An ideal T4 is 15
An ‘anti-aging’ DHEAs must be >7
A ferritin of 100 is optimal for women…
I’ve heard it all, probably you have too, and far too often & too recently from practitioners who should have rationalised & researched their way beyond these functional falsehoods, by now. I bought into these ‘optimal wellness truths’ hook line & sinker early in my career and proceeded to even propagate a few but with (not much) more experience in clinic, I had to seriously question this pursuit of ‘perfection’ & ‘perfect pathology’…in favour of reality & scientific evidence! They didn’t add up. Not with my patients – even the healthiest ones, in fact some of the really unwell ones occasionally had these kind of high-normal results and they were part of the problem!. ‘But that’s because no one is truly healthy outside of those seeing a functional medicine practitioner & supercharged on supplements & hormone replacements!!’ came the counter-argument. Ahhh, really?
How then do we reconcile this with the following: Individual genetics & biochemistry
Our biological resilience Healthy & appropriate senescence Large datasets of mixed race populations from other comparable first world countries…where these figures denote the statistical outliers?
I mean, if the 50th centile value for ferritin for actual living, breathing, bleeding, women in the US, Canada, Australia etc etc is 30-40 ng/mL and the 95th centile is 126 ng/mL and the WHO says that in fact, anyone menstruating with a ferritin > 150 ng/mL should attract suspicion for iron overload….but functional medicine men (mostly…sorry but it has to be said!) say 100 IS OPTIMAL FOR EVERY WOMAN #@^*…please tell me in which women, consuming what kind of diet, where in the world, & based on what improved or better health outcomes?
And while you’re there can someone please support this bold claim with a scrap of high quality evidence?? [Rant over🎤💧]
The falsehoods of functional medicine include the blanket belief, ‘more is better’ (ahhhhh not when it comes to many things, including iron where women’s lower levels have been found to be an evolutionary advantage…guys). But you know what, we’re better than that! We see each individual, recognising all the factors at play that make for their uniqueness, help to define what ‘healthy’ looks like for each person and don’t fall for one-size-fits-all claims without any evidence nor common sense even, to support them. What do you think?
Let’s make sense of the over-arching nutrition principles, that will profoundly change your understanding and application of this modality Truly understanding the ‘big’ concepts, so often overlooked, or incorrectly taught, ensures you get the critical ‘small’ detail in your nutritional prescriptions right. In this 4 hour recording, together with key clinical tools, we talk about the tough stuff: dose-response curves, active versus passive stores and excretory pathways and ooh lah lah…the myth of taking ‘activated vitamins’. Even those who feel satisfied with their original training – will find a lot in this critical review that is new, insightful and truly practise-changing!
It’s quite the meme of the moment and while I completely get the sentiment behind its original meaning, my take is a little different:
Results in Practice 2021!
How were yours?
Here were some of ours from the cases presented in group mentoring:
💪 We correctly identified hyperparathyroidism in several presentations of GIT, mood & musculoskeletal concerns (remember bones, stones, groans & moans?) with good response to targeted doses of D & Ca
🎯 We correctly identified BAD in a patient with ‘refractory IBS-D’ for decades – who responded well to lowering her fat intake & other support
🧐 We determined HFE mutations were present & a pathophysiological player all over the place – with presentations from psych to fatigue
🤯 We stumbled across several cases of concurrent Gilbert Syndrome & PCOS – ‘mixed messages’ in both labs & presentations – which research now suggests may be related! & should change the way we treat these PCOS patients e.g. not with CHO restriction!
But the best result of all – arguably was the growth we got to witness in all our mentees – from those in our New Graduate Program:
“I truly appreciate your compassionate way of lifting everyone up whilst stretching our brain gently to build up on knowledge, and confidence. You have such beautiful skills in navigating us – how you treat us all helped to restore my trust in this industry/naturopaths and myself 😅 so huge thank you 🙏❤️🔥” Reiko Fujike-Stirling | New Graduate Group Mentoring 2021
…to those dedicated practitioners working to build their competency & confidence in mental health:
“There’s so much to learn and stay on top of in terms of new information, I realise it is important for developing integrity and how I practice. Having a mentor, like Rachel, who I can rely on who is super on top of what’s going on in research in Mental Health. Someone I can rely on for very accurate and practical information that keeps me on my toes and challenges me and is practical for my clients. Doing mentoring and learning how to refine my understanding of case taking, mental health screening / testing, treatments and just really deepening my understanding has ignited a passion in me as a practitioner. Rachel presents everything so brilliantly and practically. Thanks so much Rachel, the content and everything is just brilliant.” Steven Judge, Naturopath, Nutrition & Herbalist | Mental Health Group Mentoring 2021
We’re sharing some of our ‘Conversations with our Community’ via our social platforms at the moment – it’s such a joy to listen to each individual practitioner’s journey…and we might end on just such a note here courtesy of Amanda Astrop – another ‘survivor and thriver’ from our 2021 New Graduate Program:
Want to join me next year so we can make RIP 2022 mean something far more positive?? Email us at [email protected], before the 22nd November, to tell us your needs, wants and desires (educational only of course 😅) & we’ll find the right group for you 🙂
New Graduate – great opportunity for New Grads to build confidence as they leap from student to practitioner, or for practitioners wanting to refresh their core clinical skills such as MindMaps, Pathology, Case Taking etc
General – our regular case presentation groups, with one practitioner presenting a case each month, or just listen in.
Mental Health Primer– topic based to build on your knowledge in the role of naturopathic medicine in Mental Health – from screening tools to key management issues, specialist diagnostics and beyond.
Mental Health Applied – this group will help you fortify and buildupon what you already know and increase your confidence when working with clients who present with myriad mental health issues & shared care arrangements. This is a case presentation group, with one practitioner presenting a case each month, or just listen in.
And not in a good way, right. While we’ve known about the potential for peripheral neuropathy with excess B6 supplementation since the 1980s, currently there’s a seismic shift in our sense of safety even with previously regarded ‘safe’ levels. You may have heard individual whispers, or the chorus of voices coming together, both here and overseas, belonging to members of the public who report suffering sensory nerve impairment with as little as 2mg/d! Is this a mess of mis-diagnosis, false attribution & nocebo? Perhaps for some, but certainly not for all.
