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A Naturopathic approach to Rosacea with Emma Sutherland and Ananda Mahony

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A Naturopathic approach to Rosacea with Emma Sutherland and Ananda Mahony

Naturopath and nutritionist, Ananda Mahony and fx Medicine ambassador Emma Sutherland deep dive into the triggers and causes of rosacea, and the intricate connection of the gut-skin axis.

Ananda helps to unravel the complex nature of this progressive inflammatory condition, the causes and risk factors of rosacea, and how the gut plays a pivotal role in symptom manifestation and progression.

She stresses the importance of treating holistically, both internally and topically, and how as clinicians we can help our patients in down-regulating inflammation associated with rosacea through diet and lifestyle and targeted supplementation.

This podcast is full of clinical pearls to support clinicians to identify, manage, and treat rosacea using a holistic approach.

Covered in this episode

(00:33) Welcoming Ananda Mahony
(03:24) Rosacea causes and presentation
(06:06) Pathophysiology of rosacea
(11:05) Rosacea as a comorbidity to autoimmune conditions
(12:48) Key differentials between rosacea and other skin conditions
(14:50) Key age and sex related risk factors
(18:25) Common medical treatments
(20:12) The skin-gut axis
(24:10) Rosacea and Helicobacter pylori
(27:03) Holistic goals for treatment
(34:56) Dietary approach to rosacea treatment
(38:25) The role of probiotics in treatment
(40:10) Supplemental treatment for rosacea
(42:22) Clinical mistakes when treating rosacea

Key takeaways

Most commonly seen in women aged 35-50 years. More strongly associated with menopause / low levels of estrogen.

Sex hormones have a direct impact on skin cell receptors. Imbalance or excess can influence skin pathology and immune function and drive inflammatory processes as well as alter skin barrier integrity.

Facial flushing/blushing is an immune response; due to changes to the vasculature and neurogenic pathways that lead to persistent, progressive inflammation.

  • Primary triggers of rosacea
    • Sun or UV exposure
    • Heat sensitivity
    • Certain medications including topical steroids
    • Emotional stress
    • Sex hormones

Diagnosis is confirmed by clinical examination and medical history

Gut dysbiotic conditions, such as SIBO, are shown to be of high prevalence in patients with rosacea. This leads to intestinal permeability and alterations in anti-inflammatory mediator production, which acts as a driver for systemic inflammation.

  • Goals of treatment
    • Avoid known triggers
    • Support vascular integrity
    • Reduce inflammation and immune dysregulation

  • Supplemental support
    • Quercetin and Baikal skullcap reduce mast cell activation and cethelicidin release, downregulating inflammatory processes.
    • Vitamin D regulates cathelicidin expression.
    • Omega-3s reduce the risk of ocular rosacea progression.
    • St. Mary's thistle and methylsulfonylmethane modulate the action of cytokines and inflammatory responses.
    • Probiotics reduce inflammation in the skin by regulating inflammatory cytokines and activating T regulatory cells, as well as increasing ceramide production in the skin.
    • Zinc can reduce the incidence of inflammatory lesions and papules.
    • Collagen may be indicated in cases of greater transepidermal water loss.

Resources discussed and further reading

Ananda Mahony

Ananda's website
Connect with Ananda: Facebook

Rosacea pathophysiology and aetiology 

Article: Rosacea pathogenesis, common triggers, and dietary role: The cause, the trigger, and the positive effects of different foods
Article: Current research and clinical trends in rosacea pathogenesis. 
Article: Incidence and prevalence of rosacea: a systematic review and meta-analysis


Article: Recent Advances in the Management of Rosacea through Natural Compounds.
Research: Phytochemical and botanical therapies for rosacea: a systematic review.
Article: Botanicals and anti-inflammatories: natural ingredients for rosacea.
Article: Rosacea: Treatment targets based on new physiopathology data.
Article: Rosacea: New Concepts in Classification and Treatment

Rosacea and autoimmunity

Research: Clustering of autoimmune diseases in patients with rosacea

Rosacea and the gut

Research: Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication
Article: Relationship between Helicobacter pylori and Rosacea: review and discussion
Research: Rosacea and gastrointestinal disorders: a population-based cohort study
Journal: Rosacea and the Microbiome: A Systematic Review


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 respects to the elders, past and present, and extend that respect to all Aboriginal and Torres Strait Islander peoples today.

