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.
If you know me, you may wonder if I’ve recently undergone a personality bypass. I am passionate about diagnostics, pride myself on ‘making the invisible visible’ through better understanding of pathology markers and confirming the true nature of the underpinning problem in order to be most effective in our management of every client. And I absolutely see that for the majority of patients ‘ knowledge is power’, so what on earth is this all about? Well, while I stand by my stubborn commitment to diagnostic sleuthing for ‘most patients most of the time’, there are occasions when I’m left wondering about the value and the likely outcome should we finally catch that elusive diagnosis by its tail…case in point:
Recently I’ve been aware of a bit of spike in ‘diagnosing’ Ehlers Danlos Syndrome for patients who present with myriad problems – from the text-book connective tissue issues (loose joints, hypermobility etc) to the seemingly more far flung like mast-cell activation syndrome and overactive pelvic floors.
Just so happens this ended up being a thought-provoking 3 way conversation. Got to love having so many wise women’s email ear..and especially such generous ones. First, I ran this case and the differential past the wisest dual qual physio/naturopath I know Alyssa Tait who specialises in pelvic conditions and any and every other bizarre – no-one-else-could-name-it, kind of conditions. And her response, breathtakingly comprehensive and punctuated by copious journal articles throughout as always, proceeded to flesh out the evidence for and against the more unusual patient features and the possibility of EDS from bladder irritability (maybe) to functional GIT disorders (definite maybe) to the dysautonomia link (patchy). But it was what she said next that struck a deep cord for me:
“This happened recently to me when I referred a very difficult Painful Bladder Syndrome (PBS) patient to a GP – suddenly she had EDS as the answer to all her problems. But we can’t change genetics. All we can change is the function, and I have seen a worrying pattern of blaming the unchangeable (EDS) at the expense of looking for the changeable (e.g. an EDS patient of mine who actually had low thyroid function which had been over-looked.)
My feeling is it’s better to evaluate and treat what we see. As soon as we start giving our patients a litany of all the possible horrible ways their health is/will be pervasively affected by a completely unchangeable genetic reality (EDS), it’s a major “thought virus” that can both reinforce the “sick person” self-image and negatively impact their health-seeking behaviour – either by making them give up, ‘cause it’s all too overwhelming, or to follow an infinite journey through rabbit holes that make health their hobby rather than experiencing their life and relationships to the full.”
So back I went to the original practitioner who was contemplating chasing this EDS diagnosis in her patient and she was not short on some of her own wisdom. Like many people who end up working in health Gabby battled her way out of her own ‘no-one-cold name-it’ health crisis before training to be a naturopath. So understandably she sees both sides:
“As a terrified 20 something who kept ending up in the emergency ward with flares – I desperately wanted to know what was wrong with me, why it was happening, why I was in so much pain and why at the time no-one could tell me. I remember being about 28 asking my Prof (of immunology) whether what I had was going to kill me. He said ‘If you want me to be honest I’m really not sure at the moment darling but I’ll do my absolute best to take care of you’. That answer changed my life. Now as a Nat with a history of chronic conditions – I can see managing the symptoms is probably really all you need plus regular monitoring. Which is what I do for myself and many of my clients. The hurdle is getting over the lack of trust these clients feel after years and YEARS of being misdiagnosed and fearing for their lives.”
So..I’m asking us all again..is a diagnosis always helpful? Perhaps with each patient we need to think this through afresh? Thanks wise women 😉
There’s a significant increase in the number of women in their 20s to 50s presenting with ‘atypical’ joint pain, that seems hard for specialists to diagnose and therefore, hard for any of us to know how best to treat. If we listen closely to these patients, however, they are often telling us that their, ‘gut isn’t right’. It doesn’t tend to grab so much attention but maybe it should! We examine 3 ‘atypical’ arthropathies that can have GIT symptoms and arguably may represent a key driver of their joint pain. The different clinical pictures & targeted investigations for these big 3 together with some key papers are covered in this audio.
Ok here’s some tough Tuesday talk..not all tests are valid. Tougher still…not all of the mainstream nor the functional pathology ones. I am talking across the board here. Each and every pathology parameter requires good knowledge about its strengths. limitations and, one of my absolute favourite nemeses, confounders. “How on earth am I supposed to learn all that and everything else I have to know too?!!” I hear you scream at your screen. Btw keep yourself nice if you’re in public while you’re reading this 😉
But rather than imagining you need to have this level of knowledge for all tests, I would suggest you set yourself a hit list of the ones you rely on most, either in terms of frequency or in terms of the degree to which they direct your decisions about patient care…can I mention (ahem) Iron studies here perhaps for us all…but maybe you have a specialist area so you use a particular investigation routinely or at least frequently…
CDSAs? Breath tests for SIBO? Oxalates?
May I please then politely suggest that you get to know these inside and out? Not based purely on the information and assistance that the test provider provides you..but you scrutinise them independently. Top to bottom. Because that’s your business, right? And your diagnoses and treatment decisions are pivoting on these results. Jason Hawrelak gave us all some great examples, including his informal experiment of sending the same stool sample to multiple labs. Don’t know about this and his findings?? If you’re in the business of ordering stool tests, you need to. I am doing this all the time with numerous pathology markers because diagnostics is my passion (alright, obsession)…and recently I put Oxalate Assessment to the test and oh boy!
