[Ahem] Ok let me explain…Several catch-cries from Australian ads have earnt themselves a lifelong place in my head and heart, taking up space where something more important should be, no doubt, but does anyone remember this SPC canned fruit (REALLY showing my age now!!) one, where the little boy chases the grape around the bowl and declares it a, ‘Slippery Little Sucker!’? Ok so this little boy is every one of us when we’re trying to ‘capture someone’s cortisol’ and just like the boy we will eventually achieve a ‘result’ – get a ‘number’ but what in fact does this mean in relation to your patient’s HPA axis, stress perception, responsivity, recovery etc etc?
Recently I was presented with 2 cortisol results for a patient taken within the same 24hrs – her blood am result was above range, while her 24hr urine flagged under-functioning of her HPA axis generally.
Both were accurate.
Had I have only have seen one, I would have formed the wrong opinion and only gleaned part of her overall HPA story. Every different type of cortisol capture – from different mediums: blood, saliva & urine – to different collection conditions: time of day, fasting V fed, specific stressor exposure etc answers a different question about our patient’s HPA axis. So to use any form of cortisol assessment well we need to start with 2 understandings: 1) it is a slippery little sucker indeed and no one test can answer all our questions – or as Miller & colleagues more eloquently put it, “Remember, all models are wrong; the practical question is, how wrong do they have to be to not to be useful” and 2) be clear about the most important question you have about your patient you are trying to answer and that will make your choice of test (& timing & & &) patent. But do you know enough about cortisol regulation to be clear about the ‘sweet spot’ of each test?
The Cortisol Awakening Response has understandably attracted the bulk of the research focus over the last decade and accordingly has risen in popularity in practice & while it remains a very valuable way to answer certain questions about patients, our understanding of its limitations continue to grow. For example there is a disconnect between CAR & diurnal cortisol secretion – so in essence your CAR can look woke but your ‘Slope’ may be broke! If you’re a fan of this method, make sure you catch up on the CAR-Expert Consensus Guidelines by Stalder et al and if you’d like to get clear about which test and when, when it comes to all the key options for Cortisol Capture..
then let’s dive in together with my latest Update in Under 30 instalment
Cortisol – Have You Been Caught Out?
I have! And just recently a stark contrast between the results from 2 different methods of cortisol capture in the same patient illustrated just how likely this is. How do we ‘capture’ something so ‘dynamic’ and interpret anything of substance from a ‘static’ assessment technique? But rather than throw up our hands and throw out the whole attempt to measure cortisol, we can improve the rigor, reliability and real-world meaningfulness of our patients’ results by refining our timing of tests, choosing the medium wisely & manipulating test conditions to answer specific questions about their HPA function. Great desktop reference included!
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The average woman & her dog (& likely every other member of her household, be they furred or otherwise), can tell you that sudden changes in sex hormones can
undermine, derange, psychopathise, impact her mind and mood. Hey, for me most days reverse parking is my mild super power, the envy of all, but on day 26 of my menstrual cycle, I can struggle with a ‘nose-to-kerb’! But if we are quick to attribute this to the fluctuating sex hormones produced by our ovaries, alone, we’d be making a mistake. A portion of these peripheral steroids do cross the BBB and act in our brain, so changes to these levels during any kind of transition: follicular to luteal, pregnant to post-partum, menstruating to menopausal, early adulthood to andropause, will be ‘felt’ but the sex (hormones) we have on our brains at any given time, are far more abundant, potent and complex than this, thanks to the brain’s ability to make its own.
So in fact, the amount of sex hormones active in the brain represent an intersection between peripheral and central steroidogenesis.
These Neurosteroids, made ‘on site’, are as much produced in response to our mood, our neurobiology, our psychological and environmental stress, to help us navigate these, as they are the creators of mood itself.
Yes, these particular sex hormones, due to their actions in our brain, belong to that growing list of CNS celebrities: the Non-Classical Neuromodulators. Which, for the otherwise neurotransmitter-centric & obsessed among us (that’s everyone), makes mental health and illness much more complex than ‘serotonin deficiency’ or ‘glutamate excess’ and a whole lot more real. We now need to consider other entities like: ‘suboptimal LDLs’, 5 alpha reductase over or under-expression & ‘xs inhibitory tone via progesterone’.
The ‘sex on the brain’ of any patient therefore is impacted by both their Endocrine (ovaries, testes, adrenals) and Synaptocrine (neural) contributions – and these demonstrate some shared dependence (for cholesterol & healthy mitochondria etc) and independence.
We all know the depressing stats in support of the ‘ovarian withdrawal hypothesis’ and the risk to women’s mental health with each reproductive transition, and also in andropause in men, but the time has come to now deepen our understanding and to recognise we can have an imbalance of ‘sex’ on the brain – regardless of the ‘balance’ we might see in the periphery and put our thinking caps on about the options we have to address steroidogenesis either side of the blood brain barrier.
When it comes to a modern take on how sex hormones impact both the structure & function of our CNS, we need to blend the ‘old’ with the ‘new’. The ‘old’ tells us, production of sex hormones is in the gonads and action at a distant target anywhere else in the body, including our brain. And the ‘new’ is in the form of the ‘Synaptocrine’ – where production of these sex steroids is actually within neural tissue itself and their immediate actions occur close-by, in the synpase and at the post-synaptic neuronal membrane. These two contributive pathways show some shared dependence but also independence from one another and the balance of both has now been recognised to be integral to the overall health of the nervous system.
