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…..”😴
The Calcium Conspiracy -Your Latest Update in Under 30
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’.
The latest Update in Under 30 has landed!!!
You can purchase The Calcium Conspiracy here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here
I 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 by Aussie researchers is: 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…
Should We Rethink High Dose Vitamin D?
Vitamin D deficiency has been associated with a long list of major health conditions: from autoimmunity to mental health & almost everything in between. This has lead to many of us recommending high dose vitamin D supplementation for a large proportion of our patients but do we understand everything we need to to be certain of the merits and safety of this? In this provocative episode Rachel outlines the key unresolved vitamin D dilemmas that should encourage us to exercise caution and outlines how adequate sun exposure is associated with improved health outcomes independent of the production & action of vitamin D.
You can purchase this UU30 episode individually here or become a subscriber and gain access to this and over 65+ episodes plus new monthly releases for 12 months here.
If you are already an Update in Under 30 Subscriber, you will have immediate access to this episode in the ‘active content’ of your online account.
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@example.com 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.
MindMaps & Timelines – Effective Integrated Patient Work-up
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.
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.
For Update in Under 30 Subscribers you will find it waiting in your online account.
-Your RAN Online Account has a NEW LOOK!!-
Next time your log in, you will experience a more user friendly way to search,
view, listen and download your resources.
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!
But always HATING to be the one to throw the baby out with the bathwater, I lose hours of my time, over and over again, trying to determine the worth in this multi-paged report and salvage some value along the way, given these patients’ significant financial outlay. So it’s handy when the test also professes to accurately determine whether these patients are nutritionally replete for basic vitamins. Aha! Now we’re talking! The science of nutritional assessment includes volumes and volumes of studies, reviews, discussion and luckily enough I happen to have a strong foundation in this area and read such research for recreation! Today I am looking at a patient’s results that flag profoundly low Vitamin B6. Several hours of reading later I can call BS. Seriously. The marker used by the company is urinary pyridoxic acid which is 1) reflective of recent intake only, failing to reflect both tissue levels and coenzyme activity 2) needs to be reviewed in light of protein intake, as high protein produces lower excretion and B2 levels because B2 deficiency will produce a secondary abnormally low B6 in the urine. There’s zero mention of any of these limitations or considerations in the report, sadly 🙁
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.
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.
-Your RAN Online Account has a NEW LOOK!!-
Next time your log in, you will experience a more user friendly way to search, view, listen and download your resources. Find out what’s new here.
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 Relief Habit
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:
These individuals drink to cope or resolve a negative experience and therefore a driven by negative reinforcement. As a group they present with more depressive features and have more anxious traits than those ‘reward drinkers’. So the key to managing these patients is to offer treatment that also appeases their negative physical and psychological experiences with sedation, anxiolytics, glutamatergic modulation. (Hint this is where Taurine really shines, in this group!!)
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? As a nation of over-consumers by nature, this is a question we need to ask all our patients
Mastering Mental Health: New Assessments and Management Resources in Your Clinic (2hrs)
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…
Setting the record straight: 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 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!
You can purchase The ABC of CDG here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account after you have logged into your account.
*****Your RAN Online Account has a NEW LOOK!!*****
Next time your log in, you will experience a more user friendly way to search, view, listen and download your resources. Find out what’s new here.
Remember the days when we had the brain all back-to-front & upside down? Anatomy & physiology told us it was an island, completely protected by the blood-brain-barrier from pathology in the rest of the body, that it was incapable of regeneration after damage and that it didn’t have its own lymphatic system. All wrong. Which presents a problem, the CNS is absolutely in trouble if other parts of our body are (!), but also some solutions: plasticity and the brain’s own capacity for cleaning up after itself. New research has revealed more about this critical CNS cleansing and what is likely to get in the way of this
The latest Medscape update on this is quite poetic, speaking to the movement of body fluids like tides within the human body.
“They found that the blood flow to the brain diminishes, allowing for an influx of cerebrospinal fluid (CSF), washing away the day’s detritus of proteins and other waste substances that might harm the brain if they aren’t cleared out.”
