How often were we told this in our training? And how often have we found this to be true in practice? And now suddenly, it seems, the medical researchers (at last!) are rapidly coming around to this core concept?? Our microbiome is suddenly the hottest property on the body block, and it seems every interested party is shouting, ‘Buy!Buy!Buy!’ As integrative health practitioners, of course, we had a major head-start, not just by appreciating the gut’s central positioning in the whole health story (iridology beliefs, maps & teasers aside!!) but also a heads-up about the damage the western diet, our medication exposures and lifestyle tend to wreak upon it. A favourite quote of Jason Hawrelak’s by Justin Sonnenburg, “The western diet starves your microbial self”, underscores the significance of just one element of this impact. And…are we all clear that the increasing number of patients reporting adverse food reactions, once again, overwhelmingly are a response to aberrant processes in the GIT?
Sounds silly it’s so obvious right, but it’s easy to get distracted & misattribute blame…for example, it’s the food that’s the problem. Well yes in a minority of situations interactions between someone’s genes, immune system and a particular food turns something otherwise healthy into something pathological, but for the majority, the food itself & in others is healthy, & could be beneficial to this individual, if only we could resolve their GIT issues…like FODMAPs for example.
Not the problem, just the messenger.
So if the ‘problem food’ is just the messenger, what’s the actual message we need to understand? Is it that this patient has medication, disease or otherwise induced hypochlorhydria, impairing ‘chopping up’ of potential antigens implicated in immune mediated food reactions? Or is that this person’s got fat maldigestion &/or malabsorption so that in addition to not tolerating fats, they may experience dietary oxalate intolerance to boot? Or are the food reactions the result of altered microflora changing what we can and can’t digest (via their critical contribution) & absorb?
So what message does the presence of IgG antibodies to consumed foods send us about the state of someone’s gut? It’s telling us 2 things: this individual exhibits abnormal intestinal permeability & currently in the context of this leaky gut, these foods may constitute a barrier to resolving this & other symptoms as well.
We’ve recently released the mp4 (that’s audio plus the movie version of the slideshow so grab your popcorn…that’s if you don’t have a corn issue!) of A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it? which details the science behind IgG, including debunking, the incorrect debunking of IgG food antibody testing!! But more than this, it overviews the whole maze of adverse food reactions, articulates a logical investigative path for practitioners through this maze, and helps us to really understand that finding the food(s) responsible for a patient’s symptoms is not the final destination..and can be in fact a distraction, if we don’t cut to the chase and find out the why…and funnily enough…my dear old iridology teachers and colleagues...it almost always comes back to the gut 😉
Confronted with the possibility of adverse food reactions in an increasing number of our patients can be an overwhelming prospect, in terms of accurately identifying and understanding the faulty mechanism underpinning these aberrant responses to healthy foods. Elimination of culprits in most situations is only a short term reliever, not an appropriate long term solution, so to optimise results we need to know the real mechanism of action. The majority of these, of course, stem from the gut, but being able to elucidate exactly which of the many things that can go wrong there, is going wrong and therefore what foods are problematic until we address this, is the key. This 2hr mp4 is all about the bigger picture and helping you find method in the madness that can be the AFR landscape. Along the way, we detail the science of where IgG reactions fit into this and it’s a fascinating story that just might be the missing puzzle in your leaky gut patients.
and watch this presentation now in your online account.
Q: If a patient says they can only tolerate 7 foods…how many did they start with?
A: Typically about 20
No, this answer doesn’t come from some complex mathematical formula…it comes from appreciating the low dietary diversity of those eating a Western diet. When we boil down these diets to the number of foods from different biological origins (families) it can be a frighteningly small number.
You see, like most practitioners, I feel utter dread when I encounter the patient who prefaces their diet story with a statement similar to the one above. It speaks to the severity of their symptoms, their attribution of these with food, that by the way is essential for their sustenance and nutritional salvation, and implies an exhaustive pursuit they’ve undertaken probably over years to find ‘safe foods’. And yes, as discussed in my recent talk A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it? – food reactions, as in more than one mechanism of food reaction, often do move in packs and that comes typically back to a poorly functioning gut…BUT…that latter assumption…’they’ve explored and exhausted all foods’ is the one we need to keep in check.
