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’ 🙄
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!
Did I mention my mentees ask the meanest (!) & most meaningful questions? Especially those early career practitioners engaged in our New Grads program! And it’s been almost a whole month minute since I’ve talked about iron, so I wanted to share this gem from Katherine Geary:
“Why are so many women seriously low in iron? Periods aren’t a modern invention and it seems a bit of a design fault to have half the population dragging themselves around with iron deficiency anaemia! So why is it so common, even in women who seem to have reasonable dietary intake and low/average menstrual blood loss?”
Well I am so glad you asked! And not because I or anyone has the definitive answer. But there are some excellent voices joining in this conversation about how iron nutriture has seemingly become the collective female Achilles and how, in fact, this might be, as opposed to a ‘design fault’…wait for it…an evolutionary advantage! Particularly hard to believe I bet for those of us ‘dragging ourselves around with iron deficiency anaemia’…to contemplate that this makes you, in fact, some kind of Superhero! But let’s back up there a bit. Firstly, in light of iron being the 4th most common element on earth and concurrently the number one micronutrient globally we struggle to stay replete in…the contradiction is striking. Add to this the fact that while women and children of developing countries experience higher rates of deficiency & IDA, those of us living the ‘good life’ in the top pastures of the developed ones, are still affected at strikingly high rates. Katherine’s right of course, periods are not new…so have the rates of iron deficiency always been so high, or if not, what’s changed?Well, a few things.
As so often seems to be the case 🙄 most of the finger-pointing is at the problem child period: the Agricultural Revolution. This radical shift in diet, away from meat towards cereals, is a clear contributor.
And then came the infections. Both the GIT ones, with bacteria (not naming any names, H.pylori!) parasites & helminths etc getting cosy and cohabiting inside no-longer nomadic humans (stealing even more of our precious iron) and then following on as well, the rise of infectious illnesses, flu, smallpox, malaria, TB, etc. [Ok this is the bit where you can don your cape!] If you have one of the latter, then having one of the former can be really handy! Let’s say this another way. Iron deficiency is considered protective against the infections that can kill.
That’s why we see that characteristic sequestering of iron during any significant inflammation in our patients – ferritin rises because in fact as much iron as possible has been removed from the blood…because our infectious foes are fans of ferrous (not Ferris..😳)
Authors like Denic and colleagues contend therefore that “humans may have ‘failed to adapt’, genetically and culturally, to continuous deficiency of iron because relative iron deficiency was protective against many infectious diseases”. So next time you find yourself cursing the ‘dragging feet deficiency’, perhaps rather than our Stone-Age genes we can blame the blinkin’ Agrarian ones! It’s food for thought. Add to that, other major changes in the lives of women over time, like more time menstruating, both with a tendency to earlier menarche and significantly less cumulative time pregnant over our lifetime but I am sure there are many other theories out there. Have you got one?
Love Getting Answers to the Iron Questions That Bug Us All? Us Too!
Hence, The Iron Package
That’s why we’re often adding new tools and resources to our Iron Package for that very reason! Already, this package provides you with an opportunity to take a significant step up with regard to identifying, lows, highs and everything in between of iron status, and how best to manage deficiencies..our number one bug bear (as per above)! So if you’re not already a proud (iron) package practitioner, maybe there’s no time like….now?
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.
About 15 years ago I was introduced to histamine, the neurotransmitter. Before that, I only knew him (come on…it has to be, right? Histamine) as an immune molecule, an allergy mediator, a chemotactic agent of chaos! Given my interest & previous work in mental health, I knew the rest of the chemical cast pretty well. There was Sunny Serotonin, Dance-Party Dopamine, Nervous Noradrenaline &Go-Go Glutamate. So it came as a bit of shock to realise that an equally important member of this cast had never had a mention in all my previous education…
‘Hype-Guy Histamine’
With 64K neurons dedicated to its production & an extensive axon network all over our brains to ensure its excitatory effects are felt everywhere…I was a bit embarrassed we hadn’t met sooner! I’m not Robinson Carusoe in that regard though, our awareness and recognition of this key neurotransmitter has been snail-like in its pace and progress. A recent review paper on the development and evolution of antihistamines kicks off the conversation with, ‘Oh, so histamine is just another neurotransmitter now’…which gave me a bit of a laugh. Seems like we were all duped…even the dudes making the drugs to block it! But once I did meet Histamine, the neurotransmitter, it really did change my clinical practise, forever. And as I have gotten to know him better and better over the last 15 years, how his excesses and deficiencies present in my patients and how best to manage these, I can confirm, it is far from the answer to every patient’s prescription for mental health but this an imbalance is evident, addressing it is exceptionally effective and I remain forever grateful to those that have contributed to my learning in this area, passing on the knowledge from its originators: Car Pfeiffer & Abraham Hoffer. These pioneers of orthomolecular psychiatry gave Histamine a platform and presence that no one else had or would for decades still to come.