You can purchase Sex (Hormones) On The Brain here.
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We’ve been talking all about the dangers of excess fuel in our blood recently. You know, just like nature…too much fuel underfoot creates a fire hazard. So too in the bloods of our patients. The key fuels I am referring to, of course, are lipids (triglycerides & cholesterol) and glucose. Our tissues need ready access to both but Balanced Blood Supply & Mastery of Management is key.
In terms of excesses, lipids play the long-game…wreaking havoc over a long period primarily via their vulnerability to form peroxides, which in turn create a chain of oxidative stress and depletes our antioxidant artillery.
In contrast, even outside of insulin dependent diabetes, for the rest of our patients, glucose plays a fast and furious game, being a highly reactive substance capable of causing both glycation and oxidation. We describe even high-normal levels of glucose as something akin to the ‘Bull in the China Shop’, disrupting the function of the endothelial linings and damaging a variety of plasma proteins (not just haemoglobin) that float within them. But do we have a way to routinely measure the level of damage occurring in our non-diabetic but somewhat glucose intolerant patients? Sure! Just check the C-CCTV footage!
The extra C stands for ‘Carb’ and yes we can potentially check the Carb-Closed-Circuit-TV ‘tape’ in every patient.
It’s called HbA1c and measuring this provides us with an opportunity to review their personal ‘tape’ of the last 2-3 months for evidence of excesses.
Helpful, hey. But we actually have so many great tools through regular routine labs at our disposal to understand the glucose disposal or dys-disposal(!) at play in our patients! You’ve just got to know where to look (urate, triglycerides, insulin, HOMA-IR etc) and what each piece of information is telling you. We’ve had SO MUCH FUN with this particular topic in the MasterCourse this month…or is that just me 🙄 No, I know it was, because our live session chatbox was full of ‘blown brain emojis’!! 🤯🤯🤯 I can’t wait to share this course content far and wide at the end of year with those of you that missed out on attending live.
In the meantime if you want to learn more about glycation which is the new inflammation, out there in research-land, you know…the source of all evil including ageing itself(!!) then check this out…
Glycation is a normal physiological process that, just like inflammation and oxidative stress, can get out of hand, contributing to disease processes. Currently there is an explosion of correlational research suggesting relationships between higher levels of Advanced Glycation End-products (AGE) in individuals who have fertility problems, psychiatric conditions, osteoporosis, premature skin ageing, cancer…you name it! New research implicates diet heavily in the determination of individual’s levels of AGE but there is devil in the detail – there are ‘4 Ps’ of dietary AGE contribution that we need to be mindful of when we are giving dietary advice and trying to move patients towards wellness. This Update in Under 30 recording: Are You Feeling Your ‘AGE’ will open the lid on the ‘new black’ in chronic health & ageing.
how the time just flies when you’re chasing answers from private pathology companies! As Brisbane based naturopath, Sandi Cooper, can attest to having recently been down the seemingly eternal email trail with a pathology company trying to ascertain if their urinary iodine result accounts for the concentration of the urine sample (via the iodine:creatinine) or doesn’t….because of course it can make the world 🌎 of difference. Like clarifying that someone who appears to have very little iodine in their urine, actually has a lot or vice versa! I wrote about this back when I was a mere ‘babe blogger’, more than 5 years ago. After recently reading this historical document, Sandi has been practising due diligence and checking with her providers whether they have already corrected for creatinine..or whether she needs to herself and she shared that multi-departmental epic email endurance event thread with me. The short answer? They used to and now they don’t. Why? Oh…formatting issues or something 🙄
But just in case you do want the ‘short answer’ regarding your particular pathology provider…without emailing enigmas…the answer is, in fact, in front of you & it’s Super Short!
mcg/g Vs mcg/L
If your patient’s urinary iodine result (random or 24hr) is reported using the units on the left, sometimes actually written mcg/grCR, then BiNGo! The pathology provider has done the creatinine correction for you. If they only report the urinary iodine results using the units on the right…it’s time for some maths to avoid misinterpretation. No one panic, the formula is easy: Iodine (mcg) ÷ Creatinine (mmol) X 8.85 = Corrected Iodine. So don’t lose time sending endless emails like poor Sandy or placing countless calls, like poor Nina on my team…who has to pursue pathology providers on an almost daily basis for answers to our zillions of sensible questions!! Just check the units! You’re welcome everyone 😉 oh thank you Sandi for chasing this again and sorry about needing to chase this again! 😳
And if all of this is nEWs to yOU, you might want to review what you thought you knew, about Comprehensive Thyroid Assessment too!
We can never rest when it comes to learning more about the individual nuances of our patients thyroid pictures! In this 90min recording, Rachel covers the key thyroid parameters both functional & autoimmune (TSH, T4, T3, rT3, TPO, TgAbs, TRAB). As well as the most accurate methods of assessing relevant thyroid nutrients: iodine & selenium & a genuinely game-changing insight on interpretation of these . Finally she pulls all the individual parameters together to illustrate common patterns of thyroid imbalance – making it almost as easy 1-2-3! Well, hey..it’s the thyroid…a fickle fellow.
I used to all the time. Especially when I noticed the Niagara-falls-sized gap between the doses I was using compared with my mainstream medico mates. I thought, hang on, for a patient with a baseline blood level of 40nmol/L, they’re recommending <1000 IU per day, but I’m thinking 5000 IU…which one of us is wrong? Then again, we might both be right!
