A few things really took up a disproportionate amount of our time & attention in 2020: Zoom, Mask Fashion & Gin based hand sanitiser.On a personal note I need to confess another: Iron. So while my one true (mineral) love remains zinc, iron answer hunting has infiltrated a lot of my days and some nights! There’s no hiding it…3 out of my 12 UU30 episodes this year have iron in the title 🙄 a sure sign its been on my and my mentees’ minds and sitting across the desk from a lot of health professionals in human form. And this affair I’ve been having, like most, started innocently… it started with a just a ‘quickie’, you know a quick question from a well meaning practitioner: “So, what’s expected in terms of ferritin levels across pregnancy?”
There are 2 answers to this. The first reflects the practice guidelines for GPs and obstetricians in most western countries: > 30 mcg/L regardless of trimester And then there’s another that is [ahem] evidence based, accounts for the essentiality of physiological anaemia in pregnancy &, naturally, trimester specific
There’s a big Fe-ar factor at play when it comes to answering the question, ‘Does this woman have enough iron for her and bub?’ Public health and practice guidelines appear to assume we are ‘guilty’ until proven innocent, patients are worried and health professionals are plagued with their own doubts about whether they’re ‘reading this right?!’ I’m sure we’ve all been in the situation where we feel our pregnant patient is doing well iron wise early in pregnancy, only for them to have that routine antenatal 28wk GP/Ob visit and discover a total panic has descended upon the patient and the rest of the health care team, with calls for ‘IV Iron STAT!’ But 28wks is the height of haemodilution right? You know, that time when ferritin, Hb and Hct should look at their lowest, right? There certainly is a limit to how low we want any pregnant woman to go – for her and her baby’s health but that limit is not the one routinely used and the truly evidenced based one is going to shock you. So what? What’s the issues if we are a little Fe-ar based about Fe, resulting in hypervigilance (calling a deficiency when there isn’t actually one) and giving them a ‘boost’ of more iron, surely this is good news ultimately for baby’s iron levels and for lactation and for…sorry what? No?
There’s a U shaped Curve for Iron supplementation & serum Ferritin levels in pregnant women?!!
It starts with a simple enough question: What should women’s ferritin levels be in pregnancy? But the answer will surprise many. There are in fact two. The first reflects the practice guidelines for GPs and obstetricians in most western countries regardless of trimester and then there’s another that is arguably more evidence based, accounts for the essentiality of physiological anaemia in pregnancy & is also, sensibly, trimester specific. To challenge the ‘noise’ and have the confidence that ‘normal’ is ‘enough’, we need to better understand the mother’s protective physiological adaptation of iron regulation and the intricate systems the foetus has to ensure its needs are met. This of course is not without limit, so we need to also be clear about the maternal serum ferritin threshold for negative impact on the foetus and newborn. Getting the balance or iron right in pregnancy for both mother and baby, is perhaps easier than we have been led to believe.
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.
When I deliver foundational nutrition training to GPs I talk tough. It’s a tough field, right? Compared with the relative certainty of pharmaceuticals, their established pharmacokinetics, their sophisticated delivery systems to ensure high bioavailability…trying to fix micronutrient deficiencies in patients can feel a lot like you’re trying to perform minor miracles. Take iron for something different, its homeostasis pivots on its tight regulation at the gut wall – and this is a wall that is very tight!! At best you get about 10% of a supplement taken up, at worst you get none and the harder you push & the higher you go with your dose…the lower the fractional uptake. Tough stuff, right?!
It’s about at this point in my talk I read their collective minds and say, “I know, you’re thinking, oral supplementation is for suckers – what about we bypass that road block and use IV?!” [Ok, I definitely use nicer words than this]
And then I put up a list of pros and cons about IV micronutrient repletion: ‘100% bioavailable’ & ‘Bypasses the body’s regulatory systems’, go on both! You see, time & time again we discover, when we think we’re outsmarting the body, it still manages to outsmart us. There are some exceptions to this – some nutrients (Vitamin C) and some contexts (late pregnancy iron deficiency) but the broader promise of ‘rapid replenishment’ for everyone, in your lunch break, via an IV infusion..is not realistic, responsible nor without risk. Don’t get me wrong, I am an advocate of appropriate IV Fe use and have encouraged a small fraction of my patients to take this path. However, given the dramatic rise in prescriptions for this since 2013, I think it’s time to stop and seriously review each element: In reality what does it achieve and in whom is it a responsible recommendation; Was a risk benefit analysis performed for & communicated to each individual & was the remaining risk mitigated?
