Ever feel like the universe has been preparing you just for this moment? Me neither really…but in this one weird way – yes!
So hear me out.
Thyroid disease as a result of a viral infection was first described in 1902 by Dr Fritz De Quervain and of course he and his ego called it De Quervain’s subacute thyroiditis. For some historical context, this predates the recognised role of iodine deficiency in thyroid disease! Skip ahead almost a century to deep in the 1990s and mini-me was sitting in a uni lecture room [front row & wearing fluro of course🤣] and over hundreds of hours (no scrap that zillions*^# of hours) of lecture content I was exposed to, the description of De Quervain’s Subacute Thyroiditis stood out and stayed stuck to me. I’ve brought it out for a twirl from time to time in the interim with some of my patients & in particular in correspondence with their docs.Skip ahead to the 2020s when we had this thing called. ‘a global pandemic’, and now everyone wants to talk viruses and their broader health implications & as a result, good ol’ Fritz, me and our buddy, De Quervain’s subacute thyroiditis, are all having a moment.
But just to recap – this is (clearly) not new.
What is new is the way this ‘virus of the moment’ has brought this Thyroid V Virus battle to the forefront. We are living an important chapter in history where all the textbook entries on De Quervain’s Subacute Thyroiditis are madly being rewritten to reflect the veracity of this viral attack on the gland and the wide-scale & varied damage that ensues over the months and years that follow. And so many of our patients are the walking embodiment of it – whether that be in the form of low or high thyroid hormones, nefarious changes to gland anatomy only evidenced on US. So what do we need to know? in short, that pathogens as goitrogens have never been more of an issue than right now for ourselves and our patients. And that compared with just our usual desire for comprehensive investigation of the HPT, taking a complete look ‘under the hood’, not only by way of a full TFT and Ab titres but also, wherever there is an additional suspicion – by way of a thyroid US – has become non-negotiable. But regardless of what you find there, once you look, do you know what to do next?
Biopsies and autopsies of diseased thyroid glands alike reveal the prevalence of many common viruses within, setting the scene perfectly for the Thyroid V Virus battle. So, what happens when a virus takes a specific liking to this gland? While there are several different possibilities, one brought to the forefront in recent years is viral thyroiditis wherein stage 1 is ‘spill’, stage 2 constitutes a gland that is now ’empty’ and while stage 3 is reported to be ‘recovery’, this is increasingly scarce – replaced with chronic or recurrent thyroiditis, relapses of previously remitted GD and a doubling of new AITD diagnoses – not to mention the wide variety of unfavourable anatomical changes being found on ultrasound. Comes with a great desktop reference with prescription examples.
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Rachel: And sometimes emails from practitioners provide me with both the question and their own answer to their question even!
Cameron Barker’s (Ex-student long-term learner & mentee)email arrives titled:Unexpected Source of Iodine in Placenta Caps?!
A 32 yo female with a 12-week-old daughter came to me as she was not feeling well, in particular, she reports fatigue, racing heartbeat, anxiety and loss of appetite. Previously, 2 years ago, I had helped her with her Hashimoto’s. I did not hear from her for a year or so and she fell pregnant and was recommended to take a well-known iodine-containing pregnancy multi.
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…
Have you been told somewhere by someone that the ‘perfect’ TSH is 1.5 mIU/L? This is a wonderful, terrible & wonderfully terrible example of ‘magical numbers medicine’. As a push-back against the published reference ranges we’re given, that are so wide you could drive a truck through them, there has been an over-correction by some, leading to the myth of ‘magic numbers’. We can narrow the reference range substantially for many parameters with good rationale, make no mistake about that but once we start setting ‘aspirational goals’ that are explicitly rigid…well we’ve done 2 things 1) forgotten about the patient to whom this result belongs and 2) disregarded viewing each result as part of a ‘pattern’, that we must piece together and make sense of.
Back to TSH then… if my obese patient had a value of 1.5 mIU/L this in fact would be woefully inadequate – so too a child at any weight.
And we expect a higher value as well in our elderly clients too and this level there may be, in fact, increased mortality.
But the same result would be excessively & worringly high in my patient who’s undergone thyroidectomy.
Realising the full value of any test result in terms of what it reveals about the person sitting in front of you, requires these more thinking and more thoughtfulness. Unfortunately, a list of ‘magic numbers’ will often lead you astray. And building your scientific knowledge about labs will not only help you avoid the pitfalls of pathology but will strengthen your pathophysiology prowess in surprising ways, saving your patients a packet in terms of additional extraneous testing and help you truly personalise your prescriptions…because the ‘invisible (biochemical individuality, oxidative stress, genetic probabilities, subclinical states, imbalanced or burdened processes etc) just became visible’. I started requesting lab results early in my career and years later was lucky enough to be taken under the wing of Dr. Tini Gruner. I found some of our shared notes, from 10 years ago, scribbled all over patient results recently and I was struck by just how lucky I was to have her encouragement to really pursue my interest and how she was a guiding force about learning to recognise pathology patterns over single parameters. A decade on I can concede, much of my clinical and educative success has come off the back of this foundational skill-set and I know, this is true for so many I’ve taught too.