Have they tried daikon? Prickly pear or jambu? Okra? Snake beans? Quail or duck eggs? Kangaroo? Crickets? Etc Etc. Etc.
Are you catching my drift? Because someone has DIY diagnosed a wheat, dairy, soy and, and, and, reaction (correctly or incorrectly) and perceive themselves to react also to most of the limited fruit and veg they can identify in Woolies…doesn’t mean they’ve remotely exhausted the global food supply! Where am I going with this? When patients tell us they’re down to 7 foods they can tolerate – some sensible follow up actions on our behalf may include:
- Check the strength and validity of their level & strength of evidence for their DIY diagnosis
- Think about the linking ‘process’ (more than likely gut) that is the real potential issue (aka don’t eliminate the messenger and do nothing more!)
- Encourage and advise them to shop anywhere other than where they normally do – somewhere that sells fresh produce they don’t recognise at all…like Asian, Indian or Middle Eastern supermarkets and grocers
My tour of A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it? (and the weeks of lit review leading up to this) provided me with enormous food for thought…and this is just one! If you want to hear more about how to find method in the madness of food reactions…you should probably listen in to the whole shebang…goodness knows with the increasing number of patients who present with self-determined food reactions and an increasingly narrow menu of safe foods…practitioners and patients alike need all the help we can get!
Confronted with the possibility of adverse food reactions in an increasing number of our patients can be an overwhelming prospect, in terms of accurately identifying and understanding the faulty mechanism underpinning these aberrant responses to healthy foods. Elimination of culprits in most situations is only a short term reliever, not an appropriate long term solution, so to optimise results we need to know the real mechanism of action. The majority of these, of course stem from the gut, but being able to elucidate exactly which of the many things that can go wrong there, is going wrong and therefore what foods are problematic until we address this, is the key. This 2hr mp4 is all about the bigger picture and helping you find method in the madness that can be the AFR landscape. Along the way we detail the science of where IgG reactions fit into this and it’s a fascinating story that just might be the missing puzzle in your leaky gut patients.
Click here to purchase A Guide to Investigating Adverse Food Reactions – What’s IgG got to do with it?
So you’ve gone to all the effort. Be that writing referral letters suggesting some pathology investigations might be warranted or you’ve coached your patients endlessly to get copies of ones done elsewhere so that you may be privy to their findings. Worse still, you’ve directly requested the pathology, with your patient paying out of pocket for the tests. Then the results come in and they look…well wrong. You, as the conscientious clinician, typically do 3 things:
Step 1 Spend hours pouring over & over the labs and back over the case notes
Step 2 Worry about the new differential diagnoses that are now suddenly seemingly a possibility in your patient. It doesn’t look good.
Step 3 Doubt your own pathology reading ability, ‘Hey maybe I just don’t understand these bloods like I thought I did’
But (often)…it’s not you, it’s them.
And that’s what I often explain to practitioners who contact me (step 4). You see sometimes what they’re losing sleep over are what I call, Bad Bloods. Occasionally, the fault of the pathology company…but way way way more often the fault of the patient and the referring practitioner, who has not educated the patient correctly about what to do and not do prior to blood collection for certain tests. I am excited to see how many practitioners are competent with pathology reading these days and building their skills and confidence all the time, that’s why it is so so disheartening for the practitioners (and for me as a mother hen mentor) when they lose time (& sleep) getting to Step 3 when they should be able to spot ‘Bad Bloods’ fast. There are 7 classic give-away patterns.
Will are unlikely to know every quirk of every blood test our patients will ever have done, but knowing what constitutes the ideal time and conditions for the most commonly performed ones, can go a long way to minimising any future Bad Bloods between you and patient as well. This includes things like exercise, alcohol intake, duration fasting and even sexual intimacy…yup!
This month’s Update in Under 30 installment Beware of Bad Bloods teaches you the 7 patterns to watch for and provides you with a great resource stipulating the best collection conditions for the most common blood tests. Don’t let Bad Blood come between you and your patient, the right diagnosis & management or just some well-deserved sleep!
