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!
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 firstname.lastname@example.org, and we’ll put you on the ‘first to know’ list.
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.
The latest Update in Under 30 has landed!!!
You can purchase The Calcium Conspiracy Continued 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.
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.
Have you been told somewhere by someone that the ‘perfect’ TSH is 1.5 mIU/L? This is a wonderful, terrible & wonderfully terrible example of ‘magical numbers medicine’. As a push-back against the published reference ranges we’re given, that are so wide you could drive a truck through them, there has been an over-correction by some, leading to the myth of ‘magic numbers’. We can narrow the reference range substantially for many parameters with good rationale, make no mistake about that but once we start setting ‘aspirational goals’ that are explicitly rigid…well we’ve done 2 things 1) forgotten about the patient to whom this result belongs and 2) disregarded viewing each result as part of a ‘pattern’, that we must piece together and make sense of.
Back to TSH then… if my obese patient had a value of 1.5 mIU/L this in fact would be woefully inadequate.
Also too low for any patient, no matter their size, if their T4 is low and we’d like a higher value as well for risk minimisation in our elderly clients too.
But the same result would be excessively & worringly high in my patient who’s undergone thyroidectomy.
Being given a list of ‘magic numbers’ will never replace learning labs correctly. When we do this, we come to truly know that meaning can only be made of the markers when you can answer the following questions:
What is this (metabolite, analyte, binding agent, plasma protein etc)?
What do I know about its physiological and biochemical context – what is its role and regulation in the blood, what moves it and to what magnitude?
How have the reference ranges been determined for this lab – who am I comparing my patient to?
Therefore, what is the significance of a result that is: ‘normal’, ‘low normal’, ‘high normal’, below or above the range?
Does this value ‘fit’ with my patient?
What else could explain an unexpected result?
How strong is my level of evidence?
What do I need to do from here to confirm or refute this?
And a few more 😉
Realising the full value of any test result in terms of what it reveals about the person sitting in front of you, requires these skills. Unfortunately, in contrast a list of magic numbers will often lead you astray. And building your scientific knowledge about labs will not only help you avoid the pitfalls of pathology but will strengthen your pathophysiology prowess in surprising ways, saving your patients a packet in terms of additional extraneous testing and help you truly personalise your prescriptions…because the ‘invisible (biochemical individuality, oxidative stress, genetic probabilities, subclinical states, imbalanced or burdened processes etc) just became visible’. I started requesting lab results early in my career and years later was lucky enough to be taken under the wing of Dr. Tini Gruner. I found some of our shared notes, from 10 years ago, scribbled all over patient results recently and I was struck by just how lucky I was to have her encouragement to really pursue my interest and how she was a guiding force about learning to recognise pathology patterns over single parameters. A decade on I can confess, much of clinical and educative success has come off the back of this foundational skill-set and I know, this is true for so many I’ve taught too.
“The guidance I’ve received over the years from Rachel in relation to pathology interpretation has been one of the most valuable (and fascinating) investments I’ve made as a clinician. Her teachings have filled gaps in my knowledge base I never knew needed filling and have significantly enhanced my understanding of the inner workings of the body! Rachel has an incredible ability to make the numbers that patient’s so often present us with, both understandable and clinically meaningful. The knowledge I’ve gained by investing in this skillset has paid off in dividends and I’m certain will continue to do so into the future.”
Stacey Curcio – Cultivating Wellness
I hope you’ll join me for the most exciting up-skilling opportunity in learning labs yet. Oh…and all this talk about thyroid testing..that’s just a serving suggestion 😉 this year my MasterCourse is focused on the most routine labs of all: ELFTs, FBE, WCC, Lipid and Glucose Panels…an absolute treasure trove of free integrative health information about your patient!
This skillset has been found by many to be biggest ‘game-changer’ in Integrative Medicine!
There are limited places. To sign up for the MasterCourse: Comprehensive Diagnostics click here. For more information about the program click here.
What does lockdown look like for you? More time spent…
A) Learning or B) Losing sleep over things outside of our control or C) Losing days just watching Tik Tok
I’m choosing ‘A’ and I know I’m keeping good company because last week many of my ‘nearest and dearest’ gathered on 2 occasions for some serious extra brain gym. The first was the ACNEM Fellowship Community of Practice that I had the privilege to co-chair with Dr. William Ferguson. A fantastic new initiative by @ACNEM to offer more hands-on mentoring and support to their doctors.
The second, our own Give-back-Gratitude Live Q & A for our Update in Under 30 Subscribers where I used the time to check-in and see if we could further the learning offered by our monthly audios and clinical tools.
