I’m such a sucker for marketing!…ZoomZoom is from an old Australian car ad – an earworm clearly conveying ‘ the speed of something’, and let me tell you, totally fitting for this little Zinc tale I’m about to tell! Many years ago, I wrote a thesis on Zinc that necessitated me reading every research paper ever written (that’s how it felt anyway!🤪) on this trace mineral. Like everything in nutritional medicine, especially in the area of our burgeoning understanding of micronutrients, this is a highly dynamic space, so regular reviews of what’s new is essential and, since my thesis, part of my regular practice. Well, I just did my latest deep dive, and HELLOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOO radical paradigm shift(s)…yep plural!
Zinc supplements should ideally be: Organic amino acid chelates Taken daily – due to the lack of Zinc stores in the body Taken fasting Taken in doses in excess of the RDI to compensate for the smaller % absorbed
Yep – nope. Or in true-blue Aussie: Yeah, nah. Can’t believe what you’re reading right now? Neither could I when I undertook this recent review but the studies are increasingly sophisticated and the resultant paradigm shifts are being echoed, reiterated & reinforced. And these have, in turn, challenged all those old ‘norms’ about how best to administer zinc for those patients with a shortfall. If you’d like to take this little journey for yourself…I suggest you start here! I immediately changed how I take it myself and now my mission is to both spread the word and get us all reflecting and reviewing our prescribing principles around Zinc…and tbh, around all micronutrients! After spending my ‘summer’ doing sufficient reading for a second thesis on everything new in micronutrients…I am armed and dangerously prepared for our upcoming *NEW* program: The Nutrient Prescriber’s Program which kicks off in late Feb for 5 months.
I truly believe that based on all this new information, we can now get so much more out of our medicines.
Nutrition represents such an extraordinary set of tools for us to work with, but it’s time to sharpen those tools in terms of how we apply them!
The Changing Zeitgeist Of Zinc Prescribing
Zinc research is a highly dynamic field and given its relative recency of discovery as being essential to humans, we’re still in the early days of truly getting to know this mineral. In just the last few years, enormous gaps have been filled-in regarding its regulation and roles that look to radically change our prescribing practices. Tune in to this essential update for some serious food for thought about doses and dosing frequency.
You can purchase The Changing Zeitgeist Of Zinc Prescribinghere. 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.
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…)
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?
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…)
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…)
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.
One of my dear friends told her husband several years ago that she had noticed he was now making, ‘old man noises’ upon standing up from couches & chairs. She told him that must simply stop. She pointed out that he was only 50 and that she neither could nor would listen to that for another 40 years!
He stopped!
But aging and old (wo)man noises are coming for all of us, right? And by the time we’re making those noises or excusing ourselves from certain activities due to sore, dodgy or NQR [insert joint or body part], we’ve spent several decades unknowingly right on course to get here! We don’t generally pay any attention to our ECM (extracellular matrix) which suffers in silence, slowly but surely losing its structural & functional integrity from the age of 18 on, until we reach the tipping point: joint degeneration, repetitive soft tissue injuries etc, and a problem that will never be silent again! Cue your choice of anti-inflammatories it seems – til death do us part!
The Ageing Matrix is a thing.
And no I haven’t seen the movie – I don’t need to – I’m living it.
When I was pregnant I thought I wanted to specialise in pre-conception & pregnancy care. Then my babies arrived and I took a fancy to paediatrics. Sound familiar to anyone? Now, unsurprisingly, I have a real thirst for knowledge expressly aimed at bettering this whole ageing-thing! So in preparation for this Update in Under 30 episode, I’ve relished the opportunity to put the Ponds Institute & all similar cosmetic companies on notice! Scrutinising their claims that every woman on the planet would do better with more Collagen, more Elastin, more Hyaluronic Acid, just more of every key ECM component really. Ok, but in accordance with my bias and my business, my lit review pertained to oral supplements, not outrageously priced magical middle-life-crisis rubs and the therapeutic action I had in mind was the integrity of our ECM, and the roughly 2kg of collagen, we rely on, for functions a lot less frivolous than stopping sag. I have to say, I started out as non-believer but the research was quite the awakening…still there’s a lot to unpack here in order to repack our ECM and prevent against the erosion of its integrity and everything we build, and rely on, upon it – to live well!
