“My 7yo daughter was frequently distressed, telling me she had that ‘throat feeling’.”
As you can imagine, mum offered up a smorgasbord of suggestions to help her try and describe it: Can you swallow ok? Does it burn or taste funny? Where is it? Is it hard, soft, moving, give me a rating out of ten….so many, but she just couldn’t. When it was really bad, her daughter said she also felt it in her sternum. The first doctor attributed it to ‘stress’ & mum understood why. Her 7yo is a bit of a worrier and while the ‘throat feeling’ was distressing, stress, itself, seemed to also perhaps bring this on. But by the time they made an appointment with their regular family GP, mum had noticed her daughter’s sx were worse with heavy, fatty, high meat meals & that she was burping excessively especially with the night time meal also. So, when their switched-on doctor heard these very careful observations, he referred her for a urea breath test (UBT) for H.pylori.
‘Miss 7’ blew 1200 on the UBT the decision limit is 200, to confirm the presence of the bacteria in significant amounts
As I’ve said previously, there are (sadly for ‘Miss 7’ & myself) no prizes for the highest score on this particular test. In fact, I spoke with a gastroenterologist last week who said, really it remains so debateable about the significance of the overall result (?size or virulence of colony) that results should probably be more considered like a pregnancy test: a simple yes or no! But this together with her sx was a clear yes. GP recommended triple antibiotic therapy which sadly produced vomiting in Ms 7 within a few days. GP contacted paediatric gastroenterologists to get some advice, which was: don’t treat unless symptomatic. Back to square 1.
“In the meantime, I had done Rachel’s two UU30 episodes on H.pylori, so I told him what ‘we’ would do (polyphenols plus cranberry juice plus Zn carnosine plus deal with the hypochlorhydria). GP says. “Ok, then let’s do it and then let’s breath test again in 3-6 months.
She has now breath tested at 200 and symptoms are non existent!”
Mum contacts me to relay the success story & give me the credit but mum is completely minimising her extraordinary actions that produced this outcome. Firstly, not resting with the ‘stress’ diagnosis. I have seen several children who present in very similar ways to Miss 7, YES! they are anxious, YES! parents might tell you they are the ‘worrying-type’ but when combined with these upper GIT sx I have found they test positive for H pylori more often than they don’t. And how clever is this mother’s medicine?
“I recognised it was worst after birthday parties where she has eaten too much and done cartwheels or run around (we now talk about recognising when she has a ‘full bucket’. We talk about the fact that her tummy takes a little bit more time to process food it means her bucket fills and she needs a bit of extra time to let it do it’s job before she adds more food to the bucket otherwise it spills over and she feels rubbish. She finds that analogy useful as she can feel her bucket getting full at birthday parties and when she gets the feeling, she knows why and doesn’t freak out.”
H.pylori – Eradicate or Rehabilitate? For a bacteria identified just a few decades ago as being a cause of chronic gastritis, atrophic gastritis and gastric carcinoma, the escalation in the number of antibiotics used to eradicate it (4 at last count + PPI) has been nothing short of breath-taking. A management approach more consistent with both integrative medicine and with an improved understanding of the delicate microbiome focuses on changing the gastric environment to ‘remove the welcome mat’. What do we know about how to do this successfully? It turns out…quite a lot.
And it will. It knocked again on a practitioner’s door last week. She in turn knocked on mine. It turned out to be a very familiar story:
Firstly:Patient presents distressed – recently a nurse applied the term ‘Chronic Kidney Disease’ to HER (note no one has ever mentioned this diagnosis) Secondly:She is in stage 3 of 5 Then: This practitioner is left to have ‘the conversation’ but wants to know where to start, ‘What do I say?’ Next up:And what else can I do for her – are we really able to make a difference?
Familiar to you too? So,1st & 2nd: Yes, this is not uncommon we would have to say and even with age-appropriate reference range adjustment, her GFR consistently in the 50s, flags premature decline. Then: What DO you say? Well this clearly is a delicate area, not only because of the level of patient distress and concern but because, at this stage the practitioner knows nothing more than what the patient tells her and her ELFTs over the last 2 years. This is not enough information, right? Chronic Kidney Disease is a heterogeneous condition, with many different causes, manifestations, comorbid conditions, and factors affecting prognosis (Levey et al., 2009) So while most individuals certainly progress from stage I to II and II to III the rate at which they do this differs dramatically.
Two years of data is not long enough for us to appreciate the trajectory of her CKD & means we are unable to provide the patient with any kind of perspective:
‘With no further decline in GFR or progression in stages over 5 years, you’re doing well, so keep doing what you’re doing!’ Vs ‘Ok, I can see what looks like a little period of accelerated decline – let’s review what’s been happening and how we can turn this around”
“Please sir can I have some more?’ Yes, back to her primary carers to request more information to fill in the gaps, and ideally more labs to calculate & observe the trajectory for yourself. Next Up: What do we have to offer the patient with CKD stage III? Soooooooooooooooooooooooooooooooooo much!! When is adequate hydration helpful? Always, except Stage V! (and these patients are not coming to see us) What are our treatment objectives & our evidence backed medicines to meet these? Hcy lowering (note often referred to as ‘folate refractory’ in renal dx), vitamin D adequacy, lowering the acid load, supporting the microbiome & in turn the Renal-GIT axis…hang on, got to go…someone’s knocking 😅 but hopefully we all can see, when they present to us, they are indeed knocking on the right door ✊
Nutritional or naturopathic support for the kidneys tends to have been over-looked in our training and yet research suggests there is much in our tool kit that can make an enormous difference to this system, in particular, slowing the progression of chronic kidney disease in patients. Rachel talks about what these key evidence based interventions are and also gives you the tools to identify the early pathology markers of renal impairment – the earlier the recognition, the earlier we can make a start on the remedy.
