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…)
Howdy hard working praccies 🙂 well I received a very interesting email this week from someone asking me if I thought her urinary iodine result was accurate or if, as I have written about previously (https://rachelarthur.com.au/concentrating-concentration-getting-urinary-iodine-right/), it needed to be corrected for the creatinine content of her urine. Her raw iodine result was 24ug/L which suggests severe iodine deficiency. Her referring doctor however had also asked for creatinine and applied the creatinine correction formula I have previously described:
Iodine (mcg) ÷ Creatinine (mmol) X 8.85 = Corrected Iodine – which changed her result to 265 mcg/gCR which suggests she is NOT iodine deficient at all
She then asked another doctor to review the result who had told her 24ug/L was correct in the first place as ‘pathology companies automatically correct for the concentration of the urine’. Naturally the individual found the difference in opinions and results absolutely striking and ultimately disconcerting so she thought she’d ask me.
It was good to get this email because it made me go and check my facts, get in touch with all the major mainstream pathology companies we deal with and ask their labs ‘Do you or do you not automatically correct for creatinine when you report urinary iodine results?’ I was worried I had given you guys some bad advice 🙁 …here’s what I found out: (more…)
No matter how long I am in practise there is always a group of patients for whom ‘vaginal thrush’ is a major problem. Most of us have some fabulous tricks up our sleeves to help resolve these issues & reduce their susceptibility – intravaginal lactulose is one of mine thanks to Jason Hawrelak. And then you come across those clients who vigilantly do every thing you ask them to and yet you fail to completely resolve the issue. Doh!
One of the most important things to do with all clients presenting with ‘thrush’ sooner rather than later is send them STAT (!) for a vaginal swab.
Not only does this clarify if it is in fact actually thrush (2/3 of self-diagnosed women get it wrong according to research!) but better again it names the actual culprit. It may come as a surprise but not all vulvovaginitis is due to Candida albicans – increasingly they are the result of other Candida species and this is something you absolutely need to know.
During a recent mentoring session, a practitioner wanted to better understand why she had a group of patients whose thrush seemed so resistant to her usually successful treatment. Here’s my initial response in a nutshell… (more…)
We had a great case in one of our graduate mentoring sessions the other day (thanks Kate 😉 ) , about a 40 something mum of 3 who reported to have cyclical mood and depression. Further investigation of the case, however, revealed that some of the key characteristics of the mood disorder were actually anger, aggression, irritability, hyperactivity, vivid nightmares etc. This particularly came to light with her responses to a mood survey that the practitioner had asked her to complete. I think validated tools like this (esp. DASS), when used appropriately, can give us enormous insight – often revealing things we might not have thought to ask about or that the client might not have voluntarily offered up, particularly if they are not socially accepted or attractive qualities.
If you practice anything like me, then Vitex is an absolute reflex response (think the very funny reflex paper ad – that’s me in my clinic!) & godsend for most cyclical mood issues. However, apart from the fact that this woman’s key period of mood aggravation, although clearly related to her menstrual cycle, was day 5-14 rather than during the late luteal phase, there was another stand out reason for me why I definitely wouldn’t use Vitex. (more…)
So…a 40 something female walks into your clinic with depression & anxiety…sounds common enough right? But here’s the twist: she’s already seen another practitioner who ran a range of investigations revealing she has pyrroles, high copper levels & is homozygous for the C677T MTHFR mutation. Her medical history includes significant use of Ecstasy and a partial thyroidectomy due to nodules & she has persistently high TSH. But wait there’s more!…The first practitioner upon discovering all of this put the patient on 12 different products which included zinc, B6, evening primrose oil, vitamin D, thyroid support etc etc. And guess what…the patient feels worse!
Frequently our patients are just as complex as this case & sometimes our attempts to narrow the treatment focus through thorough investigation instead leaves us feeling we now have even more things we need to deal with than before! Feeling overwhelmed?? Often! At risk of completely overwhelming the client as well? Definitely! And a reflex to throw your whole dispensary at a client never ends well. (more…)