A 26 year old woman suffering years of fatigue from ‘persistent iron and B12 deficiency’ repetitively treated with both oral and IV, walks into a compounding chemist and finally meets her match 🐱🏍 A naturopath with years of experience working the frontline, used to dispensing iron galore (& to a lesser extent B12) to young women with similar stories. But this naturopath requests to see all her labs, she meticulously collates them and then she comes back to the client and deals the fatal blow: Has the iron or B12 ever made you feel any better? “No,” she replies.
“I didn’t think so,” says the Naturopath…”everyone’s been barking up the wrong tree all these years!” And she was right.
First glance at her blood results has all of us reflexively reaching for the same diagnosis everyone has made before – crikey that serum B12 is terrible! And then there’s the fuzzy family history of relations ‘needing’ B12 injections and some even with confirmed pernicious anaemia. But wait up…let’s keep our critical thinking hats on once you look over the rest of the lab you see there’s no evidence of functional B12 deficiency (no rise in Hcy, MCV even RDW) and then, the statement that seals the deal, ‘B12 injections have never made me feel any better’. This woman is not feeling the pinch of pernicious anaemia, not the crush of cobalamin clinical deficiency. In spite of being told that for almost a decade.
A low serum B12 value can of course flag a deficiency and we must never ignore it. But given the serum measures, in fact, predominantly Transcobalamin I (TCI), which is the carrier or taxi for B12 that almost ‘never drops its passengers off’, we are less concerned than when we see a low active B12 (TCII aka ‘the real deal’)
So what else could leave someone with less TCI, while not in fact creating a genuine functional deficit of B12? SNPs?🤧 Bless you!…Sorry that sounded like a sneeze and this retort, as we know is almost as common as the common cold! Sure…of course it could be sexy SNPs…but wait, what about something a little less ‘zebra’…a little more horse. The COCP…oh blooming heck..she’s spent the last decade on the COCP and guess what, its impact on B12 is thought to be principally a reduction in TCI! Oh and that iron story, that supposed ‘iron hunger’ we can see with her upregulation of transferrin? Well that’s an artefact of the COCP too, right? And BINGO was her name-O 🕵️♀️
Separating the B12 from the B*S#!
B12 is a routinely under-rated and recognised micronutrient, which is in fact in high demand by many of our patients. As nutritional research pushes back against defining adequacy as simply the prevention of the deficiency-associated disease (macrocyctic anaemia, irreversible neurological damage) we enter a new landscape of more individualised approaches where we’re better able to recognise and treat those at risk of falling below ‘optimal’. But how do we accurately identify this and then choose the ‘best’ B12 (methyl- cyano- adenosyl- hyroxo-) supplement? Does it need to be this complex? Time to sort the B12 from the B*S#!! This recording comes with a bunch of great resources including a clever clinical tool.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
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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!
It’s that time of year when we tend to set our intentions both personally and professionally. For me, between the many meals, pressies and dunks in the river, I slip into some ‘silent work’. In particular, I find myself flagging a couple of key areas that I want to sharpen my knowledge in this year. I’ve already picked mine…have you identified yours?
For many practitioners if there is one topic in nutritional medicine that seems to be more generous than any other it would have to be iron: Iron gives us patients…loads of them! Patients who present with deficiency, with overload, with something in between but still noteworthy, or on iron and that’s causing them all sorts of problems.
But Iron’s generosity doesn’t end there.
It also tends to give a lot of practitioners a bit of a headache!
That’s because a) we were mistakenly taught about iron as if it were just another one of the mineral mob and accordingly allocated grossly inadequate time to do more than scratch the surface of what we need to know and b) what we need to know, thanks to it being the most researched mineral, has undergone a couple of major revelations and revolutions since then anyway! So we can benefit from Iron’s generosity most and leave its other unwanted pressies (the headaches, confusion, frustration & suboptimal management of patients) under the tree – we just need to give iron the real attention it deserves, filling in the gaps in ours and many people’s knowledge about this critical nutrient. And boy, do we (and I mean everyone!! including doctors, midwives, pharmacists…anyone who has ever called iron deficiency on a client!!) need to learn how to correctly read iron studies!!!
Because iron also gives us much needed insight into other micronutrients and just how exquisitely sophisticated their roles & regulation can be. Thanks to it being one of the ‘older minerals’ we know more about it than any other and in turn we have the most advanced assessment methods: Iron studies, a collection of 4 parameters, like 4 chapters in a book or 4 key characters in a play, that need to be viewed separately and then together to understand the whole story.