It seems almost farcical to question the merits of hydration for our renal health but is this actually the truism we have been lead to believe? Where does the recommendation of ‘8 glasses a day’ come from and what is the level of evidence to support it and in whom? Or should we in fact be setting our sights on output ie. 24 hr urinary volume, over input. Do all kidneys love water – or does this relationship change with the progressive impairment seen in CKD which affects up to 30% of our middle-aged population? When does hydration become harassment?
Most practitioners graduated with not much more than a few ‘kidney’ herbs and an under-appreciation of the contribution renal health makes to wellbeing. It’s not just about waste and water. In reality, the kidneys are pivotal in just about every major element: blood, bones, pH balance, methylation, control of oxidative stress, the GIT microbiome and more! And we are seeing the impact of this in our patients in all sorts of subtle and not so subtle presentations. This new instalment in diagnostics, brings the renal system into the spotlight so we can confidently identify and better manage its critical contribution. In addition to this, just like with other routine labs such as LFTs, we unpack how these so-called ‘renal markers’ can flag a plethora of other insights into your patients, from reflecting (un)healthy muscle mass, to calculating individual dietary protein adequacy, from key ‘danger and distress’ signals in response to disturbed metabolism, oxidative stress to certain types of GIT dysbiosis! We call this Explained, Expanded and Exploded because these routine labs can deliver XXX sized insights into your patients.
Something’s just come up today again and I think we need to talk about it. A positive result on a stool PCR microbiome test for H. pylori, understandably, might be heard as a clear call to action to go in guns blazing with an eradication approach. But is it? Trust me, I’ve had more than my fair share of battles with this bug & can understand being keen to have it be gone BUT first things first, let’s be clear about what the result speaks to.
Does it say, “Here! Look over here! Here’s the source of your patient’s GIT distress,” or even, “Here’s a pathogen that has taken up residence in their GIT and is a risk for future dx!”
No, not necessarily. It speaks to its presence.
And that may be only fleetingly, as it passes through. I’ve seen it before and so have many other experienced practitioners: a positive stool PCR that is at odds with the results of gold standard H.pylori testing, the UBT, faecal antigens or blood serology, all freely available through the GP. And the reality is, if you have a negative UBT, there’s no urease production, the trademark trouble-making of this bug. If you have negative blood serology, your immune system has never ‘met’ this bug or, in the minority of cases, you’ve tested in that brief early exposure window prior to antibody production (2wks) so you should retest within the month, to confirm or refute. And if you don’t have any faecal antigen…it ain’t in da’ house…so to speak 😅 If there’s something new here, then have a quick read of Medscape’s great work-up summary. So, clearly we need to confirm before we open fire.
We (me included) have been so single-minded about increasing the ‘sensitivity’ with our testing methods, we may have left ‘specificity’, in broader sense, behind & that creates a new problem.
This leads us and the patient down the garden path of false attribution and time and money wasted ‘treating’ a ghost gut issue. And no one wants to be put on a pylori protocol when they really didn’t need to. Trust me 🙄 But if someone does come back confirmed, well then…
For a bacteria identified just a few decades ago as being a cause of chronic gastritis, atrophic gastritis and gastric carcinoma, the escalation of number of antibiotics used to eradicate it (4 at last count + PPI) has been nothing short of breath-taking. A management approach more consistent with both integrative medicine and with an improved understanding of the delicate microbiome focuses on changing the gastric environment to ‘remove the welcome mat’. What do we know about how to do this successfully? It turns out…quite a lot.
I say: Biotin, Broccoli Sprouts & Bone Broth You say….?
If you said: ‘Sulphur’, go directly to the top of the class, passing ‘Go’ & collecting $200 on your way!🤓 If you nervously said…”I don’t know, they all start with ‘B’ ?”, you are not alone. In fact, most integrative health professionals aren’t aware of the Sulphur Strategies they’re using, probably, everyday. But it’s time we all were.
How about this list? Glycosaminoglycans (GAGs for joint, gut etc tissue integrity), Cerebroside Sulphate (Myelin), Metallothionein, Glutathione, Hydrogen Sulphide (H2S), Co-Enzyme A, Lipoic acid, SAMe, are just some things Sulphur is essential for.
