Keeping Things Real & Representative

 

Any pathology test is only of value if the result produced is ‘real’, or, representative of that individual, right? So the timing of the test is a major pivot point then: do I tell my patient to present for the test, or collect the sample themselves, on their ‘best’, their ‘worst’ or their ‘average’ day? 🤷‍♀️  Well, that all depends on the question you are trying to answer.

Whenever we reach or refer for a test, we have a question in mind we’re seeking an answer to. But the question always comes in two parts, at least.

Part 1: How much progesterone is she making?
Part 2: …When she’s ovulated & her corpus luteum should be most productive?

A third might refine the question you’re answering further by adding another contextual clarification

Part 3,4,5: …When she’s eating her regular diet, not exercising excessively or under extreme stress

Without these other parts – the answer to the first one: How much progesterone is she making (full stop), is hard to correctly interpret, right? By refining and expanding on the full extent of our question, we can be clear about which elements of this patient’s life the result likely reflects. We might say that for her, this time-point, or set of collection conditions, is a ‘real reflection’ of her generally and therefore, representative.  But what if she does occasionally undertake a 5 day fast, or train for & compete in marathons? If we were to specifically test during these times, we answer a different question, right?  Likewise every time we instruct a patient to present for their blood tests (routine or fancy schmancy): Fasted, Rested, Hydrated and off their supplements – is this sound advice or a misdirection?  Well it depends on the individual in front of you and the real question you want answered about them 🤓

Ahhhhh I love rules: both the making of them and the subsequent breaking of them 🦜🏴‍☠️

Fasted, Rested, Hydrated & Unsupplemented? Exceptions to the rule

The collection conditions for any pathology test – can refine or ruin the question you were hoping to have answered about your patient but is it always appropriate to ask everyone to ensure their preparation for the test was ‘ideal’? What if their real life is far from ‘ideal’ and contrasts dramatically with these ‘conditions’ e.g. they forget to drink water but never alcohol! Or do they run 20km every weekday and 40 on weekends?  And why would we tell some patients to stop their supplements prior to a blood-test and not others? If our goal is to ensure any pathology test answers the question we need answered we need to know how to respond to these and other scenarios.  This new update is all about keeping results ‘real’ & representative.

 

You can purchase Fasted, Rested, Hydrated & Unsupplemented? Exceptions to the Rule 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.

The GREAT Cortisol Capture! 35K Aussies Get Tested

And all 35K results have been collated, analysed & made available so we can be better informed regarding expected Cortisol values based on sex (spoiler alert: women win & when I say win I mean track higher generally🤷‍♀️), age & life-stage. This month in our Mental Health Primer program I’m talking about how to look at labs through a mental health lens – from the most routine (ELFTs, FBE etc) to those 2nd tier assessments that we might sometimes recognise to provide essential information about our patients.  HPA assessment is such a big one in mental health and depression, specifically, because of the 2 major subtypes: typical (can’t sleep, can’t eat) and ‘atypical’ (over-sleeps, over-eats).   We all know that in ‘typical’ depression – the subtype we tend to over-focus on due to its dominance (and sometimes therefore miss the atypical patient at our own peril),  there is most characteristically a hyper-cortisolism, with poor negative feedback at the HP, allowing for these higher circulating levels. But is your depressed patient with sleep disturbance experiencing higher than healthy or expected cortisol release?  No, not necessarily.

You see even the 2 subtypes can have sub- sub- types.  Patients can have a diagnosis of either form of depression but have PTSD features or other psych and non-psych comorbidities that make it more probable that their adrenals and Cortisol are turned to ‘low’.
As in unhealthily & unhelpfully low.

And that would then necessitate a very different approach to treatment – a different choice of herbs and nutrients etc., right? As we’ve discussed before, accurately capturing cortisol is a task not for the faint-hearted!  Cortisol demonstrates such dynamism – not just regarding time of day and pre-test and test exposures & experiences, but also your geographical location in the world (!), not to mention choice of medium and which aspect of the HPA story that specifically reflects.   But for some patients it is essential for best management that we ‘feel the fear & undertake an assessment of their HPA function anyway’! But we need to ensure we get results we know how to accurately interpret.

I use different cortisol captures (saliva, urine, blood) to answer different questions – but if I want to understand the HPA functionality and performance and feedback…then measuring cortisol alone is not adequate – and we are back at blood, which offers us, as always, to go beyond a simple numerical: ‘adrenal output’ & also answer the question: “What were the adrenals TOLD to do?” aka where does any actual mismanagement lie & likewise, the key to correction.

Cortisol – Have you been caught out?

I have!  And just recently a stark contrast between the results from 2 different methods of cortisol capture in the same patient illustrated just how likely this is. How do we ‘capture’ something so ‘dynamic’ and interpret anything of substance from a ‘static’ assessment technique?   But rather than throw up our hands and throw out the whole attempt to measure cortisol, we can improve the rigor, reliability, and real-world meaningfulness of our patients’ results by refining our timing of tests, choosing the medium wisely & manipulating test conditions to answer specific questions about their HPA function.  Great ready reference resource included!

 

More FODMAP Fails

Last week, yet another patient with refractory diarrhoea, up to 10 stools a day, Bristol type 5-7, for 3 decades following a diagnosis of Crohn’s at 16 years old. A range of specialists have thrown everything at ‘it’ – single & combination immunosuppressants, TNF alpha blockers, buckets of sulfasalazine and bathtubs of antibiotics – she’s been gluten and dairy free for years, trialled strict diets that are FODMAPs free, low histamine etc etc etc. She’s even had 50cm of her terminal ileum removed & the diarrhoea continues unabated – perhaps even worse than before…& therein lies a major clue.

 1/2 patients with Crohn’s exhibit bile acid malabsorption –> diarrhoea but with terminal ileum resection this jumps to > 90%

This is Type I BAD (Bile Acid Diarrhoea) & is the easiest to spot, being the result of anatomical change.  You remove the section of the small intestines responsible for 95% of the reabsorption of bile acids…a LOT of bile acids are going to be present in the colon where they act as potent osmotic laxatives, right? But there are 3 other types which are a little trickier to identify – including one that affects up to 50% of IBS-D patients. 

