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Understanding Paediatric Neurodevelopmental Disorders: A focus on PANDAS with Emma Sutherland and Keonie Moore

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Understanding Paediatric Neurodevelopmental Disorders with Emma Sutherland & Keonie Moore

Naturopath Keonie Moore shares in-depth clinical experience on managing Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS) with Ambassador Emma Sutherland. Together they define the key differences between PANDAS and PANS, as well as the the common triggers, signs and symptoms to help clinicians pinpoint the condition - including an overview of the research history backing this relatively newly understood condition. They also discuss the immune-based pathophysiology that not only involves the nervous system but centralises around gastrointestinal health, triggering systemic inflammation.  

Keonie shares several components of her Moore method; a treatment plan where specific microbiome, nutrigenomic and pathology tests are recommended to help clinicians determine PANDAS and their therapeutic recommendations. Finally, Keonie details an in-depth, informative, and practical case study of a ten-year-old boy who had severe tic disorder, outlining her strategic approach to the case, therapeutic considerations and dosages, and ultimate outcome. The case study shows the determination of the patient, his family and the clinician in order to bring him back to health.   

Covered in this episode

[00:33] Welcoming Keonie Moore
[01:33] Setting the scene on PANDAS
[05:25] Common presentations of PANDAS
[10:48] Key drivers of PANS and PANDAS
[13:52] A diagnosis of exclusion
[14:57] Can gut health be connected?
[18:28] Testing to determine the best clinical interventions
[24:23] Environmental drivers affecting gut bacteria populations
[28:12] NAC: mechanisms of action
[30:36] Nutrigenomics and how vitamin D impacts the gut microbiome
[33:24] Connections between iron deficiency and neurodevelopmental disorders
[38:15] Case study: 10 year old boy with tic disorder
[48:04] Keonie’s top tip for treating paediatric neurology
[50:13] The Moore Method
[51:21] Thanking Keonie and final remarks

Key takeaways  

  • Abbreviations
    • PANDAS - Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections 
    • PANS - Paediatric Acute-onset Neuropsychiatric Syndrome 
    • ASD – Autism Spectrum Disorder 
    • ADHD – Attention deficit hyperactivity disorder 
    • PAMPS – Pathogen associated molecular pattern molecules 
    • DAMPS – Damage associated molecular pattern molecules 
    • LPS – Lipopolysaccharides 
  • PANDAS can be triggered by any infection and (in non-infectious cases) mould exposure
  • PANDAS/PANS may present closely with other neurodevelopment conditions in children ASD, ADHD, OCD (related to food), anxiety (separation anxiety) with a typical presentation being history of an infection (not necessarily group A strep. but this is common) developmental regression (e.g., no longer speaking words, unable to recognise letters), polyuria, nocturia, and increased frequency mood lability, emotional aggression, defiance 
  • Key drivers/triggers: immune system dysregulation, triggered by PAMPs and DAMPs from the gut microbiome, followed by inflammatory cascade 


  • Current testing methods do not support diagnosis of PANS/PANDAS. Diagnosis is by exclusion. 
  • Group A Strep is not the only trigger, there can be environmental triggers as well such as mould.
  • Nutrigenomics can help assess susceptibilities to nutritional deficiencies. Investigate SNPs for vitamin D, methylation, neurotransmitters in relation to environment 
  • Gut microbiome factors: high level of Bacteroides, significant dysbiosis, clostridia species, SCFA ratio, zonulin 
  • Blood tests to consider: iron studies, ferritin 40-80, FBC, vit-D, Zn, Cu, inflammatory markers 


  • Correcting nutritional deficiencies can provide symptomatic relief. 
  • Correct gut dysbiosis, support immunity, reduce inflammation, and repair the gut for resolution. 
  • Supportive nutrients include NAC as a cysteine donor for supporting glutathione production, and GABA for reducing excess glutamate and improving the brain’s resistance to inflammation 
  • Phytotherapies include curcumin and saffron to increase BDNF and support neuroplasticity  
  • Consider an Ibuprofen challenge. Ibuprofen can aid with excluding differentials and provide short-term relief. 

Resources and further reading

Keonie Moore

Keonie Moore
ReMed PANDS and PANDAS Clinic
The Moore Method


PANS & PANDAS assessment (ReMed Clinic)
PANDAS Diagnostic Guidelines (PANDAS Physicians Network)
Group A Streptococcal overview (Better Health Channel)
Research: PAMPs and DAMPs: signal 0s that spur autophagy and immunity (Immunological Reviews, 2012)
Research: Clinical Description and Outcomes of Australian Children With Invasive Group A Streptococcal Disease (The Pediatric Infectious Disease Journal, 2020)
Research: Pediatric Autoimmune Neuropsychiatric Disorders
Associated With Streptococcal Infections: Clinical Description of the First 50 Cases (Am J Psychiatry, 1998)
Research: Clinical Presentation of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections in Research and Community Settings (J Child Adolesc Psychopharmacol., 2015)
Article: Sequence thousands of organisms in parallel: Comprehensively sample all genes in all organisms present in a complex sample (Illumina.com)
fx Medicine Article: The Rise of PANS: Paediatric Acute-Onset Neuropsychiatric Syndrome 
fx Medicine Infographic: Leaky gut, leaky brain: the role of zonulin


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 owners of the country throughout Australia. We pay our respects to elders, past and present. 