I could go on…and on and on. You see Sulphur, in spite of being an essential macromineral (adult dietary requirements > 1g per day) and critical to health, remains largely unseen. Often we don’t know when we’re writing patient prescriptions that actually we’re using a particular vehicle for Sulphur and therefore we’re also not able to discern which, of the very long list of options (dietary and supplements), makes the most sense in this patient at this time. We’re not to blame, not many ‘possess the power’ to see it, it seems. Por old essential, irreplaceable Sulphur doesn’t even have an RDI. But the time has come to take a good look. We need to know how patients are able to meet their needs, who needs more and how, very commonly, someone who is seemingly ‘consuming enough’ may still exhibit a functional Sulphur deficiency with poor musculoskeletal tissue integrity, low white cell replication capacity or higher oxidative stress load etc and in those who do have a shortfall, how to treat successfully & safely. Who needs a top down approach (more protein, methionine, cysteine, bone broth) and in whom would that be a risky path and using ‘downstream’ Sulphur products instead would be a better balance of pros and cons?
Because all Sulphur needs to be handled with care.
That’s right. Like other highly chemically reactive minerals, with reactivity comes risk – a great potency that requires careful consideration of both form and dose, so that we can harness this power for good not…well evil’s a bit strong…but how about, for not-good. I’m a bit of fan of Sulphur and using Sulphur strategies in my patients. I think it has interesting echoes with our past: the ‘healing’ waters of a Sulphur Spring and of course even further back the old ‘brimstone and treacle’ medicine of eons ago. This paper by Nimni in 2007: Are we getting enough sulfur in our diet? got me thinking about Sulphur again in a contemporary context, over a decade ago, I’ve done a lot more thinking, researching and prescribing since then but it seems that Sulphur still remains ‘unseen’ by most. But with the rise and rise and rise of popular Sulphur-based supplements (alpha lipoic acid, GSH, N-acetyl glucosamine, Brassica & Allium extracts and concentrates, N-acetyl-cysteine etc) I think it’s time to talk.
If you don’t have a clear picture of the gross daily requirements, determinants of altered individual needs, sources, regulation & associated deficiency picture of Sulphur, you’re not alone. Turns out this essential macromineral remains ‘unseen’ by most, even though you’re probably writing prescriptions everyday that have Sulphur as their key component. From the simple: Taurine, N-acetyl cysteine, Protein powders, to the sublime: Brassica extracts & concentrates, N-acetyl Glucosamine, Alpha Lipoic acid etc. In order to use these Sulphur strategies successfully and safely, however, we need to fill in the missing detail on its metabolism, the difference between the ‘organic’ and ‘inorganic pools’, how regulation regularly goes wrong, even in those seemingly consuming enough, and how to balance the risks of this reactive medicine with its substantial therapeutic value. This recording comes with a great clinical tool to help you at last see the Sulphur strategy most indicated for your patient.
The latest Update in Under 30 has landed!!!
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You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audio’s and resources here.
When I deliver foundational nutrition training to GPs I talk tough. It’s a tough field, right? Compared with the relative certainty of pharmaceuticals, their established pharmacokinetics, their sophisticated delivery systems to ensure high bioavailability…trying to fix micronutrient deficiencies in patients can feel a lot like you’re trying to perform minor miracles. Take iron for something different, its homeostasis pivots on its tight regulation at the gut wall – and this is a wall that is very tight!! At best you get about 10% of a supplement taken up, at worst you get none and the harder you push & the higher you go with your dose…the lower the fractional uptake. Tough stuff, right?!
It’s about at this point in my talk I read their collective minds and say, “I know, you’re thinking, oral supplementation is for suckers – what about we bypass that road block and use IV?!” [Ok, I definitely use nicer words than this]
And then I put up a list of pros and cons about IV micronutrient repletion: ‘100% bioavailable’ & ‘Bypasses the body’s regulatory systems’, go on both! You see, time & time again we discover, when we think we’re outsmarting the body, it still manages to outsmart us. There are some exceptions to this – some nutrients (Vitamin C) and some contexts (late pregnancy iron deficiency) but the broader promise of ‘rapid replenishment’ for everyone, in your lunch break, via an IV infusion..is not realistic, responsible nor without risk. Don’t get me wrong, I am an advocate of appropriate IV Fe use and have encouraged a small fraction of my patients to take this path. However, given the dramatic rise in prescriptions for this since 2013, I think it’s time to stop and seriously review each element: In reality what does it achieve and in whom is it a responsible recommendation; Was a risk benefit analysis performed for & communicated to each individual & was the remaining risk mitigated?
Think anaphylaxis is the major concern? It might be the most lethal but there are more serious concerns due to higher incidence with newer preparations.
So, how well do you know your different IV iron forms, and their predilection for potential problems? And have your answers ready to all the questions raised above? In order for all involved to make an informed choice (both practitioners and patients), we must.
You’re welcome 😉 and hey welcome back to tough talkin’ Tuesday…
While rates of iron deficiency and related anaemia continue to grow, the increase in prescriptions of IV Fe have expanded exponentially in western countries. What is behind this change in practice regarding how we treat iron deficiency and does it match with responsible prescribing? Do the benefits always outweigh the risks? And while we’re on the topic, who is most likely to benefit and what are all the risks? In light of a current class action in the US, relating to a lesser talked about adverse event associated with IV Fe and recent complaints here in Australia against GPs, allegedly due to inadequate information to enable informed patient consent…it’s time to answer these questions and more. When is IV Fe a means of rescue and when is it a risky repletion strategy with no evidence of advantage?