And now every practitioner and their pet poodle seems to want to talk about Histamine! But, my friends let me tell you, CNS Histamine imbalance has little to do with eating tuna, umami flavours and the state of your gut!
Hype-Guy Histamine is made on-site, in your brain. We don’t import it in over the BBB mountain range. So, in terms of a histamine imbalance in your neurochemistry, we need to narrow in on the noggin and get crystal clear about what could be behind such an imbalance and therefore how to tailor treatment to address each cause. I owe a lot to those who first taught me this model and I think it’s time the model had a mini-makeover, thanks to our vastly improved understanding of Histamine, methylation, genes, mast cells, behaviour driven biology etc etc. etc. that has been generated now mainstream medicine has finally met Histamine, the neurotransmitter! 🥳🥳 And now, be warned folks, contemporary psychiatric pharmacy has its sights set on histamine as a key target for new medication development and the improved management of mental health. Better late than never, I guess. Have you met your Hype-Guy Histamine?
Histamine Imbalances in Mental Health 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 amounts, 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 practice 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 two hugely helpful clinical resources, will give you the confidence to recognise and remedy this important imbalance in mental health.
The latest Update in Under 30 has landed!!!
You can purchase Histamine Imbalance in Mental Healthhere.
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I’ve a confession to make, I took the batteries out of our smoke detector in our kitchen. Why? You know why. Because it went off all the time, with what I like to call, friendly fires…you know, heating oil for poppadoms, a rush of steam upwards from a hot pot on the stove with its lid removed, gosh even toasting your bread a little too vigorously would do it! Taking the batteries out, stopped the alarming alarm (!) and quelled my need to always keep a tall stool and ‘whooshing’ implement nearby, in preparedness for the next smoke activated siren. But of course this is not a solution. There are consequences.
I recently realised this was the best analogy I had for many patients who have experienced significant trauma. Particularly when this trauma has occurred during childhood, there is potential that they too have effectively ‘taken the batteries out of the ‘smoke alarms’
This has been documented in a proportion of individuals affected with PTSD for example and is believed to be due to the ‘re-calibration’ or ‘rewiring’ of their HPA axis in response to excess ‘over-activation’. So because their internal ‘alarm system’ had been so consistently activated, the chronic hypercortisolism evokes a down-regulation of their glucocorticoid receptors, as a means to ‘turning down the volume’ or…removing the batteries. Let’s think about this. If your patient has, let’s say, 5 receptors for cortisol compared with 50, their receptors will be ‘filled’ quickly with only minimal amounts of cortisol. This receptor ‘fullness’ however is detected by the brain which in turn then shuts off the ACTH release. But really there was only a small amount of cortisol. The threshold for the negative feedback inhibition (cortisol –> no more cortisol) is very low and patients can end up with too little. Wouldn’t they have less stress, then, feel better then?
In spite of all the name-calling Cortisol is not the criminal he’s been made out to be.
Cortisol ≠ Stress.
Cortisol in fact offers a way out of stress – the means to physically resolve the stressor. So too little…feels awful.
Patients of mine who have been shown to be affected by this hypocortisolism present as extremely anxious with poor stress tolerance, in fact if I didn’t know differently, I would have imagined they had ‘over-activation’ of their SNS not under. When I speak with them I try to find different ways to describe why this down-regulation of their HPA can contribute to their mental health challenges. I talk about Cortisol being akin to clothes…no one wants to leave the house without it, or a raincoat that we really need because one day inevitably its going to rain and we’re going to be out in it…its protective. But from now on I think I might confess about my battery-less smoke alarms. Yes I can cook toast without getting startled by screeching sirens now…but I could also burn down my house…which clearly doesn’t rid me of stress and anxiety…
Anxiety, high stress, poor sleep – it all sounds like high cortisol right? But did you know that these are all features of abnormally low cortisol as well, which underscores why accurate adrenal assessment is so important. This Premium Audio takes you through all the investigations you have at your hands, from clinical markers (Pupil response, Rogoff’s sign etc.) to the strengths and weaknesses of blood, urine and saliva assessment. It identifies the variables you need to consider and how to accurately interpret your patients’ findings.