With us today is Ananda Mahony who is an experienced naturopath and nutritionist, helping people in both clinical practice and is a lecturer at Torrens University. Ananda works by treating a wide range of health conditions, but she has a special interest in helping problematic skin conditions such as rosacea, psoriasis, acne, and eczema as well as helping people with chronic pain. Her expertise in treating skin conditions comes from personally experiencing adult breakouts and also having chemically sensitive skin throughout her 20s.

Ananda has a lot of experience in treating the tricky skin condition, rosacea, which is what we will be discussing today. Welcome to fx Medicine, Ananda. Thank you so much for being with us today.

Ananda: Thanks, Emma. I'm really looking forward to talking about rosacea today and it's actually part of my health journey. So, it's a topic that is of keen interest to me.

Emma: Mm, near and dear to your heart, which is so, so beautiful, because it gives you that authenticity in this space.

Ananda: Yeah, absolutely.

Emma: Now, rosacea is most common in women who are fair-skinned and between the ages of 35 to 50. And because it affects the face, it can have a profoundly negative impact on a woman's quality of life, her self-esteem and her well-being. Now, I'm sure we have all had a patient in clinic with this tricky skin condition, and it is overwhelming to know how to treat it effectively. Patients are often told it's a condition of unknown cause, and there's no cure, only management. But this leads to patients feeling like their health is beyond their control and consequently they're disempowered in their quest for clear skin.

Now, in a recent systematic review, the global prevalence of rosacea was estimated at 5.5% of the adult population, but really in researching this episode, many other reviews stated that it was up to 10% prevalence. So, Ananda, what exactly is rosacea? What is the pathophysiology involved and what are the key ways it presents? Let's hit the ground running with the basics.

Ananda: Okay, great. And that statistical research is interesting, because it is higher in so me countries. Sweden had that 10% prevalence, so I find that interesting, and maybe that links into or with some of the triggers that I'll talk about. But, first, yes, what is rosacea? Well, it's a chronic inflammatory disease of the skin, and the areas of the skin that are predominantly affected are the central face. And this typically presents with flushing, persistent erythema or redness. There's pustules and papules. And, look, I love this word because it's... I'm just going to try not to trip up, but telangiectasia every time. So, that's abnormal dilation of the capillaries or venules under the skin. So, you see those darkened and enlarged capillaries. There's also secondary features. So, the skin can be burning or stinging. It can look dry or rough in appearance. There could be skin changes, and we see thickened skin with enlarged pores or an irregular surface. And the eyes can be involved, so you can actually have ocular rosacea as well.

And there are quite a few known triggers that result in that blushing, flushing effect. And that's the effect that plays a vital role in rosacea development. And so primary triggers are things like sun exposure and UV exposure, and that's in up to 81% of people presenting with rosacea that are triggered by sun exposure. But then there's also heat sensitivity, so that can be with exercise as your body heats up or in hot weather and hot baths. And I know, for me, any kind of warm, stuffy environment used to be a trigger, or wearing a roll-neck like skivvies, it just heated me up and my face would then flush and blush. There was medications such as nasal or topical steroids. And there's a big neurovascular component, so sensitivity from stress or hormones, and that might be emotional stress. There's certain foods or beverages such as alcohol and spicy foods are triggers, and I'm sure we'll go into detail on those later. And then also a combination of poor sleep and stress. So, it's a very individual presentation, and people will be triggered by several different things. But as I said, probably the most two common are sun exposure and emotional stress.

Emma: Mm, and both of those are just so hard to avoid, aren't they?

Ananda: Absolutely, yeah. And a combination of both of those, and you could have someone flushing and blushing on a regular basis.

Emma: Mm. Mm, exactly. And what's going on with the pathophysiology involved in rosacea? What's actually going on under the surface?

Ananda: Well as everything, it's complex, and it involves a variety of factors. Those factors trigger both vascular and inflammatory responses. So, there's some genetics there, and that's not clear cut, but there's also neurogenic dysregulation, immune system dysregulation. There's the potential for skin infections or skin infections maybe even just overgrowth of commensals but creating a superantigen whenever these kind of processes happen in the skin, there's also barrier function impairment and inflammatory response.

Ananda: So, firstly, with neurovascular, there are alterations in vascular responses and the blood flow to the skin. And this leads to the easier and more prolonged flushing in response to heat. But there's also an oral thermal flushing response, and that's hot foods like temperature hot, so a hot beverage or, yeah, a cup of tea or coffee. And this altered blood flow occurs more in the affected and inflamed areas of the face. So, you might get flushing across the cheeks and nose, but other areas of the face may not be as flushed. And a key driver of this process is the activation of transient receptive potential channels.