Think anaphylaxis is the major concern? It might be the most lethal but there are more serious concerns due to higher incidence with newer preparations.
So, how well do you know your different IV iron forms, and their predilection for potential problems? And have your answers ready to all the questions raised above? In order for all involved to make an informed choice (both practitioners and patients), we must.
You’re welcome 😉 and hey welcome back to tough talkin’ Tuesday…
While rates of iron deficiency and related anaemia continue to grow, the increase in prescriptions of IV Fe have expanded exponentially in western countries. What is behind this change in practice regarding how we treat iron deficiency and does it match with responsible prescribing? Do the benefits always outweigh the risks? And while we’re on the topic, who is most likely to benefit and what are all the risks? In light of a current class action in the US, relating to a lesser talked about adverse event associated with IV Fe and recent complaints here in Australia against GPs, allegedly due to inadequate information to enable informed patient consent…it’s time to answer these questions and more. When is IV Fe a means of rescue and when is it a risky repletion strategy with no evidence of advantage?
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.
Here’s a newsflash for absolutely no one, we’re all practising healthcare in racially diverse communities, right? Take Australia for example. At last count, at least 1 in 4 were not born here and of those who were, 3% are indigenous and many many more come from migrant families. This spells DiVeRSIty. Yet our pathology reference intervals are a whitewash, frequently derived from in-house samples that stratify by gender and age but not race, or adopted external data from predominantly Caucasian countries. Think it doesn’t matter? It does. I learnt this as (almost) always…on the ground.
I have had the privilege of mentoring health professionals in South East Asia for several years but in hindsight, I can see I was under-cooked for the role: Almost every patient these professionals discussed with me, had a vitamin D result that made me feel faint at their ‘rickets-like readings’.
“But all our patients have blood levels like this, that’s normal here”, they reassured me.
And of course, they were right.
I hit the books science databases to find out more and sure enough, new evidence has emerged of racial differences in relation to vitamin D binding and therefore definitions of ‘adequacy’ in terms of blood levels of 25(OH)D, and this has been particularly well documented amongst SE Asians Gopal-Kothandapani et al., 2019 But who of us knows this outside of that region? When we see patients of this background, are we alert to the strong genetic differences that drive different Vitamin D metabolism and therefore redefine healthy, or are we incorrectly comparing them to Caucasian Cohorts?! I have to confess in the past I’ve done the latter 🤦♀️ So what else are we over or under-diagnosing or just plain misunderstanding, in our patients who are not Caucasian? Chances are quite a lot. But the more I’ve dug into the topic, looking at racial differences in pathology markers, the more complex it gets, with plenty of conflation for example with increased rates of certain diseases. So it’s not an easy answer, granted, but that shouldn’t stop us from trying to achieve better clarity, for us and our patients.
We all pat ourselves on the back because we’re across the understanding that a healthy weight is defined differently depending on your racial background, we’ve nailed (hopefully!) the whole ‘healthy BMI < 23 in Asian populations and the smaller WC cutoffs’…but really…there’s so much more that needs to be done.
Want to be on the front foot with critical pathology interpretation? Join the club!
There is such a groundswell of naturopaths, nutritionists, physical therapists etc working in integrative health that are ‘lab literate’. It appears to be a combination of both a choice and consumer expectation. With patients thinking, surely, we can make sense of those numbers on the page that remain a mystery to the patient…and tbh to some doctors!? We should. We’re currently halfway through our 6 month long MasterCourse in Comprehensive Diagnostics which is custom-built for this context. It has been incredibly well attended and well-received to date and we’re excited about the amazing content that Rachel has had to redevelop along the way. If you missed out on the actual live classroom experience…your chance is coming soon. Promise. Your DIY Diagnostics version will be released at the end of this year. Let us know if you’re keen by sending an email to [email protected], and we’ll put you on the ‘first to know’ list.
