The debasing of BMI as a stand-alone assessment of weight is long overdue given its significant limitations and lack of meaningfulness with respect to overall health. This coincides with a bigger societal and cultural shift towards inclusivity which involves redressing bias against people with diverse body sizes and compositions.
And how do we, as integrative health professionals, continue to uphold our principles of prevention and treating the cause when excess adiposity may be a very real contributor? While ensuring we ‘see’ and treat each individual in front of us, not our assumptions about adiposity, not our body size bias nor blind spots?
One part of the answer: read and be led by their lab results – because pathology is nothing if not personalised.(more…)
The builder responsible for my reno arrived one day with a frown. When I asked him what was wrong – he said he’d just had his second high PSA result and now the doctor wants him to see a specialist. It was apparent that he felt this was a real cause for concern. Talk about raising a red flag to a bull 🚩🐂 Yes, of course you know what followed. I insisted on reviewing the results myself only to find the reference range provided on his report was not specific to his age – and if we adjusted up for this (as the science supports) his result is just 0.5 ng/mL above the expected value!
Now, remember he is a builder so, ‘0.5’ in his mind might well be on par with 5mm which apparently is a big deal…or so he keeps telling me every time I try asking for some weird unconventional thing for my roof, windows, walls, whatever!! So I still had to provide a little bit more detail for him to get perspective and to understand the true meaning (and lack of scary meaning) of his results.
This however is just a micro-illustration of a big problem in pathology – we all risk a lack of perspective but if we can get it back, aids us to see that seemingly ‘normal’ results are sometimes a concern, and so-called ‘concerning’ ones, non-significant. The incredible patient insights that can be gained from being able to measure & monitor actual quantities of things in our patients; nutrients to novel disease markers, precursors to end-products, all comes down to understanding how their values compare with…with what? With someone of a different sex and age? With ‘all adults 18-108!’? With any other pre-menopausal woman regardless of reproductive or cycle stage? With ‘the average’ adult given that this current definition is overweight & unwell? Who are we comparing ourselves and our patients to?
When I undertook my undergraduate training many moons ago – there was no education in blood test interpretation. But as soon as I got out into practice I found my patients had all these bits of paper filled with magic numbers that I felt certain might offer me insights and a deeper understanding of their whole health – and how to best help them.
I desperately wanted to decipher this foreign language and made it my mission to do so. I was lucky enough to meet and be paired with a kindred spirit, Dr Tini Gruner, who happened to be my supervisor when I returned to undertake my honours thesis. Together we pooled our knowledge, sought out & shared with each other yet more and found that, together with comprehensive case taking, it provided excellent scaffolding to our work-up of patient cases. Better than that, it created this baseline for patients, identified clear treatment objectives and we could measure the success of our interventions based on how their results did (or didn’t) respond to our interventions. It was (and still is) a totally thrilling way to practice.
We talk about there being both an art & science to medicine generally and certainly an integrative approach. Without the benefit of pathology interpretation, I felt too at sea at times, without quite enough of the science to check the accuracy of the ‘art’ and my speculation.
Being able to understand what each individual result represents and reflects, to know how to form meaningful comparisons – with external reference ranges that speak to healthy individuals of the same sex & life stage, derived from rigorous research – and also form a comparison with the patient themselves, to pick up on the most subtle and significant early alerts to an emerging pathophysiological or healing process – is the skill, I believe, we all need in health to complete the toolkit. That’s why I made it my mission to learn the language of labs, from a conventional & integrative interpretative perspective, and then to share this learning with everyone wanting and willing to take this baton from me (& Tini) and run with it 🏃♀️🏃
MasterCourse I: Comprehensive Diagnostics. Click here to read more and here to purchase it.
*Please note that this is the place to start for everyone wanting to add preventive diagnostics to their tool kit. It is also the pre-requisite for MasterCourse II, so make sure you have completed this before continuing with MasterCourse II: Thyroid and Adrenal Diagnostics.
MasterCourse II: Thyroid & Adrenal Diagnostics. Clickhereto read more and here to purchase it and sign up for the Free Watch Party commencing tomorrow, 3rd August 2023 with is included with each purchase of the MasterCourse II.
Heck yeah. It’s going to take a lot more than 1 push-back post to turn this ship around! Likewise, I was only getting started with my recent Update in Under 30 episode, ‘What’s Hiding Behind Histamine’ 🤓😂 & part 2 has just been released where we unpack the case of a 41yo female with chronic diarrhoea, multiple food reactions, very high stress and very high oestrogen. Sounds like she’s a walking Histamine Headline – except she isn’t.
Right now we really do need to keep this conversation going such that a healthy discourse can help us deconstruct the histamine dogma.
