Let’s play a word association game of minerals & their major roles
I say, ‘Potassium’. Maybe you say, ‘Sodium Potassium Pump’ I say, ‘Magnesium’. You say, ‘Muscles?’ I say, ‘Calcium’. You say, “Bones’….
But I say, Second Messenger. And arguably the most pervasive & potent one, at that. Remind you about second messengers? Well, sure. They are the ones who get sh*t done. Not like a boss (i.e. hormone or neurotransmitter) who shout directives from above but never step foot inside the dirty guts of the engine room itself. It’s the second messengers who run these messages from the outside of the cell to the inside and the engine room, to ensure that the directive is actually actioned! Amazing huh! And free calcium in the blood is, as I said, really a superhero even among the second messengers – with its regular responsibilities including: Insulin, TSH, Adrenaline, Oxytocin, Serotonin receptor activation etc etc
Does, it have a dark side? Well, sure. Don’t most superheroes?
If the available Calcium in blood and the extracellular environment is too high then basically bad sh*t gets done. Including vasoconstriction, clotting, deposition of calcium in the wrong place like arteries and joints and etc etc. That’s why the amount of Calcium in our blood is the MOST tightly regulated of all electrolytes and, in turn, has the NARROWEST of reference ranges. But will a Serum Calcium level always tell you when there is a problem with Calcium regulation? No. You’d need to have measured the major regulator itself, Parathyroid Hormone (PTH). Wait, am I seriously trying to tell you, that Serum Calcium alone can look completely normal in spite of really damaging Calcium dysregulation underway – leading to accelerated BMD loss, increased cardiovascular and renal risks etc.? I most certainly am.
So do you know which of your patients’ really need PTH assessment and why 1 dominant group amongst those, is any woman leading up to and following menopause?
No? Well you better pull up a pew and have a listen and a watch then! Yes this latest Update in Under 30 episode even comes with a little video tutorial!🤓🤯
Parathyroid hormone is a career criminal. In addition to buoying dropping blood calcium levels via legitimate means, it illegitimately achieves this by stealing it from our bones. But you wouldn’t know it – because like all career criminals this occurs completely under the radar. Elevated PTH, however, constitutes the most modifiable risk factor for bone mineral density loss & fracture risk and offers the biggest BMD gains secondary to its normalisation. In addition to this, even within range but ‘high-normal’ PTH correlates with a range of other cardiovascular and urinary presentations & if combined with elevated serum calcium can become a multi-systemic presentation (GIT, Mental health etc) frequently mistaken for other aetiologies. So how can we be alert to this ‘bone thief’? Which of our patients will benefit the most from PTH measurement and monitoring? This recording, resource & video tutorial on how to use a Ca PTH Nomogram answers all!
You can purchase Unmasking Hyperparathyroidism – Menopause & Morehere. 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.
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.
You can purchase ThyVIRoidhere. 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.
Just last week the sickest patient I’ve encountered this year (& for perhaps some time) asked me, if I ever see really sick people.
This 60 something-year-old farmer has a great sense of humour, so I immediately thought he was joking but as soon as I looked up from my notes, I realised my error. It kind of stumped me for a moment. I hoped he didn’t notice the gaping chasm between his question and my response as I quickly recalibrated my own internal compass… of course – our sense of our own heath is SO subjective – he is alive, he is upright & functioning and that means he is well & winning. Because it wasn’t so long ago that he was so very close to losing it all. That ‘note to self’ sent and received I replied, “No, they wouldn’t be coming to see me, they’d be in emergency.”
He liked this response – because I think he could relate. After all, when he was sick – he was in emergency & ICU. But now that he is home & free he is clearly ‘well’ again,
Back then he had had cardiomyopathy that was not picked up until he had just 20% cardiac function – underwent surgery, had a pacemaker put in and is now on the most incredible suite of meds for life. Over the interim 18 months, he has lost enormous amounts of muscle & weight and when I look at his labs I see effectively a multi-car-pile-up. He has CKD 4 that, of course, no one has mentioned, a homocysteine of 15, macrocytic anaemia, subclinical hypothyroidism etc etc And did I mention he’s a smoker, with a persistent hacking cough?
He tells me that his goal is to one day be able to come off ‘all these meds’🤯
Our sense of our own health is composed of many things – and objectivity is not necessarily one of them. But things like our expectations, our perceptions of ‘normal’ and the cultural, societal and spiritual influences upon these are big players. And of course it’s all relative – he is well; relative to how he was before. I just love working in this space – the learning goes on forever.
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…)
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.
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…)
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?
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.
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.
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…)
When it comes to the recognition of Nickel as the number one metal allergen worldwide, affecting up to 30% of adults and with a particular predilection for women, it seems like Australian health professionals really do come from the ‘land down under’, with many of us still somehow yet to read that memo.
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…)
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.
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.