I think I’m finally able to put my ‘late-90s-Creatine-frontline-trauma’ behind me. Back then, like many good nats in training, I was working the trenches of the health food stores and was faced on a daily basis with two types of men with two types of Creatine questions. The first type was scrawny and would ask, ‘will taking this help me build muscle?’, the second, built like the proverbial brick *&#@ house, asking, ‘will it help me build more muscle?’ Cue, eye roll. Come on… any of you current or ex apothecaries, pharmacy or retail assistants…you know exactly what I’m talking about!!! So deep was this trauma that I put Creatine as a supplement, into the ‘strictly sports folder’ in my brain (the bit in the deep dark back with other rarely accessed items) and never gave it much thought when I left retail and moved exclusively into private practice. Even back when I was a sub-editor for the Braun and Cohen 4th edition, it was apparently still too soon.
A great colleague of mine, Emily Bradley, had written the chapter on Creatine and, in doing so, presented compelling case to reconsider this supplement as offering great therapeutic potential well outside of the sports-field. That one was accidental 😂
I actually remember reading that chapter, especially the sections on Creatine supplementation for neurological & psychiatric conditions and thinking….WOW…who knew?! ??!! Well, clearly Emily for one 🙄 and also every author and researcher whose work she had read…so that made quite a lot of people actually! But another [ahem 😳] several years had to pass before the research into Creatine and the argument that this has been a grossly over-looked CAM option in mental health, beat down my door and finally got my full attention. Better late than never. And boy, do we all have some catching up to do!
Let’s start with 5 fun facts: 1. Creatine is critical for energy – like cellular currency it ‘tops’ back up our funds, after increased spending, everywhere, including the brain 2. The Brain consumes >20% of our resting energy expenditure & is fifth on the organ list in terms of highest concentration of this molecule 3. Creatine CNS depletion is a thing – and it happens in a wide variety of scenarios – from the seemingly benign (like chronic sleep deprivation) to the more sinister (neurodegeneration) 4. This then leads to higher Glutamate, Oxidative Stress & a spell of other sorts of ‘brain badness’ 5. Oral supplementation can cross the BBB and ‘refuel’ the brain and correct the Creatine deficit
Out of the thousand or so pages of research on this topic, I’ve just indulged in, there are several great reviews to pick from…it’s a tough call to make but perhaps this older one by Patricia Allen remains my favourite. This marks the beginning of a new era…I’m putting the trauma behind me & moving on & hope you’ll come along too!
When we recap the contemporary science of shared pathophysiology in mental health, we have: oxidative stress, impaired neurogenesis, monoamine deficits, glutamate excess, hypometabolism & mitochondrial dysfunction. When we ask researchers which of these supplemental Creatine might be able to assist with, we get hits at each and every point. Turns out, Creatine’s capacity for enhancing performance is not limited to athletes but can be capitalised on for anyone vulnerable to a CNS shortfall. Ignored for far too long, this economic and impactful brain nutrient is coming to the fore for psychiatric and neurological disorders.
The latest Update in Under 30 has landed!!!
You can purchase Creatine – The Brain Builder Part 1here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.
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.
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.
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 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 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.
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Listen to me, I’m sounding all sporty 😂. I’m not though, just in case you suffer misguided visions of my virtues! But it’s not just the self-declared serious athletes that we need to have on our radar in relation to optimising their oxygen carrying capacity (aka window to winning). Our clinics are full of people, regularly running, doing triathlons for fun (!), riding vast distances clad in Lycra to drink coffee in other town’s cafes etc. etc. whose FBE might be feeling the pinch! That’s right! All these individuals, depending on the frequency and intensity of their exercise, could have the so-called, anaemia of an athlete.
Long gone is the idea that exercise-induced changes to your haemoglobin and red blood cells and perhaps even your iron, would only affect the ultra-marathon runners among us. It’s the swimmers, the cyclists, the Roller Derbyists, the CrossFitters, the basketballers, the Gym Junkies, the lawn bowlers..ok I may have gone too far now…they all are at increased risk.
