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…)

There are few complementary medicines that come onto the market with such a bang, opening up genuinely new therapeutic options for the effective management of such a broad range of health complaints.  N-acetyl cysteine stands out for this reason and has changed the way I practice… seriously!

Recently I had the pleasure of presenting a webinar for Biomedica completely and utterly focussed on N-acetyl cysteine – its key actions, pharmacokinetics, applications and contraindications.  In the process of researching for the webinar I learnt so much and to my surprise found even I was under-utilising my favourite supplement! How familiar are you with its application in cystic fibrosis,  fertility, biofilm eradication etc. etc ?  Not to mention, it’s incredible versatility in mental health.  Recently, buoyed by some new research suggesting the efficacy in severe glutamate excess of much higher doses than previously studied for depression and bipolar, I have stepped up my doses in patients with some forms of addiction, OCD, refractory insomnia to 4g/d with great results!  I could talk all day about NAC but perhaps for a starter if you missed the webinar you might want to listen to the recording?  We have the Clinical Knack of NAC now available as a CD with audio and notes for purchase on the website:

https://rachelarthur.com.au/product-category/audio/

This in-depth 1 hour webinar offers practitioners new to NAC, the practical knowledge and tools they need to start using it effectively and for the practitioner already dispensing it, to really broaden their understanding of indications , correct many misunderstandings and get the latest research on the why, when and how to use it.  From reproductive to respiratory health, from heavy metal burdens to biofilms and athletes to addicts, this webinar covers the latest information about NAC’s real therapeutic potential.  Having been a favourite nutraceutical/prescription of Rachel’s for some time, she punctuates the presentation with many of her own cases.  

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

I briefly mentioned in a previous post Dr. Robyn Cosford’s inspiring opening speech at this year’s MINDD conference.   A key point she made was the growing gap between what’s regarded as normal and what is actually healthy. 

Having worked in general practice for decades, Robyn provided us with one illustration after another – Type 2 diabetes, previously called adult-onset diabetes, now not infrequently diagnosed in primary school aged children; delayed speech and learning difficulties in male toddlers which many increasingly regard as ‘normal’; precocious puberty in girls; escalating rates of depression and anxiety in children and adolescents…Robyn asked us as practitioners to be vigilant about helping patients to distinguish between what has become perceived as ‘normal’ and what is actually healthy.

In my MINDD presentation this year I talked about the mental health challenges faced by young men and I expressed a similar concern: that when we witness extensive aberrant behaviour in young men we are prone to rationalise it.  Are we mistakenly attributing these signs of dis-ease in males as simply being an initiation into Australian culture?  When you hear of young men exhibiting binge drinking behaviour, does it set off the same alarms as it would if your patient was female and if not….why not? 

As part of a broader discussion of the issues, I presented two cases of young men with mental health problems – both from very different sides of the tracks, one gifted and the other a struggler but one of the features they shared included the way their use of alcohol & other substances had passively been condoned by society instead of being seen as a call for help.  We can help these young men but only once we’ve acknowledged there’s a problem. So now I’m extending Robyn’s plea and ask you to be vigilant in making the distinction between ‘normal’ and healthy… when mothers relay stories of their son’s ‘antics’, when brothers, cousins & uncles temporarily ‘go off the rails’,  when young men reluctantly present for a quick fix…

If you missed the presentation and are interested in the full recording check out  https://rachelarthur.com.au/product/new-young-white-men-mental-health-challengers-face-mindd-conference1hr-total-50/

 

I’ve been curious about the push towards using so-called ‘active forms’ of B vitamins over the last 10 years in nutritional medicine – particularly with regard to B6 (pyridoxal-5-phosphate) and B2 (riboflavin 5’-phospate aka FMN) in light of substantial research demonstrating that these phosphorylated forms will in fact be dephosphorylated prior to uptake in the small intestine (Gropper, Smith & Groff Advanced Nutrition & Human Metabolism 2005) – so initially it seemed we were being encouraged to pay more for something that ultimately gave us less of the same vitamin. Funnily enough the only established scientific way to ensure uptake of the active forms in their intact active states is to use very high doses – however supplements containing either active B6 or B2 consistently offer very low doses compared with the regular supplements, so this seemed to rule this out as an explanation.