Osteoarthritis (OA), like osteoporosis, is a diagnosis made after decades of disease. Underpinning it all, is our aging Extracellular Matrix (ECM) with its characteristic compositional change that leaves us vulnerable, from the ripe old age of 18! The ECM, like all other tissues, is made from basic building block nutrients but presented in their most fanciest of forms with triple helix structures, aggregates and other large molecular weight components, that each possess remarkable physico-chemical properties & convey extraordinary functionality to structures like joints. But is prevention against, and effective intervention for, OA as easy as consuming more of these ECM biomaterials?
You can purchase Supplementing Collagen & ECM Biomaterials – What’s the story?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.
Are we doing ourselves out of a job? I’ve been talking treatment plans with my New Grads recently. Given, only recently these were major assessment items in their clinic units, they have been trained to create ALL-ENCOMPASSING (biopsychosocial) prescriptions and recommendations of utterly EPIC PROPORTIONS – to simply prove they know it all. Problem is this doesn’t work in the real world.
Emailing your client multiple pages of advice that covers: a whole sizeable supplement schedule that only a military-training could nail (2 tablets 1 XTID 1 X BID, a liquid, a powder, some with food, some definitely not with food) plus dietary advice, plus hyperlinks to exercise advice, mindfulness exercises and a request for follow up investigations before the next appointment…is…a L*O*T!!
It is also ineffectual – because it completely disregards the human on the other end. Let me ask you this, how much change are you capable of between a first and second appointment, roughly a period of 2-3 weeks? Personally, I gotta say not that much. It took my dentist years to get me just embrace flossing & I don’t think I am an exception! With all the knowledge we possess its hard not to see people as (a long list of) problems (& problematic behaviours) that we translate into, and solve via, a prescription.
Effectively we are saying to patients with this practice model, ‘Go change & come back when you’re done & then I’ll probably ask you to change some more!’ That’s both a big ask and a huge missed opportunity.
I hear from reliable sources over the ditch, that GPs are increasingly referring their patients to, or teaming up with health coaches, rather than naturopaths. Given what I’m observing, I get it. Doctors on the whole only have time (and barely then) for a finger-pointing prescription – certainly not the time and touch-points required to actually support patients with the very difficult thing that is, behaviour change. Nor the skills to truly facilitate patients making the necessary and desired changes – so they outsource this role. But we shouldn’t.
After all – I want to be on my patients’ support bench & health care team always – not a flash in the pan, that blinded them with science or my ‘smarts’ and proved to them in one over-stretching prescription – that naturopathy is not for them, or at least, they’re not fit for the task.
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!
And all 35K results have been collated, analysed & made available so we can be better informed regarding expected Cortisol values based on sex (spoiler alert: women win & when I say win I mean track higher generally🤷♀️), age & life-stage. This month in our Mental Health Primer program I’m talking about how to look at labs through a mental health lens – from the most routine (ELFTs, FBE etc) to those 2nd tier assessments that we might sometimes recognise to provide essential information about our patients. HPA assessment is such a big one in mental health and depression, specifically, because of the 2 major subtypes: typical (can’t sleep, can’t eat) and ‘atypical’ (over-sleeps, over-eats). We all know that in ‘typical’ depression – the subtype we tend to over-focus on due to its dominance (and sometimes therefore miss the atypical patient at our own peril), there is most characteristically a hyper-cortisolism, with poor negative feedback at the HP, allowing for these higher circulating levels. But is your depressed patient with sleep disturbance experiencing higher than healthy or expected cortisol release? No, not necessarily.
You see even the 2 subtypes can have sub- sub- types. Patients can have a diagnosis of either form of depression but have PTSD features or other psych and non-psych comorbidities that make it more probable that their adrenals and Cortisol are turned to ‘low’. As in unhealthily & unhelpfully low.