I'm Emma Sutherland, and joining us on the line today is Naturopath Keonie Moore. 

With four children of her own, Keonie has always worked predominantly in paediatrics throughout her career, spanning over the last 16 years. With her extensive experience with children, she has become specialised in neurological presentations, such as PANDAS, ADHD, autism, OCD, tics, and paediatric oncology. 

Today, we are going to take a deep dive into some neurodevelopmental conditions in kids. 

Welcome to fx Medicine, Keonie. Thank you so much for being with us today.

Keonie: My pleasure, Emma.

Emma: Well, paediatric neurology is a very complex field, and today, I am so keen to learn from you. You are known for your work in PANDAS, which is an acronym for Paediatric Autoimmune Neuropsychiatric Disorders associated with streptococcal infections. Wow, no wonder it's called PANDAS. 

In fact, you founded a clinic dedicated to the treatment of PANDAS in 2018, and have recently launched a practitioner training program called The Moore Method. But let's zoom out a little today, and I want to discuss the drivers, the biochemistry, and testing for neurological issues. 

But to get us started, I would love to start with what is your why? Why are you so passionate about neurological issues in children?

Keonie: Well, as you mentioned, Emma, I am a mama bear of four now-adult children. So that always guided my career as a naturopath. Initially, even when I started studying due to a recurrent illness of my son when he was an infant, and just saw the amazing results that natural medicine brought in my own children really started me on this journey. 

But I guess my specific interest in neurological conditions really started when my youngest daughter developed anxiety, aggression, and OCD after having impetigo, or school sores.

Emma: Oh, wow. Okay.

Keonie: Something that I didn't recognise until many years later was actually PANS, because back then, I had absolutely no idea what PANS was. And I guess having lived through a time of such concern about my daughter and just being totally bewildered about what was going on, and on top of what, to be honest, was judgement from those around me that not only I received, but also my daughter, about her behaviour.

Emma: Okay.

Keonie: And that has just given me an unending commitment to help parents after my own experience. But, unfortunately, a lot of parents go through, when they need support the most, it's often when they receive judgement, particularly because there's such little awareness around PANS. 

Emma: Agree.

Keonie: So I think in conditions such as autism and ADHD, because there's greater recognition and a clear diagnostic pathway, then it helps that support network. But when it's a constellation of symptoms that are poorly understood and a condition that is rarely recognised, let alone treated, then parents are often, just through sheer desperation, trying to find answers and solutions themselves.

Emma: Yeah. And I guess the empathy that you would hold for those families because you've walked that path is so authentic. You know, they feel that, so I can really understand why you're so successful in this area as well now. 

Now, I know you see many different neurodevelopmental issues in-clinic, what are the things that you see most commonly?

Keonie: So due to my recognition in the field of PANDAS, I do see a lot of that presentation. But invariably, there's a lot of crossover with ASD, ADHD, and OCD anxiety presentations. One thing that I'm really aware of is that because parents are often doing their own research and then coming into clinic, maybe they're even thinking, "Oh, does my child have PANS?" I've really got to distinguish the working diagnosis myself to ensure that I don't just have the blinkers on and, you know, if you look hard enough, you can see PANS in any child.

Emma: Yeah.

Keonie: But certainly, it's a subset of what I see, but there is a lot of crossover with those other neurodevelopmental conditions. And that is predominantly that whole spectrum of what I see in-clinic.

Emma: Yeah, well, let's start with PANDAS and just see where it takes us. How does a patient typically present when they have PANDAS?

Keonie: Yeah, so, most commonly, PANDAS is triggered by an infection. So to start with, I probably should differentiate just between the difference between PANS and PANDAS.

Emma: Please do.

Keonie: So back in the late 1980s, Dr. Susan Swedo and her team at the National Institutes of Mental Health identified that there was a subset of children with OCD that actually had onset after an infection. So even back then, they recognised that there was a whole host of different infections that could have that impact, one of which was Strep, or Group A Streptococcal Infections. But even back then, they recognised herpes simplex, Epstein-Barr virus, Coxsackie virus, a whole bunch of other infections.

They made a research decision to deliberately exclude children with PANS that were not triggered by a Group A Strep infection so that they could leverage off the body of work for well-recognised autoimmune condition rheumatic fever, which has a neurological component called Sydenham's chorea, which is actually very similar to PANS.

Emma: Okay.

Keonie: Now, the trick with that is that what has been issued in clinical practice is that the PANDAS criteria has sort of been adopted clinically. And so, we do see a lot of children that come into the clinic that have had blood test after blood test after blood test, trying to find positive streptococcal serology.

Emma: Okay.

Keonie: But that's something that I would encourage practitioners not to do, because we do know that there's actually a whole bunch of different infections that can be the trigger. So even if it is a Group A Strep infection in the first instance, it can be any kind of infection in the future that might trigger a flag.

Emma: Right. Okay.

Keonie: So certainly from that point of view, when we say that most commonly the PANS is triggered by an infection, so you can actually have non-infectious triggered PANS as well, so mould exposure is probably the most common occurrence with that. And certainly, with all the flooding that we've seen throughout Australia in the last few months, we have actually seen an increase in PANS, conditions presenting post mould exposure.

Emma: Okay.