If you’re already an Update in Under 30 Subscriber – you’ve got this! Just log on and go to your Active Content. If you’re not and would like to download this recording and resource then 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…
No. 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?
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.
I love a good iron question. It makes me emit a sound like Jack Sparrow might, when faced with something pleasingly piratey 🏴☠️ Lucky because I am asked SO MANY GOOD ONES, SO OFTEN!! Being one of the earliest minerals discovered to be essential…we know so much more about it than the other latecomers but that ABSOLUTELY DOES NOT MEAN WE KNOW IT ALL! Sorry…I also tend to shout with excitement when faced with a good iron question. Yes, run for cover, I do have an even higher volume setting 🙉🙉
Just this month, I received this little ripper: I was wondering about the expected timeframe for iron supplementation to improve ferritin levels?
Yes of all the nutritional answers we can quickly ‘google scholar‘ our way towards, actual realistic expectations for response to treatment, is rarely an easy find! And yet, this critical clinical detail seems to be the thing that can leave so many of us stranded at sea with our patient prescriptions. Did I give up too soon? Or should it have worked already by now? Some of the best naturopathic approaches are easy to execute…but when those patients come back after maybe a few repeats & perhaps minimal change you realise, you have a major piece of information MIA: what to expect. Rapid relief or a cure by Christmas?! Aka, it won’t happen overnight but it will happen. So, great, let’s talk ironing out our expectations around responses to iron repletion!!!
First – We need know where iron goes First!
So if your iron deficient individual is actually suffering from iron deficiency anaemia, no guesses who the VIP (very important priority) is during repletion! Consequently, you can throw lots of iron at somebody (oral or even IV) and find there’s limited increase in their ferritin initially, a rather ‘disappointing’ show actually but if you keep your other eye (Jack Sparrow style) on their FBE, you’ll see the iron is being funnelled into producing haemoglobin and red blood cells. Sneaky! And if sensible can ever be associated with sexy…this is it! Ferritin is for iron surpluses only and right now, we ain’t got none! Medical texts advise that in these scenarios, confirmation of efficacy equals an increase in Hb levels of approx 10g/L a week. In reality, no one wants to turn patients into pin cushions (esp when we’re trying to build iron back up not keep springing leaks!) so we might retest in a month or more. But an increase in Haemoglobin of 40g/L per month sounds rather aspirational with oral iron, doesn’t it!!
If we bring in the personalised perspective here, we recognise that most of our anaemic patients may only be just on the wrong side of the line, with values at 110g/L and tbh we would be shocked and a little worried if this grew in a month to 150 in a woman! Erythropoiesis is not the result of iron alone! But the point is, if the iron replacement is working well enough, you should be moving out of anaemia within a month not a millennium!
And only once this job is done will the ferritin start to build.
So what if your patient isn’t anaemic – just low in ferritin? Well then, if you’ve a) fixed the leaks (unintended or excessive blood loss anywhere Rectal, Renal, Repro) and b) buoyed bioavailability (HCl & prebiotics while minimising iron-blocking issues like excess Ca, tannins etc) and c) corrected for low intake via a sound supplemental approach (daily dosing for those not consuming much dietary iron and alternate days for the rest) you should be seeing ferritin increase within the month of at least 10mcg/L, but hopefully more. And if it’s not? Go back to the beginning of this little to-do list…because it means we’ve missed something. Doh!
Yes it’s true the learning doesn’t ever end and as I’ve continued to learn about new iron research I’ve added to our one-stop-iron-resource-shop..the Iron Package. Earlier this year we added a new clinical cheat sheet with some other important numbers on there you want to have at your fingertips whenever you read iron studies. So if you’ve already purchased and have access to the Iron Package…SURPRISE! 🤩 Go back and look again and if the iron package is not already on your ‘bookshelf’ there’s no time to waste!
You’ll never look at iron studies or your iron-challenged patients the same way.
Given1 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: But why? But why?? But why???!
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…🧐
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.
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Now find a comfy spot everyone & I’ll tell you a story…’Once upon a time, a long long time ago, we lived our days out in the dark, regarding potential calcium dysregulation!’But ever since serum Calcium has become a standard lab included in most routine screening tests (General Chemistry aka ELFTs) abnormal calcium handling is no longer an ambush for patients of ‘stones, moans and abdominal groans’, as the saying goes in hyperaparthyroidism. A diagnosis historically only mad, when someone presented with this constellation of rather advanced symptoms. But actually being able to identify your patients’ typical blood calcium levels offer us so much more than just a heads-up re parathyroid disease
It may tell us something about their Magnesium status, cardio cautions, be a bit of ‘bone barometer’ and probably most immediately important, flag their suitability for calcium supplementation!
