Key texts tell us, 2nd trimester Serum Ferritin may be between: 2……………………………………………………………………………………….and……………………………………………………………………………………….230 mcg/L But a 2nd trimester Ferritin even > 40 mcg/L is remarkable – and not in a good way🙄 So, ummmm what should it be and why?
Given all the attention iron gets from me alone, you would think we would be a lot clearer and a little ‘clueier’ regarding the answers to core questions like this. But we’re not. Correction, they’re not. Who is this ‘they’ of which I speak, um well, just the dudes in the top level office who write the practice guidelines for GPs, Obs, Midwives etc. Big call I know, but answer these to get my drift:
What is the average Serum Ferritin in healthy women with healthy pregnancies in the 2nd trimester? After all the routine Iron treatment given across numerous countries, in line with the WHO recommendations, is there any evidence that values higher than this have irrefutable benefits for mother or baby? Is there evidence to the contrary, that it can be harmful?
And while we’re busy asking questions that shake the flimsy foundations of the practice guidelines regarding monitoring and managing iron levels in mid-pregnancy – how about we get up to speed with the evidence that shows 1st trimester Serum Ferritin is in fact the most meaningful as an iron marker both in the short and long-run for any woman’s pregnancy. I know, right…this is all sounding very different from the, inappropriately named, ‘normal’, which is to test women at wk28, in the midst of peak haemodilution, and therefore physiological anaemia, and to then send that patient home often with a new diagnosis of iron deficiency and a sense of urgency to ‘fix this fast for you and baby’. In some instances this is appropriate and important, especially women who weren’t comprehensively cared for & whose iron status wasn’t monitored & well-managed in the first trimester. But for so many women, who are just riding the Ferritin-Fun-Bus…they are right on track with looking their very worst!
Couldn’t resist finishing this year of Update and Under 30s with a serious BANG! 🧨🧨🧨
In this continuation of our discussion about better iron balance for mum and baby we now map what is happening in each trimester with regard to requirements and regulation, and accordingly, what ‘healthy looks like’ in terms of both serum ferritin and transferrin, at every time point. This also gives us a clear practice protocol around when and how exactly to treat iron deficiency in pregnant women. Additionally, we review the risks of both under and over-treatment.
The latest Update in Under 30 has landed!!!
You can purchase Pregnancy Iron Balance Part 2 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.
I love a little temporal lobe tap. Especially the kind patients provide. This week mine came from a mentee’s patient who, while presenting with concerns about possible perimenopause, was found to have radical shifts in her thyroid hormones, largely thanks to a dramatic increase in TPO Abs (>1000). The patient’s other presenting complaint was ongoing gastritis (confirmed via scope) and reflux…and that’s when I started to deep-dive into the archaeological archives of my brain…with the…’didn’t I have somewhere in here, in some dark dusty deep recess…a connection between the two?!’
Aha! With the help of a torch [read Google Scholar] the temporal tap bore fruit. 1 in 4 patients with AITD (Hashimoto’s or Graves, you choose!) test positive to Parietal Cell Antibodies
I’ve created (clearly, not-so)SmartArt graphics on powerpoint slides on this exact topic, waxed lyrical about it in my thyroid training packages…but in fact needed a temporal tap to be reminded! And in turn thought, well gosh if this has slipped from my mind, it might just have slipped from yours too! ‘Thyrogastric autoimmunity’ as it’s called, refers to a patient group that exhibit antibodies to both and remember, the antibodies precede the condition in both disorders, so you can have a patient with established AITD, who has zero gastric symptoms but tests positive for the antibody…an important heads-up, as it speaks to significant risk of the subsequent development of gastritis in the following years. This excellent prospective study of AITD patients by Tozzoli and colleagues mapped exactly that! Jump forward just another day or so and…
I’m preparing for our final FiNAl FINAL Q & A on Haematology for our MasterCourse in Comprehensive Diagnostics and I’m wrestling with all the conflicting ‘facts’ about the anaemia that may present alongside hypothyroidism – it has been documented and described as being macrocytic, normocytic and even microcytic… how can it possibly be so diverse I wonder and then 💡 I’m guessing the presence or absence of these parietal cell Abs likely has something to do with it!!
Anyway, it’s getting towards the end of a VeRy loooooooooooooooooooooooooooooong year…thought we could all do with a temporal tap 😉
Well, obviously(!)…this has been a year heavy on pathology interpretation for me and the huge number of practitioners who’ve just spent the last 6 months taking that learning journey with me. I celebrate and congratulate them all for their commitment to their own professional development and also their investment, in what is arguably, the most potent yet overlooked set of skills of any health professional… the ability to read bloods. Basic bloods. Mainstream labs. No…but to really read them. Backed by all the scientific understanding about what these parameters actually are, how they perform and what they (dis)prove e.g. subclinical inflammation and ramped up oxidative stress – not an informed guess but mappable…right there but where no one else can apparently see it! But I digress!
Actually what I wanted to discuss was the whole erroneous notion of ‘normal’.
No, I am not speaking from the heart about my personal quirks, sense of humour or dress sense but rather the incorrect assumption that a reference range defines ‘normal’ and that our answer for each patient and each result is, a Yes or a No!
In this brilliant article by Whyte & Kelly published in the BMJ they spell out this falsehood succinctly. They note that the term ‘normal range’ has slipped into medical language from the misunderstanding that all lab results follow a Gaussian (aka bell shaped curve & later referred to as ‘normal distribution’) pattern but many simply don’t. So for some parameters a result near the ‘middle of the reference interval’ constitutes aspirational whereas for others it spells danger. Add to this, that these reference intervals are mathematically determined to reflect the expected values of 95% of your patient population (mean +/- 2 SD either side) so…that means the chance of a YES…”Your patient’s results are ABNORMAL!”… is just 5%. And hey…who said all the values within the reference range are all equally “normal” or better yet, healthy?! Not these authors, nor I, nor the praccies who’ve just done our course. So while, in many regards, these goalposts are too wide, they are also too narrow – typically only representing a subset of adults age-wise and Caucasians, yes they are both ageist and racist (yep, I said it!). And if our practitioners have learnt anything it’s about keeping an ol’ eagle eye on the sneaky intra-individual shift! Only spotted, of course, if you know your patient’s normal (not theirs compared to anyone else…just theirs) and then spot a shift. [I can hear they’re shushing 🤫me…they’ve got it already, alright!!]
