Ever been guilty of having a ‘man’s look’ for something? I have. Particularly when it comes to the online omniverse! I can be a bit flaky at finding things right there on the page…allegedly! So for those of you who have a similar experience with my website & endless educational offerings, I FEEL YOU! We do have a tonne of training options and a whole lot of (love 😉 couldn’t resist the Led Zepplin reference)… lab & diagnostics resources! This has come up in conversation a lot recently, following the release of our RAN Student Pathology Hub, for example: “I’ve done your MasterCourse in Diagnostics, does this cover something different?” or “LOVED😍 this new hub its *$@# incredible resources & extra training vids but I also wished it included your take on… [insert your pick from infinite list: thyroid, cortisol, zinc etc etc etc]
So here’s a Dummies Guide:
How to Find the Help you Need in Diagnostics
If you are just starting out on your path to pathology & true lab literacy & want an accelerated way to ensure you are starting this journey on solid ground and you have the most called-upon skills you’ll need in clinic today, then the RAN Student Pathology Hub is your perfect match. NOTE: this is not limited to actual students but anyone who considers themselves, like us, a life-long learner! This 12 part module includes some small core components of our MasterCourse, a few expanded episodes from our Update in Under 30, plus unique short training videos, covering tests and topics including: Iron studies, B12 assessment methods, Coeliac screening & much more
If you’re seeking the immersive experience – you want to maximise your competence and confidence & forge your path as a true Diagnostic Diva or Divo then look no further than our ‘mothership’, the MasterCourse in Comprehensive Diagnostics which now has a part payment option. This really is the most seminal training we offer, taking the time to dig deep into the science behind all the ‘signposts’ our patients’ results are pointing to. A big commitment for a big reward. It comprehensively covers all the routine labs you will see everyday: LFTs, Renal markers, Glucose and Lipids, FBE & WCCs & is loaded up with case illustrations for each key pathology pattern – that many practitioners say was an absolute highlight
Just have a specific question or need for upskilling in Cortisol assessment? Zinc or Zonulin? It’s probably in our vast Update in Under 30 library! Yes, with more than 100 episodes in there and my penchant for pathology…you’ll find something, if not in the UU30 episodes, then somewhere else on my website. You know how in pdfs ‘Control + F’ is a god! Ok on my site it is this fella 🔎 You can use this to search my whole site to find free information on the topic (blogs) or manifest the same magnifier🔎 magic once you have clicked ‘Catalogue’ on the top right of the tool bar on any page, to locate any specific educational offerings. Remember with the UU30, you can purchase single episodes or subscribe and get access to the whole shebang.
And for those of you primed praccies, patiently waiting for our MasterCourse II to land? Well about that…did we mention we got hit with a flood? Twice? And then got covid? Two of us? And have our beloved Nina about to depart to become a mumma!!! Yeah, so our plans to have this up and ready for May changed to Mayhem, real fast 🙄🤪 We will definitely keep you posted on any developments and new timeframes but for now we can only apologise for the delay and will do our best to get back on track with this, at the earliest opportunity. In the meantime maybe a little review of some of MasterCourse I is in order? I refer back and re-listen all the time, myself!!😂
Being a practitioner who is able to read labs will set you apart in practice. For your patients this flows from your ability to form a more sophisticated understanding of what’s happening for them, enabling you to better individualise treatment and deliver superior outcomes. Amongst other health professionals, it will attract positive regard and an increased willingness and enthusiasm for sharing the care of patients with you. Learning to be lab literate could take a lifetime…or you can enter the expressway from the very outset! We have curated the content to reflect the most essential elements, to help you hit the ground running in the shortest period of time. Spread across 12 modules which can be consumed as monthly instalments or, as an all-in-one experience for those wishing to waste no time. The teaching points, tips and tools make the complex simple, engaging, even fun!
Developed, designed and delivered with students of any health discipline in mind.
Did I say, ‘Our Brain’? 🙄 Maybe it really should be, ‘Their Brain…on Drugs: what recreational substances reveal’. While infinite self-analysis is an occupational hazard for health professionals, when we use our detective powers for good not evil, our patient work-up benefits. But of course, it is impossible (and not desirable) to avoid all self-reflection. Let me introduce myself: I am a high dopamine gal. How do I know? Because a valid accurate test of my neurotransmitters told so? Heck no – outside of lumbar puncture there isn’t one! Because my reactions to recreational drugs did.
A self-proclaimed ‘cheap date’, with amplified & protracted intoxication experiences from small amounts of any psychoactive & no, sadly, not always pleasant. I specialise in visual trails, a known trademark of dopamine surges, when under the influence of even just a few drinks – much to the bewilderment of my loved ones.
Some even famously once questioned whether I was, in fact, safe to ride a push-bike 500m on Lord Howe Island after 2 glasses of prosecco. Stop! I heard that murmur, this has nothing to do with my liver & its handling of such substances. [How rude!😆] I can cite ample other evidence in support of this. This is also not simply due to being a teetotaller and therefore having not (yet) developed tolerance. This high dopamine diva-stuff is echoed by my non-intoxicated ‘normal’: vivid dreaming, impulsivity, and bankable bad reactions to Vitex: ANGER (capitals intended). TMI? 🙄🤐
When you know the questions to ask, the answers to lean in further to, and then the way it can all come together, to create a neat little trail of breadcrumbs we can follow all the way to our their neurochemistry…you can find the gold.