Having all of those who attended, in my ‘home’ was a fabulous contrast to our social distancing ‘new norm’, and seeing all those lovely faces and buzzing brains behind them, warmed the cockles of my cortex!
For those of you that couldn’t make our UU30 date, I wanted to share a few things we learned in lockdown this week:
Copper can be absorbed through the skin and penetrate to deeper layers potentially increasing serum levels butthe degree of uptake is highly variable and more likely with prolonged contact e.g. jewellery and pastes not showers etc
Just like the Zn:Cu, when reviewing patients’ albumin:globulin, we must first look at each value individually and consider causes and consequences of low or high values, otherwise we can ‘miss the message’
When understanding labs of anybody who is not a couch potato we need to ditch reference ranges based on the general population because they essentially are…couch potatoes and ask ourselves 3 questions: 1) Whois this person outside of being ‘sporty’2) Whatis the nature of their sportiness because exercise ain’t exercise in terms of physiological effects and 3) When are the tests being done in relation to any exercise
On that last note, I am so thrilled to be able to share my brand spanking new presentation The Impact of Exercise on Pathology Tests – Beyond Artefact to Understanding which I put together B.C. (Before COVID19) for a NZ speaking engagement. This actually has been one of the most satisfying areas of research to expand my own knowledge in…explained a LOT about what labs go whacky (and why and how to navigate around and through this) not just in what you might call ‘real athletes’ but in weekend warriors, crossfit crazies, MIL (men in Lycra) and the increasing number of middle-aged or older women who just love pounding the pavement. Know the types? Our clinics are full of them…it is time to learn their labs properly.
Overwhelmingly when we look at our patients’ labs we compare their results with a reference range derived from ‘the general population’ aka couch potatoes! Therein lies our first problem. Exercise is recommended for health but we don’t know what this ‘looks like’ in terms of labs. The reference ranges reflect and assume ‘average’ muscle mass & haemodynamics & ‘average’ nutritional requirements in people consuming the SAD (standard Australian diet) none of which apply to the exercise enthusiast, weekend warrior, least of all the professional athlete! Given an increasing number of our patients are embracing exercise, this is an important instruction in what healthy looks like, how to make meaning of otherwise meaningless comparisons and ultimately enable you to distinguish between what is healthy exercise-induced adaptation, an artefact and an actual aberration that flags possible negative impact of emerging pathology for other reasons.
Click here to add The Impact of Exercise on Pathology Tests to your online RAN Library.
For all UU30 Subscribers the full Live Q&A Recording is now available in your ‘active content’ of your online account.
Listen to me, I’m sounding all sporty 😂. I’m not though, just in case you suffer misguided visions of my virtues! But it’s not just the self-declared serious athletes that we need to have on our radar in relation to optimising their oxygen carrying capacity (aka window to winning). Our clinics are full of people, regularly running, doing triathlons for fun (!), riding vast distances clad in Lycra to drink coffee in other town’s cafes etc. etc. whose FBE might be feeling the pinch! That’s right! All these individuals, depending on the frequency and intensity of their exercise, could have the so-called, anaemia of an athlete.
Long gone is the idea that exercise-induced changes to your haemoglobin and red blood cells and perhaps even your iron, would only affect the ultra-marathon runners among us. It’s the swimmers, the cyclists, the Roller Derbyists, the CrossFitters, the basketballers, the Gym Junkies, the lawn bowlers..ok I may have gone too far now…they all are at increased risk.
Why? Isn’t exercise good for you? You know I so want to say, ‘Surprise! It’s not!’ but alas. Of course it is good for us BUT there are some fascinating challenges regular exercise can throw at your dear old blood and its bestie, iron. These challenges are incredibly dynamic – having one effect during exercise, a different one immediately following, and yet another in the days of rest in between. And sometimes, in fact, often, our patients can end up on the wrong side of these seismic shifts. Here’s how the story usually goes
“Oh yeah..I’ve had anaemia for ages! You know and it doesn’t matter how much Iron I take or how I take it – it never budges. But I’ve been told to stay on the Ferrograd anyway”
Typically, being told it’s ‘Athlete’s Anaemia’ is the first, in a series, of many many errors to follow. Because in fact, there is no such thing. That’s right. Anaemia is a symptom not a disease and exercise induced anaemia comes in 4 common flavours: Dilutional, Heamolytic, Iron Deficient & Acute Anaemia of Exercise, and knowing the difference is critical to correct management. Only 1 of them will reliably improve with iron and it needs to be prescribed in a totally novel way. Others will get worse with more iron. Yep. And one is a complete illusion. So when we don’t make the right diagnosis, which of the 4 types your patient actually has, we fail to find the fix. And while all of our patients may not be overly obsessed with improving their performance or even winning, let’s face it, they all want to achieve their PB, that’s why they came to see you. So can you tell the difference?