In spite of my scepticism & encouraged by the Pfeiffer approach, I got into using P5P and had to suspend my disbelief in the face of good clinical results.

However finally at the MINDD conference last week, scientist Woody McGinnis at last made sense of this riddle for me!

McGinnis, who some of you might know as previously being a key researcher at the Pfeiffer Institute which specialises in nutritional and integrative management of mental health & behavioural disorders, confessed that he had also struggled with concept of P5P supplementation from a scientific perspective until Bill Walsh suggested that this form was particularly indicated for the ‘lean malabsorbers’.

What Woody essentially took from this was that patients with leaky guts could absorb the P5P intact &  would ultimately benefit from this form.  Adding to this is my understanding that the dephosphorylation process for P5P in the gut occurs via ALP – a zinc dependent enzyme found in the brush border of the small intestine…so here you have the double whammy – if your patient is a malabsorber AND zinc deficient (which of course commonly go together) they are the ones picking up the P5P perfectly and for the rest of us perhaps the pyridoxine will do.

Woody also attested to this with his story of his own pyrroluric son who initially only responded to P5P but in his teens (with significantly improved gut health) appeared to stop responding – at which point Woody switched him to the higher dose pyridoxine with fantastic results…..Aaahhhh at last my scientific curiosity has been quenched! 🙂

I was honoured to speak at the MINDD conference again this year.  MINDD is an organisation that really sets itself apart by providing incredible hands on support for parents, carers and practitioners in the area of integrative mental health management and one of the key strengths is the sense of community they’ve developed secondary to this.  A key message echoed by numerous speakers was the enhanced clinical benefits for patients when a truly whole health, multi-modality approach is taken – from naturopathy to psychology, from neurology to audiology, from building biology to biological markers and so on.

And just to put the brakes on the whole ‘genes are us’ movement that is currently sweeping Australian integrative medicine, Dr. Robyn Cosford (a highly-regarded integrative GP) kicked off the whole weekend with a presentation that included a study of some of the oldest Okinawan individuals and their genetic profiles.  These individuals aged well over 100 and fighting fit each possessed hundreds of genes currently thought to be associated with chronic disease: cardiovascular, diabetes, cancer.  Robyn reminds us all that while genetics loads the gun it is our diet, lifestyle and environment that actually pulls the trigger!

While I was inspired by the research and insight offered by clinicians and scientists from various modalities, I was reminded again, that no one individual can be across it all and to attempt is to fail or become exhausted in the process and this of course is where the community bit comes in – we need a network of integrative individuals to refer between and support each patient & my experience this weekend suggests these events certainly build that community.  Our job is to practice within our scope and know when and where these other therapies and approaches are indicated and to develop a good referral network.   So many great speakers this year and this time I actually managed to sit still and enjoy some of these so I’ll be bringing you the highlights over the next couple of weeks so stay tuned! 🙂

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!

A few years ago I heard Felice Jacka, Associate Professor (Deakin University), speak about her research linking mental health to certain Western dietary patterns and possibly many of you have already heard me rave about her work.  This year I had the pleasure of hearing her again at the recent Science of Nutrition in Medicine Conference and guess what I learned this time?  Felice is actually Alf Jacka’s daughter…I know I’m a bit slow sometimes. For those of you still going, “Huh?” – I am guessing you’re not from Victoria and certainly didn’t study at Southern School of Natural Therapies. Alf Jacka is considered by many, a pioneer of naturopathy in Australia and he established SSNT.  So I was thoroughly delighted when Felice, who is a very highly regarded researcher, made reference to her late father, & naturopaths generally, as being trail blazers: articulating many of the physiological drivers behind mental health decades before they turn up in the mainstream zeitgeist e.g. digestive health & the central importance of microbiota, excess glutamate activity in addiction.  Felice’s key interest lies in how we can prevent depression and mental illness at a population level via diet and she seems keen to essentially bring a more holistic perspective to the often reductionist world of health research.