Keonie: But usually, the majority are infection-triggered. So after infection, it's not necessarily while they have the infection, but in a week or two afterwards, then suddenly starting to develop OCD, anxiety, and a constellation of neuropsychiatric symptoms. So it does vary from child to child, but I guess the keynote ones are really focused around developmental regression, so maybe they could write their name and then, after developing PANS, can no longer write. Or concepts that they, you know, maybe they could read fluently and, now they're struggling to be able to read. I've had some cases where they could read fluently and then can't recognise a letter in the alphabet after the onset.

Emma: Okay.

Keonie: So then are characteristic ones. Maybe they start baby talking or being interested in games or movies that they haven't done or watched for years. So, we see that real developmental regression alongside the OCD and anxiety. Separation anxiety is a big key component. But we often see changes in urination as well. So increased frequency of urination, or suddenly starting to wet the bed at night when they've been dry for years.

Emma: Okay.

Keonie: Now, obviously, in those cases, we want to rule out urinary tract infection, but it is actually a very different presentation that, whilst a urinary tract infection might be a sense of requiring to urinate but not actually needing to, this actually is an increased volume of urination.

Emma: Right. Okay. So triggered by an infection, and then, what I'm kind of hearing, is that a week or so afterwards, symptoms such as OCD, anxiety, the developmental regression is a big one, and urination changes such as bed wetting could be key white flags for clinicians that could be, you know, seeing this in their patient demographic. And I think it can be so complex, but it also can be simple when you're looking at it the right way. So I'm really liking how you're framing this for us.

Keonie: Absolutely. Because there are a number of other symptoms such as mood lability, emotional aggression, oppositional defiance. So some of those are listed as potential symptoms within the constellation that we see with a PANS onset. But there's so much crossover with those particular symptoms with other neurodevelopmental conditions in children that I tend to look for more the unique characteristics of PANS that are going to lead me down that pathway as differentiated from other presentations.

Emma: Yeah, I love that. And, you know, it's hypothesised that one of the underlying pathology in PANS and PANDAS involves an immune-mediated mechanism with molecular mimicry. But in your opinion, your experience, what are the key drivers and triggers? You've spoken about the infection side of things, and not just infection but also mould exposure, so I guess it's anything pathogen-related. But what are the drivers for PANS and PANDAS?

Keonie: It's a great question, Emma. So for many years, the research on PANS and PANDAS has focused on trying to find an autoimmune biomarker or an antibody that proves that it's an autoimmune condition. But to date, that hasn't been found. And certainly, initially, PANDAS was considered to be an autoimmune condition, leveraging off that body of work from rheumatic fever, which we know is autoimmune based.

However, when I'm looking at PANS from a clinical perspective and the way that I treat is actually coming back from an innate immune system dysregulation as opposed to an autoimmune condition. So it's a slightly different focus. And I must point out, it's my opinion at this point in time. So I guess in terms of the work that I've done over the past 12 or 13 years that I've been working with this condition and trialling different, I guess, theories and treatment interventions in the process of developing what we now call The Moore Method is actually looking at some of those key markers. So from my perspective, it's really a dysregulated immune response. So triggered by PAMPs and DAMPs.

Emma: Okay.

Keonie: So if we think about pathogen-associated molecular patterns, or danger-associated molecular patterns, which are the triggers for that inflammatory process from the innate immune response, which is directly influenced by the gut microbiome.

Emma: Yes.

Keonie: So the change in my approach, I guess, is that I do not focus on the initiating trigger at all.

Emma: Yeah, great. Okay.

Keonie: So if someone has a virus that triggers their PANS, I don't treat with an antiviral. Because in my mind, every child should be able to get sick and not develop neurological symptoms. So we're like, "Okay, well, where..." You know, it's really the immune system that's perpetuating that effect.

Emma: Yeah, and that would be treating the noise and not the issue. I really love that because it's so naturopathic. And so, your experience, just sort of summarising, your theory is that it's an innate immune system dysregulation triggered by PAMPs and DAMPs, causing inflammation that then obviously becomes systemic from the gut through to that systemic effect. That's fascinating. I really love the differentiation there, that it is not autoimmune, it's an innate immune system dysregulation. Your lens on this is really interesting. 

You know, we know that there's no biomarkers to diagnose this, it's a diagnosis by exclusion. But, you know, do you agree with that? I mean, there's no one biomarker, but are there some things you look for?

Keonie: Yes, so I do agree that there's no test that's reliable for the assessment of PANS.

Emma: Okay.

Keonie: It really is considered to be a clinical diagnosis that requires the exclusion of other medical and neurological conditions. So any further testing that is recommended as part of the clinical diagnosis process is really to eliminate other causes. So technically, rheumatic fever should be excluded to be able to make a diagnosis of PANS, for example.

Emma: Yeah.

Keonie: We don't often see the level of testing to exclude all of the medical and neurological conditions that need to be done within the Australian population, to be honest.

Emma: Yeah, I would imagine, I mean, that would be quite exhaustive and extensive, and a little difficult for families to actually enable to be done within our medical system. Like that one is a little bit tricky. 

Let’s talk gut health, I mean, we're both naturopaths, so of course, fascinated with all things microbiome related. I want to go through a couple of studies that I looked at for this interview. A recent study suggests that Strep infections alter gut bacterial communities, leading to a pro-inflammatory state through the selection of specific bacterial strains that are associated with gut inflammation and immune response activation.