Being a child of the 80s⚡🎹 (ok a teen of the 80s but who’s counting?!) and a personal fan of fat, I NEVER thought I would EVER be recommending a ‘low fat’ diet to ANYONE🤐

But hey, that’s another ‘absolute’ that needs challenging, right? I mean this is the primary, almost only, dietary change these patients need to make and as a stand-alone intervention, is highly effective for many. We’ve had several patient successes in the last year – a total game-changer for patients in similar situations where all kinds of  ‘restriction’ had brought zero joy and reward for all their ‘good (dietary) behaviour’. While sequestrants (like cholestyramine) are recommended in BAD, and are certainly worth a trial at least, patients have very mixed results – for some, in combination with the low fat diet it’s a winner – for others these meds cause GIT upset all on their own and actually undo the good of the fat restriction. Being able to identify the true reason for their loose stools and stop them going down endless rabbit holes of ..is it? is it? is a great way to re-empower people who’ve been bossed and bullied by their bowel for far too long 🤓💪🧻

 

When is IBS BAD?

This is not a trick question. Up to 50% of all patients diagnosed with IBS-D actually have bile acid diarrhoea (BAD) underpinning their digestive complaints as well as some patients with non-resolving diarrhoea post-cholecystectomy and gastro.  Knowing which ones do and how to manage this, which requires distinctly different approaches from our general management of IBS, is the key.  As always, good lessons come from those we learn in the clinic and this story starts with a patient and how we came to recognise the BAD in her belly.

Last Words for 2021

I’m ready to zip my lips 🤐 and ride off into the sunset of silly season. But first I wanted to tell you about the BIG PLANS we have ON THE BOIL!  Noticed a bit of a thyroid theme of late?  Last month I presented training in thyroid assessment for the 4th time for ACNEM but not a slide, possibly barely a dot-point remained from the original one I wrote back in 2009.  That’s how much my ideas & understanding have changed.

Some of the assay techniques & technologies are new, there’s a river of research  & a mountain of meta-analyses published in the time between & I have had the privilege of yet more clinical encounters in this space, to really nut out how all this translates into the real world.

There’s a lot I need to catch you up on.  And as I start creating our new MasterCourse II in Comprehensive Diagnostics…which will include 🥁…you guessed it…the humongously hardworking HPT, I’m just about bursting at the seams! And will those four little friends of every good practitioner, that sit superficially atop the ‘butterfly’, make it into our MCII?? I hope so because a) they should be our besties – being the director of Ca Mg D & P regulation and b) research tells us that where we find, ‘thyroid’ dx we should have another good hard look for ‘parathyroid’ dx and vide versa and c) over the last few years it has become increasingly apparent to me that this is one incredibly common source of ‘medical mysteries’  in our patients – remember the ‘Bones, Stones, Abdominal Groans & Psychic Moans’ catch-cry?  Yep, that’s the patient who typically finds their way to us, with pervasive but hard to pinpoint gut issues (often misdiagnosed as SIBO, FGD, IBS -D or C), some significant stress perhaps even depression and insomnia and, if someone bothered to look, premature bone demineralisation.  What other pathology panels and parameters will we be able to squeeze into our MasterCourse II?

Our current plans are to deliver the MCII live from May but just a reminder, because this next instalment assumes you have the exquisite foundational knowledge we laid down in the MCI – this is a pre-requisite for attending the MCII.
So if you’ve been putting off your pathology apprenticeship now you have a hard deadline to work to!

And finally the last, last words. On topic because they came from someone who specialises in thyroid, did the original thyroid training with me, way back when, and last month was my fellow presenter & panellist on all things thyroid for ACNEM:

I’m sure I’m the 1 billionth person to reflect this back to you but I’ll do it anyway because I think we all need reminders sometimes – you have a truly special gift in critical thinking, discernment, and most importantly passing on complex knowledge in a very digestible way without making anyone feel silly for asking questions or not getting something the first (or fifth time…no, just me?). The endless analogies are a teaching tool you’ve well and truly nailed and boy am I grateful because it speaks to my way of learning very well.
So, a big thank you! Endless gratitude for your brain, passion and generosity with your time/knowledge/resources.
Natalie Douglas
Here’s to another great year of learning, teaching, sharing & mentoring in 2022 – 1 billion and counting I hope 🌟🌈😂

Urinary Iodine Curveball Corrected!

Example 1:

Example  2:

We love hearing from our fellow fearless friends on the frontline – working with lab results & pathology providers – everyday.  We recently received an SOS! from the Francesca Naish over yet another iodine assessment issue that you may need to also be alert to:

“Ever since you first drew our attention to the need to correct urinary iodine results, I have used your formula for all my patients’ results. Thank you for this.  As most GPs don’t seem to be aware of the need to do this, I find it essential to warn my patients to wait for my interpretation before acting on their doctor’s advice! For a while now, Laverty have started giving the corrected result, which complies with the calculation you recommended. However, very recently Douglass Hanly Moir have started to give a corrected result on their  result sheets, but it does not tally with the calculation I have been using (the one you recommended) and generally gives a lower figure.”

Well, as always, cluey people ask cluey questions…and this did take some back & forth with DHM to solve.  Increasingly, all the major pathology companies are coming around to the essentiality of urinary iodine correction, something I’ve been banging the drum 🥁 about now for….yikes…7 years..no wonder I’m going grey! This is a mathematical formula applied to any raw score for urinary iodine to account for the dilution/concentration of the given sample, because, as we all know, hydration status varies widely between individuals and even within an individual at different times – and this is something that can wildly lead you astray in your thoughts about their iodine status, if not accounted for. Some companies are now employing the formula we use: Iodine (mcg) ÷ Creatinine (mmol) X 8.85 = Corrected Iodine in mcg/gCr which is wonderful to see.  But DHM have taken a different path, strangely enough, using this formula BUT rather than using the patient’s own reported urinary creatinine they instead use a ‘median creatinine’ 

Which…I am going to say it… MAKES NO SENSE!^%@* aka we WILL correct this iodine for hydration status – but we’ll correct it for someone else’s no yours! – Ms/Mr average…ok?
Ahhhh no.
Just look at the difference this makes in a patient with very dilute urine, in example number 2 above!!

So Francesca & all of you on the frontline, can be assured, if you’re using the formula above – it is correct – keep up the great work and know that it is often better to do something yourself than blindly trust a 3rd party when it comes to pathology…unless that 3rd party is our RAN Patient Pathology Manager template which calculates this perfectly of course!

RAN 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, the RAN Patient Pathology Manager 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. 
This provides you with a template that can be used an infinite number of times plus a short training tutorial.