Why? Isn’t exercise good for you? You know I so want to say, ‘Surprise! It’s not!’ but alas. Of course it is good for us BUT there are some fascinating challenges regular exercise can throw at your dear old blood and its bestie, iron. These challenges are incredibly dynamic – having one effect during exercise, a different one immediately following, and yet another in the days of rest in between. And sometimes, in fact, often, our patients can end up on the wrong side of these seismic shifts. Here’s how the story usually goes
“Oh yeah..I’ve had anaemia for ages! You know and it doesn’t matter how much Iron I take or how I take it – it never budges. But I’ve been told to stay on the Ferrograd anyway”
Typically, being told it’s ‘Athlete’s Anaemia’ is the first, in a series, of many many errors to follow. Because in fact, there is no such thing. That’s right. Anaemia is a symptom not a disease and exercise induced anaemia comes in 4 common flavours: Dilutional, Heamolytic, Iron Deficient & Acute Anaemia of Exercise, and knowing the difference is critical to correct management. Only 1 of them will reliably improve with iron and it needs to be prescribed in a totally novel way. Others will get worse with more iron. Yep. And one is a complete illusion. So when we don’t make the right diagnosis, which of the 4 types your patient actually has, we fail to find the fix. And while all of our patients may not be overly obsessed with improving their performance or even winning, let’s face it, they all want to achieve their PB, that’s why they came to see you. So can you tell the difference?
WARNING: I got so enthused about this topic that I went over. The current ‘Update in Under 30’ is a ‘serving suggestion’ only! And you may need to speed up your playback to squeeze in another bonus 10 min, if you can only afford your usual 30 min car trip to listen!
Outrunning ‘Athlete’s’ Anaemia
Persistent ‘hard-to-resolve’ anaemia is a common presentation for anyone participating routinely in sport and that can be at any level, not just among the professionals. From our lovely ladies who take up running or CrossFit in their middle-age, to our MIL (men in Lycra) and ‘weekend warriors’, they may love it but their haemoglobin and their iron doesn’t! Anaemia equals reduced oxygen carrying capacity, a concern for anyone interested in optimising their performance but equally relevant to patients just trying to manage their energy throughout the day. In this important episode we identify 4 different types of anaemia seen in patients as a result of exercise, incorrectly lumped together as ‘Athlete’s Anaemia’. Each type is easy to recognise once you know how and effective treatment of each is remarkably different. This summary and the super handy clinical resource that accompanies it will help you and your patients absolutely outrun it, at last.
For all Update in Under 30 Subscribers, you will find it waiting for you in your online account and don’t forget the **EXTRA BONUS LIVE CALL WITH RACHEL.
**This live Zoom call with Rachel is for current Update in Under 30 Subscribers ONLY. A Q&A session for subscribers on the UU30 episodes released in 2020. Contact the RAN Team to reserve your spot!
Can you hear that? No it’s not some weird raucous bird-call. That’s me. A fabulous colleague of mine who also happens to be a Master MindMapper (yes it’s an official club now😂) , told me a couple of weeks back that practising naturopaths who don’t use this incredible tool for their case work-up typically say, “Oh, I’ve internalised that!” Well we laughed and laughed and yep even as I write this the giggles are back. You see between the two of us we have almost half a century of combined clinical experience between us (no telling on who has the bigger share!!) and WE haven’t managed that feat…so we’re wondering what we’re missing (bigger internalised RAM?) or indeed, what they are?! And naturally, I’m leaning towards the latter.
‘I practise holistically. I am truly integrative’, you say, ‘I consider all levels of evidence in patients, from their narrative to their neurologist’s report – from their bloods to their B vitamin SNPS – from their detailed diets to their social (dis)connections”
And I know you do.
But how on earth amongst all the information overload, that deafening white noise & distractions, can you always see the root cause and every connection?
Because for me, spending the time practising due diligence with the creating a MindMap, after I see every patient, is my reliable path to achieving this. Not just settling for the reflexive related systems that become well trodden paths in our minds…Gut to Brain (walked that track a million times, right!)…but step by step deepening my understanding of the case, adding layers I couldn’t see or hear at first, to reveal other critical connections that were unexpected. Gut to Kidney –> Kidney to Brain. It’s that time of the year when I’ve (clearly) been talking about MindMapping with my mentees and accordingly, I’m all juiced up! And my love of this process and skill-set is also getting more layers! I’ve realised that of course, beyond summarising the case in a truly integrated way, it helps me sift through my differentials, creating effectively a to-do-list about what things need follow-up assessment via questions, validated surveys, or testing. It also keeps me (and patients) accountable moving forward, as I come back to this over months and years while they remain in my care and I have to answer the question: did we address that?