And that would then necessitate a very different approach to treatment – a different choice of herbs and nutrients etc., right? As we’ve discussed before, accurately capturing cortisol is a task not for the faint-hearted! Cortisol demonstrates such dynamism – not just regarding time of day and pre-test and test exposures & experiences, but also your geographical location in the world (!), not to mention choice of medium and which aspect of the HPA story that specifically reflects. But for some patients it is essential for best management that we ‘feel the fear & undertake an assessment of their HPA function anyway’! But we need to ensure we get results we know how to accurately interpret.
I use different cortisol captures (saliva, urine, blood) to answer different questions – but if I want to understand the HPA functionality and performance and feedback…then measuring cortisol alone is not adequate – and we are back at blood, which offers us, as always, to go beyond a simple numerical: ‘adrenal output’ & also answer the question: “What were the adrenals TOLD to do?” aka where does any actual mismanagement lie & likewise, the key to correction.
I have! And just recently a stark contrast between the results from 2 different methods of cortisol capture in the same patient illustrated just how likely this is. How do we ‘capture’ something so ‘dynamic’ and interpret anything of substance from a ‘static’ assessment technique? But rather than throw up our hands and throw out the whole attempt to measure cortisol, we can improve the rigor, reliability, and real-world meaningfulness of our patients’ results by refining our timing of tests, choosing the medium wisely & manipulating test conditions to answer specific questions about their HPA function. Great ready reference resource included!
An ideal T4 is 15
An ‘anti-aging’ DHEAs must be >7
A ferritin of 100 is optimal for women…
I’ve heard it all, probably you have too, and far too often & too recently from practitioners who should have rationalised & researched their way beyond these functional falsehoods, by now. I bought into these ‘optimal wellness truths’ hook line & sinker early in my career and proceeded to even propagate a few but with (not much) more experience in clinic, I had to seriously question this pursuit of ‘perfection’ & ‘perfect pathology’…in favour of reality & scientific evidence! They didn’t add up. Not with my patients – even the healthiest ones, in fact some of the really unwell ones occasionally had these kind of high-normal results and they were part of the problem!. ‘But that’s because no one is truly healthy outside of those seeing a functional medicine practitioner & supercharged on supplements & hormone replacements!!’ came the counter-argument. Ahhh, really?
How then do we reconcile this with the following: Individual genetics & biochemistry
Our biological resilience Healthy & appropriate senescence Large datasets of mixed race populations from other comparable first world countries…where these figures denote the statistical outliers?
I mean, if the 50th centile value for ferritin for actual living, breathing, bleeding, women in the US, Canada, Australia etc etc is 30-40 ng/mL and the 95th centile is 126 ng/mL and the WHO says that in fact, anyone menstruating with a ferritin > 150 ng/mL should attract suspicion for iron overload….but functional medicine men (mostly…sorry but it has to be said!) say 100 IS OPTIMAL FOR EVERY WOMAN #@^*…please tell me in which women, consuming what kind of diet, where in the world, & based on what improved or better health outcomes?
And while you’re there can someone please support this bold claim with a scrap of high quality evidence?? [Rant over🎤💧]
The falsehoods of functional medicine include the blanket belief, ‘more is better’ (ahhhhh not when it comes to many things, including iron where women’s lower levels have been found to be an evolutionary advantage…guys). But you know what, we’re better than that! We see each individual, recognising all the factors at play that make for their uniqueness, help to define what ‘healthy’ looks like for each person and don’t fall for one-size-fits-all claims without any evidence nor common sense even, to support them. What do you think?
Let’s make sense of the over-arching nutrition principles, that will profoundly change your understanding and application of this modality Truly understanding the ‘big’ concepts, so often overlooked, or incorrectly taught, ensures you get the critical ‘small’ detail in your nutritional prescriptions right. In this 4 hour recording, together with key clinical tools, we talk about the tough stuff: dose-response curves, active versus passive stores and excretory pathways and ooh lah lah…the myth of taking ‘activated vitamins’. Even those who feel satisfied with their original training – will find a lot in this critical review that is new, insightful and truly practise-changing!
And it will. It knocked again on a practitioner’s door last week. She in turn knocked on mine. It turned out to be a very familiar story:
Firstly:Patient presents distressed – recently a nurse applied the term ‘Chronic Kidney Disease’ to HER (note no one has ever mentioned this diagnosis) Secondly:She is in stage 3 of 5 Then: This practitioner is left to have ‘the conversation’ but wants to know where to start, ‘What do I say?’ Next up:And what else can I do for her – are we really able to make a difference?
