Naturopathic support for Topical Steroidal Withdrawal with Emma Sutherland and Ben Lee

Naturopathic support for Topical Steroidal Withdrawal with Emma Sutherland and Ben Lee

Naturopath Ben Lee shares his clinical insights into the challenges associated with topical steroid withdrawal. With skin conditions so prevalent in our society, the prescribing of topical steroids is on the rise. Ben’s integrated approach to firstly identifying the condition, and then treating from the root cause addresses the mechanisms of action, the signs and symptoms to look out for, and how we as healthcare professionals can best support others to reduce symptoms and optimise skin integrity.

Covered in this episode

(00:26) Welcoming Ben Lee
(02:31) Ben’s personal experience with topical steroids
(04:30) Steroids and their mechanism of action
(06:55) Signs, symptoms and triggers of topical steroid withdrawal (TSW)
(09:45) Key underlying drivers of TSW symptoms
(12:17) Staph aureus colonisation effects on the skin
(15:07) Biologics
(18:35) Testing for TSW
(20:53) How to differentiate between eczema and TSW
(23:04) Eczema and the gut health link
(26:29) Dermal microbiome imbalances and TSW
(29:03) Holistic treatment of TSW
(34:05) Treatment options
(44:00) Thanking Ben and final remarks

Key Takeaways

Topical steroid withdrawal (TSW) is defined as rebound vasodilation from prolonged, inappropriate, and frequent use of moderate to high potency corticosteroids.
The main pathophysiology of TSW is excess nitric oxide production. High potency corticosteroids induce vasoconstriction. When topical corticosteroids are ceased, it leads to rebound vasodilation, nitric oxide increases, flushing and erythema.
Nitric oxide IL-4, IL-13 and Thymic stromal lymphopoietin (TSLP) are the main pathophysiological mediators of TSW and eczema

Common signs and symptoms of TSW

- Thermoregulation difficulties
- The red sleeve
- Headlight signs
- Elephant wrinkles on the skin
- Skin striae

Many eczema patients have a filaggrin gene mutation. This mutation can contribute to a more alkaline stratum corneum pH. This alkalinity favours the growth of staph aureus and impairs skin barrier integrity.

Treatment aims in TSW

Reduce nitric oxide production and strengthen the leaky capillaries.
Reduce staph aureus levels to reduce staph aureus super antigens from entering the epidermis and dermis and triggering T cell responses.
Calm down specific inflammatory pathways such as IL-4, IL-13 and TSLP, because these will increase when the skin barrier is impaired.
Support the nervous system and the adrenals.

Investigations to identify causes

Skin swab to identify potential staph overgrowth.

Differentiate between eczema or topical steroid withdrawal.

Treatments

Vitamin B12 topically has been shown to reduce nitric oxide levels in the endothelium.

1 to 2% methylcobalamin or hydroxycobalamin in a cream base to help with the nitric oxide.

Antimicrobial herbs to reduce staph aureus overgrowth: Coptis, goldenseal, oregon grape, myrrh, and green tea extracts

Baikal skullcap ticks all the boxes for TSW by inhibiting IL-4, IL-13, TSLP, IgE, and reducing the TH2 response.

Vitamin C, lutein, hesperidin, bioflavonoids, and maritime pine bark reduce inflammation, are anti-allergic, and enhance capillary integrity.

Nervous system support through the use of Verbena officinalis as a nervine and gentle bitter to calm/cool inflammation associated with TSW.

To improve skin barrier integrity: evening primrose oil at a dose of around 3-4 grams per day, combined with a fish oil and B-complex.

Resources discussed and further reading

Ben Lee

Connect with Ben: Instagram

Ben's Website

Transcript

Emma: Hi, and welcome to fx Medicine, where we bring you the latest in evidence based, integrative, functional, and complementary medicine. fx Medicine acknowledges the traditional custodians of country throughout Australia, where we live and work and their connections to land, sea and community. We pay our respect to their elders, past and present, and extend that respect to all Aboriginal and Torres Strait Islander peoples today.

