Helping Patients Achieve Their PB

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. 

The latest Update in Under 30 has landed.
You can purchase March’s episode, Outrunning ‘Athlete’s’ Anaemia here.
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!

 

 

Are You Being Gaslighted?

Ever suspect you’re being gaslighted by your patients’ results?  Especially when their CRP result says, ‘nothing to see here’!  But every other piece of information and every one of your senses tell you they’re inflamed and their immune system is up to something!! Me too.  You probably then look at their other results, their ESR or their white cell count searching out something that supports your hunch, but they too can look disappointingly unremarkable. That’s the moment when you wish life was like a televised sports match and you could check the video evidence rather than believe the mere mortal (and clearly blind!!) man in white on the pitch. Well guess, what…you can. 

Albumin

÷

Globulin

As long as you know how to divide one figure by another using a calculator. I’ve found it requires the same digital dexterity as pushing the ‘on’ button’ on my blender…so if you can make a smoothie, you’re sorted! So while almost every lab routinely reports these two as separate parameters that are also routinely in range…I haven’t seen many that actually do the calculation for you and give you the Albumin:Globulin (AGR) on a platter.  Yet this one step maths transforms the mundane into magic and can reveal almost all to you regarding your patient’s level of immune activation, inflammation and oxidative stress, from the largest number and variety of drivers.  That’s why I call it, 📣The Master Inflammatory Marker 👑

When factoring in your patients pathology results is at its best – it makes the invisible suddenly visible to us.  We could have sat and eyeballed that patient all month and never suspected that their Hcy was too high, or they had antiphospholipid antibodies or, or etc.

But the albumin to globulin ratio goes one step further & trumps the other inflammatory markers we’re so familiar with, because it even sees what they can’t! 

And a low AGR (≤1.2) signals just that to you. So when the patient with joint pains, or just a little bit of belly fat or an emerging yet unnamed autoimmune condition presents exasperated saying, ‘but apparently I’m not even inflamed!’…you can let them know you do see it, and it’s just that others weren’t looking in the right place, then  get busy rolling your sleeves up to move those markers!  That’s right, a low AGR is a clear call to action for practitioners engaged in risk minimisation, prevention and for working towards best outcomes in established disease and  monitoring a patient’s AGR is a series of clear sign-posts about whether you’re leading them in the right direction or not.  There’s a lot more to say on this this third umpire & ripper of a ratio – about kids, the contraceptive pill, confounders, a role in cognitive impairment prevention and what optimal might look like but hey…the cricket’s back on…gotta go 😂

Patients’ labs lie, not often, but sometimes and the inflammatory markers performed routinely like CRP and ESR have been known to tell a few.  Like when everything about a case screams inflammation but both of those say there’s none there.  Why do they miss it?…well basically it’s not their lot.  CRP and ESR have specific signals they only respond to and therefore reflect only certain immune reactions and at specific stages of that response.  But there’s a nifty little calculation you can perform with all of your patients labs and suddenly see the immune activation, inflammation and oxidative stress that was lurking beneath.  It’s called the albumin to globulin ratio and it’s going to change your understanding of what’s going on in your clients and your ability to monitor the efficacy of your management.
The latest Update in Under 30 has landed.
You can purchase February’s episode, Your Master Inflammatory Marker here.
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.

 

 

Are You A Sucker For ‘Secret Herbs & Spices’?!

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.

 

Getting More Bang From Your Patients’ BP

While we may not all be pathology proficient, overwhelmingly we do take or record blood pressure, right?  It’s such an easy but essential inroad to understand something more about patients’ cardiovascular system, and indeed their nervous system, when prone to the so-called ‘white-coat syndrome’. And it never fails to amaze me how the ‘numbers’ are so abstract and cryptic to the average patient. They’ll tell you things about previous BP readings like, ‘it’s normally fine I think, you know, like a 40 and maybe a 160, does that sound right?  Ahhhhh…not quite. But of course these two numbers are not cryptic to us.  And like all patient results, rather than our response being a simple, binary, GOOD/BAD one, we should be asking ourselves: What does this actually mean?  What is it telling me?

Consequently, I’ve been interested in the blood pressure battle going on in America.  Having traditionally placed the greater significance on a patient’s systolic pressure with comparatively little attention paid to the diastole, there have been lots of ruffled feathers following the redefined cut off for hypertension, which now flags any diastolic pressure over 80mmHg.