I also recently attended the annual Biobalance Conference one (yes I truly have nothing else to do with my weekends!) which had Jerome Sarris on the bill.  Many of you will be aware of Jerome who is a Senior Research Fellow at The University of Melbourne, following completion of his doctorate at The University of Queensland in the field of psychiatry.  Again, some of you would have heard me mention his work in previous posts – he’s attracted more than $4 million in grants and has published some very high impact papers on the use of CAM in psychiatry. Personally, I find his review papers demonstrate a deeper understanding of CAM so clearly lacking in those written by non-naturopaths i.e. the others miss the point and he generally gets it and can find a way of putting voice to naturopathic nutrition in the forum of a scientific dialogue.

Anyway, at Biobalance, another speaker on the bill essentially suggested (possibly unintentionally) that naturopaths had less of a grasp of complex nutrition than integrative GPs and much to my delight, Jerome, a keynote speaker, responded by identifying himself first and foremost as a naturopath and then saying on the matter , “Ahem…I don’t agree at all”…or something to that effect.  It was a great moment.

So fellow naturopaths and integrative practitioners, be assured that we are being beautifully represented by these trailblazers & if you’re interested in getting into research yourself – I suspect there’s never been a better time.

Also presenting at the Science of Nutrition in Medicine Conference this year was Professor Eastman who is a world-renowned Australian endocrinologist with a primary interest in global iodine deficiency. He is also Deputy Chairman elect of the International Council for the Control of Iodine Deficiency Disorders (ICCIDD) and is frequently consulted by Australian health authorities and medical groups on the issue of iodine deficiency in Australia.  Boy did he have some things to say…and it kind of went like this:

  • Substantial epidemiological research has shown that 95% of euthyroid patients have a TSH between  0.04-2.5 mIU/L  (note the current reference range suggests results < 4 mIU/L are okay, Eastman strongly refutes this)
  • The mean TSH in a disease free population is actually 1.5 mIU/L
  • In fact Professor Eastman was emphatic that the mean TSH in iodine replete individuals is actually 1 mIU/L
  • While acknowledging the limitations of spot urinary iodine testing for the assessment of individual iodine status, he genuinely seemed at a loss to understand GPs reluctance to refer for this test when patients exhibit risk factors for hypothyroidism and in his article (Screening for thyroid disease and iodine deficiency. Eastman CJ. Pathology. 2012 Feb;44(2):153-9.) he argues strongly for screening of all mature age women, pregnant women (1st trimester) and school children, using the urinary iodine and TSH together
  • And while we’re stirring the pot how about this: Professor Eastman says that hyperthyroid individuals who have a low urinary iodine result should still be given judicious iodine! Such sacrilege!!
  • But wait…before you get too excited and join the ‘too much iodine is never enough… just look how much the Japanese eat’ camp…I was very relieved to hear Professor Eastman remind the audience that while the Japanese diet does provide substantially more iodine than the Western one, it is not without problems, with very high rates of thyroid disease especially thyroid cancer and in fact, Japanese health authorities are concerned about excessive intake and are currently investigating ways to cut back.  And lastly, if you’re not convinced by this, he says perhaps you should talk to one of the many litigants in the current class action against Bonsoy, who developed severe thyroid diseases thanks to excessive iodine exposure from the milk (7.5mg/cup)!

So keep arguing for urinary iodine assessment and for addressing individuals with ‘within range reference results’ for TSH that are clearly not healthy ones.  Check out Professor Eastman’s article, there’s a goldmine of information in there and while we’re talking about incredible resources in nutritional medicine – take a moment out to thank Dr. Tini Gruner (previously from Southern Cross University) for her significant contribution to naturopathic nutrition education in Australia.  She was a mentor and inspiration to me and many others. She sadly passed away this week and we will miss her dearly.

What an absolute pleasure to attend this conference this weekend just gone, where the presenters were researchers, most of them internationally acclaimed in their respective area and to find what they had to say SO clinically relevant and to find the presenters SO unafraid of bucking the norm (be that the NHMRC dietary guidelines, folate fortification, the use of broad TSH reference ranges, the refusal by many medicos to use urinary iodine testing of individual patients etc. etc.).

Then to boot – to be able to ask them questions!  Want to know about N-acetyl cysteine? – How about asking Dr. Michael Berk the Australian researcher who ran the first human studies in psychiatry and is the most prolific research of NAC yourself?!