Emma: Joining us on the line from Singapore today is Naturopath Ben Lee, a degree qualified naturopath who has extensive training and experience in nutrition and herbal medicine. Ben has a special interest in skin conditions, particularly eczema. His personal journey of healing from severe full body eczema and topical steroid withdrawal guides his evidence-based approach towards treating eczema. Ben runs a busy clinical practice in Singapore, and he's also a consultant to eczema support groups and companies.

Emma: Today we're going to deep dive into topical steroid withdrawal, which is also known as steroid cream withdrawal or red skin syndrome. And learn how to navigate this tricky clinical condition. Welcome to fx Medicine, Ben. Thank you so much for being with us today.

Ben: And thanks Emma for having me. And it's a privilege to be here. I think TSW is very close to my heart and I'm happy to share all the protocols and about my own story about TSW.

Brilliant, I would actually love to start with your personal story and how that influenced your clinical practice. Tell us more.

Ben: Yeah, for sure. So, for myself, I had severe eczema since a child and for years and years I was on many rounds of both topical and oral corticosteroids. So, each time the skin will get better, it would clear up for a while.

But once it stopped, then it can get worse than before. And over the years there was a trend in that I had to use higher and higher potency steroids. And each time they became ineffective or less effective. And I noticed this spreading redness and burning sensation. And it got to a point where I had moved on from class seven, which includes hydrocortisone to class one, which includes clobetasol and at the highest potency, it just stopped working and eventually the immunosuppressants were suggested as a next step. And I just realised that this just wasn’t sustainable. And what happened was that one of my lowest periods in life, I then discovered the work of Dr. Marvin Rapaport who is a dermatologist and he's one of the pioneers of TSW. And so back in 2003 he published a paper about how 100 patients with chronic eczema, they didn't get better until all steroids were stopped and their story was like mine, they had used more and more steroids with increasing potency, but it just did not improve. And so similar symptoms – they had severe burning it was spreading to local and distant areas. And that's what got me into my own journey and clinical practice in TSW.

And it's realistically it's a story that we do see in clinic that patients are using more and more topical steroids to try and get the same outcome. And then we get this rebound effect. And I feel like this is such a fascinating topic and it really took me on a path of hours and hours of research. And what I did come to understand is that this condition is not well addressed in both the naturopathic world and the conventional medicine world, and we're really failing a subset of patients who are experiencing chronic severe symptoms.

You know, in a systematic review of eczema sufferers and their use of topical steroids, the topical steroid withdrawal affected 80% of the women and an amazing 99% of the women said it affected their face or genitals with the symptoms of redness, burning and stinging experienced by all the women. So, before we go any further, can you just give us a bit of a 101 on steroids on their potency, the mechanism of action so that I can understand this?

Ben: Yes, sure Emma. So topical steroids work by a few mechanisms. Our first is vasoconstriction. And number two, they reduce inflammatory prostaglandins and leukotrienes, and they reduce cell proliferation. And so many of my patients, when they come to me, they have the misimpression that when they jump from a class seven hydrocortisone to class two and class three, they think that it is an increase of two or three times.

But actually, if you compare a class one steroid to class seven steroids, so a class seven steroid is hydrocortisone and a class one is clobetasol, the jump is 600 times more potent.

Emma: Wow. Okay.

Ben: And so, one measure of steroid potency is how strongly they can constrict the blood vessels. And so, the higher we go, the stronger the vasoconstriction.

Emma: Mm. So, the higher the class then the more potent the steroid cream?

Ben: Yes. And also, the more potent the strength of the vasoconstriction becomes.

Emma: Right. Okay. All right. That makes sense. Can you explain what topical steroid withdrawal is? And then the main signs and symptoms and any triggers? And I'm kind of curious, like, why do women seem to be more affected than men with this?

Ben: Yes. So TSW is defined as rebound vasodilation from prolonged, inappropriate, and frequent use of moderate to high potency corticosteroids.