But these particular tide times are restricted to sleep – having never been identified during awake states & even more specifically only during our Deep Sleep, the period of slowest brainwave activity. The speculation is, of course, given sleep issues predate or are a feature of neurological and mental health conditions, that perhaps this comes back to the impeded process of waste removal that accompanies this and how this may contribute to accelerated negative neurological change. For example, beta-amyloid proteins are well known to be removed most rapidly during our sleep and this week I’ve been faced with a small mob of patients who have substantial cognitive impairment risk from a genetic standpoint (e.g. Apo E 4 carriers in families riddled with dementia) but their unmanaged long-standing insomnia plus or minus OSA is likely just AS risky. So here we are again back at one of the key non-negotiables for health: Sleep.
I often say to my patients, ‘There is nothing I can give you in a bottle or a blend than can do one 100th of what healthy (quantity & quality) sleep can do for your wellbeing today or for preventing health issues for you in the future’
And then I say it out loud again when no one else is around just to ensure we’re all aware of that 😉
Want an Update on Inflamed Brain Science?
The brain is no longer considered an immunoprivileged organ separated from immune cells by the blood-brain barrier, with research revealing numerous interactions between the neurological and immune systems. A large body of evidence now shows that these interactions, in particular an imbalance in pro-oxidant & antioxidant systems, play a clinically relevant role in the mental health issues of our patients and may go some way to explain why patients with chronic inflammation frequently present with mood and cognitive issues. Identifying and addressing the source of the inflammation (musculoskeletal, gastrointestinal etc.) therefore potentially addresses the underpinning cause and creates a ‘win-win’ scenario for patients. This updated recording aptly named: The Inflamed Brain, covers all this and more!
Assessing Adrenals can be hit and miss, especially given that even more so than other labs, timing is everything. That’s why endocrinologists typically won’t look at anything less than a 24hr urine collection. If the total output is deemed to be high = Cushing’s and if it’s low = Addison’s. Sounds simple right? But to say only values outside of this reference range flag a problem might just be a case of throwing the baby out with the bathwater (or urine in this case!). Especially given it has been established that humans frequently fail at correct & complete 24hr urine collection! Alternatively we can use saliva or blood assays and capture the cortisol at any given time point, comparing that to expectations based on diurnal rhythm – but again, how are the reference ranges for these ascertained and is there such as thing as low normal. high normal results for cortisol, that actually warrant follow up investigation? I’m so glad you asked.
I see a number of patients who present with possible indications of flagging adrenals: from some distinguishing, but far from definitive features, in the clinical picture, to secondary lab markers. However, when they ‘limp’ over the line with their morning blood cortisol result I am often left talking to myself in an echo chamber about the need for more follow up.
But with the RCPA a.m. reference range of 200-650 nmol/L (Some seriously wide goalposts!) and some labs even going down to 150 with their minimum acceptable level for morning cortisol…are we right to still flag hypocortisolism (for any reason) as a differential in patients with low normal results?
Well Medscape yet again delivered Christmas 🤶 early last week with the largest study to date of blood cortisol, that has narrowed what’s ‘normal’ significantly…at least in terms of how low you can go before warranting further investigation. In this study they tested blood cortisol in the morning and afternoon, in over 1200 individuals presenting at an endocrinology clinic to determine in real world terms how low is too low (and associated with an increased likelihood of genuine adrenal insufficiency). They then gave this new ‘minimum cortisol’ a bit of test-run in 2 other large cohorts of patients to check it really did work as an effective cut off and wham bang…we now have a fully validated bare minimum… and guess what…it’s 275 nmol/L in the morning and 250 nmol/L in the afternoon!
Let’s be clear, their cut-off has what’s called a low ‘positive predictive value’ – which means most people (approx 2/3) with cortisol under this cut-off, upon further investigation (typically the ACTH stimulation test) will be found to be fine. BUT the point of this study was to ensure we don’t miss patients with adrenal problems just because they have ‘within range’ cortisol…and this new cut-off delivers on that.