Functional Medicine Falsehoods ⛔️

Functional Medicine Falsehood

An ideal T4 is 15
An ‘anti-aging’ DHEAs must be >7
A ferritin of 100 is optimal for women…

I’ve heard it all, probably you have too, and far too often & too recently from practitioners who should have rationalised & researched their way beyond these functional falsehoods, by now.  I bought into these ‘optimal wellness truths’ hook line & sinker early in my career and proceeded to even propagate a few but with (not much) more experience in clinic, I had to seriously question this pursuit of ‘perfection’ & ‘perfect pathology’…in favour of reality & scientific evidence!  They didn’t add up.  Not with my patients – even the healthiest ones, in fact some of the really unwell ones occasionally had these kind of high-normal results and they were part of the problem!. ‘But that’s because no one is truly healthy outside of those seeing a functional medicine practitioner & supercharged on supplements & hormone replacements!!’ came the counter-argument.  Ahhh, really?

How then do we reconcile this with the following:
Individual genetics & biochemistry
Our biological resilience
Healthy & appropriate senescence
Large datasets of mixed race populations from other comparable first world countries…where these figures denote the statistical outliers?

I mean, if the 50th centile value for ferritin for actual living, breathing, bleeding, women in the US, Canada, Australia etc etc is 30-40 ng/mL and the 95th centile is 126 ng/mL and the WHO says that in fact, anyone menstruating with a ferritin > 150 ng/mL should attract suspicion for iron overload….but functional medicine men (mostly…sorry but it has to be said!) say 100 IS OPTIMAL FOR EVERY WOMAN #@^*…please tell me in which women, consuming what kind of diet, where in the world, & based on what improved or better health outcomes?
And while you’re there can someone please support this bold claim with a scrap of high quality evidence??

[Rant over🎤💧]

The falsehoods of functional medicine include the blanket belief, ‘more is better’ (ahhhhh not when it comes to many things, including iron where women’s lower levels have been found to be an evolutionary advantage…guys). But you know what, we’re better than that! We see each individual, recognising all the factors at play that make for their uniqueness, help to define what ‘healthy’ looks like for each person and don’t fall for one-size-fits-all claims without any evidence nor common sense even, to support them. What do you think?

Mastering Micronutrients

Let’s make sense of the over-arching nutrition principles, that will profoundly change your understanding and application of this modality  Truly understanding the ‘big’ concepts, so often overlooked, or incorrectly taught, ensures you get the critical ‘small’ detail in your nutritional prescriptions right. In this 4 hour recording, together with key clinical tools, we talk about the tough stuff: dose-response curves, active versus passive stores and excretory pathways and ooh lah lah…the myth of taking ‘activated vitamins’.  Even those who feel satisfied with their original training – will find a lot in this critical review that is new, insightful and truly practise-changing!

 

When CKD C(omes) K(nocking) at your D(oor)

And it will.  It knocked again on a practitioner’s door last week.  She in turn knocked on mine. It turned out to be a very familiar story:

Firstly: Patient presents distressed – recently a nurse applied the term ‘Chronic Kidney Disease’ to HER (note no one has ever mentioned this diagnosis)
Secondly: She is in stage 3 of 5
Then: This practitioner is left to have ‘the conversation’ but wants to know where to start, ‘What do I say?’
Next up: And what else can I do for her – are we really able to make a difference?

Familiar to you too? So,1st & 2nd: Yes, this is not uncommon we would have to say and even with age-appropriate reference range adjustment, her GFR consistently in the 50s,  flags premature decline.  Then: What DO you say?  Well this clearly is a delicate area, not only because of the level of patient distress and concern but because, at this stage the practitioner knows nothing more than what the patient tells her and her ELFTs over the last 2 years.  This is not enough information, right? Chronic Kidney Disease is a heterogeneous condition, with many different causes, manifestations, comorbid conditions, and factors affecting prognosis (Levey et al., 2009) So while most individuals certainly progress from stage I to II and II to III the rate at which they do this differs dramatically.

Two years of data is not long enough for us to appreciate the trajectory of her CKD & means we are unable to provide the patient with any kind of perspective:
‘With no further decline in GFR or progression in stages over 5 years, you’re doing well, so keep doing what you’re doing!’
Vs
‘Ok, I can see what looks like a little period of accelerated decline – let’s review what’s been happening and how we can turn this around”

“Please sir can I have some more?’ Yes, back to her primary carers to request more information to fill in the gaps, and ideally more labs to calculate & observe the trajectory for yourself.  Next Up: What do we have to offer the patient with CKD stage III? Soooooooooooooooooooooooooooooooooo much!! When is adequate hydration helpful?  Always, except Stage V! (and these patients are not coming to see us) What are our treatment objectives & our evidence backed medicines to meet these? Hcy lowering (note often referred to as ‘folate refractory’ in renal dx), vitamin D adequacy, lowering the acid load, supporting the microbiome & in turn the Renal-GIT axis…hang on, got to go…someone’s knocking 😅 but hopefully we all can see, when they present to us, they are indeed knocking on the right door ✊

Nutritional Interventions in Renal Impairment – Place & Potency

Nutritional or naturopathic support for the kidneys tends to have been over-looked in our training and yet research suggests there is much in our tool kit that can make an enormous difference to this system, in particular, slowing the progression of chronic kidney disease in patients.  Rachel talks about what these key evidence based interventions are and also gives you the tools to identify the early pathology markers of renal impairment – the earlier the recognition, the earlier we can make a start on the remedy.

Water & Our Kidneys – Helping or Harassing?

It seems almost farcical to question the merits of hydration for our renal health but is this actually the truism we have been lead to believe?  Where does the recommendation of ‘8 glasses a day’ come from and what is the level of evidence to support it and in whom?  Or should we in fact be setting our sights on output ie. 24 hr urinary volume, over input. Do all kidneys love water – or does this relationship change with the progressive impairment seen in CKD which affects up to 30% of our middle-aged population?  When does hydration become harassment?

Renal Markers – Explained, Expanded and Exploded 

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

 

Female Pattern Hair Loss ≠ A Female With Hair Loss

I’m intrigued by the silence.  Hair loss in women is frighteningly common, following pregnancy, menopause & with extreme stress (wait is that a tautology? 🙄) In fact it can strike at any age and for a multitude of reasons.  When it happened to me a few years back I also initially responded with silence, terrified that if I said it out loud it would make it real, but when my daughter suddenly asked, ‘Mum are you losing your hair?’ with her trademark attention to detail & exquisite empathy, she gave me the words & a good kick into gear, simultaneously.  Now I am fascinated by women’s silence around this generally, how little we share our stories & forewarn others, & as practitioners, the lack of adequate training we’ve had identifying the different types (hint: it involves donning gloves or if restricted to online consulting, knowing how to organise correctly positioned pics) & from there finding the right solutions. 

While Female Pattern Hair Loss (FPHL) is the dominant type in women – it only applies to the following pattern:

But alopecia due to stress, thyroid disorders, autoimmunity, contact dermatitis etc will affect different regions of the scalp and with a different onset & progression.