The thing is – and I remain annoyed and frustrated by this to this day – our ‘schooling’ was not very ‘sex, drugs and rock’n’roll’. New grads tell me nothing has changed. In fact, these kind of topics were absolutely omitted, in spite of the claim we consider the ‘whole patient’, the whole health story! Interesting, hey? Nod to those working on the ‘sex’ bit in holistic health: Moira Bradfield-Strydom, Sage King, Monica Francia, Daniel Robson…love ya work! Now for the drugs! Do you know what recreational substances can reveal about your patients’ neurochemistry?
Finding out about your patient’s historical or current psychoactive appetites and adventures (and yes that could be as commonplace as alcohol), is not purely for the purpose of collecting yet more data on their ‘health behaviours’. Nor yet another cue for casting judgement! It is an opportunity to take a can-opener to their cranium, open that baby up & take a look inside. Without making a single incision!
But there’s a bunch of background knowledge you need to polish up on re psychoactive MoA and what each part of your patients’ experience (1st vs subsequent exposures, threshold for intoxication, the nature of the intoxication itself, & the possible aftermath) can reveal – as an inventory of their CNS materials and machinery. All the while having a process to follow to ensure your evidence is leading you to the right and reasonable conclusion. Come with me and let’s follow the trail of breadcrumbs your patients recreational substance experiences have laid out for you…🐓
Our Brain On Drugs – What Recreational Substances Reveal Part 1
Ever wondered why not everyone loves MDMA given it’s the ultimate love drug? Or why some of your clients are exquisitely sensitive to the aftermath of psychoactives and routinely, reliably experience ‘rebound’, in the following days while others ‘bounce’ seamlessly from a big night into the boardroom the very next morning? What do these things tell you about the state of play of their neurotransmitters & their neurochemistry? So much more than you expect and given the only validated accurate assessment of an individual’s neurotransmitters is via lumbar puncture…with far less pain and inconvenience. This is the first of a 2 part discussion.
&
Our Brain On Drugs – What Recreational Substances Reveal Part 1 Part 2
The 2nd part of this discussion goes into the detail of the MoA of each recreational drug class and what our patients’ encounters with these reveal about their neurochemistry. It also includes a resource we’ve developed to help you follow a process, in your review and rate the quality of evidence you have, to ensure your extrapolation and interpretation are well-founded. **WARNING OVERSIZE LOAD AHEAD** There is a bonus case discussion that puts into action everything outlined in both parts and the process of qualifying the evidence.
You can purchase individually Our Brain on Drugs – What Recreational Substances Reveal Part 1here and Part 2 here
or become an Update in Under 30 Subscriber to access both episodes plus the entire library (100+ episodes) of Update in Under 30 audio’s and resources here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
And health, no matter which side you sit on, seems to be particularly plagued by them. I (incorrectly) recall my 4 year degree as being a series of deep personal losses, some favourite food, then caffeine, then alcohol etc etc.😂 Likewise, I’m aware that naturopathy & integrative health’s ‘voice’ in the ‘conversation’, could arguably be perceived as mostly a negative one – as in, ‘No. Never. Not good. No, not even a little bit?!’ But I love both playing devil’s advocate & reading the research (ALL the research – even the stuff that doesn’t support my views and position GASP!~) so I am less in favour of absolutisms. This came up recently when I suggested alcohol may improve iron uptake 😬
Practitioners’ responses were 1 of 2 types: humorous dismissal (“steak & beer for breakfast – at last a naturopathic prescription I can support!”) or horror. But why are we so attached to the absolutes in spite of contradictory evidence?
Let me ask you this: is coffee bad? Full stop? Period? The end? Or is it the most concentrated source of antioxidants consumed in the average Western diet? Does it improve bile flow, peristalsis and at higher levels actually protect the liver against damage? Clearly, we need to read all the evidence, including, the favourable and make individual decisions about ‘what serves and what sabotages’, for each patient. But do we? Or do we imagine we only get membership to the ‘Ultimate Integrative Health-club’ when we adhere to blanket bans?
Similarly I, like many of you, see a LOT of iron deficient women – & a fair chunk of these have been incorrectly labelled, ‘refractory’ because theconventional correction strategies (high doses everyday) don’t actually make sense. But like you guys too, I’m always on the hunt for new ways to improve iron absorption in these women, so I can hit them & their gut with less. That’s why I shared the research regarding alternate day dosing, and taking a supplement within an hour of exercise and now, I dare to ask if a tipple could be helpful?
While we know that both ‘GOOD’ (exercise) & ‘BAD’ (alcohol) health behaviours increase gut permeability, which sounds ‘BAD’, right?
But could this be ‘GOOD’ for some?
This has certainly been demonstrated in relation to exercise & iron but most of the research investigating how alcohol intake effects iron uptake and status is based on alcohol abuse. The study below, however, based on a large sample of non, mild, moderate & heavy drinkers captured in NHANES data – is a very well written and reasoned article, such that it can exclude liver damage, inflammation and HFE mutations as other explanations for the better iron status, in drinkers. And it found:
I challenge you to read it for yourself and challenge your absolutes!🤓
Oh and just in case you’re thinking, “Have we all misdiagnosed iron deficiency and it’s actually a Copper deficiency underneath?”because last year the fashion was everyone was copper toxic and now this year someone’s making noise saying everyone is copper deficient !!! (Absolute? Anyone?!) Ah, no. Copper deficiency, as a cause of iron deficiency and anaemia, has been around for about as long as nutritional medicine itself. It is absolutely a thing. But in the absolute minority of people. And if you go back to some basic maths & compare and contrast Fe & Cu at each level: 1) requirements almost 20mg Vs < 2mg 2) average intake (inadequate Vs adequate) 3) bioavailability (Fe < 20% more typically < 10% in a modern low meat diet Vs Cu is typically >50% ) and do some basic sums I call, ‘Menstrual Maths’ – You’ll likely deduce that inadequate iron intake and uptake, given our losses, is in fact the common culprit and a ‘coldie’ may be more beneficial than copper in most! Can y’all stop asking me about that now – pretty please?
