Calling Out The Conspiracy

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…..”😴

The Calcium Conspiracy -Your Latest Update in Under 30

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’.

 

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No One Does Nutrition Like We Do Nutrition

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 🕵️‍♀️

Separating the B12 from the B*S#!

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.

 

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Ever Wondered How Much D Will Get You There?

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 by Aussie researchers is: 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…

Should We Rethink High Dose Vitamin D?

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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Are You Thinking What I’m Thinking?

🍌 ‘Are you thinking what I’m thinking, B1?’

🍌‘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.

 

The ‘Perfect’ TSH?

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:

  1. What is this (metabolite, analyte, binding agent, plasma protein etc)?
  2. 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?
  3. How have the reference ranges been determined for this lab – who am I comparing my patient to?
  4. Therefore, what is the significance of a result that is: ‘normal’, ‘low normal’, ‘high normal’, below or above the range?
  5. Does this value ‘fit’ with my patient?
  6. What else could explain an unexpected result?
  7. How strong is my level of evidence?
  8. What do I need to do from here to confirm or refute this?
  9. 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 We Learned in Lock Down Last Week…

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:

  1. Copper can be absorbed through the skin and penetrate to deeper layers potentially increasing serum levels but the degree of uptake is highly variable and more likely with prolonged contact e.g. jewellery and pastes not showers etc
  2. 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’
  3. 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) Who is this person outside of being ‘sporty’ 2) What is 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.

 

The Impact of Exercise on Pathology Tests – Beyond Artefacts to an Understanding

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.

 

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Helping Patients Achieve Their PB

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. 

The latest Update in Under 30 has landed.
You can purchase March’s episode, Outrunning ‘Athlete’s’ Anaemia here.
For all Update in Under 30 Subscribers, you will find it waiting for you in your online account and don’t forget the **EXTRA BONUS LIVE CALL WITH RACHEL.
**This live Zoom call with Rachel is for current Update in Under 30 Subscribers ONLY. A Q&A session for subscribers on the UU30 episodes released in 2020. Contact the RAN Team to reserve your spot!

 

 

I’ve Internalised The Process

Can you hear that? No it’s not some weird raucous bird-call. That’s me. A fabulous colleague of mine who also happens to be a Master MindMapper (yes it’s an official club now😂) , told me a couple of weeks back that practising naturopaths who don’t use this incredible tool for their case work-up typically say, “Oh, I’ve internalised that!” Well we laughed and laughed and yep even as I write this the giggles are back.  You see between the two of us we have almost half a century of combined clinical experience between us (no telling on who has the bigger share!!) and WE haven’t managed that feat…so we’re wondering what we’re missing (bigger internalised RAM?) or indeed, what they are?!  And naturally, I’m leaning towards the latter.

‘I practise holistically. I am truly integrative’, you say, ‘I consider all levels of evidence in patients, from their narrative to their neurologist’s report – from their bloods to their B vitamin  SNPS – from their detailed diets to their social (dis)connections”  

And I know you do. 

But how on earth amongst all the information overload, that deafening white noise & distractions, can you always see the root cause and every connection?

Because for me, spending the time practising due diligence with the creating a MindMap, after I see every patient, is my reliable path to achieving this.  Not just settling for the reflexive related systems that become well trodden paths in our minds…Gut to Brain (walked that track a million times, right!)…but step by step deepening my understanding of the case, adding layers I couldn’t see or hear at first, to reveal other critical connections that were unexpected.  Gut to Kidney –> Kidney to Brain It’s that time of the year when I’ve (clearly) been talking about MindMapping with my mentees and accordingly, I’m all juiced up!  And my love of this process and skill-set is also getting more layers!  I’ve realised that of course, beyond summarising the case in a truly integrated way, it helps me sift through my differentials, creating effectively a to-do-list about what things need follow-up assessment via questions, validated surveys, or testing.  It also keeps me (and patients) accountable moving forward, as I come back to this over months and years while they remain in my care and I have to answer the question: did we address that?

This Master MindMapper Mate – she’s gone 1 GIANT step further, dedicating (virtually) the next few years of her life to writing a thesis on Complexity Science and, in part, how holistic medicine has now finally found its friend in science via this progressive model.  