The sexily simple formula as cited by Aussie researchers is: for every 1,000 IU of vitamin D a patient takes a day, their blood level is likely to rise approx. 17 nmol/L over 2 months, at which point it plateaus. So the medicos’ 1,000 IU supplement would bring our patient’s blood level up to 57 nmol/L which, as far as the medico might be concerned, is ‘job done’ 👍👏
My dose would be viewed as excessive but clearly I am aiming for a different set of goals (optimal rather than simple prevention of deficiency)…oh and I insist on follow up testing to know when we’ve made it!!
I encourage my patients to get their Vitamin D retested 2 months into treatment to confirm 1) they have responded and 2) their response is loosely within this predicted performance. And how many times is it not? Often. Which got me to readjust the formula I use to something more akin to: for every 10 nmol I want their blood levels to rise, I will need to increase their intake by a 1,000 IU. Now am I just making big sweeping inferences from empirical experiences of a few (hundred) patients without additional backing….well so what if I was...this is a branch of the EBM family tree! But no! I have also actually read enough studies clearly documenting the individualistic response to vitamin D, as a consequence of different adiposity levels, genes, magnesium status etc. to know that, while I am very grateful to have any kind of formula to start my thinking from…I treat individuals and goshdangit#@! they keep insisting on individualised medicine!
The whole practise of identifying a deficiency, ‘treating it’ and yet never following up with repeat labs to confirm that you actually have…BLOWS MY MIND🤯
That’s not EBM, let’s face it. Not even a distant demented cousin who has fallen from the dizzying heights of that family tree.
The one lesson I’ve learned, more than any other over 20 years in nutritional medicine, is that the more questions we ask and the more we challenge ‘established truths’, the more we uncover something much more personalised and potent about each and every nutrient …and now as the days continue to shorten into smaller and smaller slithers of sunlight between ‘bed-ends’, this is probably also a good time to ask ourselves…
Should We Rethink High Dose Vitamin D?
Vitamin D deficiency has been associated with a long list of major health conditions: from autoimmunity to mental health & almost everything in between. This has lead to many of us recommending high dose vitamin D supplementation for a large proportion of our patients but do we understand everything we need to to be certain of the merits and safety of this? In this provocative episode Rachel outlines the key unresolved vitamin D dilemmas that should encourage us to exercise caution and outlines how adequate sun exposure is associated with improved health outcomes independent of the production & action of vitamin D.
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When a teenage girl presents seeking her first oral contraceptive pill (OCP) script, what information is she privy to that enables her to make an informed decision? Read the insert inside the box? Please. Which 50 year old, let alone 15 year old does that? Forget it! What might her doctor tell her? Perhaps about clotting risk, as part of their determination of the suitability of this form of contraception for her but is there any discussion about the potential for adverse mood effects? A recent study of over 1,000 teenage girls followed over more than a decade adds to other evidence that suggests this should be flagged as a consideration prior to the prescription being written.
Most integrative health practitioners not only know about the potential negative impact on mood from OCP use in women but we’ve observed firsthand the havoc it has wreaked in some teenage girls’ and women’s lives.
A very experienced practitioner I know says, ‘if I am hearing mood instability and then I see a significantly elevated serum copper and or cortisol in these girls that’s when I just say to have to say to them, you know I don’t think this is the best contraception for you!’
This latest study did not find higher rates of depression across all OCP users in this group of 16-25 year olds but when they looked at this at different ages they found its use increased depression scores and was associated specifically with more crying, eating problems and hypersomnia. The discussion around the enhanced vulnerability at this younger age compared with older girls centres on the relative immaturity of their CNS. But wait, I hear you critical thinking clinicians ask, perhaps those teenage girls had more depressive features prior to starting the OCP. Good thinking 99! And the answer is…maybe…but the relationship goes both ways: from the related Medscape Continuing Medical Educational Activity
“For 16-year-old girls, the association was weakened after adjusting for depressive symptoms before use of OCPs, but the findings remained significant. This suggests that the relationship between OCP use and depressive symptoms could be bidirectional…For instance, 16-year-old OCP users were more sexually active and had more stressful events, as well as more menstruation-related pain and acne, than their counterparts in the nonuser group. Analyses showed that all these factors weakened the association, although none diminished it.”
The commentary surrounding this latest study is essentially 1) this is not the first study to find an association and others have been more able to demonstrate that COCP use predated the mood disorder in those affected and 2) those exhibiting higher depressive scores did not actually score strongly for anhedonia or sadness which are the most typical features in adult depression – so perhaps we are missing some of these negatively impacted young women. Awareness regarding reproductive psychology is rapidly growing and in Australia we are fortunate to have emerging hubs to seek help and specialist advice in this area, such as the important work of Professor Jayashri Kulkarni and colleagues out of the Women’s Mental Health Clinic. I’ve referred patients, both when a patient’s mental health appears to be caused or aggravated by use of hormonal agents but which they can’t not use for various reasons and for those small number of women in whom I feel hormonal management may in fact offer a psychiatric solution. So again I am asking, while we know & mainstream medicine increasingly knows about this association…who’s telling these young women?
How many of your clients are on a combination OCP? Do you know the full extent of the physiological impact as a result and are you able to identify to key pathology indicators of the size of that impact?