I know I’m showing my age here, but anyone remember when Candida was having a ‘moment in the 90s? Ok, so that ‘moment’ stretched to over a decade of a ‘Candida-contagion’. No one could eat melons or mushrooms, eat ferments or feel joy. It was a bleak time that did our profession some reputational damage. Not only because seeing an ‘alternative practitioner’ became synonymous with being put on an unbearable, unattainable restrictive diet and positioned practitioners as peddlers of punishment but also because it took some time for science, in the form of accessible (& always improving) assessment methods, to come along and save us from the folly of the 1-diagnosis-for-all mentality.
Let me ask you, how many times do you actually see Candida overgrowth on reports from stool testing performed using best practice modern methods?
In my experience – never – not as a stand-alone issue. Occasionally, as part of the overgrowth of a suite of opportunistic organisms where the real-take home is the need to ‘remove the opportunity’ via the promotion of more good guys. So not only was the diagnosis incorrect, the proposed treatment for it was a complete misdirection as well.
Can’t help thinking in the current climate of Histamine Hysteria that history is repeating itself.
How will we all individually, and as a profession, respond this time?
In this follow-up episode we observe how the 3 key elements often hiding behind a histamine intolerance diagnosis: Misunderstandings, Missed Messages & the potential for Mistaken Identity, have played out in the case of a 41yo female who presents with chronic diarrhoea, a long list of problem foods including now a suspicion of ‘histamine foods’. Rachel offers up new ways to approach the patient work-up that cut through the ‘noise’ and enable us to better identify what is hiding behind histamine in similar cases of marked gut dysfunction.
You can purchase What’s Hiding Behind Histamine? – Part 2here. If you are an Update in Under 30 Subscriber, you will find it waiting for you in youronline account. You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audios and resources here.
You’re invited to attend acnem’s 2023 Annual Conference ‘Long COVID, Navigating the Complexity, A Clinician’s Roadmap’.
Saturday 29th & Sunday 30th July 2023, Melbourne. Both face-to-face and online.
To get 25% off acnem Annual Conference USE CODE: acnem25
Never done a MasterCourse in Diagnostics with me? Is that because you’re scared of…
a) investing that much time Aren’t we all – but we can hold each others’ hands & hold each other accountable each Thursday for just 7 weeks🤝 b) investing that much money We hear over & over again from our alumni that this was the best investment they made in their practice & it paid them back in spades! 💰💰 c) your own future fully fluent – all seeing all knowing (almost!) – diagnostic diva/divo self?! Don’t be: Dare to be remarkable. This will set you up & apart.🤓 d) of Rachel Well that’s a point – hard to argue! But feel the fear and then be pleasantly surprised by the fun! 🤸♂️🤸♀️ e) all of the above you best keep reading then…
Is now the time to face your fears, save a substantial amount of $$ and get on board with this train(ing) destined for your new empowered practice model, before it leaves the station?? Yep.
The MasterCourse I: Comprehensive Diagnostics has been called the single greatest change-maker to people’s clinical practice and likened to a total brain reboot. Not only with respect to the interpretation of patients’ results but to your complete understanding of integrative physiology. Liver function tests become markers of mitochondrial function, muscle mass and much more. Patterns in routine labs make patent the otherwise ‘invisible’: central and peripheral sleep-disordered breathing, the earliest signs of bone demineralisation etc And now it has a new sibling MasterCourse II: Thyroid & Adrenal Diagnostics. (more…)
Have you had a book that is so compelling & transporting you can’t put it down?
In the last year or so I’ve rewritten my own little book of sorts, on thyroid physiology and results interpretation and during that process I came across a paper that referred to ‘the thyroid biography of each individual’. I was so struck by this concept, how it brings into life my new appreciation of how a patient’s thyroid function speaks to the totality of their exposures – from their diet to their dopamine, from their exercise regime to their environmental pollutants, from their sex hormones to their stressors.
Being immersed in the research was deeply rewarding but the obsession proper began when I started applying everything new I’d learned to patient labs. Reading the ‘thyroid biography’ of every individual is the book I just can’t put down.
Not just because it enables us to see that our clinics are full of responsive thyroids more so than rogue and that the ultimate tailored ‘treatment’ is spelt out, right there, in the nuances of each patient’s TFT & other pathology patterns but also because these results themselves are a portal into the patient’s bigger story. During a recent interview on this topic, where I had the good fortune to be interviewed by someone who really understands health, we got deep into a discussion about how differing macrophage dominance (M1 or M2) in our adipose tissue disturbs thyroid function differently. The interviewer then asked – well how do you know if your patient is M1 or M2 dominant – is it just based on different measures like waist-circumference etc? and I said something to the effect of, ‘Well these can be indicators but actually more and more in someone with excess adiposity I look to their TFTs to tell me the answer to that!’
And that was actually a Tada! moment right there!