And remember, by the time YOU, the practitioner, can spot a patient is losing hair when they simply walk into the room, they have ALREADY LOST 50% 😢 This is why I think we need to push back against the silence. The research is unflinching about the serious psychological impact this has on women – especially in cultures which place so much emphasis on looks generally, and hair, specifically as a commodity of very high value in women.  The diagram above comes from a 2019 update on the phenomenon of FHPL and it’s a good articulation of the knowns and unknowns (pssst spoiler alert…it ain’t about androgens!) but let’s never forget the other causes and cures.  So let’s make sure as the trusted practitioners women present to so often, we are sensitive enough to have this tricky conversation & skilled enough to help 💪

Stop Pulling Your Hair Out – The FPHL Answers You Need

Female Pattern Hair Loss (FPHL) is everywhere, perhaps you just haven’t been looking.  As the leading cause of alopecia in women globally and with 1 in 5 women affected at any age, we’ve all got clients who have FPHL to different degrees.   We need to be better able to recognise the early features of this condition which profoundly impairs quality of life and induces depression in its sufferers and that begins with validating patients’ concerns when they report “thinning” or “increased losses”.  But what do we do from there?  This recording talks you through the assessment, diagnosis and management of FPHL based on a combination of the most recent research and Rachel’s clinical experiences.  Once you’ve ‘seen’ FPHL.., you won’t ever ‘unsee’ it and your patients will thank you.

Following The Fenton Fall-Out

I confess I was a chemistry nerd ‘way back when’, but my skill for stoichiometric calculations had sadly slipped by the time my kids needed help with high-school science & now my son, who’s about to graduate from chemical engineering, is my ‘chem-friend’ 🙄🧐 I suspect he feels FB messenger wasn’t intended for such use – or at least there should be some veneer of, ‘Hi darling how are you?’ before…’Need to talk through these pharmacokinetic datasets’ However, the one equation that was like turning a light on in my brain & therefore never forgotten was the Fenton reaction – basically metals’ MO for messing with our biology, especially iron.  Turns out – it’s the most essential and helpful in understanding health & disease:

Endometriosis
IBD
Neurogenerative disorders: MS, PD, Alzheimer’s
Higher than healthy GGT
Impaired COMT or catechol excess for other reasons
Cardiovascular disease & Diabetes
Vitiligo
Both the Big Cs
Heavy metal burden
Iron dysregulation (Obesity, HFE mutations, Thalassaemia) & Excess (IV or oral over-treatment etc)

(almost) All roads lead to radicals & reactive species…if you follow the Fenton pathway & iron leads us down this path more often than any other metal.  Certainly sometimes for good: like protecting us against pathogens and destroying dodgy cells, but when it gets out of hand, a key pathophysiological process in a long list of disease.  So understanding how to recognise patients prone to dysregulation of this mineral, avoiding iron over-treatment at all costs (I am seeing incorrect and excessive use of IV iron in many patients make it stop!) and identifying means to contain and control its movement, are important.  Oh and in case the Fenton has faded in memory, it goes a little something like this:

The Fenton reaction. Repeated cycles of oxidation and reduction of iron in the presence of hydrogen peroxide generates reactive oxygen radicals. 

While rates of iron deficiency and related anaemia continue to grow, the increase in prescriptions of IV Fe have expanded exponentially in western countries. What is behind this change in practice regarding how we treat iron deficiency and does it match with responsible prescribing? Do the benefits always outweigh the risks?  And while we’re on the topic, who is most likely to benefit and what are all the risks? In light of a current class action in the US, relating to a lesser talked about adverse event associated with IV Fe and recent complaints here in Australia against GPs, allegedly due to inadequate information to enable informed patient consent…it’s time to answer these questions and more. When is IV Fe a means of rescue and when is it a risky repletion strategy with no evidence of advantage? Click here for this episode.

 

 

I’m Using My Inside Voice 🙄

Maybe it’s tax-time, just my wintery whinge or a tirade triggered by missing my twins’ 21st birthday due to border restrictions 😶 but I’m sorry for all the shouting of late…about interpreting iron studies, about the copper misinformed etc etc. and my gorgeous new grad mentees copped a full monologue, with links to articles, recordings & the Coeliac Society, when they asked me to expand on why we must exclude coeliac disease before removing gluten from anyone’s diet.  I was so glad they asked though!  I’m now using my inside voice.  

But I don’t want my message to be misdirected and I fear it might be.
It’s not you and it’s not me

‘We’ are doing our best.  We are working in a field that demands us to be across soooooo many domains of knowledge and information, from the basic & not-so-basic medical sciences, to pathology interpretation, nutrition, herbal medicine and beyond.  It’s a lot.  None of us are across it all. I’m certainly not.  And I’m aware, that the frustration I feel at others’ misunderstandings sometimes is unfair, because I’ve benefited from excellent early teachers all the way through to having a job now, that keeps my head in the research daily. And even still, without a doubt, the gaps & shortfalls I observe and criticise in others, I could have made of myself, earlier in my career. We don’t know what we don’t know, until we know better, right.

It’s them

Who is this ‘them’ of which I speak? Well, 25 years ago when I completed my under-graduate (and walked 10 miles to school in the rain, without shoes or breakfast 👵) I believe I received the training required to be the naturopath that I needed to be. Safe, effective, knowing my scope – which was basically coughs. colds, atopy and risk mitigation for future chronic disease.  I never saw a lab test during my under-grad. I would have read a set of iron studies badly and something like ELFTs, like it was Latin. I wasn’t made aware by my lecturers of the critical part I could play in my patients’ lives, either by advocating and advancing correct diagnosis or by obscuring, confounding and delaying it (sorry, still thinking about the gluten debate!).  But back then, I think this was appropriate for the time, the state of play of our collective medical knowledge and for the role naturopaths were playing in the health landscape. Not any more.

If you haven’t had a chance to read the extensive research about ‘us’ (Australian nats, nuts & herbalists) published of late,  who we are, what we do, how we are viewed and what our patients expect, then you could be in for a surprise.

