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.
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
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
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.
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?’
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.
This week, care of Health Masters, I am delivering the first part of a 3 part webinar called ‘Clinical Case Analyses in Women with Anxiety’.
I originally wanted to call this brand new seminar series Dis-ease.
The idea was in response to the large number of female patients who come through my clinic door, presenting mostly self-diagnosed with anxiety. Some of these women absolutely do have anxiety disorders and both the aetiology & maintenance of these fit with the regular psycho-social theories, however, many of them, upon further investigation, have something biologically going on that constitutes a plausible alternative cause of their dis-ease.
That’s where the interesting journey begins as
you start to identify what’s the physical source of sensations they have reinterpreted/translated as ‘anxiety’ and
you start to address these physical drivers and relieve their negative psychological affect and then finally
you see how the discovery and recognition of a biological rather than a purely psychological explanation behind their ‘anxiety’ challenges women to rethink their self-story.
It’s big and thrilling stuff to be a part of and one of the most satisfying aspects of my practice.
This is the latest instalment in mental health education from me but from an entirely fresh perspective.
I’ve buried my head in the journals & leant heavily on my colleague who’s a psychologist to bring to you the first instalment this week – understanding the long list of differentials for patients who present with anxiety and how to approach the work up.
The following two weeks are dedicated to presenting 2 amazingly anxious female patients of mine – with case summaries, all the pathology results etc. so that you can see the journey I took with them and why.
I hope to ‘see’ you there.
If you’re not on the Health Masters mailing list already and want to check it out click here.
Professor Andrew Sinclair, a leading Australian nutrition scientist from Deakin University, has warned that some snack foods on Australian supermarket shelves contain high levels of trans fats acids (TFAs) and is calling for mandatory labelling of TFAs in processed foods.
Societies promotion of happiness and happiness campaigns puts expectations on people of how they should feel. Expectations of happiness may be making sad people feel worse.
Upper respiratory tract infections (URTIs) are a normal part of childhood that often disturb sleep, parents and children alike, but a simple dose of honey may just be the remedy needed. A recent study published in Pediatrics (Aug 6 2012) has confirmed that honey is more effective than placebo in controlling nocturnal cough and poor sleep in children with URTI. (more…)
Parents should be aware persistent snoring is not normal in children and should be investigated. Researchers, whose results appeared in the journal Pediatrics May 2012 found that two- and three-year olds who snored loudly at least a couple of times per week tended to have more behavioural problems, especially hyperactivity, depression and inattention.
The limitations of serum B12 testing have been reported for some time.
When testing for deficiency, Serum B12 does not give an accurate picture unless there is an overt deficiency and even then not consistently. This is because the majority (approx.70%) of B12 in the blood is attached to haptocorrin, which is unable to enter cells, and is termed inactive B12 (Lloyd-Write et al 2003).
), 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 🙂