I’d attended the inaugural conference some years ago in Sydney and, while there were less attendees this time around on the Gold Coast (must be our horrible weather! ;) ), I thought the format and quality was just as good.  While I certainly saw some familiar faces – I would have loved to see more – I think we’ve got to make the most of these independent sources of information, because, while we can get some great ideas and tips from company seminars – there will always ultimately be a barrow to push and some bias. I found this to be true, most disappointingly even at last year’s NHAA conference where so many of the main speakers ultimately had a vested interest and a product to sell the audience. Given that’s supposed to be independent that was even more appalling I thought.  The Science of Nutrition in Medicine Conference is of course not free of all sponsorship but I  didn’t see any bias permeate into the presentations from this.  So major congrats to the organisers of this one (ACNEM, CSIRO & NSA), mark it on your calendar for next year as a probable must-see and over the next few weeks I’m going to bring you some of the key highlights from what I heard – that might just change the way you practice!  Very inspiring 🙂

We’ve all heard about the higher incidence of mood disorders (depression, anxiety etc.) in women and chances are we’ve all seen this reflected in the dominance of female clients who present seeking help but what’s this really telling us?  Many of us are aware that men are more likely to ‘self-medicate’ with alcohol and other substances, as a maladaptive way of dealing with the psychological stressors, however, the lesser talked about fact is that substance induced (i.e. cannabis etc.) psychotic disorders are significantly more prevalent in men and occur at younger ages than women (Bogren et al 2010) and substance use & abuse is commonly not sufficiently explored or adequately diagnosed in general practice amongst male patients.  Oh dear…what else do we need to know?

The results of a large English survey on mental health and help-seeking behaviour published in 2005 found that men were less likely than women to say that they would seek help (OR=0.78, 95% CI 0.72–0.88,P<0.001). The preferred reported source of help was friends or relatives with 63.1% saying they would seek help from this source.  In addition to this and somewhat, more alarmingly, the WHO reports that “doctors are more likely to diagnose depression in women compared with men, even when they have similar scores on standardised measures of depression or present with identical symptoms.”  https://www.who.int/mental_health/prevention/genderwomen/en/ So even when males do finally present for help, often, the mental health problem is being overlooked or missed.

One theme that keeps coming up in research is the ongoing associated stigma for men with mental health issues.  A study published in 2008, conducted by two National Institute of Mental Health postdoctoral fellows in mental health care policy at Harvard Medical School, investigated the effect of gender, race and socioeconomic status on psychosocial barriers to mental health care and found that white males were most likely to mistrust the mental health care system and were also likely to perceive mental illness as a stigma and therefore avoid formal mental health care https://www.sciencedaily.com/releases/2008/09/080908125123.htm

In my practice we actually have a high proportion of males presenting with mental health concerns, admittedly, our practice specialises in this area so that may be a key reason for this and in many instances the appointment has been instigated or driven by a concerned mother, a wife etc.  Regardless, I’ve found that many men really struggle & it’s made somewhat more complicated by the role they are expected to play in society. I think the key message is not to reinforce gender based stereotypes on our patients, have the confidence to explore mental health with male patients, their vulnerabilities, concerns etc. as much as you would your female patients. Make sure you thoroughly assess their substance use and take heart there is a lot we can do for these individuals, the first step is recognising there’s a problem.

Rachel will be speaking on Young White Men & the Mental Health Challenges They Face at the MINDD International Forum in Sydney June 14-15th.  For more information and bookings check out: https://mindd.org/forum/mind2014.html

About a decade ago there was a lot of excitement about using fish oils in the management of mental health, so much so even the American Psychiatric Association developed recommendations suggesting that people with mood, impulse control & psychotic disorders should all consume 1g EPA + DHA per day… but then what happened?  Ask most health professionals (GPs, psychiatrists, naturopaths & nutritionists alike) today whether fish oils are their first choice in mental health nutritional interventions and you’ll frequently get a, ‘No’ and I include myself in that.

Let’s retrace our steps to find out how we got here.  The epidemiological evidence linking low omega 3 intake to myriad mental health problems in terms of susceptibility, incidence and severity is almost overwhelming. For example, depression rates are 10 times higher in countries with limited seafood intake and post-partum depression 10-50 times higher (Kendall-Tackett, 2010).