Yes it’s true the learning doesn’t ever end and as I’ve continued to learn about new iron research I’ve added to our one-stop-iron-resource-shop..the Iron Package. Our very latest edition? A new clinical cheat sheet with some other important numbers on there you want to have at your fingertips whenever you read iron studies. So if you’ve already purchased and have access to the Iron Package…SURPRISE! 🤩 Go back and look again and if not, there’s never been a time like now. Oh iron, you’re sooooo generous!! 😉
Listen to these audios and download the resources straight away in your online account.
If you’ve already purchased ‘Update in Under 30: How to Read Iron Studies’ or ‘Iron Package’ you will find this new clinical cheat sheet available with these audios when you log in to your account.
Yet another super-helpful part of Iron-Land has been mapped!! Ever struggled to correct chronic iron deficiency in athletes or even just weekend warriors? Yep, me too. One of the key barriers being the 2-3 fold rise in hepcidin in response to exercise. Hepcidin whose day job is an inflammatory signal that two-times as an iron uptake blocking agent at the small intestine. In addition to other exercise-induced factors that either reduce Fe uptake or increase losses, it really is no surprise that these cases can be hard to treat. However, a recently published small Australian study has brought to light some constructive new information. Similar to the often talked about ‘anabolic window of opportunity’ whereby we encourage people to consume protein +/- CHOs within a short time-frame post-exercise to optimise exercise outcomes and negate negatives, these new findings imply the same might be true for optimal Iron uptake. But only in relation to exercise done in the morning!
The key finding was when individuals consumed iron after 90mins of exercise in the morning they exhibited higher uptake than both when they took the iron at the same time but didn’t exercise beforehand or took it after exercising at night.
This is a game-changer for potentially ALL our patients who struggle with iron absorption. With the key take-home being…not just take your iron preferably in the morning which we already know (when hepcidin is naturally lower as part of its diurnal rhythm) but before you pop that pill, pop on your sneakers and get busy sweating! How on earth might this be working? Well this study demonstrated that while hepcidin rises after exercise typically for up to 6hrs…it is not yet ‘up’ and blocking within the first hour – gotcha! But why would this mean an even greater uptake compared with the same iron at the same time in the same individual…but a resting version of themselves? Because exercise may in fact cause a transient leaky gut post exercise & enhanced nutrient uptake may be its silver lining! A small study that actually punches above its weight, this one is worth the read – via a great comprehensive summary on Medscape if you have it or you can check out the abstract.
Our ever-expanding Iron knowledge gives us great hope for the improved understanding we are likely to reach with all nutrients in the future. Let’s not forget Iron has about a 70 year head-start on other microminerals such as Zinc and almost a century on Selenium, which was identified to be essential in just 1979!
And the contrast is apparent anywhere you care to compare and contrast the ‘older’ with the ‘younger’ nutrients. Just look at iron studies. A personalised detailed account of each individual’s iron story: how much you’re consuming, how effective you are at absorbing what you’ve been offered, how hungry that makes you for more and what good stores mean to you (not some fictitious average male or female)! All told through 4 distinct but inter-related markers: serum iron, transferrin, transferrin saturation and ferritin. What can we glean from our current routine assessment of Selenium in contrast? Their short-term Se intake…yep. Looking forward to the multi-parameter markers of each individual nutrient we just might have at our fingertips in the future, thanks to iron nutrition which continues to teach us how sophisticated nutritional physiology really is 🙂
We know the most about iron and yet we know there is always more to learn. And who better to teach us this than our clients with iron deficiency or iron excess? Need some help getting across the most important aspects of recognising and correcting each iron issue in clinic? We released an Iron Package earlier this year for this very reason. It covers how to really read iron studies (with a great cheat sheet), how not to fall for a fake (deficiency) and what the best supplements and dosing regimes look like and how that differs in pregnancy, athletes, those with marked gut issues and other key groups. It’s your 1 stop iron shop.
We’re not deaf…we heard that stampede of Iron-Inundated Practitioners!
Our recordings and clinical resources for improving your skill-set in all things iron including, your accuracy of diagnosing deficiencies, pseudo-deficiencies & excesses, plus radically rethinking the best treatment approaches for each scenario…have been some of our most popular. Because nailing iron (pardon the pun) is harder than we were all lead to believe and at least 1 ‘iron maiden’ or ‘iron man’ walks into our practice every day, right? So we’ve brought together 5 extremely popular UU30’s on Iron into one bundle for the price of 4! So if you’re more than ready to graduate from ‘iron school’, now’s your best chance!