Familiar to you too? So,1st & 2nd: Yes, this is not uncommon we would have to say and even with age-appropriate reference range adjustment, her GFR consistently in the 50s, flags premature decline. Then: What DO you say? Well this clearly is a delicate area, not only because of the level of patient distress and concern but because, at this stage the practitioner knows nothing more than what the patient tells her and her ELFTs over the last 2 years. This is not enough information, right? Chronic Kidney Disease is a heterogeneous condition, with many different causes, manifestations, comorbid conditions, and factors affecting prognosis (Levey et al., 2009) So while most individuals certainly progress from stage I to II and II to III the rate at which they do this differs dramatically.
Two years of data is not long enough for us to appreciate the trajectory of her CKD & means we are unable to provide the patient with any kind of perspective:
‘With no further decline in GFR or progression in stages over 5 years, you’re doing well, so keep doing what you’re doing!’ Vs ‘Ok, I can see what looks like a little period of accelerated decline – let’s review what’s been happening and how we can turn this around”
“Please sir can I have some more?’ Yes, back to her primary carers to request more information to fill in the gaps, and ideally more labs to calculate & observe the trajectory for yourself. Next Up: What do we have to offer the patient with CKD stage III? Soooooooooooooooooooooooooooooooooo much!! When is adequate hydration helpful? Always, except Stage V! (and these patients are not coming to see us) What are our treatment objectives & our evidence backed medicines to meet these? Hcy lowering (note often referred to as ‘folate refractory’ in renal dx), vitamin D adequacy, lowering the acid load, supporting the microbiome & in turn the Renal-GIT axis…hang on, got to go…someone’s knocking 😅 but hopefully we all can see, when they present to us, they are indeed knocking on the right door ✊
Nutritional or naturopathic support for the kidneys tends to have been over-looked in our training and yet research suggests there is much in our tool kit that can make an enormous difference to this system, in particular, slowing the progression of chronic kidney disease in patients. Rachel talks about what these key evidence based interventions are and also gives you the tools to identify the early pathology markers of renal impairment – the earlier the recognition, the earlier we can make a start on the remedy.
It seems almost farcical to question the merits of hydration for our renal health but is this actually the truism we have been lead to believe? Where does the recommendation of ‘8 glasses a day’ come from and what is the level of evidence to support it and in whom? Or should we in fact be setting our sights on output ie. 24 hr urinary volume, over input. Do all kidneys love water – or does this relationship change with the progressive impairment seen in CKD which affects up to 30% of our middle-aged population? When does hydration become harassment?
Most practitioners graduated with not much more than a few ‘kidney’ herbs and an under-appreciation of the contribution renal health makes to wellbeing. It’s not just about waste and water. In reality, the kidneys are pivotal in just about every major element: blood, bones, pH balance, methylation, control of oxidative stress, the GIT microbiome and more! And we are seeing the impact of this in our patients in all sorts of subtle and not so subtle presentations. This new instalment in diagnostics, brings the renal system into the spotlight so we can confidently identify and better manage its critical contribution. In addition to this, just like with other routine labs such as LFTs, we unpack how these so-called ‘renal markers’ can flag a plethora of other insights into your patients, from reflecting (un)healthy muscle mass, to calculating individual dietary protein adequacy, from key ‘danger and distress’ signals in response to disturbed metabolism, oxidative stress to certain types of GIT dysbiosis! We call this Explained, Expanded and Exploded because these routine labs can deliver XXX sized insights into your patients.
And not in a good way, right. While we’ve known about the potential for peripheral neuropathy with excess B6 supplementation since the 1980s, currently there’s a seismic shift in our sense of safety even with previously regarded ‘safe’ levels. You may have heard individual whispers, or the chorus of voices coming together, both here and overseas, belonging to members of the public who report suffering sensory nerve impairment with as little as 2mg/d! Is this a mess of mis-diagnosis, false attribution & nocebo? Perhaps for some, but certainly not for all.
