I talk so much about iron, I feel like I’m cheating on my life partner (Zinc)…but these two are arguably the main mineral deficiencies we encounter most consistently in our patients and, don’t tell Zn, but quite frankly, in terms of who’s more well recognised out there, Iron throws some serious shade! But the truth is they’re a ‘twofor’, as a result of their similar distribution in food, with both demonstrating significantly better bioavailability (read: virtually double) from flesh foods etc, ‘Watch out, she’s on the attack again!’ I can hear the V’s (vegetarians and vegans) say and yes I think you see this one coming…but I think it’s possible to be pro moderate meat, without being, antiV.
Ethical and environmental aspects aside (just momentarily) it is hard to argue against the nutritional benefits from moderate meat for most patients.
I tried, trust me. Put my own body on the line (and my babies) to be a vegetarian for over a decade. But as the wheels fell off for me, I noticed them falling off for so many others…and these were people who were educated, with a capital ‘E’ and putting serious ‘E for effort’ into substitution etc Not everyone of course – but a LOT of women and occasionally some men. There was no denying their ‘iron hunger’ (high serum transferrin), their movement towards microcytosis (however slight that ‘smallifying’ may be…we don’t wait for anaemia, right?), their poor zinc status and more importantly, the clinical chaos of impaired immunity, some cognitive or mood issues that presented, as a result. I went back to the mineral manual, back to all the science that helps us to understand these minerals especially in a modern dietary context.
Ah yes…meat has become marginalised in our diets compared to those of our yesteryear selves (ABS data) while our consumption of potential mineral inhibitors…you know, all the good, but bad, but good foods, like legumes and grains and green tea and and and…has risen…especially among the kind of clients who come to see us, right?
Which ultimately leads to a lower iron ‘income’ with the same outgoings, again especially for menstruating, pregnant & breastfeeding women.
The books don’t balance. (So then…IV Fe to the Rescue???)
Bite me…it’s just science. There have been some wonderfully thorough studies on this very issue and thoughtful discussions. This study in particular, by Reeves et al, of Australian women in their 20s followed for 6 years to 2009, argues that just a 1mg/d increase in heme iron from flesh foods could reduce susceptibility to the subsequent development of iron deficiency amongst omnivores. So while the median daily intake of fresh red meat in these women was just 39g/d, their analysis found that an additional 70g of lamb or 60g of beef…or about 140g of chicken and 250g of fish if you prefer white over red, appeared to be the positive tipping point for women and their ability to stay iron-replete. Well below ‘dietary guidelines’, nowhere near the scary cancer correlations (which of course may be more about fat or nitrates or ??). Moderate meat intake, right? Just saying. And don’t worry, I know. The only thing worse than an evangelical ex-smoker is a rambunctious reformed vegetarian 😂
Need A Manual on Minerals?
Minerals represent a critical tool in naturopathic nutrition and there has been an explosion of research in this area over the last 10 years. In order to optimise patient care, practitioners need to keep up with the constant stream of information, updating their previous beliefs and understanding in the process. This seminal 7hr seminar (!!)…yes…seriously..it’s THE MANUAL..is designed to facilitate and accelerate this process of review and re-evaluation via a fresh look at the key minerals iodine, selenium, iron, copper, zinc, calcium and magnesium.
We’ve been talking all about the dangers of excess fuel in our blood recently. You know, just like nature…too much fuel underfoot creates a fire hazard. So too in the bloods of our patients. The key fuels I am referring to, of course, are lipids (triglycerides & cholesterol) and glucose. Our tissues need ready access to both but Balanced Blood Supply & Mastery of Management is key.
In terms of excesses, lipids play the long-game…wreaking havoc over a long period primarily via their vulnerability to form peroxides, which in turn create a chain of oxidative stress and depletes our antioxidant artillery.
In contrast, even outside of insulin dependent diabetes, for the rest of our patients, glucose plays a fast and furious game, being a highly reactive substance capable of causing both glycation and oxidation. We describe even high-normal levels of glucose as something akin to the ‘Bull in the China Shop’, disrupting the function of the endothelial linings and damaging a variety of plasma proteins (not just haemoglobin) that float within them. But do we have a way to routinely measure the level of damage occurring in our non-diabetic but somewhat glucose intolerant patients? Sure! Just check the C-CCTV footage!
The extra C stands for ‘Carb’ and yes we can potentially check the Carb-Closed-Circuit-TV ‘tape’ in every patient.
It’s called HbA1c and measuring this provides us with an opportunity to review their personal ‘tape’ of the last 2-3 months for evidence of excesses.