“The guidance I’ve received over the years from Rachel in relation to pathology interpretation has been one of the most valuable (and fascinating) investments I’ve made as a clinician. Her teachings have filled gaps in my knowledge base I never knew needed filling and have significantly enhanced my understanding of the inner workings of the body! Rachel has an incredible ability to make the numbers that patient’s so often present us with, both understandable and clinically meaningful. The knowledge I’ve gained by investing in this skillset has paid off in dividends and I’m certain will continue to do so into the future.”
Stacey Curcio – Cultivating Wellness
I hope you’ll join me for the most exciting up-skilling opportunity in learning labs yet. Oh…and all this talk about thyroid testing..this next MasterCourse series is focused on revolutionising your understanding of thyroid, adrenal, HPT & HPA markers based on the very latest research & findings & marry these together with everything you learned in MasterCourse I (ELFTs, FBE, Lipids & Glucose) to understand the ‘whole story’.
…an absolute treasure trove of free integrative health information about your patient!
DEEP DIVE INTO REAL CASE STUDIES TO DEMONSTRATE EACH PATHOLOGY PATTERN IN ACTION. ]\
There are limited places. To sign up for Rachel’s LIVE Series – MasterCourse II: Thyroid & Adrenal Diagnostics and for more information click here.
I’ve spent the best part of about 4 months recording my *NEW* Advanced Thyroid Assessment training. I told my team this would be easy and quick, given it was to be based on a great little 2-part, 2hr updated presentation I delivered just last year for ACNEM!! Sixteen weeks (like seriously…most of it) numerous rewrites and retakes later, our final product is 4 parts that goes for over 12hrs in total & has a bonus Adrenal recording! And yeah my team are impressed but unimpressed too if you know what I mean?!🙄🤪
Every time another, ‘Oh wow!’, or ‘No way!’, escaped my lips, it was a source of personal celebration, as another deeper layer of learning revealed itself.
But to the wonderful, somewhat weary and definitely wary Sally, who does all my powerpoints, it was met with, ‘Oh boy!’, because it meant many multiple new slides to build full of visual metaphors, animation acrobatics, if not an entire new Part!*#@^
Her sage advice along the infinite research road I’ve been travelling was : ‘Stop. You’re going to have to stop.’
So I didbut now I am this meme. Everything I see currently through the lens of thyroid health, I talk in tongues TFTs and my brain is one giant neural network of integrative endocrinological circuits! I have fallen in love with this topic, this neuroendocrine axis and its ‘first responder’ role all over again! Hence our little thyroid character below – all ‘antennaed’ up – is one of the many tools we’ve developed for this training, to teach us that ‘bad thyroids’ per se are extremely rare – but bad scenarios are common (too much or too little of any macronutrient, key micronutrients, a change in the internal or external environment etc etc) and this little fellow and his board of directors (no – not the hypothalamus or pituitary!) – well it’s their job to ‘read the room’, right?!
In the absence of this key understanding we risk: A lot of lazy labelling in thyroid health – ‘You have a bad thyroid – that’s why you…[can’t lose weight, feel tired, have SIBO etc]’ Misdirected treatment & especially a tendency to overload the butterfly with ‘thyroid’ nutrients – which can do more harm than good
I’ve said many times, ‘perfect number pathology is a myth’ but it runs rife in practitioners’ beliefs about TFT results with complete disregard of the person those labs belong too! Did you know, for example, that your TFTs should all be higher if your BMI is? That your T4:T3 ratio should never be 3:1 if you are on replacement, have hot nodules, are pregnant or are acutely unwell etc etc etc? How about how low your Selenium or Iron levels need to be before this factor will influence the actual levels of thyroid hormones measurable – & what the impact of these deficiencies are well before then that is far more sinister and serious? Yep…you see here I am, pouring just some of the tiny take-homes of Advanced Thyroid Assessment ALL over you!
Watch this space my new Thyroid training is just around the corner!