We’re perceived by many, if not most, of our patients to be a primary health care provider – either flying solo or co-piloting with the patient’s GP (& no auto-pilot function!!!) and as clinicians for chronic comorbid cases not the acute cold. My how times have changed and the question is – has the knowledge and level of competency of those in educational roles & the quality of what they deliver a good fit? Sorry, but if the majority of a large new graduate cohort have left their training with a mantra of ‘we must not diagnose’ and INTSEAD are likely to advocate a gluten free diet RATHER THAN Coeliac testing with the patients doctor first – then we’re falling at the first: Primum non nocere. Sorry,I forgot, inside voice 🙄🤐

Closing the Gap on Coeliac

This Update in Under 30 recording speaks to the seriousness and primacy of identifying Coeliac Disease in any patient reporting a suspected reaction to gluten and takes you through the latest evidence on the best screening protocol.  With an increased understanding about the strengths and limitations of gene testing, serology and biopsy, we have a clear map to follow now.  Along the way Rachel outlines 3 additional potential mechanisms for ‘gluten’ reactions amongst our patients, what to look for and how to tell the difference. 

Cracking At The Corners?

Name a B vitamin. Hey, Bingo! It’s on the list!   What list? The complete one from all the review papers & references to possible links between individual nutrient deficiencies & Angular Cheilitis – inflammation & cracking at the corners of the mouth. So does that mean more Bs are the answer for people presenting with this painful, recurring issue?…Ahhhhhh No.  Yes, you heard me correctly, these deficiencies rarely cause the breakdown of the integrity of this very specific area of skin in the patients we see.   So now we have a double ouch, right?

We might send patients away with a B complex and some lip balm and over a week the cheilitis resolves – which one was the most therapeutic?
…I hate to tell you 👀

What is the underpinning cause(s) & the important message we are missing with this presentation?  Well, it could be one or more of a long LONG list of differentials, ranging from anatomical, habitual, immune related to iatrogenic. And while many nutrient deficiency pictures can include this feature and therefore make the ‘possible’ list, only one makes the ‘probable’ list. And that’s iron but only in severe deficiency, aka anaemia and only affecting 1 in 5.

Me???
…Telling anyone to push the nutritional issues further down the list of differentials for any condition?
Well, that’s unexpected
…possibly unprecedented

And no, antifungals aren’t the answer either. Yep, that might be worth a listen….👂

 

Just an annoying, embarrassing, cosmetic condition or could it be the clue that helps you ‘crack the case’?  There is a surprisingly long list of differentials for this condition but most of us only know a few, reflexively reaching for either B vitamins or anti-fungal creams. Does either make sense?  Does either address the cause(s) which we now recognise to be a unique series of risk factors in each individual?  Or are we at risk of shooting the messenger and missing the message of Cracking Corners altogether?
You can purchase Cracking in the Corners – Angular Cheilitis 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.

Slippery Little Sucker Indeed!

[Ahem] Ok let me explain…Several catch-cries from Australian ads have earnt themselves a lifelong place in my head and heart, taking up space where something more important should be, no doubt, but does anyone remember this SPC canned fruit (REALLY showing my age now!!) one, where the little boy chases the grape around the bowl and declares it a, ‘Slippery Little Sucker!’? Ok so this little boy is every one of us when we’re trying to ‘capture someone’s cortisol’ and just like the boy we will eventually achieve a ‘result’ – get a ‘number’ but what in fact does this mean in relation to your patient’s HPA axis, stress perception, responsivity, recovery etc etc?

Recently I was presented with 2 cortisol results for a patient taken within the same 24hrs – her blood am result was above range, while her 24hr urine flagged under-functioning of her HPA axis generally.
Both were accurate.

Had I have only have seen one, I would have formed the wrong opinion and only gleaned part of her overall HPA story.  Every different type of cortisol capture – from different mediums: blood, saliva & urine – to different collection conditions: time of day, fasting V fed, specific stressor exposure etc answers a different question about our patient’s HPA axis.  So to use any form of cortisol assessment well we need to start with 2 understandings: 1) it is a slippery little sucker indeed and no one test can answer all our questions – or as Miller & colleagues more eloquently put it, “Remember, all models are wrong; the practical question is, how wrong do they have to be to not to be useful” and 2) be clear about the most important question you have about your patient you are trying to answer and that will make your choice of test (& timing & & &) patent. But do you know enough about cortisol regulation to be clear about the ‘sweet spot’ of each test?

The Cortisol Awakening Response has understandably attracted the bulk of the research focus over the last decade and accordingly has risen in popularity in practice & while it remains a very valuable way to answer certain questions about patients, our understanding of its limitations continue to grow.  For example there is a disconnect between CAR & diurnal cortisol secretion – so in essence your CAR can look woke but your ‘Slope’ may be broke!  If you’re a fan of this method, make sure you catch up on the CAR-Expert Consensus Guidelines by Stalder et al and if you’d like to get clear about which test and when, when it comes to all the key options for Cortisol Capture..
then let’s dive in together with my latest Update in Under 30 instalment

 

Cortisol – Have You Been Caught Out?

I have!  And just recently a stark contrast between the results from 2 different methods of cortisol capture in the same patient illustrated just how likely this is. How do we ‘capture’ something so ‘dynamic’ and  interpret anything of substance from a ‘static’ assessment technique?   But rather than throw up our hands and throw out the whole attempt to measure cortisol, we can improve the rigor, reliability and real-world meaningfulness of our patients’ results by refining our timing of tests, choosing the medium wisely & manipulating test conditions to answer specific questions about their HPA function.  Great desktop reference included!

 

You can purchase Cortisol – Have You Been Caught Out? here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.

What’s happening with Lucy’s Labs?

What’s your knee-jerk response to 52Y Lipids Lucy & Liver, whose ALT & AST suddenly jumped above range when she was put on statins?  They’re damaging her liver?  You’d be wrong.  One of the practitioners who undertook the MasterCourse in Comprehensive Diagnostics just graduated with flying colours when she was able to correctly identify the true cause of this patient’s LFT abnormalities, can you? 

[Cheeky hint: there is more than one explanation/process at play]

This naturopath now knows her pathology patterns.  She knows the interpretation of any liver enzyme must also take into account the movement in other markers, to make meaning of the whole.  Because so-called ‘liver enzymes’ are never exclusive to the liver.  They are expressed in multiple other tissues and organs – sometimes at equal concentrations to their liver-level (e.g. ALP and bone). For some, even referring to them as a ‘liver enzyme’ is a mislabelling of sorts, with minimal expression in the liver itself compared with ubiquitous distribution all over the body (e.g. GGT & LDH).  Of course this is both a blessing and a curse.  A curse if you make the mistake of only interpreting their levels through a ‘liver lens’…a blessing if you know when they are flagging problems elsewhere through the specific pattern recognition.  So back to Lucy – the statins had induced a rhabdomyolysis not hepatocellular damage. The clues?  Significant AST dominance over ALT, above range CK and LDH.

So if the statins weren’t causing increased hepatocellular damage what is that increasingly high-normal ALP pattern all about?

Bones. And again, this practitioner picked it.  And then got to win herself some pretty BIG credit and credibility points with all the other health professionals sharing care of this patient by suggesting that they clarify and confirm this by referring her for an ALP bone isoenzyme assay, which answers the question: is the elevated ALP originating from the liver, the intestines or from the bone? Bingo, bones it is!  Or was, because this practitioner was able to alert not only the patient but all the other practitioners treating her to the increased bone remodelling taking place, independent of the statin reaction, but part of her perimenopause. Left unchecked this would escalate further of course at menopause and leave her bones in bad shape. This is just one illustration of how we can show ourselves the be the incredible one we are on the shared-care team. 

Being lab literate and pathology proficient, sets you apart from the rest and enables you to practice truly preventative medicine.
How else would we have known she was experiencing increased BMD loss that may be the start of something truly tragic?

 

Realise the true value you can extract from the most commonly performed labs.
Join Rachel Arthur LIVE on the MasterCourse I: Comprehensive Diagnostics WATCH PARTY
This skill is the biggest ‘game-changer’ in Integrative Medicine!
Want to know more? Head over to my website here and check out more of the great benefits and bonuses of joining this program
This course is a fantastic learning opportunity to identify the many intricacies in cases that have previously been missed.

B12…12kms?

Is it just me or do you view everything with a trained eye?   My son always laughed when I wrote him a shopping list: I would list items under each shop and I always wrote down our local supermarket the Independent Grocers Association, like this: IgA…you all see what I was doing, right?!! It’s actually known to everyone else as IGA…well truth be told, I didn’t until he pointed it out 😂 Then there’s this relic I regularly pass, as I walk through bushy parkland near my home, ‘Hmmmmmm, B12 hey?’, I’d muse. I’d be embarrassed to tell you exactly how long it was before I realised OMG it’s not  a shrine to the vitamin but an old road sign telling you…Byron 12kms!!! 

I preferred my take on it to be honest, because invariably once past this, the remainder of my walk was full of scintillating B12 banter. Just internally, people, no one panic, I don’t walk the streets of this town spouting out crazy random nutritional tidbits…although, let’s face it, I would be in good company in, the Byron Bay region!

I have a deep respect for B12 – weird but true. As a result of my clinical experiences helping patients who had a previously ‘unseen need’ for this nutrient and the significant improvements that come with its replenishment. Plus the deep dive I did into the science of the different forms and their actions last year. In particular, I now have 2 families where the TCNII SNP is evident in mum and all her children.  No gene testing necessary, the pattern is self-evident once you know what to look for and the clear ‘call to action’ – more B12 please! And just this month, a fresh aspect has come to my attention in regard some brand spanking new research on B12 and IBD and the microbial (im)balance of this vitamin as a pivot point for the pathophysiology. Wowza!  Early days, but I think we’re headed next level on this nutrient again! And I can’t say, I’m surprised.  For while I don’t think the CHOICE of the supplemental form for B12 is complex at all (hence why we need to separate the B12 from the B*S#!) I recognise it is a complex character far beyond what regular dietetics has reduced it to. 

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.

 

Every Woman & Her Dog

The average woman & her dog (& likely every other member of her household, be they furred or otherwise), can tell you that sudden changes in sex hormones can undermine, derange, psychopathise, impact her mind and mood.  Hey, for me most days reverse parking is my mild super power, the envy of all, but on day 26 of my menstrual cycle, I can struggle with a ‘nose-to-kerb’! But if we are quick to attribute this to the fluctuating sex hormones produced by our ovaries, alone, we’d be making a mistake.  A portion of these peripheral steroids do cross the BBB and act in our brain, so changes to these levels during any kind of transition: follicular to luteal, pregnant to post-partum, menstruating to menopausal, early adulthood to andropause, will be ‘felt’ but the sex (hormones) we have on our brains at any given time, are far more abundant, potent and complex than this, thanks to the brain’s ability to make its own.

So in fact, the amount of sex hormones active in the brain represent an intersection between peripheral and central steroidogenesis. 
These Neurosteroids, made ‘on site’, are as much produced in response to our mood, our neurobiology, our psychological and environmental stress, to help us navigate these, as they are the creators of mood itself.

Yes, these particular sex hormones, due to their actions in our brain, belong to that growing list of CNS celebrities: the Non-Classical Neuromodulators.  Which, for the otherwise neurotransmitter-centric & obsessed among us (that’s everyone), makes mental health and illness much more complex than ‘serotonin deficiency’ or ‘glutamate excess’ and a whole lot more real.  We now need to consider other entities like: ‘suboptimal LDLs’, 5 alpha reductase over or under-expression & ‘xs inhibitory tone via progesterone’.

The ‘sex on the brain’ of any patient therefore is impacted by both their Endocrine (ovaries, testes, adrenals) and Synaptocrine (neural) contributions – and these demonstrate some shared dependence (for cholesterol & healthy mitochondria etc) and independence.

We all know the depressing stats in support of the ‘ovarian withdrawal hypothesis’ and the risk to women’s mental health with each reproductive transition, and also in andropause in men, but the time has come to now deepen our understanding and to recognise  we can have an imbalance of ‘sex’ on the brain – regardless of the ‘balance’ we might see in the periphery and put our thinking caps on about the options we have to address steroidogenesis either side of the blood brain barrier.

When it comes to a modern take on how sex hormones impact both the structure & function of our CNS, we need to blend the ‘old’ with the ‘new’.  The ‘old’ tells us, production of sex hormones is in the gonads and action at a distant target anywhere else in the body, including our brain. And the ‘new’ is in the form of the ‘Synaptocrine’ – where production of these sex steroids is actually within neural tissue itself and their immediate actions occur close-by, in the synpase and at the post-synaptic neuronal membrane. These two contributive pathways show some shared dependence but also independence from one another and the balance of both has now been recognised to be integral to the overall health of the nervous system.
You can purchase Sex (Hormones) On The Brain 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.

 

Present But Not The Problem

Something’s just come up today again and I think we need to talk about it.  A positive result on a stool PCR microbiome test for H. pylori, understandably, might be heard as a clear call to action to go in guns blazing with an eradication approach.  But is it?  Trust me, I’ve had more than my fair share of battles with this bug & can understand being keen to have it be gone BUT first things first, let’s be clear about what the result speaks to.  

Does it say, “Here!  Look over here!  Here’s the source of your patient’s GIT distress,”  or even, “Here’s a pathogen that has taken up residence in their GIT and is a risk for future dx!”

No, not necessarily. It speaks to its presence.