Good practitioners are being led to bad conclusions by some patients’ pathology results. Not because they can’t interpret them or the testing has no merit but because they just don’t know when to discard a set because they are ‘bad’. Occasionally, the fault of the pathology company but much more often the fault of the patient and the referring practitioner, who has not educated the patient correctly about what to do and not do prior to blood collection for certain tests. This recording clearly describes the 7 classic give-away patterns of ‘Bad Bloods’ which will enable you to spot them fast in the future. In addition to this. while we are unlikely to know the idiosyncrasies of very lab our patients will ever have done, knowing the ideal collection times and conditions for the most common ones assists you and your patients to avoid any in the future – handy clinic resource included.
Hear all about it by listening to my latest Update in Under 30: Beware of Bad Bloods.
For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
Oh no, it’s her again 🙁 I mean the chick in the photostock image not the other ‘her’, me. I know. It’s the end of another mammoth year, you’re tired, worn out, used-up all your brain-power quota (a little projection?) and I can hear you begging for mercy when I start a sentence with…”So you think you know….” followed by, “blah blah blah Iron,” but hear me out.
Correctly identifying & managing iron issues is a bread & butter part of our business, right?
With Iron deficiency affecting an estimated 1 in 5 women and Iron excess almost another 1 in 5 – patients with one form of iron imbalance or another tend to be over-represented in waiting rooms.
Anyone can spot overt iron deficiency anaemia or full-blown haemochromatosis but many health professionals find the ‘in-betweens’ confusing and fail to recognise some key patterns we see over and over again, that spell out clearly your patient’s current relationship-status with this essential mineral. This often results in giving iron when it wasn’t needed and missing it when it was. If you’re imagining someone else, i.e. the person who ordered the Iron Studies for your patient, will step in and accurately interpret the more curly results can I just say D-O-N’-T...they’re often as perplexed or even more so than you. After starting this conversation a year ago with So you think you know how to Treat Iron Deficiency, & its baby sister, So you think know the best Iron Supplements, our (imaginary) switchboard went crazy. While practitioners got the message loud and clear about how to improve the likelihood of treatment success in iron deficient patients, hot on the heels of this came email, after fax, after carrier pigeon, with examples of patients’ Iron Studies, the ‘somewhere in between ones’, accompanied by the equivalent of a dog head tilt…aka ‘I don’t get it’.
And this is to be expected.
What were you taught about reading Iron Studies? Was it made out to be all about ferritin? And TSH is a solid stand-alone marker of thyroid health, right? 😉
Were you introduced to the other essential parameters included in Iron Studies, explained how they contribute to your diagnosis and reveal important details about the patient’s ability to regulate this mineral or not? About when to dose and when to hold your fire?
Nah…I didn’t think so. But it’s up to us, people, to hone our skills in Iron Study interpretation…because individualised nutrition is our ‘thang’ and more than any other nutritional assessment, this collection of markers, actually allows us to go beyond the ‘one size fits all’ model…everyone must have X of this and Z of that in their blood tests…and see each patient’s actual individualised need and relationship with this mineral. In the latest Update in Under 30, I introduce you to 3 key players in iron assessment and the insights each offers become so clear, you’ll be able to read any combination or permutation of iron results that walk through your door. To boot, I’ve included a wizz-bang cheat-sheet of those iron patterns that are frequently seen and rarely recognised, including one totally novel one that I’ve never talked about before…to make your job even easier and put you well and truly ahead of the pack in understanding iron nutrition. It’s Christmas…and as the mantra goes…we can always fit just a little more in at Christmas time, right? 😉
Overt Iron Deficiency Anaemia or Haemochromatosis aside…do you understand the critical insights markers like transferrin and its saturation reveal about your patients iron status? Most practitioners don’t and as a result give iron when they shouldn’t and fail to sometimes when they should. This audio complete with an amazing cheat sheet for interpreting your patients Iron Study results will sharpen your skills around iron assessment, enabling you to recognise the real story of your patients’ relationship with iron.
Hear all about it by listening by my latest Update in Under 30: So You Think You Know How To Read Iron Studies? For all Update in Under 30 Subscribers, it’s now available in your online account and if you are not a subscriber you can purchase this individually here.
So we already know that thyroid problems can start in utero, right…but a recent Medscape review (the fountain of thyroid information that I frequently drinketh from 😉 ) on Hypothyroidism in childhood taught me a couple of big things I hadn’t known before!
