manage their condition long-term. Yet we start them giving them topicals to relieve their symptoms, give them a treatment approach and management program where they could look at triggers that are exacerbating their condition. And if they adhere to that, the majority of patients get excellent results.
Andrew: It's the age-old job, if you like, isn't it? The uphill battle is the continued motivation of patients, even when they've seen the results.
Michael: Of course. And it's a continuing thing, you know? Like, you've got to continue to explain to them… They're very good when their condition's doing well, and then, as soon as it rebounds, they come over and they're very sheepish about the whole thing. It's as if, "It's time for my confession." So, they've got to confess, and we've got to absolve them of their sin and start again.
Andrew: So, let's talk a little bit about psoriasis. We think we know about it, but what is psoriasis, and just how prevalent is this condition in Australia? And, you know, you went over to Vietnam. Do you see different prevalences in varying areas?
Michael: Yeah, it's certainly...in different parts of the world, it's different.
Well, psoriasis is a chronic inflammatory skin disease. It's characterised by different presentations. Plaque is the most common psoriasis. You can get papules on the skin, red papules or macules. It can be extremely pruritic, and it can lead to other comorbidities in psoriasis where you get new psoriasis, and also you could get psoriatic arthritis, which can be very severe and debilitating for the patient.
Andrew: And what are the clinical features of psoriasis? You mentioned plaque and the macular papules. What's happening with the pathophysiology here in the different presentations?
Michael: Well, you're getting keratinocyte buildup a lot faster with psoriasis than with normal skin. The turnover is about 20 times faster. Hence, you've got successive skin buildup and flakiness all over the place. So, that's what causes this different types of presentation.
You can get this parakeratotic presentation, hyperkeratotic presentation, dyskeratotic presentation. These are all different presentations that you get. And interestingly, treatment varies according to the presentation you see. I often look at when people talk about, "I have a treatment for psoriasis." "Yes, well, what type of psoriasis are you talking about?"
Michael: Because there are different presentations for psoriasis. We treat the presentations, not the name, if you understand where I'm coming from?
Andrew: So, what's the basic runaway issue here? I mean, you know, proliferative issues, you're thinking more like, you know, the cancers, the endometriosis, that sort of...you know, hyperplasias. Is there a...you know, is it a loss of apoptotic mechanisms, a loss of autophagy? What are the drivers here?
Michael: It's an auto-immune condition, so it's self-recognition of cells. So, the body basically starts attacking itself and destroying itself. So, that's basically what's going on with psoriasis and a lot of other auto-immune conditions. So, that's what's going on in the overall etiology and pathophysiology of this condition. And it can become very, very severe. And like I mentioned, especially, when it gets into the joints. With all of this, you're getting more and more build-up of skin.
So, you're going from a phase of a macular presentation where it's flat. Then it becomes papular. Then it can become parakeratotic, where it's getting thicker and thicker, and it becomes hyperkeratotic where it's actually it’s so thick on the skin, it's like, you know, crocodile skin in some presentations that we see.
So, there's this constant transformation, depending on if it's treated or not treated and how severe the condition is.
Andrew: So, the presentation that we see, that we're treating in an orthodox manner, is really the dysfunctional remodeling of an inflammatory process that goes on, much like what happens with, you know, say, osteoarthritic joints or rheumatoid arthritic joints where you get a remodeling. Is that what's happening?
Michael: Yes, correct, yeah. There are, Andrew, there are a lot of inflammatory markers and mediators that we're talking about here. Psoriasis is not a simple condition. It is a very, very complex disease where you have a lot of triggers, provoking factors, if you want to call it that. There are a lot of comorbidities involved, and there are a lot of inflammatory markers and mediators. Interleukin-1, Interleukin-2, Interleukin-6, Interleukin-8, Interleukin-12, Interleukin-11, 23, etc.
Michael: And tumor necrosis factor is playing its role. So you've got all these things converging and effecting, basically, the flare-up and the flakiness of the skin.
So, when people talk about getting a solution for psoriasis long-term and finding a molecule that will actually clear up psoriasis, there are many molecules already on the market, but because the etiology and the pathophysiology is so, so complex, it's very difficult to have one treatment that will ever fix up psoriasis. It's impossible, actually.