Here’s something for free:
If you are measuring urinary oxalates to diagnose oxalate overload in your patients and you, 1) are using a lab that does not preserve the urine as you collect it, using acidified containers or providing additional preservatives for take home testing kits….you are wasting your patients money and you are likely getting a lot of false positives, i.e. the result infers the patient has a problem when they don’t!!
And 2) if you are simply following the labs reference ranges for what ‘healthy’ urinary oxalates look like – you’re wasting your patients money again and likely getting false negatives – a failure to show a problem that is actually there! If you’re hunting oxalates…please ensure you have a current effective hunter’s licence…by getting up to speed fast regarding accurate investigation of this. Oh yes…it’s tough-talkin’-Tuesday and I’ve come out firing…watch out this may become a regular feature 🤷♀️
Update in Under 30: Oxalate Overload – Assessment and Management
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update.
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.
When patients present feeling worse every time they DIY a Green Detox, as the practitioner, you’re likely to be sniffing around reduced oxalate tolerance as a differential. Rightly so. But what about the patient with joint pains and disproportionate fatigue who has baffled their rheumatologist, or the one suffering vulvodynia that baffles everyone, or irritable bladder symptoms, or….and they all eat an exemplary colourful high plant food diet, with their only self-confessed sin…darker than dark chocolate between every mouthful? Who doesn’t? While you may have a hunch, given the goodness of those foods, we should check these out objectively rather than unnecessarily restrict or limit someone’s food choices for the rest of their natural life! If dietary oxalate overload is now on your radar for these patients you need to move to the next step. Assessment.
Spot or 24hr urine collection or plasma assay or OATS testing or imaging or joint aspirates? So many choices but which one has the greatest validity depending on your patient’s presentation? Ok how about the most general all-rounder that is truly an option in the real world? – always helpful;) Yep, 24hr urine collection…agreed.
Ok, next step.
You need to wrap around that waist of yours one seriously heavy tool belt for accurate interpretation of their results. That’s right…those random ol’ reference ranges need a serious rethink! How much? Well, given the reference ranges every lab will give you for urinary oxalates typically fail to pick up up to 1/3 of patients with oxalate overload high enough to produce oxalate kidney stones…I think you get the picture. I feel your trepidation now but can hear you pensively ask anyway…next step? Management.
Just google oxalate-rich foods, print out the list for your patient and tell them never to have these (or joy, laughter, sex or a healthy microbiome) ever again.
The ‘low oxalate lists’ will lead you astray and the ‘high oxalate foods’ should not be tossed away! The research has found greater therapeutic benefits from different dietary approaches, some nutritional supplements and most importantly targeted treatment of the cause…which is all about the…go on, try and say it without screaming…the GUT!!!!!!!!!!!!!!
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update
Hear all about it by listening to my latest Update in Under 30:
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Horses not Zebras. You’ve no doubt heard me repeat that quote which is famous in medical schools, something to the effect of, “When you hear a heard of animals outside your door, think horses not zebras”…unless of course you are practising in Africa might I suggest 😉 This of course reminds us all in short to think of the most likely explanations not the most exotic first. Likewise with our case taking. The number of times I ask practitioners for the ‘boring basics’ and am met with an embarrassed silence. Think:
Body Mass Index
There I said it…and yet these are like dirty words in integrative health. Why? Because we’re starting to ignore the ‘boring basics’ in favour of getting ‘fancy first up’, as I like to call it. Look I love a good bit of bioelectrical impedence assessment as much as the next clinician and I am not about to use this crude measure as replacement for that but I absolutely need to have these key landmark pieces of information to understand a very long list of things such as contribution to future health risks, current burdens from literally the weight on those joints leading to knee pain, to the weight/mass not pulling on their bones and therefore contributing to lower BMD their whole life. Even their likelihood of a leaky gut today, right, Brad Leech, our colleague and impressive IP researcher? BMI drives also the appropriateness and their capacity for any exercise interventions I might recommend, not to mention the frequently mentioned, accurate interpretation of their labs.
For many many labs that we routinely see for our clients…the reference range should actually be a sliding scale that moves with BMI…what do we really ‘expect’ and what is actually ‘healthy’ is different at different weights.
Like TFTs – this may be a big newsflash for most but I never want to see a patient with a BMI > 30 have a TSH anywhere < 2, unless they’re on replacement.
Say wha? You heard me. I promise I’ll tell you more about that soon.
But again…let’s not get fancy first up especially not in any of our paediatric patients and in spite of what their words or ‘tude may be telling you, that includes all the way up to 18 in our books! Brace yourself, I’m going to speak that dirty word again…BMI..boring basics before all else. We need to review their height, weight and BMI against paediatric growth charts. These oldies are goldies and can reveal so much about growth trajectories, puberty milestones when any other discussion is off the table, type 2 nutritional imbalances (protein, zinc, potassium, magnesium, sulfur) and flag all other sorts of concerns or reassurance…and you haven’t had to steal a drop of blood or any much hard earned money off mum and dad to work a lot out. Anyway, that’s my ‘boring basic beef’ for now…there’s a lot to be said for ensuring such ‘dirty words’ come before everything else.