An unhealthy high systole of course is undeniably the most meaningful in terms of short term cardiovascular consequences and we are in no doubt that lowering this is critical for risk reduction BUT a new longitudinal study of over 13,000 UK citizens just published in the Journal of the American Heart Association, suggests that perhaps patients’ high or high-normal diastole in mid-life was in fact the earliest warning sign of poor cardiovascular health in the future.  This comprehensive study followed participants for 8.5 years and essentially found that a rise in diastole in their mid-life (ahem, that’s our 40-50s 🙄) predicted the progression of arterial stiffness more strongly than any other measure. Additionally, while diastolic blood pressure tends to decrease as we move into our 6th decade and beyond, those individuals in mid-life with higher DBP –> more arterial stiffness were same people in whom their DBP drops the most significantly later in life.  What a guise!!  So, in a nutshell this substantial study teaches us:

“Prevention of arterial stiffening and the associated transition to a late-life hypertensive phenotype of falling diastolic BP is likely to depend on effective control of midlife diastolic
BP in particular.”

Fortunately, the people we see are more in their mid- than late-life, which this new understanding speaks directly to, presenting the greatest window of opportunity for prevention in terms of modifiable risks for chronic disease, especially CVD, dementia and renal disease which arterial stiffness is such a major risk for. This extraordinary separate longitudinal study following individuals born in 1946 also suggests mid-life BP(both systole & diastole) is the major modifiable factor for later brain volume, integrity and function. Maybe we need to keep our eyes on that lower figure and our ears more closely peeled to hear what in fact it’s telling us 😊

Have you also heard what’s totally NEW! for 2020 – Our Patient Pathology Manager!!

Increasingly our patients are coming armed with lab results and this cumulative data helps us to clearly see their ‘norms’ (as opposed to textbook ones) and therefore be alert to any changes. However, results from different labs at different times, and even the same lab, are unlikely to be presented side by side for easy comparison.  They certainly don’t come with all the important information about what was happening for that patient at each time point – important details pertaining to the blood collection itself (fasting, inflamed etc) which can profoundly alter results or the broader context: menstruating, breastfeeding, losing weight, on meds and supplements. The Patient Pathology Manager retains all the results for you, including the critical contextual elements, helping you to keep more accurate records to make the most correct interpretation. It also assists you to monitor changes related to various interventions. 

Previously, this tool has only ever been available to clinicians who participate in Group Mentoring but due to frequent requests for access, we thought it was time to share this great tool for those wanting a foot up with some better systems in their practice.

‘Copper Excess’ In A Child?!….Really??

Copper deficiency happens in kids, so does copper toxicity and both are serious concerns, but do we know when to accurately call either?  First, we have to know ‘normal’. If we know what normal Serum Copper values look like in children, then we can easily spot those falling below or above this, right? That’s the first hurdle we tend to knock over and break a toe on!  Being a mineral whose levels vary widely in soil from country to country, globally, the differences in reference ranges are breathtaking & absurd. Add to that, that copper is a key mineral in kids, driving huge demand for it during key periods of development, so the range for pre-schoolers isn’t the same as the primary or high schoolers – not that your lab is flagging that. Unhelpful? Yes.  Dangerous, even? Potentially.

To diagnose ‘Copper Excess’ in a child is a big call to make.

One, because most practitioners are unaware just how much Copper a child really needs at each age & two, high copper is often a messenger for something else going on and then three,  the primary objective based on this diagnosis becomes to lower their Copper but we could be either shooting the messenger or missing the mark all together…right?

Copper excess does happen but not nearly as often as practitioners believe it does.  And in kids, the fall-out from such misdiagnosis is bigger. And missing a Copper deficiency? (because we’re not as well-trained to recognise it and because Copper has been sadly demonised)  Likely to have myriad negative impacts at this vulnerable age…almost none of which generate symptoms or a distinct clinical picture e.g. secondary iron deficiency, low neutrophils without necessarily compromised immunity.  But what about the holy grail get-out of jail adjective: ‘relative’. You know, ‘this is at least a Copper excess relative to their Zinc?’

Well, to form this opinion you’re likely calculating the Zn:Cu ratio and applying an ideal adult value of 1:1 but show me the primary evidence that supports this for kids…anywhere?  The Zn & Cu relationship shifts as we move through life-stages and in fact Copper is supposed to dominate through a lot of our childhood so…ummmmm…no.

HTMA Copper side-steps all of this?..double no.

I used to make the same mistake re Zn:Cu, I may have even taught you this?!🤦‍♀️  But as so often happens, a week spent in all the original scientific data and I’ve emerged a changed practitioner! Having been part of perpetuating this problematic premise in the past, I am determined to get the correct message out there to as many practitioners as possible.  So help me spread the word on Copper in Kids – by telling others that this mineral is so critical to kids compared with adults, they will often have higher levels than ‘us’ and that until you’ve applied the right age-appropriate reference range and ruled out confounders you can’t possibly make a call on Copper. I mean, we kind of knew this all along, with healthy pregnancy Copper values being exponentially higher being a giant clue. Turns out kids’ ‘Copper Age’ extends way beyond the womb.