Michael: Because you're covering one or two pathways, but there are another 25 pathways that need to be looked at. They're each genetic, and so overall, you've got this genetic predisposition, and so far, we've identified 13 genes that are involved, and we don't even think that's all of it yet.
So, we've gotten 13 genes that have got a dysregulation going on. You've got all of these mediators working together. How are you going to get a solution with one topical or one systemic drug to fix it? That's why there are many systemic drugs, and they all play a role. They all help. But it doesn't fix it.
Michael: Now we're moving to the new age of molecules, now. We're looking at biologics. Back in 1995 to 2000, biologics were going to be the fix-all. It was called the ‘new dawn of psoriasis treatment.’ And we move on 20 years later, we're back to square one!
Andrew: Oh really?
Michael: Because we do have these molecules that have come on the market. Having said that, they do provide some benefits, but you can't fix it. You know, like, the government's just recently advised that they will be covering one of the biologics for very, very severe psoriasis. And it's a good thing. You would give some benefit to some of the patients, but not all. And it won't fix it long-term. Unless you start looking at some of the causative factors that are driving the condition.
Michael: Well, there are many types. I'll go through them. You've got plaque psoriasis, which is chronic plaque, which is the most common form. And then you have guttate psoriasis, which is a type of psoriasis that flares up following a bacterial, viral, or microbial infection. And it's very rampant, that type of psoriasis. From one day you may not have any psoriasis, to the next day, you are absolutely covered.
Michael: Because the T cell activation is so large.
Then you've got flexural psoriasis, which is in flexions where skin touches skin. That's another form of psoriasis. Then you've got annularis, psoriasis annularis. It presents on the skin like a round circle.
Then you've got pustural, a weepy type of psoriasis. Then you've got palmoplantar psoriasis, which affects both the palms and the feet. Then you've got exogenative erythrodermic psoriasis, which it's like a red man syndrome where the whole body's red-raw. Then we have scalp psoriasis. Then we've got nail psoriasis. Then we've got psoriatic arthritis.
So, there are different variants of psoriasis. For example, you mentioned when we talk about treatment. If you have plaque psoriasis which is dry and flaky, obviously, you're not going to treat it the same as pustular psoriasis which is weepy. It's not possible. You cannot get good results with a topical where you're treating, like they use a lot of different topicals on the market for the same condition, and no wonder it doesn't work. Because one is very dry and flaky, and the other one is weepy. So, how can you treat the same condition, those two conditions, with the same topical?
Michael: It's not possible.
Andrew: Yeah. When you get something like a diffuse plaque type versus the annular type, the circles, I'm trying to understand why the immune system of the body would make it a discreet presentation…
Michael: It's the nature of the beast. You know, we don't know that. We don't know why, all of a sudden, you've got all of these round little patches that are almost perfect on the body. They're so spherical and round, it's unbelievable when you look at them.
And then you have plaque psoriasis which is, like, variable, you know? You get many different presentations on the skin. So, we ask the same questions. Like, if you look at pustular psoriasis, it's like a lake of pustules on the skin. And those pustules, before they erupt, they are almost identical. And you think, how did they become like this? What's driving it to become like this? All we know is that it's flaring it because of all these mediators and markers that are going on, but the exact presentation, the exact look of it, is difficult.
What I can tell you, though, is most times, it's bilateral. So, what happens on the left side of the body happens on the right. So, we know, because of this genetic driving force behind it, if you understand what I'm saying, it's definitely a genetic condition, so that's why it's bilateral. There is a genetic pre-disposition there, so that's why you have this bilateral presentation.
Michael: With elbow, left elbow, right elbow. Left knee, right knee. So, what happens on the left happens on the right.
Michael: Now you're talking, Andrew. There are triggers. I've been working on triggers for over 30 years. There are...I've divided them into two types of triggers. There are what I call primary triggers. Primary triggers are more the initiating triggers, the...that's what starts the psoriasis the first time. And then there are secondary triggers. They are more exacerbating triggers or fueling triggers. So, they keep the condition going.
When we talk about primary triggers, there are four major ones that we deal with. The first one is Koebner phenomenon, or injury or trauma to the skin. So, if you have an accident, for example, or you have an operation where you damage the skin, where you create a portal for infection or potential release of super-antigen reactions from bacterial infections on the skin, then that can initiate a flare-up.