This Master MindMapper Mate – she’s gone 1 GIANT step further, dedicating (virtually) the next few years of her life to writing a thesis on Complexity Science and, in part, how holistic medicine has now finally found its friend in science via this progressive model.
And MindMapping, and timelines and other key tools for genuinely integrated patient work-up, are the things that enable us to consistently uphold our holistic principles and practices and keep pace with the scientific progression. So if you wanna join our club 😂 because you’re already a MindMapping enthusiast don’t forget to contact [email protected] to find out about and ideally participate in her study. And if you’re feeling like the words MindMapping are Martian-speak for something you know nothing about 😥 …then maybe you should check this out.
As integrative health practitioners, we pride ourselves on taking in the ‘whole health story’ as a means to accurately identifying all the contributors & connections to each patient’s presenting unwellness. In the process, we gather a wealth of information from each client – pathology, medical history, screening tests, diet diaries etc. that borders on information overload and often creates so much ‘noise’, we struggle to ‘hear’ what’s most important. The management of complex patient information and the application of a truly integrative approach, requires due diligence and the right tools. Mindmapping and Timelines are two key tools to help you go from vast quantities of information to a true integrated understanding of what is going on in the case and the more time we spend learning and applying these tools, the more they will write the prescription for you. Not just for today but for the next 6-12mo for that patient.
Ever suspect you’re being gaslighted by your patients’ results? Especially when their CRP result says, ‘nothing to see here’! But every other piece of information and every one of your senses tell you they’re inflamed and their immune system is up to something!!Me too. You probably then look at their other results, their ESR or their white cell count searching out something that supports your hunch, but they too can look disappointingly unremarkable. That’s the moment when you wish life was like a televised sports match and you could check the video evidence rather than believe the mere mortal (and clearly blind!!) man in white on the pitch. Well guess, what…you can.
Albumin
÷
Globulin
As long as you know how to divide one figure by another using a calculator. I’ve found it requires the same digital dexterity as pushing the ‘on’ button’ on my blender…so if you can make a smoothie, you’re sorted! So while almost every lab routinely reports these two as separate parameters that are also routinely in range…I haven’t seen many that actually do the calculation for you and give you the Albumin:Globulin (AGR) on a platter. Yet this one step maths transforms the mundane into magic and can reveal almost all to you regarding your patient’s level of immune activation, inflammation and oxidative stress, from the largest number and variety of drivers. That’s why I call it, 📣The Master Inflammatory Marker 👑
When factoring in your patients pathology results is at its best – it makes the invisible suddenly visible to us. We could have sat and eyeballed that patient all month and never suspected that their Hcy was too high, or they had antiphospholipid antibodies or, or etc.
But the albumin to globulin ratio goes one step further & trumps the other inflammatory markers we’re so familiar with, because it even sees what they can’t!
And a low AGR (≤1.2) signals just that to you. So when the patient with joint pains, or just a little bit of belly fat or an emerging yet unnamed autoimmune condition presents exasperated saying, ‘but apparently I’m not even inflamed!’…you can let them know you do see it, and it’s just that others weren’t looking in the right place, then get busy rolling your sleeves up to move those markers! That’s right, a low AGR is a clear call to action for practitioners engaged in risk minimisation, prevention and for working towards best outcomes in established disease and monitoring a patient’s AGR is a series of clear sign-posts about whether you’re leading them in the right direction or not. There’s a lot more to say on this this third umpire & ripper of a ratio – about kids, the contraceptive pill, confounders, a role in cognitive impairment prevention and what optimal might look like but hey…the cricket’s back on…gotta go 😂
Patients’ labs lie, not often, but sometimes and the inflammatory markers performed routinely like CRP and ESR have been known to tell a few. Like when everything about a case screams inflammation but both of those say there’s none there. Why do they miss it?…well basically it’s not their lot. CRP and ESR have specific signals they only respond to and therefore reflect only certain immune reactions and at specific stages of that response. But there’s a nifty little calculation you can perform with all of your patients labs and suddenly see the immune activation, inflammation and oxidative stress that was lurking beneath. It’s called the albumin to globulin ratio and it’s going to change your understanding of what’s going on in your clients and your ability to monitor the efficacy of your management.