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 😉
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!
I’ve been ruffling feathers over here while speaking at AIMA in Auckland. While I am pretty familiar and comfortable with that role (& responsibility?) – this topic ruffled my own, arguably the most. In fact, I kicked off the presentation with, ‘What I’m going to say might make some of you uncomfortable but you know what, it makes me uncomfortable and if it makes you think a little less of me, well, to be honest, contemplating these issues has already made me think less of me!”
As an educator in integrative health, I have overwhelmingly been a peddler of knowledge and skills under the headings of: ‘WHY’ and‘WHAT’
Why – as in why does this patient present in this way, at this time. I am passionate about upskilling practitioners re our powerful contribution to the diagnostics & work-up of each individual. What – as in what changes (supps, herbs, diet etc) need to happen to correct for these very unique elements of imbalance in this patient to therefore aid resolution. We might label this, ‘personalised medicine’. But after so long in practice it’s patent that the best results don’t come from being the cleverest clinician nor the biggest biochemical brainiac. Knowing the ‘why’ and even the ‘what’, while enough for a minority of patients, fall short for the rest and can still fail to be truly about, & exclusively with, the most important person, in mind.
We’ve learned this before but it needs to be said again and again and again: much of any medicine is via the therapeutic relationship – and as part of this, our ability to PLACE the patient at the centre of their own SOLUTION. And therein lies the conversation we need to have in detail with them about the ‘HOW’ But how much time in your current consults is afforded to the ‘HOW’?
Being able to effectively negotiate with out patients the ‘HOW’ is an extension of Motivational Interviewing, Behaviour Change Theory & Patient Centred Care. It returns the humanity to our list of recommendations for each patient, pushing back against the autocracy that can tend to slip in with prescription writing. It powerfully reminds us that the prescription is only ever as good as the patient’s engagement & buy-in, and that’s only ever as good as our ability to write a prescription that is accessible & readily transplantable into their existing lives: to co-create with them Patient Centred Prescriptions. Someone in the audience had been my patient in the past – double awks right – because I absolutely know, I didn’t know this well enough back then. Back then when they were unable to do exactly as I had recommended – with their diet, their supps, their sleep, their work-life balance – they had, in turn, apologised for their ‘weakness’, ‘lack of willpower or diligence’ and me, being ever so gracious, accepted those apologies only to repeat the error of my ways and write yet more scripts that set them up to fail. 🤦♀️ I am committed to getting better at this and in this endeavour, giving both more attention & time in my appointments to the ‘HOW’ & yes I think we need to think creatively about how we use our appt time and between session touch points to achieve this – keen to hear about your perspective and experiences.
At the end of an information & insight heavy appointment, formulating a list of products and doses for our patients to take can feel like a bit of a ‘tada moment’, like a magician pulling a rabbit out of the hat. “Here is the solution – now off you go!” Research tells us, however, that treatment-plans that are a co-creation between you and your patient – evolving from a discussion that not only allows them a voice, but a major role in the decision making – are far more likely to succeed. While we are the authority on our medicines, our patients are the authority on what makes them tick & what’s likely to succeed, in terms of taste, texture, temperature & timing! This is called Patient Centred Prescribing and together with some other tips tricks and hacks I share with you in this episode, can really increase patient buy-in, compliance and therefore bring your treatment plan to fruition and fulfilment!
This is not about body shaming nor body positivity. I understand the crudeness of the body mass index, as a measure of (un)healthy weight – let alone (un)healthy muscle mass, so I don’t use this as a stand-alone assessment of weight, nor rigidly adhere to the categories it allocates individuals. With only minor recognised racial adjustments for BMI, I also recognise our concept of ‘healthy weight’ is incredibly whitewashed with minimal regard and consideration for clear ethnic and racial differences in physique. Patient’s lab results tell the real story. It’s in their results that we can discover someone is thin-on-the-outside-fat-on-the-inside (TOFI) or FOTI. These are patients whose BMI, WC,WHR, Body fat% etc identify them as obese – yet there is not a whisper of what I call ‘Adiposity Patterns’: no subclinical inflammation, no reduced glucose tolerance or actual IR, no raised transaminases that we expect to correlate with girth and the corresponding fatty infiltration of their liver. In this, as in so many other aspects of clinical practice, we are reminded to see each individual, individually.
AND if we adhered to this always, listening unfiltered to the whole health story and letting the labs speak, we would not miss those patients in whom unhealthy weight really is the most important underpinning, & all impacting, issue. And we are not doing our job, when we don’t.