How could this be the case given the many RCTs employing hundreds of mgs per day over months, with no such events recorded? How could this be given, your (?), certainly my, high dose prescriptions, with only 1 case of quickly reversed, peripheral neuropathy in over 20 years, on my books? The pieces of this complex paradoxical pyridoxine puzzle are coming to light.
Is it the form?, the dose? the duration? individual differences in B6 metabolism & toxicity threshold? amplification of risk secondary to levels of other nutrients, or the use of certain medications? Yes. And we need to understand each element to better tailor every B6 prescription to the individual & mitigate risk. I have spent the best part of this month reading almost every paper on this from the 1970s to last month and I am now alarmed but more importantly, alert, to what prescription practice changes we can all make to lessen the risk, and control the power of B6. It’s been the most compelling deep-dive. Because in spite of a clear TGA warning issued last year that likely prompted the quiet removal of high dose products from market, it would seem none of the companies have the courage to have this difficult conversation with us 🙁 I invite you to ‘feel the fear & do it anyway’ & listen in to our latest Update in Under 30.
Haven’t we always known that nutritional medicine is a potent prescription? Now thanks to more sophisticated research we have a much greater understanding of this and of both the intended and unintended effects of micronutrient supplements that have the potential to achieve supra-physiological levels. B6 metabolism is arguably the most complex of the Bs – involving 6 different forms, at least 2 of which are active – and exhibiting some of the most complicated regulatory control designed to both harness the power & limit the accompanying risks. Excess B6 supplementation, however, has long been known to present as peripheral neuropathy in some individuals and case reports of this are growing, at lower and lower doses. New information has come to light to help us understand the why, the how and better still how to mitigate risk to our patients.
You can purchase Dynamics and Dangers of B6 – Controlling the Powerhere.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.
You know when you learn about a ‘new’ dis-ease driver and then you actually have to stop yourself from diagnosing every patient with it? I’ve done this dance with Gilbert’s Syndrome for over a decade, so too maybe have some of you? And while there have been many, many occasions when I’ve been certain it’s Gilbert’s (clear robust & reproducible patterns of high bilirubin without other explanation) there are other times when I’ve been left wondering, and with questions. Like – what about a fluctuating pattern – sometimes ‘within range’ sometimes above or at least high-normal – with no other explanation? What about the patient whose symptom-story is a perfect fit – prone to nausea, early satiety, gut issues, food reactions and anxiety all worse for increased oestrogen…but the total serum bilirubin is 14 micromoles/L? I mean, 14, right? that’s well below the top of that range, but remarkably higher than the majority of women of the same age, eating the same diet. And you ask yourself…could it…be??
It could.
The latest UU30 offering on Gilbert’s Syndrome constitutes a complete overhaul of everything we’ve previously been told about how to recognise and diagnose this polymorphism & it’s going to answer a lot of those ‘could it be’ questions we’ve all had! Known also as familial non-haemolytic jaundice and episodic hyperbilirubinaemia under stress – is everyone with Gilbert’s prone to jaundice? Uh, no. Total bilirubin levels typically have to get to 45 micromoles/L to evoke this effect – many of our GS patients won’t ever get there, some will with increased illness or other stress and may yellow a tad (like a fading bruise), while other patients of mine routinely have a bilirubin at this level but won’t experience jaundice unless they impair their UGT further via doing what they know they shouldn’t: extreme exercise or excess alcohol. The latest deep dive into GS diagnostics
But as much as we don’t want to miss this diagnosis we don’t want to mis-diagnose patients with it either!
Can you spot the difference? Don’t forget total serum bilirubin levels are the net result of haem catabolism – so you need to account for rate of blood production, destruction and of course rule out any biliary dx before you can take a guess at Gilbert’s. Oh and watch out for expected high bilirubin values in the fasting fan(atic)s!
For those people living with Gilbert Syndrome at last the research world & the real one are uniting – with greater detailed documentation of how this very common polymorphism presents and the mark it may make in their health story. However, given only 1/5 with Gilbert’s syndrome actually know they have this condition, who are we missing? This latest instalment rewrites our diagnostic criteria and corrects our past misunderstandings based on the very latest science, while shedding further light on what it’s like to live in Gilbert St.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
I’m 100% confident that, as a professional group, among our highest values about healthy, preferable, food choices, would be characteristics like: ‘as close to nature as possible’, ‘unrefined’, ‘unprocessed’, ‘unadulterated’. Tell me I’m wrong.