I realised the truth and gravity of what I’d just said – increasingly I’m looking to patients’ thyroid function to tell me the rest of their story – to reveal not only their totality of exposures but to shine a light into some darker corners that are otherwise hard to see or measure or know…like macrophage dominance patterns in fat tissue, or HPA setpoint recalibrations following trauma, or subinflammation that remains under the inflammatory marker radar.
We’re understandably critical of the over-stretch a name like ‘Thyroid Function Tests’ conjures up – how can 1 panel of 3 (ideally!) markers deliver on such a promise?! But I am here to tell you it can and in fact, it can deliver on far more than that once we learn to read TFTs as Thyroid First-Responder Tests, instead. And of course, we generally don’t see TFTs in isolation – so we can couple these with patient results for routine labs that add to our understanding, support our suppositions or challenge them based on their FBE, their renal or metabolic markers etc. This is integrative endocrinology within the broader framework of integrative medicine after all. This necessitates de-compartmentalisation while being able to disentangle one source of HPT directive or disruption from another. This is real-world results interpretation that optimises our insights and understanding & patient outcomes.
The back cover of my copy of this well-thumbed thyroid biography so far reads:
⇒Rather than rogue thyroids our clinics are full of responsive ones – responding to the totality of each individual’s exposures. ⇒If you don’t read patient TFTs through the lens of the HPT as a first responder – you’ll misinterpret what’s happening within their HPT. ⇒If you don’t read these results through this lens you will miss out on a much bigger understanding of their whole health story.
Of late, I’ve been woken at night to find I have been page-turning through a patient’s thyroid biography and a lightbulb moment of discovery is coming into land! I wish for everyone else the same…not the sleep disruption bit of course but those glorious Aha! moments. Oh and don’t get me started on HPA Assessments – that’s another page-turner!
MasterCourse II: Thyroid & Adrenal Diagnostics is NOW available. Clickhereto read more and here to purchase it and sign up for the Free Watch Party commencing 3rd August 2023 with is included with each purchase of the MasterCourse II.
I can barely bring myself to write the word given how overused it has been of late 🤐🙄😯😕🙃 But I gotta say something! If we have found ourselves currently in a place where every second (or indeed single!) patient has a ‘histamine issue’ then I am afraid that it is we, that have an issue. (more…)
The case of a slim 41YOF under very high stress due to marriage separation & the care of 2 young kids was presented in mentoring this month. Her a.m. Cortisol was 710 nmol/L – Rachel asked the group to identify 3 results in her routine labs that are consistent with & likely to be caused by this hypercortisolism…
Mentee & MasterCourse I & II Alumnus: In this case… – High-normal sodium – High neutrophil:lymphocyte ratio (on a few occasions) – Mildly elevated CRP
Rachel: The 3 markers you mention can indeed be consistent with and purely caused by high Cortisol: HN Na, HN Neutrophils and LN Lymphocytes producing an elevated Neutrophil Lymphocyte Ratio (NLR) and some low-level CRP elevation
I am just back from the NHAA Symposium – all informationed-up and raring to share!! LOL
I learned some great stuff about Black Pepper and that made me think about a case from mentoring last month🤓
One of the presentations was from Jason Hawrelak during which we ‘went back to school’ (as in old-school Materia Medica-based teaching – unsurprisingly I love this stuff!) and we (?re)-learned all about the herb Black Pepper and its active constituent piperine. It was brilliant and really challenged a LOT of uninformed thoughts I had about how to use this herbal medicine. It is now officially my herb of the month😆 But seriously, prior to this, I would have thought of this as being a great adjuvant and circ stim but primarily a gut irritant. Wrong. While it is contraindicated (CI) in ulcers or very active gastritis here are some GIT actions that might just surprise you as much as they did me(please remember, the below only applies to liquid (ethanol) herbal extracts at the ratio of 1:2):
Major carminative & antispasmodic for the GIT
It SLOWS transit time (TT) and hence its major indication, across different herbal medicine traditions, as anti-diarrhoeal
Coupled with very powerful stimulation of both digestive enzymes and absorption
Capable of increasing secretion of both saliva and HCl
I was most wowed by its documented positive effect on improved nutrient absorption via the saliva, HCl promotion, the slowed TT and increased villi length (true!!), increased bile flow, increased pancreatic (up to 90%) and intestinal lipase and amylase etc etc so massive increases in Ca uptake most notably along with phytonutrients (think curcumin as just one illustration of this) and, though much smaller, still improved uptake of Fe/Zn etc etc
In fact when Jason then created a profile of who he would think of Black Pepper for the one that really jumped out to me and related to this mentoring case was: the person who is eating good food but is surprisingly low in nutrient levels – esp if confirmed low pancreatic elastase. There is also evidence to support it as an effective strategy in both early and ongoing coeliac disease as well – which we still have as a differential in this patient
It is a UGT & SULT inhibitor & esp of p-glycoprotein efflux transporters however, so we need to use extreme caution in patients taking pharmaceuticals because there are loads of potential drug interactions,however, this is not an issue for this patient
Drop doses of a 1:2 liquid herbal extract of course – not pleasant to taste but not as bad as berberine (in my personal opinion!!)