We’re all aware that in theory OCP use correlates with a range of elevated risks but in reality many females will make the decision that the pros, in terms of contraception or control of acne etc., outweigh the cons. What if we could provide more individualised advice by looking to their pathology results and identifying and quantifying specific danger signs for each individual? This approach enables us to better support patients who chose this form of contraception and to accurately identify those that should be be encouraged to find other safer options more biochemically suited to them. Learn more here.
Assessing Adrenals can be hit and miss, especially given that even more so than other labs, timing is everything. That’s why endocrinologists typically won’t look at anything less than a 24hr urine collection. If the total output is deemed to be high = Cushing’s and if it’s low = Addison’s. Sounds simple right? But to say only values outside of this reference range flag a problem might just be a case of throwing the baby out with the bathwater (or urine in this case!). Especially given it has been established that humans frequently fail at correct & complete 24hr urine collection! Alternatively we can use saliva or blood assays and capture the cortisol at any given time point, comparing that to expectations based on diurnal rhythm – but again, how are the reference ranges for these ascertained and is there such as thing as low normal. high normal results for cortisol, that actually warrant follow up investigation? I’m so glad you asked.
I see a number of patients who present with possible indications of flagging adrenals: from some distinguishing, but far from definitive features, in the clinical picture, to secondary lab markers. However, when they ‘limp’ over the line with their morning blood cortisol result I am often left talking to myself in an echo chamber about the need for more follow up.
But with the RCPA a.m. reference range of 200-650 nmol/L (Some seriously wide goalposts!) and some labs even going down to 150 with their minimum acceptable level for morning cortisol…are we right to still flag hypocortisolism (for any reason) as a differential in patients with low normal results?
Well Medscape yet again delivered Christmas 🤶 early last week with the largest study to date of blood cortisol, that has narrowed what’s ‘normal’ significantly…at least in terms of how low you can go before warranting further investigation. In this study they tested blood cortisol in the morning and afternoon, in over 1200 individuals presenting at an endocrinology clinic to determine in real world terms how low is too low (and associated with an increased likelihood of genuine adrenal insufficiency). They then gave this new ‘minimum cortisol’ a bit of test-run in 2 other large cohorts of patients to check it really did work as an effective cut off and wham bang…we now have a fully validated bare minimum… and guess what…it’s 275 nmol/L in the morning and 250 nmol/L in the afternoon!
Let’s be clear, their cut-off has what’s called a low ‘positive predictive value’ – which means most people (approx 2/3) with cortisol under this cut-off, upon further investigation (typically the ACTH stimulation test) will be found to be fine. BUT the point of this study was to ensure we don’t miss patients with adrenal problems just because they have ‘within range’ cortisol…and this new cut-off delivers on that.
This is big helpful news actually. Previously with patients who had am cortisol between 150- 275 we tended to find ourselves in ‘no man’s land’ – unable to provide enough of an argument about why adrenal insufficiency should still be on the differential list but unable to abandon that suspicion entirely. Thanks Medscape! Now if all the labs, RCPA and the referring physicians can just read this study and shift their goal posts…🙄
Our Group Mentoring 2020 Doors are just…about…to…close!
So if you love labs (or want to learn to love them more), desire to be a better diagnostic detective than you already are and want truly independent mentoring in a collegiate and structured environment for next year and you haven’t applied yet…best shove your foot to hold that door open right now! We offer a range of different levels & types of special interest groups: from New Graduates & the Mental Health Primer group (for those wanting to upskill and focus on this area), from rotating case presentations in our regular groups which are a mix of funky similarly skilled clinicians, to our pure GP group…take our pick! But get in quick by emailing us right this very second: firstname.lastname@example.org
What’s the most common thyroid disease you’re seeing in practice? Nope, try again. I’m serious. There would be very few of us who’d get this right without cheating. It’s nodules. Current figures suggest 1/2 of all us middle-agers have them and by the time we’re 80 that’s risen to 90%! There’s a school of thought that says these figures have jumped purely because of increased rates of thyroid imaging and we should stop sticking our nose in places it doesn’t belong. Just because they are there doesn’t mean we need to know about them or that they are causing trouble. All this is true and yet there is a percentage of patients for whom these nodules are a whole lot of trouble, in fact, that’s why they’re coming to see you…they (& possibly you!) just don’t know it yet.
Nodules, outside of radiation exposure, have always been primarily viewed as a nutritional deficiency disease: Iodine. While this was always a bit one-dimensional (poor selenium…when will you ever get your due?) it’s an explanation that no longer fits as well as it once did because even in populations who have addressed iodine deficiency, the incidence of nodules continues to rise.
So, what now?
New nutritional drivers have been identified but rather than being about our deficiencies they speak to our nutritional excesses. And while iodine is not totally out of a job here, some people of course are still experiencing long-term suboptimal iodine which can trigger nodule development, we now need to question if there is any therapeutic role for iodine once the nodules are established. Well the answer is both ‘yes, maybe’ and ‘absolutely not’. The determinant being whether we’re dealing with Hot or Cold. Unfortunately most patients and therefore their practitioners can’t tell the difference. But it is the presence or absence of a hot nodule that radically changes what complementary medicines you can and can’t use and what an effective treatment plan looks like.
I’ve seen a lot of thyroid nodule cases pop up in mentoring this year and it’s been a great learning opportunity for everyone to get comfortable with clues in both patients’ presentation & their pathology. While iodine deficiency no longer ‘fits’ like it did, nutritional medicine should arguably remain the primary approach to their management and the new research gives even more credence to this and identifies a far greater range of dietary and supplemental tools.