1. So You Think You Know How to Read Iron Studies? (≤30 min audio + Cheat Sheet)
Overt Iron Deficiency Anaemia or Haemochromatosis aside…do you understand the critical insights markers like transferrin and its saturation reveal about your patients iron status? Most practitioners don’t and as a result give iron when they shouldn’t and fail to sometimes when they should. This audio complete with an amazing cheat sheet for interpreting your patients Iron Study results will sharpen your skills around iron assessment, enabling you to recognise the real story of your patients’ relationship with iron.
2. Pseudo Iron Deficiency (≤30 minute audio)
The most common mistake made in the interpretation of Iron Studies is this one: confusing inflammation driven iron ‘hiding’ with a genuine iron deficiency. Worse still, following through and giving such a patient oral iron – when in fact it is at its most ‘toxic’ to them.
This audio together with some key patient pathology examples will prevent you ever falling for this one! Learn how to recognise a ‘Pseudo Iron Deficiency’ in a heartbeat!
3. Iron Overload… But not as you know it (≤30 minute audio)
We’re increasingly seeing high ferritin levels in our patients and getting more comfortable referring those patients for gene testing of the haemochromatosis mutations; but, do you know how to distinguish between high ferritin levels that are likely to be genetic and those that are not? This can save you and your patient time and money and there are some strong road signs you need to know. In addition to this, what could cause ferritin results in the hundreds if it’s not genetic nor inflammation? This Update in Under 30 summary will help you streamline your investigations and add a whole new dimension to understanding iron overload…but not as you know it!
4. So You Think You Know How To Treat Iron Deficiency? (≤30 min audio)
And then you don’t. The reality is we all struggle at times with correcting low ferritin or iron deficiency anaemia – so what have we got wrong? In spite of being the most common nutritional deficiency worldwide, the traditional treatment approaches to supplementation have been rudimentary, falling under the hit hard and heavy model e.g. 70mg TIDS, and are relatively unconvincing in terms of success. New research into iron homeostasis has revealed why these prescriptions are all wrong and what even us low-dosers need to do to get it more right, more often!
5. So You Think You Know the Best Iron Supplement, Right?! (≤30 min audio + Iron Supplement Guide)
Iron supplementation, regardless of brand, presents us with some major challenges: low efficacy, poor tolerability & high toxicity – in terms of oxidative stress, inflammation (local and systemic) and detrimental effects on patients’ microbiome. What should we look for to minimise these issues & enhance our patients’ chance of success. Which nutritional adjuvants are likely to turn a non-responder into a success story and how do we tailor the approach for each patient? It’s not what you’ve been taught nor is it what you think! This comes with a bonus clinical tool, a fabulous easy reference guide – to help you individualise your approach to iron deficiency and increase your likelihood of success.
You’ll never look at iron studies or your iron-challenged patients the same way.
Listen to these audios straight away in your online account.
And then you don’t, right? Because if my experience is anything to go by, there are some patients that just don’t respond to the usual iron repletion strategies. Depending on how low their ferritin is, this can then precipitate ‘practitioner panic’ (we’ve all had it right?!) where we’re inclined to go higher & higher with the dose and number of doses per day. Typically, this also fails. I hear about this from other practitioners all the time and I see the ‘normal’ doses of iron sneaking up and up. Remember the days when we couldn’t get a non-pharmacy supplement with over 5mg elemental iron in it and now we have > 20mg? But still, I hear you say, this fades into insignificance when you think about the standard medical model for iron correction which provides 100-200mg/day and you’re right.
Gee… after hundreds of years of knowing about this deficiency and being the most common deficiency word-wide, you’d think we had our supplemental regime nailed.
But that’s where you’d be wrong. (more…)
While I did diagnose this one correctly, I didn’t get 100% in this quiz – Can you? Speaking of the devil, Medscape, has this great little visual quiz to test your knowledge about physical signs & other hidden clues of nutritional deficiencies.
While we all know there can be a lack of specificity when it comes to some deficiency signs…like glossitis…eyeyiyi..naming a nutritional deficiency that doesn’t include this sign would be a tougher question 😉 but what a great reminder of some quirky things you may have forgotten or in fact deficiency features you may not have even known about.