Helpful, hey. But we actually have so many great tools through regular routine labs at our disposal to understand the glucose disposal or dys-disposal(!) at play in our patients! You’ve just got to know where to look (urate, triglycerides, insulin, HOMA-IR etc) and what each piece of information is telling you. We’ve had SO MUCH FUN with this particular topic in the MasterCourse this month…or is that just me 🙄 No, I know it was, because our live session chatbox was full of ‘blown brain emojis’!! 🤯🤯🤯 I can’t wait to share this course content far and wide at the end of year with those of you that missed out on attending live.
In the meantime if you want to learn more about glycation which is the new inflammation, out there in research-land, you know…the source of all evil including ageing itself(!!) then check this out…
Glycation is a normal physiological process that, just like inflammation and oxidative stress, can get out of hand, contributing to disease processes. Currently there is an explosion of correlational research suggesting relationships between higher levels of Advanced Glycation End-products (AGE) in individuals who have fertility problems, psychiatric conditions, osteoporosis, premature skin ageing, cancer…you name it! New research implicates diet heavily in the determination of individual’s levels of AGE but there is devil in the detail – there are ‘4 Ps’ of dietary AGE contribution that we need to be mindful of when we are giving dietary advice and trying to move patients towards wellness. This Update in Under 30 recording: Are You Feeling Your ‘AGE’ will open the lid on the ‘new black’ in chronic health & ageing.
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.
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’.
🍌‘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.
Copper deficiency happens in kids, so does copper toxicity and both are serious concerns, but do we know when to accurately call either? First, we have to know ‘normal’. If we know what normal Serum Copper values look like in children, then we can easily spot those falling below or above this, right? That’s the first hurdle we tend to knock over and break a toe on! Being a mineral whose levels vary widely in soil from country to country, globally, the differences in reference ranges are breathtaking & absurd. Add to that, that copper is a key mineral in kids, driving huge demand for it during key periods of development, so the range for pre-schoolers isn’t the same as the primary or high schoolers – not that your lab is flagging that. Unhelpful? Yes. Dangerous, even? Potentially.
To diagnose ‘Copper Excess’ in a child is a big call to make.
One, because most practitioners are unaware just how much Copper a child really needs at each age & two, high copper is often a messenger for something else going on and then three, the primary objective based on this diagnosis becomes to lower their Copper but we could be either shooting the messenger or missing the mark all together…right?
Copper excess does happen but not nearly as often as practitioners believe it does. And in kids, the fall-out from such misdiagnosis is bigger. And missing a Copper deficiency? (because we’re not as well-trained to recognise it and because Copper has been sadly demonised) Likely to have myriad negative impacts at this vulnerable age…almost none of which generate symptoms or a distinct clinical picture e.g. secondary iron deficiency, low neutrophils without necessarily compromised immunity. But what about the holy grail get-out of jail adjective: ‘relative’. You know, ‘this is at least a Copper excess relative to their Zinc?’
Well, to form this opinion you’re likely calculating the Zn:Cu ratio and applying an ideal adult value of 1:1 but show me the primary evidence that supports this for kids…anywhere? The Zn & Cu relationship shifts as we move through life-stages and in fact Copper is supposed to dominate through a lot of our childhood so…ummmmm…no.
HTMA Copper side-steps all of this?..double no.
I used to make the same mistake re Zn:Cu, I may have even taught you this?!🤦♀️ But as so often happens, a week spent in all the original scientific data and I’ve emerged a changed practitioner! Having been part of perpetuating this problematic premise in the past, I am determined to get the correct message out there to as many practitioners as possible. So help me spread the word on Copper in Kids – by telling others that this mineral is so critical to kids compared with adults, they will often have higher levels than ‘us’ and that until you’ve applied the right age-appropriate reference range and ruled out confounders you can’t possibly make a call on Copper. I mean, we kind of knew this all along, with healthy pregnancy Copper values being exponentially higher being a giant clue. Turns out kids’ ‘Copper Age’ extends way beyond the womb.
Copper, as a kingpin in angiogenesis, brain & bone building & iron regulation is a critical mineral during paediatric development. So much so, the kind of blood levels we see in a primary schooler might cause alarm if we saw them in an adult. So too their Zn:Cu. But higher blood Copper and more Copper than Zinc are not just healthy but perhaps necessary during certain paediatric periods. This recording redefines normal, low and high with a great clinical desktop tool to help you better interpret these labs, as well as reviewing the top causes and consequences of both types of Copper imbalance in kids.