Thyroid nodules are going to explain a surprising number of our subclinical (hypo and hyper) thyroid patients and we already have a dispensary full of powerful interventions but we need to start by familiarising ourselves with their story: their why (they happen), their what (this means for patients) and their how (on earth are we going to address these effectively) Knowing your Hot from your Cold…is step one.
An increasing number of our patients have thyroid concerns but unbeknown to many of us the most likely explanation of all is thyroid nodules, whose incidence is on the rise globally.The development of nodules has always been primarily viewed as a nutritional disease. Traditionally attributed to chronic iodine deficiency but recently novel nutritional causes have emerged . Benign nodules come in 2 flavours: hot and cold and while patients can present with a mixture, it is the presence or absence of a hot nodule that radically changes what complementary medicines you can and can’t use and what an effective treatment plan looks like. The pointers, as is often the case, are there for us in the patient’s presentation and pathology, so knowing the difference is no longer a guessing game. This UU30 comes with a great visual clinical resource and includes key papers on the nutritional management of nodules.
You can purchase Are You Running Hot and Cold on Thyroid Nodules here.
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I had to say to a mentee just yesterday, “You’re going to see the topic for the Update in Under 30 this month and think it’s inspired by your patient but it was actually about the 3 other cases I’d seen this month, before yours!” Yep…I’m talking about thyroid nodules, which happen to be hot (pardon the pun) right now. But they’re not always hot, right? I mean, they are always a good topic for discussion because so many of our clients thyroid issues are due to these but nodules come in 2 flavours: hot and cold. And knowing the difference is about as important as knowing your left from your right 🤲
“Oh Iodine the panacea of all things thyroid (tongue firmly in cheek) – can you fix nodules as well?” chorus the masses
Honest (salt of the earth!) Iodine Replies, “No & in fact I may make some nodules worse!”
Sorry for the re-enactment of this little local theatre piece in my head…it’s been a big week. Hence the marionette…ah yes it’s all becoming clear now 🙄 But it seems this isn’t common knowledge because a mentee presented a case this week of a 39 year old female who has confirmed multiple thyroid nodules that had prior to seeing her, seen another practitioner who put her on high dose iodine with the reassurance “there’s nothing wrong with your gland that iodine can’t fix”..or something to that effect. Oh boy 🤨
“Tell us! Tell us what happened next!” the chorus chants
Well it looks like as a result of the iodine, her cold nodules just might have switched to hot…that’s bad news all round I am afraid 🙁 But if we all knew our nodule nutrition better, this wouldn’t happen.
Next week our October UU30 release becomes available: Can you tell you tell your Hot from your Cold in Thyroid Nodules?
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This week’s wonder-full paper and light-bulb discovery was prompted by a 34 year old woman with a history of Depo Provera injections over several years to control unruly menstrual bleeding and pain. She was subsequently diagnosed at 28 with osteoporosis. That’s not a mispelling…not -penia, -porosis. Now I may be a bit slower than some on the ol’ synthetic hormone fallout front but when it was pointed out that this is a known possible side effect of this synthetic progestin (even features in the consumer brochure), which is used for a range of indications in both pre and post-menopausal women, I did a double-take. What kind of progesterone replacement impacts your bone health negatively and how? And therein the real trouble started.
So fixated are we (myself included) on the evils of oestrogen, I think we’ve failed to notice the wolf in sheep’s clothing that can be synthetic progestins for some patients. Not just in general terms of concern regarding all synthetic hormones but as a result specifically of their interaction with glucocorticoid receptors (GR). This excellent paper reviews this aspect of the 2 most commonly used ones: medroxyprogesterone acetate (MPA) and norethisterone enanthate.
The bottom-line? MPA (which is Depo provera) is a significant GR agonist. That means it’s behaving like cortisol producing a degree of immune suppression and constituting yet another mechanism, in addition to the low oestrogen state it induces, by which negative bone effects may be mediated. This is not a mild or minor action according to this and other research. This is likely to have significant implications for some women, including this 34 year old female. Some women see reversal of this demineralisation following cessation, but not all and the younger your first exposure, the higher the likelihood it won’t correct. This woman had other osteoporotic risk factors, sure, but never enough on their own to produce such severity so young. Mind. Blown.🎆 Or is that just me?
While none of us are likely to be advocating for replacement sex hormones without very careful consideration, this has really helped me to change channels off my oestrogen obsession and become alert to the potential for broader effects from synthetic progestins. MPA…you’re firmly on my radar now in a whole new way.
As always, our patients teach us the most and thanks to Amanda Mullemeister for bringing hers to our recent mentoring session. The learning is never one-directional and I am so privileged to share in these discoveries with all of my mentees, every week. I just wanted to share some light from this particular light-bulb 💡
How To Uncover Unhealthy Bones Earlier
If you’ve heard Rachel speak ever (!) you probably know she’s on a mission to stop the late diagnosis of osteoporosis in patients and as part of this reminds us that this is a condition that develops over a lifetime not overnight – so waiting until women are 65yrs and men are 70yrs (which is the standard recommended age for BMD screening) seems a little remiss in terms of identifying our opportunity for preventative medicine. Are there earlier warning signs that we are ignoring or specific tests more sensitive and accessible than DXA scans that we could be ordering to better monitor patients who are at higher risk of bone demineralisation? The answers are of course, yes and yes! This Update in Under 30 outlines the clinical tools we should be using to uncover unhealthy bones earlier in our patients, how to implement them, their limitations and their strengths.