Yep…rather than the current-criminally-crude-calcium-checklist: 1. Patient is female 2. Patient probably doesn’t consume enough calcium 3. Patient may be at risk of osteoporosis (yup…that accounts for practically every woman, right there!)
But seriously, if you just do a full review of the vast literature on this topic, what?! Not enough time?! How about then, just skim read a couple of key papers? Still baulking at that?…maybe just a wafer-thing editorial (??!) will tell you that, consuming elemental amounts of calcium (> 250mg), that are beyond even the biggest Dairy Diva’s Diet Diary, may be deeply problematic for many. And guess what…this doesn’t pertain to supplements alone…even calcium fortified foods are not free from concern! But let’s not let yet throw all our calcium fortified foods in the same bin as the folate ones we did a while ago!! Let’s step out of the dark and into the light that shines upon us, care of fasting serum Calcium measurements, to help us recognise whether Calcium is the cause, the consequence, a cure or a curse for person sitting in front of you 🧐
The Calcium ConspiracyControversy Continued
The Calcium Conspiracy arises primarily from misperceptions about it being ‘the boss of bones’ but becomes more of a controversy when in spite of ongoing advice for broad-scale use we review the evidence and have to acknowledge that the recommendation to supplement post-menopausal women with large doses of Calcium, not only lacks strong evidence but may cause harm to some. In this detailed discussion of the two schools of thought – Rachel finds a position somewhere in between. Reinforcing the need for an individualised approach and personalised risk benefit analysis while teaching you how to undertake this in every client.
The latest Update in Under 30 has landed!!!
You can purchase The Calcium Conspiracy Continued 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.
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!
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 😉 🧐 😂
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.
You guys know I can’t help myself. For the last year or so I’ve been immersed in developing and redeveloping and redeveloping 🤓 [ahem apologies to my team!!] teaching tools for all practitioners to better understand what the routine renal markers can offer us in terms of understanding our patients…and it is far above and beyond renal function, promise. Just one example of this, is the sophisticated yet incredibly simple urea to creatinine ratio calculation that I was originally taught by Professor Mel Sydney-Smith. In adults with preserved renal function, this is the key to the kingdom, in terms of being able to objectively quantify whether patients are truly meeting their own individualised protein requirements. The Marvellous Mel (well he is, who can argue with that?!) added this one to my toolkit a long long time ago and in turn, I’ve been using it and spruiking it ever since.
In fact, I just lost 30 mins of my life listening to myself (ewww) in an old Update in Under 30 from 2013 that I recorded on this very topic.
[Sigh] I sounded so youthful…and…about 7 years younger too in terms of experience with this crafty calculation in the hundreds of labs I have encountered since!
My reliance on this ratio has remained but my wisdom regarding how to apply it has widened….and so, as I prepare to initiate another hundred or so practitioners into this secret sect 😉 via our current MasterCourse in Comprehensive Diagnostics, I couldn’t help myself and decided to re-record this UU30 episode: Using Urea & Creatinine as Markers of Protein Adequacy and also throw in a new pdf resource to boot [once again, ahem,apologies to my team!!] You see our ability to identify protein adequacy without this tool relies on the rather-rudimentary-‘rule’ that your protein requirements increase linearly with your weight…that’s the whole g/kg body weight thingo, right? But what if your weight gain is ‘all adipose’ Vs ‘mega muscle’ – are the protein requirements really the same for both people? Absolutely, not! This calculation enables us to step away from the rough approximation of the RDI and be able to determine if each individual is meeting their genuine requirements as driven by their own unique muscle mass hunger…oh and it reveals a few other very helpful things along the way to boot!
But this simple calculation comes with some caveats: 1. there are people and presentations in whom this calculation is not appropriate or accurate 2. because there are no magic numbers, right, it is about matching your labs with the patient in front of you and 3. looking (as always) for patterns.
…and a word of warning to the uninitiated: You’re going to love it!
So for those of you who are already Update in Under 30 Subscribers…happy Wednesday! Because you always benefit from any updated recordings etc. you’ll find this rejigged resource is already in your Active Content and for those of you who may have purchased this as an individual recording in the past, the same applies. And for anyone else keen to make some real meaning out of the most routine labs we see over and over again, and understand a whole world more about what they tell us about our patients’ muscle mass health, trajectory and the dietary protein piece of this puzzle…you might want to check this out too! And for those of you who think ‘total protein’ on a patient’s blood test results reflects ‘total protein’…boy have I got news for you!!