The latest Update in Under 30 has landed. You can purchase January’s episode, Copper in Kids here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
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Earlier this year at a Mental Health Training for IM doctors, 3 practitioners (myself, a doctor & a psychiatrist) walked into a bar…not really, but we did each present a case study of challenging patient & in whom we had some great outcomes. All 3 patients presented happened to have Gilbert’s Syndrome. Just in case you’re wondering if there was a secret Gilbert Syndrome Conference you didn’t get an invite to, no. Or that perhaps there was premeditation and intention on the organisers behalf for a bit of sub-theme and focus, no. While this was purely coincidental it does speak rather loudly to a couple of things though.
Patients with Gilbert’s syndrome are likely to be over-represented in our client base especially among those presenting with psychiatric and/or gut issues (and both presentations frustratingly for them, very hard to diagnose, define, pigeon hole etc) and secondly, even though their genes underpin their biological susceptibility to such health problems, great outcomes are really possible.
One of the challenges comes from the medical dismissiveness of this genetic issue as simply ‘benign hyperbilirubinemia’. This has lead to a lack of diagnosis in patients affected and when it is incidentally picked up on routine bloods, a lack of follow up education about what having approx. 30% less phase 2 glucuronidation activity, in their gut and their liver, is really likely to mean, not to mention radically altered bile composition and digestion (!) and how they can make better choices in light of this. Similarly this year in our Mental Health Specialist Mentoring Group, the issue of reduced efficacy and tolerance of psychiatric medications, in those with Gilbert’s, raised its head over and over again. Given that so many drugs within the psychiatric class add at the very least to the ‘substrate load’ of the UGT system, if not frankly inhibit some members of this enzyme family, as this paper (check out Table 2…superb!) shared by my colleague, Kate Worsfold, points out, it actually shouldn’t come as a surprise.
But there is a change a’coming with an influx of research leading to improved understanding of this seemingly mercurial malady, resolving many riddles, identifying new key ways to help these patients and at last….some exceptionally good news for those with Gilbert’s.
For example, when I started this conversation back in 2013 with the Update in Under 30 Gilbert’s Girls, that was in response to seeing so many women at the time presenting with significant imbalances in both their sex hormones and their neurobiology as a result of their UGT impairment. But of course it was never meant to imply GS is just a girl thing! In fact there is a 3:1 dominance of men with this condition and some very good reasons as to why: more red blood cells and more testosterone…the former being the primary source of bilirubin and the later a terrifically powerful UGT inhibitor. The news from the research frontier is nothing short of thrilling, rewriting our thoughts on what medications and supplements (!!) are the most problematic, improved dietary management, how to track their progress more accurately and why completely normalising their bilirubin is not the goal…hey did someone say…longer telomeres?! 😉
The latest Update in Under 30 has landed: Gilbert’s – New Goals and Good News and my team has gone all out in producing a brilliant desktop reference to go with this recording that aids better understanding and clear treatment aims for your GS patients.
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This year I heard a great quote that hit the spot for me: anyone who offers you a simple solution to a complex problem is lying or misguided, the solution to a complex problem will inherently be complex. Dang! I’m frequently reminded of this in relation to many different aspects of working in integrative health. Or even just answering work-related questions socially. Random-friend-I-haven’t-met- yet, upon finding out I work in nutrition, asks: Is [insert any given food, beverage, macronutrient, micronutrient] good for you? In spite of over 20 years of this happening, I confess, the poker face still requires concentration.
The poker face is necessary of course to
a) conceal my amusement at how predictable humans are and
b) to cushion the blow for them as I tear down the delusion that real nutritional science is simple and can be served up in a soundbyte or
c) lie and infer that it is, just to get out of there faster!
But recently, I’ve had another reminder of that ‘in here’ rather than ‘out there’, about how even as practitioners we long for things to be simpler than they are. This month in mentoring I’ve been talking about the dark side of both zinc and Akkermansia muciniphila (I know wash my mouth out right?!) in neurological issues. What, but we had them on the good guys list?! Remember the answer to a complex problem (and human health surely owns this territory) will inherently be complex, right? Similarly, I’ve been digging deep in research about beta-glucuronidase, that enzyme that undoes our phase 2 detoxification of oestrogen, bilirubin and a long list of nasty xenobiotics, earning it the informal title of ‘bad ass biomarker’…scoundrel! And well, I’ve found some really nice things to say about it…like actually it extends the half life of most of our flavonoids such as quercetin, isoflavones etc etc and that’s a great thing for increasing their positive punch given that their rapid detoxification limits how much we can benefit from them. Turns out, like everything else, even dear old beta-glucuronidase exhibits light and shade.
How I ended up losing a weekend to such papers was because I was trying to resolve some burning questions about Ca-D-glucurate (CDG) that I’ve had for as long as I’ve been recommending it to people who arguably could benefit from a little less beta-glucuronidase activity.