And MindMapping, and timelines and other key tools for genuinely integrated patient work-up, are the things that enable us to consistently uphold our holistic principles and practices and keep pace with the scientific progression. So if you wanna join our club 😂 because you’re already a MindMapping enthusiast don’t forget to contact kim.d.graham@student.uts.edu.au to find out about and ideally participate in her study. And if you’re feeling like the words MindMapping are Martian-speak for something you know nothing about 😥 …then maybe you should check this out.

MindMaps & Timelines – Effective Integrated Patient Work-up

As integrative health practitioners, we pride ourselves on taking in the ‘whole health story’ as a means to accurately identifying all the contributors & connections to each patient’s presenting unwellness.  In the process, we gather a wealth of information from each client  – pathology, medical history, screening tests, diet diaries etc. that borders on information overload and often creates so much ‘noise’, we struggle to ‘hear’ what’s most important. The management of complex patient information and the application of a truly integrative approach, requires due diligence and the right tools. Mindmapping and Timelines are two key tools to help you go from vast quantities of information to a true integrated understanding of what is going on in the case and the more time we spend learning and applying these tools, the more they will write the prescription for you. Not just for today but for the next 6-12mo for that patient.

 

Are You Being Gaslighted?

Ever suspect you’re being gaslighted by your patients’ results?  Especially when their CRP result says, ‘nothing to see here’!  But every other piece of information and every one of your senses tell you they’re inflamed and their immune system is up to something!! Me too.  You probably then look at their other results, their ESR or their white cell count searching out something that supports your hunch, but they too can look disappointingly unremarkable. That’s the moment when you wish life was like a televised sports match and you could check the video evidence rather than believe the mere mortal (and clearly blind!!) man in white on the pitch. Well guess, what…you can. 

Albumin

÷

Globulin

As long as you know how to divide one figure by another using a calculator. I’ve found it requires the same digital dexterity as pushing the ‘on’ button’ on my blender…so if you can make a smoothie, you’re sorted! So while almost every lab routinely reports these two as separate parameters that are also routinely in range…I haven’t seen many that actually do the calculation for you and give you the Albumin:Globulin (AGR) on a platter.  Yet this one step maths transforms the mundane into magic and can reveal almost all to you regarding your patient’s level of immune activation, inflammation and oxidative stress, from the largest number and variety of drivers.  That’s why I call it, 📣The Master Inflammatory Marker 👑

When factoring in your patients pathology results is at its best – it makes the invisible suddenly visible to us.  We could have sat and eyeballed that patient all month and never suspected that their Hcy was too high, or they had antiphospholipid antibodies or, or etc.

But the albumin to globulin ratio goes one step further & trumps the other inflammatory markers we’re so familiar with, because it even sees what they can’t! 

And a low AGR (≤1.2) signals just that to you. So when the patient with joint pains, or just a little bit of belly fat or an emerging yet unnamed autoimmune condition presents exasperated saying, ‘but apparently I’m not even inflamed!’…you can let them know you do see it, and it’s just that others weren’t looking in the right place, then  get busy rolling your sleeves up to move those markers!  That’s right, a low AGR is a clear call to action for practitioners engaged in risk minimisation, prevention and for working towards best outcomes in established disease and  monitoring a patient’s AGR is a series of clear sign-posts about whether you’re leading them in the right direction or not.  There’s a lot more to say on this this third umpire & ripper of a ratio – about kids, the contraceptive pill, confounders, a role in cognitive impairment prevention and what optimal might look like but hey…the cricket’s back on…gotta go 😂

Patients’ labs lie, not often, but sometimes and the inflammatory markers performed routinely like CRP and ESR have been known to tell a few.  Like when everything about a case screams inflammation but both of those say there’s none there.  Why do they miss it?…well basically it’s not their lot.  CRP and ESR have specific signals they only respond to and therefore reflect only certain immune reactions and at specific stages of that response.  But there’s a nifty little calculation you can perform with all of your patients labs and suddenly see the immune activation, inflammation and oxidative stress that was lurking beneath.  It’s called the albumin to globulin ratio and it’s going to change your understanding of what’s going on in your clients and your ability to monitor the efficacy of your management.
The latest Update in Under 30 has landed.
You can purchase February’s episode, Your Master Inflammatory Marker here.
For Update in Under 30 Subscribers you will find it waiting in your online account.
-Your RAN Online Account has a NEW LOOK!!-
Next time your log in, you will experience a more user friendly way to search,
view, listen and download your resources.