An increasing number of our patients have thyroid concerns but unbeknown to many of us the most likely explanation of all is thyroid nodules, whose incidence is on the rise globally. The development of nodules has always been primarily viewed as a nutritional disease. Traditionally attributed to chronic iodine deficiency but recently novel nutritional causes have emerged. Benign nodules come in 2 flavours: hot and cold and while patients can present with a mixture, it is the presence or absence of a hot nodule that radically changes what complementary medicines you can and can’t use and what an effective treatment plan looks like. The pointers, as is often the case, are there for us in the patient’s presentation and pathology, so knowing the difference is no longer a guessing game. This UU30 comes with a great visual clinical resource and includes key papers on the nutritional management of nodules.
Over years of delivering independent education in integrative health I have spoken to some diverse audiences. This has included health professionals from very different backgrounds: from hospital-based psychiatrists & mental health nurses, to whom I presented on site in hospitals both in Australia & NZ, to a national sparkle-arkle speaking tour, in front of large groups of aesthetic practitioners. They’re the doctors & nurses for whom botox and fillers are their tools of trade, and yes I got to see actual demonstrations of their work performed live!!!😶 More recently, I’ve had several opportunities to deliver evidence-based independent education on nutrition to pharmacists en masse – which I always enjoy because they ask some of the best questions!
Underpinning each decision to accept an invitation from a 3rd party, be that a company an organisation or an institution, to speak, is: 1.The realisation of an opportunity for nutritional medicine to reach more people, a wider audience, & ultimately expand the circle of influence amongst health professionals, who interact with & advise the public at all different levels 2. An agreement and/or contract that ensures my independence, the correct use of my materials, image, brand and IP & removes any expectation to promote their products/services etc
And my ‘door’ is open to any invitation which meets these 2 criteria. So you might have seen my name, previously associated with some brands or organisations, in the last few years disappear off their speaker announcements, or no longer connected, and in turn you might see my name pop up in new places! Like….Metagenics Congress on Autoimmune Disease!! After many invitations from this company, that I wasn’t able to previously accept, I am pleased to be speaking at this face to face event on the Gold Coast in August. What a novelty, hey? Face to face?! My talk is about the 4 Mistakes not to Make in Hashimoto’s and as always, I’ve completed a full mini-literature review in order to speak to the very latest on diagnostics and nutritional management, in this condition. Yes, to quote a Costanza, “We’re back baby, we’re back!” And to see my full current smorgasbord of speaking commitments & all the people I am ‘spreading the (nutritional) word’ to – just click here.
This previous training will take your understanding of the interplay between food, nutrition, environment and the thyroid several steps further. With more supportive research and a greater focus on the mechanisms behind the relationships between these macro- & micro nutrient & environmental factors, this presentation is for the true thyroid die-hard.
I love a little temporal lobe tap. Especially the kind patients provide. This week mine came from a mentee’s patient who, while presenting with concerns about possible perimenopause, was found to have radical shifts in her thyroid hormones, largely thanks to a dramatic increase in TPO Abs (>1000). The patient’s other presenting complaint was ongoing gastritis (confirmed via scope) and reflux…and that’s when I started to deep-dive into the archaeological archives of my brain…with the…’didn’t I have somewhere in here, in some dark dusty deep recess…a connection between the two?!’
Aha! With the help of a torch [read Google Scholar] the temporal tap bore fruit. 1 in 4 patients with AITD (Hashimoto’s or Graves, you choose!) test positive to Parietal Cell Antibodies
I’ve created (clearly, not-so)SmartArt graphics on powerpoint slides on this exact topic, waxed lyrical about it in my thyroid training packages…but in fact needed a temporal tap to be reminded! And in turn thought, well gosh if this has slipped from my mind, it might just have slipped from yours too! ‘Thyrogastric autoimmunity’ as it’s called, refers to a patient group that exhibit antibodies to both and remember, the antibodies precede the condition in both disorders, so you can have a patient with established AITD, who has zero gastric symptoms but tests positive for the antibody…an important heads-up, as it speaks to significant risk of the subsequent development of gastritis in the following years. This excellent prospective study of AITD patients by Tozzoli and colleagues mapped exactly that! Jump forward just another day or so and…
I’m preparing for our final FiNAl FINAL Q & A on Haematology for our MasterCourse in Comprehensive Diagnostics and I’m wrestling with all the conflicting ‘facts’ about the anaemia that may present alongside hypothyroidism – it has been documented and described as being macrocytic, normocytic and even microcytic… how can it possibly be so diverse I wonder and then 💡 I’m guessing the presence or absence of these parietal cell Abs likely has something to do with it!!
Anyway, it’s getting towards the end of a VeRy loooooooooooooooooooooooooooooong year…thought we could all do with a temporal tap 😉
Ever suspect you’re being gaslighted by your patients’ results? Especially when their CRP result says, ‘nothing to see here’! But every other piece of information and every one of your senses tell you they’re inflamed and their immune system is up to something!!Me too. You probably then look at their other results, their ESR or their white cell count searching out something that supports your hunch, but they too can look disappointingly unremarkable. That’s the moment when you wish life was like a televised sports match and you could check the video evidence rather than believe the mere mortal (and clearly blind!!) man in white on the pitch. Well guess, what…you can.