I feel a bit Trumpy…because whenever someone says ‘N-acetyl cysteine’, I want to reply, “Big fan, I’m a big fan”. And yes that’s an uncomfortable awareness. But unlike he who shall not be mentioned, I can qualify my statement and provide supportive evidence, both of the research and real-world varieties. So, of course, can so many of you as well. I know of fertility specialists who place it in PCOS patients’ preconception prescriptions and respiratory specialists who regard it highly in COPD, CF and a range of other conditions. And I am a signed up supporter of its adjunctive use in many psychiatric conditions. Then there’s the biofilm-breaking buffs…
This is where non-believers might be tempted to call ‘Snake-oil!’
How can one very simple tricked-up amino acid possibly contribute to the health of so many systems? Oh, just via the chameleon qualities of its chemistry of course! As a rate limiting ingredient and precursor of GSH, as well as a potent mucolytic agent and and and…we get it. We surrender! But I want us all to back up here just a few steps. As a mucolytic agent…renowned for biofilm busting…hmmm. I prescribe a lot of NAC for a lot of people for a lot of days-weeks-months….because all the research in mental health points to it being a long-term intervention. I’ve heard Professor Michael Berk say, that patients still on it at 2 years had even more improvements than they had experienced at the 6 month mark and of course mental health, for most, is a chronic illness, so no one is surprised.
But we can’t contain its chameleon chemical qualities. Given orally, it will be having effects within the gut of these individuals on the way through…and not all biofilms should be busted, right?!
So what to do? Well thankfully, NAC is not something that patients rely on for short term acute effects, that would then make missing doses problematic – like pharmaceutical psychiatric medications, and some CAM options as well potentially, like SAMe and SJW. So a regular sNAC break is likely to be free from negative impact for those with mental health issues and in fact, beneficial long term. With all this in mind, we’re now using a dosing model of taking weekends off from this supplement – which works for most. Do we have any concrete research to say this makes sense and doesn’t compromise efficacy yet? Well no, and don’t hold your breath, because research can be very reductionistic (you heard it here first LOL) and there is a lack of consideration of the effects on an individual as a whole. The psych researchers are not measuring the impact of all interventions on the microbome of patients (yet!) and the gut researchers not always monitoring the mind. But we clinicians can pioneer the path, fuelled by two old buddies of mine: first do no harm & least medicine, best medicine, right?
Oh and has anyone managed to open a tub of NAC and not accidentally snort some?…I don’t have anything else to add or a solution, I am genuinely asking if this is humanly possible 😂
“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” Rachel Arthur
🍌‘I think I am, B2! It’s time to separate the B12 from the B*S#!’
Ok, if you’re reading this and you’re not from around here you have reasonable grounds to conclude I’m the one who’s gone 🍌 but if you grew up with a show all about 2 adults dressed up as bananas and creatively known as B1 and B2, then we’re all good! Ok now for the next bit, you might need to sit down. Nothing not everything in the wildly popular, and dare I say it populist, doco The Game Changers was scientifically rigorous. I know, I’m loving the strike through a little too much today.
Goodness, when otherwise intelligent friends of mine forced me to watch this, they found the need for both restraints and duct tape over my mouth, to hear or see anything other than me jumping up and down, arms flapping, mouth yapping. People only tend to make this mistake with me once.
Among the many many dubious XXX was a terrible mis-truth about our ‘new modern reliance on animal food or supplements for B12’. Woah…back up there Game Changers Gang, say what?! Does anyone on their research team read any research? So that got me all motivated to go back to the books on our beloved B12, which is simply like no other micronutrient in human physiology or in nature, for many reasons…starting with 1) it contains a metal in the middle 2) it has dietary dopplegangers (plant forms that look just like it but actually are decoys that need to be actively removed from the body so as not to block its actions) and 3) has the most complex and sophisticated pathway for digestion and absorption, which surprising equates to brilliant average bioavailability (much better than most micronutrients)…until it doesn’t! And that’s when the trouble starts. Once you don’t have an intact IF absorption pathway, you’re down to picking up < 1% via simple diffusion, and suddenly we see why patients can be vulnerable to not meeting even the piddly required amount. Not to mention the vegans, of course.I’m on my best behaviour.
But the B*S#! about B12 is far from limited to the documentary. It’s in the words of the Methylation Mystics, making methylation sound like rocket science and in the supplements we’re being sold.