 

 

Are You A Sucker For ‘Secret Herbs & Spices’?!

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!

But always HATING to be the one to throw the baby out with the bathwater, I lose hours of my time, over and over again, trying to determine the worth in this multi-paged report and salvage some value along the way, given these patients’ significant financial outlay.  So it’s handy when the test also professes to accurately determine whether these patients are nutritionally replete for basic vitamins.  Aha!  Now we’re talking! The science of nutritional assessment includes volumes and volumes of studies, reviews, discussion and luckily enough I happen to have a strong foundation in this area and read such research for recreation! Today I am looking at a patient’s results that flag profoundly low Vitamin B6.  Several hours of reading later I can call BS. Seriously. The marker used by the company is urinary pyridoxic acid which is 1) reflective of recent intake only, failing to reflect both tissue levels and coenzyme activity 2) needs to be reviewed in light of protein intake, as high protein produces lower excretion and B2 levels because B2 deficiency will produce a secondary abnormally low B6 in the urine. There’s zero mention of any of these limitations or considerations in the report, sadly 🙁

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.

 

Is Copper the Culprit in ADHD?

Sometimes I think I must be psychic..or is that psychotic? Don’t answer that, it’s a bad Byron Bay in-joke.  I had literally just recorded my Update in Under 30 Copper in Kids and this excellent new study was published that same week, assessing and comparing trace minerals in age-matched ADHD and neurotypical kids. Snap! First, a moment of panic…because believe it or not, there are very few rigorous studies that have looked into this and so I had already read them all cover to cover and could confidently say, I had a grip on the literature. Gasp…’ will it have a different finding and challenge the much broader story about the excessive demonising of this mineral in kids health?’ Everyone take a big breath out…no. 

But if you’re someone who thinks you’re seeing Copper toxicity in kids, you can keep taking a big breath in and while you’re at it a huge bit of new information:

Copper Excess is Normal in Children.

Every investigation of blood Copper levels in kids has reached the same conclusion and this latest one by a Russian group of researchers renowned for their work in Copper agrees. So the ideas that we have about optimal in terms of mineral balance for adults may stand, but can not and should not be applied to children.  The elusive 1:1 relationship between Cu and Zn, for example, considered aspirational in optimising the mental health of big people, is absolutely not desirable or even healthy, in little ones. Why is it so? I hear you ask (…because you loved those old Cadbury chocolate ads with the crazy Professor as much as I did)  Well, essentially because kids need more Copper than us, as a simple result of their increased growth requirements: blood vessels, bones, brains…Cu is a critical player in them all and more.  And while we (and when I say ‘we’ I mean ‘I’) may be passionately passionate about Zinc’s importance, turns out, in paediatrics, it really does play second fiddle to Cu and should.

This new contribution to the Cu & Zn in ADHD kids debate did find that compared with neurotypical kids, their Cu:Zn was higher BUT – **and this is the really important bit **- as has been shown in a similar cohort before, the shift in relationship between the two was due in fact to lower Zinc levels NOT higher Copper. 

So, I guess when you think about it…Zinc perhaps really does still deserve all our loving attention we give it 😂…we just need to rethink the whole negative attention we tend to mistakenly give Copper! 

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.
-Your RAN Online Account has a NEW LOOK!!-
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.

 

Getting More Bang From Your Patients’ BP

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 😊

Have you also heard what’s totally NEW! for 2020 – Our Patient Pathology Manager!!

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 Excess’ In A Child?!….Really??

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.
-Your RAN Online Account has a NEW LOOK!!-
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.

 

In Need Of A Better System?

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 RAN Patient 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’?

 

Add this essential tool to your clinical toolkit by clicking here to purchase RAN Patient Pathology Manager
and watch this presentation now in your online account.

Ironing Out Some Old Misunderstandings

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!! 😉

 

Listen to these audios and download the resources straight away in your online account.
If you’ve already purchased ‘Update in Under 30: How to Read Iron Studies’ or ‘Iron Package’ you will find this new clinical cheat sheet available with these audios when you log in to your account.