And then you don’t. The reality is we all struggle at times with correcting low ferritin or iron deficiency anaemia – so what have we got wrong? In spite of being the most common nutritional deficiency worldwide, the traditional treatment approaches to supplementation have been rudimentary, falling under the hit hard and heavy model e.g. 70mg TIDS, and are relatively unconvincing in terms of success. New research into iron homeostasis has revealed why these prescriptions are all wrong and what even us low-dosers need to do, to get it more right, more often!
Did you know you can subscribe to these? We deliver at the end of each month, just add a 12-month subscription to your cart and Rachel’s latest research is on it’s way to you!
When was the last time you ‘got on the gear?’. Wait, am I showing my age?🙄 The afore mentioned ‘gear’ could be beers or GnTs, weed or hooch, eccies or pingers, ‘nose candy’ or blow. I could keep going! While, anything beyond alcohol, might be purely a historical tale for many of us – during a [ahem] ‘very different phase of our lives’, Australian research tells us that the patients who come to see naturopaths are just as likely to drink alcohol as those that don’t and are in fact about 40% more likely, to have used marijuana or other illicit drugs in the past 12mo. And this was the women in their 30s! You heard me.
Now, this is not a call to action, to dob in a dabbler.
This is instead a wake-up call for all of us, regarding the best insight into our patient’s neurochemistry, that is right there in the patient’s psychoactive substance encounters.
Because let’s get 1 thing clear, straight up – the ONLY valid, accurate, reliable pathology test for the measurement of neurotransmitters is a lumbar puncture. Correct. And anyway, if you’ve been following psychiatric research this millennium, you’ll know that the belief that neurotransmitter quantities are the whole story (or even main players) in neurochemistry, is fatally flawed. So, whether your patient’s ‘alcohol or other’ is purely in the past or in the present, this line of questioning and what it can reveal to you about their neurochemical nuances (high or low dopaminergic tone, shortfall in serotonin, high or low histamine etc) is gold.
Because no recreational substance BYO
Instead they raid your stocks and supplies, get your brain to develop ‘bigger ears’ for some signals over others. Their effects are purely a manipulation of the patient’s existing materials and machinery. And accordingly, here is the great reveal. So, a 30 something patient of mine reports dabbling in all sorts during her teens and twenties. She relays pretty ‘expected experiences’ with each substance – remember these psychoactives are known quantities, we know a lot about which buttons they push and I so I concur that her responses were anticipated & typical. Maybe if anything, she is able to recognise that she had a lower threshold for intoxication compared with other first time users. “But MDMA,” she says, “I don’t get it and boy I tried! Several times!” So, while everyone else felt the love in the room, danced all night to the fantazzmical beats and the orgasmic-optic light show…she felt like she’d taken nothing at all. Aha! This of course would prompt me to ask more questions to help clarify both her serotonergic tone & other instances where she might have encountered oxytocin. And the real insights about her neurochemical milieu (strengths, weaknesses, balance and imbalance) start to form, so too the best way to support her. Don’t miss the real reveal in your patient’s story – that offers to lift the lid on their cranium and let you take a look inside.
Our Brain on Drugs – What Recreational Substances Reveal Pt 1
Ever wondered why not everyone loves MDMA given it’s the ultimate love drug? Or why some of your clients are exquisitely sensitive to the aftermath of psychoactives and routinely, reliably experience ‘rebound’, in the following days while others ‘bounce’ seamlessly from a big night into the boardroom the very next morning? What do these things tell you about the state of play of their neurotransmitters & their neurochemistry? So much more than you expect and given the only validated accurate assessment of an individual’s neurotransmitters is via lumbar puncture…with far less pain and inconvenience. This is the first of a 2 part discussion.
You can purchase Our Brain on Drugs – What Recreational Substances Reveal Pt 1here.
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.
I’m ready to zip my lips 🤐 and ride off into the sunset of silly season. But first I wanted to tell you about the BIG PLANS we have ON THE BOIL! Noticed a bit of a thyroid theme of late? Last month I presented training in thyroid assessment for the 4th time for ACNEM but not a slide, possibly barely a dot-point remained from the original one I wrote back in 2009. That’s how much my ideas & understanding have changed.
Some of the assay techniques & technologies are new, there’s a river of research & a mountain of meta-analyses published in the time between & I have had the privilege of yet more clinical encounters in this space, to really nut out how all this translates into the real world.
There’s a lot I need to catch you up on. And as I start creating our new MasterCourse II in Comprehensive Diagnostics…which will include 🥁…you guessed it…the humongously hardworking HPT, I’m just about bursting at the seams! And will those four little friends of every good practitioner, that sit superficially atop the ‘butterfly’, make it into our MCII?? I hope so because a) they should be our besties – being the director of Ca Mg D & P regulation and b) research tells us that where we find, ‘thyroid’ dx we should have another good hard look for ‘parathyroid’ dx and vide versa and c) over the last few years it has become increasingly apparent to me that this is one incredibly common source of ‘medical mysteries’ in our patients – remember the ‘Bones, Stones, Abdominal Groans & Psychic Moans’ catch-cry? Yep, that’s the patient who typically finds their way to us, with pervasive but hard to pinpoint gut issues (often misdiagnosed as SIBO, FGD, IBS -D or C), some significant stress perhaps even depression and insomnia and, if someone bothered to look, premature bone demineralisation. What other pathology panels and parameters will we be able to squeeze into our MasterCourse II?