And there are a large family of non-selective calcium permeable channels, and they're expressed in the cells of the skin. So, keratinocytes, melanocytes, immune cells, and the sensory neurons. And in rosacea, there's two of these channels: TRPV1 and TRPA1. And they activate those sensory nerve endings in response to, well, for example, alcohol or spices or temperature changes. And that leads to the release of vasoactive neuropeptides such as substance P and calcitonin gene-related peptide. And then those neuropeptides cause that inflammatory response of the skin vessels and they activate mast cells, macrophages, and other immune cells within the skin. And it is this increased and prolonged expression of those transient receptor potential channels in rosacea patients that results in the facial flushing, and dysregulation of the vascularity, and neurogenic inflammation.

And that's that key factor in the development of the fixed changes. So, there's this propensity. There's more flushing and blushing. And eventually the vasculature starts to change and become fixed, which causes persistent erythema and those larger vessels or dilated vessels in the skin and the dilation of the capillaries.

So, that's one key process, and the thought is... And it's not clear cut because there's never a linear process here, but that flushing-blushing propensity is what almost kicks it off. But then of course the immune system gets involved as it always does.

Emma: Yeah.

Ananda: Yeah, and there's a dysregulation of both the innate and adaptive arms. And with the innate immune system, the augmentation in those processes leads to upregulation of the cathelicidin pathway. And then that leads to downstream inflammatory and phytochemical cascades. I'll talk to that. Now, in particular in rosacea, there's high levels of toll-like 2 receptors, and I, kind of, think that these are akin to security cameras with a very long memory like a danger recognition pathway. And so in response to a trigger, whatever that might be, UV exposure or spices, there's this augmented dangerous recognition in response to that trigger. And its signaling is involved in the key inflammatory pathways, which drive rosacea. And once that inflammatory pathway is triggered by the toll-like receptor, there's an upregulation and a release of this chemical soup that gets involved. So, there's proteolytic enzymes such as matrix metalloproteinase, in particular, 9, and kallikrein-related peptidase 5. And these, in turn, activate that cathelicidin pathway and its related peptide, LL-37. And that's one of the key inflammatory signals and acts as an angiogenic factor stimulating the vasoactive endothelial growth factor, so VEGF factor. And then we start to see there's an immune driver as part of those vascular changes as well as a neurogenic pathway. And that inflammation becomes persistent, again, when we start to see an inflammatory cascade in the skin that is maintaining those changes.

Emma: It's so complex, and it's kind of fascinating because it all is feeding each other into this big loop of inflammation that just seems to become more and more perpetuated. One study I read showed that people with rosacea specifically women though had a high incidence of autoimmune conditions such as type 1 diabetes, coeliac and rheumatoid arthritis. So, is rosacea an autoimmune disease or not? I mean, I'm confused.

Ananda: Well, I think it's a common comorbidity, but there are other common comorbidities such as gastrointestinal, cardiovascular, and mood disorders. So, it may just be that it is a comorbidity. But there are some shared associations between the genes that encode for HLA variants and that code for rosacea and diseases such as, as you mentioned, coeliac disease and type 1 diabetes. And there's a number of others.

So, there's some shared genetic pathways, but I think at this stage, the evidence doesn't suggest that it is an autoimmune condition, but there is an overlap in some of the key drivers. So, there's some common factors such as microbiota imbalance and the specific role of the immune system intolerance, immune dysregulation, inflammation, and stress. But those are common to the other comorbidities too. So, I think that there's probably common factors between autoimmune conditions and rosacea, but there's also unique features of individual conditions. So, I think maybe we'll see that there is later on, but at this stage, there's not enough evidence to suggest that.

Emma: Okay. All right, thank you for clearing that up for me once and for all. What biomarkers can we actually utilise to diagnose rosacea though? And what do you consider to be key differentials between rosacea and other skin conditions, things like acne or eczema?

Ananda: Yeah, because it is interesting. A red rash doesn't always indicate rosacea. And there's a number of other presentations, as you say, that it can be confused with. But I will say in terms of biomarkers, there's no histological or serological markers that indicate the presence of rosacea. It's done by clinical examination and medical history. So, it is actually using those... I mean, usually a patient will come with a diagnosis of rosacea, so it's not something that we do as naturopaths and nutritionists, but there are differential markers. So, for example, acne has comedones and pustules, and they may be red skin, but it doesn't include that easy flushing, burning, or stinging sensations or the changes in the blood vessels. And rosacea has pustules but no comedones. The tricky thing with both acne and rosacea is that they can both occur at the same time and that just complicates matters.