So, for example, my patients, when they have been on clobetasol or betamethasone dipropionate for like months and we do see a few things, we see that their skin happens to look more pale because of the blanching effect, because of the vasoconstriction. And then when they stop, then the rebound vasodilation happens. So, I often tell my patients, imagine that you have a water hose, and this is like a blood vessel.

And you clamp down on the hose for a long time and then you just release it all of a sudden; and a sudden water gushes through and blood goes through and then there’s a compensatory rebound vasodilation that happens. And this is actually the pathophysiology of TSW because more blood and more inflammatory mediators gush through the vessels. And so, as a result the patients get diffuse erythema, they get burning. Patients often say I feel redness everywhere and they feel cold, they have thermoregulation issues and you see oozing skin, you see all the interstitial fluid coming out and you see oedema.

So, if I may summarise this into an archetype of a TSW patient. When they walk into my room, they are usually wrapped up in layers and layers of clothing, and they feel cold. And when they come in, they will say please can you turn the fan and aircon off, I feel so chilly. You will sometimes see a classic red sleeve, so the whole arm will flush red, and this abruptly stops at the palms. And this is one of the key features of TSW, the red sleeve.

Emma: Okay.

Ben: The non skin symptoms may be major fatigue because they haven’t slept for weeks or months and there can be depression, anxiety and also not uncommonly, suicidal tendency.

Emma: That's hugely impactful, isn't it? I mean, I know how I feel if I haven't slept for a couple of nights, let alone chronic sleep disruption. And I'd imagine that that is feeding into that inflammatory process as well for sure.

Ben: For sure, Majorly, yes.

Mhm. What is the, the underlying pathophysiology. You've kind of given me a broad sweep but I want to kind of go deeper again. What's happening to this skin on a cellular level? What are the key underlying drivers that are happening.

Ben: Yes. So, there are three drivers happening. So, besides the nitric oxide increases that we discussed earlier, there are a few other areas. Firstly, there is a transient HPA-axis suppression. This happens more commonly when very potent class one steroids are used, and studies in children estimate this to be around 6% and it is reversible when the steroids are stopped. The second driver is skin atrophy because steroids inhibit fibroblast activity and inhibit collagen synthesis, so many patients may see telangiectasia, striae and thin skin.

And they say that if I scratch my skin, it breaks so easily, and they will describe the skin as sandpaper.

Emma: Mm hmm. Okay.

Ben: And the striae - a key feature. So, you see it these red indented streaks on the skin because of the skin thinning.

Emma: Okay.

Ben: Lastly, and what I see very often in my own practice is secondary infections, commonly bacterial. I can't emphasise further how important staph aureus is in the TSW pathophysiology because staph aureus produces alpha toxins and delta toxins, and these trigger major, major T-cell activation. They penetrate to the epidermis and dermis, and they trigger major inflammation.

Emma: Okay. Mm. Fascinating. So, we have a couple of mechanisms. It's the nitric oxide that you mentioned earlier. We have the HPA (Hypothalamic Pituitary Adrenal) axis suppression that is temporary. Then the skin atrophy due to the inhibition of collagen synthesis and then the added layer of the staph aureus colonisation. So, there's a lot going on there.

Ben: A lot. And then also, coupled together with the major nervous system dysregulation of patients, they are in sympathetic dominance all the time and they are stressed, often they are depressed. It's a lot to handle.

Emma: And what else is the Staph Aureus colonisation doing to the skin?

Ben: Yeah. So, if I, if I may summarise one point that I've seen, whether or not this TSW or eczema, we must treat the staph and that's so important. And at this juncture I wish to segway a bit about staph aureus because among adults with eczema, studies show that between 54% to 100% of adults have staph colonisation.

It's not just on lesional skin but it's also on non-eczema skin. And it also colonises the nose. And so, studies found that the extent of nasal colonisation is also linked to eczema severity. And I reckon that perhaps there's some translocation of the staph happening. I also read this study that showed that how gut staph overgrowth is also linked with skin staph overgrowth.