How could this be the case given the many RCTs employing hundreds of mgs per day over months, with no such events recorded? How could this be given, your (?), certainly my, high dose prescriptions, with only 1 case of quickly reversed, peripheral neuropathy in over 20 years, on my books? The pieces of this complex paradoxical pyridoxine puzzle are coming to light.
Is it the form?, the dose? the duration? individual differences in B6 metabolism & toxicity threshold? amplification of risk secondary to levels of other nutrients, or the use of certain medications? Yes. And we need to understand each element to better tailor every B6 prescription to the individual & mitigate risk. I have spent the best part of this month reading almost every paper on this from the 1970s to last month and I am now alarmed but more importantly, alert, to what prescription practice changes we can all make to lessen the risk, and control the power of B6. It’s been the most compelling deep-dive. Because in spite of a clear TGA warning issued last year that likely prompted the quiet removal of high dose products from market, it would seem none of the companies have the courage to have this difficult conversation with us 🙁 I invite you to ‘feel the fear & do it anyway’ & listen in to our latest Update in Under 30.
Haven’t we always known that nutritional medicine is a potent prescription? Now thanks to more sophisticated research we have a much greater understanding of this and of both the intended and unintended effects of micronutrient supplements that have the potential to achieve supra-physiological levels. B6 metabolism is arguably the most complex of the Bs – involving 6 different forms, at least 2 of which are active – and exhibiting some of the most complicated regulatory control designed to both harness the power & limit the accompanying risks. Excess B6 supplementation, however, has long been known to present as peripheral neuropathy in some individuals and case reports of this are growing, at lower and lower doses. New information has come to light to help us understand the why, the how and better still how to mitigate risk to our patients.
You can purchase Dynamics and Dangers of B6 – Controlling the Powerhere.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.
I’m intrigued by the silence. Hair loss in women is frighteningly common, following pregnancy, menopause & with extreme stress (wait is that a tautology? 🙄) In fact it can strike at any age and for a multitude of reasons. When it happened to me a few years back I also initially responded with silence, terrified that if I said it out loud it would make it real, but when my daughter suddenly asked, ‘Mum are you losing your hair?’ with her trademark attention to detail & exquisite empathy, she gave me the words & a good kick into gear, simultaneously. Now I am fascinated by women’s silence around this generally, how little we share our stories & forewarn others, & as practitioners, the lack of adequate training we’ve had identifying the different types (hint: it involves donning gloves or if restricted to online consulting, knowing how to organise correctly positioned pics) & from there finding the right solutions.
While Female Pattern Hair Loss (FPHL) is the dominant type in women – it only applies to the following pattern:
But alopecia due to stress, thyroid disorders, autoimmunity, contact dermatitis etc will affect different regions of the scalp and with a different onset & progression.
And remember, by the time YOU, the practitioner, can spot a patient is losing hair when they simply walk into the room, they have ALREADY LOST 50%😢 This is why I think we need to push back against the silence. The research is unflinching about the serious psychological impact this has on women – especially in cultures which place so much emphasis on looks generally, and hair, specifically as a commodity of very high value in women. The diagram above comes from a 2019 update on the phenomenon of FHPL and it’s a good articulation of the knowns and unknowns (pssst spoiler alert…it ain’t about androgens!) but let’s never forget the other causes and cures. So let’s make sure as the trusted practitioners women present to so often, we are sensitive enough to have this tricky conversation & skilled enough to help 💪
Stop Pulling Your Hair Out – The FPHL Answers You Need
Female Pattern Hair Loss (FPHL) is everywhere, perhaps you just haven’t been looking. As the leading cause of alopecia in women globally and with 1 in 5 women affected at any age, we’ve all got clients who have FPHL to different degrees. We need to be better able to recognise the early features of this condition which profoundly impairs quality of life and induces depression in its sufferers and that begins with validating patients’ concerns when they report “thinning” or “increased losses”. But what do we do from there? This recording talks you through the assessment, diagnosis and management of FPHL based on a combination of the most recent research and Rachel’s clinical experiences. Once you’ve ‘seen’ FPHL.., you won’t ever ‘unsee’ it and your patients will thank you.
I confess I was a chemistry nerd ‘way back when’, but my skill for stoichiometric calculations had sadly slipped by the time my kids needed help with high-school science & now my son, who’s about to graduate from chemical engineering, is my ‘chem-friend’ 🙄🧐 I suspect he feels FB messenger wasn’t intended for such use – or at least there should be some veneer of, ‘Hi darling how are you?’ before…’Need to talk through these pharmacokinetic datasets’ However, the one equation that was like turning a light on in my brain & therefore never forgotten was the Fenton reaction – basically metals’ MO for messing with our biology, especially iron. Turns out – it’s the most essential and helpful in understanding health & disease:
Endometriosis IBD Neurogenerative disorders: MS, PD, Alzheimer’s Higher than healthy GGT Impaired COMT or catechol excess for other reasons Cardiovascular disease & Diabetes Vitiligo Both the Big Cs Heavy metal burden Iron dysregulation (Obesity, HFE mutations, Thalassaemia) & Excess (IV or oral over-treatment etc)
(almost) All roads lead to radicals & reactive species…if you follow the Fenton pathway & iron leads us down this path more often than any other metal. Certainly sometimes for good: like protecting us against pathogens and destroying dodgy cells, but when it gets out of hand, a key pathophysiological process in a long list of disease. So understanding how to recognise patients prone to dysregulation of this mineral, avoiding iron over-treatment at all costs (I am seeing incorrect and excessive use of IV iron in many patients make it stop!) and identifying means to contain and control its movement, are important. Oh and in case the Fenton has faded in memory, it goes a little something like this:
While rates of iron deficiency and related anaemia continue to grow, the increase in prescriptions of IV Fe have expanded exponentially in western countries. What is behind this change in practice regarding how we treat iron deficiency and does it match with responsible prescribing? Do the benefits always outweigh the risks? And while we’re on the topic, who is most likely to benefit and what are all the risks? In light of a current class action in the US, relating to a lesser talked about adverse event associated with IV Fe and recent complaints here in Australia against GPs, allegedly due to inadequate information to enable informed patient consent…it’s time to answer these questions and more. When is IV Fe a means of rescue and when is it a risky repletion strategy with no evidence of advantage? Click here for this episode.