This is big helpful news actually. Previously with patients who had am cortisol between 150- 275 we tended to find ourselves in ‘no man’s land’ – unable to provide enough of an argument about why adrenal insufficiency should still be on the differential list but unable to abandon that suspicion entirely. Thanks Medscape! Now if all the labs, RCPA and the referring physicians can just read this study and shift their goal posts…🙄
Our Group Mentoring 2020 Doors are just…about…to…close!
So if you love labs (or want to learn to love them more), desire to be a better diagnostic detective than you already are and want truly independent mentoring in a collegiate and structured environment for next year and you haven’t applied yet…best shove your foot to hold that door open right now! We offer a range of different levels & types of special interest groups: from New Graduates & the Mental Health Primer group (for those wanting to upskill and focus on this area), from rotating case presentations in our regular groups which are a mix of funky similarly skilled clinicians, to our pure GP group…take our pick! But get in quick by emailing us right this very second: firstname.lastname@example.org
This week’s wonder-full paper and light-bulb discovery was prompted by a 34 year old woman with a history of Depo Provera injections over several years to control unruly menstrual bleeding and pain. She was subsequently diagnosed at 28 with osteoporosis. That’s not a mispelling…not -penia, -porosis. Now I may be a bit slower than some on the ol’ synthetic hormone fallout front but when it was pointed out that this is a known possible side effect of this synthetic progestin (even features in the consumer brochure), which is used for a range of indications in both pre and post-menopausal women, I did a double-take. What kind of progesterone replacement impacts your bone health negatively and how? And therein the real trouble started.
So fixated are we (myself included) on the evils of oestrogen, I think we’ve failed to notice the wolf in sheep’s clothing that can be synthetic progestins for some patients. Not just in general terms of concern regarding all synthetic hormones but as a result specifically of their interaction with glucocorticoid receptors (GR). This excellent paper reviews this aspect of the 2 most commonly used ones: medroxyprogesterone acetate (MPA) and norethisterone enanthate.
The bottom-line? MPA (which is Depo provera) is a significant GR agonist. That means it’s behaving like cortisol producing a degree of immune suppression and constituting yet another mechanism, in addition to the low oestrogen state it induces, by which negative bone effects may be mediated. This is not a mild or minor action according to this and other research. This is likely to have significant implications for some women, including this 34 year old female. Some women see reversal of this demineralisation following cessation, but not all and the younger your first exposure, the higher the likelihood it won’t correct. This woman had other osteoporotic risk factors, sure, but never enough on their own to produce such severity so young. Mind. Blown.🎆 Or is that just me?
While none of us are likely to be advocating for replacement sex hormones without very careful consideration, this has really helped me to change channels off my oestrogen obsession and become alert to the potential for broader effects from synthetic progestins. MPA…you’re firmly on my radar now in a whole new way.
As always, our patients teach us the most and thanks to Amanda Mullemeister for bringing hers to our recent mentoring session. The learning is never one-directional and I am so privileged to share in these discoveries with all of my mentees, every week. I just wanted to share some light from this particular light-bulb 💡
How To Uncover Unhealthy Bones Earlier
If you’ve heard Rachel speak ever (!) you probably know she’s on a mission to stop the late diagnosis of osteoporosis in patients and as part of this reminds us that this is a condition that develops over a lifetime not overnight – so waiting until women are 65yrs and men are 70yrs (which is the standard recommended age for BMD screening) seems a little remiss in terms of identifying our opportunity for preventative medicine. Are there earlier warning signs that we are ignoring or specific tests more sensitive and accessible than DXA scans that we could be ordering to better monitor patients who are at higher risk of bone demineralisation? The answers are of course, yes and yes! This Update in Under 30 outlines the clinical tools we should be using to uncover unhealthy bones earlier in our patients, how to implement them, their limitations and their strengths.
I’d love to continue this conversation with you so join me and be part of my ongoing dialogue on this and my other blogs by following my Facebook page.