WARNING: I got so enthused about this topic that I went over. The current ‘Update in Under 30’ is a ‘serving suggestion’ only! And you may need to speed up your playback to squeeze in another bonus 10 min, if you can only afford your usual 30 min car trip to listen!
Outrunning ‘Athlete’s’ Anaemia
Persistent ‘hard-to-resolve’ anaemia is a common presentation for anyone participating routinely in sport and that can be at any level, not just among the professionals. From our lovely ladies who take up running or CrossFit in their middle-age, to our MIL (men in Lycra) and ‘weekend warriors’, they may love it but their haemoglobin and their iron doesn’t! Anaemia equals reduced oxygen carrying capacity, a concern for anyone interested in optimising their performance but equally relevant to patients just trying to manage their energy throughout the day. In this important episode we identify 4 different types of anaemia seen in patients as a result of exercise, incorrectly lumped together as ‘Athlete’s Anaemia’. Each type is easy to recognise once you know how and effective treatment of each is remarkably different. This summary and the super handy clinical resource that accompanies it will help you and your patients absolutely outrun it, at last.
Ever suspect you’re being gaslighted by your patients’ results? Especially when their CRP result says, ‘nothing to see here’! But every other piece of information and every one of your senses tell you they’re inflamed and their immune system is up to something!!Me too. You probably then look at their other results, their ESR or their white cell count searching out something that supports your hunch, but they too can look disappointingly unremarkable. That’s the moment when you wish life was like a televised sports match and you could check the video evidence rather than believe the mere mortal (and clearly blind!!) man in white on the pitch. Well guess, what…you can.
As long as you know how to divide one figure by another using a calculator. I’ve found it requires the same digital dexterity as pushing the ‘on’ button’ on my blender…so if you can make a smoothie, you’re sorted! So while almost every lab routinely reports these two as separate parameters that are also routinely in range…I haven’t seen many that actually do the calculation for you and give you the Albumin:Globulin (AGR) on a platter. Yet this one step maths transforms the mundane into magic and can reveal almost all to you regarding your patient’s level of immune activation, inflammation and oxidative stress, from the largest number and variety of drivers. That’s why I call it, 📣The Master Inflammatory Marker 👑
When factoring in your patients pathology results is at its best – it makes the invisible suddenly visible to us. We could have sat and eyeballed that patient all month and never suspected that their Hcy was too high, or they had antiphospholipid antibodies or, or etc.
But the albumin to globulin ratio goes one step further & trumps the other inflammatory markers we’re so familiar with, because it even sees what they can’t!
And a low AGR (≤1.2) signals just that to you. So when the patient with joint pains, or just a little bit of belly fat or an emerging yet unnamed autoimmune condition presents exasperated saying, ‘but apparently I’m not even inflamed!’…you can let them know you do see it, and it’s just that others weren’t looking in the right place, then get busy rolling your sleeves up to move those markers! That’s right, a low AGR is a clear call to action for practitioners engaged in risk minimisation, prevention and for working towards best outcomes in established disease and monitoring a patient’s AGR is a series of clear sign-posts about whether you’re leading them in the right direction or not. There’s a lot more to say on this this third umpire & ripper of a ratio – about kids, the contraceptive pill, confounders, a role in cognitive impairment prevention and what optimal might look like but hey…the cricket’s back on…gotta go 😂
Patients’ labs lie, not often, but sometimes and the inflammatory markers performed routinely like CRP and ESR have been known to tell a few. Like when everything about a case screams inflammation but both of those say there’s none there. Why do they miss it?…well basically it’s not their lot. CRP and ESR have specific signals they only respond to and therefore reflect only certain immune reactions and at specific stages of that response. But there’s a nifty little calculation you can perform with all of your patients labs and suddenly see the immune activation, inflammation and oxidative stress that was lurking beneath. It’s called the albumin to globulin ratio and it’s going to change your understanding of what’s going on in your clients and your ability to monitor the efficacy of your management.
Me neither. I value transparency in all things impacting my health. So when the ‘Colonel’ tells us the magic is in not knowing…I think….hmmmmmmm, no thanks!