Then you have drugs, clinicals, some medications that we take, for example, mood-stabilising drug like lithium can initiate a flare-up. First-time flare-up. So, drugs can drive it alot. Like, that's why a lot of patients, when they go on medications, I always tell them, "Please get your doctor to talk to me first because none of the drugs, especially blood pressure medications, can start a flare." Beta blockers are well-known for that.
Infections. Staphylococcal, streptococcal infections, bacterial infections. What happens there is the bacteria releases toxins in the system. These type of toxins have a special name. We call them super-antigens, and normally they activate the cell, a phenomenal release of T cells, up to 20% of T cells in the body are activated, hence you get this massive flare-up…
Michael: With guttate psoriasis that I was explaining before.
Michael: Then you have stress. Well, when talk about stress, there are two types of stress that are important here. Acute stress initiates the first-time flare. Chronic stress flares it up or, like, exacerbates the condition. So, that's very important in differentiating what type of stress we are dealing with and how we manage that stress. Because that would start the condition or it would cause this chronic type of psoriasis to continue.
Andrew: So, humans aren't very good at looking at multiple causative factors. You know, like these very poorly-identified Clostridiae group of things called segmented filamentous bacteria, SFMs. They seem to inhabit the infant gut, and then they seem to prime the immune system, but as long as there's a good, copious amount of probiotics and good bacteria there, that sort of puts the brake on and says, "That's enough, thanks. You can stop now."
When we don't have that good milieu of protective bugs, there may be this priming for auto-immune disease. Any research...they've looked at rheumatoid arthritis, for instance, but is there any research that you know of with these SFMs?
Michael: Well, I think we have. We've looked at probiotics. We've looked at the gut microbiome and all of that. There really is a benefit to probiotic, Andrew. I'm not saying there isn't. But we've done a lot of work on that back in the early '90s because I had a focus on that. And we did trials where we did probiotic supplementation for a number of patients. When I'm talking about "a number," it was over 140 patients. And I'll tell you, just with probiotic supplementation alone, there was minimal improvement, less than 1% better than, when you're looking at all the markers.
So, although probiotics are important, we must establish first what kind of probiotic we're talking about. You know, some of probiotics are T1 treatments. Some probiotics are T2 treatments. So, if you have a concoction of both where, you know, a probiotic, one is T1, one is T2, and you mix them up, you get minimal effect.
And there's a lot of anecdotal evidence. I mean, I speak to a lot of people who have had probiotics, and they say, "After I take probiotics, I get some improvement." And I say, "What else are you taking?" Then they give me this long list of 5 or 10 different things that they're taking.
Andrew: Yeah, okay.
Michael: So, it's very difficult to say, well, the benefits are coming from the probiotics. And that's when we actually had our own probiotics in the early '90s. And because I didn't see the huge benefit, I didn't feel I wanted to continue down that line.
Michael: But having said that, now, we now have a lot of new thinking. There are a lot of new strains that we are looking at now. And the scheme has its own bacteria on it that are protecting it in a way, like you would know.
So, it's breaking in the barrier function that creates a lot of the problem all the time. That's why I was mentioning before the Koebner reaction where you damage the skin. Now, all of a sudden, you've created this portal where the microbes living on the skin can release toxins. And then you've got this super-antigen reaction going on. And this is very, very important.
And there is also an issue that I see coming forth now where a lot of the bacteria are becoming resistant to a lot of these topicals. That you go in every hospital, you've got to wash your hands every time, you've got to rub it everywhere.
Michael: So that, long-term, I think it's going to damage the barrier function of the skin and create more problems. I think the skin and the body has its own mechanism of defence. We've got to allow it to play a role in itself. I'm not saying we don't use topicals, we don't use medications to try and stop that. But certainly, we have an ability, an innate ability, to defend ourselves, and in a lot of cases, we are not giving ourselves that chance.
And I read an article when I was in Vietnam, actually, that was translated into English saying a lot of these Vietnamese children, they were allowed to play in the dirt, you know, all the time. That now...and they were very healthy children, but now they've got this [clipped out sound]. So, I don't know whether that's a direct relationship or not, but that's what's going on.
Andrew: Yeah, I think the "Dettol generation" handwash has got a lot to answer for. But I do wonder if, you know, perhaps with...I wasn't thinking about probiotics so much. I was thinking about repeated antibiotics, given that if somebody has, let's say, a genetic predisposition, perhaps a certain number of SNPs, and then they get hit with not one but a multiple, successive amounts of antibiotics, I wonder if that priming is lost in the gut.