Ok, so maybe I don’t quite look like this after 100 episodes & almost a decade of our Update in Under 30 series but sometimes, in the depths of researching & developing each episode I can feel like this! The idea for this subscription series came out of a desire to share little monthly snippets from my patients and was called, ‘From my desk to yours’, but over time as its following grew, I came to realise how large and valuable a resource – a library of sorts – this was to practitioners. In particular, those hungry for answers, rich in critical thinking but time poor. And so, it evolved to become ‘Update in Under 30’. The topics are remain typically ‘home-births’, from my patients or those shared with me through mentoring but I realised recently, each episode goes through 3 stages of development, something like:
1. Answer a key Clinical Question that’s out there in our professional community generally 2. Answer the often more complex questions clinicians, with significant first-hand experience, have directly asked me about this same aspect of practice 3. Then, last & most challenging, is endeavouring to answer all the questions that I have now after reading the first 50 or so articles to answer the first two questions!!
And let me tell you – that last one can take weeks!!🧐😵🧐 often stalling or stopping all together, the recording or release of an otherwise near-complete episode 🙄 Ask my team – I drive us all batty. But that’s because I recognise the great responsibility I have so wonderfully been awarded and I take that to heart. And I have these questions of yours, of ours, in the driver’s seat when I research (and research again), write and rewrite, record and re-record these [messing with the myth, hey…did you think was my passive income?!^#@}
Take this month’s topic – to celebrate our 100th episode it seemed fitting to pick a BIG one!:To NAC or Not to NAC (that is the question!):
1.In integrative medicine opinions on NAC are divided – among all the fans it has its dissenters – why? 2.If such concerns about NAC are well-founded (and they are) how do we mitigate these? 3.What risks are real & relevant to the kind of plasma values we are likely to see? How precise can we get with our prescription through changes to form, dose, dosing regime etc to ‘accentuate the positives, eliminate the negatives & not mess with Mr In-between,’ as my bestie, Bing Crosby says?
Relax – I refrained from singing this line in our latest update!! But what I do let loose on is a whole lotta juicy answers to our collective questions about a much loved nutraceutical! Happy 100th UU30 🥳
That is indeed the question for most of us working in integrative medicine. While there is hardly a nutraceutical with more therapeutic flexibility and potency – with potency comes risk and responsibility – hence NAC’s dissenters. Many of the concerns regarding the use of NAC are well-founded and come down to its dynamic chemistry in both the gut and blood together with its specific pharmacokinetics. With improved understanding of both, however, to direct dose, dosing regime & duration for more precise NAC prescribing – we can accentuate its positives, eliminate its negatives and not mess with Mr In-Between, so to speak!
And for our 100th session this is of course a SUPER SIZE ME SERVE coming in at about the 40minute mark 🙄🥳
But sadly, still not cloned! While it may sound like Big-Brother was responsible, it was the efforts of my tremendous team responding to feedback from fans – who said things like:
I just LOVED EVERY SINGLE MINUTE of the MasterCourse in Diagnostics but would love to be able find a little gem I know I’m digging for, or re-listen to a very particular section without having to RELISTEN TO EVERY SINGLE MINUTE? Someone with a life, Somewhere not in lockdown
Ok I am paraphrasing, but you get the gist. So we thought, reasonable request really. With over 24hrs of core training modules plus all the bonus sessions that you get to have & to hold for the rest of your RAN’s life, even we might be out of lockdown by then and have other things to do!! And while I personally couldn’t stomach my 99th listen…I made St Sally do it 😂 This now means you can find the time-stamp from the video on the top right hand corner of your pdf copy of the notes and go, ‘Hey, that amazing animation of what’s behind increased Neutrophil counts – here I come’ & go directly there (39minutes & 21 seconds) without listening to a single extraneous, ‘you know’, ‘right?’ & ‘ummmmmmmmmmmmmmmmmm’
So, while I am already working up a serious head sweat (too much information?) working on the development of MCII which will kick off early next year…oh boy…did I just say that?!*%#@ and already getting outrageously excited about our next adventure together – we thought we’d go back and increase the value of the investment many of you have already made…and maybe entice a few others with our trail of breadcrumbs that takes you to the best treasure trove of all in our toolkit! I think this was Western Herbalist, Penny Henderson’s experience 🤩
“I’ve been in practice as a herbalist for many years and have to say that your master course has been one of the most exciting, inspiring courses I’ve done for a very long time! What a ripper! Your understanding and love of biochemistry and pathology brought it out of the too hard basket and into the sunshine for me. I can’t thank you enough. I have piles of patients blood tests on my desk as we speak which I have to say is rather daunting. Hopefully with much practise I won’t feel quite so laboriously slow!
Anyway thanks so much Rachel -you’re an inspiration to so very many practitioners!”
You know when you learn about a ‘new’ dis-ease driver and then you actually have to stop yourself from diagnosing every patient with it? I’ve done this dance with Gilbert’s Syndrome for over a decade, so too maybe have some of you? And while there have been many, many occasions when I’ve been certain it’s Gilbert’s (clear robust & reproducible patterns of high bilirubin without other explanation) there are other times when I’ve been left wondering, and with questions. Like – what about a fluctuating pattern – sometimes ‘within range’ sometimes above or at least high-normal – with no other explanation? What about the patient whose symptom-story is a perfect fit – prone to nausea, early satiety, gut issues, food reactions and anxiety all worse for increased oestrogen…but the total serum bilirubin is 14 micromoles/L? I mean, 14, right? that’s well below the top of that range, but remarkably higher than the majority of women of the same age, eating the same diet. And you ask yourself…could it…be??