So, when I keep hearing about NEW! “Never seen before” (read: never in nature) modified (read: more processed, adulterated) nutritional supplements: water soluble vitamin D, fat soluble C, bioflavonoids with unprecedented (read unnatural) bioavailability
I’m left wondering what these companies are missing about their customer group (because we are clear about our valuing of nature & what’s natural & have a desire to minimise exposures to things that are not, right?
or what are we missing here, in the clear conflict of our core values these constitute?
I think if we find ourselves forsaking this core value & prescribing highly modified, unnatural supps, it’s the result of both hype & fear. The hype is self-explanatory and I’ve written recently on how modifications exponentially increase profit margins for companies, all the while possibly reducing ours because patients are spending more on product and therefore there is less left over for the practitioner fees 🙁 [The ones spending hours with them face to face, not to mention years & thousands on our training] The fear is perhaps less apparent, more insidious. The fear is that we’re not using the best, being the most effective, and deeper still, inevitably that we will fail to action our patients return to health. This is a big one. I think it’s pervasive, if not omnipresent, and works as a motivator for many positive actions by practitioners – like engaging in further education, reading that latest journal edition on your lonesome laptop when you could be streaming some series on a shared sofa. But this same fear can also undermine us, overwhelm us and shake our tree of trust, that we believe to be so firmly rooted within us, of the healing power of nature.
So while my position sometimes makes me feel very ‘old school’, I’m not suggesting we return to nutritional prescriptions composed exclusively of bee pollen & brewer’s yeast and I absolutely recognise and respond to an individual who has very specific barriers to benefiting from nutrients in their natural normal forms. But let’s be clear, they are a minority.
Some of you will know naturopath Dawn Whitten & know that she is one of my mentors. I’ve had the benefit of speaking with her over the years about herbal prescriptions but also about the principles & philosophy behind our practice & in one of many conversations she told me that a key objective she has with her patients is to rebuild their trust in their body, their own biological resilience (I love this concept and that’s a talk for another time!) and ultimately in nature. Well jeepers Dawn – how did you get to be so wise so young? But isn’t that central to vis medicatrix naturae? Maybe that Naturopathic Nanna’s club isn’t so fuddy-duddy after all. Want to join us?
Speaking of using nutrients in their most natural state for the best health outcomes – the best B3 is probably not what you think!!…. The Balance of B3
Most of us have been taught to ‘balance the Bs’ when supplementing, which discourages the use of single B vitamins in case this interferes with the regulation and roles of others. In reality, outside of a couple of dynamic duos like B12 and folate, there is little concrete information & evidence of this. In the case specifically of B3, however, we now know, the risk of an excess of the most common B3 forms found in supplements and fortified foods, results not only in disruption of other nutrients but imbalanced B3 biochemistry itself. Given B3, in its coenzyme form NAD+, is regarded as highly valued currency in the prevention of many diseases, as well as the key to our optimal health and longevity, it’s critical to understand the different forms and functions of the various B3 sources.
I haven’t personally seen every medical condition known to occur, nor every micronutrient deficiency & toxicity picture in the flesh but that doesn’t mean I doubt their very existence. Sadly, it would seem some practitioners due to a) not knowing ‘where’ to look in terms of best assessment medium and/or b) not knowing ‘what’ they’re looking at, when faced with an actual Copper deficiency, have declared this uncommon, but certainly not unknown, nutritional issue to be a figment of others’ imagination!
I know I’ve been fortunate to see more labs than most would want to in an entire lifetime , a collection of my own, my student’s & my mentee’s patients, so let me share just 3 sets of results from 3 different individuals: an 11Y boy, a male teenage athlete and a female in her early 20s with an eating disorder, all with Copper deficiency.
Don’t worry, I have more – just ask. What’s so dangerous about people spreading myths and misinformation in relation to copper in kids and teenagers specifically, is it shows complete disregard or ignorance of an understanding of how Copper is critical for development during these life-stages and how regardless of which developed country you live in Copper is expected to dominant over Zinc in blood, especially pre-puberty.