The diagnostic criteria for subclinical hypothyroidism are raised TSH levels in combination with a normal concentration of free serum thyroxine (FT4) but because there are some differences between accepted ranges in TSH assays, high-risk groups should be screened, especially babies with malformations, whose mum received steroid treatment during pregnancy or in the neonatal period, or who had existing thyroid dysfunction, TFTs (or at the least TSH as part of what’s called the Neonatal Screening test) should be repeated 2 weeks later. But now comes the couple of big light-bulb moments: the incidence of eutopic thyroid in twin births is nearly double compared with singletons! As you know, I’m a mother of twins and I’m guessing at 18yrs old now (and multiple peachy TFTs 😉 ) the horse has well and truly bolted for my two but geez…I had no idea of the dramatic increase in risk. And it keeps going…monozygotic twins very commonly show a delayed TSH rise and those numbers are even more prominent in multiple births. The other not-so-fun-fact is the discovery that subclinical hypothyroidism in IVF babies is approx. 10% which is noteworthy considering none were observed in the control group.
This obviously left me thinking “W.H.Y?” And of course…the first place my head goes with the latter…is iodine.
Could this phenomenon in IVF babies be due ultimately to undiagnosed or poorly managed SCH in mum or even simpler still, just basic iodine deficiency, presenting as infertility?!
The reasons behind our increasing rates of thyroid dysfunction across the life-stages are multifactorial (and don’t get me started on the very real contribution of EDCs!) and how, in spite of iodine adequacy being the first thing on the checklist for thyroid health, so many health professionals ignore this, at their patients’ peril… But now at least we know that patients with IVF babies, twins, and preterm bub, who are currently not included in the prioritised screening groups should be…and of course we should keep asking the questions, “what are the mechanisms behind this, why is it so?”
So if this has made you even more curious about the incredible butterflied-shaped gland and you’d like to go for a stroll on the vast plains of “thyroidisms” you can click on this link Thyroid Assessment in Kids and Teenagers and get completely “thyroided” up. There is always more research to come our way so keep your eyes and ears peeled.
A few months back I seriously ‘blew over’. Not on an RBT but on a UBT (Urea Breath Test). In spite of it being not the kind of test you want to score top marks for, my result was in the high 2000s, when all I needed was around 800 to confirm, and anything over 50 to be suspicious, that Helicobacter pylori had taken up residence in my stomach lining. I tell you, I knew it when I blew it! 😉 After ingesting the radioactive urea and waiting to blow up my sampling balloon, I felt like I could still fill a room full of balloons with all the gas being produced in my stomach and those balloons, I imagined, would all rise to the ceiling as if full of helium! Yep…I burped all the way home, which was representative of what I’d been experiencing daily for a month beforehand and what lead me to get the test done.
But initially, it wasn’t so clear.
The very first symptom I experienced was a sudden onset of severe tightness around my throat that lasted for minutes but started to happen multiple times in a day. Yep..no one panic. Together with a strange sensation of ‘extreme emptiness’ in my stomach on waking or delayed meals, and then mild nausea both with an empty and full stomach…only some days or weeks later the fabulously-unprecedented-&-socially-adorable-burping started, proper.
So a month or so later, I’ve solved my own mystery. Happy? Not in the least…where the heck have I picked up H.pylori from? Yes…that’s what I said because it had to come from somewhere people…right? I think there is much we have misunderstood about this bacteria with an incredibly long and interesting human history. Animals don’t and can’t carry this bacteria. The evidence suggests that it can’t survive for very long in the environment either (approx 4 days) but that is long enough to get into our food and water and maybe even onto shared chopsticks…just saying (listen in to hear the lowdown on all these and more!) Essentially hoomans are the traffickers, people! In fact one of the things that surprises people the most is the very high prevalence in young children and the clusters of positive tests & identical strains within families…but once you learn a little more about this bacteria…it won’t surprise you at all. (more…)
I’ve had my nose in all the research on Gilbert’s Syndrome again..watch this space…in the interim just thought I’d share this image and a couple of important details I may not have been able to convey when you last heard me talk (very fast!) about this important and common polymorphism:
- While the incidence is approximately 10% of Caucasian population, rates are heavily influenced by ethnic background and the highest rates (up to 1/4) are seen in Middle Eastern populations
- Gone are the days of thinking this condition only effects bilirubin levels and the enzyme responsible for its clearance – more recent research has shown over 3/4 of patients with Gilbert’s Syndrome have multiple SNPs that compromise clusters of enzymes within the glucuronidation pathway – with varying patterns – this goes a good chunk of the way to explaining the variability we see in bilirubin levels and symptom pictures across patients all deemed to have Gilbert’s Syndrome. This also explains why figures of reduced glucuronidation activity vary anywhere between 10% less to 90% less! It depends on your cluster..but the average reduction is around 50%
- UGT enzymes, the ones affected in Gilbert’s, are also expressed all the way down the GIT and constitute important food and drug handling. These UGTs are most active in the small intestines,as you can see above, but may explain why Gilbert’s patients are ‘more sensitive’ to medications than just paracetamol!