Our current plans are to deliver the MCII live from May but just a reminder, because this next instalment assumes you have the exquisite foundational knowledge we laid down in the MCI – this is a pre-requisite for attending the MCII. So if you’ve been putting off your pathology apprenticeship now you have a hard deadline to work to!
And finally the last, last words. On topic because they came from someone who specialises in thyroid, did the original thyroid training with me, way back when, and last month was my fellow presenter & panellist on all things thyroid for ACNEM:
I’m sure I’m the 1 billionth person to reflect this back to you but I’ll do it anyway because I think we all need reminders sometimes – you have a truly special gift in critical thinking, discernment, and most importantly passing on complex knowledge in a very digestible way without making anyone feel silly for asking questions or not getting something the first (or fifth time…no, just me?). The endless analogies are a teaching tool you’ve well and truly nailed and boy am I grateful because it speaks to my way of learning very well.
So, a big thank you! Endless gratitude for your brain, passion and generosity with your time/knowledge/resources. Natalie Douglas
Here’s to another great year of learning, teaching, sharing & mentoring in 2022 – 1 billion and counting I hope 🌟🌈😂
There are some things we say so often to patients we could record them and just press <PLAY> Like this daily dogma: ‘When you’re under stress, your demand for Magnesium rises and then in turn that can make you more susceptible to further stress, so we’re going to give you some to support you’. But is this actually the whole story? You guessed it, no. (I know I am fairly predictable like that 😅)
Recently, a personal new record – a patient reported ongoing daily use of a very high dose Magnesium ‘practitioner only’ product 8 years after it was prescribed by her then naturopath – and guess what, the patient still hadn’t reached nirvana* not the band! – a transcendent state in which there is neither suffering, desire, nor sense of self
Jest as I may – I think this raises some serious questions. The pervasiveness of our prescriptions when patients are not given an end-date coupled with ongoing access. How (not) effective this intervention was if someone perceives ongoing undiminished dependency on it. And specifically with Magnesium – whether our prescriptions (form, dose, adjuvants, advice) are the problem? If stress is synonymous with a shortfall of this mineral then Magnesium is not a solution to stress itself but the amplified stress response and the stress still requires its own redress, right? But do our patients hear this as well when we press <PLAY>?
Likewise – the BIG doses per serve being recommended might make sense for the minority (seeking potential NMDA antagonism) but are a real mismatch with the majority, who are just stuck in the stress loop and weathering a perfect storm of Magnesium under-supply and increased demand.
I love my minerals as much as, ok more than, the next practitioner but I’m always keen to refine my repletion approaches and oh yes, by the way, there is good data, a meta-analysis in fact, examining how long it takes to achieve repletion using oral Magnesium – and guess what, it’s not 8 years! The latest Update in Under 30 goes into all this and much MuCh MUCH more…you’re welcome 😂
Practitioners working with nutrition appreciate that Magnesium is vulnerable to depletion by the stress response and that in turn, can make people more prone to stress & keep patients stuck in a so-called ‘stress loop’. But do we understand the intricacies of this and how we, as practitioners, can get stuck in another kind of loop – one of endless Magnesium prescribing without reaching repletion? We discuss ways to improve your Magnesium prescriptions – in particular, ‘doping Vs drip-feeding’ and other things to assess & address if the long road to repletion risks becoming an endless one!
You can purchase Magnesium – Stuck in the Stress Loophere.
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.
An ideal T4 is 15
An ‘anti-aging’ DHEAs must be >7
A ferritin of 100 is optimal for women…
I’ve heard it all, probably you have too, and far too often & too recently from practitioners who should have rationalised & researched their way beyond these functional falsehoods, by now. I bought into these ‘optimal wellness truths’ hook line & sinker early in my career and proceeded to even propagate a few but with (not much) more experience in clinic, I had to seriously question this pursuit of ‘perfection’ & ‘perfect pathology’…in favour of reality & scientific evidence! They didn’t add up. Not with my patients – even the healthiest ones, in fact some of the really unwell ones occasionally had these kind of high-normal results and they were part of the problem!. ‘But that’s because no one is truly healthy outside of those seeing a functional medicine practitioner & supercharged on supplements & hormone replacements!!’ came the counter-argument. Ahhh, really?
How then do we reconcile this with the following: Individual genetics & biochemistry
Our biological resilience Healthy & appropriate senescence Large datasets of mixed race populations from other comparable first world countries…where these figures denote the statistical outliers?
I mean, if the 50th centile value for ferritin for actual living, breathing, bleeding, women in the US, Canada, Australia etc etc is 30-40 ng/mL and the 95th centile is 126 ng/mL and the WHO says that in fact, anyone menstruating with a ferritin > 150 ng/mL should attract suspicion for iron overload….but functional medicine men (mostly…sorry but it has to be said!) say 100 IS OPTIMAL FOR EVERY WOMAN #@^*…please tell me in which women, consuming what kind of diet, where in the world, & based on what improved or better health outcomes?