So, What Kind Of Drunk Are You?

I know, timing, huh?! It’s almost like I’ve been sniffing around your recycling bins but I didn’t need to of course, at this time of year it’s a fairly safe bet you’re madly winding it back a tad from your most outrageous annual alcohol imbibing. And so are all our patients.  To me, extracting accurate information succinctly from patients regarding their alcohol use can be one slippery little sucker. It’s one of the questions people tend to give you a very tidied up answer to, or in fact they’re in such denial they can’t be considered a reliable witness.  Think about it.  Being a non-habitual drinker myself, I can appear almost saintly when reporting my daily consumption, “None”…but that omits the ‘other me’ that might show up at a conference gala dinner or some live music event, with my volume controls adjusted significantly up…ergh…firsthand accounts anyone? And how often does that happen?  Well anywhere between 4 times a week and once a month.  See what I mean?

While I’m sure you’ve probably heard me say before, I ask every patient who does drink, what kind of drunk they are because it can hint at their underlying neurobiology, there is a new study that suggests, using a very short 4 item UCLA RRHDS survey, we can categorise patients alcohol use and misuse into 3 types:

Reward  Relief Habit

and in doing so, also be better able to identify the best way to manage them as well.

I’ve been interested in addiction neurobiology for a long time and very much resonate with the work of Koob, which in layman’s terms proposes that we seek intoxication initially for the ‘high’ and then with dependence, we continue to seek it to appease the terrible lows of withdrawal.  It has long been known that alcohol use disorder is heterogeneous – there are different types and accordingly the kind of generalised treatment of these individuals proves extremely hit and miss. But articulating the different types and their distinct drivers and solutions has been fraught. Like what makes one alcoholic the functional type who in addition to their long-lunches is a CEO and the one who can’t keep their job?  Is it just socioeconomic context or something more?  Why are some types of alcoholism deemed also to run more in families and while others aren’t? There are clearly major difference in pathophysiology but what are they?  More recently these 3 groups have emerged and this recent study confirms the value particularly in the distinction between those who drink driven by reward and those for relief + habit. It’s a great read but here are some key take-homes:

Relief Habit

These individuals drink to cope or resolve a negative experience and therefore a driven by negative reinforcement. As a group they present with more depressive features and have more anxious traits than those ‘reward drinkers’. So the key to managing these patients is to offer treatment that also appeases their negative physical and psychological experiences with sedation, anxiolytics, glutamatergic modulation. (Hint this is where Taurine really shines, in this group!!)

Reward

These individuals drink to feel good so they are driven by positive reinforcement and therefore the approach to the helping them should be quite different, with lifestyle recommendations that offer other options for  mood elevation such as exercise etc as well and herbal and nutritional approaches.( Hint hint…not the key group for Taurine, more like Tyrosine and Saffron etc)

So….back to my question…what kind of drunk are you? As a nation of over-consumers by nature, this is a question we need to ask all our patients

Mastering Mental Health: New Assessments and Management Resources in Your Clinic (2hrs)

Rachel introduces you to new clinical tools that has been developing to help us all better master the maze of mental health. With so many possible biological drivers: from methylation to inflammation and from gonads to gut, these tools can help you quickly identify those most relevant to each patient and also outline the strategies necessary for redressing these. This presentation comes with an extensive library of resources including pdf of Assessments Tools and Case Study Notes.

How Low Can You Go…With Cortisol?

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! 

TODAY!

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: admin@rachelarthur.com.au

Does Holistic Health Include The Hardest Workers?

Did someone explain the kidneys are like a really important, not to be forgotten, under-estimated, ignored or under-valued kind of organ in your training as a naturopath? No, me neither.  I mean I know Buchu and Uva and Zea (on a first name basis only, clearly!) and …no actually, I’m done.  But seriously, it didn’t take too long in practice to stumble across a whole lot of bad when kidneys aren’t getting the attention they warrant and equally to develop a slight obsession with renal markers in all of my patients not just because of their incredible impact on whole health but also because of what ‘lay beneath’.

As you might suspect, I get sent labs all the time from practitioners. Stop no! That is not an invitation!   