The latest UU30 offering on Gilbert’s Syndrome constitutes a complete overhaul of everything we’ve previously been told about how to recognise and diagnose this polymorphism & it’s going to answer a lot of those ‘could it be’ questions we’ve all had! Known also as familial non-haemolytic jaundice and episodic hyperbilirubinaemia under stress – is everyone with Gilbert’s prone to jaundice? Uh, no. Total bilirubin levels typically have to get to 45 micromoles/L to evoke this effect – many of our GS patients won’t ever get there, some will with increased illness or other stress and may yellow a tad (like a fading bruise), while other patients of mine routinely have a bilirubin at this level but won’t experience jaundice unless they impair their UGT further via doing what they know they shouldn’t: extreme exercise or excess alcohol. The latest deep dive into GS diagnostics
But as much as we don’t want to miss this diagnosis we don’t want to mis-diagnose patients with it either!
Can you spot the difference? Don’t forget total serum bilirubin levels are the net result of haem catabolism – so you need to account for rate of blood production, destruction and of course rule out any biliary dx before you can take a guess at Gilbert’s. Oh and watch out for expected high bilirubin values in the fasting fan(atic)s!
For those people living with Gilbert Syndrome at last the research world & the real one are uniting – with greater detailed documentation of how this very common polymorphism presents and the mark it may make in their health story. However, given only 1/5 with Gilbert’s syndrome actually know they have this condition, who are we missing? This latest instalment rewrites our diagnostic criteria and corrects our past misunderstandings based on the very latest science, while shedding further light on what it’s like to live in Gilbert St.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
Are we all just a bit prone to panic at the moment? I received a 9pm call from my 21year old son. Trying desperately to disguise my reflexive s’mothering, I ask in a voice feigning carefree, ‘Everything ok?’ to which he replies, ‘Well, [long pause] not really…”
My fingers are poised to dial 000, I just know I’m not going to sleep tonight now (or possibly ever again!!) I become aware of a lot of background noise around him (?is he at hospital), my heart is in my throat as I ask, “What’s goingon?!!”
“There’s no organic kale
…I mean there’s rainbow chard, but that has things in it that reduce the absorption of minerals, right, mum? But is it ok to buy just once?”
Ok everyone exhale. He’s not in ER just the produce aisle of his local late-night supermarket and his main concern is optimising his nutrition 🙄😂 Oh and not overly relying on food delivery services because, “well that’s just depressing and I know whatever I cook is so much better’. And while he might be the scientific one of the siblings his area is oxy-fuel combustion as opposed to oxalates so he thought he’d call a friend 😅 My children have demonstrated the most incredible resilience under some trying times in their young lives of late but good to know their #kidsofnaturopaths qualities are alive & well 🥰 Now I could have kept him on the line for longer to explain all the ins and outs of oxalates and how to keep the levels low…but nah…with my heartrate returned to normal I was suddenly very ready to sleep, he can just listen to the recording😂 …and so can you!
Oxalates are found in high concentrations in many of the ‘healthy food choices’ we promote and are even higher again, when these are organically farmed! Given the importance of individualising therapeutic diets are we able to quickly recognise those who need to lower their level of these naturally occurring plant products? Who shouldn’t be drinking green juices? And which of our patients might benefit from being educated about different food combinations and preparation to lower the oxalate load from these otherwise fabulous foods?
“After our group session I suggested the low fat trial but she was ‘no, no, no….I can’t take anything more out of my diet’. It was at the beginning of lockdown & she had other stressors as well. So I asked her to be mindful of her fat intake & if one meal was higher in fat then go low fat for the rest of the day. I saw her last week & she did this & guess what her diarrhoea has dramatically improved. She is not experiencing watery diarrhoea nor the sense of urgency nor leakage. Mostly 4, sometimes 5 on Bristol Stool. She’s now happy to trial low fat (<40g/d)”
This is the story of a 50-something female who has battled IBS-D for over 30 years. Along the way she has diligently sought the help of so many health professionals and tried numerous ‘tried and true’ IBS approaches, like FODMAPS minimisation, gluten minimisation, dairy minimisation & joy minimisation with hardly any minimisation of her symptoms!Why? Because her loose stools and urgency were BAD. A very particular form of bile acid dysregulation that is present in almost half of IBS-D patients and responds best to low fat intake, together with a few other tricks.
And with the corresponding slowed transit time, we now can more clearly see if there are additional actual food reactions at play – without all the background BAD confounding and now that her gut has time at last to actually correctly absorb things that she couldn’t before due to inadequate time in contact with digestive enzymes and absorptive surfaces.
Ahhhhh we love a great ending – especially one that reminds us the most powerful prescription is getting to the root cause such that we can empower patients 💪🧐 This patient and her practitioner inspired the recent Update in Under 30 on how we can all learn to recognise….
This is not a trick question. Up to 50% of all patients diagnosed with IBS-D actually have bile acid diarrhoea (BAD) underpinning their digestive complaints as well as some patients with unresolving diarrhoea post-cholecystectomy and gastro. Knowing which ones do and how to manage this, which requires distinctly different approaches from our general management of IBS, is the key. As always, good lessons come from those we learn in the clinic and this story starts with a patient and how we came to recognise the BAD in her belly. Get this as a single download here.
No, this is not a trick question & it’s certainly not a silly one. IBS, as many of us know, has a very loose diagnostic criteria: visceral hypersensitivity coupled with altered motility in the absence of organic disease. Hence it tends to ‘loosely’ fit a vast number of patients struggling with GIT issues. The differential diagnostic algorithm all health professionals are encouraged to use for patients presenting with GIT issues leads us to this IBS label, just as soon as we’ve excluded the red flags. But this ‘early opt out’ according to many experts, including Schiller et al in the American Journal of Gastroenterology, tends to propagate the illusion we’ve reached our diagnostic destination: practitioners stop thinking about the ‘why’ & stop looking for the real drivers & causes, which is the key to shifting the refractory patient into remission.