But don’t get me wrong…effective B12 treatment in the right patient is a total wow moment. I’ve literally seen all the lights go on⚡ in some . So what do we need to do to find our way out of the dark? Go back to the solid science. Come on. There’s nothing else you need to do and nowhere else you need to be… we all know it…so start by reading this and this. There’s plenty more of course but these are excellent appetisers. And if you want to cut to the chase and get the lowdown on what’s B*S#! versus what’s the real magic of B12, you can always settle in and listen to my latest Update in Under 30 – complete with a very cool clinical tool to help you choose the best B12 for each individual, but spoiler alert, it ain’t rocket science.🤫
B12 is a routinely under-rated and recognised micronutrient, which is in fact in high demand by many of our patients. As nutritional research pushes back against defining adequacy as simply the prevention of the deficiency-associated disease (macrocyctic anaemia, irreversible neurological damage) we enter a new landscape of more individualised approaches where we’re better able to recognise and treat those at risk of falling below ‘optimal’. But how do we accurately identify this and then choose the ‘best’ B12 (methyl- cyano- adenosyl- hyroxo-) supplement? Does it need to be this complex? Time to sort the B12 from the B*S#!! This recording comes with a bunch of great resources including a very handy clinical tool
The latest Update in Under 30 has landed!!!
You can purchase April’s episode, Separating the B12 from the B*S#! is here.
If you are an Update in Under 30 Subscriber, you will find it waiting for you in your online account.
Have you been told somewhere by someone that the ‘perfect’ TSH is 1.5 mIU/L? This is a wonderful, terrible & wonderfully terrible example of ‘magical numbers medicine’. As a push-back against the published reference ranges we’re given, that are so wide you could drive a truck through them, there has been an over-correction by some, leading to the myth of ‘magic numbers’. We can narrow the reference range substantially for many parameters with good rationale, make no mistake about that but once we start setting ‘aspirational goals’ that are explicitly rigid…well we’ve done 2 things 1) forgotten about the patient to whom this result belongs and 2) disregarded viewing each result as part of a ‘pattern’, that we must piece together and make sense of.
Back to TSH then… if my obese patient had a value of 1.5 mIU/L this in fact would be woefully inadequate.
Also too low for any patient, no matter their size, if their T4 is low and we’d like a higher value as well for risk minimisation in our elderly clients too.
But the same result would be excessively & worringly high in my patient who’s undergone thyroidectomy.
Being given a list of ‘magic numbers’ will never replace learning labs correctly. When we do this, we come to truly know that meaning can only be made of the markers when you can answer the following questions:
What is this (metabolite, analyte, binding agent, plasma protein etc)?
What do I know about its physiological and biochemical context – what is its role and regulation in the blood, what moves it and to what magnitude?
How have the reference ranges been determined for this lab – who am I comparing my patient to?
Therefore, what is the significance of a result that is: ‘normal’, ‘low normal’, ‘high normal’, below or above the range?
Does this value ‘fit’ with my patient?
What else could explain an unexpected result?
How strong is my level of evidence?
What do I need to do from here to confirm or refute this?
And a few more 😉
Realising the full value of any test result in terms of what it reveals about the person sitting in front of you, requires these skills. Unfortunately, in contrast a list of magic numbers will often lead you astray. And building your scientific knowledge about labs will not only help you avoid the pitfalls of pathology but will strengthen your pathophysiology prowess in surprising ways, saving your patients a packet in terms of additional extraneous testing and help you truly personalise your prescriptions…because the ‘invisible (biochemical individuality, oxidative stress, genetic probabilities, subclinical states, imbalanced or burdened processes etc) just became visible’. I started requesting lab results early in my career and years later was lucky enough to be taken under the wing of Dr. Tini Gruner. I found some of our shared notes, from 10 years ago, scribbled all over patient results recently and I was struck by just how lucky I was to have her encouragement to really pursue my interest and how she was a guiding force about learning to recognise pathology patterns over single parameters. A decade on I can confess, much of clinical and educative success has come off the back of this foundational skill-set and I know, this is true for so many I’ve taught too.
“The guidance I’ve received over the years from Rachel in relation to pathology interpretation has been one of the most valuable (and fascinating) investments I’ve made as a clinician. Her teachings have filled gaps in my knowledge base I never knew needed filling and have significantly enhanced my understanding of the inner workings of the body! Rachel has an incredible ability to make the numbers that patient’s so often present us with, both understandable and clinically meaningful. The knowledge I’ve gained by investing in this skillset has paid off in dividends and I’m certain will continue to do so into the future.”
Stacey Curcio – Cultivating Wellness
I hope you’ll join me for the most exciting up-skilling opportunity in learning labs yet. Oh…and all this talk about thyroid testing..that’s just a serving suggestion 😉 this year my MasterCourse is focused on the most routine labs of all: ELFTs, FBE, WCC, Lipid and Glucose Panels…an absolute treasure trove of free integrative health information about your patient!
This skillset has been found by many to be biggest ‘game-changer’ in Integrative Medicine!
There are limited places. To sign up for the MasterCourse: Comprehensive Diagnostics click here. For more information about the program click here.
This year I heard a great quote that hit the spot for me: anyone who offers you a simple solution to a complex problem is lying or misguided, the solution to a complex problem will inherently be complex. Dang! I’m frequently reminded of this in relation to many different aspects of working in integrative health. Or even just answering work-related questions socially. Random-friend-I-haven’t-met- yet, upon finding out I work in nutrition, asks: Is [insert any given food, beverage, macronutrient, micronutrient] good for you? In spite of over 20 years of this happening, I confess, the poker face still requires concentration.