Need help with wrestling all the most important patient information into a clear management plan?
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.
With the increasing weight of evidence pointing to a potent pathogenic portal between our mouths and every other part of the body, whether that be in terms of cardiovascular disease, rheumatoid arthritis, appendicitis, even a growing case for Alzheimer’s disease, we need to ensure we’re not overlooking the condition of each patient’s oral cavity. I got very excited about the recent Medscape article: A rapid non-invasive tool for periodontitis screening in a medical care setting. It’s true, I live a quiet life 😉 But seriously, a validated tool for all non-dentists to accurately pick up on the likelihood of this condition would be a nifty little thing indeed, so we can narrow down just who we quick-march off the dentist as well as understand their whole health story. But then I read the 8 actual questions which included gems such as: Do you think you have gum disease? and Have you ever had treatment for gum disease such as scaling and root planing, sometimes called “deep cleaning”? I thought, ok, this is not rocket (dental) science.
But that’s the point, I guess, right?
So while I encourage you to check out & employ this screening tool by all means, we can also be reassured that just by ensuring that when we ask about someone’s digestion (and when don’t we?!) we start at the very top of the tube, we’re doing a good job!! As my new grad mentees learnt this year…following the patient’s GIT from mouth to south anatomically, is my rather simplistic way of guaranteeing I cover everything digestive..without using formal consultation script. So in the case of the mouth, my questions include things like: last trip to the dentist; any prior dental diagnoses, number of amalgams, implants, root canals etc & their routine dental care techniques, any signs of bleeding on brushing & all foods they avoid for dental or oral reasons? Look, it hasn’t undergone the rigorous validation that the Self-Reported Oral Health Questionnaire has..but I think it’s a good start.
Whether we’re being picky about pathogens and exactly how they got access to the rest of the body (and gums make a great entry point!!) or just concerned about chronic low level inflammation, a ‘gurgling’ CRP between 1-5 in an otherwise ‘healthy adult’, picking up on periodontitis is a pivotal.
Oh and if you’ve ever wondered about possible health implications from mouth metals other than amalgams…don’t worry, soon I’ll be getting to that with a forthcoming UU30.
Want to hear more about how certain microbiota (from the mouth to the south) are being implicated in joint diseases such as rheumatoid arthritis and ankylosing spondylitis and how we can investigate these individuals? Getting to the Guts of Women with Joint Pain is a recent UU30 instalment that gets down & dirty on the detail.
Integrative Psychiatry is an inspiring area to work in & its evidence base, acceptance and recognition of potency is rapidly growing & offering more patients, more. Going beyond the ‘neurotransmitter imbalance model’ for each presenting diagnosis helps us to see the unique mix of biological & psychological drivers in each individual who presents seeking our help. However sometimes I believe, we find ourselves falling into looking through the lens of just another short-list of alternate models: What kind of methylation imbalance does this person have? What sort of Zn, Cu issues?
While I am so grateful for having learned these tools and watched them be very successful in a portion of my mental health clients, they are simply not the answer for everyone. We need to keep our thinking and practices dynamic and up to date, to reflect the incredible increase in research in new areas of integrative psychiatry, such that more of our patients can benefit and that we can continue to think beyond the box…even if that box itself was originally so progressive!
What do you know, for example, about abnormal purine metabolism in mania and using serum urate as a BPAD prognostic marker in depressed patients? Think you can simply be guided by the reference range provided, think again. What could good old LFTs reveal about our patient’s mental health vulnerabilities and what have we potentially misunderstood about copper in this area, particularly in children?
I appreciate Zinc’s role in mental health as much as the next integrative practitioner. Okay, given my 20K word thesis manifesto, more. But increasingly I am seeing mental health patients who need treatment with different tools. This upcoming ACNEM Mental Health Module in Perth is on point: thinking outside of, outside the box!
While the above only speaks to what I’m presenting, I know Dr. Sanjeev Sharma will also be sharing his wealth of individualised management insights and he’s a big fan of addressing Chronic MIld Metabolic Acidosis as an early treatment objective. Maybe we all need to hear why? And I am so looking forward to getting a PTSD update from Christabelle and hear all about the research into therapeutic keto-diets in psychiatry from Cliff Harvey…haven’t read all those papers to know which conditions and when this approach shows merit? No, most of us haven’t. That’s the point of outsourcing our up-skilling to colleagues who we know are across these more than us and to boot have the clinical experience to ‘make real the research’. As I’ve said before, given the content of this upcoming ACNEM Mental Health program, I wish I wasn’t presenting really, so I could just kick back and take it all in, uninterrupted. But alas, I have some important new information on reading basic bloods through a mental health lens to share! I really hope to see you all there. Let’s get out of the rut of 3-4 nutritional approaches to mental health and make the most of the explosion of research and shared clinical experience.