Often it’s client’s renal markers which I do appreciate because it tells me there is an increasing number of praccies that absolutely have done some post-grad DIY knowledge building about these bean-shaped babies and their critical contribution to health. The results might come with a question like, “What’s going on with their kidneys?!” [insert worried face emoji of choosing] 

To which my reply is often… “not much but boy do we need to talk about your patient’s GIT microbiome! [or] mental health! [or] sarcopenia!”

Say what?  Yes abnormalities within the renal markers: urea, creatinine and uric acid may be a reflection of renal issues.  But if you know where each of these molecules enters the blood,exits the body and all the interesting good & bad they can get up to in between…then the patterns speak less (if at all in some instances) to what’s going down in the kidneys but instead give you an incredible insight into key issues all over the body: from the gut to the brain.  But wait there’s more!  Want to know what’s the latest and greatest in management of advanced renal disease? Treat the gut to lower the urea.  What about managing mania? Add in a gout treatment to lower uric acidDang!  This is holistic health at its best with those poor kidneys no longer being left out in the cold!

“Who knew urea, creatinine, GFR and uric acid could be such a Goldmine….Mind…officially…blown!” New Graduate Mentee 2019

Want an Opportunity for ‘XXX sized’ up-skilling in Renal Markers & Health?

Most practitioners graduated with not much more than a few ‘kidney’ herbs and an under-appreciation of the contribution renal health makes to wellbeing. It’s not just about waste and water.  In reality, the kidneys are pivotal in just about every major element: blood, bones, pH balance, methylation, control of oxidative stress, the GIT microbiome and more!  And we are seeing the impact of this in our patients in all sorts of subtle and not so subtle presentations.  This new instalment in diagnostics, brings the renal system into the spotlight so we can confidently identify and better manage its critical contribution.  In addition to this, just like with other routine labs such as LFTs, we unpack how these so-called ‘renal markers’ can flag a plethora of other insights into your patients, from reflecting (un)healthy muscle mass to calculating  individual dietary protein adequacy, from key ‘danger and distress’ signals in response to disturbed metabolism, oxidative stress to certain types of GIT dysbiosis!  We call this Renal Markers: Explained, Expanded and Exploded because these routine labs can deliver XXX sized insights into your patients.

Iron – Another Important Discovery

Yet another super-helpful part of Iron-Land has been mapped!!  Ever struggled to correct chronic iron deficiency in athletes or even just weekend warriors?  Yep, me too. One of the key barriers being the 2-3 fold rise in hepcidin in response to exercise. Hepcidin whose day job is an inflammatory signal that two-times as an iron uptake blocking agent at the small intestine.  In addition to other exercise-induced factors that either reduce Fe uptake or increase losses, it really is no surprise that these cases can be hard to treat. However, a recently published small Australian study has brought to light some constructive new information. Similar to the often talked about ‘anabolic window of opportunity’ whereby we encourage people to consume protein +/- CHOs within a short time-frame post-exercise to optimise exercise outcomes and negate negatives, these new findings imply the same might be true for optimal Iron uptake. But only in relation to exercise done in the morning! 

The key finding was when individuals consumed iron after 90mins of exercise in the morning they exhibited higher uptake than both when they took the iron at the same time but didn’t exercise beforehand or took it after exercising at night.

This is a game-changer for potentially ALL our patients who struggle with iron absorption.  With the key take-home being…not just take your iron preferably in the morning which we already know (when hepcidin is naturally lower as part of its diurnal rhythm) but before you pop that pill, pop on your sneakers and get busy sweating! How on earth might this be working?  Well this study demonstrated that while hepcidin rises after exercise typically for up to 6hrs…it is not yet ‘up’ and blocking within the first hour – gotcha! But why would this mean an even greater uptake compared with the same iron at the same time in the same individual…but a resting version of themselves?  Because exercise may in fact cause a transient leaky gut post exercise & enhanced nutrient uptake may be its silver lining!  A small study that actually punches above its weight, this one is worth the read – via a great comprehensive summary on Medscape if you have it or you can check out the abstract.

Our ever-expanding Iron knowledge gives us great hope for the improved understanding we are likely to reach with all nutrients in the future.  Let’s not forget Iron has about a 70 year head-start on other microminerals such as Zinc and almost a century on Selenium, which was identified to be essential in just 1979! 