Albumin
÷
Globulin
As long as you know how to divide one figure by another using a calculator. I’ve found it requires the same digital dexterity as pushing the ‘on’ button’ on my blender…so if you can make a smoothie, you’re sorted! So while almost every lab routinely reports these two as separate parameters that are also routinely in range…I haven’t seen many that actually do the calculation for you and give you the Albumin:Globulin (AGR) on a platter. Yet this one step maths transforms the mundane into magic and can reveal almost all to you regarding your patient’s level of immune activation, inflammation and oxidative stress, from the largest number and variety of drivers. That’s why I call it, 📣The Master Inflammatory Marker 👑
When factoring in your patients pathology results is at its best – it makes the invisible suddenly visible to us. We could have sat and eyeballed that patient all month and never suspected that their Hcy was too high, or they had antiphospholipid antibodies or, or etc.
But the albumin to globulin ratio goes one step further & trumps the other inflammatory markers we’re so familiar with, because it even sees what they can’t!
And a low AGR (≤1.2) signals just that to you. So when the patient with joint pains, or just a little bit of belly fat or an emerging yet unnamed autoimmune condition presents exasperated saying, ‘but apparently I’m not even inflamed!’…you can let them know you do see it, and it’s just that others weren’t looking in the right place, then get busy rolling your sleeves up to move those markers! That’s right, a low AGR is a clear call to action for practitioners engaged in risk minimisation, prevention and for working towards best outcomes in established disease and monitoring a patient’s AGR is a series of clear sign-posts about whether you’re leading them in the right direction or not. There’s a lot more to say on this this third umpire & ripper of a ratio – about kids, the contraceptive pill, confounders, a role in cognitive impairment prevention and what optimal might look like but hey…the cricket’s back on…gotta go 😂
Patients’ labs lie, not often, but sometimes and the inflammatory markers performed routinely like CRP and ESR have been known to tell a few. Like when everything about a case screams inflammation but both of those say there’s none there. Why do they miss it?…well basically it’s not their lot. CRP and ESR have specific signals they only respond to and therefore reflect only certain immune reactions and at specific stages of that response. But there’s a nifty little calculation you can perform with all of your patients labs and suddenly see the immune activation, inflammation and oxidative stress that was lurking beneath. It’s called the albumin to globulin ratio and it’s going to change your understanding of what’s going on in your clients and your ability to monitor the efficacy of your management.
Have you still got some thyroid patients that don’t fit any sort of traditional thyroid disease model and are difficult to get results with? Oh yes me too… and watch out…I’ve been spending the last few weeks with my nose firmly embedded in hundreds of articles digging around for more answers. As I am presenting on thyroid conditions for ACNEM in Adelaide March 18-19th, I couldn’t resist going back to the literature to see if by delving a little deeper again I could come up with some more answers to these weird, wacky and hard to treat thyroid presentations that we’re increasingly seeing and guess what…I think I’ve found a few gems.(more…)
Back a few weeks ago I had the pleasure of presenting at the Integria Symposium and the even greater pleasure of listening to some of the fabulous speakers …you see I’ve heard my stuff before! 😉The ‘Mosaic of Autoimmunity’ was delivered by the very funny and knowledgeable Professor Yehuda Shoenfeld, who reiterated the sequence of events now well recognised to precede and precipitate autoimmunity: genetic susceptibility + endocrine context + environmental trigger –>autoimmunity.
Clinicians know that overwhelmingly women dominate when it comes to autoimmune disease epidemiology and most understand that this is a consequence of oestrogen’s immunostimulatory effects. Professor Shoenfeld, described the female, or E2 dominant, immune system as being ‘super charged’ and that increased rates of autoimmune diseases were a reflection of this. Sometimes practitioners do initially great work with a/immune clients – clearing up the diet & gut, ensuring vitamin D adequacy etc and then get ‘stuck’ or plateau with antibody levels that ‘won’t budge’. Going back and checking the hormonal contribution in the case is often indicated. If the patient has an unhealthy E2 dominance and /or impaired detoxification and clearance of this hormone then working on this aspect often kickstarts the next stage of improvement.
A new thing to me (I know I’m a bit slow sometimes 🙁 ) was his mention of the potential link also with high prolactin (PRL). The literature on this is extensive and hyperprolactinemia (HPRL), even just mild elevations, have been correlated with a very long list of both systemic and organ specific diseases including: (more…)
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