ACNEM Face-to-Face Training
Fremantle, 27-28 July 2019 at the Esplanade Hotel Fremantle by Rydges
Oh and while you’re here…did you know the research into both beta-casomorphins and IgG casein reactions in relation to certain mental health diagnoses has taken some giant steps forward in the last couple of years? You should. Milk Madness is back and it’s via two distinct mechanisms – identifying which might be at play in your patients & correct management is now clearer than before. Want to get up to date in this area of mental health – check out our UU30 recordings: Milk Madness part 1 & part 2
No you’re right, it’s not long enough to be a Hemsworth’s mobile number but actually it’s more sought after 😉 If you’re up to date with reading & recognising all the different patterns of Iron Studies & the stories they tell, which is a daily business for most of us, then you will know by heart the striking pattern we call, ‘Pseudo Iron Deficiency’. You know the one where your patient’s serum iron & transferrin saturation are mischievously trying to trick you into thinking you need to give this patient iron…when in fact this is absolutely not what they need!
This is of course the result of the redistribution of iron during inflammation – iron is actively removed from the blood and sequestered in the liver instead. It’s designed to protect us from bacterial bogeymen, which is how our stone-age bodies interpret all inflammation of course.
Doesn’t sound familiar? Ok you need to start here or even embrace a full overhaul of all things iron here.
But for those of you nodding so hard you’re at risk of doing yourself an injury, this number is for you. We’ve often talked about the redistributional increase in patients’ ferritin levels in non-specific terms: it goes up..but by how much? Of course we would like to know because no one is fooling us with this transiently inflated value…but can we make an estimation as to what this person’s ferritin will drop to once this inflammation is resolved? Yes.
Write it down. Consider a tattoo, perhaps?
This glorious magic number comes from Thurnham et al paper in 2010 who did the number crunching on over 30 studies involving almost 9,000 individuals to determine the mathematical relationship between inflammatory states & markers and the reciprocal increases in ferritin. Their work is exceptional in that it also differentiates between incubation (pre-symptoms), early and late coalescence periods (if you want to differentiate your patients in this way and get even more specific then you need to read the paper), however, overall when we see a patient who has a CRP ≥5 mg /dL , we can multiply their ferritin by 0.67 and get a lot closer to the truth of their iron stores. Oh and another important detail they revealed, this magnitude of ferritin increase is more likely seen in women or those with baseline (non-inflamed) values < 100 ug/L..so generally more applicable to women than men. Thanks Thurnham and colleagues and the lovely Cheryl, my previous intern who brought this paper to my attention…you just took the guessing out of this extremely common clinical scenario 🙂
We’re not deaf…we heard that stampede of Iron-Inundated Practitioners! The Iron Package is for you!
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!
What makes integrative health professionals stand out is that we take the time and have the attention to detail to capture the ‘whole health story’ of each patient. As a result, however, we tend to end up with vast amounts of information for every client: detailed medical histories, broad systems-reviews, condition specific validated screening surveys, in-house physical assessment data, not to mention a pile of past pathology results…and that’s before we start our own investigative path!
So as you sit at your desk with a plethora of information in front of you, you’re probably thinking, ‘Great, so much valuable information – Oh dear…so much valuable information!’ and struggling to separate the critical narrative from the noise.
Plagued by circular questions: ‘Where do I start?’, ‘What needs to come first?’, ‘Which treatment objectives will pack the most punch for this patient right now?’, ‘What really requires further investigation and what can wait?’ … your thoughts jump around, from one shiny thing to the next…you can ‘see’ so many of the connections… but can you see them all, the whole interconnectedness, and therefore the prescription, laid out in front of you like a road map to follow?
Introducing the two essential tools (aka secret weapons)…
MindMapping & Timelines
… the actual practice of gathering vast amount of a patients case onto one piece of paper.
Yes, that’s what I said ONE PIECE of paper!
Sounds too good to be true?? Well, they don’t quite give you super powers but they will help you write the patient prescription for you and not just one prescription but typically, for the next 12 months. These tools can turn good clinicians into great ones and, once you master them, save enormous amount of your time on your patient work-ups. Relevant to all health professionals who use an integrated approach, the utilisation of these tools, will also reveal to you much about what you know, but didn’t immediately realise (e.g. the means by which gut dysbiosis contributes to impaired oestrogen detoxification), and just as importantly, highlight your knowledge gaps & therefore opportunities for further growth along the way (e.g. how do inflamed joints disrupt GIT tight junctions?).
As ‘whole picture people’ we bite off a lot! It’s these systems, timelines and MindMapping, that Rachel has found help her, and so many other clinicians, truly ‘digest’ the case, optimising our understanding and management.
“I loved this session and think it’s very relevant. I have used these tools before, but never mastered them or used them regularly. I have mostly used mind maps for study, so I love this application and with practice, think I will get used to using them for every case.”
“AMAZING!!! Fantastic health links that I did not know and really consolidated my knowledge on how to produce a Mindmap and how to be better at it! Fabulous session. Thank you”
“Most difficult is challenging existing patterns of thinking around mindmaps and training my brain to approach it more effectively (plus getting faster). This will come with practice. Most satisfying is seeing how useful they can be when done well at the start in terms of time saving in the overall case (across years) and getting to the core (s) of the case. Great session!”