This comprehensive analysis of two standard indicators, urea and creatinine, that are often part of the patient’s standard blood chemistry tests. These commonly available results can provide insight into protein ingestion and uptake as well as muscle mass and, in extreme cases, kidney and liver function.
The walls of books you can see behind me in my office, during webinars etc are not stage-props. Not a single day would go by without me pulling multiple core texts down off these shelves to caress their paper pages. I recite the most often used ones: Shils Shike, Olsen (Modern Nutrition in Health & Disease), Mosby’s (Manual of Diagnostics and Lab Tests), Gibson (Principles of Nutritional Assessment) like members of my extended family. But I know I am a bit of a relic in this way and nowadays that’s seen as a very slow solution…
I’ve seen young people unconsciously spread their fingers wider on the paper page in front of them, trying in vain to ‘zoom out’. I’ve watched them frantically search for the ‘Control F’ function that is nowhere to be found. That’s what we old folk liked to call an index.
But I have to concede Control F stands for flippin’ fantastic…when some of even my most beloved books have turned using the index into some kind of combative sport…not naming any names, MOSBY’S 😵😫🥴 where the page number listed for each lab is just a rough ballpark indication that the information you’re seeking features somewhere in the book but possibly specifically not on that page! And in terms of a resource for drug herb nutrient interactions, I alone (apparently…!) love another book by Stargrove, for the reason that it exquisitely details every scrap of original evidence that is behind a theoretical or actual interaction potential and for exactly the same reason…it is never a fast find! Then Nina from my team showed me this nifty little tool Evidence-Based Drug-Induced Nutrient-Depletion Checker. I haven’t exhaustively played with this one but on first glance it’s solid. This search engine is referenced and you can access the reference list and source of information by simply clicking on the indicated reference number.It is an American based database so specific Australian pharmaceutical branding will not be included, just use generics. Finding fast facts is important when patients are in front of you so this might just make your job a bit easier.
So, will I make the leap into this century at last and end up burning all my books? Just try me…I’m the one in the front of this picture, guarding my stash 🙉
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.
I don’t know about you but I don’t count myself among the conspiracy theorists. While I may have been partial to the occasional one over my lifetime, you have my word, I never inhaled. Or at least not since I learned the practise of scientific enquiry and the application of critical thinking to all evidence. The two together tend to put a dampener on the whole: earth is flat & the moon-landing was a hoax…kind of notions. But there is one conspiracy I think all of us in nutritional medicine have been the victim of: The Calcium Conspiracy.
Not in the vein of speculations regarding excessive lobbying & undue influence of the Dairy Corporation on dietary guidelines. Nor even arguments that this has gone so far as to inflate the RDIs for this nutrient. Nope, I am actually good with the RDIs for this mineral. High level evidence confirms that our intake of Calcium was enormous even before the Agricultural Revolution, and therefore BD (Before Dairy) 😂
Man, those roots and tubers and other bushfoods sure were nutrient dense, not like the stuff we consume these days!
No, the Calcium Conspiracy we’ve all been lead to believe is that it is the boss. The boss of bones. The boss of the parathyroid. The boss of the other minerals. And especially the boss of Magnesium. While you might have heard me describe Calcium as a ‘bully’ in the GIT (let’s call this the slide 😅) and I stand by that, it is far from being the boss of the rest of the playground! In fact its regulation is largely at the hands of other nutrients..not naming any names…[Magnesium😳] So while, all of us trained in nutrition have had the significance of the Calcium-Magnesium relationship & the mantra “2:1, 2:1, 2:1” drilled into us, which we repeat at night to get ourselves to sleep (or did they mean to take not just ‘talk’ these minerals, to help with sleep?!) Our teaching created this conspiracy – a misperception that Calcium is the boss and Magnesium its long-forgotten lackey. Well guess who’s really calling the shots and on whom?!
Have you ever heard the saying, ‘It can take Magnesium to fix a Calcium problem”? I’ve not just heard it but seen it many, many times in my patients.