- And are you still thinking you need to run an $$$ gene test to confirm your Gilbert’s hunch in a client whose bilirubin sits consistently high normal or high? Think again… here’s a great little diagnostic short-cut that even the Royal College of Pathologists Australasia cites as sufficient evidence to confirm the polymorphism:
In the face of elevated total bilirubin levels and in the absence of liver pathology or increased haemolysis to explain this..”If the diagnosis is uncertain the serum bilirubin fasting level can be measured and should exceed the non-fasting level by >50%.”
Nice. So that means you only need to demonstrate that the patient’s fasting total bilirubin levels go up by at least 50% compared with their fed levels and BINGO you have your diagnosis. Much easier. Oh and this image comes from an interesting paper from Tukey & Strassburg 2001 – but is probably not for the faint-hearted 😉
Stay tuned for more 🙂
Just new to this condition and need a soft place to land with understanding Gilbert’s Syndrome? This previous UU30 is just the thing! Affectionately called Gilbert’s Girls because in particular it details a set of twins with this condition, this short audio explains the basics about this common polymorphism and why we tend to see a lot of patients who have this…even if no one has pointed it out to them yet! You could be the first to provide them with this important understanding about how genetics is impacting their detox pathways, changing their sex hormone handling and perhaps setting them up for both mental health issues and some serious upset guts! Better still, what to do once we have that diagnosis.
These little blighters are getting a lot of airplay this month and rightly so…..! Oh Em Geeeeeeeee….so much misinformation out there!! It’s time to set the record straight
Worm infestations never conjure up a pretty picture in our minds although a video of humans trying to bum slide across the floor like some dogs we know would get a fair few laughs (…will share that vid later)
Despite much talk of the potential therapeutic activity of helminths for things like autoimmune diseases and allergies due to their immuosuppressive effects, there’s nothing nice, friendly or ‘good for us’ about a chronic Enterobius vermicularis (threadworm) infestation in a child or adult (YES! You heard me). Oh and don’t forget the possible link with your D.fragilis patients…you just might need to treat these guys instead.
It was great to get down and dirty on worms with Andrew at FX Medicine. This podcast has us uncovering and debunking myths on these creepy critters that have more to answer for than you probably realise…
The outcry from the public is enormous, in terms of their need for help and the gaps that are there at the moment in terms of getting it. There is an online resource called thewormwhisperer.com.au, which is primarily there for the public to meet this need and practitioners can learn a lot by going on there as well.
You know I’m not one to raise my voice and make scene.
Ok, I always raise my voice and make a scene, but only when I think something really warrants our attention and the issue of under-recognised, under-estimated and mismanaged chronic worms, demands our attention. I’ve been talking about this ever since the first patient stepped into my clinic, a young girl with severe mood issues who just happened to also have treatment-resistant chronic threadworm, and since then, as the volume of patients I see affected by this has grown, so too has the volume of my message. And there’s actually so much to say.
Chronic worm problems don’t always come with an itchy bottom calling card. In fact, many individuals don’t have any of the telltale signs you might be used to screening for. Recent research suggests adult men, in particular, are commonly asymptomatic when infected with them (Boga et al 2016)
So what alerts us as practitioners to the possibility of chronic worms – so many things…but here’s just some thought bubbles to get you started.
Are you treating patients with recurrent or treatment-resistant Dientamoeba fragilis?
Are you seeing women who have thrush-like symptoms, in spite of negative swabs and no benefit from antifungals?