MindMaps & Timelines – Effective Integrated Patient Work-Up
In the Part 1 Video, Rachel teaches you how to effectively perform a case work-up that does justice to the holistic framework and model. At the end of this presentation there is a practice run for you to create a MindMap and Timeline. PDF sample case notes, MindMap and timelines are included.
In the Part 2 Video, Rachel demonstrates in detail how to put a MindMap together from case notes. You’ll be able to see ‘in action’ how to apply all the information from Video 1 and have all your questions answered. PDF’s of both slideshows are included.
and watch this presentation now in your online account.
Remember biochemical individuality folks? That great core underpinning principle of naturopathic & integrative nutrition. We should always keep this in front of mind, when something utterly fabulous for absolutely everyone pops its head up. Like every month or so, in the area of health, correct?
Fasting, in all its forms, is having a lot of time centre-stage right now. What a novel & truly prehistoric notion in this era of food 24/7! I get it and I agree, most of us would do much better by regularly moving out of the top paddock.
BUT…and there has to be a but…or we are no longer treating the individual…
Some of whom, due to specific conditions or biochemical tendencies, do utterly horribly with any sort of prolonged periods between feeds. I already have a hit-list of conditions where fasting and food restriction is a no-no…then I saw a set of labs the other day from a patient who self-initiates regular, 4-6 day fasts during one of said fasts,whose alarming results jumped out in bold, italicized CAPITALS, illuminated itself in neon pink and reminded me to remind you! This patient’s (extended) fasting labs went a little like this… total bilirubin 48 (normally 15 umol/L), bicarbonate 18 (normally 26 mmol/L), corresponding anion gap 20 (normally 12), uric acid 0.62 (normally 0.4 mmol/L). Are you thinking what I am thinking B1?
So here’s my hit-list of ‘fasting = foe’ for – still subject to case by case assessment (of course!! because we treat the individual, right?!)…but
- Any individual with a history of, or currently risk factors for, disordered eating, e.g. orthorexia, bulimia, binge eating disorder, anorexia
- Gilbert’s Syndrome
- Low T3 – thyroid ‘hibernation’
- Anxiety and PTSD
- Drug addiction
- Children, pregnant women, the elderly…of course!
In short: any patient whose condition or biochemistry may be too negatively impacted even in the short term by any of the following: higher cortisol release, significant slowing of phase II detoxification, or radically elevated acidosis, should step away from the fast and towards the fridge! 🙂 🙂
Got any you want to add to this list?
What’s this you say about a hibernating thyroid?
Thyroid hibernation produces a low T3 value coupled with a ‘lowish’ TSH and typically a clinical picture of hypothyroidism. As the practitioner we are faced with the conundrum of how to effectively ‘wake up’ the pituitary which appears to be sleeping on the job. This audio connects up the dots between this type of thyroid dysfunction, dietary patterns, restrictive eating (including a history of eating disorders), carbohydrate intake and disturbed iodine nutrition of the thyroid gland. This pattern is increasingly seen in practice and this audio is a must for anyone working in the area.
Q: If a patient says they can only tolerate 7 foods…how many did they start with?
A: Typically about 20
No, this answer doesn’t come from some complex mathematical formula…it comes from appreciating the low dietary diversity of those eating a Western diet. When we boil down these diets to the number of foods from different biological origins (families) it can be a frighteningly small number.
You see, like most practitioners, I feel utter dread when I encounter the patient who prefaces their diet story with a statement similar to the one above. It speaks to the severity of their symptoms, their attribution of these with food, that by the way is essential for their sustenance and nutritional salvation, and implies an exhaustive pursuit they’ve undertaken probably over years to find ‘safe foods’. And yes, as discussed in my recent talk A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it? – food reactions, as in more than one mechanism of food reaction, often do move in packs and that comes typically back to a poorly functioning gut…BUT…that latter assumption…’they’ve explored and exhausted all foods’ is the one we need to keep in check.
Have they tried daikon? Prickly pear or jambu? Okra? Snake beans? Quail or duck eggs? Kangaroo? Crickets? Etc Etc. Etc.
Are you catching my drift? Because someone has DIY diagnosed a wheat, dairy, soy and, and, and, reaction (correctly or incorrectly) and perceive themselves to react also to most of the limited fruit and veg they can identify in Woolies…doesn’t mean they’ve remotely exhausted the global food supply! Where am I going with this? When patients tell us they’re down to 7 foods they can tolerate – some sensible follow up actions on our behalf may include:
- Check the strength and validity of their level & strength of evidence for their DIY diagnosis
- Think about the linking ‘process’ (more than likely gut) that is the real potential issue (aka don’t eliminate the messenger and do nothing more!)
- Encourage and advise them to shop anywhere other than where they normally do – somewhere that sells fresh produce they don’t recognise at all…like Asian, Indian or Middle Eastern supermarkets and grocers
My tour of A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it? (and the weeks of lit review leading up to this) provided me with enormous food for thought…and this is just one! If you want to hear more about how to find method in the madness of food reactions…you should probably listen in to the whole shebang…goodness knows with the increasing number of patients who present with self-determined food reactions and an increasingly narrow menu of safe foods…practitioners and patients alike need all the help we can get!