My two most pressing ones were: How much is required to be effective & Where’s the evidence?
And that’s when the fight broke out [just in my head] You see every review I’ve read, every piece of product information too, repeats the mantra CDG 500mg TID but turns out this is based on…not much. More uncomfortable still, is that even our assumption that we can convert CDG into its active form has been strongly challenged. The new research, which is not the work from the 1990s that everyone cites, is a must read…or if you actually have a life, and other ways to spend a weekend then maybe just spend 30 mins with me in my Update in Under 30 this month 😂 I wanted to keep it simple and neat and tidy. I tried I promise. But in the end…wouldn’t you know it…it’s complex.
So to bring everyone up to speed, including myself!, I recorded an UU30 on…
The ABC of CDG We often identify patients who could do with a little glucuronidation first aid: marked dysbiosis, Gilbert’s syndrome, oestrogen excess, cancer risk (especially bowel, breast & prostate) and one of our nutritional go-to’s has typically been Calcium D Glucurate. While there is ample evidence that one of CDG’s metabolites : 1,4 GL – inhibits beta-glucuronidase, is an antioxidant, platelet activation inhibitor and generally all round good guy to have on board, new research strongly challenges that oral CDG will convert to this at levels sufficient to support our detoxification pathways. Sounds like we’re overdue for an update on this supplement and when and where it might be useful in addition to how to find the real deal in real food!
Yet another super-helpful part of Iron-Land has been mapped!! Ever struggled to correct chronic iron deficiency in athletes or even just weekend warriors? Yep, me too. One of the key barriers being the 2-3 fold rise in hepcidin in response to exercise. Hepcidin whose day job is an inflammatory signal that two-times as an iron uptake blocking agent at the small intestine. In addition to other exercise-induced factors that either reduce Fe uptake or increase losses, it really is no surprise that these cases can be hard to treat. However, a recently published small Australian study has brought to light some constructive new information. Similar to the often talked about ‘anabolic window of opportunity’ whereby we encourage people to consume protein +/- CHOs within a short time-frame post-exercise to optimise exercise outcomes and negate negatives, these new findings imply the same might be true for optimal Iron uptake. But only in relation to exercise done in the morning!
The key finding was when individuals consumed iron after 90mins of exercise in the morning they exhibited higher uptake than both when they took the iron at the same time but didn’t exercise beforehand or took it after exercising at night.
This is a game-changer for potentially ALL our patients who struggle with iron absorption. With the key take-home being…not just take your iron preferably in the morning which we already know (when hepcidin is naturally lower as part of its diurnal rhythm) but before you pop that pill, pop on your sneakers and get busy sweating! How on earth might this be working? Well this study demonstrated that while hepcidin rises after exercise typically for up to 6hrs…it is not yet ‘up’ and blocking within the first hour – gotcha! But why would this mean an even greater uptake compared with the same iron at the same time in the same individual…but a resting version of themselves? Because exercise may in fact cause a transient leaky gut post exercise & enhanced nutrient uptake may be its silver lining! A small study that actually punches above its weight, this one is worth the read – via a great comprehensive summary on Medscape if you have it or you can check out the abstract.
Our ever-expanding Iron knowledge gives us great hope for the improved understanding we are likely to reach with all nutrients in the future. Let’s not forget Iron has about a 70 year head-start on other microminerals such as Zinc and almost a century on Selenium, which was identified to be essential in just 1979!
And the contrast is apparent anywhere you care to compare and contrast the ‘older’ with the ‘younger’ nutrients. Just look at iron studies. A personalised detailed account of each individual’s iron story: how much you’re consuming, how effective you are at absorbing what you’ve been offered, how hungry that makes you for more and what good stores mean to you (not some fictitious average male or female)! All told through 4 distinct but inter-related markers: serum iron, transferrin, transferrin saturation and ferritin. What can we glean from our current routine assessment of Selenium in contrast? Their short-term Se intake…yep. Looking forward to the multi-parameter markers of each individual nutrient we just might have at our fingertips in the future, thanks to iron nutrition which continues to teach us how sophisticated nutritional physiology really is 🙂
We know the most about iron and yet we know there is always more to learn. And who better to teach us this than our clients with iron deficiency or iron excess? Need some help getting across the most important aspects of recognising and correcting each iron issue in clinic? We released an Iron Package earlier this year for this very reason. It covers how to really read iron studies (with a great cheat sheet), how not to fall for a fake (deficiency) and what the best supplements and dosing regimes look like and how that differs in pregnancy, athletes, those with marked gut issues and other key groups. It’s your 1 stop iron shop.