And while you’re there can someone please support this bold claim with a scrap of high quality evidence?? [Rant over🎤💧]
The falsehoods of functional medicine include the blanket belief, ‘more is better’ (ahhhhh not when it comes to many things, including iron where women’s lower levels have been found to be an evolutionary advantage…guys). But you know what, we’re better than that! We see each individual, recognising all the factors at play that make for their uniqueness, help to define what ‘healthy’ looks like for each person and don’t fall for one-size-fits-all claims without any evidence nor common sense even, to support them. What do you think?
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 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 Powerhere.
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??
It could.
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!
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.
Maybe it’s tax-time, just my wintery whinge or a tirade triggered by missing my twins’ 21st birthday due to border restrictions 😶 butI’m sorry for all the shouting of late…about interpreting iron studies, about the copper misinformed etc etc. and my gorgeous new grad mentees copped a full monologue, with links to articles, recordings & the Coeliac Society, when they asked me to expand on why we must exclude coeliac disease before removing gluten from anyone’s diet. I was so glad they asked though! I’m now using my inside voice.
But I don’t want my message to be misdirected and I fear it might be. It’s not you and it’s not me
‘We’ are doing our best. We are working in a field that demands us to be across soooooo many domains of knowledge and information, from the basic & not-so-basic medical sciences, to pathology interpretation, nutrition, herbal medicine and beyond. It’s a lot. None of us are across it all. I’m certainly not. And I’m aware, that the frustration I feel at others’ misunderstandings sometimes is unfair, because I’ve benefited from excellent early teachers all the way through to having a job now, that keeps my head in the research daily. And even still, without a doubt, the gaps & shortfalls I observe and criticise in others, I could have made of myself, earlier in my career. We don’t know what we don’t know, until we know better, right.
It’s them
Who is this ‘them’ of which I speak? Well, 25 years ago when I completed my under-graduate (and walked 10 miles to school in the rain, without shoes or breakfast 👵) I believe I received the training required to be the naturopath that I needed to be. Safe, effective, knowing my scope – which was basically coughs. colds, atopy and risk mitigation for future chronic disease. I never saw a lab test during my under-grad. I would have read a set of iron studies badly and something like ELFTs, like it was Latin. I wasn’t made aware by my lecturers of the critical part I could play in my patients’ lives, either by advocating and advancing correct diagnosis or by obscuring, confounding and delaying it (sorry, still thinking about the gluten debate!). But back then, I think this was appropriate for the time, the state of play of our collective medical knowledge and for the role naturopaths were playing in the health landscape. Not any more.
If you haven’t had a chance to read the extensive research about ‘us’ (Australian nats, nuts & herbalists) published of late, who we are, what we do, how we are viewed and what our patients expect, then you could be in for a surprise.
We’re perceived by many, if not most, of our patients to be a primary health care provider – either flying solo or co-piloting with the patient’s GP (& no auto-pilot function!!!) and as clinicians for chronic comorbid cases not the acute cold. My how times have changed and the question is – has the knowledge and level of competency of those in educational roles & the quality of what they deliver a good fit? Sorry, but if the majority of a large new graduate cohort have left their training with a mantra of ‘we must not diagnose’ and INTSEAD are likely to advocate a gluten free diet RATHER THAN Coeliac testing with the patients doctor first – then we’re falling at the first: Primum non nocere. Sorry,I forgot, inside voice 🙄🤐
This Update in Under 30 recording speaks to the seriousness and primacy of identifying Coeliac Disease in any patient reporting a suspected reaction to gluten and takes you through the latest evidence on the best screening protocol. With an increased understanding about the strengths and limitations of gene testing, serology and biopsy, we have a clear map to follow now. Along the way Rachel outlines 3 additional potential mechanisms for ‘gluten’ reactions amongst our patients, what to look for and how to tell the difference.
Name a B vitamin. Hey, Bingo! It’s on the list! What list? The complete one from all the review papers & references to possible links between individual nutrient deficiencies & Angular Cheilitis – inflammation & cracking at the corners of the mouth. So does that mean more Bs are the answer for people presenting with this painful, recurring issue?…Ahhhhhh No. Yes, you heard me correctly, these deficiencies rarely cause the breakdown of the integrity of this very specific area of skin in the patients we see. So now we have a double ouch, right?
We might send patients away with a B complex and some lip balm and over a week the cheilitis resolves – which one was the most therapeutic? …I hate to tell you 👀
What is the underpinning cause(s) & the important message we are missing with this presentation? Well, it could be one or more of a long LONG list of differentials, ranging from anatomical, habitual, immune related to iatrogenic. And while many nutrient deficiency pictures can include this feature and therefore make the ‘possible’ list, only one makes the ‘probable’ list. And that’s iron but only in severe deficiency, aka anaemia and only affecting 1 in 5.
Me???
…Telling anyone to push the nutritional issues further down the list of differentials for any condition? Well, that’s unexpected
…possibly unprecedented
And no, antifungals aren’t the answer either. Yep, that might be worth a listen….👂
Just an annoying, embarrassing, cosmetic condition or could it be the clue that helps you ‘crack the case’? There is a surprisingly long list of differentials for this condition but most of us only know a few, reflexively reaching for either B vitamins or anti-fungal creams. Does either make sense? Does either address the cause(s) which we now recognise to be a unique series of risk factors in each individual? Or are we at risk of shooting the messenger and missing the message of Cracking Corners altogether?
You can purchase Cracking in the Corners – Angular Cheilitishere.
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.