Confronted with the possibility of adverse food reactions in an increasing number of our patients can be an overwhelming prospect, in terms of accurately identifying and understanding the faulty mechanism underpinning these aberrant responses to healthy foods. Elimination of culprits in most situations is only a short term reliever, not an appropriate long term solution, so to optimise results we need to know the real mechanism of action. The majority of these, of course stem from the gut, but being able to elucidate exactly which of the many things that can go wrong there, is going wrong and therefore what foods are problematic until we address this, is the key. This 2hr mp4 is all about the bigger picture and helping you find method in the madness that can be the AFR landscape. Along the way we detail the science of where IgG reactions fit into this and it’s a fascinating story that just might be the missing puzzle in your leaky gut patients.
Click here to purchase A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it?
So you’ve gone to all the effort. Be that writing referral letters suggesting some pathology investigations might be warranted or you’ve coached your patients endlessly to get copies of ones done elsewhere so that you may be privy to their findings. Worse still, you’ve directly requested the pathology, with your patient paying out of pocket for the tests. Then the results come in and they look…well wrong. You, as the conscientious clinician, typically do 3 things:
Step 1 Spend hours pouring over & over the labs and back over the case notes
Step 2 Worry about the new differential diagnoses that are now suddenly seemingly a possibility in your patient. It doesn’t look good.
Step 3 Doubt your own pathology reading ability, ‘Hey maybe I just don’t understand these bloods like I thought I did’
But (often)…it’s not you, it’s them.
And that’s what I often explain to practitioners who contact me (step 4). You see sometimes what they’re losing sleep over are what I call, Bad Bloods. Occasionally, the fault of the pathology company…but way way way more often the fault of the patient and the referring practitioner, who has not educated the patient correctly about what to do and not do prior to blood collection for certain tests. I am excited to see how many practitioners are competent with pathology reading these days and building their skills and confidence all the time, that’s why it is so so disheartening for the practitioners (and for me as a mother hen mentor) when they lose time (& sleep) getting to Step 3 when they should be able to spot ‘Bad Bloods’ fast. There are 7 classic give-away patterns.
Will are unlikely to know every quirk of every blood test our patients will ever have done, but knowing what constitutes the ideal time and conditions for the most commonly performed ones, can go a long way to minimising any future Bad Bloods between you and patient as well. This includes things like exercise, alcohol intake, duration fasting and even sexual intimacy…yup!
This month’s Update in Under 30 installment Beware of Bad Bloods teaches you the 7 patterns to watch for and provides you with a great resource stipulating the best collection conditions for the most common blood tests. Don’t let Bad Blood come between you and your patient, the right diagnosis & management or just some well-deserved sleep!
Good practitioners are being led to bad conclusions by some patients’ pathology results. Not because they can’t interpret them or the testing has no merit but because they just don’t know when to discard a set because they are ‘bad’. Occasionally, the fault of the pathology company but much more often the fault of the patient and the referring practitioner, who has not educated the patient correctly about what to do and not do prior to blood collection for certain tests. This recording clearly describes the 7 classic give-away patterns of ‘Bad Bloods’ which will enable you to spot them fast in the future. In addition to this. while we are unlikely to know the idiosyncrasies of very lab our patients will ever have done, knowing the ideal collection times and conditions for the most common ones assists you and your patients to avoid any in the future – handy clinic resource included.
Hear all about it by listening to my latest Update in Under 30: Beware of Bad Bloods.
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.
Virginal skin, as my sister calls it, is on the endangered list. She also predicts that as a result, it will be a highly sort after commodity in the future and I agree but our reasons are a little different. Hers are aesthetic and mine are well, health-based.
I dislike spreading fear in the wellness world, especially around the area of autoimmunity, which is already plagued with podcasting puritans, espousing the notion that people with autoimmune conditions need to give up every single source of joy in their lives and then, and only then, they will be healed
[Silent Scream !!!!!!]
The essential formula for autoimmunity is generally thought to be: genetic susceptibility + environmental trigger = Bingo! i.e. Hashimoto’s or Grave’s or AS or or or…There are already so many candidates, both confirmed and speculated, on the environmental triggers list, from individual nutrient deficiencies, to food groups, from infectious organisms to of course, the big monster under the bed and everywhere else (!), environmental toxins. But wait there’s one more.
“Black inks likewise have been shown to induce production of reactive oxygen species (ROS) such as singlet oxygen or peroxyl radicals, which are free-radicals that can steal electrons from neighboring molecules and damage cell constituents. One study by Regensberger and colleagues (2010) found that in the presence of ultraviolet light, some black inks reduced activity of the energetic powerhouses of the cell, the mitochondria, of human dermal keratinocytes, the type of cell that predominates in the outermost layer of skin”
Recently I was prompted to ask one of my mentors whether tattoo inks contained heavy metals. His reply, “I seriously doubt that heavy metal-free tattoo inks even exist.” Then someone on my team forwarded me this well referenced article that contains the above quote titled, Toxic Chemicals Found in Tattoos: Links to Autoimmune & Inflammatory Diseases. I haven’t had a chance to read their citations and understand the real implications of this very plausible biological threat and I can’t do anything about the skull & crossbones on my back but I can warn my kids, my patients and anyone else with virginal skin to rethink the ink.