Now, the research into neurodegenerative diseases, like Alzheimer's, is really interesting, and I was wondering if this kind of research could provide some insights. Now, a 2020 paper stated that Lipopolysaccharides derived from Gram-negative bacteria in the gut are believed to play a role in causing neurodegeneration by increasing the level of oxidative stress and inflammation. And fascinating to me was the subjects that had neurodegeneration had higher levels of zonulin, indicating increased gut permeability. Now, you know, as naturopaths, we know that leaky gut can drive leaky brain. But what is the biochemistry? Or, I guess, what are the mechanisms behind the way the gut impacts neurological health?

Keonie: Yeah, absolutely. And to be honest, that is definitely the lead that I follow when considering PANS. So if we look at Lipopolysaccharides, or LPS, that is a well-known PAMP, so one of the pathogen-associated molecular patterns that will actually trigger that inflammatory response that we've been talking about. So certainly clinically, I found that gut dysbiosis is the real underlying driver of PANS. And as I mentioned, that with any old infection that comes along, it's a trigger but not the cause. So, it really stands to reason in my mind that when we have an inflammatory state that favours bacterial strains, that promote a persistent inflammatory situation alongside increased gut permeability, and then the blood-brain barrier as well, that anything that can stimulate that inflammatory response is going to be a really important underlying factor. So when we consider that the gut barrier is made of a single layer of epithelial cells held together by tight junctions, we know that tight junctions are made leaky by a number of factors, including gluten exposure and changes in that microbial balance, and that's via that increased production of zonulin.

But the blood-brain barrier is also held together by tight junctions and will also be impacted by serum levels of zonulin. So it really stands to reason that anything that causes the gut barrier to be leaky that is circulating systemically, it's also going to induce leakiness of the blood-brain barrier. And they're core components of what I work with before I get to balancing gut flora when it comes to neurodevelopmental conditions, not only PANS but also particularly ASD, so autism spectrum disorders.

Emma: Okay. Well, I'm just digesting. That's a lot, isn't it? But it makes sense to me that gut dysbiosis will have that systemic effect. But the main thing is the inflammation, the increased zonulin levels, the increased permeability of the blood-brain barrier, and the resulting neurodevelopmental symptoms. As we know, we have to start in the gut. 

And when you're looking at testing, I mean, do you do gut tests? Do you do DNA tests? What do you do to help direct your treatment? Because as you've stated, there isn't a test for this. We have to work out other ways to direct our treatment.

Keonie: Absolutely. So I would consider PANS to be a clinical diagnosis, but then I'm going to use testing to help me elicit which interventions are going to be most useful for that particular individual. So I could have ten children with PANS or ten children with ASD present, and the treatment that they respond to best is different. So there's no protocol where you can give everyone the same supplements and dietary plan and get the same results. It's just not that simple. It's complex by nature. But when we really start to kind of work with a foundation of the underlying drivers, I look at two testings that I do with pretty much all of my patients. One is nutrigenomics and the other is gut microbiome testing.

Emma: Okay.

Keonie: And I consider with the nutrigenomics testing that it's really setting the scene for why was this child predisposed in the first place. So sure, there is environmental triggers, the perfect storm, multiple things aligning at a point to trigger that, but what was the susceptibility that was sitting there in the first place to develop those conditions? Because not every child that gets an infection develops PANS.

Emma: Exactly.

Keonie: And even children that might have the predisposing risk factors for autism don't develop autism. So, certainly those triggers of the environment that caused that condition to happen are certainly important, but it actually starts before that point. So really looking at how is the methylation gene SNPs working? Is there a susceptibility to anxiety and OCD through elevated MAOA activity, for example? So they're all the things that I will be looking at of going, "Okay, genetically, I can understand why they were predisposed to a neurodevelopmental condition in the first place."

Emma: And I think that would give a lot of understanding to the parents if they were talked through that explanation as to why, because parents are often so baffled, "Why my child?"

Keonie: Absolutely, absolutely. And so, when you can start putting a process together where there is that understanding, but not only the understanding, but some actions of, "Okay, this is what we're going to do about it," it's incredibly reassuring to parents to know that there's a plan going forward.

Emma: Yes, yes, I agree. And the gut microbiome testing, what are you looking for? What kind of aberrations are you seeing?

Keonie: Yes, so generally I will prefer to use shotgun metagenomics over 16S rRNA as a technology so that I can get down to strain level of understanding the bacterial populations. But certainly, we do see patterns. So from a PANS perspective, we do see higher levels of Bacteroides, particularly Bacteroides Fragilis, not in 100% of the children, but in a high proportion. So really seeing some pro-inflammatory bacterial populations. Significant amounts of dysbiosis that is driving, I guess, the leaky gut in the first place, but also triggering the immune system in a certain way that is pushing it towards more pro-inflammatory.

Emma: Yes.

Keonie: So for me, every single documented case that I have of complete resolution of PANS, and we're approaching 50 now, has been based on treating the gut based on microbiome testing. So we might get a lot of symptomatic improvements based on correcting nutritional deficiencies and then nutrigenomics test results. So that generally is what brings about symptomatic relief. But when you're talking about actually being able to resolve things on a deeper level, and I would say this is true of ASD as well as PANS, it really comes down to correcting that dysbiotic picture and then normalising the gut-brain axis and how the central nervous system is being stimulated or treated from the gut.