The poker face is necessary of course to
a) conceal my amusement at how predictable humans are and
b) to cushion the blow for them as I tear down the delusion that real nutritional science is simple and can be served up in a soundbyte or
c) lie and infer that it is, just to get out of there faster!
But recently, I’ve had another reminder of that ‘in here’ rather than ‘out there’, about how even as practitioners we long for things to be simpler than they are. This month in mentoring I’ve been talking about the dark side of both zinc and Akkermansia muciniphila (I know wash my mouth out right?!) in neurological issues. What, but we had them on the good guys list?! Remember the answer to a complex problem (and human health surely owns this territory) will inherently be complex, right? Similarly, I’ve been digging deep in research about beta-glucuronidase, that enzyme that undoes our phase 2 detoxification of oestrogen, bilirubin and a long list of nasty xenobiotics, earning it the informal title of ‘bad ass biomarker’…scoundrel! And well, I’ve found some really nice things to say about it…like actually it extends the half life of most of our flavonoids such as quercetin, isoflavones etc etc and that’s a great thing for increasing their positive punch given that their rapid detoxification limits how much we can benefit from them. Turns out, like everything else, even dear old beta-glucuronidase exhibits light and shade.
How I ended up losing a weekend to such papers was because I was trying to resolve some burning questions about Ca-D-glucurate (CDG) that I’ve had for as long as I’ve been recommending it to people who arguably could benefit from a little less beta-glucuronidase activity.
My two most pressing ones were: How much is required to be effective & Where’s the evidence?
And that’s when the fight broke out [just in my head] You see every review I’ve read, every piece of product information too, repeats the mantra CDG 500mg TID but turns out this is based on…not much. More uncomfortable still, is that even our assumption that we can convert CDG into its active form has been strongly challenged. The new research, which is not the work from the 1990s that everyone cites, is a must read…or if you actually have a life, and other ways to spend a weekend then maybe just spend 30 mins with me in my Update in Under 30 this month 😂 I wanted to keep it simple and neat and tidy. I tried I promise. But in the end…wouldn’t you know it…it’s complex.
So to bring everyone up to speed, including myself!, I recorded an UU30 on…
The ABC of CDG We often identify patients who could do with a little glucuronidation first aid: marked dysbiosis, Gilbert’s syndrome, oestrogen excess, cancer risk (especially bowel, breast & prostate) and one of our nutritional go-to’s has typically been Calcium D Glucurate. While there is ample evidence that one of CDG’s metabolites : 1,4 GL – inhibits beta-glucuronidase, is an antioxidant, platelet activation inhibitor and generally all round good guy to have on board, new research strongly challenges that oral CDG will convert to this at levels sufficient to support our detoxification pathways. Sounds like we’re overdue for an update on this supplement and when and where it might be useful in addition to how to find the real deal in real food!
Did someone explain the kidneys are like a really important, not to be forgotten, under-estimated, ignored or under-valued kind of organ in your training as a naturopath?No, me neither. I mean I know Buchu and Uva and Zea (on a first name basis only, clearly!) and …no actually, I’m done. But seriously, it didn’t take too long in practice to stumble across a whole lot of bad when kidneys aren’t getting the attention they warrant and equally to develop a slight obsession with renal markers in all of my patients not just because of their incredible impact on whole health but also because of what ‘lay beneath’.
As you might suspect, I get sent labs all the time from practitioners. Stop no! That is not an invitation!
Often it’s client’s renal markers which I do appreciate because it tells me there is an increasing number of praccies that absolutely have done some post-grad DIY knowledge building about these bean-shaped babies and their critical contribution to health. The results might come with a question like, “What’s going on with their kidneys?!” [insert worried face emoji of choosing]
To which my reply is often… “not much but boy do we need to talk about your patient’s GIT microbiome! [or] mental health! [or] sarcopenia!”
Say what? Yes abnormalities within the renal markers: urea, creatinine and uric acid may be a reflection of renal issues. But if you know where each of these molecules enters the blood,exits the body and all the interesting good & bad they can get up to in between…then the patterns speak less (if at all in some instances) to what’s going down in the kidneys but instead give you an incredible insight into key issues all over the body: from the gut to the brain. But wait there’s more! Want to know what’s the latest and greatest in management of advanced renal disease? Treat the gut to lower the urea. What about managing mania? Add in a gout treatment to lower uric acid. Dang! This is holistic health at its best with those poor kidneys no longer being left out in the cold!
“Who knew urea, creatinine, GFR and uric acid could be such a Goldmine….Mind…officially…blown!” New Graduate Mentee 2019
Most practitioners graduated with not much more than a few ‘kidney’ herbs and an under-appreciation of the contribution renal health makes to wellbeing. It’s not just about waste and water. In reality, the kidneys are pivotal in just about every major element: blood, bones, pH balance, methylation, control of oxidative stress, the GIT microbiome and more! And we are seeing the impact of this in our patients in all sorts of subtle and not so subtle presentations. This new instalment in diagnostics, brings the renal system into the spotlight so we can confidently identify and better manage its critical contribution. In addition to this, just like with other routine labs such as LFTs, we unpack how these so-called ‘renal markers’ can flag a plethora of other insights into your patients, from reflecting (un)healthy muscle mass to calculating individual dietary protein adequacy, from key ‘danger and distress’ signals in response to disturbed metabolism, oxidative stress to certain types of GIT dysbiosis! We call this Renal Markers: Explained, Expanded and Exploded because these routine labs can deliver XXX sized insights into your patients.