Copper, as a kingpin in angiogenesis, brain & bone building & iron regulation is a critical mineral during paediatric development. So much so, the kind of blood levels we see in a primary schooler might cause alarm if we saw them in an adult. So too their Zn:Cu.  But higher blood Copper and more Copper than Zinc are not just healthy but perhaps necessary during certain paediatric periods.  This recording redefines normal, low and high with a great clinical desktop tool to help you better interpret these labs, as well as reviewing the top causes and consequences of both types of Copper imbalance in kids. 
The latest Update in Under 30 has landed. You can purchase January’s episode, Copper in Kids here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
-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.

 

In Need Of A Better System?

When you start doing this with your patients’ pathology results, you know your client records are turning into a big hot mess and more importantly your ability to see the wood for the trees is seriously under threat!  Private labs don’t play nicely with one another and if your patient has  been to more than 1 pathology provider you lose an enormous amount of their potential value, blindsiding you to their patterns, & the most accurate interpretations.  I have a saying when it comes to getting the most out of pathology in your practice: Cumulative Data is King & Context is Queen.

Increasingly we’re in in the fortunate position of patients taking responsibility for their health and coming armed with lab results – this cumulative data helps us to clearly see their ‘norms’ (as opposed to textbook ones) and therefore also any noteworthy variations. 

But even in this luxurious position of multiple results across a variety of time points & stages of their life – our ability to derive the greatest understanding from these is greatly stunted if we don’t have the context.

For example: if he was ‘cross-fit-keto-crazy’ at the time, if she’d stopped being pregnant & started breastfeeding, if in light of a major shift in thyroid hormone results, they were on biotin, or iodine, or changed their dose of thyroxine or were drinking straight from the udder of a soybean (!) these all seem like fairly critical contextual details to be across, right?   All of these factors: diet, acute health context, medications, reproductive state, even season… impact the lab results we expect to see and therefore should be captured and considered to form the most accurate interpretation.  But how do we pull it all together in a systematic way that SAVES us time and SAVES your sanity and can keep growing alongside your ever-growing patient notes?  Cue the: RAN Patient Pathology Manager!

Systems for sorting through huge amounts of patient information help us make sense of what we’re seeing…and help us spot the source & solutions.

Systematised patient timelines for a better overview of the chronology of any case, the RAN Patient Pathology Manager not only holds all the data for you, helping you keep more accurate records & make the most  correct interpretation from these,  but also maps and monitors changes related to various interventions.  Lastly there’s my old BFF, Mindmaps and Timelines not ancient torture tools of clinical supervisors (!) but rather what distinguishes us as integrative, enabling us a to work up a case in a truly holistic fashion instead of: symptom–> solution, symptom –> solution. These are the 3 key clinic systems I really wished I’d had from the get-go…so, me and my team created them!  We’ve re-crafted them with each year and this year our RAN Patient Pathology Manager has undergone a significant evolutionary leap and it comes with a comprehensive video explaining how to easily get the most out of this resource for all your patients.  We always share these tools with all our mentees but we’re frequently asked how others can access them so this year we thought those of you out there just wanting a foot up with some better systems might like to get your hands on them too!  Maybe this is one very practical part of the ‘new year new you’?

 

Add this essential tool to your clinical toolkit by clicking here to purchase RAN Patient Pathology Manager
and watch this presentation now in your online account.

…& Stop Giving Them Manganese!

 

It’s like that split-second you close the door and realise you’ve locked the car with the keys still inside, or the whole reason you rang someone pops back into your head just after you put the phone down.  Yes after the opportunity to draw breath over the break I went, ‘Doh! …I forgot to mention manganese!!’ So some of you may already know I am not a super fan of manganese.  Well actually, that’s not accurate, I am perhaps just less of a fan than the people who are formulating a lot of our supplements! A place for everything and everything in its place. While this saying is completely foreign to my office, my house, my domestics and the rest of my life, it is a mantra I abide by with all micronutrients Having enough of each micronutrient is good, having optimal (if we know what that is, which often we don’t) is wonderful but an excess is bad news.

And as I’ve spoken to before, with our increasing use of multi-nutritional formulas and the frequent inclusion of significant amounts Mn somewhere towards the bottom of those long ingredient lists…we very much run this risk with patients who are taking multiple supplements, at which point Manganese can become a serious meddler.