Emma: Yeah, it fascinates me because I see a lot of kids in clinical practice, and when I start asking all the questions, hundreds of questions we ask around that gut health parents are often a little perplexed about why I'm asking so many questions about their child's gut health, because they're kind of, "Well, we're not here for constipation." I really have to explain to them the importance of the gut, and your child may not be what you feel symptomatic of a gut issue, but it's much more complex than that. So I would agree, we have to really dive deep on this side of things.

Keonie: You raised such a good point, Emma, because I think that when a child has diarrhoea or constipation, they're like, "Oh, okay, yeah, I can see there's going to be a gut problem here." But when you start talking about other conditions where they don't have that presentation, they are a bit perplexed, like, "Why are you talking about gut health?" But, some of the things that I might talk to them about is actually, you'd be hard pressed finding any health condition that in some way hasn't been linked to gut microbiome.

Emma: Yeah.

Keonie: So it's much more... Certain bacterial overgrowth will impact transit time, but there are plenty that absolutely have no impact on that. So it really depends on which bacterial population is overgrown to see what the impact is on health generally.

Emma: Yeah, good point. Looking at environmental drivers, now, I found this paper. It was a 2018 systematic review on the role of glyphosate. We know glyphosate is a broad spectrum herbicide that can reduce beneficial bacteria such as lactobacillus and bifidobacteria. But this paper showed that it doesn't affect clostridium. Now, there is an association between clostridium and ASD, but do you see that coming up when you do gut testing in-clinic, that link?

Keonie: Absolutely, we do.

Emma: Okay.

Keonie: So I think it's important to recognise that not only has technology around gut microbiome testing evolved, but also our understanding. We don't want to generalise too much. Some clostridia species are considered to be commensal or normal habitants of the gut.

Emma: Yeah.

Keonie: And so, that's why my preference is to know what bacteria is in the gut down to the strain level. However, saying that, we do see higher populations of clostridia species in children with ASD. But probably even more importantly a higher ratio of propionate, so one of the short-chain fatty acids. So typically, we see low butyrate and high propionate.

Emma: Yeah.

Keonie: Now, what's interesting is that the bacterial populations that have been linked to autism include the clostridium species, Bacteroides and Desulfovibrio. They are bacteria populations where propionate is the short-term fatty acid that's most produced in those ASD prevalent bacteria, which is interesting. And even last week in clinic, I do a lot of mentoring practitioners, and a practitioner brought a gut test to me to review. And I could see the high propionate low butyrate. I saw high populations of clostridia species. I was like, "Oh, is this child on the spectrum?" They're like, "Yes, you picked it." So again, nothing's 100%. We got complex combinations. But we do see pretty strong patterns around those short-chain fatty acids. And certainly, when we see it, we can be assured that that diagnosis has usually already been made.

Emma: Yeah, fascinating. The role of gut dysbiosis in ASD is really fascinating. I was reading a 2019 study that looked at the effect of short-chain fatty acids, as you've just been talking, on human neural stem cells. And it showed definite benefits to these cells' proliferation and differentiation. So we can see that there's such an interaction here between the gut and the brain. I mean, you must see that kind of thing clinically.

Keonie: Absolutely. And it's really interesting when we start thinking about the impact of short-chain fatty acids when they stimulate the neural stem cells to differentiate from the neuroepithelial progenitor cells into neuronal or glial cells. So glial cells we know tend to be the ones that are thought to release the inflammatory cytokines and may be pivotal in that disturbed neuronal circuitry that we see in autism.

Emma: Right.

Keonie: Interesting that study showed that the ASD brain also seems to have a higher population of glial cells, far exceeding the number of neuronal cells. So really I guess leaning itself towards that gut microbiome is having a definite impact on that neuronal circuitry.

Emma: Yeah, yeah, yeah. This is where...yes, this is a very complex topic, but being able to glean from you these little snapshots is so helpful to put everything in its place in my mind. 

Now, there was a small 2020 paper on NAC and OCD, and it showed really positive outcomes after the eight-week point. The daily dose was 2700 milligrams per day. But how do you think N-Acetyl Cysteine is helping here? What is the mechanism of action that is showing those positive outcomes?

Keonie: Yeah, absolutely. So one of the main reasons that NAC is so useful in OCD is because of its ability to modulate glutamate.

Emma: Okay.

Keonie: So NAC will increase GABA and reduce glutamate in the central nervous system. But honestly, I think the benefits of NAC really go past even that central action. So we know, for example, that NAC is going to provide more cysteine to the body, and cysteine is the rate-limiting step in glutathione production. And the brain is incredibly sensitive, even more so in children, to inflammation. So when we're talking about things like lipopolysaccharides, we know that they cross the blood-brain barrier, interact with microglial cells, and microglial cells, when they're activated, can be a main source of that excessive glutamate in the first place.
So we're really seeing how we can modulate not only the GABA-glutamate ratio, but also actually make the brain less sensitive to neuroinflammation. And this is important, like obviously, I've delved into it with autism and PANS, but even looking at the research on anxiety and depression has shown links to inflammation. So we know herbs like curcumin and saffron actually increase brain-derived neurotrophic factor, and then change the expression of the amygdala to be more fear, anxiety-provoking and calm that down through modulating inflammatory processes.

Emma: It's interesting, isn't it? It keeps coming back to inflammation. Yeah, I love that explanation on the NAC, of how it modulates glutamate, it can increase GABA, but it also is providing cysteine, which is that rate-limiting step in producing glutathione, which could be helping protect the brain from the effects of lipopolysaccharides, i.e., reducing inflammation. Yeah, that makes sense completely. Thank you.