How might your patients’ Nickel exposure wreak havoc with their health? What might that look like? It may be lurking behind labels like IBS, non-coeliac gluten sensitivity, contact dermatitis of unknown origin,(with or without alopecia) or even CFS. “Then how does Nickel, which can’t even claim fame as a heavy metal, manage such diverse detrimental effects’? I hear you ask. In 3 easy steps 1) exposure…we’re all exposed, Ni is ubiquitous in our soil, our food, our environment so don’t bother trying to run from it 2) it hits our gut where our microbiome and intestinal lining may constitute the first fallen soldiers 3) exposure to our immune system can lead to sensitisation, and the subsequent development of a hypersensitivity response to each following exposure …and at worst precipitation of an autoimmune process. You got all that?
So therein lies the big question: how can we help patients whose health problems stem from Noxious Nickel? We could run and hide…from our jewellery, our mobile phones, dental interventions, most food (!), but we’d be wasting our time…we’re surrounded!
In this instalment it’s time to get down and dirty and detailed about how to best identify those patients who may have Nickel related pathology and presentations. We cover testing options, typical systems affected from GIT to autoimmunity and the most extreme form: Systemic Nickel Allergy Syndrome. We outline Nickel management strategies in a world full of it (!) and we include several key papers for additional resources and support. How noxious is Nickel for some of your patients? Well by the end of this you’ll know and better still, know what to do once that’s established.
Hear all about it by listening to my latest Update in Under 30:
Ok here’s some tough Tuesday talk..not all tests are valid. Tougher still…not all of the mainstream nor the functional pathology ones. I am talking across the board here. Each and every pathology parameter requires good knowledge about its strengths. limitations and, one of my absolute favourite nemeses, confounders. “How on earth am I supposed to learn all that and everything else I have to know too?!!” I hear you scream at your screen. Btw keep yourself nice if you’re in public while you’re reading this 😉
But rather than imagining you need to have this level of knowledge for all tests, I would suggest you set yourself a hit list of the ones you rely on most, either in terms of frequency or in terms of the degree to which they direct your decisions about patient care…can I mention (ahem) Iron studies here perhaps for us all…but maybe you have a specialist area so you use a particular investigation routinely or at least frequently…
CDSAs? Breath tests for SIBO? Oxalates?
May I please then politely suggest that you get to know these inside and out? Not based purely on the information and assistance that the test provider provides you..but you scrutinise them independently. Top to bottom. Because that’s your business, right? And your diagnoses and treatment decisions are pivoting on these results. Jason Hawrelak gave us all some great examples, including his informal experiment of sending the same stool sample to multiple labs. Don’t know about this and his findings?? If you’re in the business of ordering stool tests, you need to. I am doing this all the time with numerous pathology markers because diagnostics is my passion (alright, obsession)…and recently I put Oxalate Assessment to the test and oh boy!
Here’s something for free:
If you are measuring urinary oxalates to diagnose oxalate overload in your patients and you, 1) are using a lab that does not preserve the urine as you collect it, using acidified containers or providing additional preservatives for take home testing kits….you are wasting your patients money and you are likely getting a lot of false positives, i.e. the result infers the patient has a problem when they don’t!!
And 2) if you are simply following the labs reference ranges for what ‘healthy’ urinary oxalates look like – you’re wasting your patients money again and likely getting false negatives – a failure to show a problem that is actually there! If you’re hunting oxalates…please ensure you have a current effective hunter’s licence…by getting up to speed fast regarding accurate investigation of this. Oh yes…it’s tough-talkin’-Tuesday and I’ve come out firing…watch out this may become a regular feature 🤷♀️
Update in Under 30: Oxalate Overload – Assessment and Management
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update.
When patients present feeling worse every time they DIY a Green Detox, as the practitioner, you’re likely to be sniffing around reduced oxalate tolerance as a differential. Rightly so. But what about the patient with joint pains and disproportionate fatigue who has baffled their rheumatologist, or the one suffering vulvodynia that baffles everyone, or irritable bladder symptoms, or….and they all eat an exemplary colourful high plant food diet, with their only self-confessed sin…darker than dark chocolate between every mouthful? Who doesn’t? While you may have a hunch, given the goodness of those foods, we should check these out objectively rather than unnecessarily restrict or limit someone’s food choices for the rest of their natural life! If dietary oxalate overload is now on your radar for these patients you need to move to the next step. Assessment.
Spot or 24hr urine collection or plasma assay or OATS testing or imaging or joint aspirates? So many choices but which one has the greatest validity depending on your patient’s presentation? Ok how about the most general all-rounder that is truly an option in the real world? – always helpful;) Yep, 24hr urine collection…agreed.
Ok, next step.