But how do you tell which patients need both and which ones, just one? It comes down to understanding the exquisitely sophisticated way Magnesium lords it over Calcium – via the parathyroid and Vitamin D metabolism and how we can see this patently in the pathology (regular screening labs) of your clients. I think there is a bias in integrative nutrition – we favour Magnesium – it goes into our supplement recommendations for so many of our patients and while the rationale for this is valid – all dietary surveys show magnesium under-consumption to be rampant in the SAD – I don’t actually think all of us know 1) how much we should be giving (yes there is a limit) 2) how to discern who needs what, in spite of a lack of a good Magnesium assay and 3) the true potency in the prescription when we get these things right or wrong! This study by Sahota et al is so far my favourite for 2020..it’s 14 years old and the sample size is small but its methodology and examination of when Magnesium can fix a Calcium issue and when it can’t, is superb. Together with about 50 other papers I’ve just imbibed…they’ve refined my thinking, tremendously. There’s a Calcium Conspiracy, alright, but just throwing Magnesium at everyone in arbitrary doses is not the solution…. “2:1, 2:1, 2:1…..”😴
There’s a conspiracy going on regarding Calcium but it’s probably not the one you imagine. We have been lead to believe that Calcium is the boss: the boss of the bones, of the other minerals and certainly of its often over-looked lackey, Magnesium. But the truth is, we have it all the wrong way round. There is a sophisticated synergism between these two minerals but the brains and the brawn in this relationship are held by the latter and we need to understand how to recognise when Magnesium is ‘pulling the strings’, to produce low calcium, in our patients and how to find the sweet spot of their synergy. This recording comes with a great resource to use in your clinic, with explicit redefinition of ‘what healthy looks like’.
A 26 year old woman suffering years of fatigue from ‘persistent iron and B12 deficiency’ repetitively treated with both oral and IV, walks into a compounding chemist and finally meets her match 🐱🏍 A naturopath with years of experience working the frontline, used to dispensing iron galore (& to a lesser extent B12) to young women with similar stories. But this naturopath requests to see all her labs, she meticulously collates them and then she comes back to the client and deals the fatal blow: Has the iron or B12 ever made you feel any better? “No,” she replies.
“I didn’t think so,” says the Naturopath…”everyone’s been barking up the wrong tree all these years!” And she was right.
First glance at her blood results has all of us reflexively reaching for the same diagnosis everyone has made before – crikey that serum B12 is terrible! And then there’s the fuzzy family history of relations ‘needing’ B12 injections and some even with confirmed pernicious anaemia. But wait up…let’s keep our critical thinking hats on once you look over the rest of the lab you see there’s no evidence of functional B12 deficiency (no rise in Hcy, MCV even RDW) and then, the statement that seals the deal, ‘B12 injections have never made me feel any better’. This woman is not feeling the pinch of pernicious anaemia, not the crush of cobalamin clinical deficiency. In spite of being told that for almost a decade.
A low serum B12 value can of course flag a deficiency and we must never ignore it. But given the serum measures, in fact, predominantly Transcobalamin I (TCI), which is the carrier or taxi for B12 that almost ‘never drops its passengers off’, we are less concerned than when we see a low active B12 (TCII aka ‘the real deal’)
So what else could leave someone with less TCI, while not in fact creating a genuine functional deficit of B12? SNPs?🤧 Bless you!…Sorry that sounded like a sneeze and this retort, as we know is almost as common as the common cold! Sure…of course it could be sexy SNPs…but wait, what about something a little less ‘zebra’…a little more horse. The COCP…oh blooming heck..she’s spent the last decade on the COCP and guess what, its impact on B12 is thought to be principally a reduction in TCI! Oh and that iron story, that supposed ‘iron hunger’ we can see with her upregulation of transferrin? Well that’s an artefact of the COCP too, right? And BINGO was her name-O 🕵️♀️
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.
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
I used to all the time. Especially when I noticed the Niagara-falls-sized gap between the doses I was using compared with my mainstream medico mates. I thought, hang on, for a patient with a baseline blood level of 40nmol/L, they’re recommending <1000 IU per day, but I’m thinking 5000 IU…which one of us is wrong? Then again, we might both be right!
The sexily simple formula as cited byAussie researchersis: for every 1,000 IU of vitamin D a patient takes a day, their blood level is likely to rise approx. 17 nmol/L over 2 months, at which point it plateaus. So the medicos’ 1,000 IU supplement would bring our patient’s blood level up to 57 nmol/L which, as far as the medico might be concerned, is ‘job done’ 👍👏
My dose would be viewed as excessive but clearly I am aiming for a different set of goals (optimal rather than simple prevention of deficiency)…oh and I insist on follow up testing to know when we’ve made it!!