Me neither. I value transparency in all things impacting my health. So when the ‘Colonel’ tells us the magic is in not knowing…I think….hmmmmmmm, no thanks!
Similarly, when the provider of a test tells us, ‘We’d like to give you independent scientific support for our markers and our method but we just can’t because it’s patented!’…well that’s as good as the so-called ‘Colonel’ and his mysterious unidentified herbs and spices, as far as I’m concerned.
It’s effectively like they have created for themselves a ‘Get out of jail free card’ but unlike in Monopoly, they can play it over and over again. Trouble is, as the referring or just ‘reading’ practitioner (many of my patients present with results of these tests in hand) you have to practice either utter blind faith and believe every word that report tells you or you feel like you have to disregard the entire thing because you don’t have the time to sift through every parameter, searching out any independent scientific discussion of their markers, to distinguish fact from fiction. Utterly exasperating. Because of course, a test that offers a huge panel of results may consist of both – some of high value, some utter nonsense and some somewhere in between.
There’s one 24hr urine test from an OS company that I tend to see increasingly and it purports to be able to assess just about everything from gut health, to neurotransmitter levels, to your antioxidant capacity, mitochondrial health and beyond! How is this even possible in one 24 hr non-preserved urine sample that goes off-shore to be analysed? Well they can’t say…it’s a secret. 🤐 Pu-lease!
To boot all the lights and sirens are on for this patient who appears to have such little vitamin C in their urine, they’re at risk of scurvy! That is except for the fact that Vitamin C readily oxidises in urine only to turn into….wait for it….Oxalic acid! So, anyone surprised to hear she is also reported to have an exceptionally high oxalate load?!
Secret herbs and spices? No thanks, I’d prefer science. As the saying goes, “Keep an open mind but not so open your brain falls out!” Sorry but tough-talkin’ Tuesday is back and it’s gotten all toothy!
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.
Sometimes I think I must be psychic..or is that psychotic? Don’t answer that, it’s a bad Byron Bay in-joke. I had literally just recorded my Update in Under 30 Copper in Kids and this excellent new study was published that same week, assessing and comparing trace minerals in age-matched ADHD and neurotypical kids. Snap! ✨ First, a moment of panic…because believe it or not, there are very few rigorous studies that have looked into this and so I had already read them all cover to cover and could confidently say, I had a grip on the literature. Gasp…’ will it have a different finding and challenge the much broader story about the excessive demonising of this mineral in kids health?’ Everyone take a big breath out…no.
But if you’re someone who thinks you’re seeing Copper toxicity in kids, you can keep taking a big breath in and while you’re at it a huge bit of new information:
Copper Excess is Normal in Children.
Every investigation of blood Copper levels in kids has reached the same conclusion and this latest one by a Russian group of researchers renowned for their work in Copper agrees. So the ideas that we have about optimal in terms of mineral balance for adults may stand, but can not and should not be applied to children. The elusive 1:1 relationship between Cu and Zn, for example, considered aspirational in optimising the mental health of big people, is absolutely not desirable or even healthy, in little ones. Why is it so? I hear you ask (…because you loved those old Cadbury chocolate ads with the crazy Professor as much as I did) Well, essentially because kids need more Copper than us, as a simple result of their increased growth requirements: blood vessels, bones, brains…Cu is a critical player in them all and more. And while we (and when I say ‘we’ I mean ‘I’) may be passionately passionate about Zinc’s importance, turns out, in paediatrics, it really does play second fiddle to Cu and should.
This new contribution to the Cu & Zn in ADHD kids debate did find that compared with neurotypical kids, their Cu:Zn was higher BUT – **and this is the really important bit **- as has been shown in a similar cohort before, the shift in relationship between the two was due in fact to lower Zinc levels NOT higher Copper.
So, I guess when you think about it…Zinc perhaps really does still deserve all our loving attention we give it 😂…we just need to rethink the whole negative attention we tend to mistakenly give Copper!
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.