Stop press. No, seriously. This new research warrants the attention of every practitioner working with children & teenagers. In the largest paediatric study of its kind to date, which included 2,480 children aged 10-18yrs diagnosed with hyperthyroidism (Grave’s or otherwise), Zader & colleagues found
Double the rate of ADHD diagnoses
5 times the rate of Bipolar diagnoses (almost 7 times in males)
5 times the rate of suicidality
That’s what I said: in 10-18 year olds
What is most alarming of course is that these mental health diagnoses were made in half of these children >3 months prior to the diagnosis of hyperthyroidism. What does this mean? It means we are missing this critical biological driver in this patient group. We all recognise the potential for some psychological presentations people affected with thyroid conditions, however, perhaps we are more alert to this in adults and letting it slip off our radar in kids? There’s been renewed talk about the over- and mis-diagnosing of ADHD lately and given that research has found up to 80% of hyperthyroid children meet ADHD diagnostic criteria this is one of the 1st place arguably to look! It also means, as these researchers discuss in detail, these kids are being medicated with psychiatric meds that in fact may, at the least mask their abnormal thyroid, lead to the incorrect diagnosis of hypothyroidism (lithium & even stimulants for example) or exacerbate their hyperthyroidism (quetiapine). But wait there’s more and it’s essential to understand.
Zadar & colleagues note that while we can not be 100% clear about the direction of the relationship…e.g. were these children already at risk psychologically and the hyperthyroidism just exacerbated that, they note that correction of the TFTs does not always equate to ‘cure’ of the mental health issues. This is not entirely surprising of course. What the problem emerges via a combination of biology and psychology & we resolve or remedy the biology…guess what you have left? PLUS the learned behaviours etc from suffering from anxiety, impaired cognition, suicidality they’ve been battling at the hands of excess T3 and a subsequent tsunami of reactive oxygen species.
This is one of those papers we should all have to read top to toe and therefore ideally be able to access for free but alas 🙁 What you can read is the Medscape review of this, which is a reasonable summary but the full paper is worth it if you can. You know the other key take home here…the diagnosis of hyperthyroidism was only made with overt out of range TFTs… which begs the question what about all those subclinical hyperthyroid cases we know exist? Yes, no wonder this paper has RACHEL’ S FAVOURITE written all over it…paediatric thyroid assessment and missed biological drivers of mental health and the opportunity to get better at both…can my research reading get any better this week?!🤓
Do you know how paediatric thyroid assessment differs from adults? Thyroid Assessment in Kids & Teenagers – Why, When & How
Currently in Australia there is limited use of age specific reference ranges for thyroid parameters in children & teenagers yet they are essential for correct interpretation and diagnosis. Even doctors & specialists seem to be at a loss with diagnosing thyroid problems in kids unless they are extreme presentations. Subclinical thyroid presentations, however, are increasing in both children and adults. Many practitioners competent in adult thyroid identification & management are less familiar and confident with knowing when why and how to test in this population. Make sure you’re not missing thyroid imbalance in your paediatric patients…early detection makes treatment easy.
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 ‘Devil’s Copper’. 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.
There I said it. It was always going to happen. I’m ok, thanks for asking. This week we had a case of a woman diagnosed with MS in her late 20s. That was 5 years ago and she’s been medicated ever since with an immunosuppressant and she is understandably very nervous about taking any complementary medicine that would pull against this medication, interfering with its actions. Her concerns extended to zinc supplementation in spite of her plasma zinc being 7 umol/L. That’s right, 7. Zinc STAT, right? But slow up there everyone, her apprehension is not necessarily unfounded.
The top nutritional research topics in MS are: Vitamin D (for der…we all knew that, right?), Vitamin A and Zinc. The fan-mail for the first two, as key immuno-modulators in both prevention and in established conditions, is almost at stalker level.
In contrast Zinc attracts both fan and hate mail.