Emma: Yeah.

Ananda: Yeah. And there's other conditions such as seborrhoeic dermatitis and perioral dermatitis that also overlap, and they may have similar areas of redness but they'll be differential. So, seborrhoeic dermatitis, again, no pustules of rosacea and no flushing, and same with perioral dermatitis. Flushing is not common, and the presentation of perioral dermatitis is around the mouth or in the nose and labial folds, not centrally as with rosacea. So, there are markers that, kind of, tell us that it's a rosacea picture rather than some of those other conditions.

Emma: Okay, and it sounds like a couple of those key differential markers are the flushing and the central location of the flushing.

Ananda: Yeah, absolutely.

Emma: Yeah, okay, fantastic. And with the drivers for rosacea, what do you think helps it or causes it to kick off during the key ages of 35 to 50? And why are women more affected than men? What's going on here?

Ananda: So, I'll talk about the key ages, and I think that rosacea is a condition that progressively gets worse across time. So, you might have someone, and I was a bit like this. I stopped it in its tracks, I like to think that I did, but I started with a really flushing-blushing propensity and then started to get more persistent redness or erythema. And if you say that that is a gradual process that occurs over time, and then there's further chronicity that occurs, it may not be that until 35 or 50 that we start to see the full presentation of rosacea.

But there are other things that impact and more women than men. I think sex hormones play a role. They have a direct impact on skin cell receptors, and any imbalance or excess can influence skin pathology as well as immune function. And in rosacea, in particular, it's more strongly associated with menopause and low levels of estrogen. And they can promote that shift towards T helper 1 status in the immune system and the increases in TNF alpha and natural killer cells.

And some of those processes might drive into an inflammatory processes in the skin. They can't find a specific link between hot flushes as part of the picture, but again, it might just be that gradual contribution to the flushing-blushing effect because hot flushes don't necessarily specifically... You don't specifically see that in just the face. It's a full body experience.

But women also tend to have less skin hydration and greater transepidermal water loss. And, also, the skin thickness losses with hormonal changes. And we say those hormonal changes aren't just happening at menopause. There's up to 10 years lead up of a change in hormonal factors. So, those may predispose them to skin barrier dysfunction and allow, for example, skin microbial shifts or barrier dysfunction is linked with a greater predisposition to inflammation and sensitivity. So, it might be those factors that we start to see this gradual onset of rosacea and then it more likely to be prevalent in women than men.

Emma: Yeah, I really like that little insight there around the ages, because if I think about it, I do have patients that are younger than 35 and they do often come to their appointment looking a little flushed. And it could just be that we just pass it off as something else until then it gets to the point where we just can't ignore it anymore. So, I really like that insight. And I feel for women, this change in sex hormones can really promote that shift to the pro-inflammatory processes. And then you've got less skin hydration, you've got thinner skin, and you get skin microbial shifts and skin barrier changes. It seems like almost the perfect storm, doesn't it?

Ananda: Yes, it does. And look, we know that, with those hormonal changes and women heading to menopause, there are other inflammatory shifts. You see it in joint changes. And so why not skin basically?

Emma: Yeah, exactly. Now for a patient, can you outline the medical treatment that's usually offered to patients so we know?

Ananda: Yeah, often it's topical, but it depends on the subtype. So, if it's just flushing-blushing, they might have topical agents such as azelaic acid or oral beta blockers to reduce the emotional component of that flushing-blushing. With the erythemato...

Emma: That one.

Ananda: With the first subtype where you get persistent flushing or persistent redness and the changes in the blood vessel, they might use flagyl. That can be seen to reduce inflammation. There's also alpha-adrenergic agonists to reduce sympathetic drive. And then with each one, progressive stage is slightly different approaches. So, papulopustular rosacea, again, they might use those topicals. They also might use ivermectin or other oral antibiotics. And then where you see that thickening and changes in the density of the skin and more scar tissue and the phymatous rosacea, they might use things like isotretinoin or laser. And then for oral rosacea, if it's severe, they'll consider oral or local antibiotic therapy. So, it depends on the subtype. There's a lot of more topical approaches to rosacea that tend to be offered such as niacinamide and, as I said, azelaic acid, isotretinoin. So, yes, there's a lot.