A gem I love and apply frequently, is about zinc the ALP levels…watch out for the that later in the slideshow quiz.
Also note the distinct difference in opinion when it comes to vitamin D adequacy – with Medscape citing blood vitamin D result < 75 nmol/L unequivocally associated with osteoporotic change…in contrast to the …’anything over 50 nmol/L is a bonus’ line we’re being fed here in Aus and NZ! While we may not ever see some of these severe deficiency presentations walking through our doors – you can’t be so sure…given the reported resurfacing of scurvy in good ol’ Sydney just last year!
Is it just me? I love going back to nutrition 101. So tomorrow with your cuppa…test yourself and then let us know how you go 😉
Are you keen to keep developing your naturopathic knowledge in areas of diagnostics and nutrition? Rachel has a range of services that can help accelerate your learning. From the long list of great downloadable recordings in the store, that help fill your ‘knowledge potholes’ in a fun and engaging way that really brings these topics to life, to our Update in Under 30 Subscription: 30 mins of power-packed up-skilling delivered to your inbox every month, as well as our individual and group mentoring programs! There’s content galore and a delivery format to suit every clinician – come check out what’s on offer.
Cheesy I know! 😉 However, recently the issue of knowing when to use Withania somnifera & when not to, came up again in mentoring so I thought it’s probably a good one to share. Withania, aka Aswagandha or Indian Ginseng, has become a favourite adaptogenic prescription for many practitioners, myself included. I remember learning specifically (about a million years ago!!) that this herb is ‘warming’ & ‘nourishing’, thanks in part to its iron content. In a traditional medicine context, it’s used for those particularly vulnerable populations such as children, the pregnant, the elderly and the malnourished, boiled in milk as a tonic. These ideas always stayed with me, and lead me to only use Withania in similar patients and presentations with good results. (more…)
Well here’s a thought…the ‘Superfood’ nutrition movement has just about eaten the South Americans out of quinoa and the Pacific Islanders out of coconuts..isn’t it time for a local hero? I get a bit despondent when any new food is touted as a ‘Superfood’ anyway for all the obvious reasons but this is heavily compounded when this so-called ‘Superfood’ and the bankable gross exploitation of this foodstuff comes at a huge cost: whether that be in terms of food-miles, another population’s access to their food staple or the radical change in land management in these countries that often follows, e.g. think palm oil plantations.
“I need a (Local) Hero!” – cue Bonnie Tyler soundtrack & wind machine 🙂
These days it seems like patients can almost be divided into two groups: those that have a tendency to iron overload and those that struggle most of their lives just to keep ferritin in the red…and what a struggle it can be. So many clients have spent years taking every form of iron there is in high doses, trying to improve their intake of dietary sources, working on their digestion etc etc but still those numbers can fail to really pick up. (more…)
We’ve just had another mentoring case in which a 40 something female with deficiencies of almost all other minerals but ‘pretty normal ferritin levels’ presented with a range of endocrine problems and arthralgia. Sounds as if iron’s not the problem right? Except that in this case her iron studies also tell us that her transferrin saturation % on last check was 48%. The diagnostic criteria for hereditary haemachromatosis (HH) necessitates elevated ferritin – to indicate that the iron stores are reaching saturation, however, while this becomes evident at relatively young ages in men (20s-40s), who have no specific excretory pathway for iron, is this still appropriate in menstruating female, whose monthly periods may mask the HH tendency with regard to ferritin? I’m guessing you know what my answer is already! 😉
Some would argue that HH, in spite of being an inherited disorder, is only clinically meaningful once the ferritin is elevated ( earlier and more potent elevations are seen in people possessing the C282Y genotype) but again this is very much up for debate in the current scientific literature, with a lot of research concluding that the transferrin saturation (also referred to as the transferrin ratio) being an important prognostic indicator for various chronic diseases including CVD.
When we go back to basics and remember the higher the transferrin percentage the more iron is being delivered to tissues around the body (whether they like/want it or not! so we refer to this as being ‘iron dumping’) and the higher the serum iron, the more unbound iron is in the system – a key source of oxidative stress..it becomes patently clear that these two parameters are important early warning signs of a tendency to iron overload, increased risk of heavy metal toxicity and already active mineral imbalance. So in future keep your eyes open for women with fasting transferrin saturation values that consistently sit above 35% and men, > 40% and if you do see a series of suspicious values – consider the genotype test through mainstream labs.