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??
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?
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!
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!’
‘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 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.
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?
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.
And not in a good way, right. While we’ve known about the potential for peripheral neuropathy with excess B6 supplementation since the 1980s, currently there’s a seismic shift in our sense of safety even with previously regarded ‘safe’ levels. You may have heard individual whispers, or the chorus of voices coming together, both here and overseas, belonging to members of the public who report suffering sensory nerve impairment with as little as 2mg/d! Is this a mess of mis-diagnosis, false attribution & nocebo? Perhaps for some, but certainly not for all.
How could this be the case given the many RCTs employing hundreds of mgs per day over months, with no such events recorded?
How could this be given, your (?), certainly my, high dose prescriptions, with only 1 case of quickly reversed, peripheral neuropathy in over 20 years, on my books?
The pieces of this complex paradoxical pyridoxine puzzle are coming to light.
Is it the form?, the dose? the duration? individual differences in B6 metabolism & toxicity threshold? amplification of risk secondary to levels of other nutrients, or the use of certain medications? Yes. And we need to understand each element to better tailor every B6 prescription to the individual & mitigate risk. I have spent the best part of this month reading almost every paper on this from the 1970s to last month and I am now alarmed but more importantly, alert, to what prescription practice changes we can all make to lessen the risk, and control the power of B6. It’s been the most compelling deep-dive. Because in spite of a clear TGA warning issued last year that likely prompted the quiet removal of high dose products from market, it would seem none of the companies have the courage to have this difficult conversation with us 🙁 I invite you to ‘feel the fear & do it anyway’ & listen in to our latest Update in Under 30.
Haven’t we always known that nutritional medicine is a potent prescription? Now thanks to more sophisticated research we have a much greater understanding of this and of both the intended and unintended effects of micronutrient supplements that have the potential to achieve supra-physiological levels. B6 metabolism is arguably the most complex of the Bs – involving 6 different forms, at least 2 of which are active – and exhibiting some of the most complicated regulatory control designed to both harness the power & limit the accompanying risks. Excess B6 supplementation, however, has long been known to present as peripheral neuropathy in some individuals and case reports of this are growing, at lower and lower doses. New information has come to light to help us understand the why, the how and better still how to mitigate risk to our patients.
You can purchase Dynamics and Dangers of B6 – Controlling the Power 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.
You know when you learn about a ‘new’ dis-ease driver and then you actually have to stop yourself from diagnosing every patient with it? I’ve done this dance with Gilbert’s Syndrome for over a decade, so too maybe have some of you? And while there have been many, many occasions when I’ve been certain it’s Gilbert’s (clear robust & reproducible patterns of high bilirubin without other explanation) there are other times when I’ve been left wondering, and with questions. Like – what about a fluctuating pattern – sometimes ‘within range’ sometimes above or at least high-normal – with no other explanation? What about the patient whose symptom-story is a perfect fit – prone to nausea, early satiety, gut issues, food reactions and anxiety all worse for increased oestrogen…but the total serum bilirubin is 14 micromoles/L? I mean, 14, right? that’s well below the top of that range, but remarkably higher than the majority of women of the same age, eating the same diet. And you ask yourself…could it…be??
The latest UU30 offering on Gilbert’s Syndrome constitutes a complete overhaul of everything we’ve previously been told about how to recognise and diagnose this polymorphism & it’s going to answer a lot of those ‘could it be’ questions we’ve all had! Known also as familial non-haemolytic jaundice and episodic hyperbilirubinaemia under stress – is everyone with Gilbert’s prone to jaundice? Uh, no. Total bilirubin levels typically have to get to 45 micromoles/L to evoke this effect – many of our GS patients won’t ever get there, some will with increased illness or other stress and may yellow a tad (like a fading bruise), while other patients of mine routinely have a bilirubin at this level but won’t experience jaundice unless they impair their UGT further via doing what they know they shouldn’t: extreme exercise or excess alcohol. The latest deep dive into GS diagnostics
But as much as we don’t want to miss this diagnosis we don’t want to mis-diagnose patients with it either!
Can you spot the difference? Don’t forget total serum bilirubin levels are the net result of haem catabolism – so you need to account for rate of blood production, destruction and of course rule out any biliary dx before you can take a guess at Gilbert’s. Oh and watch out for expected high bilirubin values in the fasting fan(atic)s!
Living on Gilbert Street
For those people living with Gilbert Syndrome at last the research world & the real one are uniting – with greater detailed documentation of how this very common polymorphism presents and the mark it may make in their health story. However, given only 1/5 with Gilbert’s syndrome actually know they have this condition, who are we missing? This latest instalment rewrites our diagnostic criteria and corrects our past misunderstandings based on the very latest science, while shedding further light on what it’s like to live in Gilbert St.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can purchase Living on Gilbert Street here…
OR 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.
100% confident that, as a professional group, among our highest values about healthy, preferable, food choices, would be characteristics like: ‘as close to nature as possible’, ‘unrefined’, ‘unprocessed’, ‘unadulterated’. Tell me I’m wrong.
So, when I keep hearing about NEW! “Never seen before” (read: never in nature) modified (read: more processed, adulterated) nutritional supplements: water soluble vitamin D, fat soluble C, bioflavonoids with unprecedented (read unnatural) bioavailability
I’m left wondering what these companies are missing about their customer group (because we are clear about our valuing of nature & what’s natural & have a desire to minimise exposures to things that are not, right?
or what are we missing here, in the clear conflict of our core values these constitute?