So this is music 🎻to my ears, from Whyte & Kelly: “The intraindividual variation in laboratory values is usually much smaller than the interindividual variability (ie, the variation in the population). Variation in the concentration of an analyte, if significantly outside of a patient’s usual values (but still within the reference interval), could be a sign of early or latent disease”
So if you want to tap into the power of pathology…start with Whyte & Kelly, maybe even dip your pinky in the pool by checking out Accurate Pathology Results Interpretation Starts Here – an easy little 1.5hr kickstarter…or jump right in the deep end with the rest of us pathology reading polo players and sign up for the MasterCourse 1: Comprehensive Diagnostics for some DIY summer fun 🌊
ps I know your type and know that is EXACTLY the kind of weird nerdy thing you have planned for your break…you should see my summer fun list!!! 😅
MasterCourse 1: Comprehensive Diagnostics is a self-paced online program due for release in December. The course has pver 18 hours of video presentations plus 2 free bonus sessions 1) Accurate Pathology Interpretation Starts Here and 2) Patient Pathology Manager and access to resources and tools within, for your own use. This is a pre-requisite for MasterCourse II that will be delivered live in 2021.
This skillset has been found by many to be biggest ‘game-changer’ in Integrative Health You can view the full course outline here.
When I deliver foundational nutrition training to GPs I talk tough. It’s a tough field, right? Compared with the relative certainty of pharmaceuticals, their established pharmacokinetics, their sophisticated delivery systems to ensure high bioavailability…trying to fix micronutrient deficiencies in patients can feel a lot like you’re trying to perform minor miracles. Take iron for something different, its homeostasis pivots on its tight regulation at the gut wall – and this is a wall that is very tight!! At best you get about 10% of a supplement taken up, at worst you get none and the harder you push & the higher you go with your dose…the lower the fractional uptake. Tough stuff, right?!
It’s about at this point in my talk I read their collective minds and say, “I know, you’re thinking, oral supplementation is for suckers – what about we bypass that road block and use IV?!” [Ok, I definitely use nicer words than this]
And then I put up a list of pros and cons about IV micronutrient repletion: ‘100% bioavailable’ & ‘Bypasses the body’s regulatory systems’, go on both! You see, time & time again we discover, when we think we’re outsmarting the body, it still manages to outsmart us. There are some exceptions to this – some nutrients (Vitamin C) and some contexts (late pregnancy iron deficiency) but the broader promise of ‘rapid replenishment’ for everyone, in your lunch break, via an IV infusion..is not realistic, responsible nor without risk. Don’t get me wrong, I am an advocate of appropriate IV Fe use and have encouraged a small fraction of my patients to take this path. However, given the dramatic rise in prescriptions for this since 2013, I think it’s time to stop and seriously review each element: In reality what does it achieve and in whom is it a responsible recommendation; Was a risk benefit analysis performed for & communicated to each individual & was the remaining risk mitigated?
Think anaphylaxis is the major concern? It might be the most lethal but there are more serious concerns due to higher incidence with newer preparations.
So, how well do you know your different IV iron forms, and their predilection for potential problems? And have your answers ready to all the questions raised above? In order for all involved to make an informed choice (both practitioners and patients), we must.
You’re welcome 😉 and hey welcome back to tough talkin’ Tuesday…
While rates of iron deficiency and related anaemia continue to grow, the increase in prescriptions of IV Fe have expanded exponentially in western countries. What is behind this change in practice regarding how we treat iron deficiency and does it match with responsible prescribing? Do the benefits always outweigh the risks? And while we’re on the topic, who is most likely to benefit and what are all the risks? In light of a current class action in the US, relating to a lesser talked about adverse event associated with IV Fe and recent complaints here in Australia against GPs, allegedly due to inadequate information to enable informed patient consent…it’s time to answer these questions and more. When is IV Fe a means of rescue and when is it a risky repletion strategy with no evidence of advantage?
As a health practitioner, you are always actively building: your reputation, your practice and your knowledge.There’s theoretical …and then there’s applied. Some of the biggest leaps we take forward as practitioners come with being shown how (rather than told) & then being forced to ‘do the work’ ourselves, rather than being exposed to simply more information, be that about pathology, patient prescriptions or practice structure! The slogan ‘Just Do It!’, might have already been nabbed and TMed by a huge corporate beast, but this doesn’t undo the universal truth of it! Prefer your mantras to come from mystical philosophers rather than monster multinationals? How about this then?
I hear and I forget. I see and I remember. I do and I understand. Confucius
This mentoring community that I am a part of, we are about applied learning. We learn by doing. We learn, not just through each individual’s patient encounters but through the collective clinical experience. We make what can otherwise be an isolating experience of constantly, seemingly, reinventing the wheel, if not many wheels (!), into one of collegiality and ‘using the force’. If you haven’t experienced Group Mentoring with me previously and are thinking about next year being your year (see below to find out more about our 2021 offerings), we put together this fun little video here to get across that mentoring isn’t about a conversation between just two people.
With Group Mentoring you’ll be learning, through the application of core clinical skills, improved patient questioning, methodical information gathering, evidence based answer finding & getting access to resources that you can apply in real-time in your own practice.
“Having the group session each month, as well as having Basecamp to bounce ideas around in, is a reassuring connection to know is there if I need it. Having just started practice this year and working in an environment without other Nats around, I have noticed the occasional feeling of isolation. So having the monthly catch up keeps me feeling connected to other clinicians and gives me exposure to other cases and perspectives that I wouldn’t have otherwise had.” – Georgie
We have a range of groups on offer to suit all levels and most types of integrative health modalities. Go to our Group Mentoring page to discover the groups and bonus extras on offer for 2021.
Going by the landslide registrations for 2020, our ongoing excellent retention rate of practitioners from year to year & our already overflowing waitlist for 2021, the reputation of RAN Group Mentoring is highly regarded and a popular choice.
So, if being part of our community excites you and if the thought of learning and applying collective knowledge from expertise outside of our own, now’s the time to put your hat 🎩 in the ring, put your hand up ✋🏼 & join the conversation 📣 through Group Mentoring.
We’ve been talking all about the dangers of excess fuel in our blood recently. You know, just like nature…too much fuel underfoot creates a fire hazard. So too in the bloods of our patients. The key fuels I am referring to, of course, are lipids (triglycerides & cholesterol) and glucose. Our tissues need ready access to both but Balanced Blood Supply & Mastery of Management is key.
In terms of excesses, lipids play the long-game…wreaking havoc over a long period primarily via their vulnerability to form peroxides, which in turn create a chain of oxidative stress and depletes our antioxidant artillery.
In contrast, even outside of insulin dependent diabetes, for the rest of our patients, glucose plays a fast and furious game, being a highly reactive substance capable of causing both glycation and oxidation. We describe even high-normal levels of glucose as something akin to the ‘Bull in the China Shop’, disrupting the function of the endothelial linings and damaging a variety of plasma proteins (not just haemoglobin) that float within them. But do we have a way to routinely measure the level of damage occurring in our non-diabetic but somewhat glucose intolerant patients? Sure! Just check the C-CCTV footage!