AM I SHOUTING???!!!
I’m sorry it’s just that my blood tends to hit boiling when exposed to the misinformed, misinforming others… and that can make one call out in pain 🤯
You see, I literally heard a practitioner in an “educational” webinar purport that
‘Copper Toxicity is so prevalent in kids in her clinic’ and I was like,
OH. EM. GEEE.
Because if you start with that misunderstanding, and are unclear about what constitutes an accurate Copper assessment and how to recognise the pattern that follows low serum levels (each of these patients above had abnormalities in their FBE consistent with Copper deficiency) you are not only going to miss the thing you need to make a priority to fix, you’re going to make it worse! Take ‘Volatile Vince’ the gorgeous sensitive 11Y boy I saw, whose increasing mood volatility had been misattributed to pyrroles and given large doses of Zinc! So, Copper Crimes are a thing. Guilty until proven innocent but in fact, never found innocent by some practitioners it would seem. The ramifications of unchecked Copper deficiency include negative effects on mood and cognition, immunity, and the balance of other nutrients and kids are going to feel this impact the most! What are the causes? Inadequate intake being uncommon outside of eating disorders, and excessive Zinc rarely the cause, we’re likely looking at a marker of malabsorption or a genetic issue. Don’t buy into the confirmatory bias many use when they choose which research to read (risk of excess) and which to ignore (Copper as an essential mineral, critical to kids) and let’s not discredit something as not being a thing because we haven’t seen it ourselves, yet, hey, anyway, at least, now we all have, right?!😵🥴😆
Copper, as a kingpin in angiogenesis, brain & bone building & iron regulation is a critical mineral during paediatric development. So much so, the kind of blood levels we see in a primary schooler might cause alarm if we saw them in an adult. So too their Zn:Cu. But higher blood Copper and more Copper than Zinc are not just healthy but perhaps necessary during certain paediatric periods. This recording redefines normal, low and high with a great clinical desktop tool to help you better interpret these labs, as well as reviewing the top causes and consequences of both types of Copper imbalance in kids.
Name a B vitamin. Hey, Bingo! It’s on the list! What list? The complete one from all the review papers & references to possible links between individual nutrient deficiencies & Angular Cheilitis – inflammation & cracking at the corners of the mouth. So does that mean more Bs are the answer for people presenting with this painful, recurring issue?…Ahhhhhh No. Yes, you heard me correctly, these deficiencies rarely cause the breakdown of the integrity of this very specific area of skin in the patients we see. So now we have a double ouch, right?
We might send patients away with a B complex and some lip balm and over a week the cheilitis resolves – which one was the most therapeutic? …I hate to tell you 👀
What is the underpinning cause(s) & the important message we are missing with this presentation? Well, it could be one or more of a long LONG list of differentials, ranging from anatomical, habitual, immune related to iatrogenic. And while many nutrient deficiency pictures can include this feature and therefore make the ‘possible’ list, only one makes the ‘probable’ list. And that’s iron but only in severe deficiency, aka anaemia and only affecting 1 in 5.
Me???
…Telling anyone to push the nutritional issues further down the list of differentials for any condition? Well, that’s unexpected
…possibly unprecedented
And no, antifungals aren’t the answer either. Yep, that might be worth a listen….👂
Just an annoying, embarrassing, cosmetic condition or could it be the clue that helps you ‘crack the case’? There is a surprisingly long list of differentials for this condition but most of us only know a few, reflexively reaching for either B vitamins or anti-fungal creams. Does either make sense? Does either address the cause(s) which we now recognise to be a unique series of risk factors in each individual? Or are we at risk of shooting the messenger and missing the message of Cracking Corners altogether?
You can purchase Cracking in the Corners – Angular Cheilitishere.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.
[Ahem] Ok let me explain…Several catch-cries from Australian ads have earnt themselves a lifelong place in my head and heart, taking up space where something more important should be, no doubt, but does anyone remember this SPC canned fruit (REALLY showing my age now!!) one, where the little boy chases the grape around the bowl and declares it a, ‘Slippery Little Sucker!’? Ok so this little boy is every one of us when we’re trying to ‘capture someone’s cortisol’ and just like the boy we will eventually achieve a ‘result’ – get a ‘number’ but what in fact does this mean in relation to your patient’s HPA axis, stress perception, responsivity, recovery etc etc?