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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.
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.
Tonic. Homeostatic modulator. These terms and concepts, which have a long tradition in herbal medicine (and let’s be clear, were considered yet another example of the wishy-washiness of the modality) are being appropriated by some areas of mainstream medicine right now. Cheer up ‘leaky gut’, you’re no longer alone! And arguably misappropriated by the public’s very ‘lay’ interpretation of the science on medicinal cannabis and its subsequent elevation to panacea, of late.
“So many of my patients are telling me they’re taking Cannabis now, just as a tonic”, says yet another practitioner to me recently, “No, not for pain, they’re young and fit but they take it because it’s a homeostatic regulator!!”
The capacity to maintain homeostasis, and particularly in the face of adversity or imbalance, is a sign of the vitality of the individual, according to what I remember from naturopathic philosophy (and have truly taken on and observed firsthand)…so just back up there a tad and explain to me how this one herb proposes to do this for everyone on a one-size-fits-all-fashion? As confessed in an earlier communication, I am a cannabis convert. But only in the sense of appreciating the niche areas where it is likely to offer true therapeutic benefits. I still have the words of warning from the brilliant Professor Michael Lintzeris, the Director of the Drug & Alcohol Services, South East Sydney Local Health District; Conjoint Professor, Division of Addiction Medicine etc., ringing in my ears, pleading with health practitioners to not ‘fall’ for cannabis in the way we have previously ‘fallen’ (so far and landed so badly) for the panaceas of the past: opiates and benzodiazepines. Most notable major omission for me, in an otherwise rigorous scientific debate of late, is any discussion about its potential for impacting fertility.
I’ve been aware of the potential negative effect on male fertility, in particular, for over a decade and while we undoubtedly need more targeted research on this topic to reach a consensus, the evidence base to date points to lower LH +/- testosterone and impaired sperm quality and motility. Certainly not perhaps what tonic-seeking patients know they’re signing up for.
There is in fact evidence to suggest ‘sperm under the influence’…’lose their way’ and are less effective at finding and fertilising the egg. Sorry but the image always makes me chuckle…stoned sperm. ‘Hey, dude where’s my egg?!’ style. But it’s not funny when impaired fertility is a problem affecting so many these days, and we still are guilty of over-focusing on ‘her’ and under-assessing ‘him’…and lo and behold it could be his chronic cannabis use to blame. We had a case recently, years of unprotected sex, daily cannabis, no baby, no dots connected. We may think this is a handy incidental contraceptive for young men sitting on couches with cones (one mum recently said as much to me) but for the rest…?
Getting Men’s Hormones Right
As practitioners we should know as much about investigating and treating male hormone imbalances as we do female ones, yet this is often not the case. While we are increasingly aware of everyone’s exposure to lifestyle & environmental endocrine disruptors and the fragility of the HPO axis, we sometimes fail to recognise that the reproductive health of our male patients is equally under threat. This is clearly demonstrated by generally diminishing levels of testosterone amongst men and increasingly early onset of andropause. These issues then become barriers to achieving success in other health areas with your clients, mood, metabolism, fertility and beyond. Learn more here
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Did you and all your patients survive Spring? Have you had a chance to restock the shelves with all the big-gun-Quercetin-products for the next allergy onslaught…or maybe for patients presenting with other conditions that respond well to this, like leaky gut, asthma, MCAS, Grave’s disease? Either way…can I ask you a Quiet Quercetin Question…how high do you go?
I ask this because I know myself to be pretty heavy-handed at times, especially in those severely affected by traditional allergies..and the results are so impressive for patients and practitioners alike, it’s easy to perhaps get very enthusiastic with this approach, with doses sneaking higher and higher… if a little is so good then a lot must be great!
“Severe eczema and allergic asthma – [Insert preferred big-gun-Quercetin-product] 2 three times a day – STAT!”
And we use it across all patients, right? I love it in kids, teens and adults, men and women. So I kind of stopped dead in my tracks when a colleague recently said…”I do the same…buckets of Quercetin especially over hayfever season but Rach, what about it’s phyto-oestrogenic effects? Should we be worried?” Ah…yup…that’s right…being a flavanoid…it has them. Now let’s be clear about one thing, unlike some practitioners I am NOT, I repeat, NOT against phytoestrogens nor even (ahem) soy 😉 but the question was great because it got me thinking…at high-end supplement doses we are producing levels in the body 100s if not 1000s of times higher than a fruit and vegetable rich diet ever can….is it time we knew a little bit more about what Quercetin does at this level, or is suspected of doing and not just the benefits. Therefore we can be more informed about who we should not be so generous or so long-term with our big Quercetin prescriptions?
So I started busying myself in the literature and it turns out THERE IS A LOT OF LITERATURE!
[Note to said colleague who asked me question, you owe me some sleep] But at least I got an answer!
If you want a bit of DIY drilling then this Andes et al paper is an excellent overview of quercetin supplementation safety concerns…but it doesn’t cover everything. We need to talk. We need to talk about that dang estrogen aspect but it’s bigger than that – you see Quercetin doesn’t just engage with oestrogen receptors like a ‘normal’ phytoestrogen…it messes with levels of this hormone via several other paths…and where does that lead us…? Listen in to the latest UU30 Querctin – Are We Pushing the Limits? and you’ll know exactly our destination. This is important for the Quercetin Queens (both male and female) among us…and that’s like…everyone…right? 🙂
Quercetin has become an absolute go-to treatment for many practitioners faced with patients affected with allergies and high histamine. It is in this context, that often we find ourselves using large amounts over long periods. Supplemental quercetin exhibits a 5-20 fold higher bioavailability than its dietary counterpart, therefore increasing body levels beyond what a diet could ever achieve. This introduces more potent novel actions: anti-thyroid, pro-oestrogenic, detoxification disrupting…are we pushing the limits of desirable effects and introducing some undesirable ones and who should we be most conservative in?