There’s a short list of patients for whom I am particularly conservative regarding their Manganese exposure and near the top of that list is those with Gilbert’s Syndrome.  Do you get my ‘Doh!’ moment now?  Because at the end of last year I released the Gilbert’s Syndrome: New Goals & Good News Update in Under 30…only to realise after ‘I’d put the phone down’ that I’d left this important one out of the dos and don’ts of managing these patients. So why am I saying no to chronic routine use of Manganese in those with GS? Well here’s the deal…

There are very few micronutrients that rely on bile to leave the body but of course Manganese is one of these – so in cases of reduced bile flow, altered bile composition etc the capacity to excrete and therefore regulate levels of this trace mineral become compromised and a lower toxicity threshold ensues.  Same goes for Copper as well of course, but we’re not including this in as large of number of supplements.

That’s why we need to be clear to cap the Mn for these patients as part of being across the cumulative subtotals of all micronutrients.  While there is no established Upper Tolerable Limit (UL) set for Mn, adequate intake has been determined as 5mg/d for an adult. I agree, this is probably inadequate for some but I’ve seem individual patient prescriptions with cumulative Mn totals over 20 and 30mg per day! In spite of being generally regarded as having a low acute toxicity profile there is increasing research documenting Mn as a meddler when it comes to thyroid function in particular.  So who else is on my watch and wait list for Mn excess?  You’ve probably got some ideas…

The latest Update in Under 30 has landed: Gilbert’s – New Goals and Good News and my team has gone all out in producing a brilliant desktop reference to go with this recording that aids better understanding and clear treatment aims for your GS patients.

You can purchase Gilbert’s: New Goals & Good News here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
**But if you’re just joining us & this important conversation now,
ideally get the basics and backstory first and purchase all 3 key episodes in
‘A Guide to Gilbert’s Package’

Ironing Out Some Old Misunderstandings

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.

How Low Can You Go…With Cortisol?

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! 

TODAY!

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: admin@rachelarthur.com.au

Are We Missing A Different Kind of ‘Hyper’ Child?

 

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.

Will Hair Testing Nail Your Patient’s Nickel Problem?

How might your patients’ Nickel exposure wreak havoc with their health?  What might that look like?  It may be lurking behind labels like IBS, non-coeliac gluten sensitivity, contact dermatitis of unknown origin,(with or without alopecia) or even CFS. “Then how does Nickel, which can’t even claim fame as a heavy metal, manage such diverse detrimental effects’? I hear you ask. In 3 easy steps 1) exposure…we’re all exposed, Ni is ubiquitous in our soil, our food, our environment so don’t bother trying to run from it 2) it hits our gut where our microbiome and intestinal lining may constitute the first fallen soldiers 3) exposure to our immune system can lead to sensitisation, and the subsequent development of a hypersensitivity response to each following exposure …and at worst precipitation of an autoimmune process.  You got all that?

So therein lies the big question: how can we help patients whose health problems stem from Noxious Nickel? We could run and hide…from our jewellery, our mobile phones, dental interventions, most food (!), but we’d be wasting our time…we’re surrounded!

As always, we go back to the science and we find others have done the work for us. Not google though.  Google ‘low nickel diet’ and like ‘low oxalate diet’, you’re likely to get a whole heap of hogwash!  How reassuring then that there is a validated dietary scoring tool to assist patients lower their dietary Nickel and that numerous other studies can show us the way in terms of use of mineral balancing strategies, probiotics etc.  These resources plus more are all included in the latest Update in Under 30: Noxious Nickel part 2 as well as a discussion of what assessments we have available to confirm nickel as the culprit.  But here’s something for free: hair nickel concentration (HTMA) is not by any means diagnostic in these cases, because it’s not necessarily about an issue of overall higher exposure it’s about an aberrant immune response to Nickel at any level.  Just saying.  You know me….not scared of controversy in the pursuit of improved patient outcomes. Ok a bit scared… 😁

In this instalment it’s time to get down and dirty and detailed about how to best identify those patients who may have Nickel related pathology and presentations.  We cover testing options, typical systems affected from GIT to autoimmunity and the most extreme form: Systemic Nickel Allergy Syndrome. We outline Nickel management strategies in a world full of it (!) and we include several key papers for additional resources and support. How noxious is Nickel for some of your patients?  Well by the end of this you’ll know and better still, know what to do once that’s established.
Hear all about it by listening to my latest Update in Under 30:
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.

Are You Dancing With The ‘Devil’s…Copper’?

 

KupfernickelIt’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.

Is A Diagnosis Always Helpful?

 

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.

 

 

 

Are You Being Foxed By An Ox…alate Result?