How might your patients’ Nickel exposure wreak havoc with their health? What might that look like? It may be lurking behind labels like IBS, non-coeliac gluten sensitivity, contact dermatitis of unknown origin,(with or without alopecia) or even CFS. “Then how does Nickel, which can’t even claim fame as a heavy metal, manage such diverse detrimental effects’? I hear you ask. In 3 easy steps 1) exposure…we’re all exposed, Ni is ubiquitous in our soil, our food, our environment so don’t bother trying to run from it 2) it hits our gut where our microbiome and intestinal lining may constitute the first fallen soldiers 3) exposure to our immune system can lead to sensitisation, and the subsequent development of a hypersensitivity response to each following exposure …and at worst precipitation of an autoimmune process. You got all that?
So therein lies the big question: how can we help patients whose health problems stem from Noxious Nickel? We could run and hide…from our jewellery, our mobile phones, dental interventions, most food (!), but we’d be wasting our time…we’re surrounded!
As always, we go back to the science and we find others have done the work for us. Not google though. Google ‘low nickel diet’ and like ‘low oxalate diet’, you’re likely to get a whole heap of hogwash! How reassuring then that there is a validated dietary scoring tool to assist patients lower their dietary Nickel and that numerous other studies can show us the way in terms of use of mineral balancing strategies, probiotics etc. These resources plus more are all included in the latest Update in Under 30: Noxious Nickel part 2 as well as a discussion of what assessments we have available to confirm nickel as the culprit. But here’s something for free: hair nickel concentration (HTMA) is not by any means diagnostic in these cases, because it’s not necessarily about an issue of overall higher exposure it’s about an aberrant immune response to Nickel at any level. Just saying. You know me….not scared of controversy in the pursuit of improved patient outcomes. Ok a bit scared… 😁
In this instalment it’s time to get down and dirty and detailed about how to best identify those patients who may have Nickel related pathology and presentations. We cover testing options, typical systems affected from GIT to autoimmunity and the most extreme form: Systemic Nickel Allergy Syndrome. We outline Nickel management strategies in a world full of it (!) and we include several key papers for additional resources and support. How noxious is Nickel for some of your patients? Well by the end of this you’ll know and better still, know what to do once that’s established.
Hear all about it by listening to my latest Update in Under 30:
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Remember when I said you say tomatoes… equal histamine but I say, well maybe oxalates, maybe Nickel? So in the UU30 released just last week How Noxious is Nickel we get down and dirtily detailed with just why Nickel, which is almost ubiquitous in soils and therefore the food and water we consume, may prove to be a catalyst for change in the digestive systems of our patients and beyond. While we humans don’t have any actual use for this metal, many bacteria do and this means in a Nickel rich diet or environment, some will thrive and others struggle, potentially creating unrest in our very own microbiotic megacity.
It’s bigger & broader than this though, with Ni triggered contact allergies not just possible on the skin like we commonly see for some individuals with cheap jewellery. The gastrointestinal lining may also manifest a similar reaction. Yes, you heard me right.
What would this look like? Well, a patient who ‘reacts to’ tomatoes, legumes, nuts maybe and given the chance (!) chocolate cake with icing especially, which happens to be highest containing Ni food documented 👀 Someone who has been given an IBS label, or has even been diagnosed with gastritis. Still a non-believer? Check out these papers to get you started. The labyrinth of potential food reactions makes us dizzy yet again! We seriously need a map and compass to find our way through this with patients!
While nickel sits rather benignly among its mineral mates in the transition metals of the periodic table, it is a metal that humans are constantly exposed to yet have no need for. What could possibly go wrong? Well, a lot it seems. Nickel is the most prevalent metal allergen worldwide and beyond this, there is strong evidence of its potential to trigger autoimmunity, major endocrine pathology and a raft of GIT problems that masquerade as other conditions like IBS & NCGS. This episode captures the dance we all do with the ‘Devil’s Copper’ and why some of our patients are likely to end up with a bigger dose and a much bigger disease picture as a result of noxious nickel.
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Kupfernickel. It’s the original German name for Nickel and it literally translates to ‘Copper Nickel’ which inferred it to be the ‘Copper Nickel’ aka ‘Devil’s Copper’…because each metal can masquerade and be mistaken for the other! There’s an interesting story behind this of course and lo and behold the explanation (as is often the case with minerals and metals) is revealed by looking at where Nickel sits in the periodic table. Haven’t heard me rave on before about how all the key nutritional relationships are illustrated in that cornerstone of chemistry?? Where have you been?! Nickel is a transition metal and that tells us many things – including that its key relationships and interactions are likely to be with Iron, Cobalt, Zinc and Copper. And guess what? It’s all true. Still, I’ve had another Nickel-centric chemistry lesson of late because I actually had not the slightest appreciation of how noxious this can make it for us humans.