And the contrast is apparent anywhere you care to compare and contrast the ‘older’ with the ‘younger’ nutrients. Just look at iron studies. A personalised detailed account of each individual’s iron story: how much you’re consuming, how effective you are at absorbing what you’ve been offered, how hungry that makes you for more and what good stores mean to you (not some fictitious average male or female)!  All told through 4 distinct but inter-related markers: serum iron, transferrin, transferrin saturation and ferritin.  What can we glean from our current routine assessment of Selenium in contrast?  Their short-term Se intake…yep. Looking forward to the multi-parameter markers of each individual nutrient we just might have at our fingertips in the future, thanks to iron nutrition which continues to teach us how sophisticated nutritional physiology really is 🙂

We know the most about iron and yet we know there is always more to learn.  And who better to teach us this than our clients with iron deficiency or iron excess?  Need some help getting across the most important aspects of recognising and correcting each iron issue in clinic?  We released an Iron Package earlier this year for this very reason. It covers how to really read iron studies (with a great cheat sheet), how not to fall for a fake (deficiency) and what the best supplements and dosing regimes look like and how that differs in pregnancy, athletes, those with marked gut issues and other key groups. It’s your 1 stop iron shop.

Are You Going Hot & Cold On Thyroid Cases?

What’s the most common thyroid disease you’re seeing in practice?  Nope, try again. I’m serious.  There would be very few of us who’d get this right without cheating. It’s nodules.  Current figures suggest 1/2 of all us middle-agers have them and by the time we’re 80 that’s risen to 90%!  There’s a school of thought that says these figures have jumped purely because of increased rates of thyroid imaging and we should stop sticking our nose in places it doesn’t belong. Just because they are there doesn’t mean we need to know about them or that they are causing trouble. All this is true and yet there is a percentage of patients for whom these nodules are a whole lot of trouble, in fact, that’s why they’re coming to see you…they (& possibly you!) just don’t know it yet.

Nodules, outside of radiation exposure, have always been primarily viewed as a nutritional deficiency disease: Iodine.  While this was always a bit one-dimensional (poor selenium…when will you ever get your due?) it’s an explanation that no longer fits as well as it once did because even in populations who have addressed iodine deficiency, the incidence of nodules continues to rise. 

So, what now?

New nutritional drivers have been identified but rather than being about our deficiencies they speak to our nutritional excesses.  And while iodine is not totally out of a job here, some people of course are still experiencing long-term suboptimal iodine which can trigger nodule development, we now need to question if there is any therapeutic role for iodine once the nodules are established. Well the answer is both ‘yes, maybe’ and ‘absolutely not’. The determinant being whether we’re dealing with Hot or Cold Unfortunately most patients and therefore their practitioners can’t tell the difference. But it is the presence or absence of a hot nodule that radically changes what complementary medicines you can and can’t use and what an effective treatment plan looks like.  

I’ve seen a lot of thyroid nodule cases pop up in mentoring this year and it’s been a great learning opportunity for everyone to get comfortable with clues in both patients’ presentation & their pathology. While iodine deficiency no longer ‘fits’ like it did, nutritional medicine should arguably remain the primary approach to their management and the new research gives even more credence to this and  identifies a far greater range of dietary and supplemental tools.

Thyroid nodules are going to explain a surprising number of our subclinical (hypo and hyper) thyroid patients and we already have a dispensary full of powerful interventions but we need to start by familiarising ourselves with their story: their why (they happen), their what (this means for patients) and their how (on earth are we going to address these effectively) Knowing your Hot from your Cold…is step one.

 An increasing number of our patients have thyroid concerns but unbeknown to many of us the most likely explanation of all is thyroid nodules, whose incidence is on the rise globally.The development of nodules has always been primarily viewed as a nutritional disease. Traditionally attributed to chronic iodine deficiency but recently novel nutritional causes have emerged . Benign nodules come in 2 flavours: hot and cold and while patients can present with a mixture, it is the presence or absence of a hot nodule that radically changes what complementary medicines you can and can’t use and what an effective treatment plan looks like.  The pointers, as is often the case, are there for us in the patient’s presentation and pathology, so knowing the difference is no longer a guessing game. This UU30 comes with a great visual clinical resource and includes key papers on the nutritional management of nodules.
You can purchase Are You Running Hot and Cold on Thyroid Nodules here.
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