Emma: Yes, exactly. I was just about to say my experience is not vast in this space, but what I have noticed is a theme of treatment failure, unfortunately. So, we will be diving into your ideas on treatment. But I wanted to talk about a population-based cohort study. It was on 50,000 Danish patients with rosacea, and the prevalence of coeliac disease, Crohn's disease, ulcerative colitis, small intestinal bacterial overgrowth, and irritable bowel syndrome were all significantly higher among patients with rosacea compared to controls.

Now, this points to the skin-gut axis, and I do just want to press pause so we can deep dive in here. A study evaluating the role of small intestinal bacterial overgrowth in patients with rosacea demonstrated that eradication of SIBO with rifaximin resulted in complete resolution of rosacea in the vast majority of patients. So, let's talk about this. Can you discuss with us what is the mechanism of action between SIBO, rosacea, and medications like rifaximin? How is this working here?

Ananda: Yeah, absolutely. So, I will say firstly with SIBO, there is found to be a higher prevalence in rosacea patients and controls. But as you say, there's a number of gut conditions that are associated with rosacea, and I think... I'll look at it from a number of different angles. If we have a dysbiotic state, and fundamentally that's what SIBO is, it can lead to a compromised intestinal mucosal layer and impaired epithelial tight junctions. And then we see this, kind of, worsening intestinal barrier function and intestinal permeability. So, that allows things that should stay in the gut to move into the bloodstream. So, we see the translocation of bacteria or harmful compounds of bacterial origin. They're, kind of, spilling over into the bloodstream. And those spillover products, if you like, may influence the immune system. We see this in other conditions. We see a hyperresponsiveness of B cells and impaired differentiation of T cells.

And so those dysbiotic bacteria or bacterial compounds, along with altered immune cells, can reach the skin from the bloodstream. So, they can actually directly impact skin physiology, pathology, and immune responses in the skin. And then we kick off local skin immunity and local skin inflammation. And if we just, again, think about SIBO, it's been linked with high levels of inflammatory cytokines, including TNF alpha, which is seen to be something that contributes to rosacea as well.

But also, in dysbiotic guts, there is a less production of beneficial, say, short-chain fatty acids such as butyrate. And if we think about just butyrate, it has this anti-inflammatory effect because it suppresses immune responses by inhibiting proliferation, and migration, and inhibiting cytokine production by those inflammatory cells. So, we've got more potential for inflammatory drivers from those bacterial and bacterial byproducts in the immune system but also less capacity to dampen that down. And if we think about the pathophysiology of rosacea, it involves activation of the skin, the immune system, and the nervous system in response to physical, chemical, biological triggers.

And so these gut dysbiosis-driven changes could lead to that progression or even just increase severity and flare-ups or sustain symptomology. So, it might not be that they're a primary trigger or primary driver of the condition. It may be or it may not be. It could all just be that they increase severity and aggravate the condition, so we just don't know yet.

Emma: Yeah. Like most things, we just don't know enough yet, but I love those insights around the dysbiotic state and truly we really just need to work on the gut, don't we? The impaired gut lining, the increase in intestinal permeability, the translocation of bacteria into the bloodstream resulting in localised skin inflammation while at the same time having less production of beneficial and protective compounds like butyrate that are anti-inflammatory. So, I feel like that's a really good insight on that front. But what about rosacea and Helicobacter pylori? So, studies have found that H. pylori infection is associated with the occurrence of rosacea. What do you see clinically in that space?

Ananda: Well, from a research perspective, it's unclear. But, I mean, I think that I'm going to look for any history of gut overgrowth or dysbiosis, whether it be H. pylori or SIBO. But it is unclear. It's long been suspected because there's a high prevalence of seropositivity in rosacea population. So, is it a smoking gun? So, there's conflicting evidence of its role, and the pathogenetic link is difficult to establish because antibiotics independently are helpful for both conditions.

So, if you're treating H. pylori, maybe you'll just see a dampening down in rosacea because of the antibiotic effect and vice versa, but there are some mechanisms that have been probiotic. So, Helicobacter pylori drives increased reactive oxygen species and inflammation in the gut. And among those reactive oxygen species is nitric oxide. And that can specifically induce intestinal mucosal inflammation but also it's got a big role in altering the physiological processes in the skin, driving vasodilation, inflammation, and immune changes.

