Ever had those patients… young, slim, fit…I won’t go so far as to say ‘well’ or otherwise they probably wouldn’t be seeing us right? But not overtly inflamed and yet when you measure their CRP, it registers. The average CRP of ‘healthy’ adult populations is reported to be between 1 and 3 mg/L but we know that even values within this range positively correlate with long-term CVD risk and most of us believe that unless there’s a good reason for immune activation at the time of the test, we’d like to see values < 1mg/L.
I saw one of my patients who fits this bill just the other day – an updated CRP and there it was again bubbling away at 1mg/L. This guy is young (20s), slim (BMI of 19 kg/m2), non-smoker (another classic driver of this sort of brewing CRP), doesn’t report any acute illness e.g. URTI, at the time of each test (we would expect a much higher value with this anyway)…so why is there any CRP? (more…)
We now suspect that many of the drivers behind PCOS are heritable components – a genetic vulnerability passed from parents, possibly one but often both. This growing understanding has identified a phenomenon referred to as ‘PCOS families’ i.e. a family in which at least one female has confirmed PCOS.
Being a primary biological relative of someone with PCOS, it would seem, suggests a shared risk, even if you are a son, or brother or father.
So beyond the very high rates of undiagnosed PCOS in sisters of someone already diagnosed, there is much talk now about a male PCOS phenotype equivalent. (more…)
As we head rapidly towards the change over of our calendars we would like to offer you a special on the very best educational recordings from 2014 – buy 2 CDs before Jan 31st and receive one complimentary Premium Audio Recording of your choice OR purchase 4 CDs and receive a 3 month Premium Audio subscription for free.
It’s been a busy year during which Rachel has delivered 7 very successful new seminars in the area of mental health and beyond, most notably fortifying her role as a leader in the field of diagnostics and pathology interpretation. This has included collaborations with ACNEM, Biomedica, Health Masters Live, MINDD and Nutrition Care, however, each recording is classic Rachel – full of fresh perspectives on diagnosis & treatment, colourful analogies & humour. In case you missed some of these this year or want a copy for keeps – here’s a quick summary of the 2014 recordings included in this end of year offer: (more…)
We’ve just had another mentoring case in which a 40 something female with deficiencies of almost all other minerals but ‘pretty normal ferritin levels’ presented with a range of endocrine problems and arthralgia. Sounds as if iron’s not the problem right? Except that in this case her iron studies also tell us that her transferrin saturation % on last check was 48%. The diagnostic criteria for hereditary haemachromatosis (HH) necessitates elevated ferritin – to indicate that the iron stores are reaching saturation, however, while this becomes evident at relatively young ages in men (20s-40s), who have no specific excretory pathway for iron, is this still appropriate in menstruating female, whose monthly periods may mask the HH tendency with regard to ferritin? I’m guessing you know what my answer is already! 😉
Some would argue that HH, in spite of being an inherited disorder, is only clinically meaningful once the ferritin is elevated ( earlier and more potent elevations are seen in people possessing the C282Y genotype) but again this is very much up for debate in the current scientific literature, with a lot of research concluding that the transferrin saturation (also referred to as the transferrin ratio) being an important prognostic indicator for various chronic diseases including CVD.
When we go back to basics and remember the higher the transferrin percentage the more iron is being delivered to tissues around the body (whether they like/want it or not! so we refer to this as being ‘iron dumping’) and the higher the serum iron, the more unbound iron is in the system – a key source of oxidative stress..it becomes patently clear that these two parameters are important early warning signs of a tendency to iron overload, increased risk of heavy metal toxicity and already active mineral imbalance. So in future keep your eyes open for women with fasting transferrin saturation values that consistently sit above 35% and men, > 40% and if you do see a series of suspicious values – consider the genotype test through mainstream labs.
“Two great speakers – inspirational in the first half and bang on in the second – I now know how much I don’t know”
Just out now in time for Christmas…no seriously though… this year I had the good fortune to team up with Biomedica and in particular Rachel McDonald and we delivered a 3 hour seminar called Mental Health in Holistic Practice. The intention behind this collaboration was to shift the education focus for practitioners from a prescription based approach, to one really about the clinical reality of managing mental health clients. Probably most of you will agree that the ‘treatment’ counts for only a portion of the positive outcomes in your patients and this is particularly true in clients challenged with mental health issues. After more than 20 years in practice working in this area, I’m keen to share what I’ve learned so other practitioners can get there much much faster! (more…)
Apologies for having a one-track mind currently but yes I’m still banging on about the thyroid this week. You see, this year in my own clinic I connected up some dots I hadn’t connected before via a series of young female patients. Each of these women presented with some hypothyroid features, most notably, low basal body temperatures, fatigue and weight gain and while their thyroid hormones (TSH, T4 and T3) were all technically ‘within range’, their T3 levels were very low (low 3s) and the TSH seemed to sit low as well (<1.5). Normally of course, when T3 levels drop we expect TSH secretion from the pituitary to rise in response, as a means to correcting this dip, however, this part of regulation appeared ‘blunted’ or even ‘broken’ in these women.
