Seeing female patients with anxiety/depression, irregular menstrual cycles and perhaps marked PMS? How about male clients with decreased libido, low measurable testosterone and perhaps even impotence or infertility? All of these signs and symptoms could actually be the result of elevated prolactin.
Our patients are faced by more health & nutrition messages via multiple mediums than ever before yet escalating rates of obesity & lifestyle related disease highlight the failure of these. It would seem behavioural psychologists are right when they assert that information does not change behaviour in the majority of people. Therefore if we too simply add to our patients’ information overload, we’ve missed the point. One of my favourite & at the same time terrible illustrations of this was when I walked into a local café and saw a man sitting at a table by himself having just finished a cup of coffee and something sweet. On the table next to his coffee was a very recognisable ‘prescription’ from a naturopath he’d obviously just been to see.
- Reduce coffee
- Reduce sugar
- Reduce fat
- Increase exercise
Oh the power of such words!! If we spit out advice/instructions/directives at our patients, even with all the best intentions, we seem to make very little progress or only create short-term change. In contrast, if we take the time to focus in on each change we wish the patient to make, individualise the approach and solutions then we may have only given them a small fraction of the ‘advice’ we ultimately want to but at least this time it’s actually met it’s mark and created life-long healthy habits.
An understanding of the components behind successful behavioural change (readiness, empowerment, barrier identification & resolution etc.) is essential to improving patients’ health & wellbeing. If you want to hear more about how to successfully promote behavioural change in your patients follow this link https://rachelarthur.com.au/product-category/premium-audio/ to a premium audio download I recorded on this topic last February. I really believe it can make the difference between success and failure with individual patient’s treatment & the success of your practice overall. Enjoy and remember more information isn’t the answer!
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?
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
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.
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