I mean – we all know the detrimental effects of excessive adiposity – that’s like Pathology Unit 1 topic 1, right? I know we know it. Yet there are so many reasons why we might down-play, step-around, or even ignore its enormous contribution in our patient work-up and certainly the discussion that follows with our patients. That too is a no-brainer. Who wants to say to someone whose come seeking your help, as an explanation for their complex health concerns, ‘There’s no zebras here just a horse – one really over-weight horse!’ Knowing too that unhealthy weight results from the most complex constellation of factors (biopsychosocial) unique to each individual and that change in this health determinant, is arguably the slowest and hardest to sustain. But how are we serving our patients if we don’t?.
A practitioner presented this case of a 48yo F seeking help with the work-up: Self-reported inability to lose weight after 1st pregnancy = ‘obesity’ ongoing – now BMI 33.1 –> 25yo Reflux & Hiatus hernia Tx Omeprazole initiated – ongoing –> 26yo Depression Tx Venlafaxine initiated – ongoing –> 30s Back and other musculoskeletal injuries Tx Surgery & Opiates – ongoing –> 40s Hypertension & elevated resting HR –> Last 12mo – changes in Mx cycles suggestive of perimenopause & substantial weight gain
This patient didn’t ‘have’ any lab results but I think I can make an educated guess about how they would look and in particular whether they show the characteristic ‘adiposity patterns’ I mentioned before. What was my first thought about the most impactful element of the case? Obesity. What was my second thought? Where is all the weight (diet & intervention) history that would help us to understand how she is where she is, right now? We didn’t have any. The practitioner informed me that the patient was ‘not very interested in talking about her weight’ – in fact, according to her, it didn’t seem like losing weight was one of her goals. Now this could be several things: the fear of judgement, even her own self-loathing, the paralysing awareness of the enormity of such a goal, the dashed hopes of the past, or it could just be that her weight, as the key negative determinant of the majority of her health concerns & quality of life, has just never been brought to her attention, nor the connections explained to her in simple accessible language. So over to us, right?
There were other health determinants at play in this patient but the centrality of the adiposity was undeniable & the practitioner said this was the greatest take-home. She’d been ready to don some jungle gear and go hunting some zebras – but there was a horse right here in front of her and that could not and should not, ever be ignored.
What else became apparent was the lack of knowledge & skills regarding how to take a comprehensive weight history & why this is crucial. Not only for this type of unhealthy weight, the underweight require exquisite attention, as do those with a more labile weight than expected as an adult. This brilliant article by Kushner et al from 2020 is a total gift in that regard and a must-read for every clinician. We feel uncomfortable asking about certain things when a) a patient feels uncomfortable which is usually because b) we are uncomfortable and this ultimately comes from not being clear about WHY this information is so important and HOW this will ultimately enable us to better help THEM.
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Gone are the days, thankfully, when we could all easily identify any individual taking an antipsychotic 1) because they were the marginalised ‘mad’ and 2) stigma and shame were rife. With the seismic shift that has occurred both in psychiatry & society we now know so many of the people we live or work with just might be taking ‘something’ & under any number of diagnostic labels. And increasingly the ‘anti-psychotics’ are not reserved for the psychotic nor the ‘mood stabilisers’ for the manic. Which can complicate things – especially when it comes to their thyroid.
You see it’s a mistake to think that only Lithium spells trouble for thyroid function
The latest piece of evidence from a study of over 25K BPAD patients in the US tells us this common misunderstanding makes us prone to not recognise all the other patients in whom their psych meds are disrupting and in fact driving thyroid (dys)function. Though Lithium carbonate remains the most noxious goitrogen due to its multiple disruptive mechanisms – the rest of a large group of Psych meds (yes even antidepressants!) are impacting to the point of effecting the thyroid function test results you are likely to see in patients taking these. And this is something we need to be alert to – these medications are essential, non-negotiable in most scenarios, but a secondary hypothyroidism is not their intended goal and can make matters worse.
Cue our growing understand of psychoneuroendocrinology, of course. Your HPT is influenced by your mood & vice versa
I told you I’ve rekindled my love and passion for thyroid pathology and this is one of the many elements I got to include in our latest updated training * Advanced Thyroid Assessment* and the upcoming MasterCourse. But I just had to hit record on this one aspect immediately – because if we don’t recognise the cause we are likely to be throwing all the wrong things at the thyroid – to no avail. This kind of subclinical or overt hypothyroidism is not due to nutrition per se, or due to some other kind of HPT re-setting influence like inflammation…it’s the meds & that necessitates different solutions & a much bigger conversation…so join me…
Many of us recognise the bidirectionality between thyroid function and psychiatry wherein ‘stress’ and mental illness can produce a predictable pattern and shift in TFTs and vice versa but regarding the question of psych meds as potential goitrogens, many of us are mistaken in thinking this issue begins and ends with the use of Lithium carbonate. As it turns out, an increasing number of these pharmaceuticals are recognised to disrupt thyroid health & activity via a variety of mechanisms both centrally and peripherally & as a result many patients may get stuck in a vicious loop of worsening thyroid function and mental wellbeing. – until someone calls it – someone like us.