So why would their pituitary be sleeping on the job, allowing them effectively to experience long term suboptimal thyroid function? (more…)
I learned to drive more than 20 years ago in a mustard yellow VW beetle with my ageing father beside me playing the dual role of instructor and slightly hysterical passenger. The one catch-cry that he screamed over and over again was, “Where’s the fire? Where’s the fire?” In case you require translation, this was his way of indicating that I was almost travelling at 60kmph & essentially meant, ‘unless you are part of the emergency services & on your way to a crisis there is no reason to be travelling this fast!’ I know, it’s a wonder I ever learned to drive! But I’ve actually come to love that catch-cry, “Where’s the fire?” because for me it has become a pressing question in clinic every day. (more…)
I’ve learned a lot (!) and as always that learning has principally driven by my clients – their pathology, the diagnostic investigations we’ve employed to better understand the drivers behind their conditions, their response to various treatment approaches & of course a million other subtle thing we’re learning along the way. The other teachers are the many practitioners I interact with on a daily basis as part of our individual or group mentoring sessions – whether it’s some curly question or problem they bring that throws me into the scientific literature searching for answers or a fabulous bit of wisdom they bring to the table themselves, it’s a great reciprocal learning environment. You know, the most common thing I hear from naturopaths is the frustration they feel at the limitations of their under-graduate education and how it is only since graduating that they’re ‘learning all this stuff” but in reality, as with most health professions, the bulk of the learning has to happen on the ground.
I’ve been in practice for about 20yrs (ouch!) and I don’t think my rate of learning has slowed at all. It’s great if we can view this as the eternal fountain of inspiration that keeps us motivated and engaged in our profession…no not every minute of every day…let’s be realistic now…but overall it’s a strength not a weakness 🙂
Over the next month I’m being let loose on the major capital cities thanks to Nutrition Care to for a series of evenings of case study discussions – bringing together quick teaching points from all the things my clients have taught me this calendar year. Whether it’s from a diagnostic or treatment & management perspective I’ve got some juicy morsels to share! I hope you can come along and we can learn from each other yet again as a nice way to reflect on the year and our ever –growing profession…. If you’re interested in attending contact your local Nutrition Care representative for more information or call them on (03) 9769 0811
- Brisbane – 12th November
- Melbourne – 20th November
- Sydney – 26th November
- Adelaide – 27th November
I’ve been re-reading lots of studies for a talk I’m delivering at ACNEM in Melbourne, investigating the relationship between selenium and a myriad of thyroid pathologies: from hypo- to hyperthyroidism and from subclinical thyroiditis to cancer. The sheer number of trials is overwhelming & increasing, in fact I think there’s more every time I go back and look (!) and the bulk of the findings keep telling us yes! yes! yes!…selenium plays a pivotal protective & corrective role unmatched by any other nutrient. Whether it’s buffering the oxidative stress that comes with high TPO antibodies or lowering antibody titres, preventing or minimising the orbitopathy associated with Grave’s or simply maintaining a better level of T3 in euthyroid individuals, there are numerous potential positive effects from selenium supplementation …in the right patient… and therefore this is the bit we need to be clear about: while the majority of both epidemiological and interventional studies all concur that low selenium levels equate with a greater risk of thyroid issues in all our patients & poorer outcomes in patients with already established thyroid disease, the big question is how low are we talking?? (more…)
When I grow up I’d like to be a few different things, forget any ballerina or astronaut aspirations, my list includes a clinical psychologist, an integrative psychiatrist and last but by no means least, an endocrinologist. I’m fascinated by hormones, their regulation & incredible interconnectedness and the longer I’m in practice and the more patients I see with hormonal issues, the deeper I dive into the endocrinology texts (Endocrinology by Greenspan & Baxter is an absolute favourite of mine and you can now purchase this as a download to your computer which is super handy). I think (more…)
So far this year I’ve been doing most of my presenting online which has been fantastic because we can all be in our PJs and no one’s the wiser (except now!!) but I do miss the face to face seminars where sometimes the real magic happens thanks to the two-way dynamic between you and me!