It’s summer time for all of us in the southern hemisphere & that means….Slip Slop Slap?!
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 podcast, Should We Rethink High Dose Vitamin D, Rachel outlines the key unresolved vitamin D dilemmas that should encourage us to exercise caution with supplementation and outlines how adequate sun exposure is associated with improved health outcomes independent of the production and action of vitamin D.
Oh no, it’s her again 🙁 I mean the chick in the photostock image not the other ‘her’, me. I know. It’s the end of another mammoth year, you’re tired, worn out, used-up all your brain-power quota (a little projection?) and I can hear you begging for mercy when I start a sentence with…”So you think you know….” followed by, “blah blah blah Iron,” but hear me out.
Correctly identifying & managing iron issues is a bread & butter part of our business, right?
With Iron deficiency affecting an estimated 1 in 5 women and Iron excess almost another 1 in 5 – patients with one form of iron imbalance or another tend to be over-represented in waiting rooms.
Anyone can spot overt iron deficiency anaemia or full-blown haemochromatosis but many health professionals find the ‘in-betweens’ confusing and fail to recognise some key patterns we see over and over again, that spell out clearly your patient’s current relationship-status with this essential mineral. This often results in giving iron when it wasn’t needed and missing it when it was. If you’re imagining someone else, i.e. the person who ordered the Iron Studies for your patient, will step in and accurately interpret the more curly results can I just say D-O-N’-T...they’re often as perplexed or even more so than you. After starting this conversation a year ago with So you think you know how to Treat Iron Deficiency, & its baby sister, So you think know the best Iron Supplements, our (imaginary) switchboard went crazy. While practitioners got the message loud and clear about how to improve the likelihood of treatment success in iron deficient patients, hot on the heels of this came email, after fax, after carrier pigeon, with examples of patients’ Iron Studies, the ‘somewhere in between ones’, accompanied by the equivalent of a dog head tilt…aka ‘I don’t get it’.
And this is to be expected.
What were you taught about reading Iron Studies? Was it made out to be all about ferritin? And TSH is a solid stand-alone marker of thyroid health, right? 😉
Were you introduced to the other essential parameters included in Iron Studies, explained how they contribute to your diagnosis and reveal important details about the patient’s ability to regulate this mineral or not? About when to dose and when to hold your fire?
Nah…I didn’t think so. But it’s up to us, people, to hone our skills in Iron Study interpretation…because individualised nutrition is our ‘thang’ and more than any other nutritional assessment, this collection of markers, actually allows us to go beyond the ‘one size fits all’ model…everyone must have X of this and Z of that in their blood tests…and see each patient’s actual individualised need and relationship with this mineral. In the latest Update in Under 30, I introduce you to 3 key players in iron assessment and the insights each offers become so clear, you’ll be able to read any combination or permutation of iron results that walk through your door. To boot, I’ve included a wizz-bang cheat-sheet of those iron patterns that are frequently seen and rarely recognised, including one totally novel one that I’ve never talked about before…to make your job even easier and put you well and truly ahead of the pack in understanding iron nutrition. It’s Christmas…and as the mantra goes…we can always fit just a little more in at Christmas time, right? 😉
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.
Hear all about it by listening by my latest Update in Under 30: So You Think You Know How To Read Iron Studies? 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.
A few months back I seriously ‘blew over’. Not on an RBT but on a UBT (Urea Breath Test). In spite of it being not the kind of test you want to score top marks for, my result was in the high 2000s, when all I needed was around 800 to confirm, and anything over 50 to be suspicious, that Helicobacter pylori had taken up residence in my stomach lining. I tell you, I knew it when I blew it! 😉 After ingesting the radioactive urea and waiting to blow up my sampling balloon, I felt like I could still fill a room full of balloons with all the gas being produced in my stomach and those balloons, I imagined, would all rise to the ceiling as if full of helium! Yep…I burped all the way home, which was representative of what I’d been experiencing daily for a month beforehand and what lead me to get the test done.
But initially, it wasn’t so clear.
The very first symptom I experienced was a sudden onset of severe tightness around my throat that lasted for minutes but started to happen multiple times in a day. Yep..no one panic. Together with a strange sensation of ‘extreme emptiness’ in my stomach on waking or delayed meals, and then mild nausea both with an empty and full stomach…only some days or weeks later the fabulously-unprecedented-&-socially-adorable-burping started, proper.