It started with one patient then, as is always the way, I’ve had about 3 in the past few months: predominantly women, some with ‘known’ nickel allergies, in the form of jewellery-related dermatitis and sometimes not, many with significant gut disturbance (IBS like, non-infectious gastritis) and most with early or advanced autoimmunity.
And the vast amount of scientific literature on the prevalence of Ni allergy (conservative figures suggest 15% population with a very high female:male) and its capacity to go beyond the ‘cosmetic’ and trigger gross immunological aberrations in Th1 cells, well, the case for Noxious Nickel is one of those things that once you see it, you can’t ‘unsee’, ever. Think if you or your patients have never had an issue with wearing cheap jewellery we can rule this one out? Think again. While the jewellery reaction might be the helpful clue in some patients, there are also 3 other ways that the old Kupfernickel may be undermining your health. And yes! The fact that contact dermatitis to nickel-containing silver jewellery is such a common issue tells us straight up, that its absorbed via our skin, think: watches, mobile phones, e-cigarettes, hair clips, and…yes I am having another crack at these again…tattoos! We also inhale and consume it via a wide variety of food and drink we consume. Oh and did I mention dental interventions, yet? 👀 Sheesh….
So while we all accept humans have zero requirement for Nickel, it’s in us all the time and the question is (always) how each individual inner chemistry lab (!) is interacting with it and to what extent this may explain some pretty potent health problems, from GIT disturbance to Hashimotos and from skin conditions and alopecia to CFS & Fibromyalgia-like conditions.
My latest Update in Under 30: How Noxious is Nickel – highlights the fundamentals of Nickel in terms of our sources of exposure and who is most susceptible and just how this can play out as a driver of disease. Next month we move onto our testing options, drilling down into the myriad signs & symptoms and how to effectively manage the patient dancing with the Devil’s Copper. This one has been a real ‘sleeper’ for me, but it’s time to wake the beast for us all 👀
While nickel sits benignly among its mineral mates in the transition metals of the periodic table, it is a metal that humans are constantly exposed to yet have no need for. What could possibly go wrong? Well, a lot it seems. Nickel is the most prevalent metal allergen worldwide and beyond this there is strong evidence of its potential to trigger autoimmunity, major endocrine pathology and a raft of GIT problems that masquerade as other conditions like IBS & NCGS. This episode captures the dance we all do with the ‘Devil’s Copper’ and why some of our patients are likely to end up with a bigger dose and a much bigger disease picture as a result of noxious nickel.
Hear all about it by listening to my latest Update in Under 30:
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Ok here’s some tough Tuesday talk..not all tests are valid. Tougher still…not all of the mainstream nor the functional pathology ones. I am talking across the board here. Each and every pathology parameter requires good knowledge about its strengths. limitations and, one of my absolute favourite nemeses, confounders. “How on earth am I supposed to learn all that and everything else I have to know too?!!” I hear you scream at your screen. Btw keep yourself nice if you’re in public while you’re reading this 😉
But rather than imagining you need to have this level of knowledge for all tests, I would suggest you set yourself a hit list of the ones you rely on most, either in terms of frequency or in terms of the degree to which they direct your decisions about patient care…can I mention (ahem) Iron studies here perhaps for us all…but maybe you have a specialist area so you use a particular investigation routinely or at least frequently…
CDSAs? Breath tests for SIBO? Oxalates?
May I please then politely suggest that you get to know these inside and out? Not based purely on the information and assistance that the test provider provides you..but you scrutinise them independently. Top to bottom. Because that’s your business, right? And your diagnoses and treatment decisions are pivoting on these results. Jason Hawrelak gave us all some great examples, including his informal experiment of sending the same stool sample to multiple labs. Don’t know about this and his findings?? If you’re in the business of ordering stool tests, you need to. I am doing this all the time with numerous pathology markers because diagnostics is my passion (alright, obsession)…and recently I put Oxalate Assessment to the test and oh boy!
Here’s something for free:
If you are measuring urinary oxalates to diagnose oxalate overload in your patients and you, 1) are using a lab that does not preserve the urine as you collect it, using acidified containers or providing additional preservatives for take home testing kits….you are wasting your patients money and you are likely getting a lot of false positives, i.e. the result infers the patient has a problem when they don’t!!
And 2) if you are simply following the labs reference ranges for what ‘healthy’ urinary oxalates look like – you’re wasting your patients money again and likely getting false negatives – a failure to show a problem that is actually there! If you’re hunting oxalates…please ensure you have a current effective hunter’s licence…by getting up to speed fast regarding accurate investigation of this. Oh yes…it’s tough-talkin’-Tuesday and I’ve come out firing…watch out this may become a regular feature 🤷♀️
Update in Under 30: Oxalate Overload – Assessment and Management
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update.