Noaghiul & Hibbeln postulated that countries where individuals consumed less than ≈ 450-680g of seafood per person per week demonstrated the highest rates of affective disorders (2003). One study of 33 000 women with low omega-3 intake were found to have an increased risk of psychotic symptoms (Goren & Tewksbury 2011) and it goes on.  Then, we have other evidence also pointing in the direction of fish oils, such as the general consensus that excess unchecked inflammation is evident in many mental health conditions (Maes et al 2013).  Numerous intervention studies using fish oils as stand-alone or adjunctive treatments have been published. Interventions have included high dose omega 3 (no specific EPA/DHA breakdown), EPA alone, ethyl-EPA, high DHA, blends with high DHA:EPA ratio, flaxseed oil etc. etc.

These studies are quickly followed by the systematic reviews, meta-analyses etc. which almost invariably conclude that supplementation with fish oils isn’t effective  –   or more correctly,  based on this terrible mish–mosh of evidence no firm conclusions can be reached. 

Take the Cochrane Review on the use of fish oils in Bipolar Disorder for example, which based their negative conclusion on the results of one study (Frangou et al 2006), while > 23 others failed to meet their inclusion criteria (Montgomery & Richardson 2008).

The big take home message should actually be: Fish oils ain’t fish oils! 

If you understand some of the key structural & biochemical differences between EPA (precursor to eicosanoids, able to generate DHA, little structural contribution to the brain) and DHA (major structural brain fat, precursor to the docosanoids including resolvins,  mild reuptake inhibitor of 5HT and DOP), the superior bioavailability of triglyceride forms over ethyl esters and the seriously limited ability of humans to convert plant omega 3 precursors to the LCPUFAs, then you can start to see your way through the  research mess and step away from the broad brush stroke conclusions of the Cochrane review and similar.

Check out some of the better written and more insightful reviews – especially this one by Sublette (2011) which found that in  successful treatment of depression fish oil supplements must have >60% EPA compared with DHA and read her theories on this. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3534764/   So we need to get reading and get clearer about which specific omega 3 fatty acid or blend (and in what ratios) works for which mental health problem – its definitely not a case of one-size-fits-all  –  do your homework and pick your products well and most importantly let’s not throw the fish out with all that fishy research!

Do you still eat & recommend fish as part of a healthy diet? I do.  Of course these recommendations have now become species-specific and include other key criteria such as ‘wild not farmed’ and ‘local not imported’ in response to increasing concerns about contaminants especially organic methyl-mercury (MeHg) and the organohalogen pollutants (OHPs or POPs).  Most of us understand about biomagnification of MeHg in the food chain which results in the highest levels in the largest fish but did you also know that as the MeHg content rises, the relative Selenium content drops? What are we worried about?  Lots actually.  A key mechanism behind MeHg toxicity that has come to light is due to its negative interaction with selenium.  Now, as many of you know, I just love a good nutritional interaction and this is a great example of one!

It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes required to prevent and reverse oxidative damage throughout the body (i.e. glutathione peroxidase & thioredoxin reductase), particularly in the brain and neuroendocrine tissues. In fact inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity.

MeHg binds tightly to Se rendering it unavailable for selenoenzyme activities and their synthesis.  This makes sense in terms of the cardiovascular, thyroid and oxidative consequences associated with MeHg toxicity.  So essentially what MeHg is doing in one sense is inducing a profound selenium deficiency which funnily enough shares a lot of the features of MeHg toxicity: thyroid dysregulation, immune system dysfunctions, & infertility!  But wait there’s more…several pieces of research highlight the potency of this relationship showing that we can predict who will manifest Hg toxicity features following exposure by the individual’s Se status e.g. those that maintained reasonable Se levels in spite of the Hg exposure didn’t manifest the toxicity picture.  One study on this topic looked specifically at Hg amalgams.  Another study fed juvenile rats a diet of fish with a known content of MeHg, and a variable amount of natural or supplemental Se. They found that Se in blood, brain, & spinal cord was positively correlated (r between 0.69 and 0.90) with protection from neurological damage attributable to MeHg.