Ok here’s some tough Tuesday talk..not all tests are valid.  Tougher still…not all of the mainstream nor the functional pathology ones.  I am talking across the board here. Each and every pathology parameter requires good knowledge about its strengths. limitations and, one of my absolute favourite nemeses, confounders.  “How on earth am I supposed to learn all that and everything else I have to know too?!!” I hear you scream at your screen. Btw keep yourself nice if you’re in public while you’re reading this 😉 

But rather than imagining you need to have this level of knowledge for all tests, I would suggest you set yourself a hit list of the ones you rely on most, either in terms of frequency or in terms of the degree to which they direct your decisions about patient care…can I mention (ahem) Iron studies here perhaps for us all…but maybe you have a specialist area so you use a particular investigation routinely or at least frequently…

CDSAs? Breath tests for SIBO?  Oxalates?  

May I please then politely suggest that you get to know these inside and out? Not based purely on the information and assistance that the test provider provides you..but you scrutinise them independently.  Top to bottom.   Because that’s your business, right? And your diagnoses and treatment decisions are pivoting on these results. Jason Hawrelak gave us all some great examples, including his informal experiment of sending the same stool sample to multiple labs.  Don’t know about this and his findings?? If you’re in the business of ordering stool tests, you need to.  I am doing this all the time with numerous pathology markers because diagnostics is my passion (alright, obsession)…and recently I put Oxalate Assessment to the test and oh boy! 

Here’s something for free:

If you are measuring urinary oxalates to diagnose oxalate overload in your patients and you, 1) are using a lab that does not preserve the urine as you collect it, using acidified containers or providing additional preservatives for take home testing kits….you are wasting your patients money and you are likely getting a lot of false positives, i.e. the result infers the patient has a problem when they don’t!!

And 2) if you are simply  following the labs reference ranges for what ‘healthy’ urinary oxalates look like – you’re wasting your patients money again and likely getting false negatives – a failure to show a problem that is actually there! If you’re hunting oxalates…please ensure you have a current effective hunter’s licence…by getting up to speed fast  regarding accurate investigation of this.  Oh yes…it’s tough-talkin’-Tuesday and I’ve come out firing…watch out this may become a regular feature 🤷‍♀️

Update in Under 30: Oxalate Overload – Assessment and Management

Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues.  We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update.

When the Body Attacks the Mind

 

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.

Milk Madness – Is it a thing?

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.

Oxalate Overload? The next steps…

When patients present feeling worse every time they DIY a Green Detox, as the practitioner, you’re likely to be sniffing around reduced oxalate tolerance as a differential. Rightly so.  But what about the patient with joint pains and disproportionate fatigue who has baffled their rheumatologist, or the one suffering vulvodynia that baffles everyone, or irritable bladder symptoms, or….and they all eat an exemplary colourful high plant food diet, with their only self-confessed sin…darker than dark chocolate between every mouthful? Who doesn’t? While you may have a hunch, given the goodness of those foods, we should check these out objectively rather than unnecessarily restrict or limit someone’s food choices for the rest of their natural life! If dietary oxalate overload is now on your radar for these patients you need to move to the next step. Assessment. 

Spot or 24hr urine collection or plasma assay or OATS testing or imaging or joint aspirates? So many choices but which one has the greatest validity depending on your patient’s presentation? Ok how about the most general all-rounder that is truly an option in the real world? – always helpful;)   Yep, 24hr urine collection…agreed.

Ok, next step.

You need to wrap around that waist of yours one seriously heavy tool belt for accurate interpretation of their results. That’s right…those random ol’ reference ranges need a serious rethink! How much? Well, given the reference ranges every lab will give you for urinary oxalates typically fail to pick up up to 1/3 of patients with oxalate overload high enough to produce oxalate kidney stones…I think you get the picture.  I feel your trepidation now but can hear you  pensively ask anyway…next step? Management.  

Just google oxalate-rich foods, print out the list for your patient and tell them never to have these (or joy, laughter, sex or a healthy microbiome) ever again.

Not.

The ‘low oxalate lists’ will lead you astray and the ‘high oxalate foods’ should not be tossed away!   The research has found greater therapeutic benefits from different dietary approaches, some nutritional supplements and most importantly targeted treatment of the cause…which is all about the…go on, try and say it without screaming…the GUT!!!!!!!!!!!!!!

Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues.  We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update

 

Hear all about it by listening to my latest Update in Under 30: 
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.

 

Lots to be Said for Boring Basics

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.

 

It’s Not Rocket (Dental) Science!

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. 

Thank You (ACNEM), Next!

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
https://www.acnem.org/events/training

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

 

 

 

You Might Want to Write This Number Down

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.

X 0.67

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!

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