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.
Let’s play a little word association game:
I say ‘Fibroids’ – you say, ‘Oestrogen’.
I say ‘Cyclic Breast Pain’ and you say, ‘Ouch!’ [because it just slipped out] but then you say, ‘Prolactin’, right? Me too.
Prolactin driven breast pain’s most characteristic form is the premenstrual ‘oh my goodness get these off me!!’ kind, with patients experiencing anything from burning, aching, bruised feelings and acute hypersensitivity to touch, which builds in intensity for days leading up to their bleed. Of course cyclic mastalgia can progress to being full-time mastalgia in women whose breasts start to exhibit structural tissue change in the form of cysts, fibrosis and ultimately fibrocystic breast disease. If you’ve ever experienced even a day of mastalgia it is truly hard to conceive there are so many women (about 50% of premenopausal women!!) living with it daily.
Adding to our concerns about this so-called ‘benign breast disease’ (BBD) is that researchers are now certain it’s a significant risk factor for breast cancer, with women with any form of BBD experiencing at least a doubling of risk of a subsequent breast cancer diagnosis, while those women with proliferative BBD exhibiting a risk of 3.5X that of women without BBD. Castells et al 2015 (more…)
Duck duck GOOSE! Do you know this game? That’s how I’m feeling with oestrogen – high-high-high-LOW!-of late. Likely similar to your experience, the majority of my female clients battle with oestrogen dominance, therefore I get so used to looking for it, expecting it: the high Cu, the profoundly elevated SHBG, maybe a raised ESR. So much so that sometimes the low ones can catch you out, especially of course when it happens in women way way before menopause.
We’re so resolved to hear bad press about oestrogen and to be armed ready to saturate our patients with broccoli extracts of the highest order – do we remember the clinical features and markers of an oestrogen deficit and know what to do with those women who simply don’t have enough? (more…)
Got any patients on Natural Thyroid Extracts (NTE)? Me too…and I am finding it’s on the increase. What’s the deal? What do we need to understand about this form of thyroid replacement therapy to best monitor and manage those patients already on it or contemplating taking it? Does it really offer advantages to all hypothyroid patients or just to a subset of those and how would we recognise these people who might benefit the most?
NTE are marketed as being superior to synthetic thyroxine primarily based on the fact that they provide the patient with some T3 as well as T4 and in addition to that, being extracts of pig thyroid glands, there are other thyroid and iodine based actives e.g. mono and diiodotyrosine, present in the extracts. So in essence this is giving us more iodine and more of the other ingredients we need to make our own thyroid hormones. Based on this, many proponents of NTE say this is a major advantage over synthetic thyroxine replacement because it is more ‘holistic’ and it supports the patient’s gland in its own hormonogenesis. (more…)
That’s the word on integrative medicine street. I had a sense this was coming, not just a tightening of our terminology but also a challenge of the very concept of ‘adrenal burnout’. Hear me out. (more…)
I just want to scream with joy…and then keep on screaming with utter frustration! Last week I presented the culmination of months of work looking into the extraordinary manifold relationships between thyroid health, fertility, pregnancy & post-partum health for mum and bub.
The findings are breathtaking: whether it’s about being able to put thyroid Abs firmly on the ‘Must Screen’ list for preconception care, given their ability to double-quadruple the rate of early miscarriage or their propensity for triggering post-partum thyroiditis in 50% of women who possess them or being able to state emphatically that maternal low iodine (prior to conception as well as during pregnancy) remains the number one risk for the thyroid’s healthy transition to pregnancy. The evidence is overwhelming that we need to pay very close attention to the thyroid. (more…)
Have you still got some thyroid patients that don’t fit any sort of traditional thyroid disease model and are difficult to get results with? Oh yes me too… and watch out…I’ve been spending the last few weeks with my nose firmly embedded in hundreds of articles digging around for more answers. As I am presenting on thyroid conditions for ACNEM in Adelaide March 18-19th, I couldn’t resist going back to the literature to see if by delving a little deeper again I could come up with some more answers to these weird, wacky and hard to treat thyroid presentations that we’re increasingly seeing and guess what…I think I’ve found a few gems. (more…)
Back a few weeks ago I had the pleasure of presenting at the Integria Symposium and the even greater pleasure of listening to some of the fabulous speakers …you see I’ve heard my stuff before! 😉 The ‘Mosaic of Autoimmunity’ was delivered by the very funny and knowledgeable Professor Yehuda Shoenfeld, who reiterated the sequence of events now well recognised to precede and precipitate autoimmunity: genetic susceptibility + endocrine context + environmental trigger –>autoimmunity.
Clinicians know that overwhelmingly women dominate when it comes to autoimmune disease epidemiology and most understand that this is a consequence of oestrogen’s immunostimulatory effects. Professor Shoenfeld, described the female, or E2 dominant, immune system as being ‘super charged’ and that increased rates of autoimmune diseases were a reflection of this. Sometimes practitioners do initially great work with a/immune clients – clearing up the diet & gut, ensuring vitamin D adequacy etc and then get ‘stuck’ or plateau with antibody levels that ‘won’t budge’. Going back and checking the hormonal contribution in the case is often indicated. If the patient has an unhealthy E2 dominance and /or impaired detoxification and clearance of this hormone then working on this aspect often kickstarts the next stage of improvement.
A new thing to me (I know I’m a bit slow sometimes 🙁 ) was his mention of the potential link also with high prolactin (PRL). The literature on this is extensive and hyperprolactinemia (HPRL), even just mild elevations, have been correlated with a very long list of both systemic and organ specific diseases including: (more…)
During mentoring sessions over the last week I’ve been prompted to ask a few practitioners if their patient had any signs, either clinically or in their pathology results, of high oestrogen. Each time it kind of caught the practitioner off guard because their patients weren’t presenting with conditions overtly related to an oestrogen excess and they hadn’t specifically ‘tested’ for this. However, in each instance the information was already there in the case, it was just a matter of knowing what markers to look for.
So some patients scream ‘high oestrogen’ right from the minute they enter the room? But often others present with health problems that don’t necessarily appear related at first glance. Regardless, their condition absolutely could be being compounded by this background imbalance – think thyroid & other autoimmune conditions for example.
There are plenty of patients who don’t have the exaggerated clinical presentation but still have this imbalance as a significant compounder or perpetuating issue in terms of their pathology.
Relax – I am not suggesting salivary hormones or any form of expensive testing all round (!) – in fact what I am saying is before you even consider yet another pay out of pocket test, costing your patient more time and money, we should look to the clues that are already there, in standard blood tests. Amazingly, you can infer a lot not just about the overall oestrogenic load but also pick up some clues as well about where the excess might be coming from.
In this Update Rachel brings together her 10 quick tips on how to recognise either high oestrogen and/or the potential underpinning reason behind the excess, in a range of easily accessible markers. A great refresher and synthesis of ideas on this important aspect of diagnosis and clinical management. This Update in Under 30 is now available to purchase as a download, click here to find out more or if you’re interested in a 12mo subscription click here
We kicked off mentoring this year with some great cases last week. One was a pregnant hyperthyroid client. During the session the wonderful practitioner mentions that the client is using Withania somnifera as required for anxiety.
Insert sound of brakes screeching to a dangerous squealing crash! Here’s a situation where I would give Withania a miss. (more…)