Michael: Yes, that plays a big role because if you are on an excessive amount of antibiotics, like we see in the patients with acne, after a while, their condition becomes worse. Not better. Worse.
Michael: Because you're destroying the gut flora. To a certain degree, the balance is destroyed. And even if you incubate and you start with new probiotics, the gut flora, individually, everybody's got its own gut flora. Now, you could change it, but if you change it for a little while and then you pull back and you don't provide a probiotic, it returns back to what it used to be. Because that's...you are born to be like that. You are an individual. Everybody's different.
So, we're trying to normalise and make everybody the same. And it's like saying everybody's going to be treated with steroid for psoriasis. Well, a steroid might help 5%, but 95%, it's not going to get [inaudible].
Michael: Because… I hear it a lot of the time, patients will come and say, "Ah, my friend used X, and he got great results, but I've used it and I didn't get any results. Can you tell me why?" Well, because you're different. That's why.
Andrew: Yeah. I wonder if the future will include the use of faecal microbial transplants for things like psoriasis.
Michael: Well, there are talks about that, and there are investigations. I know in Russia they've looked at that. There's part of India that have also looked at that. It could provide some benefits, yes, of course.
But there's a bigger thing that we are faced with now because a lot of the bacteria, the microbes, are becoming resistant to even the strongest antibiotics we have now, Andrew.
Michael: A lot of the treatments that I look at topical, treating inflammation or infection with staphylococcal infections, now, on the skin. And vancomycin is not treating it.
Andrew: I'm aware of VRE, vancomycin-resistant enteritis, but you're talking about skin infections now?
Andrew: Ahh, right.
Michael: So, a lot of the skin infections about 20 years ago which responded to a lot of these strong antibiotics are not responding now. So, now you have this issue that you have an infection on the skin...I've just come to a hospital in Hungary where there was severe, severe bacterial infection. Started on the foot. Now, they could not resolve it and it started eating up. From the foot, it started eating into the leg. So, they amputated the foot. So, it worked with a knee.
Andrew: Now, the knee was...basically, something is eating the leg, and it's apoptotic, so it's no good, so they had to amputate at the knee.
Next thing, it went into...towards the pelvic area. So, it's not one, it was a ward full of these people. There were at least 27 of them there. Now, what is the future for these people? You know? Like, you've got these bacteria who are becoming resistant, and it's not the bacteria that cause the problem, it's the toxins that the bacteria release. So, it's an indirect relationship there. So we're looking at, all right, we can't cure the bacteria now. We must look at how we're going to complex or deactivate the toxins that are causing all of the massive T cell response that potentially...that's how toxic shock happens, and you can kill the patient, like, you know?
Michael: But, this massive release of toxins. And that's where the problem is. And these toxins can stay in your system for years. We've looked at patients who have had very severe conditions, and they tell you, they had the condition five or six years ago, and yet the toxins are still floating around. So, the toxins are not being mopped up by the immune system for whatever reason. We don't know.
So, we must...that's where my research is pushing me now. To look at all these super-antigens and how we can target them, and deactivate them, and complex them, and whatever we can do with them. And there are very strong results that we are getting at the moment, but they are obviously starting results. We've got to look further into how they're working.
Michael: Yeah, so what happens is that when you have a bacterial infection, the bacteria releases different types of toxins. Staphylococcal, for example, infections, the main toxins will be staphylococcal enterotoxin B, and that plays a huge role in atopic dermatitis. It's actually what drives atopic dermatitis.
Now, if you have an infection, the doctor gives you some antibiotics, but the antibiotics are not clearing up atopic dermatitis. They may improve the staphylococcal infection, but most of the time, they don't get rid of it fully.
But further on, the bacteria has already released the toxins into your system, and that's what causes the psoriasis or the eczema to flare up. Now because they cause massive T cell activation, so, what do we do now? We've got these toxins that we have floating around in the system. The body, for whatever reason, managed to get rid of some of it, but not all of it. And as long as he got...that's why it becomes chronic.