Recently I was presented with 2 cortisol results for a patient taken within the same 24hrs – her blood am result was above range, while her 24hr urine flagged under-functioning of her HPA axis generally. Both were accurate.
Had I have only have seen one, I would have formed the wrong opinion and only gleaned part of her overall HPA story. Every different type of cortisol capture – from different mediums: blood, saliva & urine – to different collection conditions: time of day, fasting V fed, specific stressor exposure etc answers a different question about our patient’s HPA axis. So to use any form of cortisol assessment well we need to start with 2 understandings: 1) it is a slippery little sucker indeed and no one test can answer all our questions – or as Miller & colleagues more eloquently put it, “Remember, all models are wrong; the practical question is, how wrong do they have to be to not to be useful” and 2) be clear about the most important question you have about your patient you are trying to answer and that will make your choice of test (& timing & & &) patent. But do you know enough about cortisol regulation to be clear about the ‘sweet spot’ of each test?
The Cortisol Awakening Response has understandably attracted the bulk of the research focus over the last decade and accordingly has risen in popularity in practice & while it remains a very valuable way to answer certain questions about patients, our understanding of its limitations continue to grow. For example there is a disconnect between CAR & diurnal cortisol secretion – so in essence your CAR can look woke but your ‘Slope’ may be broke! If you’re a fan of this method, make sure you catch up on the CAR-Expert Consensus Guidelines by Stalder et aland if you’d like to get clear about which test and when, when it comes to all the key options for Cortisol Capture..
then let’s dive in together with my latest Update in Under 30 instalment
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.
Is it just me or do you view everything with a trained eye? My son always laughed when I wrote him a shopping list: I would list items under each shop and I always wrote down our local supermarket the Independent Grocers Association, like this: IgA…you all see what I was doing, right?!! It’s actually known to everyone else as IGA…well truth be told, I didn’t until he pointed it out 😂 Then there’s this relic I regularly pass, as I walk through bushy parkland near my home, ‘Hmmmmmm, B12 hey?’, I’d muse. I’d be embarrassed to tell you exactly how long it was before I realised OMG it’s not a shrine to the vitamin but an old road sign telling you…Byron 12kms!!!
I preferred my take on it to be honest, because invariably once past this, the remainder of my walk was full of scintillating B12 banter. Just internally, people, no one panic, I don’t walk the streets of this town spouting out crazy random nutritional tidbits…although, let’s face it, I would be in good company in, the Byron Bay region!
I have a deep respect for B12 – weird but true. As a result of my clinical experiences helping patients who had a previously ‘unseen need’ for this nutrient and the significant improvements that come with its replenishment. Plus the deep dive I did into the science of the different forms and their actions last year. In particular, I now have 2 families where the TCNII SNP is evident in mum and all her children. No gene testing necessary, the pattern is self-evident once you know what to look for and the clear ‘call to action’ – more B12 please! And just this month, a fresh aspect has come to my attention in regard some brand spanking new research on B12 and IBD and the microbial (im)balance of this vitamin as a pivot point for the pathophysiology. Wowza! Early days, but I think we’re headed next level on this nutrient again! And I can’t say, I’m surprised. For while I don’t think the CHOICE of the supplemental form for B12 is complex at all (hence why we need to separate the B12 from the B*S#!) I recognise it is a complex character far beyond what regular dietetics has reduced it to.
B12 is a routinely under-rated and recognised micronutrient, which is in fact in high demand by many of our patients. As nutritional research pushes back against defining adequacy as simply the prevention of the deficiency-associated disease (macrocyctic anaemia, irreversible neurological damage) we enter a new landscape of more individualised approaches where we’re better able to recognise and treat those at risk of falling below ‘optimal’. But how do we accurately identify this and then choose the ‘best’ B12 (methyl- cyano- adenosyl- hyroxo-) supplement? Does it need to be this complex? Time to sort the B12 from the B*S#!! This recording comes with a bunch of great resources including a clever clinical tool.
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.