When patients present feeling worse every time they DIY a Green Detox, as the practitioner, you’re likely to be sniffing around reduced oxalate tolerance as a differential. Rightly so. But what about the patient with joint pains and disproportionate fatigue who has baffled their rheumatologist, or the one suffering vulvodynia that baffles everyone, or irritable bladder symptoms, or….and they all eat an exemplary colourful high plant food diet, with their only self-confessed sin…darker than dark chocolate between every mouthful? Who doesn’t? While you may have a hunch, given the goodness of those foods, we should check these out objectively rather than unnecessarily restrict or limit someone’s food choices for the rest of their natural life! If dietary oxalate overload is now on your radar for these patients you need to move to the next step. Assessment.
Spot or 24hr urine collection or plasma assay or OATS testing or imaging or joint aspirates? So many choices but which one has the greatest validity depending on your patient’s presentation? Ok how about the most general all-rounder that is truly an option in the real world? – always helpful;) Yep, 24hr urine collection…agreed.
Ok, next step.
You need to wrap around that waist of yours one seriously heavy tool belt for accurate interpretation of their results. That’s right…those random ol’ reference ranges need a serious rethink! How much? Well, given the reference ranges every lab will give you for urinary oxalates typically fail to pick up up to 1/3 of patients with oxalate overload high enough to produce oxalate kidney stones…I think you get the picture. I feel your trepidation now but can hear you pensively ask anyway…next step? Management.
Just google oxalate-rich foods, print out the list for your patient and tell them never to have these (or joy, laughter, sex or a healthy microbiome) ever again.
Not.
The ‘low oxalate lists’ will lead you astray and the ‘high oxalate foods’ should not be tossed away! The research has found greater therapeutic benefits from different dietary approaches, some nutritional supplements and most importantly targeted treatment of the cause…which is all about the…go on, try and say it without screaming…the GUT!!!!!!!!!!!!!!
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update
Hear all about it by listening to my latest Update in Under 30:
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Black Tea & Green Tea & All My Dark Chocolate Sins
These are a few of my favourite things!!
Sounds like a kitchen roll-call at my house…how about yours? And your patients?!! You see I’ve been working away researching Oxaluria – a condition whereby individuals end up with too many oxalates in their body and ultimately their urine – which can be a problem in a proportion of people suffering with kidney stones, vulvodynia, joint pain etc and anyone with CKD and on my travels I came across this article on how the regular intake of green smoothies could in fact turn someone with normal oxlate levels and handling, into someone who has an acute induced Oxaluria. Yup.
Nobody panic. Remember this is not going to be problematic in all patients but just might be in some. But it left me wondering if we ‘clean-diet-prescribing-practitioners’ know all we really need to about, who not to prescribe green drinks to (or beetroot juice for that matter) and cap ‘ye olde’ dark chocolate quota for!
Or…keep them eating all these fabulous generally healthy foods but mitigate any elevated oxalate risk through correct food preparation & combinations?
There’s so much more to this topic than meets the eye. Because on top of what you eat, there’s the huge variability in terms of what you absorb…think it’s as simple as, whether someone has Oxalobacter in their bowel or not? Nope. Oh…and then there’s the 3rd element: how much you make yourselves…that’s where we need to have a serious chat about collagen, high dose turmeric & vitamin C supplements in susceptible individuals, people. Want to read more yourself? Here’s somewhere to start on the giant pile of papers here.
Oxalates are found in high concentrations in many of the ‘healthy food choices’ we promote and are even higher again, when these are organically farmed! Given the importance of individualising therapeutic diets are we able to quickly recognise those who need to lower their low of these naturally occurring plant products? Who shouldn’t be drinking green juices? And which of our patients might benefit from being educated about different food combinations and preparation to lower the oxalate load from these otherwise fabulous foods?
Hear all about it by listening to my latest Update in Under 30:
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Histamine, Oxalates & Nickel…any of which may be at fault when your patient reports they experience adverse reactions from eating them.The same can be said for legumes, with a few extra contenders thrown in like oligosaccharides for those farty on FODMAPs. Additionally, in either case, there could be a bona fide allergy (IgE) or an intolerance (IgG) at play. Tricky, right?
I hear from practitioners often, though, that their interpretation of food reactions like these are at risk of being 1 dimensional, like a food word association game: tomato = histamine; legumes = FODMAPS; gluten = NCGS.
The labyrinth of possible pathways for food reactions is just that, a labyrinth!! So, we have to always be on our toes and try and approach each case methodologically.
