Ever suspect you’re being gaslighted by your patients’ results? Especially when their CRP result says, ‘nothing to see here’! But every other piece of information and every one of your senses tell you they’re inflamed and their immune system is up to something!! Me too. You probably then look at their other results, their ESR or their white cell count searching out something that supports your hunch, but they too can look disappointingly unremarkable. That’s the moment when you wish life was like a televised sports match and you could check the video evidence rather than believe the mere mortal (and clearly blind!!) man in white on the pitch. Well guess, what…you can.
As long as you know how to divide one figure by another using a calculator. I’ve found it requires the same digital dexterity as pushing the ‘on’ button’ on my blender…so if you can make a smoothie, you’re sorted! So while almost every lab routinely reports these two as separate parameters that are also routinely in range…I haven’t seen many that actually do the calculation for you and give you the Albumin:Globulin (AGR) on a platter. Yet this one step maths transforms the mundane into magic and can reveal almost all to you regarding your patient’s level of immune activation, inflammation and oxidative stress, from the largest number and variety of drivers. That’s why I call it, 📣The Master Inflammatory Marker 👑
When factoring in your patients pathology results is at its best – it makes the invisible suddenly visible to us. We could have sat and eyeballed that patient all month and never suspected that their Hcy was too high, or they had antiphospholipid antibodies or, or etc.
But the albumin to globulin ratio goes one step further & trumps the other inflammatory markers we’re so familiar with, because it even sees what they can’t!
And a low AGR (≤1.2) signals just that to you. So when the patient with joint pains, or just a little bit of belly fat or an emerging yet unnamed autoimmune condition presents exasperated saying, ‘but apparently I’m not even inflamed!’…you can let them know you do see it, and it’s just that others weren’t looking in the right place, then get busy rolling your sleeves up to move those markers! That’s right, a low AGR is a clear call to action for practitioners engaged in risk minimisation, prevention and for working towards best outcomes in established disease and monitoring a patient’s AGR is a series of clear sign-posts about whether you’re leading them in the right direction or not. There’s a lot more to say on this this third umpire & ripper of a ratio – about kids, the contraceptive pill, confounders, a role in cognitive impairment prevention and what optimal might look like but hey…the cricket’s back on…gotta go 😂
Patients’ labs lie, not often, but sometimes and the inflammatory markers performed routinely like CRP and ESR have been known to tell a few. Like when everything about a case screams inflammation but both of those say there’s none there. Why do they miss it?…well basically it’s not their lot. CRP and ESR have specific signals they only respond to and therefore reflect only certain immune reactions and at specific stages of that response. But there’s a nifty little calculation you can perform with all of your patients labs and suddenly see the immune activation, inflammation and oxidative stress that was lurking beneath. It’s called the albumin to globulin ratio and it’s going to change your understanding of what’s going on in your clients and your ability to monitor the efficacy of your management.
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Copper deficiency happens in kids, so does copper toxicity and both are serious concerns, but do we know when to accurately call either? First, we have to know ‘normal’. If we know what normal Serum Copper values look like in children, then we can easily spot those falling below or above this, right? That’s the first hurdle we tend to knock over and break a toe on! Being a mineral whose levels vary widely in soil from country to country, globally, the differences in reference ranges are breathtaking & absurd. Add to that, that copper is a key mineral in kids, driving huge demand for it during key periods of development, so the range for pre-schoolers isn’t the same as the primary or high schoolers – not that your lab is flagging that. Unhelpful? Yes. Dangerous, even? Potentially.
To diagnose ‘Copper Excess’ in a child is a big call to make.
One, because most practitioners are unaware just how much Copper a child really needs at each age & two, high copper is often a messenger for something else going on and then three, the primary objective based on this diagnosis becomes to lower their Copper but we could be either shooting the messenger or missing the mark all together…right?
Copper excess does happen but not nearly as often as practitioners believe it does. And in kids, the fall-out from such misdiagnosis is bigger. And missing a Copper deficiency? (because we’re not as well-trained to recognise it and because Copper has been sadly demonised) Likely to have myriad negative impacts at this vulnerable age…almost none of which generate symptoms or a distinct clinical picture e.g. secondary iron deficiency, low neutrophils without necessarily compromised immunity. But what about the holy grail get-out of jail adjective: ‘relative’. You know, ‘this is at least a Copper excess relative to their Zinc?’
Well, to form this opinion you’re likely calculating the Zn:Cu ratio and applying an ideal adult value of 1:1 but show me the primary evidence that supports this for kids…anywhere? The Zn & Cu relationship shifts as we move through life-stages and in fact Copper is supposed to dominate through a lot of our childhood so…ummmmm…no.
HTMA Copper side-steps all of this?..double no.
I used to make the same mistake re Zn:Cu, I may have even taught you this?!🤦♀️ But as so often happens, a week spent in all the original scientific data and I’ve emerged a changed practitioner! Having been part of perpetuating this problematic premise in the past, I am determined to get the correct message out there to as many practitioners as possible. So help me spread the word on Copper in Kids – by telling others that this mineral is so critical to kids compared with adults, they will often have higher levels than ‘us’ and that until you’ve applied the right age-appropriate reference range and ruled out confounders you can’t possibly make a call on Copper. I mean, we kind of knew this all along, with healthy pregnancy Copper values being exponentially higher being a giant clue. Turns out kids’ ‘Copper Age’ extends way beyond the womb.
Copper, as a kingpin in angiogenesis, brain & bone building & iron regulation is a critical mineral during paediatric development. So much so, the kind of blood levels we see in a primary schooler might cause alarm if we saw them in an adult. So too their Zn:Cu. But higher blood Copper and more Copper than Zinc are not just healthy but perhaps necessary during certain paediatric periods. This recording redefines normal, low and high with a great clinical desktop tool to help you better interpret these labs, as well as reviewing the top causes and consequences of both types of Copper imbalance in kids.
The latest Update in Under 30 has landed. You can purchase January’s episode, Copper in Kids here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
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Just finished talking with the fearless fertility naturopathic specialist, Rhiannon Hardingham, who wanted to let me know that after listening to my Update in Under 30: Silent Reflux she’s had a lot of success treating both GORD and insomnia in her pregnant patients. That calls for double the celebration …YAY! YAY!
‘What’s the magic answer?’, I hear you ask… (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…)
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…)
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…)
Like all thyroid disease, post-partum thyroid conditions seem to be on the rise – and often they rewrite the rule book when it comes to thyroid pathology & its management. Therefore for many of us it can add an extra element of uncertainty about how to help these clients.
One of our graduate practitioners has a great example of this, a 33yo female who developed late gestational diabetes and is now struggling with a new baby and an autoimmune thyroid disease! What would you do? Does post-partum thyroiditis have unique triggers/drivers that require specific treatment? What can you/should you be doing differently because she is still breastfeeding? What’s the likely progression/prognosis?
This is your invitation to come along and find out the answers to these questions and more. During our live graduate mentoring session on Monday 15th June at 3.30pm AEST we’ll work through all aspects of the case, from history to presentation and from looking for clues in her pathology results to where to start with treatment. (more…)
Thyroid function is critical to successful conception, healthy pregnancies, babies and mum’s post-partum wellbeing, so we need to take the time to ensure we’re monitoring it properly.
First of all you need the right tool for the right job & that means we need trimester specific reference ranges – which unfortunately many pathology companies don’t use in Australia. Due to the thyrotropic action of HCG (acting a bit like TSH), TSH should actually decrease in the 1st trimester and while TSH is less affected in 2nd and 3rd trimesters it should still actually sit lower than in non-pregnant females. (more…)