Anyway – clearly I am a convert & keen to start trialling this in a variety of cases and want to spread the Black Pepper word right now!! Let me know your thoughts 🙂
Iron issues are an everyday encounter for those of us working in nutrition. As a result, we need to constantly attend to our skill set regarding iron assessment and refine our knowledge regarding best management.
This 5 episode compilation builds upon the foundations established in Iron package I and is unashamedly women-centric with 2 episodes on the complex area of iron balance in pregnancy, however, men and children do get a little look-in in other episodes!
You can purchase UU30 Iron Package II here. 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 audios and resources here.
What level of Serum Ferritin represents ’empty’? As in complete depletion of iron stores?
Is it any value below the minimum of the reference range? e.g. < 30 mcg/L Or does the bottom of the reference range allow for a buffer and ’empty’ is substantially lower than this? Could patients actually be ’empty’ but still have Serum Ferritin values within the normal range? Could the same Serum Ferritin value occur in one patient on ’empty’ but with adequate stores in another?
Practitioner: I haven’t yet done the MasterCourse II in Thyroid & Adrenal Diagnostics but I want to better understand the HPA of that patient we discussed with significant sleep disorders. Waking blood? Saliva? Urine? Which one?
Rachel: Well, you’ve heard me say I am sure, that depends on the specific question you are trying to answer by way of this test result. For example, see this slide from MasterCourse II
which considers the best tests to answer qualitative questions about HPA behaviour and function (of course sometimes we just have quantitative ones like maximum or minimum output but I know you want to look beyond this)
Lastly, if I am running a <9am blood cortisol (which remains a good marker in most cases) then I always would add in DHEAs in the same sample which adds a WHOLE other layer of understanding: our capacity to weather the stress storm, to buffer the HPA activation or not! And if we’re collecting blood <9am why not include ACTH and then you can determine if there is a contribution from (mis)management…just saying…🤓
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 desktop reference included!
You can purchase Cortisol– Have You Been Caught Out?here.
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.
Just as optimal integration of lab results into our patient work-ups makes ‘the invisible visible’ we thought we might make visible some of the everyday Q & A that we engage in with wonderful practitioners who are fast becoming Diagnostic Divas & Divos.
Praccie email arrives with subject header ‘Graves Help’ (or is that ‘Graves…HELP!’🤔)
Practitioner: I have a Grave’s patient who required Propylthiouracil (PTU) for a few months from late 2022 until Jan 2023 which obviously took her thyroid in the opposite direction (see labs). Following a miscarriage last year, she has conceived and is around 6/40 and her current TSH result has come in at 3.3mIU/L, her TPO Abs > 1000 and she also has low-level Tg Abs (TRAbs not measured this time) and this is what she just said to me:
“I just had my specialist session this morning – and she has put me on thyroxine (50mcg) as my thyroid is quite low. I also asked her about the prenatal vitamin and she said it was safe for me to be on iodine at this time, as the Graves isn’t present and baby needs it for the development of its own thyroid.”
Oh gawd! Preg? Iodine? Graves? Antibodies? Antenatal or postnatal aggravation?!
Is there an UU30 I can listen to to help me understand this?… sorry for the panicked email…
Just as optimal integration of lab results into our patient work-ups makes ‘the invisible visible’ we thought we might make visible some of the everyday Q & A that we engage in with wonderful practitioners who are fast becoming Diagnostic Divas & Divos.
Practitioner: I am currently doing the MasterCourse I & loving it! I just want to clarify time-frames for change with respect to high liver enzymes e.g. male client has made awesome diet changes & lost about 10kg over 12 weeks but I’m slightly disappointed some of his markers are still high. You’ve said that most liver enzymes have a half-life between 2-10 days so, I guess it just takes more time to repair any damage/reduce fatty filtration of liver and ALT reducing by 10 is great and with the weight off and healthy eating it will continue to decrease?
Rachel: This is a great question you ask and one worth clarifying:
So the half-life of the LFTs is most meaningful with respect to a transient effect or artefact – raised GGT with drinking EtoH or raised AST/ ALT post strenuous exercise – this aids us in recognising the ‘window’ to allow for normalisation following a time-specific event/action or interference
But when raised levels reflect chronic change/pathology/or a pathophysiological process, at the very least – of course, it is no longer about how long that enzyme remains in the b/stream but about the time it takes to turn this unhealthy state of the liver around. I know you know this because you basically answered your own question🤓💪 I would say you are making GREAT progress with this patient not only by the reduction in ALT (and corresponding increase in De Ritis ratio) but also by the impressive drop in triglycerides and GGT!