Similarly, when the provider of a test tells us, ‘We’d like to give you independent scientific support for our markers and our method but we just can’t because it’s patented!’…well that’s as good as the so-called ‘Colonel’ and his mysterious unidentified herbs and spices, as far as I’m concerned.
It’s effectively like they have created for themselves a ‘Get out of jail free card’ but unlike in Monopoly, they can play it over and over again. Trouble is, as the referring or just ‘reading’ practitioner (many of my patients present with results of these tests in hand) you have to practice either utter blind faith and believe every word that report tells you or you feel like you have to disregard the entire thing because you don’t have the time to sift through every parameter, searching out any independent scientific discussion of their markers, to distinguish fact from fiction. Utterly exasperating. Because of course, a test that offers a huge panel of results may consist of both – some of high value, some utter nonsense and some somewhere in between.
There’s one 24hr urine test from an OS company that I tend to see increasingly and it purports to be able to assess just about everything from gut health, to neurotransmitter levels, to your antioxidant capacity, mitochondrial health and beyond! How is this even possible in one 24 hr non-preserved urine sample that goes off-shore to be analysed? Well they can’t say…it’s a secret. 🤐 Pu-lease!
To boot all the lights and sirens are on for this patient who appears to have such little vitamin C in their urine, they’re at risk of scurvy! That is except for the fact that Vitamin C readily oxidises in urine only to turn into….wait for it….Oxalic acid! So, anyone surprised to hear she is also reported to have an exceptionally high oxalate load?!
Secret herbs and spices? No thanks, I’d prefer science. As the saying goes, “Keep an open mind but not so open your brain falls out!” Sorry but tough-talkin’ Tuesday is back and it’s gotten all toothy!
Update in Under 30: Oxalate Overload – Assessment and Management
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update.
While we may not all be pathology proficient, overwhelmingly we do take or record blood pressure, right? It’s such an easy but essential inroad to understand something more about patients’ cardiovascular system, and indeed their nervous system, when prone to the so-called ‘white-coat syndrome’. And it never fails to amaze me how the ‘numbers’ are so abstract and cryptic to the average patient. They’ll tell you things about previous BP readings like, ‘it’s normally fine I think, you know, like a 40 and maybe a 160, does that sound right? Ahhhhh…not quite. But of course these two numbers are not cryptic to us. And like all patient results, rather than our response being a simple, binary, GOOD/BAD one, we should be asking ourselves: What does this actually mean? What is it telling me?
Consequently, I’ve been interested in the blood pressure battle going on in America. Having traditionally placed the greater significance on a patient’s systolic pressure with comparatively little attention paid to the diastole, there have been lots of ruffled feathers following the redefined cut off for hypertension, which now flags any diastolic pressure over 80mmHg.
An unhealthy high systole of course is undeniably the most meaningful in terms of short term cardiovascular consequences and we are in no doubt that lowering this is critical for risk reduction BUT a new longitudinal study of over 13,000 UK citizens just published in the Journal of the American Heart Association, suggests that perhaps patients’ high or high-normal diastole in mid-life was in fact the earliest warning sign of poor cardiovascular health in the future. This comprehensive study followed participants for 8.5 years and essentially found that a rise in diastole in their mid-life (ahem, that’s our 40-50s 🙄) predicted the progression of arterial stiffness more strongly than any other measure. Additionally, while diastolic blood pressure tends to decrease as we move into our 6th decade and beyond, those individuals in mid-life with higher DBP –> more arterial stiffness were same people in whom their DBP drops the most significantly later in life. What a guise!! So, in a nutshell this substantial study teaches us:
“Prevention of arterial stiffening and the associated transition to a late-life hypertensive phenotype of falling diastolic BP is likely to depend on effective control of midlife diastolic BP in particular.”
Fortunately, the people we see are more in their mid- than late-life, which this new understanding speaks directly to, presenting the greatest window of opportunity for prevention in terms of modifiable risks for chronic disease, especially CVD, dementia and renal disease which arterial stiffness is such a major risk for. This extraordinary separate longitudinal study following individuals born in 1946 also suggests mid-life BP(both systole & diastole) is the major modifiable factor for later brain volume, integrity and function. Maybe we need to keep our eyes on that lower figure and our ears more closely peeled to hear what in fact it’s telling us 😊
Increasingly our patients are coming armed with lab results and this cumulative data helps us to clearly see their ‘norms’ (as opposed to textbook ones) and therefore be alert to any changes. However, results from different labs at different times, and even the same lab, are unlikely to be presented side by side for easy comparison. They certainly don’t come with all the important information about what was happening for that patient at each time point – important details pertaining to the blood collection itself (fasting, inflamed etc) which can profoundly alter results or the broader context: menstruating, breastfeeding, losing weight, on meds and supplements. The Patient Pathology Manager retains all the results for you, including the critical contextual elements, helping you to keep more accurate records to make the most correct interpretation. It also assists you to monitor changes related to various interventions.