I encourage my patients to get their Vitamin D retested 2 months into treatment to confirm 1) they have responded and 2) their response is loosely within this predicted performance. And how many times is it not? Often. Which got me to readjust the formula I use to something more akin to: for every 10 nmol I want their blood levels to rise, I will need to increase their intake by a 1,000 IU. Now am I just making big sweeping inferences from empirical experiences of a few (hundred) patients without additional backing….well so what if I was...this is a branch of the EBM family tree! But no! I have also actually read enough studies clearly documenting the individualistic response to vitamin D, as a consequence of different adiposity levels, genes, magnesium status etc. to know that, while I am very grateful to have any kind of formula to start my thinking from…I treat individuals and goshdangit#@! they keep insisting on individualised medicine!
The whole practise of identifying a deficiency, ‘treating it’ and yet never following up with repeat labs to confirm that you actually have…BLOWS MY MIND🤯
That’s not EBM, let’s face it. Not even a distant demented cousin who has fallen from the dizzying heights of that family tree.
The one lesson I’ve learned, more than any other over 20 years in nutritional medicine, is that the more questions we ask and the more we challenge ‘established truths’, the more we uncover something much more personalised and potent about each and every nutrient …and now as the days continue to shorten into smaller and smaller slithers of sunlight between ‘bed-ends’, this is probably also a good time to ask ourselves…
Vitamin D deficiency has been associated with a long list of major health conditions: from autoimmunity to mental health & almost everything in between. This has lead to many of us recommending high dose vitamin D supplementation for a large proportion of our patients but do we understand everything we need to to be certain of the merits and safety of this? In this provocative episode Rachel outlines the key unresolved vitamin D dilemmas that should encourage us to exercise caution and outlines how adequate sun exposure is associated with improved health outcomes independent of the production & action of vitamin D.
You can purchase this UU30 episode individually here or become a subscriber and gain access to this and over 65+ episodes plus new monthly releases for 12 months here.
If you are already an Update in Under 30 Subscriber, you will have immediate access to this episode in the ‘active content’ of your online account.
🍌‘I think I am, B2! It’s time to separate the B12 from the B*S#!’
Ok, if you’re reading this and you’re not from around here you have reasonable grounds to conclude I’m the one who’s gone 🍌 but if you grew up with a show all about 2 adults dressed up as bananas and creatively known as B1 and B2, then we’re all good! Ok now for the next bit, you might need to sit down. Nothing not everything in the wildly popular, and dare I say it populist, doco The Game Changers was scientifically rigorous. I know, I’m loving the strike through a little too much today.
Goodness, when otherwise intelligent friends of mine forced me to watch this, they found the need for both restraints and duct tape over my mouth, to hear or see anything other than me jumping up and down, arms flapping, mouth yapping. People only tend to make this mistake with me once.
Among the many many dubious XXX was a terrible mis-truth about our ‘new modern reliance on animal food or supplements for B12’. Woah…back up there Game Changers Gang, say what?! Does anyone on their research team read any research? So that got me all motivated to go back to the books on our beloved B12, which is simply like no other micronutrient in human physiology or in nature, for many reasons…starting with 1) it contains a metal in the middle 2) it has dietary dopplegangers (plant forms that look just like it but actually are decoys that need to be actively removed from the body so as not to block its actions) and 3) has the most complex and sophisticated pathway for digestion and absorption, which surprising equates to brilliant average bioavailability (much better than most micronutrients)…until it doesn’t! And that’s when the trouble starts. Once you don’t have an intact IF absorption pathway, you’re down to picking up < 1% via simple diffusion, and suddenly we see why patients can be vulnerable to not meeting even the piddly required amount. Not to mention the vegans, of course.I’m on my best behaviour.
But the B*S#! about B12 is far from limited to the documentary. It’s in the words of the Methylation Mystics, making methylation sound like rocket science and in the supplements we’re being sold.
But don’t get me wrong…effective B12 treatment in the right patient is a total wow moment. I’ve literally seen all the lights go on⚡ in some . So what do we need to do to find our way out of the dark? Go back to the solid science. Come on. There’s nothing else you need to do and nowhere else you need to be… we all know it…so start by reading this and this. There’s plenty more of course but these are excellent appetisers. And if you want to cut to the chase and get the lowdown on what’s B*S#! versus what’s the real magic of B12, you can always settle in and listen to my latest Update in Under 30 – complete with a very cool clinical tool to help you choose the best B12 for each individual, but spoiler alert, it ain’t rocket science.🤫
B12 is a routinely under-rated and recognised micronutrient, which is in fact in high demand by many of our patients. As nutritional research pushes back against defining adequacy as simply the prevention of the deficiency-associated disease (macrocyctic anaemia, irreversible neurological damage) we enter a new landscape of more individualised approaches where we’re better able to recognise and treat those at risk of falling below ‘optimal’. But how do we accurately identify this and then choose the ‘best’ B12 (methyl- cyano- adenosyl- hyroxo-) supplement? Does it need to be this complex? Time to sort the B12 from the B*S#!! This recording comes with a bunch of great resources including a very handy clinical tool
The latest Update in Under 30 has landed!!!