The primary objective of MasterCourse I is to realise the true value we can extract from the most commonly performed labs (ELFTs, FBE, WCC, Lipids & Glucose) which constitute the largest biochemical dataset we have on almost every patient. By learning how to comprehensively interpret these labs in an integrated medical framework, using the very latest science, we can extract the gold often buried in this goldmine. Accordingly, we prove ourselves to be the greatest asset to our patients, to other health professionals we are sharing care of patients with and we cut the cost of additional expensive testing, that is less well understood and validated.
MasterCourse I will help you access that gold and has been intentionally designed to match each lesson with real learning– with the time spent in theory and in application. Delivered across 24+ hrs of streaming video sessions with bonus pre-sessions, audios, resources and tools – this MasterCourse is likely to be a genuine game-changer for the way you practise and the potency of your patient prescriptions.
6 sessions of online learning video presentations (total 24+hours)
Rachel provides you with questions, mini-assessments & lots of opportunities for case study application, testing your comprehension & understanding as you go.
Included BONUS preparatory videos: Patient Pathology Manager + Accurate Pathology Interpretation Starts Here!
Included BONUS audios, notes, desktop resources and templates you can use in your clinic with your own patients.
You get to keep all content in your online account forever and replay as often as you like.
There’s a bit of a backstory – play along at home if you want – by ticking off the steps in this journey we have travelled together! 😂
14 years ago I was first asked to contribute to ACNEM’s thyroid training module 9 years ago I put together a little Masterclass on Diagnostics & 6 years ago co-created another one on Thyroid 3 years ago I dived deep into new literature to update my ideas & my teaching for ACNEM again & was reinspired by all I had discovered 2 year ago I promised a new MasterCourse, for all those eagerly awaiting the next instalment: Thyroid & Adrenals Diagnostics and 6mo ago I delivered!! [phew…exhale] Today I am launching our Update in Under 30 Thyroid Collective for those of you that want more ready resources at your fingertips!
This is a curated retrospective collection of under 30mins (ok…mostly!) recordings & accompanying resources that cover a wide breadth of aspects that affect all of us working in thyroid health… btw… that’s everyone 😉 With individual episodes covering everything from patient presentations to lab interpretations and iatrogenic to metabolic drivers of thyroid dis-ease, from T3 hibernation to high-normal T3 as a response to adiposity & so much more in between!… that we’ve put it all in the one spot for ease and convenience as your go-to thyroid library.
The updated content covered across this collective puts a firm stop to all the lazy labelling around thyroid: ‘You have a bad thyroid – that’s why you…[can’t lose weight, feel tired, have SIBO etc]’ And misdirected management, especially a tendency to overload the butterfly with ‘thyroid’ nutrients – which can do more harm than good
‘When will she ever stop challenging us all to stay up to date with the research revolutionising our understanding of thyroid health & disease?’ I hear you say. ‘Never,’ she replied!!🌈❤️
UU30 The Thyroid Collective
Welcome to UU30 The Thyroid Collective!! Over more than a decade, Rachel’s work in thyroid health has gained an enormous following & an impressive reputation for its excellence in quality practitioner education. You may have up-skilled alongside Rachel, undertaking her substantial MasterCourse II in Thyroid & Adrenal Diagnostics or completed smaller instalments on an as-needed basis. Either way this collection of 10 Update in Under 30 episodes provides you with your very own library of thyroid resources & research summaries on a juicy selection of thyroid presentations, investigations and treatment approaches. These are not new episodes but a curated collection of those previously released which have been reviewed to ensure they stand up in the context of all the new research and we can officially declare them – ‘good to go and full of gold!’
Just as optimal integration of lab results into our patient work-ups makes ‘the invisible visible’ we thought we might make visible some of the everyday Q & A that we engage in with wonderful practitioners who are fast becoming Diagnostic Divas & Divos.
Practitioner : I thoroughly enjoyed taking a deep dive into your Mastercourse II Thyroid & Adrenal Diagnostics and have also tuned into your Update in Under 30 episode on Thyroid Nodules – thank you so much for consolidating the research and helping us to become better practitioners. I just have one question, if you wouldn’t mind. (more…)
Ever met a set of thyroid results you didn’t like? Because you couldn’t work them out? Because they defied your expectations, & therefore your understanding, of how they should look in this patient given their weight, nutrition, meds, diagnoses? Yeah – me too.
In simple terms this is because we are taught ‘perfect patterns’ in thyroid interpretation: * Iodine deficiency produces HN (high-normal) TSH and a shift towards T3 *Inflammation produces low TSH and T3 with a shift towards rT3 *Viral attack of the thyroid itself causes HN levels of both T4 & T3 due to spillage of preformed hormones, & secondary suppression of TSH
So can I ask: What about the patient who has a virus that is causing significant inflammation, attacking the gland directly but has a pre-existing Iodine deficiency? Seriously. What would you expect to see as the HPT responds to all of these concurrent disruptors?(more…)
Did you know that your thyroid expresses more ACE 2 receptors than your lungs? So while there is nothing new about the potential for a virus (or indeed even a vaccine against a virus) to impact thyroid form and function, the particular predilection this recent virus has demonstrated for this gland, and in turn, the wide spectrum of thyroid dysfunction and disease that has now been documented in response to this, is unparalleled and warrants our attention.