Previously, this tool has only ever been available to clinicians who participate in Group Mentoring but due to frequent requests for access, we thought it was time to share this great tool for those wanting a foot up with some better systems in their practice.
Copper deficiency happens in kids, so does copper toxicity and both are serious concerns, but do we know when to accurately call either? First, we have to know ‘normal’. If we know what normal Serum Copper values look like in children, then we can easily spot those falling below or above this, right? That’s the first hurdle we tend to knock over and break a toe on! Being a mineral whose levels vary widely in soil from country to country, globally, the differences in reference ranges are breathtaking & absurd. Add to that, that copper is a key mineral in kids, driving huge demand for it during key periods of development, so the range for pre-schoolers isn’t the same as the primary or high schoolers – not that your lab is flagging that. Unhelpful? Yes. Dangerous, even? Potentially.
To diagnose ‘Copper Excess’ in a child is a big call to make.
One, because most practitioners are unaware just how much Copper a child really needs at each age & two, high copper is often a messenger for something else going on and then three, the primary objective based on this diagnosis becomes to lower their Copper but we could be either shooting the messenger or missing the mark all together…right?
Copper excess does happen but not nearly as often as practitioners believe it does. And in kids, the fall-out from such misdiagnosis is bigger. And missing a Copper deficiency? (because we’re not as well-trained to recognise it and because Copper has been sadly demonised) Likely to have myriad negative impacts at this vulnerable age…almost none of which generate symptoms or a distinct clinical picture e.g. secondary iron deficiency, low neutrophils without necessarily compromised immunity. But what about the holy grail get-out of jail adjective: ‘relative’. You know, ‘this is at least a Copper excess relative to their Zinc?’
Well, to form this opinion you’re likely calculating the Zn:Cu ratio and applying an ideal adult value of 1:1 but show me the primary evidence that supports this for kids…anywhere? The Zn & Cu relationship shifts as we move through life-stages and in fact Copper is supposed to dominate through a lot of our childhood so…ummmmm…no.
HTMA Copper side-steps all of this?..double no.
I used to make the same mistake re Zn:Cu, I may have even taught you this?!🤦♀️ But as so often happens, a week spent in all the original scientific data and I’ve emerged a changed practitioner! Having been part of perpetuating this problematic premise in the past, I am determined to get the correct message out there to as many practitioners as possible. So help me spread the word on Copper in Kids – by telling others that this mineral is so critical to kids compared with adults, they will often have higher levels than ‘us’ and that until you’ve applied the right age-appropriate reference range and ruled out confounders you can’t possibly make a call on Copper. I mean, we kind of knew this all along, with healthy pregnancy Copper values being exponentially higher being a giant clue. Turns out kids’ ‘Copper Age’ extends way beyond the womb.
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.
The latest Update in Under 30 has landed. You can purchase January’s episode, Copper in Kids here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
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Next time your log in, you will experience a more user friendly way to search, view, listen and download your resources. Find out what’s new here.
When you start doing this with your patients’ pathology results, you know your client records are turning into a big hot mess and more importantly your ability to see the wood for the trees is seriously under threat! Private labs don’t play nicely with one another and if your patient has been to more than 1 pathology provider you lose an enormous amount of their potential value, blindsiding you to their patterns, & the most accurate interpretations. I have a saying when it comes to getting the most out of pathology in your practice: Cumulative Data is King & Context is Queen.
Increasingly we’re in in the fortunate position of patients taking responsibility for their health and coming armed with lab results – this cumulative data helps us to clearly see their ‘norms’ (as opposed to textbook ones) and therefore also any noteworthy variations.
But even in this luxurious position of multiple results across a variety of time points & stages of their life – our ability to derive the greatest understanding from these is greatly stunted if we don’t have the context.
For example: if he was ‘cross-fit-keto-crazy’ at the time, if she’d stopped being pregnant & started breastfeeding, if in light of a major shift in thyroid hormone results, they were on biotin, or iodine, or changed their dose of thyroxine or were drinking straight from the udder of a soybean (!) these all seem like fairly critical contextual details to be across, right? All of these factors: diet, acute health context, medications, reproductive state, even season… impact the lab results we expect to see and therefore should be captured and considered to form the most accurate interpretation. But how do we pull it all together in a systematic way that SAVES us time and SAVES your sanity and can keep growing alongside your ever-growing patient notes? Cue the: RAN Patient Pathology Manager!