Michael: Because these things are still there. You can't get rid of it. So, that's where...the direction I'm going. I'm going at how am I going to get rid of these toxins? And I'm looking at a lot of bio-herbal active ingredients to try and mop them up. Because with conventional medicine, normally, you've got a single molecule. You've got a steroid, you know? Or you've got cyclosporine, or you've got methotrexate. So, they’re...single molecule, and the pathway of activation, and binding, and the mechanism of action is very...it's one-directional. But when you've got a lot of toxins which different surface markers binding, how can you use one molecule to deactivate all these different toxins? It's not possible.
Michael: So, that's why I'm looking at complex molecules that we can put together. Different ingredients that could potentially target different areas, different binding sites, and hopefully deactivate those molecules.
And we're doing a lot of work on that. We're looking at X-rays, crystallography to look, potentially, how these molecules bind. And interestingly, they have two binding sites. They've got what we call a low binding site and then a high binding site, and you must bind both for you to be activated. So, just taking this probiotic or whatever we're taking, I'm not putting probiotics down by any way, shape, or form, because I use them myself. But it's too simple. It's very, very complex.
And that's what we're looking at at the moment. We've moving into...into a time, actually, that takes us back in history. We're looking at back into natural medicine because of these very complex molecules going out there, and then you can look at one… For example, Rosmarinus who contains a lot of ingredients, like, you would know. So, we are identifying the structures in these products, what structures they have in crystallographically, how we can use these structures to bind the super-antigen molecules. And it's a very complex situation, but if we can, then from there, we would want to go and do vaccines from it. But at that point, it would be very, very exciting. And that's what my work is doing at the moment. That's what I'm working on.
Andrew: Have super-antigens been, you know, well-classified and identified in, say, you know, biopsies of plaques? Or, you know, nummular…
Michael: I was going to talk to you earlier about this because I've done this. If you take involved skin and uninvolved skin and you do biopsies, you will find that in involved skin, there are at least 375 times more super-antigens than in uninvolved skin.
Andrew: Whoa, yeah.
Michael: Yeah. So, it's very well tested and shown, yeah. And there are different ones, obviously. Different types of super-antigens. In psoriasis the main one is streptococcal pyogenes exotoxin C, and in atopic dermatitis, it's staphylococcal enterotoxin B.
So, and there are many of them. I could list you a hundred of them. But they play minor roles compared to major roles. Their structures are totally different. Their binding sites are totally different. So, that's why I'm saying, we've got to look for complex different types of ingredients to mix together that would hopefully bind and deactivate those molecules.
Andrew: And are we talking about a circulating serum load because of priming, or...like, or how are they being furthered? Are we talking about chronic infection feeding it?
Michael: They are in the blood serum, also, but they tend to be localised in lesions.
Michael: Recirculating initially, but they go to a point where they...like, target or directional to where the lesions are.
So, they start with the initiation of psoriasis and these molecules, and then, once it's like migrating factors. So they migrate into this. They are skin-homing. They skin-home. They go to the skin and eventually end up in keratinocytes and all that.
Andrew: Yeah, yeah. I'm just wondering about, you know, when you get the waxing and waning of the presentation of psoriasis, if they're drawn to, if you like, or concentrated, in the lesions? Do you see a corresponding waxing and waning in the serum levels? And if so, what's feeding them?
Michael: Yes, there is a waxing pattern, also, in serum and lesional super-antigen. But the waxing and waning pattern when psoriasis gets better is more directed towards triggers.
Michael: So, if your triggers are getting better, then your skin will get better. And if your skin is getting better, then there is less super-antigens in the lesions, like that.
Andrew: So, then we go back to the nutritional and dietary aspects that you've employed over what, 20-odd years, 30-odd years. Tell us a little about that. How does diet and nutrition affect psoriasis quantitatively?
Michael: Well, we know very well that a diet that's very good, strong anti-inflammatory, is very good antioxidant, has huge benefits on psoriasis.
In one of the papers that I wrote a couple of years ago, we looked at strong antioxidant powers of some of the essential oil molecules that we use. And interestingly, everybody around the world is surprised that these little of molecules that I put together and we tested, have seven times more antioxidant power than the strongest. Even Trolox, which is a very strong antioxidant on the market, more than seven times.
Now, it's not the amount that you are using, it's how it's combined together that we find. Because we're not using grams of the material, we're using milligrams of the material. And yet, for whatever reason, it has huge impact on rough species and it has huge impact on fibroblasts for psoriasis. And we did all that. We got a study from that. We got skin of all the lesions, the biopsies that were done, and it's very, very clear.