Are you faced with families coming undone because of one child’s behaviour whether that’s aggression, defiance, emotional lability or just serious sleep problems? (more…)
Sometimes we wonder who put the invisible sign up out the front of our practice, right? The one that says…absolutely everyone with Condition ‘Z’ come and see me, now! I’m sure you know what I’m describing. Well this week I have hit the trifecta, performed a neat little hat-trick and diagnosed 3 patients with Gilbert’s Syndrome who all present in their own individual way but actually each one also with quite a textbook Gilbert’s picture, it almost beggars belief. Have a little look
70yo Female says: Since childhood she has felt like she has had a rock in her stomach after she eats. This ‘rock’ is there for hours. Her stools are never the same in spite of a regular diet and she has always been uptight and anxious. All her bilirubin results are in the 20s & she reports she’s ‘always’ had high values
55yo Male with severe ‘constitutional anxiety’ and surprisingly high oestrogen and a worrisome profile of oestrogen metabolites. His bilirubin is in the 20s
30yo something Female presents with unexplained severe unwellness for 20yrs that mostly involves nausea, bloating, a functional gut disorder without a real diagnosis, anxiety, depression and poor stress tolerance. Her bilirubin fluctuates between 30 to high 40s. (more…)
I have a good friend…who happens to be a naturopath…who happens to also be a patient of mine. Have you got a few of these as well? A month ago, looking over her recent bloods which included fasting lipids that had been steadily climbing for the last couple of years, post-menopause, she said, ‘do you think I should take something for that?’ Ahhhhhh no. My reasoning went like this:
“You love saturated fat right? You eat butter and cheese and and and…and the type of elevated lipid pattern you have LOOKS like it is at least partially the result of this, your triglycerides are low, your HDLs are good it’s just this LDL component that is too high. You could add in another supplement…and take it…forever…or you could do a little n=1 experiment and just lower your butter, cheese & coconut oil intake for a month and repeat the test.”
The horror on her face! You see I didn’t know exactly how much she loved butter but it all became clear with the first text a few hours after I had thrown down the gauntlet…which included a sobbing emoji and the comment that her afternoon snack will never be the same…turns out it was a shortbread biscuit with butter on it!!! But as a practitioner who does pride herself on walking the talk…off she went determined to give it a good go for a month. But boy did it hurt! (more…)
They’ve just come from the immunologist, having presented with extensive vitiligo in dad and early stage vitiligo now in their primary school aged son. The immunologist, without running a single blood test, told them, ‘Bad news, you both have autoimmune issues and watch this space because the vitiligo is just the first presentation, there will be more to come’. Slightly unsatisfied with this dead-end conclusion and non-existent management plan, the family then presents at a long established naturopathic clinic to see Anna Sangster, a fabulously sleuth-like detective, who takes her patients’ health very seriously and has the knowledge and skills that make her one of the best at what she does. I can say that because I’ve been mentoring Anna for a long time & she is one of the clueiest practitioners I know.
For example, she knows about the substantial research demonstrating the overlap between thyroid autoimmunity and vitiligo and, in addition to comprehensive case taking, decides some blood tests may provide valuable insight that would help to understand the degree of self-attack from their immune systems, identify if there are in fact already concurrent autoimmune targets and perhaps even provide a clue as to underpinning drivers. Well, look what she found! (more…)
Is this the way of the future for health practitioners interested in patients’ digestion…?
“The team developed an ingestible electronic capsule to monitor gas levels in the human gut. When it’s paired with a pocket-sized receiver and a mobile phone app, the pill reports tail-wind conditions in real time as it passes from the stomach to the colon…The authors are optimistic that the capsule’s gas readings can help clear the air over the inner workings of our intricate innards and the multitudes of microbes they contain. Such fume data could clarify the conditions of each section of the gut, what microbes are up to, and which foods may cause problems in the system. “ (more…)
Recognise your own name or someone else’s on this list?
Dear 2017 Group Minties aka Mentees. I have always struggled with the term, ‘mentees’…seems too American or something and this morning when I was out walking, I had a light-bulb moment – I am proposing a re-branding to something much closer to home (!)… I propose we rename you Minties!! Because you are always fresh and you give me & your fellow Minties always something; cases, questions, clinical conundrums, ethical dilemmas, every month to seriously get our teeth stuck into! Cheesy but true 😉
Congratulations on completing your full year of group mentoring – and if this is your 2nd, your 3rd even your 4th year then I bow to you even more deeply.