Last week I had my say about acknowledging our elders & mentors, this week I want to speak to the power of the young peeps. Just like a younger sibling, nipping at your heels can act as a great motivator to move faster, or having children can inspire us to do more to improve the ‘world’ we’re welcoming them into, my interactions with naturopaths, nutritionists & herbalists of the younger generations generally effect both responses in me! The best of these come from cluey ‘youngsters’ (mature-age-second-career-new-nats included!!) who ask the most difficult questions & show dogged determination in getting answers to these either via me or in spite of!
This is exactly what’s been in play over the last few years (yes, you heard me…years) while I’ve been under the watchful gaze of Jostling Josh Weymouth! He’s a youngun’ – it’s all relative right – who has kept us both on the straight and narrow writing:The accuracy and interpretation of plasma selenium in our patients: a literature review,which hasjust been published in the the Australian Journal of Herbal & Naturopathic Medicine.
At the outset I was able to hand over a substantial selenium research hoard I had obsessively compiled, Josh was able to build on this, refine some fledgling theories I had and then completely redefine my appreciation & understanding of how chronic over-treatment (not toxicity…) is so deleterious to human health. Check this out:
When Selenium (Se) saturation point occurs in plasma, there is a potential reduction in health protection… Se will progressively pool within plasma non-specifically as SeMet in lieu of regular, sulphur containing methionine, in albumin and other proteins…inducing oxidative stress via a complex disruption of cell reactions/signalling This is likely to be how Selenium over-treatment increases the risk of both CVD and T2DM
Many of you may ‘Know Your Numbers’ when it comes to Serum Se targets in thyroid health or just generally know how to Stay Safe with Selenium Supplementation because I’ve spoken extensively about these in the past and you will be relieved to know neither my ‘numbers nor my message’ have changed BUT I encourage everyone to read this new article because Josh has added so much more, including the interplay between our microbiota and our individual selenium needs, handling and tolerance and and and….I could go on but…what I really want to say is, thanks Josh for your academic rigor, your firm determination & diligence and for nipping at my heels all this time. This important piece of work just wouldn’t have happened without it 🐶
[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 aland 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
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.
I’m experiencing some serious POTTS exhaustion – how about you? No, not POTS, POTTS: Preposterous Over The Top Selling of supplements, which seems to be at an all time high even amongst our practitioner brands. I saw a product name recently that included the word, ‘supreme’!*^# Is the choice of nutritional supplements now on par with selecting our pizza toppings?
When I previously delivered university lectures on population nutrition & the role of the food industry – we acknowledged that all the processing, packaging, and promoting the food industry invests in, creates a market and a source of competition that essentially doesn’t exist for their primary whole-food ingredients.
Take apples. How can we increase the profit margin on a humble apple? Aside from organic V conventional farming, the price that any of us would pay is pretty narrow and fixed. But send that apple to the factory to make juice (and chuck in some added vitamins to boot so you can feature this on the label!!), puree and package it in the most non-biodegradable way for kiddies, dice and stew the stuff and put it in little plastic tubs for the slightly older or throw in a long list of nasties with ‘essence of apple’ to make sauce for idk and suddenly you have the capacity for mark-up, an exponentially expanded profit margin & ‘something to say and something to sell’. In supplement companies, it’s not as far from this as you might imagine. Because nutrition (**WHAT A SURPRISE**) is a lot like primary whole-food ingredients – how does vitamin C compete with vitamin C? Hey, make it liposomal!! And the nanoparticles that we’re fearful of in our sunscreens and cosmetics..let’s use the same technology for our ingestives!! YES!!! Ummm any one recall, our fears re folic acid? Just asking…
I propose that ‘practitioner only supplements’ come under the same plain packaging restrictions placed on tobacco in Australia [I am joking but only just]. Remove the bright shiny distracting graphics and hyperbolic descriptors and only state the full ingredients and excipients list plus source where relevant. Let’s bring it back to simple(?) science, basic quality ingredients and affordable effective products for our patients. Then let’s see if we can spot the difference 🧐
Rachel loves nothing better than breaking through marketing babble and spin to get to the truth about supplements – their real strengths, niches, weaknesses, contraindications, therapeutic doses and best forms & therefore there is a dedicated section of her website with resources and recordings that do just this,here. These include reviews onB3, B12, Folate, Selenium, Zinc & Iron (of course!),Calcium D Glucurate,Co Q10, Quercetin, high doseVitamin DandFish oilsfor Mental health. These are a mix of Update in Under 30 recordings and longer presentations and her library is ever expanding! So, if you have a supplement you think needs some serious sleuthing on – send us an email…we’re always sniffing around for more!!
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.
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.
The average woman & her dog (& likely every other member of her household, be they furred or otherwise), can tell you that sudden changes in sex hormones can undermine, derange, psychopathise, impact her mind and mood. Hey, for me most days reverse parking is my mild super power, the envy of all, but on day 26 of my menstrual cycle, I can struggle with a ‘nose-to-kerb’! But if we are quick to attribute this to the fluctuating sex hormones produced by our ovaries, alone, we’d be making a mistake. A portion of these peripheral steroids do cross the BBB and act in our brain, so changes to these levels during any kind of transition: follicular to luteal, pregnant to post-partum, menstruating to menopausal, early adulthood to andropause, will be ‘felt’ but the sex (hormones) we have on our brains at any given time, are far more abundant, potent and complex than this, thanks to the brain’s ability to make its own.