Hear all about it by listening by my latest Update in Under 30: Quercetin – Are We Pushing the Limits?
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.
Never say never, right. Back in my old uni teaching days, I scorned the very notion of treating someone with ‘actual melatonin’. Always in favour of upstream approaches over downstream, I was keen instead to give patients the ‘ingredients & cofactors’ so they could whip the right amount up themselves. Well fast forward another decade in clinical experience, and research too, and while I refuse to give in with many other ‘replacement remedies’, melatonin, has snuck well and truly into my list of treatment considerations for some very specific presentations such as silent reflux, treatment refractory GORD and Barrett’s oesophagus, buoyed by some amazing clinical successes. So much so…that in fact I’ve embraced this replacement approach, whose results in this setting especially, can’t be replicated by treating with ingredients and cofactors. Turns out of course I am not alone – melatonin has won a lot of fans over the last decade.
A recent Australian article from 6 minutes revealed a significant increase in GPs prescribing melatonin for sleeping issues in children and then of course, there is its substantial use in cancer and typically at mega-doses that will make your toes curl.
But always in the back of my mind is the old me. Whispering things like, ‘ but melatonin isn’t a nutrient, nor a herb, so it’s not naturopathic’ – hence we can’t even prescribe it, needing to refer patients to others for access and yet more pressing, ‘what do we really know about the full implications of replacing such a potent and ubiquitous neurotransmitter?’ I know. This old me, she’s annoying, right.
But she’s also important.
So absolutely perfect timing then to hear about a homegrown (2 Aussie Naturopaths in fact) systematic review on the adverse effects & safety of melatonin which is full of important and surprising info and I think ….everyone…single…one…of…us needs to read it:
“While this review reveals a high degree of safety for melatonin with few adverse events that cannot be easily avoided or managed in most populations, it also reveals lack of clarity regarding melatonin’s relationship to endocrine processes, and its effect on hypertensive patients and potential drug interactions in this population.”
But the devil is in the detail.
So here’s a newsflash for you – 4 human studies found melatonin had negative effects on key aspects of reproduction, like sperm counts and ovulation and not at mega-doses my friends, no…at 2mg/d over several months. We shouldn’t be surprised, right, melatonin is critical to fertility cycles in all other animals…but how many health professionals know this, or not just know it…but make our recommendations with this in mind? Other studies reported fascinating impacts on insulin sensitivity (5mg) and amazingly, (or not being the king of all things circadian), opposing effects depending on the time of administration. Then there’s the drug interaction with anti-hypertensives…a negative one, I must add. No information still unfortunately about the impact of long-term replacement on our own endogenous production. Anyway…enough spoilers… READ THE ARTICLE. This hasn’t wiped melatonin off my list of potential recommendations all together but it has given me some serious food for thought and much greater clarity about in whom this suggestion should be off the menu.
‘Melatonin – Misunderstandings and Mistakes’ – this important 2017 clinical update about what we are getting right and wrong with Melatonin answers in particular, one of the most common sources of fascination & frustration for clinicians, the reasons behind the Melatonin non-responder. We’ve all encountered patients who have taken Melatonin for sleep problems and reported no benefit, or initially responded and then lost efficacy quickly, or even patients who experienced insomnia after taking. What does this tell you about your patient and what should you do to resolve this and better still, prevent it? This UU30 from 2017 reveals all!
So we already know that thyroid problems can start in utero, right…but a recent Medscape review (the fountain of thyroid information that I frequently drinketh from 😉 ) on Hypothyroidism in childhood taught me a couple of big things I hadn’t known before!
The diagnostic criteria for subclinical hypothyroidism are raised TSH levels in combination with a normal concentration of free serum thyroxine (FT4) but because there are some differences between accepted ranges in TSH assays, high-risk groups should be screened, especially babies with malformations, whose mum received steroid treatment during pregnancy or in the neonatal period, or who had existing thyroid dysfunction, TFTs (or at the least TSH as part of what’s called the Neonatal Screening test) should be repeated 2 weeks later. But now comes the couple of big light-bulb moments: the incidence of eutopic thyroid in twin births is nearly double compared with singletons! As you know, I’m a mother of twins and I’m guessing at 18yrs old now (and multiple peachy TFTs 😉 ) the horse has well and truly bolted for my two but geez…I had no idea of the dramatic increase in risk. And it keeps going…monozygotic twins very commonly show a delayed TSH rise and those numbers are even more prominent in multiple births. The other not-so-fun-fact is the discovery that subclinical hypothyroidism in IVF babies is approx. 10% which is noteworthy considering none were observed in the control group.
This obviously left me thinking “W.H.Y?” And of course…the first place my head goes with the latter…is iodine.
Could this phenomenon in IVF babies be due ultimately to undiagnosed or poorly managed SCH in mum or even simpler still, just basic iodine deficiency, presenting as infertility?!