Systems for sorting through huge amounts of patient information help us make sense of what we’re seeing…and help us spot the source & solutions.
Systematised patient timelines for a better overview of the chronology of any case, the RAN Patient Pathology Manager not only holds all the data for you, helping you keep more accurate records & make the most correct interpretation from these, but also maps and monitors changes related to various interventions. Lastly there’s my old BFF, Mindmaps and Timelines not ancient torture tools of clinical supervisors (!) but rather what distinguishes us as integrative, enabling us a to work up a case in a truly holistic fashion instead of: symptom–> solution, symptom –> solution. These are the 3 key clinic systems I really wished I’d had from the get-go…so, me and my team created them! We’ve re-crafted them with each year and this year our RANPatient Pathology Manager has undergone a significant evolutionary leap and it comes with a comprehensive video explaining how to easily get the most out of this resource for all your patients. We always share these tools with all our mentees but we’re frequently asked how others can access them so this year we thought those of you out there just wanting a foot up with some better systems might like to get your hands on them too! Maybe this is one very practical part of the ‘new year new you’?
It’s like that split-second you close the door and realise you’ve locked the car with the keys still inside, or the whole reason you rang someone pops back into your head just after you put the phone down. Yes after the opportunity to draw breath over the break I went, ‘Doh! …I forgot to mention manganese!!’ So some of you may already know I am not a super fan of manganese. Well actually, that’s not accurate, I am perhaps just less of a fan than the people who are formulating a lot of our supplements! A place for everything and everything in its place. While this saying is completely foreign to my office, my house, my domestics and the rest of my life, it is a mantra I abide by with all micronutrients. Having enough of each micronutrient is good, having optimal (if we know what that is, which often we don’t) is wonderful but an excess is bad news.
And as I’ve spoken to before, with our increasing use of multi-nutritional formulas and the frequent inclusion of significant amounts Mn somewhere towards the bottom of those long ingredient lists…we very much run this risk with patients who are taking multiple supplements, at which point Manganese can become a serious meddler.
There’s a short list of patients for whom I am particularly conservative regarding their Manganese exposure and near the top of that list is those with Gilbert’s Syndrome. Do you get my ‘Doh!’ moment now? Because at the end of last year I released the Gilbert’s Syndrome: New Goals & Good News Update in Under 30…only to realise after ‘I’d put the phone down’ that I’d left this important one out of the dos and don’ts of managing these patients. So why am I saying no to chronic routine use of Manganese in those with GS? Well here’s the deal…
That’s why we need to be clear to cap the Mn for these patients as part of being across the cumulative subtotals of all micronutrients. While there is no established Upper Tolerable Limit (UL) set for Mn, adequate intake has been determined as 5mg/d for an adult. I agree, this is probably inadequate for some but I’ve seem individual patient prescriptions with cumulative Mn totals over 20 and 30mg per day! In spite of being generally regarded as having a low acute toxicity profile there is increasing research documenting Mn as a meddler when it comes to thyroid function in particular. So who else is on my watch and wait list for Mn excess? You’ve probably got some ideas…
The latest Update in Under 30 has landed: Gilbert’s – New Goals and Good News and my team has gone all out in producing a brilliant desktop reference to go with this recording that aids better understanding and clear treatment aims for your GS patients.
You can purchase Gilbert’s: New Goals & Good News here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
**But if you’re just joining us & this important conversation now,
ideally get the basics and backstory first and purchase all 3 key episodes in ‘A Guide to Gilbert’s Package’
It’s that time of year when we tend to set our intentions both personally and professionally. For me, between the many meals, pressies and dunks in the river, I slip into some ‘silent work’. In particular, I find myself flagging a couple of key areas that I want to sharpen my knowledge in this year. I’ve already picked mine…have you identified yours?
For many practitioners if there is one topic in nutritional medicine that seems to be more generous than any other it would have to be iron: Iron gives us patients…loads of them! Patients who present with deficiency, with overload, with something in between but still noteworthy, or on iron and that’s causing them all sorts of problems.
But Iron’s generosity doesn’t end there.
It also tends to give a lot of practitioners a bit of a headache!