So in fact, the amount of sex hormones active in the brain represent an intersection between peripheral and central steroidogenesis. These Neurosteroids, made ‘on site’, are as much produced in response to our mood, our neurobiology, our psychological and environmental stress, to help us navigate these, as they are the creators of mood itself.
Yes, these particular sex hormones, due to their actions in our brain, belong to that growing list of CNS celebrities: the Non-Classical Neuromodulators. Which, for the otherwise neurotransmitter-centric & obsessed among us (that’s everyone), makes mental health and illness much more complex than ‘serotonin deficiency’ or ‘glutamate excess’ and a whole lot more real. We now need to consider other entities like: ‘suboptimal LDLs’, 5 alpha reductase over or under-expression & ‘xs inhibitory tone via progesterone’.
The ‘sex on the brain’ of any patient therefore is impacted by both their Endocrine (ovaries, testes, adrenals) and Synaptocrine (neural) contributions – and these demonstrate some shared dependence (for cholesterol & healthy mitochondria etc) and independence.
We all know the depressing stats in support of the ‘ovarian withdrawal hypothesis’ and the risk to women’s mental health with each reproductive transition, and also in andropause in men, but the time has come to now deepen our understanding and to recognise we can have an imbalance of ‘sex’ on the brain – regardless of the ‘balance’ we might see in the periphery and put our thinking caps on about the options we have to address steroidogenesis either side of the blood brain barrier.
When it comes to a modern take on how sex hormones impact both the structure & function of our CNS, we need to blend the ‘old’ with the ‘new’. The ‘old’ tells us, production of sex hormones is in the gonads and action at a distant target anywhere else in the body, including our brain. And the ‘new’ is in the form of the ‘Synaptocrine’ – where production of these sex steroids is actually within neural tissue itself and their immediate actions occur close-by, in the synpase and at the post-synaptic neuronal membrane. These two contributive pathways show some shared dependence but also independence from one another and the balance of both has now been recognised to be integral to the overall health of the nervous system.
Just like Kevin, ‘Niacin’ is profoundly misunderstood and consequently runs the risk of doing us harm. Unlike ‘Kevin’, we can’t watch the movie to see how this (our arguably excessive use of the wrong forms of B3 in supplements and fortified foods) is all going to play out, so that we can be suitably alarmed and start making some different choices. The risks that follow from our B3 ignorance are twofold:
One comes essentially from our gross under-estimation of this B vitamin – we’re stuck in the Pellagra Paradigm, believing that prevention of the 4 D’s is confirmation of adequacy.
The second, is our lack of discernment when it comes to the different forms or precursors of B3 & our unfamiliarity with their very specific physiological roles – good and bad.
In this regard we’re all likely to say, ‘Well back up there 1 second, we do know that Niacin (aka nicotinic acid) is different from the other forms!’ Producing flushing, yes. Used as a lipid lowering agent in pharmacological doses, yes. But can you tell me, which serious concerns and biochemical disruption is shared between both gram doses of niacin and everyday ‘routine’ mg doses of niacinamide? Yep, that one, the so-called ‘safe’ one. Better still, can we all list the various B3 forms in order from most to least potent, in regard to their capacity for NAD+ promotion in the human body?
Because this is now the definition of B3 ‘adequacy’ or ‘optimisation’ according to modern scientific understanding & it is a long long way from the absence of Diarrhoea, Dermatitis, Dementia and Death!
In fact, the boosting and optimisation of NAD+ pools in the human body is key to life – a long and healthy one according to the current research consensus – and its depletion is akin to ‘death’, or a faster one, anyway. From increased metabolic disorders, mitochondrial dysfunction, impaired gene stability (cancer, infertility etc) and higher rates of neurodegenerative disorders, just to start, these take up the lion’s share of our chronic health burden and battle that currently dominates the dis-ease landscape. And more niacinamide might just make that worse.
I didn’t mean to to alarm you. I am alarmed. Want to deep dive into this yourself? Start with this older but still brilliant review article by Bogan & Brenner. Want me to hold your hand while we jump off the high platform diving board together into this vastly different and powerful new understanding of B3? Let’s do it!
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.
‘Hey Alexa, What’s that formula for correcting urinary iodine for hydration status?’ Oh yes, if only she could answer these kind of questions!
There’s no one here by that name but we get these kind of emails all the time [Oh and also for Freya who hasn’t worked here in like 5 years!!😂] But we love them because it means our blogs provide useful, sought after and (we like to think!) really really hard to get anywhere else answers . But hey try it, Ask Siri! We’re always forthcoming with references – not just citations but the full low down and dirty full texts (as long as we’ve managed to get our hands on it!!) and we know which topics particularly hit a spot across our professional group by not just the number of enquiries but how far the actual blog they’re referring to, dates back. So we’ve just received more comms regarding one that’s often on high rotation…a post I wrote on urinary Iodine Assessment & how and why we should adjust for hydration! That was 2014…what a vintage 🤩 Show’s though how topical and tricky this little test is.
The iodine landscape has undergone radical change recently. We’ve moved from recognising the resurfacing of a widespread deficiency, to large-scale food fortification that has failed to correct deficiency in most and produced excesses in a few. Parallel to this, we have the ever growing incidence of thyroid disorders and some radically contrasting ideas regarding iodine’s role in both aetiology and treatment. Micrograms V milligrams? Random urinary iodine or iodine loading test? Important new evidence and clinical experience helps us understand more about how to accurately assess patients’ need for iodine and know when & how to use it therapeutically & when not to!