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I know, timing, huh?! It’s almost like I’ve been sniffing around your recycling bins but I didn’t need to of course, at this time of year it’s a fairly safe bet you’re madly winding it back a tad from your most outrageous annual alcohol imbibing. And so are all our patients. To me, extracting accurate information succinctly from patients regarding their alcohol use can be one slippery little sucker. It’s one of the questions people tend to give you a very tidied up answer to, or in fact they’re in such denial they can’t be considered a reliable witness. Think about it. Being a non-habitual drinker myself, I can appear almost saintly when reporting my daily consumption, “None”…but that omits the ‘other me’ that might show up at a conference gala dinner or some live music event, with my volume controls adjusted significantly up…ergh…firsthand accounts anyone? And how often does that happen? Well anywhere between 4 times a week and once a month. See what I mean?
While I’m sure you’ve probably heard me say before, I ask every patient who does drink, what kind of drunk they are because it can hint at their underlying neurobiology, there is a new study that suggests, using a very short 4 item UCLA RRHDS survey, we can categorise patients alcohol use and misuse into 3 types:
Reward ReliefHabit
and in doing so, also be better able to identify the best way to manage them as well.
I’ve been interested in addiction neurobiology for a long time and very much resonate with the work of Koob, which in layman’s terms proposes that we seek intoxication initially for the ‘high’ and then with dependence, we continue to seek it to appease the terrible lows of withdrawal. It has long been known that alcohol use disorder is heterogeneous – there are different types and accordingly the kind of generalised treatment of these individuals proves extremely hit and miss. But articulating the different types and their distinct drivers and solutions has been fraught. Like what makes one alcoholic the functional type who in addition to their long-lunches is a CEO and the one who can’t keep their job? Is it just socioeconomic context or something more? Why are some types of alcoholism deemed also to run more in families and while others aren’t? There are clearly major difference in pathophysiology but what are they? More recently these 3 groups have emerged and this recent study confirms the value particularly in the distinction between those who drink driven by reward and those for relief + habit. It’s a great read but here are some key take-homes:
ReliefHabit
Relief/Habit: You predominantly drink to cope with, or resolve a negative physical and emotional experience (negative reinforcement). You have more depressive features and have more anxious traits than those ‘reward drinkers’.The key to managing this type of pattern is to target negative physical and psychological experiences with ‘downers’ (they calm down an overactive brain that’s on ‘alert’) such as sedatives, anxiolytics, and glutamatergic modulation. (Hint for practitioners: this is where Taurine & Glycine really shine)
Reward
These individuals drink to feel good so they are driven by positive reinforcement and therefore the approach to the helping them should be quite different, with lifestyle recommendations that offer other options for mood elevation such as exercise etc as well and herbal and nutritional approaches.( Hint hint…not the key group for Taurine, more like Tyrosine and Saffron etc)
So…back to my question…what kind of drunk are you & what drives you to drink? As a nation of over-consumers by nature, this is a question we need to ask all our patients
Rachel introduces you to new clinical tools that has been developing to help us all better master the maze of mental health. With so many possible biological drivers: from methylation to inflammation and from gonads to gut, these tools can help you quickly identify those most relevant to each patient and also outline the strategies necessary for redressing these. This presentation comes with an extensive library of resources including pdf of Assessments Tools and Case Study Notes.
I take my job to heart. When someone asked me recently to choose the single value that spoke most to me personally I couldn’t seem to go past, ‘Purpose’. I feel very honoured to have contributed to the learning of so many health professionals in their undergraduate and so many more in their professional careers following graduation and I know that with this comes huge responsibility. Second on my values list (again, possibly unsurprising) is Empowerment & coming in with a photo finish at 3rd:Integrity. Discernment and critical thinking (about information, about research, about reflective practice) are perhaps the eggs in this souffle, helping us all to rise up.