For those presenting with chronic diarrhoea, Bile Acid Diarrhoea (BAD) is in the diagnostic algorithm & there is strong evidence it’s at play in almost half of these patients! It’s just that BAD, is the next station along the line after IBS-D, which means most clinicians have sadly disembarked already 🙁
Bile acids, as key biological agents, in both the behaviour & health of the gut & metabolic dx, are getting a lot of attention right now. While Bile acid malabsorption (BAM) in disorders of the small intestine such as Crohn’s & undiagnosed or refractory Coeliac dx, as well as other miscellaneous GIT disorders that clearly disrupt the bile acid balancing act of the gut-liver axis, have been known for a long time, there’s a new kid on the gut block, previously only known as the idiot, I mean, idiopathic BAD. But us idiots have finally worked it out! This is not about malabsorption but about excess production of bile acids and this pathophysiology is drastically over-represented in IBS-D patients.
And knowing if your IBS-D patient has a ‘BAD-thing’ going on, every researcher wants you to know, is game-changing. Explaining the strong heritability of this particular IBS subtype and the reason so many patients are refractory to standard IBS approaches.
We need to use distinctly different dietary strategies when IBS is BAD. Once again patients are our greatest teachers & I’ve relished the excuse one practitioner and her patient gave me to deep dive into the enormous body of BAD research, that is ‘so hot right now’! The way I look at, ask questions about and assess patients with chronic diarrhoea, especially IBS-D, is forever changed 💪🙏
When is I.B.S. B.A.D?
This is not a trick question. Up to 50% of all patients diagnosed with IBS-D actually have bile acid diarrhoea (BAD) underpinning their digestive complaints as well as some patients with unresolving diarrhoea post-cholecystectomy and gastro. Knowing which ones do and how to manage this, which requires distinctly different approaches from our general management of IBS, is the key. As always, good lessons come from those we learn in the clinic and this story starts with a patient and how we came to recognise the BAD in her belly.
I’m 100% confident that, as a professional group, among our highest values about healthy, preferable, food choices, would be characteristics like: ‘as close to nature as possible’, ‘unrefined’, ‘unprocessed’, ‘unadulterated’. Tell me I’m wrong.
So, when I keep hearing about NEW! “Never seen before” (read: never in nature) modified (read: more processed, adulterated) nutritional supplements: water soluble vitamin D, fat soluble C, bioflavonoids with unprecedented (read unnatural) bioavailability
I’m left wondering what these companies are missing about their customer group (because we are clear about our valuing of nature & what’s natural & have a desire to minimise exposures to things that are not, right?
or what are we missing here, in the clear conflict of our core values these constitute?
I think if we find ourselves forsaking this core value & prescribing highly modified, unnatural supps, it’s the result of both hype & fear. The hype is self-explanatory and I’ve written recently on how modifications exponentially increase profit margins for companies, all the while possibly reducing ours because patients are spending more on product and therefore there is less left over for the practitioner fees 🙁 [The ones spending hours with them face to face, not to mention years & thousands on our training] The fear is perhaps less apparent, more insidious. The fear is that we’re not using the best, being the most effective, and deeper still, inevitably that we will fail to action our patients return to health. This is a big one. I think it’s pervasive, if not omnipresent, and works as a motivator for many positive actions by practitioners – like engaging in further education, reading that latest journal edition on your lonesome laptop when you could be streaming some series on a shared sofa. But this same fear can also undermine us, overwhelm us and shake our tree of trust, that we believe to be so firmly rooted within us, of the healing power of nature.
So while my position sometimes makes me feel very ‘old school’, I’m not suggesting we return to nutritional prescriptions composed exclusively of bee pollen & brewer’s yeast and I absolutely recognise and respond to an individual who has very specific barriers to benefiting from nutrients in their natural normal forms. But let’s be clear, they are a minority.
Some of you will know naturopath Dawn Whitten & know that she is one of my mentors. I’ve had the benefit of speaking with her over the years about herbal prescriptions but also about the principles & philosophy behind our practice & in one of many conversations she told me that a key objective she has with her patients is to rebuild their trust in their body, their own biological resilience (I love this concept and that’s a talk for another time!) and ultimately in nature. Well jeepers Dawn – how did you get to be so wise so young? But isn’t that central to vis medicatrix naturae? Maybe that Naturopathic Nanna’s club isn’t so fuddy-duddy after all. Want to join us?
Speaking of using nutrients in their most natural state for the best health outcomes – the best B3 is probably not what you think!!…. The Balance of B3
Most of us have been taught to ‘balance the Bs’ when supplementing, which discourages the use of single B vitamins in case this interferes with the regulation and roles of others. In reality, outside of a couple of dynamic duos like B12 and folate, there is little concrete information & evidence of this. In the case specifically of B3, however, we now know, the risk of an excess of the most common B3 forms found in supplements and fortified foods, results not only in disruption of other nutrients but imbalanced B3 biochemistry itself. Given B3, in its coenzyme form NAD+, is regarded as highly valued currency in the prevention of many diseases, as well as the key to our optimal health and longevity, it’s critical to understand the different forms and functions of the various B3 sources.
Maybe it’s tax-time, just my wintery whinge or a tirade triggered by missing my twins’ 21st birthday due to border restrictions 😶 butI’m sorry for all the shouting of late…about interpreting iron studies, about the copper misinformed etc etc. and my gorgeous new grad mentees copped a full monologue, with links to articles, recordings & the Coeliac Society, when they asked me to expand on why we must exclude coeliac disease before removing gluten from anyone’s diet. I was so glad they asked though! I’m now using my inside voice.
But I don’t want my message to be misdirected and I fear it might be. It’s not you and it’s not me
‘We’ are doing our best. We are working in a field that demands us to be across soooooo many domains of knowledge and information, from the basic & not-so-basic medical sciences, to pathology interpretation, nutrition, herbal medicine and beyond. It’s a lot. None of us are across it all. I’m certainly not. And I’m aware, that the frustration I feel at others’ misunderstandings sometimes is unfair, because I’ve benefited from excellent early teachers all the way through to having a job now, that keeps my head in the research daily. And even still, without a doubt, the gaps & shortfalls I observe and criticise in others, I could have made of myself, earlier in my career. We don’t know what we don’t know, until we know better, right.
