I love a little temporal lobe tap. Especially the kind patients provide. This week mine came from a mentee’s patient who, while presenting with concerns about possible perimenopause, was found to have radical shifts in her thyroid hormones, largely thanks to a dramatic increase in TPO Abs (>1000). The patient’s other presenting complaint was ongoing gastritis (confirmed via scope) and reflux…and that’s when I started to deep-dive into the archaeological archives of my brain…with the…’didn’t I have somewhere in here, in some dark dusty deep recess…a connection between the two?!’
Aha! With the help of a torch [read Google Scholar] the temporal tap bore fruit.
1 in 4 patients with AITD (Hashimoto’s or Graves, you choose!) test positive to Parietal Cell Antibodies
I’ve created (clearly, not-so)SmartArt graphics on powerpoint slides on this exact topic, waxed lyrical about it in my thyroid training packages…but in fact needed a temporal tap to be reminded! And in turn thought, well gosh if this has slipped from my mind, it might just have slipped from yours too! ‘Thyrogastric autoimmunity’ as it’s called, refers to a patient group that exhibit antibodies to both and remember, the antibodies precede the condition in both disorders, so you can have a patient with established AITD, who has zero gastric symptoms but tests positive for the antibody…an important heads-up, as it speaks to significant risk of the subsequent development of gastritis in the following years. This excellent prospective study of AITD patients by Tozzoli and colleagues mapped exactly that! Jump forward just another day or so and…
I’m preparing for our final FiNAl FINAL Q & A on Haematology for our MasterCourse in Comprehensive Diagnostics and I’m wrestling with all the conflicting ‘facts’ about the anaemia that may present alongside hypothyroidism – it has been documented and described as being macrocytic, normocytic and even microcytic… how can it possibly be so diverse I wonder and then 💡
I’m guessing the presence or absence of these parietal cell Abs likely has something to do with it!!
Anyway, it’s getting towards the end of a VeRy loooooooooooooooooooooooooooooong year…thought we could all do with a temporal tap 😉
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The course has over 18 hours of video presentations plus 2 free bonus sessions 1) Accurate Pathology Interpretation Starts Here and 2) Patient Pathology Manager and access to resources and tools within, for your own use.
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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.
No doubt you’ve heard me refer to the thyroid Abs by their nicknames, TRAb is one I mention often, or Thyroid Receptor Antibody, as its mum calls it, when it’s in trouble. And it’s always in trouble! But TRAb is actually the collective name for several flavours of trouble. What these auto-antibodies share in common is the ability to bind the TSH receptors throughout the body. They differ however, in terms of whether, once engaged, they stimulate this receptor (mimicking the action of the real-deal TSH) or they block it, so that the real-deal can’t in fact dock and do its job. The contrasting consequence is clear: stimulating ones drive up thyroid hormone production, while the blocking variety contribute to low thyroid hormone levels – and what was meaningful was each patients (im)balance of the two to produce a net effect. Because yes…a proportion of patients make both.
In Australia, and many other countries, we previously measured TRAb as a sum total and then specified what fraction was each ‘flavour’ but then the ‘flavours went out of favour’!
So for a long time now, TRAb has been measured, undifferentiated, and the assumption is, they’re stimulating…because this is in fact a) more common and b) the most common reason this test would be referred for…a set of TFTs that look suspiciously on the high-side aka Grave’s disease.
But a new era has dawned, with many mainstream laboratories now opting for the more specific assay: Thyroid Stimulating Immunoglobulins (TSI)* over the old TRAb. Fancy schmanzy, I know. Considered more accurate in the detection of autoimmune hyperthyroidism and in this regard, we’re told we’ve made a diagnostic step forward and nothing has been lost. Except the much less common type of antibodies that bind the TSH receptor only to fill it full of gum so it won’t work. That apparently, due to its low incidence and reduced clinical impact is no longer something worth testing. So consider the TSI results for your patients, the new version of your old (drab) TRAb, with similar cut-offs etc. And remember detectable levels of this may be seen in toxic nodules, and acute toxic Hashimoto’s, as well as prodromal and active Grave’s disease.
AND DON’T FORGET
(and yes, I am screaming because it is so easy to forget!!)
Biotin!! Patients on biotin at the time of the test (even as little as 1mg as part of a formula) can produce False Positives for the TSI!!! And give you and your patient the ‘fright of your life’ with a pseudo hyperthyroid set of labs to match!
Need to read more on this because you’re left thinking WTF about the TSI?!@#%^ Check out Mayo Medical Labs (always a good go-to for info on pathology) or this recent review paper 🙂
*Note TSI does not stand for Turbo fuel stratified injection in this scenario!!
Want to learn all the thyroid antibody alphabet??!! Start Here!
Learn the ropes of Thyroid Dysfunction Assessment & Identification, including all the related thyro-nutrition! 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 as easy 1-2-3!…almost!
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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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.
Remember biochemical individuality folks? That great core underpinning principle of naturopathic & integrative nutrition. We should always keep this in front of mind, when something utterly fabulous for absolutely everyone pops its head up. Like every month or so, in the area of health, correct?
Fasting, in all its forms, is having a lot of time centre-stage right now. What a novel & truly prehistoric notion in this era of food 24/7! I get it and I agree, most of us would do much better by regularly moving out of the top paddock.