And on this point, whenever I run a gut microbiome test in the clinic, I very often see the majority of cases have high staph aureus in the gut.

Emma: mm Yeah.

Ben: So, if I may expand a bit more about what inflammatory mediators this can produce. Staph aureus entry into the epidermis is linked with increased interleukin-4, interleukin-13 and Thymic stromal lymphopoietin or TSLP. And IL-4 and IL-13 are two very important mediators because if you see the biologics today, one of the most common ones that many of our patients may come in and tell us about is Dupixent or Dupilumab.

And Dupixent works exactly on the IL-4 and IL-13 pathways and both of which are TH-2 cytokines. And we find these two cytokines majorly over expressed in eczema skin. And I'm sure in TSW skin also. They do a few things. Their purpose is to actually stimulate the itch receptors and the increase neurogenic itch. They also increase trans epidermal water loss.

It makes the skin dry, and they perpetuate this constant cycle of mast cell recruitment and makes the patients very itchy.

Emma: Okay so just going back a bit, you mentioned a biologic. Now, I just wanted to I have had an increasing amount of patients over the last six, maybe 12 months that are starting to use biologics. So, I was yeah, I was just so fascinated to see how it was working because I have to say, they do seem to give good results.

Ben: Yes, they do, actually. And if I may caveat at this point, I think as naturopaths, we are not against the use of biologics but only if they are used indiscriminately for long term, then it may cause potential issues. So, I have seen in practice that when there is a big flare up, sometimes there's a role for biologics because it calms down and breaks the cycle.

And when the inflammation has calmed down, you can then go in with our herbs and nutrients to then address the inflammation. But when the skin is so flared up, sometimes the patients have so many allergies and sensitivities, and we cannot go in with many herbs or nutrients without causing a flare. To cycle back to your point Emma, I fully agree that there can be a role for biologics, and in fact we can complement biologics with herbs and nutrients at the same time and make it synergistic.

Emma: Yes. And I do see that that role is being quite powerful. And sometimes these medications can give us the space we need to start working on those underlying drivers.

Ben: Exactly, because the cycle must be broken somewhere. And sometimes when we have tried all the interventions naturally, the biologics may be the higher force intervention that we have to go through. And that's okay, because I've actually seen patients wean off biologics with the blessing of their dermatologists after we address the gut, address the liver, address the nervous system.

And I had this case, after six months off biologics, the skin remained fully clear, because when she was on Dupixent we did all the internal work and now her skin is fully clear.

Emma: Mm Isn't that amazing. That's exactly the kind of case outcome that you want. Yeah. Yeah. And anything else we need to know, you know, in, in that space of the cellular pathophysiology.

Ben: So, one other mediator is TSLP or Serum thymic stromal lymphopoietin. So, studies have shown that the most severe the eczema the higher the serum TSLP levels. And so TSLP activates dendritic cells, and it promotes the mast cell growth and survival and therefore this enhances the itching and the epidermal inflammation.

So, in summary, nitric oxide IL-4, IL-13 and TSLP are the main pathophysiological mediators of TSW and eczema and in fact later on I discuss some herbs that work on same pathways.

Emma: Yes. And we will be definitely be diving into treatment, but before we go to the treatment side of things, how do we test for topical steroid withdrawal?

Are there biomarkers that you're using? Clinic How do we know when to test? You know, is there a diagnosed diagnostic process for these? Because I find it confusing on this front.

Ben: Yeah, 100%. There is no test for TSW. And it's mainly based on clinical signs and symptoms, And I had a few patients say to me Ben, I have TSW but then we actually sent them to the GP for a swab.

And we found that it was actually a bacterial infection and once we cleared the bacterial infection, the skin cleared within one or two months and they could even go swimming and cycling again. So I find that sometimes TSW can be mistaken for a staph aureus infection.