So guess what? I’m coming to Sydney on the 31st August (and then Brisbane 6th September and then Melbourne 13th September) to touch base with many of you again. I’m joining forces with Rachel McDonald from Biomedica to talk about the real world application of naturopathy in mental health conditions. (more…)
In spite of several advantages of salivary hormone assessment, one important piece of information you miss out on when you do this rather than blood assays, is the SHBG result. Sex hormone binding globulin is a protein produced in the liver that, as the name suggests, binds our sex hormones rendering them inactive and therefore buffering us against their full potency. They bind the sex hormones to different degrees – the androgens most potently and oestradiol to a lesser extent but curiously it’s higher oestrogen that represents the major hormonal driver of increased SHBG production (including synthetic oestrogens). (more…)
Globulins…ever thought much about them? Me neither really unless they were clearly below range which made me consider immune impairment but recently Dr. Michael Hayter, who I am co-presenting the Diagnostics Master Class (Health Masters Live) with, inspired me to take a closer look! Globulins are typically reported in your patients’ E/LFTs or standard chemistry and they refer to a big group of molecules including CRP, transferrin, lipoproteins and yes all the immunoglobulins/antibodies. (more…)
I often say that if my surname was Rubin I wouldn’t be able to resist calling my son Billy. I am sure the joke would be lost on 90% of people & certainly on my poor child who might never forgive me but never on me – I get a giggle every time 🙂 Recently, I’ve been reading a lot of scientific literature on bilirubin, previously regarded as simply the end waste product of haem, it’s now attracting huge interest as a biomarker of oxidative stress. There’s still lots of ongoing debate & contradictory research findings but here’s the general consensus so far…bilirubin is an antioxidant (particularly protective against peroxyl radicals & lipid oxidation although the latter is still being hotly debated). Not surprisingly then, several studies have shown that smokers for example, consistently have lower total bilirubin blood values, indicative of their greater oxidative stress & yes, smoking cessation leads to partial correction of this (O’Malley et al. 2014 Smoking Cessation Is Followed by Increases in Serum Bilirubin, an Endogenous Antioxidant Associated With Lower Risk of Lung Cancer and Cardiovascular Disease) A recent study also found a positive correlation between higher flavonoid rich fruit & vegetable intake and total bilirubin (Laprinzi & Mahoney 2014 Association Between Flavonoid-Rich Fruit and Vegetable Consumption and Total Serum Bilirubin).
On top of this, there is a wave of epidemiological research to currently surf, suggesting inverse relationships between total bilirubin levels and several diseases: hypertension & CVD, T2DM, metabolic syndrome, MS, renal disease, IBD, lung cancer and the list goes on. The sort of cut-off point being talked about is a result < 10 µmol/L being associated with the highest risk. What remains unclear is whether lower bilirubin levels are actually risk-promoting or whether they are just a signal of the individual’s oxidative stress.
Total bilirubin (aka Indirect or Unconjugated bilirubin) values are typically included in most pathology company’s basic general chemistry or E/LFT panels which means most of your patients already have had this test performed in the previous 12 months. So next time you’re looking at patient results check out their bilirubin values and if they have bilirubin levels consistently <10µmol/Lconsider how you might better support your patient manage their oxidative burden to reduce risk of future disease and if you’re hitting the mark the bilirubin level should rise 🙂
Want to know more about Bilirubin and Pathology interpretation in general – Rachel is collaborating with Dr. Michael Hayter to present an online Master Class in Diagnostics starting this week. For more information check out Health Masters Live https://www.healthmasterslive.com/product/clinical-diagnostics-masterclass/?mc_cid=cfd82dd367&mc_eid=014c831228
Many of you would now be aware of the shift from culture (stool MCS) to gene-based stool testing (stool PCR) which has now become available under Medicare subsidy. While this has been an exciting development that promised greater accuracy for the detection of parasites in our patients, there remains limitations. One of the biggest is the fact that the PCR test is based on just one stool sample compared to the 3 day samples used in the culture test.
While this is rationalised, both by the pathology companies and some doctors, by higher test sensitivity and specificity, it flies in the face of our understanding about the irregular shedding of parasites i.e. the presence of the parasite in an infected individual’s stool can vary from nothing to severe, just day to day, therefore diagnosis must be based on several days of stool collection to account for this.
A practitioner I mentor, faced with several patients with negative PCR results but a clinical picture and other pathology results (raised eosinophils, impaired iron levels etc.) that strongly suggested the presence of parasites has been debating this with her shared care providers trying to encourage them to still refer patients for the stool PCR but performed over several samples.
She came across this article as a nice piece of supportive evidence Irregular shedding of Blastocystis hominis (Venilla et al 1999): ncbi.nlm.nih.gov/pubmed/9934969
While there are numerous other studies confirming the irregular shedding of most parasites this is a handy paper perhaps to use to strengthen the case for PCR stool tests performed over 3 days rather than 1. Let’s face it – it’s a big enough ask to get our patients to collect stool – we should really ensure we have optimised their chances of getting an accurate result!