So nutritionally, now, we can see with diet… we try as much as possible to follow the Mediterranean diet. We believe that has huge benefits for psoriasis sufferers. Except for some of areas of that where they use a lot of tomatoes. Well, tomatoes are very well-known to exacerbate psoriasis. So, with psoriasis, we've got to look at a diet which is very low in histamine. Because histamine plays a big force in it. You don't want to be eating materials that contain histamine because histamine will cause psoriasis, and the minute you start scratching the skin, if you didn't have psoriasis there, because of the Koebner reaction, like I mentioned before, if you scratch an area and damage an area where you didn't have psoriasis, well, very soon you will. Because the Koebner phenomenon is a primary trigger.
So, obviously, we're looking at diet, or nutrition, which takes away from a lot of histamine. We look at a diet which contains very few diuretics. Because the skin legions are already very hot, very dry, very flaky. You don't want to be drinking a lot of alcohol because it's a diuretic. It's going to make it worse. I've been talking about alcohol, and coffee, and sugar for at least 30 years.
Michael: And back in the '80s, they all thought I was nuts. But now, finally, about three years ago, they admitted, even the medical professional, they've admitted that, yes, alcohol and coffee can definitely play a role in psoriasis.
Michael: So, you want to keep away from all these high levels of sugar or take away these type of fast foods, because it's not the best.
I'll add… because I find that back in the '80s, high concentration or high levels of green vegetables in your diet, this is absolutely crucial. So crucial that I stayed two years at Monash trying to find out how it worked and why. Because we had a trial where we had 37 patients who were vegetarian. And those 37 patients, 26 of them cleared up roughly in about three months compared to the others which took a lot longer. So, there was a definite benefit with these vegetarians.
So, I followed up, and I thought, "Well, what is it? Is it different chlorophylls? Is it different phytonutrients in there?" After spending two years, I just decided, "Look, I'll just tell the patients to eat plenty green vegetables," rather than try to find out what it was.
Michael: It was impossible. I just couldn't find out. But I think right now, my patients, they consume at least 30% of their diet are green, leafy vegetables. That's very, very important.
Andrew: It's really interesting. Like, you mentioned tomatoes earlier with one of the nightshade group of plants, and that was popularised by Paavo Airola. Tomatoes, eggplant, chili, capsicum…
Michael: Most of these are very...not very...you wouldn't want to be having those if you've got psoriasis unfortunately.
Michael: There are other reasons, but because the histamine levels are very high.
Andrew: Right. Okay, got you. And the other thing was, you just spoke about green vegetables, and this smacks of what Clint Paddison has been using with his rheumatoid arthritis, and he's developed a program. It seems very, very similar. Do you find that some fats, even healthy fats, can be inflammatory?
Michael: Well, some healthy fats can be inflammatory. We talk about, you know, like...I would go as much as saying, you know, like, they only...you know, the fatty acids, some of the better ones, are all right, but the fish oils, then, I would say they are okay, but again, I'm sitting on the fence with a lot of these. Because I did a trial back in '93 where...I really believed in fish oil in those days and found out that we just give fish oil for psoriasis and eczema, and the benefit was minimal. It was so disappointing.
Andrew: This is really interesting.
Michael: We actually made our own fish oil. And then we decided, "Well, how can I now give the fish oil to my patients when I've just found the results to be basically ineffective?" So, we discontinued our line.
But about seven years ago, a friend of mine in Italy, we looked at this again. To make fish oil effective, it can be effective Andrew, you need to get 9,000 milligrams three times a day. Otherwise, it didn't have any benefit.
Andrew: Yeah, the anti-inflammatory actions, you need really high doses.
Michael: You need high doses. How many people are going to take 27,000 milligrams of fish oil a day?
But the other thing that's very, very useful is vitamin D. So, I’ll just talk to you about that, because that's really, really important. That's why sunlight is so effective. So I would encourage patients, especially during winter months, to increase their dosage of vitamin D, because that's very, very helpful.
Most of the vitamin D that you have in the shop, they tell you to take one capsule. Well, you're not going to get vitamin D poisoning unless you're taking high levels of vitamin D. But generally, with the amounts, I will increase it maybe to two to three capsules per day. It has enormous benefit.