The extra C stands for ‘Carb’ and yes we can potentially check the Carb-Closed-Circuit-TV ‘tape’ in every patient.
It’s called HbA1c and measuring this provides us with an opportunity to review their personal ‘tape’ of the last 2-3 months for evidence of excesses.
Helpful, hey. But we actually have so many great tools through regular routine labs at our disposal to understand the glucose disposal or dys-disposal(!) at play in our patients! You’ve just got to know where to look (urate, triglycerides, insulin, HOMA-IR etc) and what each piece of information is telling you. We’ve had SO MUCH FUN with this particular topic in the MasterCourse this month…or is that just me 🙄 No, I know it was, because our live session chatbox was full of ‘blown brain emojis’!! 🤯🤯🤯 I can’t wait to share this course content far and wide at the end of year with those of you that missed out on attending live.
In the meantime if you want to learn more about glycation which is the new inflammation, out there in research-land, you know…the source of all evil including ageing itself(!!) then check this out…
Glycation is a normal physiological process that, just like inflammation and oxidative stress, can get out of hand, contributing to disease processes. Currently there is an explosion of correlational research suggesting relationships between higher levels of Advanced Glycation End-products (AGE) in individuals who have fertility problems, psychiatric conditions, osteoporosis, premature skin ageing, cancer…you name it! New research implicates diet heavily in the determination of individual’s levels of AGE but there is devil in the detail – there are ‘4 Ps’ of dietary AGE contribution that we need to be mindful of when we are giving dietary advice and trying to move patients towards wellness. This Update in Under 30 recording: Are You Feeling Your ‘AGE’ will open the lid on the ‘new black’ in chronic health & ageing.
My how the time just flies when you’re chasing answers from private pathology companies! As Brisbane based naturopath, Sandi Cooper, can attest to having recently been down the seemingly eternal email trail with a pathology company trying to ascertain if their urinary iodine result accounts for the concentration of the urine sample (via the iodine:creatinine) or doesn’t….because of course it can make the world 🌎 of difference. Like clarifying that someone who appears to have very little iodine in their urine, actually has a lot or vice versa! I wrote about this back when I was a mere ‘babe blogger’, more than 5 years ago. After recently reading this historical document, Sandi has been practising due diligence and checking with her providers whether they have already corrected for creatinine..or whether she needs to herself and she shared that multi-departmental epic email endurance event thread with me. The short answer? They used to and now they don’t. Why? Oh…formatting issues or something 🙄
But just in case you do want the ‘short answer’ regarding your particular pathology provider…without emailing enigmas…the answer is, in fact, in front of you & it’s Super Short!
mcg/g Vsmcg/L
If your patient’s urinary iodine result (random or 24hr) is reported using the units on the left, sometimes actually written mcg/grCR, then BiNGo! The pathology provider has done the creatinine correction for you. If they only report the urinary iodine results using the units on the right…it’s time for some maths to avoid misinterpretation. No one panic, the formula is easy: Iodine (mcg) ÷ Creatinine (mmol) X 8.85 = Corrected Iodine. So don’t lose time sending endless emails like poor Sandy or placing countless calls, like poor Nina on my team…who has to pursue pathology providers on an almost daily basis for answers to our zillions of sensible questions!! Just check the units! You’re welcome everyone 😉 oh thank you Sandi for chasing this again and sorry about needing to chase this again! 😳
And if all of this is nEWs to yOU, you might want to review what you thought you knew, about Comprehensive Thyroid Assessment too!
We can never rest when it comes to learning more about the individual nuances of our patients thyroid pictures! In this 90min recording, Rachel covers the key thyroid parameters both functional & autoimmune (TSH, T4, T3, rT3, TPO, TgAbs, TRAB). As well as the most accurate methods of assessing relevant thyroid nutrients: iodine & selenium & a genuinely game-changing insight on interpretation of these . Finally she pulls all the individual parameters together to illustrate common patterns of thyroid imbalance – making it almost as easy 1-2-3! Well, hey..it’s the thyroid…a fickle fellow.
Here’s a newsflash for absolutely no one, we’re all practising healthcare in racially diverse communities, right? Take Australia for example. At last count, at least 1 in 4 were not born here and of those who were, 3% are indigenous and many many more come from migrant families. This spells DiVeRSIty. Yet our pathology reference intervals are a whitewash, frequently derived from in-house samples that stratify by gender and age but not race, or adopted external data from predominantly Caucasian countries. Think it doesn’t matter? It does. I learnt this as (almost) always…on the ground.
I have had the privilege of mentoring health professionals in South East Asia for several years but in hindsight, I can see I was under-cooked for the role: Almost every patient these professionals discussed with me, had a vitamin D result that made me feel faint at their ‘rickets-like readings’.
“But all our patients have blood levels like this, that’s normal here”, they reassured me.
And of course, they were right.
I hit the books science databases to find out more and sure enough, new evidence has emerged of racial differences in relation to vitamin D binding and therefore definitions of ‘adequacy’ in terms of blood levels of 25(OH)D, and this has been particularly well documented amongst SE Asians Gopal-Kothandapani et al., 2019 But who of us knows this outside of that region? When we see patients of this background, are we alert to the strong genetic differences that drive different Vitamin D metabolism and therefore redefine healthy, or are we incorrectly comparing them to Caucasian Cohorts?! I have to confess in the past I’ve done the latter 🤦♀️ So what else are we over or under-diagnosing or just plain misunderstanding, in our patients who are not Caucasian? Chances are quite a lot. But the more I’ve dug into the topic, looking at racial differences in pathology markers, the more complex it gets, with plenty of conflation for example with increased rates of certain diseases. So it’s not an easy answer, granted, but that shouldn’t stop us from trying to achieve better clarity, for us and our patients.
We all pat ourselves on the back because we’re across the understanding that a healthy weight is defined differently depending on your racial background, we’ve nailed (hopefully!) the whole ‘healthy BMI < 23 in Asian populations and the smaller WC cutoffs’…but really…there’s so much more that needs to be done.
Want to be on the front foot with critical pathology interpretation? Join the club!
There is such a groundswell of naturopaths, nutritionists, physical therapists etc working in integrative health that are ‘lab literate’. It appears to be a combination of both a choice and consumer expectation. With patients thinking, surely, we can make sense of those numbers on the page that remain a mystery to the patient…and tbh to some doctors!? We should. We’re currently halfway through our 6 month long MasterCourse in Comprehensive Diagnostics which is custom-built for this context. It has been incredibly well attended and well-received to date and we’re excited about the amazing content that Rachel has had to redevelop along the way. If you missed out on the actual live classroom experience…your chance is coming soon. Promise. Your DIY Diagnostics version will be released at the end of this year. Let us know if you’re keen by sending an email to [email protected], and we’ll put you on the ‘first to know’ list.