In response to these findings, there is some discussion about grading the health and safety of fish for human consumption according to their Se:Hg ratio (ideally >1), however, further research in this area suggests this is complicated with evidence that this is not simply species-specific but strongly influenced also by locality (Jones, Butler & Macleod 2013).  While an American study found for both saltwater and freshwater fish, some species with ratios >1 had a significant proportion of individual fish with ratios < 1 (Burger & Gochfeld 2013).  So what’s the upshot of all this and where do fish oil supplements fit in?  Well MeHg levels in TGA approved supplements are extremely low so this is really a non-issue as long as your patients are not shopping for their fish oils overseas and with all our fish eating friends – keep an eye on their mercury levels (blood or hair) – we’ve picked up a few with extremely high levels from seafood intake alone and consider Se the logical first step in addressing high levels.

Want to read more?  Check out… https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760827/pdf/pone.0074695.pdf

As Rachel says in this month’s From My Desk to Yours, “I had to do it sooner or later, we have to talk about Zinc.”

Rachel has been talking about Zinc for years.

Here are some of the items you might like to catch up on to brush up your background on this important mineral.

Do we need to rethink zinc?

Dynamic Balance I – Iodine, Selenium, Iron, Zinc, Calcium & Magnesium

Coeliac disease presents as behavioural problems

 

Ok – I’m excited!! A recent meta-analysis of seventeen epidemiological studies (n=1,643 depressed individuals and 804 controls) investigating zinc levels and depression found that depressed individuals had lower plasma/serum zinc levels than non –depressed people (Swardfager et al., 2013)   While the actual difference in plasma/serum zinc was found to be small, approximately -1.85 umol/L lower in depressed compared with control individuals, the effect size increased in individuals with more severe depression, inpatients and studies with more robust methodology.  

It is important to note that the lower levels  seen in depressed patients were typically still within the established reference range….and this is the bit where I get excited because in fact, all 16 studies that found a correlation between lower plasma/serum zinc and depression found a mean zinc level  i.e. 10-14mmol/L that according to the reference range used here in Australia (9-19 umol/L) – would be deemed adequate! 

This research suggests that a) the reference range for zinc testing needs serious review and b) when some health professionals insist that there’s nothing wrong with your patient’s zinc result because “it’s within range” – we now have a great piece of very significant evidence to support our different interpretation and the need for zinc supplementation. 

If you want to hear more about these new findings and the key things you need to know about plasma and serum zinc testing and interpretation then have a listen to the latest premium audio here https://rachelarthur.com.au/product-category/premium-audio/

The last two decades have seen the introduction and rapid rise in popularity of the proton pump inhibitors (PPI) for GORD & gastric ulcers.  While clinical trials prior to their approval and release didn’t reveal much in terms of adverse reactions, being not dissimilar to the side effects of the previous acid suppressing drugs, more recent studies involving larger numbers of individuals and post-marketing surveillance have raised several concerns about their chronic use.  The three key current areas of concern are

  • the potential for increased bone fracture
  • increased susceptibility to infections
  • altered gastric function – digestive and nutritional consequences

While more targeted research is needed to fully clarify any causal role of the PPIs, there is a growing body of evidence which points to potentially serious detrimental effects for some long-time users.  Increased rates of small intestinal overgrowth (SIBO), Clostridium difficile associated diarrhoea (CDAD) and other enteric infections highlight the negative impact gastric acid suppression has on host defence & eubiosis.  While the nutritional consequences, initially thought to be limited to impaired nutrient digestion and absorption are now extending to the sudden development of IgE food allergies in PPI–taking patients.  There is also new information about how PPIs interact with other medications both within the GIT and via CYP450 system.  If you’re interested in learning more about this widely prescribed class of drugs check out a recent Medscape review on the topic https://www.medscape.com/viewarticle/730747

Downloadable audio

Head on over to the down loadable audio page, now.

Many of you have been asking if we could make my presentations available for download instead of on CD. You can now do both!

The Rachel Arthur Nutrition (RAN) store on the website now has downloadable audio and CD-audio sections where you can buy my presentations. You can also get the regular case-study premium audio product from its own page.

If you have been waiting for presentations in this form, or you just want to have a look around, please go to the downloadable audio page now.

Facebook page

The Rachel Arthur Nutrition page is our first new project for 2014

We have finally taken the step into the brave new world of social media with the Rachel Arthur Nutrition facebook page.

The first step is to reflect the posts that we add to this site and our newsletter. We will let you guide us as to what you would like to see us do with it in the future.

In the meantime please “like” us so that we can start to get traction in that corner of the online world.