I outlined how to approach this in clinic in A Guide to Investigating Food Reactions, released earlier this year. We cover a lot in this 2hr recording, but let’s face it, it’s an area that needs yet more time and a field that we never stop learning in. Next week, as part of our UU30 series on Getting to the Guts of Joint Pain, we need to take a little scenic detour along Oxalate Boulevard! Keep your eyes open peeps, because our very own food prescriptions tend to be full of them!! Not naming any names….berries, green smoothies, sweet potato &…
Need to catch up on investigating adverse food reactions??
Elimination of suspected food culprits in most situations is only a short term reliever, not an appropriate long term solution, so to optimise results we need to know the real mechanism of action. The majority of these, of course, stem from the gut, but being able to elucidate exactly which of the many things that can go wrong there, is going wrong and therefore what foods are problematic until we address this, is the key. This 2hr mp4 is all about the bigger picture and helping you find method in the madness that can be the adverse food reactions landscape.
Those ‘still-believers’ look away now. One of the great myths, misconceptions and misunderstandings in nutritional medicine is that supplementation with specific nutrients will produce change specifically in one system, or pathway, which just happens to be the one that the practitioner has determined would benefit most/is targeting. Let me explain myself a bit better. When we give patients any nutrient, in the cases where it’s not simply to correct a global deficiency & therefore improve levels all round, it’s typically on the basis of a specific desirable therapeutic benefit, e.g. some magnesium to help their GABA production…, additional B3 would improve their mitochondria. Beautiful on paper…but like sending a letter to Santa in reality (I did warn you!)
Truth Bomb No.1: There are nutrient distribution pecking orders that have nothing to do with who you ‘addressed’ it to
This dictates that when something is given orally, for most nutrients, the gut itself has first dibs. So the cells of your digestive tract meet their needs before any other part of your body gets a look in. Sometimes the digestive system’s needs can be quite substantial and leave little for any other part of the body…not mentioning any names (ahem) Glutamine!
Truth Bomb No.2: En route to the ‘target’, these nutrients get delivered and distributed to many other tissues – with possibly not so desirable or intended effects!
You may determine that a patient needs iron because their ferritin hasn’t got a pulse…so you keep giving them daily high dose oral iron to ‘fix’ this…not realising you’re making their GIT dysbiosis and gut inflammation worse in the process. Or you feel their mysterious ‘methylation cycle’, happening predominantly in the liver and kidneys, could do with a folate delivery…perhaps ignoring the very worrying fact that their colon may have already had a ‘gut full’. Literally. Hence the concerns and caution against supplementing with folate in patients with established colorectal cancer. So is bypassing the gut via IM or IV nutrients the answer…well yes and no…but mostly no. Read on…
Truth Bomb No.3: Those pathways that use the nutrient you’re supplementing, that are most active in the patient’s body currently – which is determined by many factors (genes, physiology, feedback circuits, pathophysiology) and rarely simply by the availability of nutrients – will take take the next lion’s share of that nutrient
Wanting to nutritionally support someone’s thyroid, you know tyrosine is the backbone of the thyroid hormones, so you include this in the hypothyroid prescription. Will it help? Who knows? Being a non-essential amino acid the body exhibits very complex regulation of its distribution and use – with thyroid precursor availability being only one job on a very long list! And if this was in a patient who is regularly smoking cannabis, due to upregulation of the tyrosine hydroxylase enzyme – there is likely to be more of the supplement headed for even more dopamine production and very little or none reaching in fact your intended target. And don’t get me (re)started on Glutamine – supplements of which in an anxious and glutamate dominated patient will make…G.L.U.T.A.M.A.T.E…right…not GABA! 🙁
Sorry, I know, it hurts right? But these are essential teachings, that tend to have been over-looked or under-played I find, in nutrition education, regardless of training: nutritionists, naturopaths, IM doctors, dual qualification practitioners remedial therapists. Nutritional medicine is a wonderful and potent modality when it’s done well…but we need to revisit some core truths and principles that many of us have missed out on, to ensure we’re not writing letters to Santa.
Let’s start with Micronutrients. Let’s talk make sense of the over-arching nutrition principles, that will profoundly change your understanding and application of this modality Truly understanding the ‘big’ concepts, so often overlooked, or incorrectly taught, ensures you get the critical ‘small’ detail in your nutritional prescriptions right. In this 4 hour recording, together with key clinical tools, we talk about the tough stuff: dose-response curves, active versus passive stores and excretory pathways and ooh lah lah…the myth of taking ‘activated vitamins’. Even those who felt well trained – will find a lot in this critical review that is new, insightful and truly practise-changing!