I think I’m finally able to put my ‘late-90s-Creatine-frontline-trauma’ behind me. Back then, like many good nats in training, I was working the trenches of the health food stores and was faced on a daily basis with two types of men with two types of Creatine questions. The first type was scrawny and would ask, ‘will taking this help me build muscle?’, the second, built like the proverbial brick *&#@ house, asking, ‘will it help me build more muscle?’ Cue, eye roll. Come on… any of you current or ex apothecaries, pharmacy or retail assistants…you know exactly what I’m talking about!!! So deep was this trauma that I put Creatine as a supplement, into the ‘strictly sports folder’ in my brain (the bit in the deep dark back with other rarely accessed items) and never gave it much thought when I left retail and moved exclusively into private practice. Even back when I was a sub-editor for the Braun and Cohen 4th edition, it was apparently still too soon.
A great colleague of mine, Emily Bradley, had written the chapter on Creatine and, in doing so, presented compelling case to reconsider this supplement as offering great therapeutic potential well outside of the sports-field. That one was accidental 😂
I actually remember reading that chapter, especially the sections on Creatine supplementation for neurological & psychiatric conditions and thinking….WOW…who knew?! ??!! Well, clearly Emily for one 🙄 and also every author and researcher whose work she had read…so that made quite a lot of people actually! But another [ahem 😳] several years had to pass before the research into Creatine and the argument that this has been a grossly over-looked CAM option in mental health, beat down my door and finally got my full attention. Better late than never. And boy, do we all have some catching up to do!
Let’s start with 5 fun facts: 1. Creatine is critical for energy – like cellular currency it ‘tops’ back up our funds, after increased spending, everywhere, including the brain 2. The Brain consumes >20% of our resting energy expenditure & is fifth on the organ list in terms of highest concentration of this molecule 3. Creatine CNS depletion is a thing – and it happens in a wide variety of scenarios – from the seemingly benign (like chronic sleep deprivation) to the more sinister (neurodegeneration) 4. This then leads to higher Glutamate, Oxidative Stress & a spell of other sorts of ‘brain badness’ 5. Oral supplementation can cross the BBB and ‘refuel’ the brain and correct the Creatine deficit
Out of the thousand or so pages of research on this topic, I’ve just indulged in, there are several great reviews to pick from…it’s a tough call to make but perhaps this older one by Patricia Allen remains my favourite. This marks the beginning of a new era…I’m putting the trauma behind me & moving on & hope you’ll come along too!
When we recap the contemporary science of shared pathophysiology in mental health, we have: oxidative stress, impaired neurogenesis, monoamine deficits, glutamate excess, hypometabolism & mitochondrial dysfunction. When we ask researchers which of these supplemental Creatine might be able to assist with, we get hits at each and every point. Turns out, Creatine’s capacity for enhancing performance is not limited to athletes but can be capitalised on for anyone vulnerable to a CNS shortfall. Ignored for far too long, this economic and impactful brain nutrient is coming to the fore for psychiatric and neurological disorders.
The latest Update in Under 30 has landed!!!
You can purchase Creatine – The Brain Builder Part 1here.
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.
No doubt you’ve heard me refer to the thyroid Abs by their nicknames, TRAb is one I mention often, or Thyroid Receptor Antibody, as its mum calls it, when it’s in trouble. And it’s always in trouble! But TRAb is actually the collective name for several flavours of trouble. What these auto-antibodies share in common is the ability to bind the TSH receptors throughout the body. They differ however, in terms of whether, once engaged, they stimulate this receptor (mimicking the action of the real-deal TSH) or they block it, so that the real-deal can’t in fact dock and do its job. The contrasting consequence is clear: stimulating ones drive up thyroid hormone production, while the blocking variety contribute to low thyroid hormone levels – and what was meaningful was each patients (im)balance of the two to produce a net effect. Because yes…a proportion of patients make both.
In Australia, and many other countries, we previously measured TRAb as a sum total and then specified what fraction was each ‘flavour’ but then the ‘flavours went out of favour’!
So for a long time now, TRAb has been measured, undifferentiated, and the assumption is, they’re stimulating…because this is in fact a) more common and b) the most common reason this test would be referred for…a set of TFTs that look suspiciously on the high-side aka Grave’s disease.
But a new era has dawned, with many mainstream laboratories now opting for the more specific assay: Thyroid Stimulating Immunoglobulins (TSI)* over the old TRAb. Fancy schmanzy, I know. Considered more accurate in the detection of autoimmune hyperthyroidism and in this regard, we’re told we’ve made a diagnostic step forward and nothing has been lost. Except the much less common type of antibodies that bind the TSH receptor only to fill it full of gum so it won’t work. That apparently, due to its low incidence and reduced clinical impact is no longer something worth testing. So consider the TSI results for your patients, the new version of your old (drab) TRAb, with similar cut-offs etc. And remember detectable levels of this may be seen in toxic nodules, and acute toxic Hashimoto’s, as well as prodromal and active Grave’s disease.
AND DON’T FORGET
(and yes, I am screaming because it is so easy to forget!!)
Biotin!! Patients on biotin at the time of the test (even as little as 1mg as part of a formula) can produce False Positives for the TSI!!! And give you and your patient the ‘fright of your life’ with a pseudo hyperthyroid set of labs to match!
Need to read more on this because you’re left thinking WTF about the TSI?!@#%^ Check out Mayo Medical Labs (always a good go-to for info on pathology) or this recent review paper 🙂
*Note TSI does not stand for Turbo fuel stratified injection in this scenario!!
Want to learn all the thyroid antibody alphabet??!! Start Here!
Learn the ropes of Thyroid Dysfunction Assessment & Identification, including all the related thyro-nutrition! Rachel covers the key thyroid parameters both functional & autoimmune (TSH, T4, T3, rT3, TPO, TgAbs, TRAB). As well as the most accurate methods of assessing relevant thyroid nutrients: iodine & selenium & a genuinely game-changing insight on interpretation of these . Finally she pulls all the individual parameters together to illustrate common patterns of thyroid imbalance – making it as easy 1-2-3!…almost!
Recently a mentee reported that when attending an in-person training event (remember those, everyone?!) she approached a sponsor’s stand, promoting practitioner training in the nutritional management of mental health, based on the pioneering work of American scientist, Carl Pfeiffer. But when she and her nat buddy started asking questions, those manning the stand asked whether they were doctors and then, upon finding out they were naturopaths, encouraged them ‘to move along – this information isn’t for you then’. Or something to that effect…Ouch!