That’s because a) we were mistakenly taught about iron as if it were just another one of the mineral mob and accordingly allocated grossly inadequate time to do more than scratch the surface of what we need to know and b) what we need to know, thanks to it being the most researched mineral, has undergone a couple of major revelations and revolutions since then anyway! So we can benefit from Iron’s generosity most and leave its other unwanted pressies (the headaches, confusion, frustration & suboptimal management of patients) under the tree – we just need to give iron the real attention it deserves, filling in the gaps in ours and many people’s knowledge about this critical nutrient. And boy, do we (and I mean everyone!! including doctors, midwives, pharmacists…anyone who has ever called iron deficiency on a client!!) need to learn how to correctly read iron studies!!!
Because iron also gives us much needed insight into other micronutrients and just how exquisitely sophisticated their roles & regulation can be. Thanks to it being one of the ‘older minerals’ we know more about it than any other and in turn we have the most advanced assessment methods: Iron studies, a collection of 4 parameters, like 4 chapters in a book or 4 key characters in a play, that need to be viewed separately and then together to understand the whole story.
Yes it’s true the learning doesn’t ever end and as I’ve continued to learn about new iron research I’ve added to our one-stop-iron-resource-shop..the Iron Package. Our very latest edition? A new clinical cheat sheet with some other important numbers on there you want to have at your fingertips whenever you read iron studies. So if you’ve already purchased and have access to the Iron Package…SURPRISE! 🤩 Go back and look again and if not, there’s never been a time like now. Oh iron, you’re sooooo generous!! 😉
Assessing Adrenals can be hit and miss, especially given that even more so than other labs, timing is everything. That’s why endocrinologists typically won’t look at anything less than a 24hr urine collection. If the total output is deemed to be high = Cushing’s and if it’s low = Addison’s. Sounds simple right? But to say only values outside of this reference range flag a problem might just be a case of throwing the baby out with the bathwater (or urine in this case!). Especially given it has been established that humans frequently fail at correct & complete 24hr urine collection! Alternatively we can use saliva or blood assays and capture the cortisol at any given time point, comparing that to expectations based on diurnal rhythm – but again, how are the reference ranges for these ascertained and is there such as thing as low normal. high normal results for cortisol, that actually warrant follow up investigation? I’m so glad you asked.
I see a number of patients who present with possible indications of flagging adrenals: from some distinguishing, but far from definitive features, in the clinical picture, to secondary lab markers. However, when they ‘limp’ over the line with their morning blood cortisol result I am often left talking to myself in an echo chamber about the need for more follow up.
But with the RCPA a.m. reference range of 200-650 nmol/L (Some seriously wide goalposts!) and some labs even going down to 150 with their minimum acceptable level for morning cortisol…are we right to still flag hypocortisolism (for any reason) as a differential in patients with low normal results?
Well Medscape yet again delivered Christmas 🤶 early last week with the largest study to date of blood cortisol, that has narrowed what’s ‘normal’ significantly…at least in terms of how low you can go before warranting further investigation. In this study they tested blood cortisol in the morning and afternoon, in over 1200 individuals presenting at an endocrinology clinic to determine in real world terms how low is too low (and associated with an increased likelihood of genuine adrenal insufficiency). They then gave this new ‘minimum cortisol’ a bit of test-run in 2 other large cohorts of patients to check it really did work as an effective cut off and wham bang…we now have a fully validated bare minimum… and guess what…it’s 275 nmol/L in the morning and 250 nmol/L in the afternoon!
Let’s be clear, their cut-off has what’s called a low ‘positive predictive value’ – which means most people (approx 2/3) with cortisol under this cut-off, upon further investigation (typically the ACTH stimulation test) will be found to be fine. BUT the point of this study was to ensure we don’t miss patients with adrenal problems just because they have ‘within range’ cortisol…and this new cut-off delivers on that.
This is big helpful news actually. Previously with patients who had am cortisol between 150- 275 we tended to find ourselves in ‘no man’s land’ – unable to provide enough of an argument about why adrenal insufficiency should still be on the differential list but unable to abandon that suspicion entirely. Thanks Medscape! Now if all the labs, RCPA and the referring physicians can just read this study and shift their goal posts…🙄
Our Group Mentoring 2020 Doors are just…about…to…close!