There’s a push to publish right now such that information and knowledge regarding anything and everything to do with the Covid 19 pandemic can be quickly shared.
While we need to balance this with the deeper appreciation that research that reflects the entirety of the story will take a lot longer to come to light – the data already in, speaking to this strong pathophysiological relationship between Covid 19 & thyroid health, is hard to look away from – especially when patients are already presenting with this chapter in their ‘thyroid health biography’.
That might sound like a patient who tells you their ‘thyroid was affected’ by the virus when they were really sick, but apparently is ‘ok’ now (but don’t feel it!), or someone post vaccination who has had some ‘funny results’. Or it might look like reactivation of a previously under control or quiescent Grave’s or Hashimoto’s disease, or, in fact, a new AITD diagnosis all together post 2020. There’s a lot of candidates & contenders for the ‘next NEXT wave’ in this pandemic – but even higher numbers of even more diverse thyroid issues is a strong one.
Once you learn about the about the interplay between thyroid anatomy and physiology, viruses generally (yes viruses are *BIG* news in many patient’s progression to thyroid pathology) and this virus, specifically, it becomes clear that we need to tune-in even more than before, to our patients’ potential for thyroid issues, as a contributor to why they’re seeking help for health concerns.
While there’s nothing new about the potential for viral driven thyroid disturbance, both acutely during infection and chronically following ‘recovery’, what is new and making news in the aftermath of the Covid 19 pandemic is the particular predilection this virus has shown for this gland. Thanks to its naturally high expression of ACE2 receptors (far more than seen in the lungs for example) the potential impacts, covering a wide spectrum of thyroid dysfunction & disease, have been observed and documented. This ranges from unprecedented rates of Euthyroid Sick Syndrome & Thyrotoxicosis during the acute phase to either activation (in an individual with a personal hx) or provocation (no previous hx or diagnosis) of autoimmune thyroid conditions as a result of either the infection or vaccination. Although there will be much more research to come that will help us clarify and confirm some of this detail, the data already in existence is undeniable and warrants our attention.
To purchase Thyroid Health in a Time of Covid, click here.
If I wrote down these 2 elements on a MindMap: Thyroid dysfunction and Adiposity, how would you connect them? Would you reflexively draw an arrow from the former to the latter to flag that the thyroid underpins the weight management issues? My arrow would be the other way around.
According to every scrap of data, the likelihood that someone’s subclinical or even frank hypothyroidism is the source of the excess weight is quite low, while the probability that their excess adiposity has had profound effects on both the anatomy of the gland and the physiology of the HPT is much higher.
And the change in the direction of this relationship – adiposity as the cause not the consequence – changes everything, from what we tell our patients, to what effective management, and success, in terms of follow-up TFT patterns, actually looks like. It’s far from semantics. Because while we may not encounter any cassava excesses in our practice, an established goitrogen with a long history, we do see unhealthy adiposity often and it is the ‘newest’ goitrogen on the block, so to speak.
The definition of a goitrogen is something that interferes with thyroid hormonogenesis and thyroid function in any way.
Abdominal adiposity, that is excessive for that individual, (I don’t believe this can be simply determined by BMI alone but requires us to apply a more sophisticated lens & metric) interferes in many many ways.
Aligned with this recognition is the seismic shift in understanding that we’ve undergone regarding ‘who or what’ is the boss of the thyroid. Hypothalamus & pituitary, I hear you say? Nope. These guys are just the middle managers – and the real bosses are a board of directors that includes adipose tissue. Stop and think about this – makes sense, right? The HPT is attributed with being the major endocrine axis that determines how much ‘energy’ we have to spend – so of course it’s taking direct messaging and direction from the adipocytes! Add to this, that excess energy consumption drives up TSH, a trophic agent for the gland – a stimulator of proliferation without differentiation and with no guarantee of an adequate supply of the greater requirements for micronutrients required to ‘grow a bigger gland’ without architectural or functional disturbance. These are just the 1st two stages of goitrogenic effect resulting from over-nutrition, that I refer to as The Over-Feed and The Under-Resourced Thyroid…
But what can follow are 2 more stages: ‘The Disturbed’ and finally, ‘The Diseased’ thyroid – which include pathophysiological processes such as adipocyte infiltration of the actual gland (akin to the liver infiltration in NAFLD) seronegative thyroiditis, as well as epigenetic changes impairing DNA correction etc etc all a consequence of weight gain…not the cause.
Thyroid dysfunction –> weight gain or Weight gain –> thyroid dysfunction…Time to rethink this relationship?
According to every scrap of research, the likelihood that someone’s subclinical or even frank hypothyroidism is the source of their excess weight is quite low, while the probability that their excess weight has had profound effects on both the anatomy of the gland and the physiology of the HPT is much higher. So rather than a reflexive assumption that someone who presents with weight gain or ongoing unhealthy weight should have their thyroid checked to see if that is the cause – the TFTs absolutely should be performed but instead to understand one of the key consequences of this excess adiposity. In this recording we highlight the 4 stages of impact, moving from: the ‘Overfed’ to the ‘Under-Resourced’, the ‘Disturbed’ and finally the ‘Diseased Thyroid’. The reversal of this relationship – adiposity as the cause not the consequence of thyroid dysfunction – changes everything, from what we tell our patients, to what effective management, and success, in terms of follow-up TFT patterns, actually looks like. We need to be alert and responsive to the most common and contemporary thyroid disruptor in our patients: fat is a goitrogen.
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Over the years I’ve observed an increase in the incidence of practitioner paralysis. This occurs typically & understandably in the face of fearmongering. A good example is in the area of so-called ‘methylation medicine’ where we’ve been lead to believe that writing ‘the right’ nutritional prescription for patients requires a) their full gene profile, b) a knowledge of biochemistry that no one outside of a legit biochemist should have (!) and c) a bordering on perverse interest in in vitro research looking at how these pathways interact with different nutrients. And if we, as mere mortals (and naturopaths, nutritionists, herbalists or integrative pharmacists or GPs at that), are lacking in any of these WE WILL STUFF THIS UP GLOBALLY and put them on THE WRONG THING THAT WILL BE CATASROPH*C! Note: fearmongering always uses caps 😉
This stems from the misguided belief that ‘biochemistry alone maketh the man’ and ‘SNPs should write the ‘script!’
And the source of these falsisms are, what I refer to as, ‘Wallys with wall charts’. As impressed as we might be by individuals with brains for biochemistry or genetics, we should not let this overshadow the knowledge that health and disease are much more than 1 or 2 facets of your gene profile and how this may predict the pace of a few out of a million chemical reactions. Right? I mean I doubt any of us working in integrative health would intend to be so reductionistic and yet here we are with practitioners forgoing clinical (and RCT) evidence over that derived from in vitro with respect to supplements like SAMe and N-acetyl cystine, or worse still, taking as gospel, ideas that have come from pure hypotheses, based on 1 SNP out of an individual’s whole gene profile! This has infiltrated many areas of naturopathic and integrative medicine and certainly gotten the best of me at times too. But I am pushing back. Enough is enough. We humans are not our gene profile and holistic practitioners like us – know the manifold influences upon our health and wellbeing better than just about anyone else. And if you feel a bit lambasted by my little tirade – know that I have to give myself this very same talking- to every now and then – when I fall under the spell of Wallys and their wall charts!
In part one, we discovered the pro-drug nature of SAMe, revealing why evidence obtained from in vitro evidence can not be used to support either favourable claims or warnings. In the 2nd instalment we examined up close the misunderstandings about SAMe use in conjunction with antidepressants and clarified the real causes for concern in mental health clients. In this 3rd and final part we dissect claims and ideas about the success or safety of SAMe as a supplement with respect to methylation genetics and stages of pregnancy. All up this is indeed one BIG SAMe rethink that we reshape and re-inspire you about its prescription.
You know the saying, ‘If I had a dollar…’, well there’s so many ways I could finish that sentence, especially in relation to the most common questions I’m asked by praccies on a weeklybasis and ‘Can my patient on antidepressant ‘X’ take SAMe?’, would be in the top 10! While many of you might be mouths agape reading this, I bet the cause of that comical expression is not the same for everyone. Yes, like you, they’ve read the mandatory label warning: ‘individuals who are using prescription antidepressants or suffer from bipolar depression should not use this product unless under the supervision of a healthcare practitioner’ – but let me ask you, how do you interpret that? Turns out there are several interpretations and the most common is the most incorrect.
Yes you heard me. It’s time to remove that stain on SAMe’s reputation and take this nutraceutical, lauded amongst researchers and clinicians internationally for its excellent safety profile exactly in that scenario, in combination with antidepressants and other psych meds, out of the naughty corner – where it was mistakenly put in the first place! [No one puts SAMe in the corner 😂]
But I’m in no doubt many of you will take some convincing and while I am armed and dangerous ready with the answers, some will want to hear it from more than just me (and I 🙌 you ) Easy then – just read the research – take these for starters this one, that one, oh and this one – but there’s plenty more! Once you have, you’ll likely be scratching your head and asking yourself as I did, ‘How did we come to be so misinformed and come to a place where SAMe is so misunderstood?!’
I can answer that too 😉 And then for good measure I hope your brain pings you straight back to that warning on the SAMe label to follow up with – and what is the actual correct meaning and take-home of that label warning then?!🤔
In the previous Update in Under 30 episode we established where are lot of the misunderstanding originates with SAMe, in particular from lab based research that has little-no relevance on the effects of taking SAMe as a supplement, given what we understand now about its bioavailability and pharmacokinetics. While this helped us contextualise such ideas and get some serious perspective on the camp that exudes mild-moderate SAMe hysteria (arms flailing like the robot from Lost in Space, ‘Danger Will Robinson!”), supplemental SAMe is not right nor safe for all. And that is indeed something we need to sharpen our tools and our skills in recognising, monitoring and managing. Just a little somethin’ for your Christmas stocking & all those lazy hours on the beach you’re banking on over the break 😉
You’re welcome🤶
The Big SAMe Rethink Part 2
In part 1 we established where a lot of the misunderstanding originates with SAMe, in particular from lab-based research that has little-no relevance regarding the effects of taking SAMe as a supplement, given what we now understand about its behaviour in the body. In this instalment we go on to examine the evidence that led to the mistaken belief that SAMe was not safe in combination with pharmaceutical antidepressants and explore what the real safety concerns are with respect to its use in mental health patients. This audio comes with a great resource that helps you to both prescribe and supervise the taking of SAMe in your depressed patients, minimising risk and optimising outcomes.
Recently a very experienced practitioner who uses SAMe frequently and successfully in her patients and also delivers education said to me, “I don’t know what I am doing wrong – practitioners still come back to me with cases where they’re throwing 8 different products at a patient to ‘lower histamine, improve mental health and support methylation’ instead of using just one – SAMe!” I laughed and said, whatever you’re doing WRONG in trying to teach people about SAMe I am doing WRONGER and for LONGER!! I’ve been trying to encourage and inspire confidence in prescribing SAMe for 2 decades now and still some of my most loyal listeners, are like, ‘I still haven’t prescribed it, I am too scared.’ 🤯
But I think the fear factor around SAMe occurs for several reasons: Misinformation – there is a LOT of misinformation about HOW SAMe works and WHAT kind of power it wields therapeutically Misunderstanding – this comes from a couple of key misunderstandings about drug interactions and SAMe pharmacokinetics & pharmacodynamics Mystery – even for me, SAMe has had an air of mystery about it, nagging, seemingly unanswerable questions that can undermine our confidence and certainty about its appropriate use and safety
I get it. And given the studies employing SAMe as a therapeutic agent date all the way back to the 1970s and continue to today – in psychiatry, hepatobiliary disease, cancer etc – there is a LOT of information that has been gathered overall and a LOT of old ideas/theories/speculation replaced by understanding thanks to better methods and models of scientific enquiry. So I decided it was time for me to confront this ‘man/molecule/medicine of mystery’ head on, conduct a completely updated literature review of SAMe and along the way – challenge many of my long held beliefs.
I thought about calling this latest episode, ’30 Things You Don’t Know About SAMe’ – and calling it like a horse race because in all honesty I learned THAT MUCH!
But I settled for: The Big SAMe Rethink – inspired by one of many pivotal papers which helped to revolutionise my understanding & approach to this nutraceutical which you can read yourself here. Misinformation, misunderstandings and mystery be gone (ok well most of it anyway!) – by filling in the gaps in our information that previously fuelled these – we can move forward with much greater confidence and clarity and we now know where the real safety concerns exist.
The Big SAMe Rethink Part1 Do you feel like you need to pick a SAMe side? Researchers and clinicians, alike, seem divided in their opinion about its therapeutic capacity and certainly its safety. One side are the ‘naysayers’: ‘SAMe can’t possibly be effective for both depression and in hepatobiliary conditions and and and’. Keeping them company are the ‘doomsayers’, preaching danger and destruction should we prescribe this ‘universal methyl donor’. But the other camp can seem just as fanatical and far-fetched at times: ‘it’s good for just about everything with zero safety concerns’. The divide and differences come down to origins of evidence and, once again, the truth lay somewhere in the middle. This new information on SAMe’s behaviour as a supplement will prompt you to rethink so much of what you thought you knew, whatever side you’re on!
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You know the saying, ‘If I had a dollar…’, well there’s so many ways I could finish that sentence, especially in relation to the most common questions I’m asked by praccies on a weekly basis and ‘Can my patient on antidepressant ‘X’ take SAMe?’, would be in the top 10! While many of you might be mouths agape reading this, I bet the cause of that comical expression is not the same for everyone. Yes, like you, they’ve read the mandatory label warning: ‘individuals who are using prescription antidepressants or suffer from bipolar depression should not use this product unless under the supervision of a healthcare practitioner’ – but let me ask you, how do you interpret that? Turns out there are several interpretations and the most common is the most incorrect.