While I know a little about the decision behind offering this training only to doctors and specialists at this time, and I do understand that organisation’s reasoning, I also want to reassure you, this doesn’t mean that Pfeiffer’s important work, and the efforts of those that have followed him, is out of bounds to others.
No one can copyright cortisol or TM TSH, right? Equally, Histamine is his own man. Carl Pfeiffer and others brought histamine, the neurotransmitter to centre stage and many of us working in mental health remain eternally grateful for this. But CNS histamine has come a long way since then…and is currently a very hot topic in modern molecular psychiatry where they are always looking for new drug targets, given shooting at the previous ones, risked taking ‘an eye out’! The recognition of histamine as a key player in mood, cognitive and behaviour has been long overdue but is absolutely here now! Just give this search term a whirl in PubMed: histamine AND psychiatry, and you’ll be hit with quite the crush of citations!
An abundance of important info at your fingertips…no secret handshake required.
It was, in part, this story that inspired me to record an Update in Under 30 on Histamine Imbalance in Mental Health. Just the proverbial straw on the proverbial camel really, after years of examining, experimenting and experiencing the incredible results some patients can achieve when this imbalance is identified and redressed. So I’ve done my darndest to pull together those years of hands-on helping histamine imbalanced patients with the latest literature in under 30 minutes!! Surprise! I failed!There is a lot to convey but you’ll also be surprised by what I don’t say…there’s no infinitely long list of personality peculiarities that fit with too much or too little. Nor is there a didactic discourse about absolute treatment dos and don’ts. I’m communicating the common ground between the original evidence, clinical empiricism and contemporary neuroscience. So this month, consider the ‘under 30’ bit, merely a ‘Serving suggestion’…which would necessitate you playing it 1.5 X speed…go on, I dare you!!😅
About 15 years ago I was introduced to Histamine as a neurotransmitter. Not the allergy mediator or the ‘basophil baddy’ but rather this prolific and potent neurochemical we all produce in our brains which, in the right amount, regulates almost every biological rhythm, helps with memory and mood & much more. Being able to recognise excesses or deficiencies of CNS histamine in mental health presentations and, ever since then, fine-tuning my ability to support patients with these, has changed my practise forever and has been the key to some of my patients’ greatest recovery stories. Forever grateful to the pioneers of this model, 70 years on, the model is ready for a mini-makeover, to bring it in line with the current scientific understanding of histamine, methylation, genes and much more. This recording, together with a hugely helpful clinical resource, will give you the confidence to recognise and remedy this important imbalance in mental health. If you want to download this recording click here.
I’ve a confession to make, I took the batteries out of our smoke detector in our kitchen. Why? You know why. Because it went off all the time, with what I like to call, friendly fires…you know, heating oil for poppadoms, a rush of steam upwards from a hot pot on the stove with its lid removed, gosh even toasting your bread a little too vigorously would do it! Taking the batteries out, stopped the alarming alarm (!) and quelled my need to always keep a tall stool and ‘whooshing’ implement nearby, in preparedness for the next smoke activated siren. But of course this is not a solution. There are consequences.
I recently realised this was the best analogy I had for many patients who have experienced significant trauma. Particularly when this trauma has occurred during childhood, there is potential that they too have effectively ‘taken the batteries out of the ‘smoke alarms’
This has been documented in a proportion of individuals affected with PTSD for example and is believed to be due to the ‘re-calibration’ or ‘rewiring’ of their HPA axis in response to excess ‘over-activation’. So because their internal ‘alarm system’ had been so consistently activated, the chronic hypercortisolism evokes a down-regulation of their glucocorticoid receptors, as a means to ‘turning down the volume’ or…removing the batteries. Let’s think about this. If your patient has, let’s say, 5 receptors for cortisol compared with 50, their receptors will be ‘filled’ quickly with only minimal amounts of cortisol. This receptor ‘fullness’ however is detected by the brain which in turn then shuts off the ACTH release. But really there was only a small amount of cortisol. The threshold for the negative feedback inhibition (cortisol –> no more cortisol) is very low and patients can end up with too little. Wouldn’t they have less stress, then, feel better then?
In spite of all the name-calling Cortisol is not the criminal he’s been made out to be.
Cortisol ≠ Stress.
Cortisol in fact offers a way out of stress – the means to physically resolve the stressor. So too little…feels awful.
Patients of mine who have been shown to be affected by this hypocortisolism present as extremely anxious with poor stress tolerance, in fact if I didn’t know differently, I would have imagined they had ‘over-activation’ of their SNS not under. When I speak with them I try to find different ways to describe why this down-regulation of their HPA can contribute to their mental health challenges. I talk about Cortisol being akin to clothes…no one wants to leave the house without it, or a raincoat that we really need because one day inevitably its going to rain and we’re going to be out in it…its protective. But from now on I think I might confess about my battery-less smoke alarms. Yes I can cook toast without getting startled by screeching sirens now…but I could also burn down my house…which clearly doesn’t rid me of stress and anxiety…
Anxiety, high stress, poor sleep – it all sounds like high cortisol right? But did you know that these are all features of abnormally low cortisol as well, which underscores why accurate adrenal assessment is so important. This Premium Audio takes you through all the investigations you have at your hands, from clinical markers (Pupil response, Rogoff’s sign etc.) to the strengths and weaknesses of blood, urine and saliva assessment. It identifies the variables you need to consider and how to accurately interpret your patients’ findings.
If you’re already an Update in Under 30 Subscriber – you’ve got this! Just log on and go to your Active Content. If you’re not and would like to download this recording and resource then click here!
We’re midway through mentoring 2020 and we’ve temporarily shifted gear out of case presentations and into dedicated time for answering praccies toughest questions…and oh man, I love these opportunities! This year in our Mental Health Primer Group, there are clinicians whose questioning…nEVeR sTOps. [insert: excited squeal] and that means I have an excuse to dig deeper, go further, read more research and ensure I can provide answers confident of their comprehensiveness and that they reflect all the contemporary information to date. So amongst stiff competition – here’s my favourite from the gIAnT piLE on my desk right now…
“We often hear that the bulk of our body’s serotonin is in our platelets – so do platelets (counts, activity etc) have a role in mental health?”
Well, I’m so glad you asked! Yes, 99% of your body’s serotonin is found inside your platelets. Where did this come from? From the plasma. How did it get there? Using the identical transporter mechanisms that your neurons do. Sounds like all the pieces fit right…oooooh so low platelets might drive low serotonin and poor mood and and and…
No. You may get excited when you get a box of jigsaw pieces but you must first complete the puzzle and ensure everything is in its rightful place.