For TSW there are a few key clinical signs and symptoms. Number one, the red sleeve, so the whole arm flushes red, but it stops abruptly at the palms. Number two, but I don't see this so much in clinic, this is called the headlight sign, so the nose and the perioral area are spared from the erythema and the flushing. And number three, you see elephant wrinkles on the skin, with many folds and they appear sandpaperish.

Emma: Mm. Okay. So, we've got the red sleeve where the redness stops at the wrist, but the headlight sign where the nose and the peripheral area is not red. And then the elephant wrinkles on the skin. So, an abundance of sandpaper-like skin. So, no diagnostic criteria from a blood test perspective, but we're looking at those signs and symptoms.

Ben: Yes, that's right.

Emma: Now, if the condition is usually confused for eczema, then how do we differentiate between the two?

Ben: You know, that's a very good question, Emma. And so there are some ways to differentiate. Eczema is usually on the flexors. On the antecubital fossa, and behind the knees. And this is a very atopic presentation. TSW can be everywhere. So, you see a generalised erythema on the chest, on the back, flushing everywhere. And number two is, and I see this in clinic a lot, eczema patients, they don’t report a burning sensation. But TSW patients often do, and they'll say I feel I’m burning up and some of them, they'll be in the bathtub for hours because they feel so hot.

And lastly, eczema patients, they often have no issue if a fan is on them for a short while or if the aircon is a bit cold, they can thermoregulate pretty well. But with TSW, they feel cold at the slightest draft. So, I recall one patient who came into clinic, but she asked for like two or three blankets and she was wearing a jacket already, and she needed more blankets above a jacket because she felt so cold.

Emma: Yeah. Yeah. That's profound, isn't it? Wow. So, they're actually quite, quite different when you look at it like that, that eczema is usually on the fold like this. The elbow folds, the, you know, eczema patients don't say they're burning up and they're not super sensitive to the cold. So, I love that you've painted that clinical picture really nicely.

Ben: No problem. And I also wish to say that sometimes it is hard to differentiate because patients can have TSW plus eczema plus a staph infection all at once.

Emma: Oh, goodness. Now that's confusing. And I guess that's where getting a skin swab done to work out the first step is probably a good idea, right?

Ben: Yes. 100%.

Emma: Now as complementary health practitioners, we, I feel, often have a bias for believing that gut health is the root cause of everything. But are we correct in this instance or is this a classic case of confirmation bias? What are your thoughts?

Ben: Yes, I think this is a great question. So, in my own experience, in my own journey of severe eczema and TSW many years ago, I saw many good practitioners.

They, addressed the gut, they gave me antimicrobials, digestive enzymes, and betaine hydrochloride. But this had no impact on my skin at all. And in my own practice I had a few patients come to me and they had done the various gut microbiome mapping tests and SIBO tests; and had addressed all the issues in the tests and the skin had no shift, in fact it got worse.

So, I think we often discuss the gut-skin axis. But the key point is that it is actually bidirectional. So let me talk about skin-gut axis instead. Okay. So, some studies have shown that food allergy can develop through an impaired skin barrier. So, for example, when children apply a moisturiser with oats on the skin, this was linked with a higher rate of oat allergy and there are even case reports in the literature about anaphylaxis.

And so, I advise my patients, be very cautious of putting food proteins like oats and goat’s milk on the skin, which are very common in moisturisers and body washes nowadays, because when the epidermal barrier is impaired, the proteins enter the skin. The dendritic cells pick it up and they trigger the T cell responses, and it can lead to a systemic allergy and even anaphylaxis.

Emma: Okay. It's quite fascinating, isn't it? I've just had a case of a little girl with eczema, pop into my brain who had a similar thing with Sesame. She had a skin/gut reaction to a sesame. Sesame oil in a moisturiser. So, it's really one to be considering,

Ben: 100% Emma. The research has shown that even for eggs or peanuts, when kids apply peanut oil products on their skin, they have a higher risk of peanut allergy. So yes. Any food-based proteins on the skin can increase the risk of systemic allergies.