So a month or so later, I’ve solved my own mystery. Happy? Not in the least…where the heck have I picked up H.pylori from? Yes…that’s what I said because it had to come from somewhere people…right? I think there is much we have misunderstood about this bacteria with an incredibly long and interesting human history. Animals don’t and can’t carry this bacteria. The evidence suggests that it can’t survive for very long in the environment either (approx 4 days) but that is long enough to get into our food and water and maybe even onto shared chopsticks…just saying (listen in to hear the lowdown on all these and more!) Essentially hoomans are the traffickers, people! In fact one of the things that surprises people the most is the very high prevalence in young children and the clusters of positive tests & identical strains within families…but once you learn a little more about this bacteria…it won’t surprise you at all. (more…)
I was lucky enough to hear Jason Hawrelak’s excellent presentation at the Australian Naturopathic Summit last weekend, titled: A Case of Blastocystis Infection – Or Is It? Timely, highly valuable, immediately usable, provocative education (just how I like it 😉 ) on how perhaps often Blasto is playing the scapegoat for another condition/cause of patients’ GIT symptoms. During this case study, Jason detailed the shonky diagnostic work-up of his current patient by a naturopath 12 years prior…that naturopath was him.
There was so much to love about his telling of this case study and the discourse around it but here are my Top 3 Takes:
- None of us know everything or practice perfectly but rather we do what we do, until we know to do differently…even Jason 😉
- As there are 9 strains of B.hominis found in humans and many of these are in fact benign commensals, even perhaps important ‘apex predators’ for the microbiome, attributing someone’s health problems (digestive or otherwise) to the presence of this parasite should in fact be a diagnosis of exclusion…always asking yourself first, what else could it be?? e.g. coeliac, SIBO, food reactions etc etc
- The cost of being a ‘premature evaluator’, to your patients and to yourself, can be very high…
Too many times we see thyroxine treated patients on the ‘set and forget’ setting. Often, they’re taking the same dose they started on a decade or so ago, in spite of weight changes, ageing of course and new comorbidities. They’ve undergone limited monitoring, with just an annual in-range TSH viewed as confirmation of efficacy. But is it? Many patients’ re-emerging hypothyroid signs and symptoms would suggest not.
A recent Medscape review article of a large study by Gullo et al 2017, identifies another shortcoming in the rudimentary way we ‘replace thyroid hormone’, in all patients but especially in those who’ve had their thyroid removed. (more…)
I’ve had my nose in all the research on Gilbert’s Syndrome again..watch this space…in the interim just thought I’d share this image and a couple of important details I may not have been able to convey when you last heard me talk (very fast!) about this important and common polymorphism:
- While the incidence is approximately 10% of Caucasian population, rates are heavily influenced by ethnic background and the highest rates (up to 1/4) are seen in Middle Eastern populations
- Gone are the days of thinking this condition only effects bilirubin levels and the enzyme responsible for its clearance – more recent research has shown over 3/4 of patients with Gilbert’s Syndrome have multiple SNPs that compromise clusters of enzymes within the glucuronidation pathway – with varying patterns – this goes a good chunk of the way to explaining the variability we see in bilirubin levels and symptom pictures across patients all deemed to have Gilbert’s Syndrome. This also explains why figures of reduced glucuronidation activity vary anywhere between 10% less to 90% less! It depends on your cluster..but the average reduction is around 50%
- UGT enzymes, the ones affected in Gilbert’s, are also expressed all the way down the GIT and constitute important food and drug handling. These UGTs are most active in the small intestines,as you can see above, but may explain why Gilbert’s patients are ‘more sensitive’ to medications than just paracetamol!
- And are you still thinking you need to run an $$$ gene test to confirm your Gilbert’s hunch in a client whose bilirubin sits consistently high normal or high? Think again… here’s a great little diagnostic short-cut that even the Royal College of Pathologists Australasia cites as sufficient evidence to confirm the polymorphism:
In the face of elevated total bilirubin levels and in the absence of liver pathology or increased haemolysis to explain this..”If the diagnosis is uncertain the serum bilirubin fasting level can be measured and should exceed the non-fasting level by >50%.”
Nice. So that means you only need to demonstrate that the patient’s fasting total bilirubin levels go up by at least 50% compared with their fed levels and BINGO you have your diagnosis. Much easier. Oh and this image comes from an interesting paper from Tukey & Strassburg 2001 – but is probably not for the faint-hearted 😉
Stay tuned for more 🙂
Just new to this condition and need a soft place to land with understanding Gilbert’s Syndrome? This previous UU30 is just the thing! Affectionately called Gilbert’s Girls because in particular it details a set of twins with this condition, this short audio explains the basics about this common polymorphism and why we tend to see a lot of patients who have this…even if no one has pointed it out to them yet! You could be the first to provide them with this important understanding about how genetics is impacting their detox pathways, changing their sex hormone handling and perhaps setting them up for both mental health issues and some serious upset guts! Better still, what to do once we have that diagnosis.
Ever feel like you’re chasing your own tail trying to treat & find the source of GIT parasites in some patients?! Well guess what, you just might be!
We’re seeing more & more patients test positive for Dientamoeba fragilis and increasingly patients struggling to eradicate it and prevent relapse. And then there’s Blastocystis hominis affected patients… and then those lucky enough to have both.
Well, while we might have been grouping D.frag together with B.hominis, being the two most common GIT parasites in humans, looking for what they share in common, they are worlds apart (we think!) in terms of how they are transmitted to humans. (more…)