Platelets are linked to depression but not as a cause but as a consequence. Because their transporter systems & receptors for serotonin are virtually identical to those in the CNS, they suffer from the same serotonin deficit…in spite of a relative abundance in the plasma they’re floating in. So really platelets are of interest in mental health as a more accessible way of studying and understanding neurochemical regulation in the brains of those affected. Did she just say neurochemicalS…as in, plural. I sure did. Because healthy platelets contain a whole plethora of substances, even a relatively large quantity BDNF, the concentration of which also becomes severely compromised in the platelets of depressed individuals. So it seems like its tough-talkin’ Tuesday and just to bust a few more moves myths while we’re here…
Your platelets get their 5HT from the plasma
Your neurons make it themselves
Platelet numbers are not indicative of your 5HT producing capacity…anywhere
Therefore treatment objectives that speak to platelet numbers or platelet activity are clearly non-sensical A bit like measuring serotonin derivatives in your urine…and imagining that reflects the <1% from your CNS….hey?
Don’t be fooled by the false promises of functional tests. Make sure all the pieces of the puzzle fit to actually make something sensible, accurate, reproducible and meaningful. Mainstream pathology results actually offer a goldmine of information and insight about your patients However to realise their full value and make the most accurate interpretations we need to first learn more about ‘lab language’, upskill in finding our way around reports which are packed with a surprising amount of hidden extras, demystify reference ranges and then develop a logical critical process we can apply to every result of any patient to get the real take-home. Packaged with numerous specifically developed resources to aid in your application of these skills this is a foundational offering that changes practices.
Now find a comfy spot everyone & I’ll tell you a story…’Once upon a time, a long long time ago, we lived our days out in the dark, regarding potential calcium dysregulation!’But ever since serum Calcium has become a standard lab included in most routine screening tests (General Chemistry aka ELFTs) abnormal calcium handling is no longer an ambush for patients of ‘stones, moans and abdominal groans’, as the saying goes in hyperaparthyroidism. A diagnosis historically only mad, when someone presented with this constellation of rather advanced symptoms. But actually being able to identify your patients’ typical blood calcium levels offer us so much more than just a heads-up re parathyroid disease
It may tell us something about their Magnesium status, cardio cautions, be a bit of ‘bone barometer’ and probably most immediately important, flag their suitability for calcium supplementation!
Yep…rather than the current-criminally-crude-calcium-checklist: 1. Patient is female 2. Patient probably doesn’t consume enough calcium 3. Patient may be at risk of osteoporosis (yup…that accounts for practically every woman, right there!)
But seriously, if you just do a full review of the vast literature on this topic, what?! Not enough time?! How about then, just skim read a couple of key papers? Still baulking at that?…maybe just a wafer-thing editorial (??!) will tell you that, consuming elemental amounts of calcium (> 250mg), that are beyond even the biggest Dairy Diva’s Diet Diary, may be deeply problematic for many. And guess what…this doesn’t pertain to supplements alone…even calcium fortified foods are not free from concern! But let’s not let yet throw all our calcium fortified foods in the same bin as the folate ones we did a while ago!! Let’s step out of the dark and into the light that shines upon us, care of fasting serum Calcium measurements, to help us recognise whether Calcium is the cause, the consequence, a cure or a curse for person sitting in front of you 🧐
The Calcium ConspiracyControversy Continued
The Calcium Conspiracy arises primarily from misperceptions about it being ‘the boss of bones’ but becomes more of a controversy when in spite of ongoing advice for broad-scale use we review the evidence and have to acknowledge that the recommendation to supplement post-menopausal women with large doses of Calcium, not only lacks strong evidence but may cause harm to some. In this detailed discussion of the two schools of thought – Rachel finds a position somewhere in between. Reinforcing the need for an individualised approach and personalised risk benefit analysis while teaching you how to undertake this in every client.
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Gotta love all the clever inquisitive minds among our integrative health practitioner community. I think each of us, as children may have been that one kid who just never stopped asking questions. What a great quality to have because it prompts us to think outside the box, then outside the triangle, then the hexagon and beyond! Simultaneously, busy minds that never stop questioning and never quiet down can also feel like a curse! None of us have the time to go find the answer independently to every single question that our patient, prescription & pathology encounters raise for us. We need to use the force. Our colleagues, our workmates, our informal and formal practitioner networks, our mentors, our associations, our educators etc.A lot of practitioners recently got some questions answered with the Update in Under 30: Separating the B12 from the B*S#!...and then guess what…they had some more B12 related questions 😂😂
Q: What might a normal or even high serum B12 together with low Active B12 combination flag in a patient?
A: Exclude COCP use, & gross liver pathology, refer for B12 antibodies if possible & review the case for other evidence of functional B12 deficiency, as TCII values are more specific and sensitive than serum
Q: What evidence do we have to use a higher cut-off value than the labs give us for Serum B12 (< 400 pmol/L), as a decision limit for follow-up investigation for B12 deficiency
A: Just the findings of some of the biggest studies on B12 assessment – correlating serum values and markers of functional deficiency such as Harrington et al 2017, Spence et al 2016, which flag that there is already metabolic impairment typically when serum values drop below 400, well before the classic features such as macrocytic anaemia
You’re welcome 🙂 It’s nice to be surrounded by like-minded curious kids (disguised in big people’s bodies!) I love playing my part in adding to the collective knowledge in different ways and for those of you who are our Update in Under 30 subscribers, and of course anyone that purchased this as a single download, well we’ve gone that extra step and put together a nice little pdf: A B 12 Assessment Decision Tree for you and added that in as a bonus to your Separating the B12 from the B*S#! episode. So go take a look now and hopefully that answers just a couple more questions and we can all have at least 1 good night’s sleep… before you come back with more 😉 🧐 😂
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.
And now a new one to boot!!
________
You can purchase Separating the B12 from the B*S#!here
If you are an Update in Under 30 Subscriber, you will find the new resource 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 guys know I can’t help myself. For the last year or so I’ve been immersed in developing and redeveloping and redeveloping 🤓 [ahem apologies to my team!!] teaching tools for all practitioners to better understand what the routine renal markers can offer us in terms of understanding our patients…and it is far above and beyond renal function, promise. Just one example of this, is the sophisticated yet incredibly simple urea to creatinine ratio calculation that I was originally taught by Professor Mel Sydney-Smith. In adults with preserved renal function, this is the key to the kingdom, in terms of being able to objectively quantify whether patients are truly meeting their own individualised protein requirements. The Marvellous Mel (well he is, who can argue with that?!) added this one to my toolkit a long long time ago and in turn, I’ve been using it and spruiking it ever since.
In fact, I just lost 30 mins of my life listening to myself (ewww) in an old Update in Under 30 from 2013 that I recorded on this very topic.
[Sigh] I sounded so youthful…and…about 7 years younger too in terms of experience with this crafty calculation in the hundreds of labs I have encountered since!