So, we see that leading to those clinical manifestations of blushing and erythema, and that's what they think one of the predominant roles of Helicobacter pylori is, if it is a factor. And I think it's probably likely. And also H. pylori can drive proinflammatory cytokines: TNF alpha, Interleukin 8. And again, you can see that gastric mucosal inflammation, intestinal permeability, and the spillover that I talked about before with SIBO. So, we might have a number of mechanisms with H. pylori.

Emma: It seems there's a lot of commonalities between the two. And I think it's just a question to make sure that you do, in your case-taking, that have you ever experienced Helicobacter pylori? Have you been diagnosed with it? Have you been treated for it? So, a really nice addition there if you're not already doing that.

Now I want to shift the focus to holistic treatment for rosacea. Can you give us a bit of an overview of specific goals of treatment that we should be aiming for?

Ananda: Yes. So, I think the first and most obvious one is avoid known triggers where you can, so UV exposure, temperature changes, and alcohol, for example, are the most common triggers apart from emotional stress but that will be individual. So, just work out what the triggers are. And usually a patient will come to you, and they say, "I know these are my triggers, and I already avoid them." But if they haven't, some discussion around that.

I think the second is—there's some key priorities here—support vascular integrity, so stabilise and support the blood vessels in the skin and reduce inflammation and immune dysregulation. And, those, I would say, would be my top three. But then, of course, rule out Helicobacter pylori or SIBO or other gastrointestinal issues. But if they're present, treat them and generally support a healthy skin and gut microbiome.

Probably what I didn't mention before is, in addition to gut microbiome changes, there's often skin microbiome changes and wherever there's skin barrier dysfunction, there's going to be changes in the skin microbiome. And so you can even consider antimicrobial strategies for the skin microbiome. Many of those are topical, but there are some key herbs that may assist with that or key strategies that might assist with that. I think support skin barrier function. And then there's that trail of other things like eye health, stress management if identified, hormonal changes if identified. But really addressing the key drivers, so inflammation and dysregulation and vascular integrity and barrier function are those key four that need to be addressed.

Emma: And when we're looking at vascular integrity, what are your go-tos in this space?

Ananda: Yeah. So, I love a couple of things. One is green tea or if you get... Sorry, I'm crashing words today.

Emma: That one, that acid.

Ananda: EGCG.

Emma: Yep, got you.

Ananda: And that is really useful topically. So, there's some research that around 2.5% of EGCG can reduce the redness but also the blood vessel changes. It's got so many impacts to the skin. It's antioxidant, immunomodulatory, photoprotective, anti-angiogenic, and anti-inflammatory. And it suppresses that VEGF pathway.

So, I often will talk about holistic treatment and internal, but in this case, I'm also going to really emphasise that some of the topical strategies that we use can be important. And I describe this to my patients, it's like, "We can put in supplements, and we want them to go to the skin." But the body does what the body does with those supplements. And often we have to get some sustained higher doses or high therapeutic doses to really meet the needs of all the critical organs like the brain, and the heart, and liver and everything else before it gets to the skin.

So, I like to use oral treatments as well as topical treatments where I can.

Emma: Yeah. I just wanted to dive into vascular integrity and you said the green tea, which sounds like it's ticking every box, but using it topically, which I was not aware of.

Ananda: I mean, I'd also use it orally. Depending on whether hot drinks are an issue, they could have green tea, iced green tea or just cool green tea. And I will often get patients to make up a spritzer of green tea and put a couple of teabags and steep them for five minutes and then pour it into a spritzer and put it in the fridge. And that will last up to a week and then I'd make a new batch, but spray it on their face whenever it feels hot or inflamed.

Emma: Yeah, great. I love that. And anything else that you use to support the vascular integrity side of things?

Ananda: I do like Centella asiatica, and there has been, again, some research in the topical space, but I often will use it as part of a mix like a herbal liquid mix to support the vasculature of the skin and skin health generally.

Emma: Mm, mm, beautiful. And then your go-to's in relation to inflammation?

Ananda: Well, I don't know if I mentioned this, I think I briefly mentioned mast cells, but there is a big positive feedback loop with mast cells because they are producers of cathelicidin and then the LL-37, which is one of the key inflammatory drivers. And then of course that LL-37 triggers more mast cell degranulation, so it's this positive feedback loop. So, I do like quercetin in this space and Baikal skullcap just to reduce mast cell activation and cathelicidin release and therefore inflammatory processes. And vitamin D is also a regulator of cathelicidin expression, so quercetin, Baikal skullcap, omega-3, and it also can help reduce the risk of progression to ocular rosacea. Yeah, so I like those.