BUT…and there has to be a but…or we are no longer treating the individual…
Some of whom, due to specific conditions or biochemical tendencies, do utterly horribly with any sort of prolonged periods between feeds. I already have a hit-list of conditions where fasting and food restriction is a no-no…then I saw a set of labs the other day from a patient who self-initiates regular, 4-6 day fasts during one of said fasts,whose alarming results jumped out in bold, italicized CAPITALS, illuminated itself in neon pink and reminded me to remind you! This patient’s (extended) fasting labs went a little like this… total bilirubin 48 (normally 15 umol/L), bicarbonate 18 (normally 26 mmol/L), corresponding anion gap 20 (normally 12), uric acid 0.62 (normally 0.4 mmol/L). Are you thinking what I am thinking B1?
So here’s my hit-list of ‘fasting = foe’ for – still subject to case by case assessment (of course!! because we treat the individual, right?!)…but
- Any individual with a history of, or currently risk factors for, disordered eating, e.g. orthorexia, bulimia, binge eating disorder, anorexia
- Gilbert’s Syndrome
- Low T3 – thyroid ‘hibernation’
- Anxiety and PTSD
- Drug addiction
- Children, pregnant women, the elderly…of course!
In short: any patient whose condition or biochemistry may be too negatively impacted even in the short term by any of the following: higher cortisol release, significant slowing of phase II detoxification, or radically elevated acidosis, should step away from the fast and towards the fridge! 🙂 🙂
Got any you want to add to this list?
What’s this you say about a hibernating thyroid?
Thyroid hibernation produces a low T3 value coupled with a ‘lowish’ TSH and typically a clinical picture of hypothyroidism. As the practitioner we are faced with the conundrum of how to effectively ‘wake up’ the pituitary which appears to be sleeping on the job. This audio connects up the dots between this type of thyroid dysfunction, dietary patterns, restrictive eating (including a history of eating disorders), carbohydrate intake and disturbed iodine nutrition of the thyroid gland. This pattern is increasingly seen in practice and this audio is a must for anyone working in the area.
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.
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…)
They’ve just come from the immunologist, having presented with extensive vitiligo in dad and early stage vitiligo now in their primary school aged son. The immunologist, without running a single blood test, told them, ‘Bad news, you both have autoimmune issues and watch this space because the vitiligo is just the first presentation, there will be more to come’. Slightly unsatisfied with this dead-end conclusion and non-existent management plan, the family then presents at a long established naturopathic clinic to see Anna Sangster, a fabulously sleuth-like detective, who takes her patients’ health very seriously and has the knowledge and skills that make her one of the best at what she does. I can say that because I’ve been mentoring Anna for a long time & she is one of the clueiest practitioners I know.
For example, she knows about the substantial research demonstrating the overlap between thyroid autoimmunity and vitiligo and, in addition to comprehensive case taking, decides some blood tests may provide valuable insight that would help to understand the degree of self-attack from their immune systems, identify if there are in fact already concurrent autoimmune targets and perhaps even provide a clue as to underpinning drivers. Well, look what she found! (more…)
That’s me…always questioning the ‘status quo’ and Iodine is the perfect example! The interview I did on this important subject with Andrew Whitfield-Cook from FxMedicine, covers a lot of key areas of confusion & underscores why it’s so critical all health practitioners get clarity on this topic. ‘It’s just a matter of geography’.
You know, I say to people, we can make vitamins ourselves, we can get all sorts of other organisms including animals, bacteria and plants to make vitamins for us, and then eat those…but minerals…our source of minerals…well it all comes down to the rocks and the soil our food itself is grown or fed on. And iodine is profoundly influenced by these factors. (more…)
“Researchers followed more than 500 women trying to conceive over about five years and found that, overall, those with moderate to severe iodine deficiency had 46% lower odds, per cycle, of becoming pregnant.”
All researchers dream of generating the kind of results that are ground-breaking but sometimes you read about the latest study’s findings and you think, ‘Really, you spent all your time & cleverness for years on this and that’s all you have to show for it!’ Like the study that finally confirmed dog’s can feel empathy (at last thank goodness …phew…cos I had my doubts until they crunched the numbers!)
So too a study published this month on the possibility that iodine deficiency is common in women trying to conceive in developed countries and may be connected to increasing fertility issues.
Stop press! I know…that made you spill your coffee! (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…)
Whenever I talk to practitioners about thyroid health, like I recently did at MINDD, I can guarantee I’m going to get 2 questions:
- Shouldn’t we aim for the high iodine intake of Japanese?
- Can we use the patch test for testing iodine levels in our patients?
I am so glad you asked. The answers are no and no.
I am a nutter for minerals and iodine just won’t go away right now. Too little = a problem, too much = often the same problems. To boot we are faced with radically contrasting views on assessment and dosage and just about everything iodine related. It’s not you – it’s iodine. Trust me it’s a complex little mineral that requires some extra thought and caution. If you imagine the Japanese have no thyroid problems – correct that big myth right now by reading this scientific paper that refers to health problems that result from too much dietary iodine. It also explains that the typical first step in treating hypothyroidism in Japan is to reduce their iodine intake! (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…)
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…)