Emma: Mm. Okay. But first you need to have an impaired skin barrier function.

Ben: Yes. That's right. One of my top treatment aims is to repair the skin barrier. Oftentimes, I think as naturopaths or as integrative practitioners, we go for the gut barrier first. But I think we must repair the two barriers concurrently.

Emma: Yes. So, thinking about that and then thinking about the skin microbiome, how do dermal microbiome imbalances like staph impact topical steroid withdrawal? And on the skin, you know, staph aureus has been dubbed a marker of eczema severity and higher fecal concentrations have been found in eczema patients. But is it an issue with the pH? I mean, what exactly is going on here?

Ben: Yeah. So, there are two things that are going on, first our skin pH should be around pH 4 to 6. And in this range, the skin can produce anti-microbial peptides like dermicidin and it produces ceramides for skin barrier integrity.

And number two, on this point of ceramides, in many eczema patients, they have a filaggrin gene mutation and there are some studies that show that this mutation can contribute to a more alkaline stratum corneum pH. And therefore, the alkalinity favours the growth of staph aureus and impairs the skin integrity. So, one thing I find useful in my practice is I'll ask patients to show me their palms.

And so, there is term called palmar hyperlinearity. if you see that the patients have very clear deep lines on their palms, this may correlate with a filaggrin mutation. It means that these patients have a more impaired skin barrier and are more prone to atopy with more allergies and sensitivities.

Emma: Right. Because can you do a blood test for filigree and gene mutation?

Ben: I recall seeing in the literature that there were blood tests done before, but I haven't seen that in clinical practice. So usually, I find that if the patients have the palmar signs coupled with an atopic presentation; asthma, eczema, rhinitis, I often presume that they have a higher propensity to the filaggrin gene mutation.

Emma: Okay. All right. That's a good clinical tip. I'm going to start doing that one. Now I want to dive into holistic treatment. Can you take a step by step through the aims of what treatment should look like about the order of treatment that we should be prioritizing? How do we treat this effectively?

Ben: Yeah. So, if I may add one step prior

So, I think that oftentimes before we even treat TSW, assess whether it is TSW or not. So, have you done a skin swab for staph overgrowth, and also could there be other triggers, let's say could there be mould exposure? I had a patient that said that after she cleaned a big mouldy patch in her bedroom, she began having full body flushing, redness, cellulitis, this actually mimicked TSW. Do we see elevated high white blood cells that may indicate an infection. Also where is the rash location? Is it full body, or is it only on the head and neck. If it’s just on the head and neck, could the differentials be seborrheic dermatitis, could it be fungal in aetiology. If it’s more on the lower legs, could it be stasis dermatitis and issues with venous return. So therefore, getting a proper diagnosis and being clear on differentials is very important because many of my patients come to me and they may been misdiagnosed with TSW, when it was actually staph, or it may have been a mycotoxin issue.

So, moving on to your question Emma, there are five broad aims, first is support the endothelium. The main pathophysiology is the excess nitric oxide production. And going back to our water hose analogy, we have clamped it down for so long because of the vasoconstriction from the high potency steroids, and when it’s released, the vasodilation, flushing and erythema increases.

So, reduce nitric oxide and strengthen the leaky capillaries. Number two, reduce staph aureus levels to reduce the staph aureus super antigens from entering the epidermis and dermis and triggering the T cell responses. Number three to calm down the TSW and eczema specific inflammatory pathways like IL-4, IL-13 and TSLP, because these are increased when the skin barrier is impaired. Number four, support the nervous system and the adrenals.

This is where naturopathic medicine and integrative medicine really flourishes because we can support the nervous system and help them through this period of intense stress. And number five is repair the skin barrier. If the skin barrier is repaired, then the antigens - there is less antigen entry and T cell activation. So, the gut support, liver support that we do in naturopathic medicine, it’s important still. But put down the fire on the skin first.

Emma: Hmm. I really like that, that analogy. So, the first step is, I guess, doing a skin swab for a staph overgrowth and ruling that out. Second, it would be to distinguish if it's actually eczema or topical steroid withdrawal.

And then if it is indeed topical steroid withdrawal, then we would first support the endothelium by reducing excess nitric oxide, strengthen the capillaries, then look at reducing the staph aureus overgrowth, calm the inflammatory mediators like IL-4 and of course support the nervous system and adrenals and repair the skin barrier. So, I find it really interesting that the gut and liver support is not at the bottom of the priorities, but you're right, you've got to kind of put the fire on the skin out first before moving to those deeper levels.

Ben: And also, I’ve seen in TSW cases and even severe eczema cases, when patients are put on milk thistle or liver support, not uncommonly I’ve seen flare ups happen.

Emma: Yeah, Yeah, I would say exactly, because that's where we tend to head is the liver and it just blows everything up. So, looking at the nitty gritty of treatment, I want to know, let's start with the internal actually internal treatment options. Can you give us some little cheat sheets around what you use in each of those treatment aims? Let's start with the nitric oxide.

Ben: For nitric oxide, the treatments that I use are mainly external, because the research is strongest on a few things - So vitamin B12 itself has been shown to reduce nitric oxide levels in the endothelium. In the studies, which was an RCT, they used only 0.07% of cyanocobalamin in a cream base. And after four weeks the eczema decreased by around three points more in the treatment group versus the placebo group. In my practice, I use methylcobalamin and hydroxycobalamin and I find both work quite well. My favourite dilution is around 1-2%. And so if your cream looks a bit pinkish, I think that's a correct dilution and I call it the pink cream.

Emma: Yeah. Great. So, 1 to 2% methylcobalamin or hydroxycobalamin in a cream base to help with the nitric oxide. I haven't tried that myself, so thank you. That's a great addition to my tool kit. What else would you use in treatment options?

Ben: And in this pink cream, I also like to add herbs to reduce staph aureus. And so, I include different antimicrobial herbs to broaden the range of actions on the receptors, so let’s say alkaloids: for alkaloids I use berberine, and I like to use coptis because of the higher berberine content. If you don’t have it in the dispensary I use golden seal or Oregon grape.

And then for the resins, I love to use myrrh, and for the tannins I use green tea extracts. And for the volatile oils I use thyme and rosemary liquids. I favour the liquids more for the volatile oils because I find essential oils a bit too strong and sensitising for eczema skin, so I use fluid extracts of thyme and rosemary and I find those well tolerated.

Commonly I get asked why do you not use chamomile and calendula because these are our textbook herbs. I have found quite commonly that many patients - because of the impaired skin barrier, when they run IgE RAST tests, they react to pollens, so I avoid using these because of this reason. I get good results without using calendula and chamomile in my practice.

Emma: Okay, okay that's good to know. That's good to know. What else would you use?

Ben: Yeah. So internally my favourite herb is Bacal skullcap or Scutellaria baicalensis for a few reasons. It ticks all the boxes for TSW - It inhibits IL-4, IL-13, TSLP, IgE, it just calms down the whole TH2 response. The flavonoids, the baicalin and wogonin, have been so well researched for these purposes, and so one big part of my herbal prescribing is energetics. And if we see Bacal skullcap from a Chinese medicine angle, it's used to clear damp-heat in Chinese medicine. And TSW is a hot condition. It's hot, there’s oozing, there’s dampness, there’s heat, and so it’s a perfect fit for TSW.

And to segway into herbal compounding, I always favour the more cooling herbs. I have seen that patients get worse with the warming herbs like ginger, astragalus, ginseng, and a few patients told me that when they tried curcumin on its own they felt more hot and dry, and when you see the ayurvedic energetics, curcumin is more to the pitta side, and that may perhaps aggravate an already pitta condition.

Emma: Okay. So, watch the energetics of the herbs? I love that angle as well. What about for the capillaries? Strengthening the capillaries?