So if you love labs (or want to learn to love them more), desire to be a better diagnostic detective than you already are and want truly independent mentoring in a collegiate and structured environment for next year and you haven’t applied yet…best shove your foot to hold that door open right now! We offer a range of different levels & types of special interest groups: from New Graduates & the Mental Health Primer group (for those wanting to upskill and focus on this area), from rotating case presentations in our regular groups which are a mix of funky similarly skilled clinicians, to our pure GP group…take our pick! But get in quick by emailing us right this very second: email@example.com
Stop press. No, seriously. This new research warrants the attention of every practitioner working with children & teenagers. In the largest paediatric study of its kind to date, which included 2,480 children aged 10-18yrs diagnosed with hyperthyroidism (Grave’s or otherwise), Zader & colleagues found
Double the rate of ADHD diagnoses
5 times the rate of Bipolar diagnoses (almost 7 times in males)
5 times the rate of suicidality
That’s what I said: in 10-18 year olds
What is most alarming of course is that these mental health diagnoses were made in half of these children >3 months prior to the diagnosis of hyperthyroidism. What does this mean? It means we are missing this critical biological driver in this patient group. We all recognise the potential for some psychological presentations people affected with thyroid conditions, however, perhaps we are more alert to this in adults and letting it slip off our radar in kids? There’s been renewed talk about the over- and mis-diagnosing of ADHD lately and given that research has found up to 80% of hyperthyroid children meet ADHD diagnostic criteria this is one of the 1st place arguably to look! It also means, as these researchers discuss in detail, these kids are being medicated with psychiatric meds that in fact may, at the least mask their abnormal thyroid, lead to the incorrect diagnosis of hypothyroidism (lithium & even stimulants for example) or exacerbate their hyperthyroidism (quetiapine). But wait there’s more and it’s essential to understand.
Zadar & colleagues note that while we can not be 100% clear about the direction of the relationship…e.g. were these children already at risk psychologically and the hyperthyroidism just exacerbated that, they note that correction of the TFTs does not always equate to ‘cure’ of the mental health issues. This is not entirely surprising of course. What the problem emerges via a combination of biology and psychology & we resolve or remedy the biology…guess what you have left? PLUS the learned behaviours etc from suffering from anxiety, impaired cognition, suicidality they’ve been battling at the hands of excess T3 and a subsequent tsunami of reactive oxygen species.
This is one of those papers we should all have to read top to toe and therefore ideally be able to access for free but alas 🙁 What you can read is the Medscape review of this, which is a reasonable summary but the full paper is worth it if you can. You know the other key take home here…the diagnosis of hyperthyroidism was only made with overt out of range TFTs… which begs the question what about all those subclinical hyperthyroid cases we know exist? Yes, no wonder this paper has RACHEL’ S FAVOURITE written all over it…paediatric thyroid assessment and missed biological drivers of mental health and the opportunity to get better at both…can my research reading get any better this week?!🤓
Currently in Australia there is limited use of age specific reference ranges for thyroid parameters in children & teenagers yet they are essential for correct interpretation and diagnosis. Even doctors & specialists seem to be at a loss with diagnosing thyroid problems in kids unless they are extreme presentations. Subclinical thyroid presentations, however, are increasing in both children and adults. Many practitioners competent in adult thyroid identification & management are less familiar and confident with knowing when why and how to test in this population. Make sure you’re not missing thyroid imbalance in your paediatric patients…early detection makes treatment easy.
How might your patients’ Nickel exposure wreak havoc with their health? What might that look like? It may be lurking behind labels like IBS, non-coeliac gluten sensitivity, contact dermatitis of unknown origin,(with or without alopecia) or even CFS. “Then how does Nickel, which can’t even claim fame as a heavy metal, manage such diverse detrimental effects’? I hear you ask. In 3 easy steps 1) exposure…we’re all exposed, Ni is ubiquitous in our soil, our food, our environment so don’t bother trying to run from it 2) it hits our gut where our microbiome and intestinal lining may constitute the first fallen soldiers 3) exposure to our immune system can lead to sensitisation, and the subsequent development of a hypersensitivity response to each following exposure …and at worst precipitation of an autoimmune process. You got all that?
So therein lies the big question: how can we help patients whose health problems stem from Noxious Nickel? We could run and hide…from our jewellery, our mobile phones, dental interventions, most food (!), but we’d be wasting our time…we’re surrounded!
In this instalment it’s time to get down and dirty and detailed about how to best identify those patients who may have Nickel related pathology and presentations. We cover testing options, typical systems affected from GIT to autoimmunity and the most extreme form: Systemic Nickel Allergy Syndrome. We outline Nickel management strategies in a world full of it (!) and we include several key papers for additional resources and support. How noxious is Nickel for some of your patients? Well by the end of this you’ll know and better still, know what to do once that’s established.
Hear all about it by listening to my latest Update in Under 30: