[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.
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.
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…
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.
Well, obviously(!)…this has been a year heavy on pathology interpretation for me and the huge number of practitioners who’ve just spent the last 6 months taking that learning journey with me. I celebrate and congratulate them all for their commitment to their own professional development and also their investment, in what is arguably, the most potent yet overlooked set of skills of any health professional… the ability to read bloods. Basic bloods. Mainstream labs. No…but to really read them. Backed by all the scientific understanding about what these parameters actually are, how they perform and what they (dis)prove e.g. subclinical inflammation and ramped up oxidative stress – not an informed guess but mappable…right there but where no one else can apparently see it! But I digress!
Actually what I wanted to discuss was the whole erroneous notion of ‘normal’.
No, I am not speaking from the heart about my personal quirks, sense of humour or dress sense but rather the incorrect assumption that a reference range defines ‘normal’ and that our answer for each patient and each result is, a Yes or a No!
In this brilliant article by Whyte & Kelly published in the BMJ they spell out this falsehood succinctly. They note that the term ‘normal range’ has slipped into medical language from the misunderstanding that all lab results follow a Gaussian (aka bell shaped curve & later referred to as ‘normal distribution’) pattern but many simply don’t. So for some parameters a result near the ‘middle of the reference interval’ constitutes aspirational whereas for others it spells danger. Add to this, that these reference intervals are mathematically determined to reflect the expected values of 95% of your patient population (mean +/- 2 SD either side) so…that means the chance of a YES…”Your patient’s results are ABNORMAL!”… is just 5%. And hey…who said all the values within the reference range are all equally “normal” or better yet, healthy?! Not these authors, nor I, nor the praccies who’ve just done our course. So while, in many regards, these goalposts are too wide, they are also too narrow – typically only representing a subset of adults age-wise and Caucasians, yes they are both ageist and racist (yep, I said it!). And if our practitioners have learnt anything it’s about keeping an ol’ eagle eye on the sneaky intra-individual shift! Only spotted, of course, if you know your patient’s normal (not theirs compared to anyone else…just theirs) and then spot a shift. [I can hear they’re shushing 🤫me…they’ve got it already, alright!!]
So this is music 🎻to my ears, from Whyte & Kelly:
“The intraindividual variation in laboratory values is usually much smaller than the interindividual variability (ie, the variation in the population). Variation in the concentration of an analyte, if significantly outside of a patient’s usual values (but still within the reference interval), could be a sign of early or latent disease”
So if you want to tap into the power of pathology…start with Whyte & Kelly, maybe even dip your pinky in the pool by checking out Accurate Pathology Results Interpretation Starts Here – an easy little 1.5hr kickstarter…or jump right in the deep end with the rest of us pathology reading polo players and sign up for the MasterCourse 1: Comprehensive Diagnostics for some DIY summer fun 🌊
ps I know
your type and know that is EXACTLY the kind of weird nerdy thing you have planned for your break…you should see my summer fun list!!! 😅
MasterCourse 1: Comprehensive Diagnostics is a self-paced online program due for release in December.
The course has pver 18 hours of video presentations plus 2 free bonus sessions 1) Accurate Pathology Interpretation Starts Here and 2) Patient Pathology Manager and access to resources and tools within, for your own use.
This is a pre-requisite for MasterCourse II that will be delivered live in 2021.
This skillset has been found by many to be biggest ‘game-changer’ in Integrative Health
You can view the full course outline here.
I feel a bit Trumpy…because whenever someone says ‘N-acetyl cysteine’, I want to reply, “Big fan, I’m a big fan”. And yes that’s an uncomfortable awareness. But unlike he
who shall not be mentioned, I can qualify my statement and provide supportive evidence, both of the research and real-world varieties. So, of course, can so many of you as well. I know of fertility specialists who place it in PCOS patients’ preconception prescriptions and respiratory specialists who regard it highly in COPD, CF and a range of other conditions. And I am a signed up supporter of its adjunctive use in many psychiatric conditions. Then there’s the biofilm-breaking buffs…
This is where non-believers might be tempted to call ‘Snake-oil!’
How can one very simple tricked-up amino acid possibly contribute to the health of so many systems? Oh, just via the chameleon qualities of its chemistry of course! As a rate limiting ingredient and precursor of GSH, as well as a potent mucolytic agent and and and…we get it. We surrender! But I want us all to back up here just a few steps. As a mucolytic agent…renowned for biofilm busting…hmmm. I prescribe a lot of NAC for a lot of people for a lot of days-weeks-months….because all the research in mental health points to it being a long-term intervention. I’ve heard Professor Michael Berk say, that patients still on it at 2 years had even more improvements than they had experienced at the 6 month mark and of course mental health, for most, is a chronic illness, so no one is surprised.
But we can’t contain its chameleon chemical qualities. Given orally, it will be having effects within the gut of these individuals on the way through…and not all biofilms should be busted, right?!
So what to do? Well thankfully, NAC is not something that patients rely on for short term acute effects, that would then make missing doses problematic – like pharmaceutical psychiatric medications, and some CAM options as well potentially, like SAMe and SJW. So a regular sNAC break is likely to be free from negative impact for those with mental health issues and in fact, beneficial long term. With all this in mind, we’re now using a dosing model of taking weekends off from this supplement – which works for most. Do we have any concrete research to say this makes sense and doesn’t compromise efficacy yet? Well no, and don’t hold your breath, because research can be very reductionistic (you heard it here first LOL) and there is a lack of consideration of the effects on an individual as a whole. The psych researchers are not measuring the impact of all interventions on the microbome of patients (yet!) and the gut researchers not always monitoring the mind. But we clinicians can pioneer the path, fuelled by two old buddies of mine: first do no harm & least medicine, best medicine, right?
Oh and has anyone managed to open a tub of NAC and not accidentally snort some?…I don’t have anything else to add or a solution, I am genuinely asking if this is humanly possible 😂
The Clinical Knack of NAC
“There are few complementary medicines that come onto the market with such a bang, opening up genuinely new therapeutic options for the effective management of such a broad range of health complaints. N-acetyl cysteine stands out for this reason and has changed the way I practice” Rachel Arthur
Want to learn more about its diverse applications? Check this out
I didn’t catch that Zonulin wave that hit Australian integrative health practitioners a few years back. I think it might have been after Dr. Frassano himself, made an appearance at one of our big conferences. Like the true bloody sceptic I am, I stayed dry on the shore. In fact, I chucked my board in my panel van and drove straight for the library to do some research. Yep…boy do I know how to have fun in the sun 😎 But I am really glad I did.
While I am forever grateful to researchers like Frassano and so many others, who pioneer new perspectives, if not paradigms, in health, I also know that research is a long, long, long road and sometimes we get a little over-excited trying to ‘catch that wave’ too early.
This was especially the case with Zonulin testing.
When I finally left the library about a year later in 2017, I flagged my concerns. As always, my stand was
subtle: Mind the Gap with Zonulin Testing. This was my Update in Under 30 offering, encouraging us all to think about this test more critically and make a balanced review of the evidence both for and against it, as a marker of increased intestinal permeability, especially in comparison with the Lactulose Mannitol Test, considered the gold standard of IP assessment.
I also flagged that not every individual has the capacity to make Zonulin no matter how ‘gappy their guts is’…and this was something most struggled to comprehend or accept. But guess what? This fact has now gone mainstream along with even more concerns regarding the inaccuracy of commercial Zonulin testing.
“Three genetic polymorphisms in human haptoglobin expression, Hp1-1, Hp2-1, and Hp2-2, are determined by the HP1 and HP2 alleles harboured by chromosome 16q22. As zonulin is the precursor to haptoglobin-2, individuals who bear the heterozygous Hp2-1 or homozygous Hp2-2 polymorphism are zonulin-producers whereas those with the homozygous Hp1-1 polymorphism are unable to produce zonulin.” But wait, Ajamian et al 2019 has so much more in store for any remaining believers. “In conclusion, the current commercial zonulin ELISA assays investigated in this study detect different proteins, neither of which was zonulin.” Yes, that’s what they found. Two different big commercial kit assays – one from China, one from Germany…neither actually measured zonulin. I am passionate about CAM and passionate about testing…but cautious & concerned about the CAM-Sham that does get peddled to us at times, under the guise of ‘cutting edge functional testing’. Another name for that..unfounded, not yet validated, waste of money and source of possible misdirection for the practitioner. It’s tough talkin’ Tuesday…just sayin’ 🙄
Need some more help to Mind the Gap with Zonulin Testing?
Following the important discovery of the role of intestinal Zonulin in the pathophysiology of coeliac disease our fascination with measuring zonulin in non-coeliac patients suspected of ‘leaky gut’, has moved faster than the facts. It’s time to critically reassess what value, if any, there is in testing serum Zonulin – which patients and when? Let’s talk about its false positives (flagging a IP problem when there isn’t one) and negatives (failing to flag a problem when there is one) and how it compares with the gold standard for detecting increased intestinal permeability, in our patients.
No doubt you’ve heard me refer to the thyroid Abs by their nicknames, TRAb is one I mention often, or Thyroid Receptor Antibody, as its mum calls it, when it’s in trouble. And it’s always in trouble! But TRAb is actually the collective name for several flavours of trouble. What these auto-antibodies share in common is the ability to bind the TSH receptors throughout the body. They differ however, in terms of whether, once engaged, they stimulate this receptor (mimicking the action of the real-deal TSH) or they block it, so that the real-deal can’t in fact dock and do its job. The contrasting consequence is clear: stimulating ones drive up thyroid hormone production, while the blocking variety contribute to low thyroid hormone levels – and what was meaningful was each patients (im)balance of the two to produce a net effect. Because yes…a proportion of patients make both.
In Australia, and many other countries, we previously measured TRAb as a sum total and then specified what fraction was each ‘flavour’ but then the ‘flavours went out of favour’!
So for a long time now, TRAb has been measured, undifferentiated, and the assumption is, they’re stimulating…because this is in fact a) more common and b) the most common reason this test would be referred for…a set of TFTs that look suspiciously on the high-side aka Grave’s disease.
But a new era has dawned, with many mainstream laboratories now opting for the more specific assay: Thyroid Stimulating Immunoglobulins (TSI)* over the old TRAb. Fancy schmanzy, I know. Considered more accurate in the detection of autoimmune hyperthyroidism and in this regard, we’re told we’ve made a diagnostic step forward and nothing has been lost. Except the much less common type of antibodies that bind the TSH receptor only to fill it full of gum so it won’t work. That apparently, due to its low incidence and reduced clinical impact is no longer something worth testing. So consider the TSI results for your patients, the new version of your old (drab) TRAb, with similar cut-offs etc. And remember detectable levels of this may be seen in toxic nodules, and acute toxic Hashimoto’s, as well as prodromal and active Grave’s disease.
AND DON’T FORGET
(and yes, I am screaming because it is so easy to forget!!)
Biotin!! Patients on biotin at the time of the test (even as little as 1mg as part of a formula) can produce False Positives for the TSI!!! And give you and your patient the ‘fright of your life’ with a pseudo hyperthyroid set of labs to match!
Need to read more on this because you’re left thinking WTF about the TSI?!@#%^ Check out Mayo Medical Labs (always a good go-to for info on pathology) or this recent review paper 🙂
*Note TSI does not stand for Turbo fuel stratified injection in this scenario!!
Want to learn all the thyroid antibody alphabet??!! Start Here!
Learn the ropes of Thyroid Dysfunction Assessment & Identification, including all the related thyro-nutrition! Rachel covers the key thyroid parameters both functional & autoimmune (TSH, T4, T3, rT3, TPO, TgAbs, TRAB). As well as the most accurate methods of assessing relevant thyroid nutrients: iodine & selenium & a genuinely game-changing insight on interpretation of these . Finally she pulls all the individual parameters together to illustrate common patterns of thyroid imbalance – making it as easy 1-2-3!…almost!
Recently a mentee reported that when attending an in-person training event (remember those, everyone?!) she approached a sponsor’s stand, promoting practitioner training in the nutritional management of mental health, based on the pioneering work of American scientist, Carl Pfeiffer. But when she and her nat buddy started asking questions, those manning the stand asked whether they were doctors and then, upon finding out they were naturopaths, encouraged them ‘to move along – this information isn’t for you then’. Or something to that effect…Ouch!
While I know a little about the decision behind offering this training only to doctors and specialists at this time, and I do understand that organisation’s reasoning, I also want to reassure you, this doesn’t mean that Pfeiffer’s important work, and the efforts of those that have followed him, is out of bounds to others.
No one can copyright cortisol or TM TSH, right? Equally, Histamine is his own man. Carl Pfeiffer and others brought histamine, the neurotransmitter to centre stage and many of us working in mental health remain eternally grateful for this. But CNS histamine has come a long way since then…and is currently a very hot topic in modern molecular psychiatry where they are always looking for new drug targets, given shooting at the previous ones, risked taking ‘an eye out’! The recognition of histamine as a key player in mood, cognitive and behaviour has been long overdue but is absolutely here now! Just give this search term a whirl in PubMed: histamine AND psychiatry, and you’ll be hit with quite the crush of citations!
An abundance of important info at your fingertips…no secret handshake required.
It was, in part, this story that inspired me to record an Update in Under 30 on Histamine Imbalance in Mental Health. Just the proverbial straw on the proverbial camel really, after years of examining, experimenting and experiencing the incredible results some patients can achieve when this imbalance is identified and redressed. So I’ve done my darndest to pull together those years of hands-on helping histamine imbalanced patients with the latest literature in under 30 minutes!! Surprise! I failed! There is a lot to convey but you’ll also be surprised by what I don’t say…there’s no infinitely long list of personality peculiarities that fit with too much or too little. Nor is there a didactic discourse about absolute treatment dos and don’ts. I’m communicating the common ground between the original evidence, clinical empiricism and contemporary neuroscience. So this month, consider the ‘under 30’ bit, merely a ‘Serving suggestion’…which would necessitate you playing it 1.5 X speed…go on, I dare you!!😅
About 15 years ago I was introduced to Histamine as a neurotransmitter. Not the allergy mediator or the ‘basophil baddy’ but rather this prolific and potent neurochemical we all produce in our brains which, in the right amount, regulates almost every biological rhythm, helps with memory and mood & much more. Being able to recognise excesses or deficiencies of CNS histamine in mental health presentations and, ever since then, fine-tuning my ability to support patients with these, has changed my practise forever and has been the key to some of my patients’ greatest recovery stories. Forever grateful to the pioneers of this model, 70 years on, the model is ready for a mini-makeover, to bring it in line with the current scientific understanding of histamine, methylation, genes and much more. This recording, together with a hugely helpful clinical resource, will give you the confidence to recognise and remedy this important imbalance in mental health. If you want to download this recording click here.
We’re midway through mentoring 2020 and we’ve temporarily shifted gear out of case presentations and into dedicated time for answering praccies toughest questions…and oh man, I love these opportunities! This year in our Mental Health Primer Group, there are clinicians whose questioning…nEVeR sTOps. [insert: excited squeal] and that means I have an excuse to dig deeper, go further, read more research and ensure I can provide answers confident of their comprehensiveness and that they reflect all the contemporary information to date. So amongst stiff competition – here’s my favourite from the gIAnT piLE on my desk right now…
“We often hear that the bulk of our body’s serotonin is in our platelets – so do platelets (counts, activity etc) have a role in mental health?”
Well, I’m so glad you asked! Yes, 99% of your body’s serotonin is found inside your platelets. Where did this come from? From the plasma. How did it get there? Using the identical transporter mechanisms that your neurons do. Sounds like all the pieces fit right…oooooh so low platelets might drive low serotonin and poor mood and and and…
You may get excited when you get a box of jigsaw pieces but you must first complete the puzzle and ensure everything is in its rightful place.
Platelets are linked to depression but not as a cause but as a consequence. Because their transporter systems & receptors for serotonin are virtually identical to those in the CNS, they suffer from the same serotonin deficit…in spite of a relative abundance in the plasma they’re floating in. So really platelets are of interest in mental health as a more accessible way of studying and understanding neurochemical regulation in the brains of those affected. Did she just say neurochemicalS…as in, plural. I sure did. Because healthy platelets contain a whole plethora of substances, even a relatively large quantity BDNF, the concentration of which also becomes severely compromised in the platelets of depressed individuals. So it seems like its tough-talkin’ Tuesday and just to bust a few more
moves myths while we’re here…
Your platelets get their 5HT from the plasma
Your neurons make it themselves
Platelet numbers are not indicative of your 5HT producing capacity…anywhere
Therefore treatment objectives that speak to platelet numbers or platelet activity are clearly non-sensical
A bit like measuring serotonin derivatives in your urine…and imagining that reflects the <1% from your CNS….hey?
Yes. That’s what I said. Want to learn more? Please do. A great review paper by Marlene Williams, from the World Journal of Psychiatry, for starters, anyone? 🙂
If this last point is news to you…sounds like you really Need to Start Here! Accurate Pathology Interpretation
Don’t be fooled by the false promises of functional tests. Make sure all the pieces of the puzzle fit to actually make something sensible, accurate, reproducible and meaningful. Mainstream pathology results actually offer a goldmine of information and insight about your patients However to realise their full value and make the most accurate interpretations we need to first learn more about ‘lab language’, upskill in finding our way around reports which are packed with a surprising amount of hidden extras, demystify reference ranges and then develop a logical critical process we can apply to every result of any patient to get the real take-home. Packaged with numerous specifically developed resources to aid in your application of these skills this is a foundational offering that changes practices.
Given 1 in 8 Australians right now are taking an antidepressant, chances are you’re seeing a lot of clients on these, especially the SSRIs. Erica McIntyre (fellow naturopath) and colleagues, found that in fact, mental health diagnoses affect about 43% of individuals who choose to seek help from a naturopath or herbalist, so clearly this is across all of our waiting rooms. Accordingly, by this stage in your clinical career you’ve probably seen more than 1 patient taking the identical SSRI – e.g. Citalopram (aka Lexapro or Cipramil) Have you also by now, therefore come to ‘expect the unexpected’, when it comes to patients on the same prescription, in terms of ‘weight effects’? The majority not reporting this to be a major concern or issue but the occasional client, experiencing such significant weight gain, they may even have seen this as a reason to discontinue the medication. So what’s up with that then? Don’t we all wish we knew for certain! But getting our heads around the potential mechanisms is important for our patients, in terms of making more informed choices, as well as offering us insight perhaps into their neurobiological nuances.
Some of you will know, this used to be my place of business.
I have a background in the pharmaceutical industry, specifically psychiatric meds, more specifically SSRIs and even I find every time I duck-dive back into the literature I come up with more ‘fish’ – critical new information about mechanisms, secondary and unexpected actions, unforeseen benefits, barriers and yes, some sad or bad new detail. Consequently, I always field lots of questions about SSRIs in our mentoring sessions & one that often comes up is why some patients gain weight on SSRIs. What’s most curious to many, is how the weight effects of antidepressants can be hard to predict. There is not a consistent pattern across any specific antidepressant class, nor just 1 or 2 medications within a class, that will do it, while the others never will. This is in contrast to the many determinations and drivers for who will or won’t get discontinuation syndrome. So what mechanisms might be behind such an individualistic weight response and is there any way to predict or prevent this?
Here we find ourselves again with the question that keeps all IM practitioners awake at night:
A worthy question indeed. According to comprehensive reviews of this issue: there are still multiple candidates – one is the incidental histamine blocking that some SSRIs exhibit (could this flag someone low in histamine to start with??), while others still hold some suspicion over an old foe, elevated prolactin, that we can see in a minority of patients on these meds…easy to measure and confirm or refute, right? But always ask your patients first, How has your diet changed over this same period? How has your activity changed? You may of course find, you need look no further. People can give you the answer on a platter with things like, “I just relaxed a lot more: about what I ate and my weight”…Bingo! As always, the patient in front of you is their own little ultimate black-box…🧐
Leaving Anti-Depressants Behind
Never our call to make, but with 1 in 8 Australians at any time taking antidepressants, playing a supportive role for patients wishing to discontinue their antidepressant medication is common. So what do we know, about how to really do this well, what to expect and how to perhaps mitigate some of the bumps that might lie ahead. What in our artillery should we go in armed with either during the discontinuation or, better still, beforehand? This Update in Under 30 outline the key principles of patient prescriptions in this context and may assist patients, in their desire to truly leave the antidepressants behind.
If you are an Update in Under 30 Subscriber, this is a previously release episode and you will need to search for it to find this in your library of UU30’s that are in your online account.
Not an Update in Under 30 Subscriber? To access this episode and the entire library of Update in Under 30 audio’s and resources become a subscriber here.
Trends in mineral supplements are like music genres, you can pick which ‘decade’ they were formulated very quickly. But instead of going by clothes, hairstyles or even the style of accompanying music video, it’s all about the form – the ‘thing’ the mineral is bound to, that gives the game away. While mineral carbonates , sulphates and oxides seem to many of us contemporary clinicians, pre even MTV, amino acid chelates take me back to a time when I was wearing shoulder pads in everything, even my pyjamas. It was called power-dressing and needed to be adhered to 24/7, you see. Then along came fancy forms like orotates, aspartates, hydroxyapatites as we moved confidently into the 90s…well, as confidently as you can, when the Y2K bug may ‘end life as we know it’ come NYE. The dawn of the new millennium saw us embracing picolinates and bis-glycinates in a big way and for the last little while, citrates have really been having their time in the sun. But you know what…here’s a few things you MUST know…
- These are trends, not truths
- Every mineral has its Mrs Rights and Mrs Wrongs, in terms of chelates and ligands, and these are not the same from one mineral to the next e.g. Zn sulphate is a decent form of available Zn, Mg sulphate, an over-priced laxative
- In almost every case, there is simply NO strong consistent body of evidence that one form of a mineral is superior in terms of bioavailability, regardless of what companies tell you..go on I dare you…check their references and then do your own quick literature search away from the cherry picker
- Nor is there one mineral form that is above adverse effects in everyone
Brutal. Welcome back to ‘tough talkin’ Tuesday’ 😉 But we have to state these facts because we need effective supplements for our patients and not understanding the different forms that are better (but not ‘best’) compared with those that are inferior (this we do have some evidence of) threatens the integrity and efficacy of an otherwise well thought out prescription. So here’s where you might want to move into a room away from everyone and lock the door…because you’re likely to scream. One of, if not the most commonly used single nutrient supplement almost across the world, is calcium. After almost 30 years of studying supplemental forms side by side, can we conclude which form is best? No. How about ‘better’….hmmmmm yes…maybe…citrates look good going by some markers but not all and vice versa for other commonly seen forms. I can say this, because I have followed the research over the decades, reading the primary papers, like this excellent one by Bristow et al from 2015 that should burst quite a few people’s ‘best!’ bubbles. Have you screamed yet?
I scream. Often.
Because I am frustrated by the lack of research that we need, to be more certain of our preferred forms and then even more frustrated by companies’ claims that the evidence is already in, and guess what, theirs wins!
But it comes back to the same call to action for us – know your nutrients and specifically, where possible, get familiar with the Mrs Right and Wrong for each mineral! Know that the supplemental forms that work for zinc will not necessarily be a good match with iron, that any company that formulates their minerals in the vain of ‘one form for all’, be that glycinates, citrates, picolinates…well they’ve probably got a good fit for some of those minerals and a shocker for others. And as always truly check efficacy with follow up bloods, if you had baseline deficiencies evident in lab tests. I know, that’s not everyone’s model of practice right, or ideal but not always ‘real’, so alternatively, if you are prescribing based on clinical signs of mineral deficiencies that should respond quickly to repletion e.g. white spots on nails in the case of Zn deficiency, then ensure that they do!! If they don’t and your patient is compliant then consider switching form! When I see good practitioners’ prescriptions let down by poor choices of nutrient forms, well, that’s when I need to go into that separate room once more….can you hear me? Ooh that reminds me of something else dated by Mike and the Mechanics: Silent running “Can you hear me?!”😂
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’. And yes we even mention Mrs Right/Wrong forms for minerals. 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!
Click here to gain immediate access to Mastering Micronutrients – 4 hours & clinical tools that will seriously change the way you work in Nutrition
Gotta love all the clever inquisitive minds among our integrative health practitioner community. I think each of us, as children may have been that one kid who just never stopped asking questions. What a great quality to have because it prompts us to think outside the box, then outside the triangle, then the hexagon and beyond! Simultaneously, busy minds that never stop questioning and never quiet down can also feel like a curse! None of us have the time to go find the answer independently to every single question that our patient, prescription & pathology encounters raise for us. We need to use the force. Our colleagues, our workmates, our informal and formal practitioner networks, our mentors, our associations, our educators etc. A lot of practitioners recently got some questions answered with the Update in Under 30: Separating the B12 from the B*S#!...and then guess what…they had some more B12 related questions 😂😂
Q: What might a normal or even high serum B12 together with low Active B12 combination flag in a patient?
A: Exclude COCP use, & gross liver pathology, refer for B12 antibodies if possible & review the case for other evidence of functional B12 deficiency, as TCII values are more specific and sensitive than serum
Q: What evidence do we have to use a higher cut-off value than the labs give us for Serum B12 (< 400 pmol/L), as a decision limit for follow-up investigation for B12 deficiency
A: Just the findings of some of the biggest studies on B12 assessment – correlating serum values and markers of functional deficiency such as Harrington et al 2017, Spence et al 2016, which flag that there is already metabolic impairment typically when serum values drop below 400, well before the classic features such as macrocytic anaemia
You’re welcome 🙂 It’s nice to be surrounded by like-minded curious kids (disguised in big people’s bodies!) I love playing my part in adding to the collective knowledge in different ways and for those of you who are our Update in Under 30 subscribers, and of course anyone that purchased this as a single download, well we’ve gone that extra step and put together a nice little pdf: A B 12 Assessment Decision Tree for you and added that in as a bonus to your Separating the B12 from the B*S#! episode. So go take a look now and hopefully that answers just a couple more questions and we can all have at least 1 good night’s sleep… before you come back with more 😉 🧐 😂
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.
And now a new one to boot!!
You can purchase Separating the B12 from the B*S#! here
If you are an Update in Under 30 Subscriber, you will find the new resource in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here
A conscientious early career practitioner digging deep into GS research and upskilling, recently sent me a message to ask if I knew that the correct pronunciation of the condition was ‘Zheelbairs’…as in..imagine you’re French and say the word through a pencil moustache and barely opened lips! My answer? ‘Yes (or should that be Oui Oui!), but I gave up pronouncing it correctly when I realised no one in my very Aussie audience could make the connection between my fickle French impersonation and the word G-I-L-B-E-R-T-S on the screen”… 😂😂😂
Ok I know many of you imagine I read nothing else but Gilbert’s Syndrome guff and that not a day would pass without those sweet words passing my lips! But you know what? That’s not completely true 😂 But my series of mentoring sessions yesterday did end on another happy note, with both the final case presented being a Gilbert’s one (overt oestrogen excess, likely bile stasis etc) and then stumbling across this paper that I hadn’t seen before a longitudinal study of 100 Egyptians with GS, tracking their bloods and health experiences. I know you also imagine that I have a direct line with God in terms of receiving Gilbert’s research the second it gets published…again not completely true 😂 and somehow I had missed this one!
It’s not the greatest research in terms of sample size and methodology but hey beggars can’t be choosers and when you’re a condition with whom the word BENIGN is so commonly associated…you’re always begging for something: attention, validation, research crumbs!
So the practitioner presenting this case, actually asked a great question…”do I put these patients on everything you’ve talked about as having potential efficacy in GS and set and forget?” The answer of course is no. But it is good to clarify. The bulk of the heavy therapeutic lifting is always the education of these patients – what choices they need to make and perhaps make differently to get the best out of their body. The non-negotiable for me, is the direct glucuronidation support which for me typically would be cruciferae based and then if needed glucomannan (I now use this as much as possible instead of Calcium D glucurate…missed the reason why?…check this out). The next treatment tier is dictated by how the GS principally presents for the patient in front of me: GIT – choose any additional treatments to work on this aspect of the disorder (motility agents, bile thinners, fat digestion support) or Psych: mitigating and managing the longer half life of both dopamine and oestrogen and the potential imbalances that ensue. Throwing the entire dispensary at these patients (like any other) is often unpopular…especially when we know this is not something ‘solvable’ so in fact we need to aim for sustainable instead.
But following this approach has brought so many of my patients long-lasting benefits and a far better experience of their health that they are super grateful for. Now that’s a happy note to end on 🙂
A Guide to Gilberts Package
It all started way back when with ‘Gilberts Girls’…then came ‘Gilberts Guts’ because that is such a common source of unexplained hard to define gut dysfunction in patients…then latest instalment was news from the research frontier in Gilbert’s Syndrome, which is nothing short of thrilling, rewriting our thoughts on what medications and supplements (!!) are the most problematic, significantly improved dietary management of these clients, how to track their progress more accurately and why completely normalising their bilirubin is not the goal…hey did someone say…longer telomeres?! 😉 Included are kickass desktop clinical reference that comes with this months UU30 that aids a better understanding and clear treatment directives in your GS patients. All of these are combined for the newcomers in this Guide to Gilbert’s Package
A Guide to Gilbert’s package is 3 Update in Under 30 episodes combined into one
– Gilbert’s Girls; Gilbert’s Guts and Gilbert’s – New Goals & Good News.
If you are already an UU30 Subscriber you will already have access to these episodes in your ‘active content of your online’ account. Or you can purchase this complete package here
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.
Our knowledge is subject to constant change, and it is oh so necessary to stay up to date in our field for a bazillion reasons, give or take a few 😉 So sometimes we can feel like we need eight arms (for the visual amongst us) to manage and keep up with it all. However, if we ‘use the force’ together we are stronger, learn faster and can stop with the whole ‘recreating the wheel thingo’ that so many practitioners find themselves doing out there in solo practice. Like, like…well, how confident do you feel about putting pen to paper? How good are you at your inter-professional communicating?
*Cue* the release of a brand spanking new version of our
“Dear Doctor – Upskilling in Referral Writing & Inter-Professional Communications”
Referrals and inter-professional communication are just lightly touched on in the current undergraduate degrees (if at all!). But it’s actually such an important way to grow your own professional reputation while simultaneously the credibility of our whole profession. One might even argue, a pillar that stabilises the castle of shared patient-centred care & the future of true integrative health. I hear from my “New Graduates” as well as seasoned mentees about the unease that starts to creep in at the thought of writing the dreaded referral letter. I’ve been writing referral letters for 20+ years and it’s given me a lot of time to think! And refine. And refine again! To make inter-professional care a positive experience for everyone, we need to correct some misperceptions and ensure that our patients are everyone’s priority. And to fulfil our duty of care, communicating with the other practitioners on your patient’s healthcare team is fundamental. Sometimes, as you’ll learn, it’s about modelling the best kind of shared care to boot and being the bigger person 😉
Better still, positive experiences of inter-professional communication will bring collaborators out of the woodwork. Medicos and other allied health professionals you may never have been aware of otherwise, with a desire and openness to shared care tend to rise to the surface.
To get you even more excited about referral letters (you didn’t think that was going to be possible, right?!) and unlearn that Pavlovian procrastination you may have developed, Rachel has completely redesigned an older presentation to ensure it’s truly reflective of the contemporary healthcare landscape (oh yes, RACGP position statement included!). Expect to roll up your sleeves and get seriously practical advice with loads of examples about how to medico-speak naturopathic concepts, explain your role in the patient’s care, provide rationale for consideration of investigations and present ‘red flags’ with punch but minus the sensationalism. And above all else, reveal yourself as the asset you really are to the rest of the healthcare team.
“Thank you so much for a wonderful presentation yesterday, Rachel. It gave me a new perspective on how it must feel as a GP to receive incessant demands from Naturopaths/Nutritionists to order pathology for their clients. I am in awe of your integrity, desire for patient empowerment, humility and respect for other professionals in the mainstream health arena. I felt that every single naturopath and nutritionist out in the big wide world ought to have listened to your insightful words of wisdom when it comes to shared care of our clients. We are blessed to have you as our teacher.” – Michelle Blum (Mentee 2019)
If you’re interested in integrative care, want to learn the language of letter writing and follow Rachel’s SMART objectives to craft your comms and communicate clearly then you should take a listen to “Dear Doctor – Upskilling in Referral Writing & Inter-Professional Communications”
If my dispensary was on an island and could only stock 3 items, S-adenosyl-methionine would make the cut. That’s how important this nutraceutical is to my practice and has proved itself to be to so many of my patients. Regularly, I cross paths with practitioners who declare similar favouritism and then there are many others who remain apprehensive and uninitiated in its use. Often this results from 7 myths and misunderstandings, such as…
No.1 Giving someone SAMe will impair their own synthesis of it
No.2 If it’s not ‘right’ for your patient it could go horribly wrong – the risks are big!
No. 3 SAMe will increase homocysteine in your patients & shouldn’t be used if the homocysteine is high, or high-normal, to begin with
Wrong. Wrong &, you guessed it, wrong. But many of us don’t believe anything till we see it with our own eyes. Like a mentee of mine who is a seasoned SAMe savant but, like us all, continues learning more all the time through her own prescribing experience. Case in point:
“Remember when we discussed my patient with stubborn high homocysteine, who has not responded to high dose methyl factors? You suggested a trial of SAMe because other things pointed to her being an under-methylator. You were right (standard!)- it came down from 9 to 5 with 2 months of 400mg/day SAMe. She’s also been able to stop other supplements she was using for her mood and overall is much more stable emotionally, so turned out to be the perfect solution. Thanks as always :)”
So exciting to bring SAMe, together with other important CAM options in mental health management, to the attention of an increasing number of psychiatrists and other health professionals of late. It easily makes my top 3, and the other 2 supplements in my island dispensary?…well if we’re still talking mental health, Zinc and N-acetyl-cysteine, due to their versatility, potency and accessibility regardless of income. But I think you could have guessed those & likely have shared confidence, right?
This 3hr recording & resource is overflowing with case studies and the latest research relating not only to psychiatric presentations but also as a key nutraceutical to consider in liver pathology, Gilbert’s syndrome and some pain presentations. Together with this ‘literature lowdown’ we clear up a lot of misunderstandings practitioners tend to have about its prescription – busting the 7 SAMe myths along the way and giving you the confidence to know when SAMe is likely to be the solution and exactly how to prescribe and what to expect.
I’d love to continue this conversation with you…
so join me and be part of my ongoing dialogue on this and my other blogs by following my Facebook page.
Ok here’s some tough Tuesday talk..not all tests are valid. Tougher still…not all of the mainstream nor the functional pathology ones. I am talking across the board here. Each and every pathology parameter requires good knowledge about its strengths. limitations and, one of my absolute favourite nemeses, confounders. “How on earth am I supposed to learn all that and everything else I have to know too?!!” I hear you scream at your screen. Btw keep yourself nice if you’re in public while you’re reading this 😉
But rather than imagining you need to have this level of knowledge for all tests, I would suggest you set yourself a hit list of the ones you rely on most, either in terms of frequency or in terms of the degree to which they direct your decisions about patient care…can I mention (ahem) Iron studies here perhaps for us all…but maybe you have a specialist area so you use a particular investigation routinely or at least frequently…
CDSAs? Breath tests for SIBO? Oxalates?
May I please then politely suggest that you get to know these inside and out? Not based purely on the information and assistance that the test provider provides you..but you scrutinise them independently. Top to bottom. Because that’s your business, right? And your diagnoses and treatment decisions are pivoting on these results. Jason Hawrelak gave us all some great examples, including his informal experiment of sending the same stool sample to multiple labs. Don’t know about this and his findings?? If you’re in the business of ordering stool tests, you need to. I am doing this all the time with numerous pathology markers because diagnostics is my passion (alright, obsession)…and recently I put Oxalate Assessment to the test and oh boy!
Here’s something for free:
If you are measuring urinary oxalates to diagnose oxalate overload in your patients and you, 1) are using a lab that does not preserve the urine as you collect it, using acidified containers or providing additional preservatives for take home testing kits….you are wasting your patients money and you are likely getting a lot of false positives, i.e. the result infers the patient has a problem when they don’t!!
And 2) if you are simply following the labs reference ranges for what ‘healthy’ urinary oxalates look like – you’re wasting your patients money again and likely getting false negatives – a failure to show a problem that is actually there! If you’re hunting oxalates…please ensure you have a current effective hunter’s licence…by getting up to speed fast regarding accurate investigation of this. Oh yes…it’s tough-talkin’-Tuesday and I’ve come out firing…watch out this may become a regular feature 🤷♀️
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.
Horses not Zebras. You’ve no doubt heard me repeat that quote which is famous in medical schools, something to the effect of, “When you hear a heard of animals outside your door, think horses not zebras”…unless of course you are practising in Africa might I suggest 😉 This of course reminds us all in short to think of the most likely explanations not the most exotic first. Likewise with our case taking. The number of times I ask practitioners for the ‘boring basics’ and am met with an embarrassed silence. Think:
Body Mass Index
There I said it…and yet these are like dirty words in integrative health. Why? Because we’re starting to ignore the ‘boring basics’ in favour of getting ‘fancy first up’, as I like to call it. Look I love a good bit of bioelectrical impedence assessment as much as the next clinician and I am not about to use this crude measure as replacement for that but I absolutely need to have these key landmark pieces of information to understand a very long list of things such as contribution to future health risks, current burdens from literally the weight on those joints leading to knee pain, to the weight/mass not pulling on their bones and therefore contributing to lower BMD their whole life. Even their likelihood of a leaky gut today, right, Brad Leech, our colleague and impressive IP researcher? BMI drives also the appropriateness and their capacity for any exercise interventions I might recommend, not to mention the frequently mentioned, accurate interpretation of their labs.
For many many labs that we routinely see for our clients…the reference range should actually be a sliding scale that moves with BMI…what do we really ‘expect’ and what is actually ‘healthy’ is different at different weights.
Like TFTs – this may be a big newsflash for most but I never want to see a patient with a BMI > 30 have a TSH anywhere < 2, unless they’re on replacement.
Say wha? You heard me. I promise I’ll tell you more about that soon.
But again…let’s not get fancy first up especially not in any of our paediatric patients and in spite of what their words or ‘tude may be telling you, that includes all the way up to 18 in our books! Brace yourself, I’m going to speak that dirty word again…BMI..boring basics before all else. We need to review their height, weight and BMI against paediatric growth charts. These oldies are goldies and can reveal so much about growth trajectories, puberty milestones when any other discussion is off the table, type 2 nutritional imbalances (protein, zinc, potassium, magnesium, sulfur) and flag all other sorts of concerns or reassurance…and you haven’t had to steal a drop of blood or any much hard earned money off mum and dad to work a lot out. Anyway, that’s my ‘boring basic beef’ for now…there’s a lot to be said for ensuring such ‘dirty words’ come before everything else.
Need help with wrestling all the most important patient information into a clear management plan?
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.
No you’re right, it’s not long enough to be a Hemsworth’s mobile number but actually it’s more sought after 😉 If you’re up to date with reading & recognising all the different patterns of Iron Studies & the stories they tell, which is a daily business for most of us, then you will know by heart the striking pattern we call, ‘Pseudo Iron Deficiency’. You know the one where your patient’s serum iron & transferrin saturation are mischievously trying to trick you into thinking you need to give this patient iron…when in fact this is absolutely not what they need!
This is of course the result of the redistribution of iron during inflammation – iron is actively removed from the blood and sequestered in the liver instead. It’s designed to protect us from bacterial bogeymen, which is how our stone-age bodies interpret all inflammation of course.
Doesn’t sound familiar? Ok you need to start here or even embrace a full overhaul of all things iron here.
But for those of you nodding so hard you’re at risk of doing yourself an injury, this number is for you. We’ve often talked about the redistributional increase in patients’ ferritin levels in non-specific terms: it goes up..but by how much? Of course we would like to know because no one is fooling us with this transiently inflated value…but can we make an estimation as to what this person’s ferritin will drop to once this inflammation is resolved? Yes.
Write it down. Consider a tattoo, perhaps?
This glorious magic number comes from Thurnham et al paper in 2010 who did the number crunching on over 30 studies involving almost 9,000 individuals to determine the mathematical relationship between inflammatory states & markers and the reciprocal increases in ferritin. Their work is exceptional in that it also differentiates between incubation (pre-symptoms), early and late coalescence periods (if you want to differentiate your patients in this way and get even more specific then you need to read the paper), however, overall when we see a patient who has a CRP ≥5 mg /dL , we can multiply their ferritin by 0.67 and get a lot closer to the truth of their iron stores. Oh and another important detail they revealed, this magnitude of ferritin increase is more likely seen in women or those with baseline (non-inflamed) values < 100 ug/L..so generally more applicable to women than men. Thanks Thurnham and colleagues and the lovely Cheryl, my previous intern who brought this paper to my attention…you just took the guessing out of this extremely common clinical scenario 🙂
We’re not deaf…we heard that stampede of Iron-Inundated Practitioners! The Iron Package is for you!
Our recordings and clinical resources for improving your skill-set in all things iron including, your accuracy of diagnosing deficiencies, pseudo-deficiencies & excesses, plus radically rethinking the best treatment approaches for each scenario…have been some of our most popular. Because nailing iron (pardon the pun) is harder than we were all lead to believe and at least 1 ‘iron maiden’ or ‘iron man’ walks into our practice every day, right? So we’ve brought together 5 extremely popular UU30’s on Iron into one bundle for the price of 4! So if you’re more than ready to graduate from ‘iron school’, now’s your best chance!
Those ‘still-believers’ look away now. One of the great myths, misconceptions and misunderstandings in nutritional medicine is that supplementation with specific nutrients will produce change specifically in one system, or pathway, which just happens to be the one that the practitioner has determined would benefit most/is targeting. Let me explain myself a bit better. When we give patients any nutrient, in the cases where it’s not simply to correct a global deficiency & therefore improve levels all round, it’s typically on the basis of a specific desirable therapeutic benefit, e.g. some magnesium to help their GABA production…, additional B3 would improve their mitochondria. Beautiful on paper…but like sending a letter to Santa in reality (I did warn you!)
Truth Bomb No.1: There are nutrient distribution pecking orders that have nothing to do with who you ‘addressed’ it to
This dictates that when something is given orally, for most nutrients, the gut itself has first dibs. So the cells of your digestive tract meet their needs before any other part of your body gets a look in. Sometimes the digestive system’s needs can be quite substantial and leave little for any other part of the body…not mentioning any names (ahem) Glutamine!
Truth Bomb No.2: En route to the ‘target’, these nutrients get delivered and distributed to many other tissues – with possibly not so desirable or intended effects!
You may determine that a patient needs iron because their ferritin hasn’t got a pulse…so you keep giving them daily high dose oral iron to ‘fix’ this…not realising you’re making their GIT dysbiosis and gut inflammation worse in the process. Or you feel their mysterious ‘methylation cycle’, happening predominantly in the liver and kidneys, could do with a folate delivery…perhaps ignoring the very worrying fact that their colon may have already had a ‘gut full’. Literally. Hence the concerns and caution against supplementing with folate in patients with established colorectal cancer. So is bypassing the gut via IM or IV nutrients the answer…well yes and no…but mostly no. Read on…
Truth Bomb No.3: Those pathways that use the nutrient you’re supplementing, that are most active in the patient’s body currently – which is determined by many factors (genes, physiology, feedback circuits, pathophysiology) and rarely simply by the availability of nutrients – will take take the next lion’s share of that nutrient
Wanting to nutritionally support someone’s thyroid, you know tyrosine is the backbone of the thyroid hormones, so you include this in the hypothyroid prescription. Will it help? Who knows? Being a non-essential amino acid the body exhibits very complex regulation of its distribution and use – with thyroid precursor availability being only one job on a very long list! And if this was in a patient who is regularly smoking cannabis, due to upregulation of the tyrosine hydroxylase enzyme – there is likely to be more of the supplement headed for even more dopamine production and very little or none reaching in fact your intended target. And don’t get me (re)started on Glutamine – supplements of which in an anxious and glutamate dominated patient will make…G.L.U.T.A.M.A.T.E…right…not GABA! 🙁
Sorry, I know, it hurts right? But these are essential teachings, that tend to have been over-looked or under-played I find, in nutrition education, regardless of training: nutritionists, naturopaths, IM doctors, dual qualification practitioners remedial therapists. Nutritional medicine is a wonderful and potent modality when it’s done well…but we need to revisit some core truths and principles that many of us have missed out on, to ensure we’re not writing letters to Santa.
Want to revisit your core nutritional knowledge which will cover this and much much more?
Let’s start with Micronutrients. Let’s talk 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 felt well trained – will find a lot in this critical review that is new, insightful and truly practise-changing!