Keonie: Absolutely.

Emma: Now, I want to take a moment to just stop here and talk a little about nutrigenomics and the gut microbiome. Are there maybe one or two clinical pearls that you could highlight for us?

Keonie: Yeah, absolutely. So, certainly, let's say with nutrigenomics, for example, a test, as I said, I'm really doing in majority of my patients.

Emma: Yeah.

Keonie: So you get so much information from nutrigenomics. Profiles can be a bit overwhelming for practitioners to kind of know where to start. But one of my key areas that I'm going to be looking at and what I can glean so wonderfully from a clinical aspect is the vitamin D panel. So when we're looking at the Vitamin D panel, we're looking at the activation of vitamin D and the breakdown as well as the vitamin D receptor. So it's fascinating because we all have those patients where they're on vitamin D, and no matter what, it doesn't seem to go up.

Emma: Yes.

Keonie: And so, understanding those gene SNPs, we can really understand the variable requirements for vitamin D from one individual to the next. But even with perfect vitamin D status, if someone has a vitamin D receptor, particularly homozygous gene SNP, then it doesn't even matter if their vitamin D levels are perfect, there's still going to be a reduced impact of that vitamin D. So understanding those genes SNPs is really important because when I look at any neurodevelopmental condition in a child, I want to know that their vitamin D status is optimal, but also that they're utilising that vitamin D because we know it's so important for regulation of mood.

In fact, it's been directly linked to OCD and PANS. So having a vitamin D deficiency will increase the severity in alignment with how severe the vitamin D deficiency is of that OCD severity in PANS, plus the barrier function. So looking at vitamin D's critical role in having nice healthy integrity of our gut barrier and our blood-brain barrier. So understanding, not just the surface level of, okay, we might have, in the case that we've been able to get a blood test, which is not always the situation.

Emma: That is true.

Keonie: And we know, "Okay, well, what's happening with the vitamin D status?" But really going to that next level of understanding what we can do to optimise.

Emma: Yeah, that's a good insight. So Vitamin D is a key focus point that we should be looking at in that nutrigenomics. That's a really good clinical pearl. 

But kids aren't always fans of getting blood tests done. But if you do recommend a blood test, the child is sort of reasonably happy enough to get it done, what markers are you tracking and what do you tend to see? Any sort of... Yeah, trends that you tend to see.

Keonie: Absolutely. So when I am able to get a blood test, and so often we can't, especially with, I guess, a subset of children I'm working with, there's usually high levels of anxiety, certainly sensitivities to touch. There can be a whole myriad of reasons where it's just a no-go zone. In the case where I am able to though, there's some key things that I'm looking for. Number one on my list is iron, so looking at iron studies, and particularly ferritin for iron stores. We know that iron deficiency is globally the most common deficiency in children. And they have a high prevalence of that deficiency. So when we see studies that link... So, for example, tic disorders such as Tourette's have been shown that if you have iron deficiency, the tic severity will be worse.

Emma: Okay.

Keonie: So understanding what the iron status is is going to be really important for any child with a tic disorder, whether that's a part of PANS or not. But also that iron deficiency in children has been shown to elicit a constellation of symptoms very similar to ADHD. And I have personally seen in clinic a number of cases where the child has come to me already diagnosed with ADHD, we've found a very significant iron deficiency, we've corrected it, and then the parents have come back to me and go, "You know what, Keonie? I don't think my child has ADHD at all." Because once we corrected the iron deficiency, those symptoms went away. Now, I'm not suggesting that ADHD doesn't exist, but I am suggesting that there's probably a subset of children that have been diagnosed with ADHD where they actually have an iron deficiency.

Emma: Yeah. And this, you know, shows the importance of basic nutrition and how we can... Don't get too fancy, just cover the basics and start there. But when we're looking at ferritin, what kind of number are you wanting to see?

Keonie: So my optimal range for ferritin is between 40 and 80.

Emma: Yeah. Great. 

Keonie: So I don't like to see it too high, above 100. I'm like, "Okay, that's a bit...it's indicating inflammation."

Emma: Yes.

Keonie: And then anything under 40, I would consider to be suboptimal.

Emma: Yeah, fantastic. And if you can't get a blood test that lets you know their ferritin, what are you monitoring in that case?

Keonie: Yeah, this is always tricky, isn't it?

Emma: Yeah.

Keonie: Because I guess when it comes to blood tests, I always like to also have a full blood count, vitamin D levels, zinc and copper if I can get it, B12 and folate. And so, I guess particularly with vitamin D and iron, whilst deficiency is more common, nature is all about balance. As much as we don't want too little, we also don't want too much. So what I might do is trial...if there's a child that I think they're at high risk, so I'll look at the risk factors. Have they had recurrent threadworm infestations? Are they a picky eater? Like how much iron are they actually eating as part of their diet? Particularly because if OCD is part of their presentation. OCD often presents a focus around food for children. So they don't check if the doors are locked, even though most people would recognise that as OCD, because it's not part of their everyday activities. But I think about that. I think a lot about food, so often that's what they can be focused around. So that may be impacting their nutritional intake. Whether they have any signs. So pica, so eating, you know, unusual objects, including soil or dirt. I would say, "Okay, that's a clear sign." The problem is that I see that as more of a severe end symptom of iron deficiency, whereas children are going to be potentially symptomatic well before that actually occurs.