My reliance on this ratio has remained but my wisdom regarding how to apply it has widened….and so, as I prepare to initiate another hundred or so practitioners into this secret sect 😉 via our current MasterCourse in Comprehensive Diagnostics, I couldn’t help myself and decided to re-record this UU30 episode: Using Urea & Creatinine as Markers of Protein Adequacy and also throw in a new pdf resource to boot [once again, ahem,apologies to my team!!] You see our ability to identify protein adequacy without this tool relies on the rather-rudimentary-‘rule’ that your protein requirements increase linearly with your weight…that’s the whole g/kg body weight thingo, right? But what if your weight gain is ‘all adipose’ Vs ‘mega muscle’ – are the protein requirements really the same for both people? Absolutely, not! This calculation enables us to step away from the rough approximation of the RDI and be able to determine if each individual is meeting their genuine requirements as driven by their own unique muscle mass hunger…oh and it reveals a few other very helpful things along the way to boot!
But this simple calculation comes with some caveats: 1. there are people and presentations in whom this calculation is not appropriate or accurate 2. because there are no magic numbers, right, it is about matching your labs with the patient in front of you and 3. looking (as always) for patterns.
…and a word of warning to the uninitiated: You’re going to love it!
So for those of you who are already Update in Under 30 Subscribers…happy Wednesday! Because you always benefit from any updated recordings etc. you’ll find this rejigged resource is already in your Active Content and for those of you who may have purchased this as an individual recording in the past, the same applies. And for anyone else keen to make some real meaning out of the most routine labs we see over and over again, and understand a whole world more about what they tell us about our patients’ muscle mass health, trajectory and the dietary protein piece of this puzzle…you might want to check this out too! And for those of you who think ‘total protein’ on a patient’s blood test results reflects ‘total protein’…boy have I got news for you!!
This comprehensive analysis of two standard indicators, urea and creatinine, that are often part of the patient’s standard blood chemistry tests. These commonly available results can provide insight into protein ingestion and uptake as well as muscle mass and, in extreme cases, kidney and liver function.
I don’t know about you but I don’t count myself among the conspiracy theorists. While I may have been partial to the occasional one over my lifetime, you have my word, I never inhaled. Or at least not since I learned the practise of scientific enquiry and the application of critical thinking to all evidence. The two together tend to put a dampener on the whole: earth is flat & the moon-landing was a hoax…kind of notions. But there is one conspiracy I think all of us in nutritional medicine have been the victim of: The Calcium Conspiracy.
Not in the vein of speculations regarding excessive lobbying & undue influence of the Dairy Corporation on dietary guidelines. Nor even arguments that this has gone so far as to inflate the RDIs for this nutrient. Nope, I am actually good with the RDIs for this mineral. High level evidence confirms that our intake of Calcium was enormous even before the Agricultural Revolution, and therefore BD (Before Dairy) 😂
Man, those roots and tubers and other bushfoods sure were nutrient dense, not like the stuff we consume these days!
No, the Calcium Conspiracy we’ve all been lead to believe is that it is the boss. The boss of bones. The boss of the parathyroid. The boss of the other minerals. And especially the boss of Magnesium. While you might have heard me describe Calcium as a ‘bully’ in the GIT (let’s call this the slide 😅) and I stand by that, it is far from being the boss of the rest of the playground! In fact its regulation is largely at the hands of other nutrients..not naming any names…[Magnesium😳] So while, all of us trained in nutrition have had the significance of the Calcium-Magnesium relationship & the mantra “2:1, 2:1, 2:1” drilled into us, which we repeat at night to get ourselves to sleep (or did they mean to take not just ‘talk’ these minerals, to help with sleep?!) Our teaching created this conspiracy – a misperception that Calcium is the boss and Magnesium its long-forgotten lackey. Well guess who’s really calling the shots and on whom?!
Have you ever heard the saying, ‘It can take Magnesium to fix a Calcium problem”? I’ve not just heard it but seen it many, many times in my patients.
But how do you tell which patients need both and which ones, just one? It comes down to understanding the exquisitely sophisticated way Magnesium lords it over Calcium – via the parathyroid and Vitamin D metabolism and how we can see this patently in the pathology (regular screening labs) of your clients. I think there is a bias in integrative nutrition – we favour Magnesium – it goes into our supplement recommendations for so many of our patients and while the rationale for this is valid – all dietary surveys show magnesium under-consumption to be rampant in the SAD – I don’t actually think all of us know 1) how much we should be giving (yes there is a limit) 2) how to discern who needs what, in spite of a lack of a good Magnesium assay and 3) the true potency in the prescription when we get these things right or wrong! This study by Sahota et al is so far my favourite for 2020..it’s 14 years old and the sample size is small but its methodology and examination of when Magnesium can fix a Calcium issue and when it can’t, is superb. Together with about 50 other papers I’ve just imbibed…they’ve refined my thinking, tremendously. There’s a Calcium Conspiracy, alright, but just throwing Magnesium at everyone in arbitrary doses is not the solution…. “2:1, 2:1, 2:1…..”😴
There’s a conspiracy going on regarding Calcium but it’s probably not the one you imagine. We have been lead to believe that Calcium is the boss: the boss of the bones, of the other minerals and certainly of its often over-looked lackey, Magnesium. But the truth is, we have it all the wrong way round. There is a sophisticated synergism between these two minerals but the brains and the brawn in this relationship are held by the latter and we need to understand how to recognise when Magnesium is ‘pulling the strings’, to produce low calcium, in our patients and how to find the sweet spot of their synergy. This recording comes with a great resource to use in your clinic, with explicit redefinition of ‘what healthy looks like’.
A 26 year old woman suffering years of fatigue from ‘persistent iron and B12 deficiency’ repetitively treated with both oral and IV, walks into a compounding chemist and finally meets her match 🐱🏍 A naturopath with years of experience working the frontline, used to dispensing iron galore (& to a lesser extent B12) to young women with similar stories. But this naturopath requests to see all her labs, she meticulously collates them and then she comes back to the client and deals the fatal blow: Has the iron or B12 ever made you feel any better? “No,” she replies.
“I didn’t think so,” says the Naturopath…”everyone’s been barking up the wrong tree all these years!” And she was right.
First glance at her blood results has all of us reflexively reaching for the same diagnosis everyone has made before – crikey that serum B12 is terrible! And then there’s the fuzzy family history of relations ‘needing’ B12 injections and some even with confirmed pernicious anaemia. But wait up…let’s keep our critical thinking hats on once you look over the rest of the lab you see there’s no evidence of functional B12 deficiency (no rise in Hcy, MCV even RDW) and then, the statement that seals the deal, ‘B12 injections have never made me feel any better’. This woman is not feeling the pinch of pernicious anaemia, not the crush of cobalamin clinical deficiency. In spite of being told that for almost a decade.