And that may be only fleetingly, as it passes through.  I’ve seen it before and so have many other experienced practitioners: a positive stool PCR that is at odds with the results of gold standard H.pylori testing, the UBT, faecal antigens or blood serology, all freely available through the GP.  And the reality is, if you have a negative UBT, there’s no urease production, the trademark trouble-making of this bug. If you have negative blood serology, your immune system has never ‘met’ this bug or, in the minority of cases, you’ve tested in that brief early exposure window prior to antibody production (2wks) so you should retest within the month, to confirm or refute. And if you don’t have any faecal antigen…it ain’t in da’ house…so to speak 😅 If there’s something new here, then have a quick read of Medscape’s great work-up summary.  So, clearly we need to confirm before we open fire.

 We (me included) have been so single-minded about increasing the ‘sensitivity’ with our testing methods, we may have left ‘specificity’, in broader sense, behind & that creates a new problem.

This leads us and the patient down the garden path of false attribution and time and money wasted ‘treating’ a ghost gut issue. And no one wants to be put on a pylori protocol when they really didn’t need to.  Trust me 🙄 But if someone does come back confirmed, well then…

H.pylori – Eradicate or Rehabilitate?

For a bacteria identified just a few decades ago as being a cause of chronic gastritis, atrophic gastritis and gastric carcinoma, the escalation of number of antibiotics used to eradicate it (4 at last count + PPI) has been nothing short of breath-taking.  A management approach more consistent with both integrative medicine and with an improved understanding of the delicate microbiome focuses on changing the gastric environment to ‘remove the welcome mat’. What do we know about how to do this successfully? It turns out…quite a lot.

Real-time Diagnostics on the Couch!

Well, this is different, now I’m watching you! 😆 In early 2021 we released our very popular MasterCourse I: Comprehensive Diagnostics, as a ‘self-paced’ online offering for the many who missed out on attending live in 2020.  Many have grabbed this opportunity with both hands (& a headset and some hardcore Do Not Disturb! signs) but we know that for some, doing the entire course on your own, >24hrs of video presentations, can be a tad onerous & overwhelming. We want to remove these barriers and empower & upskill as many practitioners in pathology interpretation as are keen, and as a means to achieve this, we’re offering the MasterCourse I Watch Party.  So bring your bhujia and a beverage and let’s do this!!

Practitioners who sign up for this will be able to watch each session’s video replay live with other practitioners and have the opportunity to ask Rachel questions & participate in case discussions at the end. Another key detail is that we will run the sessions weekly, so that the full course is covered in just 6wks, from July 8th to August 12th.

MasterCourse I: Comprehensive Diagnostics LIVE WATCH PARTY
24 hours of live Zoom sessions + Bonus sessions!
8, 15, 22, 29 July & 5, 12 August on Thursday at 3.30pm to 7.30pm AEST.
Each Thursday, the video presentation for that week will be played so we can watch it together. Then Rachel will open up her webcam and mic, inviting you to do the same, to participate in a Q&A  as well as set case discussionsWhen you register, you get immediate access to watch our preliminary/preparatory sessions, prior to 8 July: Accurate Pathology Interpretation Starts Here and the RAN Patient Pathology Manager Tutorial.

Below is an overview of the Watch Party schedule.

Week 1 – 8 July | SESSION 1: Acid Base Balance & Electrolytes
Week 2 – 15 July | SESSION 2: Renal Markers
Week 3 – 22 July | SESSION 3: Liver Enzymes
Week 4 – 29 July | SESSION 4: Lipids & Glucose
Week 5 – 5 August | SESSION 5: Immune Markers
Week 6 – 12 August | SESSION 6: Haematology

“I thought my pathology skills were pretty up there until I did Rachel’s Diagnostic Masterclass course!  Nothing like being knocked off my perch by a literal avalanche of new information, especially when it comes from the most commonly tests that we all use so often.  The course has been a fantastic learning opportunity for me, and has since helped me pick out many intricacies in cases that have previously been missed.  

The course structure was great, the level of detail was right up my alley, and the case studies were entertaining (in true RA fashion).  Once again Rachel has increased my knowledge base, and help me provide way better service to my patients.” – Rohan Smith, Naturopath


Join Rachel on MasterCourse I: Comprehensive Diagnostics Watch Party and register here.
MasterCourse I is a pre-requisite to join MasterCourse II which will be delivered live in 2022.

Well…Does He Need Iron?!

If I could be granted 1 wish regarding all health professionals, it would be that we were all competent in reading Iron Studies.  Think that’s overstating the issue? Or not a bodacious enough way to ‘spend’ my wish? I don’t. Especially when you consider the impact of GPs in this space. 

This 57Y male was asked to make a follow up appointment with his doctor, to discuss his ‘abnormal’ results which he was informed constitute Iron deficiency. 
Consequently he was was advised to start an iron supplement! #@!*

Your thoughts?  Revoke this doctors medical licence?  Insist on some very du jour ‘re-training’ at the very least?  I mean, if you think this Iron pattern flags a deficiency or shortfall, then you’re as good as reading a map upside down and back to front…and written in a foreign language!! The ‘Ls’ in his latest labs flag he has suppressed transferrin, indicative of negative feedback inhibition of GIT uptake of this mineral, secondary to healthy stores or inflammation. And it’s not just that more iron is not indicated but that more iron in fact presents a patient like this with increased and unnecessary risk: to their microbiome, intestinal wall health, even according to the larger longer studies a potential correlation with colorectal cancer risk, if taken long term. Let alone the whole cardiovascular conundrum.  Better still this same patient was told a few years back that he might have iron overload!  Again the ‘map’ could only have been being read, upside down, back to front to reach such a conclusion! 

So the one patient in just a few years by 2 different doctors has been diagnosed incorrectly with 2 different iron issues. Yep.

And sadly I have sooooo many more cases of missed and mis-diagnoses with regard to this mineral.  The latest RCPA Position Statement on the Use of Iron Studies, underscores that assessment of iron status and GPs competence in knowing when to do this and how to interpret, is an important part of core general practice. Given it “is the commonest nutritional deficiency state in Australia and is significantly under-diagnosed” This succinct document offers a quick crash course in Iron nutrition for doctors and it hits all the right marks with advice about not ordering ferritin as a stand-alone because “the interactive nature of the three components allows for more accurate interpretation” and this simple but sage advice:

Transferrin, iron transport protein, tends to increase in ID…
A better strategy (than being tricked by Serum Fe) is to report transferrin saturation.
A low transferrin saturation in the setting of an equivocal ferritin level is suggestive of iron deficiency.
An elevated transferrin saturation is the first manifestation of iron overload.