Who is this ‘them’ of which I speak? Well, 25 years ago when I completed my under-graduate (and walked 10 miles to school in the rain, without shoes or breakfast 👵) I believe I received the training required to be the naturopath that I needed to be. Safe, effective, knowing my scope – which was basically coughs. colds, atopy and risk mitigation for future chronic disease. I never saw a lab test during my under-grad. I would have read a set of iron studies badly and something like ELFTs, like it was Latin. I wasn’t made aware by my lecturers of the critical part I could play in my patients’ lives, either by advocating and advancing correct diagnosis or by obscuring, confounding and delaying it (sorry, still thinking about the gluten debate!). But back then, I think this was appropriate for the time, the state of play of our collective medical knowledge and for the role naturopaths were playing in the health landscape. Not any more.
If you haven’t had a chance to read the extensive research about ‘us’ (Australian nats, nuts & herbalists) published of late, who we are, what we do, how we are viewed and what our patients expect, then you could be in for a surprise.
We’re perceived by many, if not most, of our patients to be a primary health care provider – either flying solo or co-piloting with the patient’s GP (& no auto-pilot function!!!) and as clinicians for chronic comorbid cases not the acute cold. My how times have changed and the question is – has the knowledge and level of competency of those in educational roles & the quality of what they deliver a good fit? Sorry, but if the majority of a large new graduate cohort have left their training with a mantra of ‘we must not diagnose’ and INTSEAD are likely to advocate a gluten free diet RATHER THAN Coeliac testing with the patients doctor first – then we’re falling at the first: Primum non nocere. Sorry,I forgot, inside voice 🙄🤐
This Update in Under 30 recording speaks to the seriousness and primacy of identifying Coeliac Disease in any patient reporting a suspected reaction to gluten and takes you through the latest evidence on the best screening protocol. With an increased understanding about the strengths and limitations of gene testing, serology and biopsy, we have a clear map to follow now. Along the way Rachel outlines 3 additional potential mechanisms for ‘gluten’ reactions amongst our patients, what to look for and how to tell the difference.
I haven’t personally seen every medical condition known to occur, nor every micronutrient deficiency & toxicity picture in the flesh but that doesn’t mean I doubt their very existence. Sadly, it would seem some practitioners due to a) not knowing ‘where’ to look in terms of best assessment medium and/or b) not knowing ‘what’ they’re looking at, when faced with an actual Copper deficiency, have declared this uncommon, but certainly not unknown, nutritional issue to be a figment of others’ imagination!
I know I’ve been fortunate to see more labs than most would want to in an entire lifetime , a collection of my own, my student’s & my mentee’s patients, so let me share just 3 sets of results from 3 different individuals: an 11Y boy, a male teenage athlete and a female in her early 20s with an eating disorder, all with Copper deficiency.
Don’t worry, I have more – just ask. What’s so dangerous about people spreading myths and misinformation in relation to copper in kids and teenagers specifically, is it shows complete disregard or ignorance of an understanding of how Copper is critical for development during these life-stages and how regardless of which developed country you live in Copper is expected to dominant over Zinc in blood, especially pre-puberty.
AM I SHOUTING???!!!
I’m sorry it’s just that my blood tends to hit boiling when exposed to the misinformed, misinforming others… and that can make one call out in pain 🤯
You see, I literally heard a practitioner in an “educational” webinar purport that
‘Copper Toxicity is so prevalent in kids in her clinic’ and I was like,
OH. EM. GEEE.
Because if you start with that misunderstanding, and are unclear about what constitutes an accurate Copper assessment and how to recognise the pattern that follows low serum levels (each of these patients above had abnormalities in their FBE consistent with Copper deficiency) you are not only going to miss the thing you need to make a priority to fix, you’re going to make it worse! Take ‘Volatile Vince’ the gorgeous sensitive 11Y boy I saw, whose increasing mood volatility had been misattributed to pyrroles and given large doses of Zinc! So, Copper Crimes are a thing. Guilty until proven innocent but in fact, never found innocent by some practitioners it would seem. The ramifications of unchecked Copper deficiency include negative effects on mood and cognition, immunity, and the balance of other nutrients and kids are going to feel this impact the most! What are the causes? Inadequate intake being uncommon outside of eating disorders, and excessive Zinc rarely the cause, we’re likely looking at a marker of malabsorption or a genetic issue. Don’t buy into the confirmatory bias many use when they choose which research to read (risk of excess) and which to ignore (Copper as an essential mineral, critical to kids) and let’s not discredit something as not being a thing because we haven’t seen it ourselves, yet, hey, anyway, at least, now we all have, right?!😵🥴😆
Copper, as a kingpin in angiogenesis, brain & bone building & iron regulation is a critical mineral during paediatric development. So much so, the kind of blood levels we see in a primary schooler might cause alarm if we saw them in an adult. So too their Zn:Cu. But higher blood Copper and more Copper than Zinc are not just healthy but perhaps necessary during certain paediatric periods. This recording redefines normal, low and high with a great clinical desktop tool to help you better interpret these labs, as well as reviewing the top causes and consequences of both types of Copper imbalance in kids.
Name a B vitamin. Hey, Bingo! It’s on the list! What list? The complete one from all the review papers & references to possible links between individual nutrient deficiencies & Angular Cheilitis – inflammation & cracking at the corners of the mouth. So does that mean more Bs are the answer for people presenting with this painful, recurring issue?…Ahhhhhh No. Yes, you heard me correctly, these deficiencies rarely cause the breakdown of the integrity of this very specific area of skin in the patients we see. So now we have a double ouch, right?