Emma: Yep.

Keonie: So sometimes we just have to put it together in terms of clinical history. How likely is it? And then try a small dose of iron and see if they respond.

Emma: Yeah. And look, in my experience, in similar situations the parents will often come back or they'll email and say, "Oh, there is a difference." Like it is quite obvious to parents when the child is iron deficient and then they start taking an iron supplement that they're absorbing. It's quite obvious, isn't it?

Keonie: I've seen that, even with what is relatively a small dose. There is a substantial improvement, even within a week or two.

Emma: Yes, absolutely. Yeah. I would love, Keonie, for you to take us through a case study. Now, I know you published a case of a three-and-a-half-year-old in the Journal of Child and Adolescent Psychopharmacology in 2018. Congratulations. That is incredible for our industry. But could you just briefly tell us about a case study so that our listeners can really understand what this looks like? All these things that we're talking about.

Keonie: Absolutely. So firstly, I would encourage any practitioners working in this field to publish their case studies, because I think if we look at clinically how much data there is on the interventions that we utilise and the results that we get, it's unfortunate saying, especially in the field of PANS, that none of the research is really leaning towards natural interventions.

Emma: Yes.

Keonie: So if we can actually start to document what we're doing in-clinic and have that published, then that starts to build on the body of evidence that will actually help get researchers to pick up some of those themes within their own research projects, which I think would be amazing.

Emma: Yeah.

Keonie: And the case that I'd like to share with you today, though, was a ten-year-old boy that presented to me with a very severe tic disorder. And I love this case study because it wasn't clear cut whether it was PANS or not. The reason for that is that the new clinical diagnosis for PANS, the central requirement is OCD sufficient to meet DSM-5 criteria. Okay, so he had quite severe vocal tics, complex motor tics, and coprolalia, so repetitive swearing. But he had minor OCD that was just really insufficient to meet that criteria. The thing that kind of alerted me to thinking, "Is this really Tourette's?" Which he has been diagnosed with, is that he had very sudden onset. So the onset was suddenly after he had a lumbar puncture three years prior, which he had because of a history of severe migraines.

Emma: Okay.

Keonie: And he was on a number of medications. So he was on fluoxetine, topiramate, riboflavin for the migraines, clonidine, melatonin at bedtime, and then the paediatrician had just recently recommended risperidone, which is an antipsychotic. That's actually what made the parents go, "Oh, we have to look at a different way here." So they had tried risperidone with him at an earlier stage and he had a really bad reaction to it.

Emma: Okay.

Keonie: Now, these parents were not parents that would normally seek natural medicine as their kind of first port of call, but they just got to the point where they're like, "Okay, what we've been trying is just not working." It was getting more and more severe, to the point that the tics were so severe he couldn't write with a pen, couldn't ride a bike, had missed a whole term of school, couldn't eat with a knife and fork, really couldn't enjoy those activities that you would expect of a ten-year-old, if that makes sense. Given that he had been neurotypical three years prior and then suddenly had this onset of tics.

Now, initially, he would have the tics for three or four months, then they would go away and then would come back every winter. So that was the other thing that sort of made me think, "Oh, I wonder if this really is Tourette's," because that's not typical of Tourette's. So that remitting-relapsing clinical course is very much more characteristic of PANS.

Emma: Right. Okay.

Keonie: So, what I decided to do... So he had had actually some blood test done. So he had tested negative to group A Strep infections. And he'd had an EEG, MRI, and multiple lumbar punctures and they were all normal, so that is the testing that should be done to exclude other medical and neurological conditions. So he'd been diagnosed with Tourette's accordingly. But what I decided to do was to do an ibuprofen challenge.

Emma: Love this.

Keonie: Now, ibuprofen is not something as a naturopath that I recommend as a whole treatment, of course, but it is reliable for getting clinical improvement in PANS. So I'll use it for one of two reasons. So if I just am not 100% sure that they have PANS or not, and I need to know because it's going to Tourette's treatment, then I'll use it, or in acute flares where it's crisis point for the family and things are going totally sideways, then we'll put a five-day limit on it. It's really important that parents understand that it's a short-term circuit breaker. Because as we know, ibuprofen thins the gastric lining, increases the risk of gastric bleeding and gastric ulcers. We certainly don't want to be creating problems for the gut when actually our long-term goal is to improve it.

Emma: Yeah, true.

Keonie: However, given this little guy had such severe tics, 24/7 at every waking moment, to the point at the end of the day it almost looked like he was having seizures because his body was so exhausted from ticking all the time.

Emma: Yeah.

Keonie: Within one day of ibuprofen, he had a 50% reduction in his tics.

Emma: Incredible.

Keonie: And 60% on day two. So you can imagine the bewilderment after being also on a whole bunch of psychiatric medications.

Emma: Yeah.

Keonie: And then just taking something as simple as ibuprofen make such a big difference for him. Thankfully, I had pre-framed it with them, "Look, this is not a long-term strategy. It's just to test my theory." Once we have a positive or negative, then you stop, we're not going to continue. And they followed that. So that was fantastic. So I sort of took him through the plan of what I use for the Moore Method, which is, number one, protect the brain.

Emma: Yes.