The reasons behind our increasing rates of thyroid dysfunction across the life-stages are multifactorial (and don’t get me started on the very real contribution of EDCs!) and how, in spite of iodine adequacy being the first thing on the checklist for thyroid health, so many health professionals ignore this, at their patients’ peril… But now at least we know that patients with IVF babies, twins, and preterm bub, who are currently not included in the prioritised screening groups should be…and of course we should keep asking the questions, “what are the mechanisms behind this, why is it so?”
So if this has made you even more curious about the incredible butterflied-shaped gland and you’d like to go for a stroll on the vast plains of “thyroidisms” you can click on this link Thyroid Assessment in Kids and Teenagers and get completely “thyroided” up. There is always more research to come our way so keep your eyes and ears peeled.
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…)
The words together with the horror on her face made me feel instantly nauseous. I’d been internally debating for months now if I was simply imagining things and intellectualising about how this just might be the case… observing myself looking in the mirror more often, getting closer to the mirror, brushing my hair more often, cleaning the brush more frequently…in psychology it’s called something like confirmatory bias…ah yes just enough psych knowledge to be a danger to myself!
But louder than the chronic self-analysis and attempts at reassurance was the voice that said, ‘You’re losing your hair like an old woman. You’re not even menopausal. You eat fabulous food and have too much energy for your own good but you’re starting to look like you’re ill’. The horror. I felt instantly like a fraud. (more…)
Just because most of us have been on holidays doesn’t mean the thyroid knowledge wagon has stopped or even slowed! Always amazed at what we continue to discover about the complex working of this amazing gland and how its health impacts so much of the rest of the body and of course our babies’ bodies! So I thought I’d give you a quick recap of an important study published while you were at the beach/in the bush/in bed ;)…
- A Finnish prospective cohort study of over 3000 pregnancies by Heikkinnen et al has revealed that at 16yo, offspring from these pregnancies, had a 1.56 increased rate of unhealthy weight and a 2.5 greater likelihood of meeting criteria for metabolic syndrome, if their mothers were thyroperoxidase antibody (TPO) positive during their first trimester
- TPO antibodies affect up to 20% of pregnancies but in this study they defined ‘TPO positive’ as those women with levels ≥ 167.7 IU/mL (the 95th centile in this sample)
- What adds to the noteworthiness of this news is that:
- More than half (55%) of the TPO positive mothers were classified as euthyroid during their pregnancy, suggesting that the effect was not driven by maternal hormone concentrations
- The offspring of mothers with actual thyroid dysfunction did not show any statistically significantly greater risk of cardiometabolic issues
- The offspring of hyperthyroid mothers in fact demonstrated significantly better insulin sensitivity at 16yo than children of euthyroid mothers
- Thyroglobulin Abs over the 95th centile (≥ 47.7 IU/mL) did not correlate with any increase in cardiometabolic risks for their children
When we consider the substantial evidence of poorer maternal cardiometabolic outcomes for women who are hypothyroid during pregnancy – it would seem that the abnormal thyroid hormones are most impacting for mum but in fact the TPO Abs the most detrimental for bub! (more…)
Another young female presents in my clinic with a newly diagnosed thyroid cancer and has been recommended urgent thyroidectomy. Her story is increasingly common. If you’re not seeing it in your clinic, you will, because thyroid cancer, and almost exclusively papillary thyroid carcinoma (the form my patient and most young patients have), is dramatically increasing. Since the 1970s there has been a 67% increase in the incidence in women and a 48% increase in men documented in 5 continents (Peterson et al 2012). Australia, though less up to date with its data collection, found a similar increase between 1982-1997 (Burgess 2002). The question begging to be answered is why.
Increased screening and more effective detection of smaller tumours was the going theory for years. New research rejects this absolutely and concludes instead this is a ‘true increase in occurrence’. Increased radiation exposure? Mutation studies say no. Many researchers are pointing to is a ‘new environmental chemical and/or dietary factor’ and EDCs (Endocrine Disrupting Chemicals) that target the thyroid such as perchlorates, phthalates, parabens and phenols are the likely suspects. And, more than likely, with iodine deficiency to explain the increased susceptibility to these EDCs.
But wait there’s more. These ‘new goitrogens’ aren’t only implicated in thyroid cancer, a large number of human studies confirm the higher your urinary metabolites of these, the lower your thyroid function. More worryingly is that they might be doing this ‘without a trace’. With myriad impacts at the receptor level, altered hormone excretion rates, impaired peripheral conversion etc. the data to date suggest these patients TFT results might only look ‘slightly low’ or even ‘normal’ but the reality is they are suffering hypothyroidism. Sound familiar?
There is a HUGE body of scientific evidence we can pull from to understand the role of EDCs in thyroid problems in our patients, how to maximise prevention and minimise impact – even when your patient, like mine, is perhaps already in the full grip of the consequences. I’ve read all the papers and summarised them in this 30min recording: Hypothyroid without a trace – the role of EDCs.
Have you got patients with hypothyroid symptoms but normal results? Or results that suggest the HPT axis just seems to be broken? Could it be the result of a combination of Endocrine Disrupting Chemicals (EDCs)? How do you assess for these ‘new goitrogens’, which act more potently and more insidiously, inducing hypothyroidism ‘without a trace’. How do you maximise prevention for all of your clients and the most at risk sub-populations or minimise impact for those already in the full grip of their consequences.
This latest Update in Under 30 audio comes with 3 key related scientific articles and a bonus larger powerpoint presentation that Rachel presented at the ASLM 2017 conference.