Andrew: What about the different forms of vitamin D? There's the vitamin D3 and there's the drug form. Which one do you prefer?
Michael: Yeah. If you could just recommend to the patients to get a bit of sunlight, you know? Because that's the best form, you know? The improvement in sunlight and a bit of salt water is amazing. Now salt water, it's sea water, not salt put in a bath. That's totally different. But certainly, it's sunlight has the big...that's why phototherapy is still being used after, you know, hundreds or even thousands of years.
Michael: It's primarily the best treatment. It's just not possible to go in and take all your clothes off and...you can, but the police might catch you when you. Run around on the beach and get a bit of salt water, because that's the best treatment. Phototherapy is still the best treatment.
Andrew: And you mentioned some herbs before, or you mentioned the use of herbs. What herbs are most beneficial in psoriasis? Do you find various combinations more successful? And, indeed, you mentioned dosing. Do you find that, you know, going lightly, treading lightly, has a better effect than going in rather heroically?
Michael: Yeah, definitely, because sometimes, the patient may respond negatively to your herb. So it's not good doing heavy handed. Like calendula is very effective. We'll use...soleirolia is very effective. There are far more very effective… Baicalin is useful. All these herbs are very...back in the late '80s, I was just mixing all these herbs together. And sometimes I would get good results, sometimes I wouldn't. I didn't really know why until I started classifying the different types of psoriasis.
So, different psoriasis, you would give different variations of the herb. So, that's one thing it taught me. But then, I've always thought, like, the conventional medicine is not always better. So, if you take 5 milligrams, seeing some result, if you take 20 milligrams, you will get a better result.
Andrew: Yeah, nup.
Michael: It doesn't work, you see? It's almost the reverse of it. It almost works on the principles of homeopathy, I suppose. Because keep in mind that a lot of these cytokines and chemokines in your system are at the levels of nanoparticles 10-9, 10-12. A lot of the chemokines and cytokines concentrations in the body, the Interleukins and all them, it's 10-10. It's a very low amounts. So, if you've got a low amount of molecule floating around and you're trying to hit it with a sledgehammer of 5 milligram of something, it doesn't bind. Somehow, it just doesn't respond.
So, small amount. And it's good to only test one thing at a time because you won't know the benefit otherwise. Like, if I give a patient some medications, now that I've got more experience, I know which ones maybe I could mix together, or different ones. But in the initial stages we being a researcher, you want to test one thing and see that that one thing works or you see some benefit. And then you would test another, and then you would test another. And then you would look at, all right, what happens, then, if I combine two together? You don't want to combine 10 in one pill, but how would you know which one works?
Andrew: I wonder, though, if the future of herbal medicine will include, you know, lower dose. And medicine always looks for a dramatic significant response, and maybe that's not the way we need to go. I'm wondering if the future of herbal medicine will include more elegant responses and that the combinations will show, you know, one herb might have an effect on, let's say, CD4. Another might have an effect on CD8, or various Interleukins. And I wonder if that concert… naturopaths think of as the beauty of herbal medicine in its entirety, not giving a sledgehammer, as you mentioned. And so, I wonder if that might be borne out by this sort of more elegant repertoire rather than a significant punch?
Michael: Well, I think that direction is definitely what you just said. You know? I believe that, especially with the type of work I'm doing on super-antigens, I know the molecule that will target that particular super-antigen, for example. But if I was to go now and say, "This is the molecule I want to turn into a medication," it becomes a drug because it's a single molecule. Now, for it to become a drug, I've got to put on the table at least $500 million.
Michael: Now, if I had $500 million, I would be at the Gold Coast, lying on the beach. So, you understand where I'm coming from?
Michael: So, what I'd prefer to do is we will keep it as herbal medicine, and I would tweak the formula as much as possible to delivery the concentration or the ingredients that I'm looking for. That's how I see the future of herbal medicine, actually, if it's done systematically and scientifically, is very, very powerful. We must do it like that. We cannot just say, "All right, Thomas, come in. I gave John a very good formula that worked well for his psoriasis." Now I'm going to give the same one to Tom.
Michael: It doesn't work like that. You've got to evaluate what's behind Tom's psoriasis. What type of psoriasis? What is the presentation? What is the potentially...if the presentation parakeratotic, hyperkeratotic, then you try and evaluate...well, super-antigens, I know for sure would be playing a role in it.