I think if we find ourselves forsaking this core value & prescribing highly modified, unnatural supps, it’s the result of both hype & fear. The hype is self-explanatory and I’ve written recently on how modifications exponentially increase profit margins for companies, all the while possibly reducing ours because patients are spending more on product and therefore there is less left over for the practitioner fees 🙁 [The ones spending hours with them face to face, not to mention years & thousands on our training] The fear is perhaps less apparent, more insidious. The fear is that we’re not using the best, being the most effective, and deeper still, inevitably that we will fail to action our patients return to health. This is a big one. I think it’s pervasive, if not omnipresent, and works as a motivator for many positive actions by practitioners – like engaging in further education, reading that latest journal edition on your lonesome laptop when you could be streaming some series on a shared sofa. But this same fear can also undermine us, overwhelm us and shake our tree of trust, that we believe to be so firmly rooted within us, of the healing power of nature.
So while my position sometimes makes me feel very ‘old school’, I’m not suggesting we return to nutritional prescriptions composed exclusively of bee pollen & brewer’s yeast and I absolutely recognise and respond to an individual who has very specific barriers to benefiting from nutrients in their natural normal forms.
But let’s be clear, they are a minority.
Some of you will know naturopath Dawn Whitten & know that she is one of my mentors. I’ve had the benefit of speaking with her over the years about herbal prescriptions but also about the principles & philosophy behind our practice & in one of many conversations she told me that a key objective she has with her patients is to rebuild their trust in their body, their own biological resilience (I love this concept and that’s a talk for another time!) and ultimately in nature. Well jeepers Dawn – how did you get to be so wise so young? But isn’t that central to vis medicatrix naturae? Maybe that Naturopathic Nanna’s club isn’t so fuddy-duddy after all. Want to join us?
Speaking of using nutrients in their most natural state for the best health outcomes – the best B3 is probably not what you think!!….
The Balance of B3
Most of us have been taught to ‘balance the Bs’ when supplementing, which discourages the use of single B vitamins in case this interferes with the regulation and roles of others. In reality, outside of a couple of dynamic duos like B12 and folate, there is little concrete information & evidence of this. In the case specifically of B3, however, we now know, the risk of an excess of the most common B3 forms found in supplements and fortified foods, results not only in disruption of other nutrients but imbalanced B3 biochemistry itself. Given B3, in its coenzyme form NAD+, is regarded as highly valued currency in the prevention of many diseases, as well as the key to our optimal health and longevity, it’s critical to understand the different forms and functions of the various B3 sources.
I haven’t personally seen every medical condition known to occur, nor every micronutrient deficiency & toxicity picture in the flesh but that doesn’t mean I doubt their very existence. Sadly, it would seem some practitioners due to a) not knowing ‘where’ to look in terms of best assessment medium and/or b) not knowing ‘what’ they’re looking at, when faced with an actual Copper deficiency, have declared this uncommon, but certainly not unknown, nutritional issue to be a figment of others’ imagination!
I know I’ve been fortunate to see more labs than most
would want to in an entire lifetime , a collection of my own, my student’s & my mentee’s patients, so let me share just 3 sets of results from 3 different individuals: an 11Y boy, a male teenage athlete and a female in her early 20s with an eating disorder, all with Copper deficiency.
Don’t worry, I have more – just ask. What’s so dangerous about people spreading myths and misinformation in relation to copper in kids and teenagers specifically, is it shows complete disregard or ignorance of an understanding of how Copper is critical for development during these life-stages and how regardless of which developed country you live in Copper is expected to dominant over Zinc in blood, especially pre-puberty.
AM I SHOUTING???!!!
I’m sorry it’s just that my blood tends to hit boiling when exposed to the misinformed, misinforming others…
and that can make one call out in pain 🤯
You see, I literally heard a practitioner in an “educational” webinar purport that
‘Copper Toxicity is so prevalent in kids in her clinic’ and I was like,
OH. EM. GEEE.
Because if you start with that misunderstanding, and are unclear about what constitutes an accurate Copper assessment and how to recognise the pattern that follows low serum levels (each of these patients above had abnormalities in their FBE consistent with Copper deficiency) you are not only going to miss the thing you need to make a priority to fix, you’re going to make it worse! Take ‘Volatile Vince’ the gorgeous sensitive 11Y boy I saw, whose increasing mood volatility had been misattributed to pyrroles and given large doses of Zinc! So, Copper Crimes are a thing. Guilty until proven innocent but in fact, never found innocent by some practitioners it would seem. The ramifications of unchecked Copper deficiency include negative effects on mood and cognition, immunity, and the balance of other nutrients and kids are going to feel this impact the most! What are the causes? Inadequate intake being uncommon outside of eating disorders, and excessive Zinc rarely the cause, we’re likely looking at a marker of malabsorption or a genetic issue. Don’t buy into the confirmatory bias many use when they choose which research to read (risk of excess) and which to ignore (Copper as an essential mineral, critical to kids) and let’s not discredit something as not being a thing because we haven’t seen it ourselves, yet, hey, anyway, at least, now we all have, right?!😵🥴😆
Copper In Kids
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.
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.
…Telling anyone to push the nutritional issues further down the list of differentials for any condition?
Well, that’s unexpected
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.
[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