Thank you for including me on your support team and entrusting me with helping you grow & develop as exceptional practitioners.
You should be celebrated for your commitment to your own learning & your endeavour to always improve your knowledge and skills. (more…)
Standing at the podium, I looked down at my notes & slowly read out the title of my presentation to the hundreds of people attending, ‘Paediatric Digestive Issues & Neurocognitive Abnormalities’ and briefly froze thinking, Holy Heck (!) this is someone else’s presentation! Seriously. No, this is not one of my work stress dreams. This happened. I thought…oh my how am I going to deliver this, it sounds very complex and lofty and scary!!
Then I saw my scribbled hand notes on the page, the unofficial name I had affectionately given this presentation as I researched, compiled my case studies and brought it into being, months prior and I instantly relaxed…oh…Kids’ Guts Are Mental…now that I have some serious experience with and something to say about! (more…)
Have you been a bit vitamin D trigger happy? Does a patient’s low blood 25(OH)D test result have you reaching for a vitamin D supplement like the rest of us? Yes…you might need to listen up then. Sunshine doesn’t come in a bottle. That’s right, if your patient’s problem stems from inadequate sun exposure, have a guess what the best remedy is. I’m not meaning to sound flippant but I think in all my ‘complex highbrow nutritional understanding’, occasionally (ahem), I have lost sight of the simple truths. (more…)
Chronic coughs, rhinitis, postnasal drip or even asthma? Have you ruled out silent reflux? Aka laryngopharyngeal reflux. Patients experiencing silent reflux don’t present with heartburn or any typical GORD features but ultimately suffer from a similar failure of the lower oesophageal sphincter (LOS) – with their complications manifesting higher up, into the upper digestive and respiratory systems. An overlooked and under-recognised condition, medical opinion has fluctuated about its name, prevalence, significance, management…you name it…however there is now a strong body of evidence that says this condition should be diagnosed and investigated as a cause of many of these otherwise unexplained chronic symptom pictures.
Take this case from group mentoring last month: (more…)
I had the privilege of presenting at the Integria GIT Symposium last weekend. For those of you who attended, you’ve gone back to your clinic with a bunch of new ideas and inspiration I hope…oh and a new respect, terror and watchfulness for threadworm thanks to me! In my presentation I outlined the many presentations of this infestation, what to watch for and the risk of chronic recurrence due,in particular, to a reduced ability for some individuals to produce chondroitin sulfate which renders the GIT environment hostile to worms.
Chronic threadworm is a huge & grossly under-recognised issue in paediatrics, often presenting as behavioural & cognitive disorders (and these can be severe), bruxism, enuresis etc. of course, but another presentation typically missed is vulvovaginitis, vulval pain or UTI like sx in young girls. (more…)
Can you help me out here? My memory has failed me. Someone, somewhere (Mel? Syd? Auckland? Online during a mentoring session? In a Mullumbimby supermarket?!), in the past month asked me for this paper documenting the increased pain perception reported by subjects given IV saline with a slightly acidic pH compared to a neutral preparation. Quite an extraordinary illustration of the potency of small pH changes in the ECF and the impact this can have on our pain perception. This study is one Professor Vormann has previously talked about and as I’m touring with the fabulous German Professor right now I said, ‘Sure!’…then seemingly instantly erased from my mind who made this request! Is it you?
This month is a fabulous blur of travelling & speaking, getting back face to face with everyone at a bunch of seminars & conferences, which I love but I do forget some days where I am, who I am and exactly what I have promised and to whom! (more…)
…Chronic Kidney Disease (CKD) that is! That’s the ad we really need broadcast on prime time tv. On par with osteoporosis and other conditions that ‘seemingly appear out of nowhere’ in people’s 60s and beyond, there’s a potent combination of ignorance (patients) and denial (health professionals) at play it seems, when it comes to discussing the earliest signs of CKD that typically start decades before you’ll ever get a ‘diagnosis’. Being specialists in preventative health care – this is something we need to have firmly on our radar in terms of early identification and also in our repertoire when it comes to risk reduction. Most of us know about water intake and all the medical risks for renal impairment but are we equally onto the critical role that mild acidosis plays in driving this condition?
It’s not just me. Promise.
Check this out. (more…)