We might send patients away with a B complex and some lip balm and over a week the cheilitis resolves – which one was the most therapeutic? …I hate to tell you 👀
What is the underpinning cause(s) & the important message we are missing with this presentation? Well, it could be one or more of a long LONG list of differentials, ranging from anatomical, habitual, immune related to iatrogenic. And while many nutrient deficiency pictures can include this feature and therefore make the ‘possible’ list, only one makes the ‘probable’ list. And that’s iron but only in severe deficiency, aka anaemia and only affecting 1 in 5.
…Telling anyone to push the nutritional issues further down the list of differentials for any condition? Well, that’s unexpected
And no, antifungals aren’t the answer either. Yep, that might be worth a listen….👂
Just an annoying, embarrassing, cosmetic condition or could it be the clue that helps you ‘crack the case’? There is a surprisingly long list of differentials for this condition but most of us only know a few, reflexively reaching for either B vitamins or anti-fungal creams. Does either make sense? Does either address the cause(s) which we now recognise to be a unique series of risk factors in each individual? Or are we at risk of shooting the messenger and missing the message of Cracking Corners altogether?
You can purchase Cracking in the Corners – Angular Cheilitishere.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.
I’m a fluoro gal myself. I take copious notes the old school way, on paper with pen and vast swathes of highlighted sections….I deface research articles much the same way. [And resist drawing moustaches on author pics😆] so I LOVE Ang’s hot tip with her hot tab system in her GIANT exercise book, that she filled (yes FILLED) with notes from our MasterCourse in Comprehensive Diagnostics last year. Angela Haldane was one of many people I saw firsthand making the absolute most of the course, applying something we’d just learned immediately in her patients and being rewarded with results 🤩
And now with another ‘EOFY- Lockdown-Cocktail’ upon us, maybe we can put our time to good use with 6 wks of intensive learning & up-skilling that will pop you out the other side of this – with a whole new skillset for patient work-up, prescription development, effective, objective monitoring of treatment & a common ground for us to walk, when we’re communicating about patients, with their GPs.
And there’s just just a week to go til 🐱🏍
And whether you’re a Onenote Wonder, a Diagram Diva, or anything outside of a savant, Good News!!! We are in the process of ‘time-stamping’ these MasterCourse recordings. That means that whether you have the recordings already, or purchase them in the future as a DIY package or, jump in now while you still have a chance and attend our Weekly Live Watch–Party that kicks off on the 8th July… over the coming months we will be adding in time-stamps or bookmarks on your powerpoint notes, a la Angela tab style! This means that you can more easily go back to a particular section of any presentation in the video and find the spot you need to rewatch. This development was off the back of some lovely feedback we received from a package purchaser, who requested this, or even transcripts….yeah about transcripts…Some of these sessions go for 4 hrs and I speak on average a million words a minute (sligexaggerationion) and we still don’t have software that can understand my accent apparently 🙄 But we know this is going to make life a lot easier for you all because we hear from so many, they have these recordings on high rotation 🤩
This MasterCourse in Diagnostics is a goldmine of information and, as always, we’ll keep working on ways to help you reap even more from your investment!
Starts on 8 July 2021 at 3.30pm AEST Every Thursday for 6 weeks. Each session starts with video presentation Plus each session has LIVE Q&A with Rachel Arthur
You get to keep the 24+ hours of video presentations in your online account to watch anytime in the future. Bonus video presentations, audio, notes and resources as well. Live Q&A’s will not be recorded.
While many of us have made it our business to ensure we are competent IN the business of understanding patients’ iron studies, it sadly seems, many even in teaching and training positions, still have not 🙁 I was sent 2 messages this week that had me lost for words (other than expletives). The first, an email from a final year nat in student clinic with the subject: Please tell me I’m not crazy!!
“Fasted male with high ferritin & high-normal transferrin saturation at two time points, with constantly raised Liver enzymes & neurological Sx. He is currently being treated for blasto in student clinic because they think the high ferritin comes from “blasto infection!!! He needs to be checked for an HFE mutation, right??”
Ok so high ferritin because of ‘blasto’ is NOT A THING! And on the HFE front…Correct! I ask, “Have you mentioned this to the supervisor? What do they say?” Student’s reply, “They say HFE mutations are uncommon so, in a word, it’s not it. But THANK YOU!!!!!!!!!!!!!!!!!!!!! I feel sane again” So, what do I do? The student is studying at a leading institution, one that has sought advice and input from me in the past regarding their diagnostics curriculum, but it would seem, the clinicians they allow to supervise our precious next gen of nats are not expected to be even as competent as the students themselves. Danger Will Robinson! Danger! [old tv show reference…apologies, young folk!] I’ve [not] recovered from this when I get hit with the old 1-2! A naturopath messages me with a screenshot of a FB group exchange over a set of iron results: Ferritin over 400 but low serum iron and transferrin saturation values…which another health professional, who offers training to naturopaths, says is ‘Iron Deficiency’
Email says, “Please help me, I’ve worked so hard to understand iron studies and this has just CONFUSED THE #@*^ out of me!”
Again someone who would typically defer to the voice of authority here, fortunately knows enough to know to question this (mis)interpretation.
I tell you…you may have thought that when I previously wished for all health professionals to be competent in reading studies…but it’s actually a big ask, it would seem 🤔 Could we just, as a start, get anyone who professes to teach, train or mentor health professionals, to actually get up to speed on this themselves or…keep their mouths 🤐
Overt Iron Deficiency Anaemia or Haemochromatosis aside…do you understand the critical insights markers like transferrin and its saturation reveal about your patients iron status? Most practitioners don’t and as a result give iron when they shouldn’t and fail to sometimes when they should. This audio complete with an amazing cheat sheet for interpreting your patients Iron Study results will sharpen your skills around iron assessment, enabling you to recognise the real story of your patients’ relationship with iron.
Last week I had my say about acknowledging our elders & mentors, this week I want to speak to the power of the young peeps. Just like a younger sibling, nipping at your heels can act as a great motivator to move faster, or having children can inspire us to do more to improve the ‘world’ we’re welcoming them into, my interactions with naturopaths, nutritionists & herbalists of the younger generations generally effect both responses in me! The best of these come from cluey ‘youngsters’ (mature-age-second-career-new-nats included!!) who ask the most difficult questions & show dogged determination in getting answers to these either via me or in spite of!