Although the jury is far from in, there’s growing concern that while extracellular levels of Zinc may appear low in MS (that includes of course plasma/serum values) the same individual may actually have elevated levels inside their cells and more specifically inside their CNS. Gulp. But wait there’s more. There is a hypothesis that Zinc dysregulation may be a pathophysiological driver in MS. Double Gulp. My (nutritional) soul mate has shown a potential dark side finally and is sitting under a cloud of suspicion. So what do we need to do differently?
If you’re seeing MS patients you need to be up on the sizeable pile of research into CM in this condition. A brilliant place to start is this very readable review of ‘Vitamins in MS’.
And specifically in regard to Zinc status in your MS patients? Well my advice is don’t rely on a plasma/serum Zinc alone – but couple this with an rbc Zn to ensure there is no sign of intracellular accumulation at play before you make a decision about treatment. Not a perfect solution, but while we’re unlikely outside of research to ever be able to measure CNS zinc concentrations, a reasonable approach. An unchecked zinc deficiency is in no-one’s interests either, including your MS patients – so it’s about gathering the best quality information you can to walk that fine line of adequacy not excess. And if you’re still reeling at the very thought that Zinc has a dark side – remember I did warn you…in Mastering Micronutrients – which is essentially a series of truth-bombs one of which, is every nutrient has a sting in its tail, a U-shaped dose response and a dark side. We need to get to know them all.
Mastering Micronutrients – An Upskilling Opportunity for Old and New Hands
Let’s make sense of the over-arching nutrition principles, that will profoundly change your understanding and application of this modality Truly understanding the ‘big’ concepts, so often overlooked, or incorrectly taught, ensures you get the critical ‘small’ detail in your nutritional prescriptions right. In this 4 hour recording, together with key clinical tools, we talk about the tough stuff: dose-response curves, active versus passive stores and excretory pathways and ooh lah lah…the myth of taking ‘activated vitamins’. Even those who feel satisfied with their original training – will find a lot in this critical review that is new, insightful and truly practise-changing!
Tonic. Homeostatic modulator. These terms and concepts, which have a long tradition in herbal medicine (and let’s be clear, were considered yet another example of the wishy-washiness of the modality) are being appropriated by some areas of mainstream medicine right now. Cheer up ‘leaky gut’, you’re no longer alone! And arguably misappropriated by the public’s very ‘lay’ interpretation of the science on medicinal cannabis and its subsequent elevation to panacea, of late.
“So many of my patients are telling me they’re taking Cannabis now, just as a tonic”, says yet another practitioner to me recently, “No, not for pain, they’re young and fit but they take it because it’s a homeostatic regulator!!”
The capacity to maintain homeostasis, and particularly in the face of adversity or imbalance, is a sign of the vitality of the individual, according to what I remember from naturopathic philosophy (and have truly taken on and observed firsthand)…so just back up there a tad and explain to me how this one herb proposes to do this for everyone on a one-size-fits-all-fashion? As confessed in an earlier communication, I am a cannabis convert. But only in the sense of appreciating the niche areas where it is likely to offer true therapeutic benefits. I still have the words of warning from the brilliant Professor Michael Lintzeris, the Director of the Drug & Alcohol Services, South East Sydney Local Health District; Conjoint Professor, Division of Addiction Medicine etc., ringing in my ears, pleading with health practitioners to not ‘fall’ for cannabis in the way we have previously ‘fallen’ (so far and landed so badly) for the panaceas of the past: opiates and benzodiazepines. Most notable major omission for me, in an otherwise rigorous scientific debate of late, is any discussion about its potential for impacting fertility.
I’ve been aware of the potential negative effect on male fertility, in particular, for over a decade and while we undoubtedly need more targeted research on this topic to reach a consensus, the evidence base to date points to lower LH +/- testosterone and impaired sperm quality and motility. Certainly not perhaps what tonic-seeking patients know they’re signing up for.