Ben: Yeah, for sure. So, the capillaries are so important, because in TSW we often see oozing, because of the capillary permeability, we must enhance capillary integrity.

So, vitamin C, lutein, hesperidin, our bioflavonoids, and I like to use maritime pine bark because it reduces inflammation, it’s also anti-allergic and enhances capillary integrity. And also, for the nervous system, my top herb for TSW, whenever we think of vervain or Verbena officinalis, being a nervine and gentle bitter, it fits the TSW person-picture of someone who is (constitutionally) hot, who is frustrated, who has not slept for days. So, in our TSW patients they are overheated, they are frustrated. And so, I love to use vervain teas. I have found that liquid herbs with the ethanol content have not uncommonly caused more heat and dryness among my patients, so I find teas a lovely addition to the treatment plan.

Emma: And such a gentle way to introduce a herb into patients as well.

Ben: For sure. And verbena, passionflower, skullcap are my favourite combinations. And the last point for the skin barrier, I love to use evening primrose oil and I dose this at around 3-4 grams per day. And I combine this with a fish oil and a B-complex. The reason being that primrose oil contains gamma linolenic acid or GLA and studies have found that eczema patients, they can’t quite convert LA or linoleic acid to GLA very well because of a mutation in the delta-6-desaturase enzyme.

And in my earlier days in the clinical practice, I would run the essential fatty acid profile for my patients, and I'll find that almost all of them had the mutation in the delta-6-desaturase enzyme, and it got so common that now I don’t run the test anymore, I just give them primrose oil.

Emma: So, Ben on the favourite topic of mine which is food is medicine, what do you think the most important thing for us practitioners to know is?

Ben: Yes, so many TSW patients, they tell me they have major food fear. Because they’ve done food intolerance testing – removed all the foods that were high on the test, and the eczema or TSW did not improve, or it got better for a while then got worse again. My main goal is that we will not take out foods as much but rather add in foods.

For example, if clients have a reaction to salicylates - if they flare up with berries and avocado and tomato, mushrooms, citrus fruits, I suspect salicylates. I use glycine, calcium, magnesium. If I see a histamine reaction to canned fish and fermented foods, I use the DAO enzyme.

So that gives our patients some wiggle room because their headspace is already so maxed out. So, I avoid doing major food elimination. Perhaps reducing some gluten and dairy, but not a full elimination diet. That way we avoid having to stress out our patients even further.

Emma: Yeah, and I love that approach because there can be a lot of fear around food for these patients, for all skin patients, actually. But I love that, you know, you'll help support their body to tolerate the foods and just minimise what's really necessary to.

Emma: Ben, I have learned so much today on topical steroid withdrawal and how to look at it at in a very strategic what are a couple of key take home messages you want us all to learn today? I mean what can help us get better patient outcomes?

Ben: Yeah, sure. So, number one is to address the endothelium first and foremost before going to the gut. Number two, we must address the staph, whether it’s eczema or TSW, staph is a major contributor for eczema and TSW flare-ups. Number three, set timelines and expectations for the patient because TSW is a long journey and we can quicken the process, but the process must still run its course. Therefore, setting expectations early will help. So, in conclusion, I think that what is most important is to reassure the patient that they are in a safe space, that this will pass and that they will see better days again, they can wear their shorts and T-shirt again after this journey passes.

And so, I think that combining naturopathic care and even conventional care together can give us the best outcomes in TSW treatments.

Emma: Amazing. Ben, thank you so much for sharing your expertise on this very tricky clinical skin condition.

Ben: You’re welcome, Emma, it's a pleasure to be here and thank you for having me. And I'm glad to share my experience with all of you. Thank you so much.

Emma: My pleasure. Thank you, everyone, for listening today. Don't forget that you can find all the show notes, transcripts, and other resources from today's episode on the fx medicine website. If fx medicine.com.au. I'm Emma Sutherland. Thanks for joining us. See you next time.

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