There’s enormous potency in nutritional medicine for mental health but it ain’t in the form of a ‘dash of precursor here and a sprinkle of co-factor there’, like some may have you believe. Many nutritional prescriptions can look good on paper but that’s the extent of it, take the suggested use of glutamine for GABA production, for example. Sure it can be said to be a precursor (so is glucose!) – so will higher intake of this equate to higher production of this neurotransmitter? Ah, no. The reasons relate to distribution and hierarchy of use for this amino acid, as well as determinants of glutamatergic neuron activity.
Why would we limit our prescriptions to precursors, anyway, when we have 2 amino acids at our disposal, whose oral supplementation is known to translate to higher CNS levels and their actions and efficacy as major inhibitors of neuronal firing (akin to GABA), involves no modification nor maybes?!
Hello, Taurine & Glycine, where have you been all this time?
While, many of us may have been using taurine in combination formulas for mood, chances are you’re not entirely clear why sometimes those work and sometimes they don’t. The answer may be in the regulation of CNS taurine transfer & balance- sometimes the people who need it most, have the least capacity for its uptake across the BBB. This is well-established in neurobiology, but news to many nutritional and integrative health professionals, who have been using it in patients where Glycine, in fact, makes more sense. So while taurine has myriad impressive strings to its bow in relation to mood-modulation and powerful protection of brain structure & function, Glycine, has an extensive network of receptors throughout the brain and spinal chord, enabling it to exert inhibitory effects, second only to GABA itself. And, most importantly, BBB transfer of this amino is not subject to the same impediments that we see with taurine. These are two of my most frequent and favourite mood-modulators, affordable and accessible when used as single ingredients, for patients, with anxiety, addiction & sleep disorders etc but understanding how they work (and when they won’t) is essential in choosing which one to use, when.
For example, do you know the Tmax for either of these oral supplements? How long it takes, to create a spike in patients’ plasma, better still their CSF, and therefore speed of onset of action? What about their elimination half-lives to guide your understanding their duration of action and therefore the timing of follow-up doses?
When we’re trying to realise the full potency of our medicines – these are important details to know that convert our ‘prescription potential’ into something powerful. Just like die-hard herbalists will tell you, its an art and a science and this is true in nutritional medicine as well. Don’t skimp on the science!🤓
Both taurine & glycine have a claim-to-fame as amino acids that effectively calm an over-revving brain, via their net inhibitory actions within the CNS. They achieve this via different means and while in some circumstances, one, either or both will is the result of differences in the regulation of their BBB transfer, pharmacokinetics, as well as add-on benefits or detractors, unique to each. Learn how to use both of these powerful and affordable mood-modulators, to their fullest, and be more able to know ‘which one when’, by listening to this latest narrative review.
The latest Update in Under 30 has landed!!!
You can purchase Take A Fresh Look: Taurine & Glycine in the CNS 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.
Key texts tell us, 2nd trimester Serum Ferritin may be between: 2……………………………………………………………………………………….and……………………………………………………………………………………….230 mcg/L But a 2nd trimester Ferritin even > 40 mcg/L is remarkable – and not in a good way🙄 So, ummmm what should it be and why?
Given all the attention iron gets from me alone, you would think we would be a lot clearer and a little ‘clueier’ regarding the answers to core questions like this. But we’re not. Correction, they’re not. Who is this ‘they’ of which I speak, um well, just the dudes in the top level office who write the practice guidelines for GPs, Obs, Midwives etc. Big call I know, but answer these to get my drift:
What is the average Serum Ferritin in healthy women with healthy pregnancies in the 2nd trimester? After all the routine Iron treatment given across numerous countries, in line with the WHO recommendations, is there any evidence that values higher than this have irrefutable benefits for mother or baby? Is there evidence to the contrary, that it can be harmful?
And while we’re busy asking questions that shake the flimsy foundations of the practice guidelines regarding monitoring and managing iron levels in mid-pregnancy – how about we get up to speed with the evidence that shows 1st trimester Serum Ferritin is in fact the most meaningful as an iron marker both in the short and long-run for any woman’s pregnancy. I know, right…this is all sounding very different from the, inappropriately named, ‘normal’, which is to test women at wk28, in the midst of peak haemodilution, and therefore physiological anaemia, and to then send that patient home often with a new diagnosis of iron deficiency and a sense of urgency to ‘fix this fast for you and baby’. In some instances this is appropriate and important, especially women who weren’t comprehensively cared for & whose iron status wasn’t monitored & well-managed in the first trimester. But for so many women, who are just riding the Ferritin-Fun-Bus…they are right on track with looking their very worst!
Couldn’t resist finishing this year of Update and Under 30s with a serious BANG! 🧨🧨🧨
In this continuation of our discussion about better iron balance for mum and baby we now map what is happening in each trimester with regard to requirements and regulation, and accordingly, what ‘healthy looks like’ in terms of both serum ferritin and transferrin, at every time point. This also gives us a clear practice protocol around when and how exactly to treat iron deficiency in pregnant women. Additionally, we review the risks of both under and over-treatment.
The latest Update in Under 30 has landed!!!
You can purchase Pregnancy Iron Balance Part 2 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.
I’m experiencing some serious POTTS exhaustion – how about you? No, not POTS, POTTS: Preposterous Over The Top Selling of supplements, which seems to be at an all time high even amongst our practitioner brands. I saw a product name recently that included the word, ‘supreme’!*^# Is the choice of nutritional supplements now on par with selecting our pizza toppings?