But then I've used SPMs and a bit of curcumin, particularly if I'm multitasking with other conditions...

Emma: Which is often the case. It's often the case.

Ananda: Yeah.

Emma: Yes.

Ananda: And another big one, which I think is quite specific to rosacea, is niacinamide.

Emma: Okay, tell us more.

Ananda: And while it's not a direct anti-inflammatory internally, it is one topically and both niacinamide cream and oral dosing have showed benefit. And so there's some of an anti-inflammatory response there, but I think the big thing here is it improves skin barrier function and then, by improving skin barrier function, it will dampen down inflammatory processes.

Emma: I really like they're coming from the outside and the inside but in a very strategic way, Ananda.

Ananda: Yeah, thanks. It was probably through my own experience that I learnt that. I was doing a lot of oral support or support for the skin from the inside out but then had to find things that would actually just dampen down redness and inflammation. So, I didn't have to walk around with makeup on all the time. I thought that was for my own sense of self-worth but, you know... Yeah.

There is another study, which I found quite interesting that I will just mention. It's a 2008 study which found that a combination of St. Mary's thistle and MSM, methylsulfonylmethane. And that was shown to have a direct modulating action on cytokines and inflammatory responses. So, along with some of green tea and Centella asiatica, St. Mary's thistle is one that I will really frequently use in the management of rosacea because of that research. And it led to significant reductions in papule count, in redness, and stinging itch scores. So, I'm a big fan of that. I have seen good outcomes. Well, not just with methylsulfonylmethane but with a combination of things.

Emma: Mm, yeah, it sounds like the liquid herbs really get a run at your clinic, Ananda.

Ananda: Yeah, they do.

Emma: Now, you've mentioned some foods to stay away from and the triggers, but do you find any particular foods that are beneficial for patients to be adding into their diet from that food as medicine aspect?

Ananda: Yes, but I'd probably just take a more general anti-inflammatory approach, dietary approach, because what it's showing is those trigger foods. And then there's also diets that contain a large amount of fatty foods showing positive correlations with rosacea and that's possibly due to their role in chronic inflammation. So, a general anti-inflammatory dietary approach.

Sometimes I use a lower histamine approach, but that just depends on what their triggers are. But I'll include really specifically foods that support a healthy microbiome and then foods that support skin health. And in the research, it's the red, yellow, green and orange-pigmented fruit and vegetables that really support skin health. And I think that's around carotenoids and photoprotection, because the more carotenoids there are in the skin, the greater the photoprotection you have in your skin.

But then I just, kind of, laugh at myself because I've got red, yellow, green, and orange, but then when I couple this with the foods that support a healthy microbiome, like those folic polyphenols, which are purple, dark red, black, and brown, I'm like, "Yeah, you might as well just get them to eat the rainbow."

Emma: Exactly. I was just thinking the same thing. We can go back to that easy tenant for patients to remember and not make it so complicated.

Ananda: Yeah, yeah, absolutely but is an inflammatory condition. So, starting with that as a dietary approach I think is pretty important and even... I don't talk about absolutes with my patients, and I'm really careful around restricting foods too much, so like a crowding out approach instead of a cutting out approach. And I just tend to say, "Okay, if we can get 80% or 85% increase their, kind of, total percentage of the overall anti-inflammatory diet, we start to get to this tipping point where it does make inroads and starts to decrease inflammation generally."

Emma: Mm, I love that. And you mentioned before around short-chain fatty acids, but I wanted to get your opinion on prebiotics. Which prebiotics do you recommend if you do? And can you tell us the dose, the duration, and how long is it going to take until a patient starts seeing some improvements?

Ananda: Oh, I hate to be disappointing in this space, but I haven't seen any specific research looking at the role of prebiotics. It doesn't mean that I don't use them, but there's none that are in rosacea specifically. There's more in acne and even that's more around probiotics.

Emma: Yes.

Ananda: But I think we can probably assume they have a positive effect because of the promotion of the short-chain fatty acids. I use them all in my clinic. I use partially hydrolyzed guar gum, GOS, inulin, and lactulose. And it all just depends on the clinical presentation of the patient or if I've done any things like GI mapping, what are the specific indicated prebiotics to support the growth of probiotics of all of their native populations. So, yes, I use them. No, there's nothing that's rosacea-specific, but I think it's more individual approaches.