At the outset I was able to hand over a substantial selenium research hoard I had obsessively compiled, Josh was able to build on this, refine some fledgling theories I had and then completely redefine my appreciation & understanding of how chronic over-treatment (not toxicity…) is so deleterious to human health. Check this out:
When Selenium (Se) saturation point occurs in plasma, there is a potential reduction in health protection… Se will progressively pool within plasma non-specifically as SeMet in lieu of regular, sulphur containing methionine, in albumin and other proteins…inducing oxidative stress via a complex disruption of cell reactions/signalling This is likely to be how Selenium over-treatment increases the risk of both CVD and T2DM
Many of you may ‘Know Your Numbers’ when it comes to Serum Se targets in thyroid health or just generally know how to Stay Safe with Selenium Supplementation because I’ve spoken extensively about these in the past and you will be relieved to know neither my ‘numbers nor my message’ have changed BUT I encourage everyone to read this new article because Josh has added so much more, including the interplay between our microbiota and our individual selenium needs, handling and tolerance and and and….I could go on but…what I really want to say is, thanks Josh for your academic rigor, your firm determination & diligence and for nipping at my heels all this time. This important piece of work just wouldn’t have happened without it 🐶
I stand on the shoulders of my elders. [I hope it’s not too painful for them, it’s been going on a long time now!!] And I regularly lean on my mentors – who are often my peers, practitioners specialising in areas different from mine. I recite their names often like a little mantra in our mentoring sessions: Kate Worsfold, Dawn Whitten, Tini Gruner, Michael Hayter, Jason Hawrelak and a few others that are on high rotation like ‘Rhiannon-repro’ Hardingham and I feel this is important to reaffirm that learning is lifelong for us all and to make clear the passing on and around of knowledge in our profession. There’s been a long history of honouring our history, so to speak, in naturopathy.
My training definitely acknowledged, paid homage to & revered elders past and present & while I’ve never been one to participate in the making of herbal preps by a full moon, at solstice, in a field somewhere, in the company of said herbal elders (you know who you are!!)…
I do try to continue & foster this important collegiate quality of our professional community by reciting the names of the saints source of clinical pearls I have been given so generously by others.
Lately, I’ve been wondering if we’re losing this tradition. I’m hearing practitioners present concepts as ‘theirs’, ‘develop’ & distribute teaching tools ‘adapted’ from others work, parrot identical ‘catch-cries’ even, with no mention of the origin, the source – even the inspiration. Now perhaps I am showing my age, reflecting a very different time in naturopathic training when we were so fortunate to be taught by some of these amazing (solstice honouring, field dwelling, herbal making) elders, but even by today’s standards and the dominant EBM model, surely every emerging clinician understands the need to cite their sources?
The green tea & lactulose intravaginal wash recipe I use and frequently share with mentees always comes with the prelude – “I got this from Gould’s” The tips on testing tools in mental health, I propagate like mad, has the epilogue – “All that I know, is because Kate taught me so!”
Of course I say more than I cite (otherwise the sessions would be impenetrable!) but I like the way it helps us all to see we are a part of something bigger.
I have! And just recently a stark contrast between the results from 2 different methods of cortisol capture in the same patient illustrated just how likely this is. How do we ‘capture’ something so ‘dynamic’ and interpret anything of substance from a ‘static’ assessment technique? But rather than throw up our hands and throw out the whole attempt to measure cortisol, we can improve the rigor, reliability and real-world meaningfulness of our patients’ results by refining our timing of tests, choosing the medium wisely & manipulating test conditions to answer specific questions about their HPA function. Great ready reference resource included!
If you’re already an Update in Under 30 Subscriber – go directly to your Active Content…it’s already there!
If you’re not and want to improve the accuracy of your Cortisol Capture in patients gohere!
What’s your knee-jerk response to 52Y Lipids Lucy & Liver, whose ALT & AST suddenly jumped above range when she was put on statins? They’re damaging her liver? You’d be wrong. One of the practitioners who undertook the MasterCourse in Comprehensive Diagnostics just graduated with flying colours when she was able to correctly identify the true cause of this patient’s LFT abnormalities, can you?
[Cheeky hint: there is more than one explanation/process at play]
This naturopath now knows her pathology patterns. She knows the interpretation of any liver enzyme must also take into account the movement in other markers, to make meaning of the whole. Because so-called ‘liver enzymes’ are never exclusive to the liver. They are expressed in multiple other tissues and organs – sometimes at equal concentrations to their liver-level (e.g. ALP and bone). For some, even referring to them as a ‘liver enzyme’ is a mislabelling of sorts, with minimal expression in the liver itself compared with ubiquitous distribution all over the body (e.g. GGT & LDH). Of course this is both a blessing and a curse. A curse if you make the mistake of only interpreting their levels through a ‘liver lens’…a blessing if you know when they are flagging problems elsewhere through the specific pattern recognition. So back to Lucy – the statins had induced a rhabdomyolysis not hepatocellular damage. The clues? Significant AST dominance over ALT, above range CK and LDH.
So if the statins weren’t causing increased hepatocellular damage what is that increasingly high-normal ALP pattern all about?
Bones. And again, this practitioner picked it. And then got to win herself some pretty BIG credit and credibility points with all the other health professionals sharing care of this patient by suggesting that they clarify and confirm this by referring her for an ALP bone isoenzyme assay, which answers the question: is the elevated ALP originating from the liver, the intestines or from the bone? Bingo, bones it is! Or was, because this practitioner was able to alert not only the patient but all the other practitioners treating her to the increased bone remodelling taking place, independent of the statin reaction, but part of her perimenopause. Left unchecked this would escalate further of course at menopause and leave her bones in bad shape. This is just one illustration of how we can show ourselves the be the incredible one we are on the shared-care team.
Being lab literate and pathology proficient, sets you apart from the rest and enables you to practice truly preventative medicine. How else would we have known she was experiencing increased BMD loss that may be the start of something truly tragic?