A low serum B12 value can of course flag a deficiency and we must never ignore it. But given the serum measures, in fact, predominantly Transcobalamin I (TCI), which is the carrier or taxi for B12 that almost ‘never drops its passengers off’, we are less concerned than when we see a low active B12 (TCII aka ‘the real deal’)
So what else could leave someone with less TCI, while not in fact creating a genuine functional deficit of B12? SNPs?🤧 Bless you!…Sorry that sounded like a sneeze and this retort, as we know is almost as common as the common cold! Sure…of course it could be sexy SNPs…but wait, what about something a little less ‘zebra’…a little more horse. The COCP…oh blooming heck..she’s spent the last decade on the COCP and guess what, its impact on B12 is thought to be principally a reduction in TCI! Oh and that iron story, that supposed ‘iron hunger’ we can see with her upregulation of transferrin? Well that’s an artefact of the COCP too, right? And BINGO was her name-O 🕵️♀️
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.
I used to all the time. Especially when I noticed the Niagara-falls-sized gap between the doses I was using compared with my mainstream medico mates. I thought, hang on, for a patient with a baseline blood level of 40nmol/L, they’re recommending <1000 IU per day, but I’m thinking 5000 IU…which one of us is wrong? Then again, we might both be right!
The sexily simple formula as cited byAussie researchersis: for every 1,000 IU of vitamin D a patient takes a day, their blood level is likely to rise approx. 17 nmol/L over 2 months, at which point it plateaus. So the medicos’ 1,000 IU supplement would bring our patient’s blood level up to 57 nmol/L which, as far as the medico might be concerned, is ‘job done’ 👍👏
My dose would be viewed as excessive but clearly I am aiming for a different set of goals (optimal rather than simple prevention of deficiency)…oh and I insist on follow up testing to know when we’ve made it!!
I encourage my patients to get their Vitamin D retested 2 months into treatment to confirm 1) they have responded and 2) their response is loosely within this predicted performance. And how many times is it not? Often. Which got me to readjust the formula I use to something more akin to: for every 10 nmol I want their blood levels to rise, I will need to increase their intake by a 1,000 IU. Now am I just making big sweeping inferences from empirical experiences of a few (hundred) patients without additional backing….well so what if I was...this is a branch of the EBM family tree! But no! I have also actually read enough studies clearly documenting the individualistic response to vitamin D, as a consequence of different adiposity levels, genes, magnesium status etc. to know that, while I am very grateful to have any kind of formula to start my thinking from…I treat individuals and goshdangit#@! they keep insisting on individualised medicine!
The whole practise of identifying a deficiency, ‘treating it’ and yet never following up with repeat labs to confirm that you actually have…BLOWS MY MIND🤯
That’s not EBM, let’s face it. Not even a distant demented cousin who has fallen from the dizzying heights of that family tree.
The one lesson I’ve learned, more than any other over 20 years in nutritional medicine, is that the more questions we ask and the more we challenge ‘established truths’, the more we uncover something much more personalised and potent about each and every nutrient …and now as the days continue to shorten into smaller and smaller slithers of sunlight between ‘bed-ends’, this is probably also a good time to ask ourselves…
Vitamin D deficiency has been associated with a long list of major health conditions: from autoimmunity to mental health & almost everything in between. This has lead to many of us recommending high dose vitamin D supplementation for a large proportion of our patients but do we understand everything we need to to be certain of the merits and safety of this? In this provocative episode Rachel outlines the key unresolved vitamin D dilemmas that should encourage us to exercise caution and outlines how adequate sun exposure is associated with improved health outcomes independent of the production & action of vitamin D.
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🍌‘I think I am, B2! It’s time to separate the B12 from the B*S#!’
Ok, if you’re reading this and you’re not from around here you have reasonable grounds to conclude I’m the one who’s gone 🍌 but if you grew up with a show all about 2 adults dressed up as bananas and creatively known as B1 and B2, then we’re all good! Ok now for the next bit, you might need to sit down. Nothing not everything in the wildly popular, and dare I say it populist, doco The Game Changers was scientifically rigorous. I know, I’m loving the strike through a little too much today.
Goodness, when otherwise intelligent friends of mine forced me to watch this, they found the need for both restraints and duct tape over my mouth, to hear or see anything other than me jumping up and down, arms flapping, mouth yapping. People only tend to make this mistake with me once.
Among the many many dubious XXX was a terrible mis-truth about our ‘new modern reliance on animal food or supplements for B12’. Woah…back up there Game Changers Gang, say what?! Does anyone on their research team read any research? So that got me all motivated to go back to the books on our beloved B12, which is simply like no other micronutrient in human physiology or in nature, for many reasons…starting with 1) it contains a metal in the middle 2) it has dietary dopplegangers (plant forms that look just like it but actually are decoys that need to be actively removed from the body so as not to block its actions) and 3) has the most complex and sophisticated pathway for digestion and absorption, which surprising equates to brilliant average bioavailability (much better than most micronutrients)…until it doesn’t! And that’s when the trouble starts. Once you don’t have an intact IF absorption pathway, you’re down to picking up < 1% via simple diffusion, and suddenly we see why patients can be vulnerable to not meeting even the piddly required amount. Not to mention the vegans, of course.I’m on my best behaviour.
But the B*S#! about B12 is far from limited to the documentary. It’s in the words of the Methylation Mystics, making methylation sound like rocket science and in the supplements we’re being sold.
But don’t get me wrong…effective B12 treatment in the right patient is a total wow moment. I’ve literally seen all the lights go on⚡ in some . So what do we need to do to find our way out of the dark? Go back to the solid science. Come on. There’s nothing else you need to do and nowhere else you need to be… we all know it…so start by reading this and this. There’s plenty more of course but these are excellent appetisers. And if you want to cut to the chase and get the lowdown on what’s B*S#! versus what’s the real magic of B12, you can always settle in and listen to my latest Update in Under 30 – complete with a very cool clinical tool to help you choose the best B12 for each individual, but spoiler alert, it ain’t rocket science.🤫
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 very handy clinical tool
The latest Update in Under 30 has landed!!!
You can purchase April’s episode, Separating the B12 from the B*S#! is here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
A 26 year old woman suffering years of fatigue from ‘persistent iron and B12 deficiency’ repetitively treated with both oral and IV, walks into a compounding chemist and finally meets her match 🐱🏍 A naturopath with years of experience working the frontline, used to dispensing iron galore (& to a lesser extent B12) to young women with similar stories. But this naturopath requests to see all her labs, she meticulously collates them and then she comes back to the client and deals the fatal blow: Has the iron or B12 ever made you feel any better? “No,” she replies. 