As part of our critical thinking we need to accept a few truisms:
Research changes Experience changes Knowledge changes
Information is not static. So we need to ask ourselves, how long ago did I learn this? How long since I’ve checked it is still correct? And just because perhaps this information came out of the mouth of our mentors or teachers, makes it no less up for regular review. I’m trying to undertake these internal audits on a regular basis. Typically they’re prompted by bloody good questions my mentees have asked me. A question I can’t answer or, more to the point, I can’t answer with full confidence I’ve double-checked my old beliefs and understandings against new evidence recently…these almost always provoke a lost night of sleep for me. Not from sleeplessness per se but due to immersing myself in the latest research and performing a mini informal lit review, bringing out all my old beliefs/evidence etc. Marie Kondo style and asking do they still spark joy✨ (in light of the latest evidence)?! And yes sometimes there’s a little bit of heartache when you have to let your old tightly held beliefs and understandings go 😢
The 1st update is about N-acetyl cysteine. Some of you may have heard me previously question the efficacy of the vegan form. Now that all but 1 Australian product is vegan, produced from bacterial fermentation or purely synthetic, I was wayyyyyyyy overdue to check the validity of my old ideas. Let the record show, I was wrong. Unlike some other nutraceuticals like chondroitin sulphate, wherein the source radically changes the overall structure of the molecule and therefore its uptake and actions – the same is simply not true for NAC.
So those ducks, & their NAC rich feathers, can all sleep a little easier at last…phew! Now the 2nd internal audit well that did cause some tears for me…
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 onboard, new research strongly challenges that oral CDG will convert to this at levels sufficient to support this detoxification pathway. 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!
When a teenage girl presents seeking her first oral contraceptive pill (OCP) script, what information is she privy to that enables her to make an informed decision? Read the insert inside the box? Please. Which 50 year old, let alone 15 year old does that? Forget it! What might her doctor tell her? Perhaps about clotting risk, as part of their determination of the suitability of this form of contraception for her but is there any discussion about the potential for adverse mood effects? A recent study of over 1,000 teenage girls followed over more than a decade adds to other evidence that suggests this should be flagged as a consideration prior to the prescription being written.
Most integrative health practitioners not only know about the potential negative impact on mood from OCP use in women but we’ve observed firsthand the havoc it has wreaked in some teenage girls’ and women’s lives.
A very experienced practitioner I know says, ‘if I am hearing mood instability and then I see a significantly elevated serum copper and or cortisol in these girls that’s when I just say to have to say to them, you know I don’t think this is the best contraception for you!’
This latest study did not find higher rates of depression across all OCP users in this group of 16-25 year olds but when they looked at this at different ages they found its use increased depression scores and was associated specifically with more crying, eating problems and hypersomnia. The discussion around the enhanced vulnerability at this younger age compared with older girls centres on the relative immaturity of their CNS. But wait, I hear you critical thinking clinicians ask, perhaps those teenage girls had more depressive features prior to starting the OCP. Good thinking 99! And the answer is…maybe…but the relationship goes both ways: from the related Medscape Continuing Medical Educational Activity
“For 16-year-old girls, the association was weakened after adjusting for depressive symptoms before use of OCPs, but the findings remained significant. This suggests that the relationship between OCP use and depressive symptoms could be bidirectional…For instance, 16-year-old OCP users were more sexually active and had more stressful events, as well as more menstruation-related pain and acne, than their counterparts in the nonuser group. Analyses showed that all these factors weakened the association, although none diminished it.”
The commentary surrounding this latest study is essentially 1) this is not the first study to find an association and others have been more able to demonstrate that COCP use predated the mood disorder in those affected and 2) those exhibiting higher depressive scores did not actually score strongly for anhedonia or sadness which are the most typical features in adult depression – so perhaps we are missing some of these negatively impacted young women. Awareness regarding reproductive psychology is rapidly growing and in Australia we are fortunate to have emerging hubs to seek help and specialist advice in this area, such as the important work of Professor Jayashri Kulkarni and colleagues out of the Women’s Mental Health Clinic. I’ve referred patients, both when a patient’s mental health appears to be caused or aggravated by use of hormonal agents but which they can’t not use for various reasons and for those small number of women in whom I feel hormonal management may in fact offer a psychiatric solution. So again I am asking, while we know & mainstream medicine increasingly knows about this association…who’s telling these young women?
How many of your clients are on a combination OCP? Do you know the full extent of the physiological impact as a result and are you able to identify to key pathology indicators of the size of that impact?
We’re all aware that in theory OCP use correlates with a range of elevated risks but in reality many females will make the decision that the pros, in terms of contraception or control of acne etc., outweigh the cons. What if we could provide more individualised advice by looking to their pathology results and identifying and quantifying specific danger signs for each individual? This approach enables us to better support patients who chose this form of contraception and to accurately identify those that should be be encouraged to find other safer options more biochemically suited to them. Learn more here.
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!