So, the concentrations of super-antigens, unless you start doing a modeling where you can do tests to work out super-antigens. In the future, if they can, it would be costly, but you still could. Because there are big laboratories now that are opening up to...for researchers to do a lot of these tests. So, sometimes once we search it, get in to it, and down the lines, I think patients would follow.
But it's a very, very interesting area, because you talked about rheumatoid arthritis before. Well, super-antigens are involved in rheumatoid arthritis.
Andrew: Right, right.
Michael: We talked about congestive heart disease. They are involved. They are involved in skin cancers. They are involved in so many things. So, primarily, if you look at what is the biggest cause of disease around, I'll put my hand up straight away and I'll tell you, "super-antigens."
Andrew: But obviously, at some stage, you've got to offer them some succour, some relief from their symptoms. So, what about treating topically versus internally? And, you know, I'm wondering about if you employ things like honey when you might suspect that there's an infection in the skin.
Michael: Yes. You must pick out your own approach, you see? Because if you're going to treat them with herbal medicine orally, it takes a while to get a response. It can take four weeks, six weeks, eight weeks. So, if the patients initially doesn't see that improvement, they lose faith. Because, remember, they tried everything before they come and see you.
So, now you're giving them some medications, some probiotics from whatever else the practitioner decides, and if that patient is not getting a response after three or four weeks, they don't believe in the treatment again. And that belief, it's very, very important.
So, we have this dual-action approach. We treat the skin. We know very well with our topicals, Andrew, our topicals are better than anything on the market. I'll put money on that, too. Topically, we can get a response with psoriasis in seven days. They can see a benefit in seven days.
Michael: So, once patients have benefit in seven days, then they become positive about the treatment. Then, long-term, then, we can target those triggers.
I mean, it's very difficult to tell a patient, "All right, look, go and make these dietary modifications." And basically, if they are on a pretty bad diet, you have to change their diet, change their lives upside down. So now they've tried different, like, treatments in the past with minimal response. They've come to see you. Now you're turning their lives upside-down by telling them to make so many changes, lose weight, do this, do that. And after four weeks, they don't see anything. Because you're not going to get a result in four weeks if you just do that.
Michael: So, we need to do something that gives them that quick result and then work on them and give them the trust, build the trust in natural medicine. That's how you've got to do it. And that's why we're very positive about what we do, obviously, because the business has been so successful. We've got...internationally, we've got treatments in Europe. We've got professors of dermatology using my treatments. We've got clinics in Vietnam. We've got clinics in Singapore. We've got clinics in Czech Republic. We've got America who's knocking on the door wanting us. I've just come back from Malaysia where the Malaysian government is involved. So, they all see the future of dermatology as integrative dermatology.
Michael: This is the future.
Andrew: Yeah. I think your ATMS webinar in June is going to be fantastic and deliver some real clinical pearls. All the info on how to attend is on the ATMS website. And I've got to say, Michael, thank you so much for taking us through what is more than a complex disorder and requires, you know, a real understanding of the variations so that you can offer a concerted approach, a sort of directed approach to relieve symptoms in your patients. So, I just thank you so much for joining us.
Michael: Well, this is my work. And basically, what we’ve just touched on it, Andrew, you know? Like, this was...it's been ongoing for years…
Michael: So, I'm more than happy. We're looking at maybe doing courses for practitioners to get everybody involved. My knowledge is not just for me. My knowledge is to be shared.
Like, in the past, we used to have a franchise in Australia. We had 37 practitioners at one stage working with us. But for whatever reason, people get a bit older, they retire, etc. And my focus now has turned to Europe because, being a professor of dermatology in Europe, I've got attend so many conferences, so I spend a lot of time internationally.
But it’s my demeanor, I love teaching, I love talking, like you can see. I've got a passion about what I do. I like to share the knowledge.
Andrew: But it's also a passion for your patients. I really thank you for sharing that.
Michael: Absolutely. Our patients are number one, you know? Without a patient, we don't have a job. So, I still tell my staff that all the time. So, patient is number one, and this is what I worked for. I work to help him.
Andrew: Brilliant words. This is FX Medicine, I'm Andrew Whitfield-Cook.
Michael: Thank you very much.