I mean seriously, do doctors read these RAGCP resources & recommendations, or is it just me? 🤓😂  

Need a rip-roaring review on how to really read iron studies?  Or know another health professional who does?!! Consider this Easter Educational Gift Instead of Eggs!!
So You Think You Know How To Read Iron Studies?
Overt Iron Deficiency Anaemia or Haemochromatosis aside…do you understand the critical insights markers like transferrin and its saturation reveal about your patients iron status?  Most practitioners don’t and as a result give iron when they shouldn’t and fail to sometimes when they should.  This audio complete with an amazing cheat sheet for interpreting your patients Iron Study results will sharpen your skills around iron assessment, enabling you to recognise the real story of your patients’ relationship with iron.

 

Ask Alexa?

‘Hey Alexa, What’s that formula for correcting urinary iodine for hydration status?’
Oh yes, if only she could answer these kind of questions!

There’s no one here by that name but we get these kind of emails all the time [Oh and also for Freya who hasn’t worked here in like 5 years!!😂]  But we love them because it means our blogs provide useful, sought after and (we like to think!) really really hard to get anywhere else answers . But hey try it, Ask Siri!  We’re always forthcoming with references – not just citations but the full low down and dirty full texts (as long as we’ve managed to get our hands on it!!) and we know which topics particularly hit a spot across our professional group by not just the number of enquiries but how far the actual blog they’re referring to, dates back.  So we’ve just received more comms regarding one that’s often on high rotation…a post I wrote on urinary Iodine Assessment & how and why we should adjust for hydration!  That was 2014…what a vintage 🤩 Show’s though how topical and tricky this little test is. 

So I dove back into the musty archives (no seriously we don’t use parchment) and thought it might be good to create a central source for all things Iodine…because…well there’s a LOT!
If you haven’t read the original post on the iodine creatinine correction – the fun starts HERE!
We named names (the companies that did correct for creatine and those that didn’t) – way back in 2015
We told you companies may change their reporting style but there’s one easy way to tell if the correction for hydration has been done for your patient’s results
I clarified, the Pitfalls of (so-called) Patch Testing for Iodine Status
And we linked you to my Free-for-all-FxMed talk on the Intricacies of Iodine – which discussed assessment & so much more!

Then there’s iodine and breast pain, iodine and sub-fertility & & &…& [ahem] turns out I perhaps have been a little Iodine Infatuated.  But you know, it’s still 100% warranted, right?  I mean here’s that latest Newsflash post Australia’s ‘genius’ bread fortification: Women Remain at Risk of Iodine Deficiency during Pregnancy: The Importance of Iodine Supplementation before Conception and Throughout Gestation. Oops, Britney style, I think I just did it again! Oh and don’t forget our website does have a search function – top right 😉

Iodine Deficiency, Toxicity & Treatment – Where are we now?

The iodine landscape has undergone radical change recently.  We’ve moved from recognising the resurfacing of a widespread deficiency, to large-scale food fortification that has failed to correct deficiency in most and produced excesses in a few. Parallel to this, we have the ever growing incidence of thyroid disorders and some radically contrasting ideas regarding iodine’s role in both aetiology and treatment.  Micrograms V milligrams?  Random urinary iodine or iodine loading test? Important new evidence and clinical experience helps us understand more about how to accurately assess patients’ need for iodine and know when & how to use it therapeutically & when not to!

Are You Ready To Be Lab Literate?

The first time I saw a set of lab results was when a patient brought them in to her appointment.  True.  In spite of the comprehensive training I’d received in nutrition and biochemistry and pathophysiology my undergraduate did not include one single lesson on lab interpretation & now here I was faced with some badly formatted inkjet printed document full of numbers I was supposed to make sense of.  Was the patient right to expect me to be lab literate?

We profess to be proficient in identifying and correcting nutritional deficiencies, as much as, cardiovascular risk, chronic inflammation, methylation imbalance etc etc so surely these ‘numbers’  are essential to informing our baseline understanding of & decision making regarding the management of our patients, as well as tools for monitoring their progress & safety.

Let alone the knowledge we need to work collaboratively with other health care professionals and show ourselves to be the asset that we are. 

And herein lies the golden opportunity, I believe.  Most of us do possess excellent foundational knowledge in nutritional biochemistry etc, much more so than other health professionals, who are ordering and seeing these results routinely, they will often tell you this themselves. And while more recent naturopathic, nutritional & herbal medicine graduates have had some basic orientation and education in pathology, are we really making the most of this powerful marriage of knowledge areas? What would we see, if we made it our business to view the same labs? So much more.

We can see warning signs well before the diagnosis, we can see the process behind the emerging or established pathology rather than simply a disease label, and accordingly, the individualisation of our patients’ presentations and their prescriptions. 

But first we need to learn our labs.

That very first patient who turned up with results in her hot little hand started me on this path to lab literacy. Later, I was lucky enough to find a kindred spirit  & mentor during my time at SCU, with Dr. Tini Gruner and then Dr. Michael Hayter, whom I co-presented my first diagnostics course with many years ago, and every day my patients and my mentees’ deepen my understanding.  This path to lab literacy goes on forever I suspect, but with every new corner I turn, I am reminded of and rewarded by all that it has gifted me and my patients. 

I’d like to share that gift with you through stories filled with new favourite characters, like ‘Mr More More More Monocyte’ above, engaging animations, loads of real cases, heaps of humour and plenty of practice in pattern-recognition, that make remembering, what can be very detailed content, doable.

In other words: The MasterCourse in Comprehensive Diagnostics I is finally here as a self-paced learning program you can undertake yourself.  We know you’ll get as much out of it as those who attended live:

 

“I thought my pathology skills were pretty up there until I did Rachel’s Diagnostic MasterCourse! Nothing like being knocked off my perch by a literal avalanche of new information, especially when it comes from the most commonly tests that we all use so often. The course has been a fantastic learning opportunity for me, and has since helped me pick out many intricacies in cases that have previously been missed.”
– Rohan Smith | Clinical Nutritionist

 

MasterCourse 1: Comprehensive Diagnostics is a self-paced online program
Gives you access to 24+ hours of streamed video presentations2 x Bonus Update in Under 30 episodes (The Calcium Conspiracy & Using Urea to Creatinine Values for Protein Adequacy) PLUS resources, a template and pdfs of all presentations. This package includes $200 worth of bonus material and remains forever in your online account. You will also receive access to any future updates of resources and our template. More information can be found here.

This is a pre-requisite for MasterCourse II that will be delivered live in 2021.