You can purchase April’s episode, Separating the B12 from the B*S#! is here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
Have you been told somewhere by someone that the ‘perfect’ TSH is 1.5 mIU/L? This is a wonderful, terrible & wonderfully terrible example of ‘magical numbers medicine’. As a push-back against the published reference ranges we’re given, that are so wide you could drive a truck through them, there has been an over-correction by some, leading to the myth of ‘magic numbers’. We can narrow the reference range substantially for many parameters with good rationale, make no mistake about that but once we start setting ‘aspirational goals’ that are explicitly rigid…well we’ve done 2 things 1) forgotten about the patient to whom this result belongs and 2) disregarded viewing each result as part of a ‘pattern’, that we must piece together and make sense of.
Back to TSH then… if my obese patient had a value of 1.5 mIU/L this in fact would be woefully inadequate.
Also too low for any patient, no matter their size, if their T4 is low and we’d like a higher value as well for risk minimisation in our elderly clients too.
But the same result would be excessively & worringly high in my patient who’s undergone thyroidectomy.
Being given a list of ‘magic numbers’ will never replace learning labs correctly. When we do this, we come to truly know that meaning can only be made of the markers when you can answer the following questions:
What is this (metabolite, analyte, binding agent, plasma protein etc)?
What do I know about its physiological and biochemical context – what is its role and regulation in the blood, what moves it and to what magnitude?
How have the reference ranges been determined for this lab – who am I comparing my patient to?
Therefore, what is the significance of a result that is: ‘normal’, ‘low normal’, ‘high normal’, below or above the range?
Does this value ‘fit’ with my patient?
What else could explain an unexpected result?
How strong is my level of evidence?
What do I need to do from here to confirm or refute this?
And a few more 😉
Realising the full value of any test result in terms of what it reveals about the person sitting in front of you, requires these skills. Unfortunately, in contrast a list of magic numbers will often lead you astray. And building your scientific knowledge about labs will not only help you avoid the pitfalls of pathology but will strengthen your pathophysiology prowess in surprising ways, saving your patients a packet in terms of additional extraneous testing and help you truly personalise your prescriptions…because the ‘invisible (biochemical individuality, oxidative stress, genetic probabilities, subclinical states, imbalanced or burdened processes etc) just became visible’. I started requesting lab results early in my career and years later was lucky enough to be taken under the wing of Dr. Tini Gruner. I found some of our shared notes, from 10 years ago, scribbled all over patient results recently and I was struck by just how lucky I was to have her encouragement to really pursue my interest and how she was a guiding force about learning to recognise pathology patterns over single parameters. A decade on I can confess, much of clinical and educative success has come off the back of this foundational skill-set and I know, this is true for so many I’ve taught too.
“The guidance I’ve received over the years from Rachel in relation to pathology interpretation has been one of the most valuable (and fascinating) investments I’ve made as a clinician. Her teachings have filled gaps in my knowledge base I never knew needed filling and have significantly enhanced my understanding of the inner workings of the body! Rachel has an incredible ability to make the numbers that patient’s so often present us with, both understandable and clinically meaningful. The knowledge I’ve gained by investing in this skillset has paid off in dividends and I’m certain will continue to do so into the future.”
Stacey Curcio – Cultivating Wellness
I hope you’ll join me for the most exciting up-skilling opportunity in learning labs yet. Oh…and all this talk about thyroid testing..that’s just a serving suggestion 😉 this year my MasterCourse is focused on the most routine labs of all: ELFTs, FBE, WCC, Lipid and Glucose Panels…an absolute treasure trove of free integrative health information about your patient!
This skillset has been found by many to be biggest ‘game-changer’ in Integrative Medicine!
There are limited places. To sign up for the MasterCourse: Comprehensive Diagnostics click here. For more information about the program click here.
A 26 year old woman suffering years of fatigue from ‘persistent iron and B12 deficiency’ repetitively treated with both oral and IV, walks into a compounding chemist and finally meets her match 🐱🏍 A naturopath with years of experience working the frontline, used to dispensing iron galore (& to a lesser extent B12) to young women with similar stories. But this naturopath requests to see all her labs, she meticulously collates them and then she comes back to the client and deals the fatal blow: Has the iron or B12 ever made you feel any better? “No,” she replies. 
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”… 