Keonie: So he was on some curcumin and some N-Acetyl Cysteine, so 2400 milligrams per day. And it is important to recognise that the prescribing of NAC for dosage does tend to be at that higher end of what we would normally prescribe.

Emma: Yeah, definitely. That is a higher-end dose, yes.

Keonie: Yeah, and if you look at that research that you were referring to before, it was 2700 milligrams. So it was sort of more at that end of the spectrum. Whereas, you know, for an adult in clinic, maybe we'd be doing between one and three grams. And then if you calculated it to body weight, it would be a lot less. But if you're wanting to use it OCD, you do need to be at that kind of dosing.

Emma: Okay.

Keonie: I would then use some probiotics with him to improve barrier function of the gut. He did have quite a severe vitamin D deficiency at 36, so we're correcting that. Gluten-free diet is a common recommendation for me to reduce that zonulin inactivity and improve barrier function of both the gut and the blood-brain barrier. We identified that he had a food intolerance to dairy, so he actually was dairy and gluten-free. But one thing I should mention is he was only opening his bowels every ten days when he first started seeing me.

Emma: Wow.

Keonie: And what we found is when we took dairy out of his diet, he started opening his bowels every day.

Emma: It's classic, isn't it? Yeah.

Keonie: Yeah, so they were like, "Okay, we're happy to continue with this because it's making such a difference to how he felt." And then I did some antimicrobial herbs, so I did a combination of juniper berry, usnea and liquorice.

Emma: Yeah.

Keonie: And I generally will do a pulsing regime. So two or three days per week, killing off the bad bacteria, and then four to five days per week going, "Okay, how are we going to influence what grows back?"

Emma: Yeah.

Keonie: It's not just about going in there and killing off as many of the dysbiotic bacteria as possible, it's actually about shifting the diversity and the populations to be a healthier balance. So...

Emma: I love that diversity comment there because I think, you know, we can be guilty as naturopaths of going in a bit hard with the antimicrobials and not understanding the full picture of the diversity and how those antimicrobial herbs can affect the diversity of our patients gut. So nice point there. Can I just ask, how on earth did you get him to take those herbs?

Keonie: He was very committed. He was very committed.

Emma: Okay.

Keonie: Saying that, I do generally recommend mixing liquid herbs with honey.

Emma: Yeah, okay.

Keonie: Usually manuka honey so that we're getting some therapeutic benefit from it. But because honey will dissolve in the herbs, it actually makes it quite palatable.

Emma: Nice tip.

Keonie: Or pear concentrates, the other one that I use.

Emma: Yeah, okay, great. So that's a remarkable case study. I mean, it really just walks us through how incredibly beneficial holistic treatment can be for these children. It's absolutely fascinating. 

I could talk to you all day, Keonie. I think we might have to get you back. But before we finish up, is there anything else that you would like us to know about paediatric neurology?

Keonie: So I think the most important thing for paediatric neurology is to treat what you see.

Emma: Okay.

Keonie: So what I mean by that is sometimes I've had some very complex, challenging, genetically-based conditions in children where sitting in front of me with their diagnosis, I'm like, "How much can I actually help this family?" And then I go through my process. So I look at nutrigenomics, I look at the gut microbiome, I look at nutritional deficiencies. And so I had a child who had very, very low muscle tone, to the point that, even at three, she couldn't sit or stand. And that was something that was considered genetic, from birth, this is your life, end of story.

So I combined that normal approach with some organic acids testing as well. And then I just went through a process. I found that she was vitamin D deficient. I corrected that. I found that she was under methylating. I corrected that, you know, put in nutrients to support methylation. We found that she had low protein levels. We worked on that. So I just went through the process and was able to identify those things. So I say, "Okay, well, that's not going to be supporting her optimal health."

Emma: Yeah.

Keonie: Within three months, she walked.

Emma: Fascinating. Yeah.

Keonie: So certainly, from my perspective, sometimes understanding that the nutrients, the gut microbiome, methylation, they're having such an overall impact on children's health, that sometimes even the simplest things make a really big difference.

Emma: Yeah, yes, yes. It's so true. Because I think, yeah, we can get a bit fancy, but we've got to make sure we cover those basics. 

And what it sounds like to me is that you have now developed the Moore Method, which is a very step-by-step process from the sounds of it. And I love, I would encourage people to do that course and become proficient in that area. And you also offer mentoring for clinicians as well. So I think that that is such a good opportunity for people out there listening to jump on either of those or both.

Keonie: Absolutely. It's something that I feel incredibly passionate about, because, you know, I really did hold back with stopping taking new patients personally for a long time because I wanted this option to be available to more and more families. And then just realising that actually this, unless I clone myself, then there is a limit to how much that I can do in that one-on-one work. So the, I guess, the flow on effect is naturally just to help other practitioners in this way. It makes a lot of sense because the results that I've seen with these families, I would love for more families to have access to that.

Emma: Yeah, I would agree. Well, thank you so much for joining us today, Keonie. There's some key points that I've taken away today. The first is that PANS and PANDAS are driven by an innate immune system dysregulation. And the second is gut dysbiosis is a main driver for neurodevelopmental issues due to the resulting gut permeability and neurological inflammation. So rule number one is correct the dysbiotic picture, but also ensure that nutrients are optimised. For example, you know, the ferritin levels being between 40 and 80. 

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, fxmedicine.com.au. I'm Emma Sutherland and thanks for joining us, we'll see you next time.


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