 

Scenario: Patient presents with low baseline 25(OH)D levels, let’s say 40 nmol/L and you prescribe a high  dose (e.g. 5000IU/day) bioavailable vitamin D supplement and retest in 3 months but the 25(OH)D levels haven’t improved…what do you do now?

Sound familiar?  It does to me. Once we have ruled out the usual suspects like taking the supplement at the wrong time (must be taken with a full stomach to ensure optimum fat digestion & uptake), inadequate dose (keep in mind that due to altered pharmacokinetics individuals with  obese BMI will require a significantly higher dose) etc. then according to new research from Deng et al. Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III, we should be reviewing the patient’s magnesium status pronto! Deng et al remind us that magnesium is the co-factor for 3 critical enzymes central to vitamin D metabolism. Previous in vitro research suggests that magnesium status regulates both 1α-hydroxylase and 24-hydroxylase activity and the binding of vitamin D to its transport protein and 25-hydroxylase might also be magnesium dependent. You might remember as well that the synthesis and metabolism of PTH (the critical cue for activating 25(OH)D to 1,25(OH)2D are reliant on health magnesium status.

All in all this places magnesium front row for a starring role in vitamin D metabolism.

Only isolated previous research showed the strength of this relationship with a 1974 study describing ‘magnesium-dependent vitamin-D-resistant rickets’, which was effectively treated with magnesium & vitamin D, while vitamin D alone was completely ineffective. 

This recent research has demonstrated in a large cohort inadequate magnesium intake was more potently related to the presence of vitamin D insufficiency in individuals than vitamin D intake!

While this is only epidemiological research at this stage – it’s certainly a scientifically plausible concept and adds another element to the strong relationship between low 25(OH)D levels and increased all-cause mortality which numerous studies point to.

So next time when a patient’s 25(OH)D levels appear non-responsive to vitamin D supplementation – ask yourself, ‘Have they got enough magnesium?’

 Read the full paper by Deng et al here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765911/pdf/1741-7015-11-187.pdf

Over the last year, I’ve seen paediatric patients with various presentations (alopecia, behavioural issues etc.) whose thyroid results have seemed out of whack e.g. TSH values in the 3s and 4s.  I noticed as well that each pathology company provided a slightly altered reference range but on the whole they weren’t significantly different from expected adult results (0.4-4.8 mU/mL). It left me wondering if there should be in fact specific reference ranges for kids given the striking developmental endocrine milieu.  So began a brief search of the scientific literature and lo and behold (!) there is such a thing and guess what?  Kids’ thyroid results do differ from adult ones!!  One piece of research that was intended to establish kids’ reference ranges was conducted in Austria, where routine results (serum TSH, fT3, and fT4) were collated from existing laboratory data of 2,194 serum samples from a hospital based population of children aged 1 day – 18 years (Kapelari et al. 2008 Pediatric reference intervals for thyroid hormone levels from birth to adulthood: a retrospective study. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645400/)) Granted, these children are in hospital and yet deemed ‘healthy’ – which is a bit befuddling, however, the ranges found by these researchers were consistent with other previous studies in different cohorts, which adds strength to their findings.  They revealed that TSH should be highest at birth and in the first month (e.g. 3.5 is the 50th percentile for this age group) and progressively decline throughout childhood and adolescence.  So 50th percentile results across the age groups looks like this:

Age

TSH 50th percentile values

TSH Range

0-1mo

3.5

0.75-16.89

1-12mo

2.85

1.30-7.09

1-5yr

2.1

1.00-5.42

6-10yr

2.3

0.90-4.40

11-14yr

2.1

0.09-4.10

15-18yr

1.7

0.70-3.93

 

While there is a clear pattern of declining TSH with age throughout childhood, there were less changes across the ages with regard to fT4 and fT3 values, with the 50th percentile value for fT4 being approx. 15 pmol/L in all ages except 1mo and fT3 being high 5s to mid 6s.  These are more robust values than we’ve come to expect and accept in many of our adult patients.

So next time you see thyroid results for a child – check out where they sit according to these percentiles, because where there’s smoke there’s typically a fire and further investigation of a marginally high TSH can reveal, antibodies, incorrect T4/T3 ratios and deficiencies of critical thyroid nutrients which might be central to helping resolve the health issues.