Emma: Yeah, and I definitely think shifting, skewing to a more anti-inflammatory profile is going to be the key thing to be aiming for here. But what about the role of probiotics? Because I've read about the strain Lactobacillus paracasei, which inhibits some substance P-induced skin inflammation. What do you think of probiotics in this space for rosacea?

Ananda: Yeah, I'm a big fan of specific probiotics rather than just broad-spectrum use of probiotics, so as in, "Here's..." I tend not to say, "Well, here's a probiotic that's got 10 different strains, use that." I'm more likely to go, "Here's a probiotic that's got a high amount of lactobacillus paracasei. We'll go with this one." And there's some other research on the E. coli Nissle, that one as well, and a few other bits and pieces.

Often that research is quite...they might have done one paper, but there's not the depth of research. That's okay. It doesn't stop me using them because I think probiotics generally reduce inflammation in the skin, and they do that by regulating inflammatory cytokines and activating T regulatory cells or some of the suspected mechanisms but they also increase ceramide production in the skin. And so it has that strengthening barrier function effect as well. So, I'm more, as I said, more likely to go with the lactobacillus paracasei than a general one, but I will use that where I think it's indicated.

Emma: Yeah, and I love your approach of being strain-specific. It's very respectful towards the strains of using them in that way. Now, anything else around naturopathic treatment for rosacea? I know there's a big trend of beauty from within. So, I'd love to know your thoughts on ingestibles like collagen or zinc. Do we use them? Do we not use them? What are your thoughts?

Ananda: Yes, absolutely. I think zinc... And there's research in zinc. It shows that it can reduce incidence of inflammatory lesions and papules over a three-month period. So, I use zinc in a lot of skin conditions. It's got so many various, different effects in the skin. And collagen, I like but I would use collagen where the skin's dry and sensitive because dry, sensitive skin is easily inflamed and it's more likely to trigger those rosacea processes. So, if I perceive that it's just the skin's not holding water or the bigger transepidermal water loss, that's when I'd use collagen because it does increase the water-holding capacity of the skin.

Emma: Mm, yeah. I love that insight. And with your zinc, Ananda, what kind of dosage are you using?

Ananda: Well, look, the research used zinc sulfate at 100 milligrammes 3 times a day. And I think that's a pretty hefty dose and also not an ideal form. So, I'm more likely to use another standard zinc.

Emma: Citrate?

Ananda: Yes, yes, or an amino acid chelate form of zinc and between 25 and 50 milligrams. If I do go to that 50 milligrams a day, it'll be shorter term and then sustained with about a 25 milligram zinc dose. But not forever and ever. So, again, I'm conscious that I want to use it as a tool to elicit change in the skin state and reduce inflammation, and then bringing food sources of zinc when we've seen enough benefit from using zinc.

Emma: I love that. Food is medicine once again. Always a good baseline, isn't it? Now, my last question for you, Ananda, is do you see any big mistakes that we tend to make when we tackle rosacea as clinicians?

Ananda: I think probably something that I haven't talked about strongly is that we can see some subtyping with rosacea because there's four different subtypes. And there are some drivers of... Look, those subtypes are also based on perhaps progression and severity of rosacea. So, for example, with the papulopustular subtype, we see a greater incidence of Demodex and more SIBO in that subtype.

So, I guess the thing that I would say is we can't treat all rosacea the same. And even though it's a progressive condition, we'd look at where that patient is at and treat them according to their presentation. Is it predominantly flushing-blushing and can we do something about supporting those blood vessels and reducing the triggers? Is it where there's actual changes in the blood vessels and a persistent state of erythema or are they getting progressive changes and do we need to take a broader look? So, check for everything in your assessment that I've discussed but then really try to pick your treatment to what's presenting in that patient.

Emma: And as always, patients are complex. They're multifactorial. But I think the insights that you've shared with us today are going to make it a little bit more easier for us to tackle those tricky rosacea cases that come walking in our door. I'm going to have a goal. I've just made a goal now that, for each rosacea patient I treat, the goal would be that she feels comfortable going and doing her shopping makeup-free.

Ananda: Yeah, great.

Emma: Thank you.

Ananda: That's a good goal.

Emma: It is. Thank you so much for joining us today, Ananda. Really appreciate your time.

Ananda: Thanks, Emma, for having me. It was great.

Emma: 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. I'm Emma Sutherland. Thanks for joining us, and we'll see you next time.

This podcast is intended as healthcare practitioner education only, and it is not a substitute for medical advice, diagnosis, or treatment.


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