There is in fact evidence to suggest ‘sperm under the influence’…’lose their way’ and are less effective at finding and fertilising the egg. Sorry but the image always makes me chuckle…stoned sperm. ‘Hey, dude where’s my egg?!’ style. But it’s not funny when impaired fertility is a problem affecting so many these days, and we still are guilty of over-focusing on ‘her’ and under-assessing ‘him’…and lo and behold it could be his chronic cannabis use to blame. We had a case recently, years of unprotected sex, daily cannabis, no baby, no dots connected. We may think this is a handy incidental contraceptive for young men sitting on couches with cones (one mum recently said as much to me) but for the rest…?
Getting Men’s Hormones Right
As practitioners we should know as much about investigating and treating male hormone imbalances as we do female ones, yet this is often not the case. While we are increasingly aware of everyone’s exposure to lifestyle & environmental endocrine disruptors and the fragility of the HPO axis, we sometimes fail to recognise that the reproductive health of our male patients is equally under threat. This is clearly demonstrated by generally diminishing levels of testosterone amongst men and increasingly early onset of andropause. These issues then become barriers to achieving success in other health areas with your clients, mood, metabolism, fertility and beyond. Learn more here
I’d love to continue this conversation with you…
so join me and be part of my ongoing dialog on this and my other blogs by following my Facebook page.
Following an important weekend of discussing mental health from a more balanced perspective (that’s my new less provocative term for ‘integrative’ or dare I even mumble…holistic) in Perth for ACNEM, I remain alert but not alarmed of how much is still to be revealed in this area. Recently, for example, in our mental health dedicated mentoring group, we discussed a case of a somewhat atypical schizophrenia presentation in a middle-age female migrant. Fortunately, I co-chair these sessions with an incredible clinical psychologist who was quick to pick up that no CNS auto-antibodies had been tested, and given the peculiarities of the case they should have. This is a relatively new area, in terms of more mainstream acceptance of this as a differential in some psychiatric presentations and provision of these tests now through mainstream labs, but it would appear it is far from common knowledge. Then I read this brilliant article and…well I think we all need to read it. Here are some snippets…
“Scientists had previously noted that certain autoimmune diseases, such as lupus, were associated with psychosis. And they’d begun to suspect that some infections might, by activating the immune system, contribute to psychiatric conditions. But Dalmau provided meticulous proof that the immune system could attack the brain. The development of a test for the disorder, and the fact that very sick patients could recover with treatment, prompted a wave of interest in autoimmune conditions of the central nervous system. In total, scientists have identified about two dozen others—including dementia-like conditions, epilepsies, and a Parkinson’s-like “stiff person” syndrome—and many experts suspect that more exist…
Robert Yolken, a scientist at Johns Hopkins University, estimates that about one-third of schizophrenics show signs of immune activation (though he adds that this could be related to other factors, such as smoking and obesity). And autoimmune diseases are more common among schizophrenics and their immediate families than among the general population, which could hint at a shared genetic vulnerability.”
There are some potent practical take-homes in this article embedded especially within the story of an 11-year-old boy who was admitted to hospital with profound psychiatric features – initially misdiagnosed and managed as BPAD and later found to have autoimmune encephalitis. First and foremost: psychiatric conditions develop gradually. When there is an acute onset in the absence of an acute trauma – the possibility of a biological (esp autoimmune) driver should be elevated in your differentials. And the mother of this boy, now aged 21 and having undergone 5 relapses and recoveries in between, virtually echoes the thoughts and findings of Carl Pfeiffer half a century ago, when she says, “Too often, psychosis is seen as the disease itself but psychosis is like a fever, it’s a symptom of a lot of different illnesses.” Important for thought.
Could dairy intake in susceptible individuals be a risk promoter for mental health problems? In addition to evidence of the exorphin derivatives from certain caseins interacting with our endogenous opiate system discussed in part 1, we now look at the evidence in support of other milk madness mechanisms. Specifically, the IgG and IgA antibodies about what this tells us about the patient sitting in front of us about their gut generally and about their mental health risks, specifically. The literature in this area dates back to the 1970s but the findings of more recent and more rigorous research are compelling. Find out more here.