You need to wrap around that waist of yours one seriously heavy tool belt for accurate interpretation of their results. That’s right…those random ol’ reference ranges need a serious rethink! How much? Well, given the reference ranges every lab will give you for urinary oxalates typically fail to pick up up to 1/3 of patients with oxalate overload high enough to produce oxalate kidney stones…I think you get the picture. I feel your trepidation now but can hear you pensively ask anyway…next step? Management.
Just google oxalate-rich foods, print out the list for your patient and tell them never to have these (or joy, laughter, sex or a healthy microbiome) ever again.
The ‘low oxalate lists’ will lead you astray and the ‘high oxalate foods’ should not be tossed away! The research has found greater therapeutic benefits from different dietary approaches, some nutritional supplements and most importantly targeted treatment of the cause…which is all about the…go on, try and say it without screaming…the GUT!!!!!!!!!!!!!!
Oxalates are present in many healthy foods and in all healthy people, but when ‘normal’ levels are exceeded they can spell trouble in a whole raft of different ways due to their extensive distribution across the body. Some tissues, however, have more problems than others, especially the urinary system and soft tissue and joints but now there are also questions about oxalates’ relationship with thyroid and breast issues. We review the latest evidence about the health consequences, blow the lid on accurate assessment for oxalate excess and talk management in this jam-packed update
Hear all about it by listening to my latest Update in Under 30:
With the increasing weight of evidence pointing to a potent pathogenic portal between our mouths and every other part of the body, whether that be in terms of cardiovascular disease, rheumatoid arthritis, appendicitis, even a growing case for Alzheimer’s disease, we need to ensure we’re not overlooking the condition of each patient’s oral cavity. I got very excited about the recent Medscape article: A rapid non-invasive tool for periodontitis screening in a medical care setting. It’s true, I live a quiet life 😉 But seriously, a validated tool for all non-dentists to accurately pick up on the likelihood of this condition would be a nifty little thing indeed, so we can narrow down just who we quick-march off the dentist as well as understand their whole health story. But then I read the 8 actual questions which included gems such as: Do you think you have gum disease? and Have you ever had treatment for gum disease such as scaling and root planing, sometimes called “deep cleaning”? I thought, ok, this is not rocket (dental) science.
But that’s the point, I guess, right?
So while I encourage you to check out & employ this screening tool by all means, we can also be reassured that just by ensuring that when we ask about someone’s digestion (and when don’t we?!) we start at the very top of the tube, we’re doing a good job!! As my new grad mentees learnt this year…following the patient’s GIT from mouth to south anatomically, is my rather simplistic way of guaranteeing I cover everything digestive..without using formal consultation script. So in the case of the mouth, my questions include things like: last trip to the dentist; any prior dental diagnoses, number of amalgams, implants, root canals etc & their routine dental care techniques, any signs of bleeding on brushing & all foods they avoid for dental or oral reasons? Look, it hasn’t undergone the rigorous validation that the Self-Reported Oral Health Questionnaire has..but I think it’s a good start.
Whether we’re being picky about pathogens and exactly how they got access to the rest of the body (and gums make a great entry point!!) or just concerned about chronic low level inflammation, a ‘gurgling’ CRP between 1-5 in an otherwise ‘healthy adult’, picking up on periodontitis is a pivotal.
Oh and if you’ve ever wondered about possible health implications from mouth metals other than amalgams…don’t worry, soon I’ll be getting to that with a forthcoming UU30.
Want to hear more about how certain microbiota (from the mouth to the south) are being implicated in joint diseases such as rheumatoid arthritis and ankylosing spondylitis and how we can investigate these individuals?Getting to the Guts of Women with Joint Pain is a recent UU30 instalment that gets down & dirty on the detail.
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.
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?
Let’s talk turkey about our pharmaceutical Pet Hates, mine are Proton Pump Inhibitors (PPIs). They irk me more than any other drug class. It’s not entirely rational. Let’s face it, they have some stiff competition but for some reason, in my mind, they almost always win: helping so little & at such a high cost to patients. What fuels my fire of course is their over-prescription, followed closely by the complete disregard for the prescribing guidelines which state:
“When clinically indicated, PPIs should be used for the shortest duration necessary and chronic use is not recommended except for treatment of pathological hypersecretory conditions including Zollinger-Ellison syndrome and maintenance healing of erosive oesophagitis.”
Sorry…did I hear you correctly?Chronic use is not recommended – yet this is one of the drugs most commonly on ‘set and forget mode’ in general practice. To boot, their chronic use has been associated with a number of serious concerns, which I’ve touched on before, from osteoporosis to increased rates of GIT infections. not to mention just the little ol’ detail of malabsorption of multiple nutrients! But this week, yet another health concern has popped up and into my inbox…and well..I found myself shouting at the medical newsfeed on my screen…[again] 🙁
“In their analysis, more than 42,500 adverse events reported to the US Food and Drug Administration by patients on PPI monotherapy were compared with more than 8300 reports from patients on histamine-2 receptor antagonists (H2RAs)….Patients on PPIs alone were 28 times more likely to report chronic kidney disease than those taking H2RAs, while the frequency of acute kidney injury reports was around four times higher…Reports of end-stage renal disease were 35-fold higher among PPI users, while reports of renal nephrolithiasis were three times higher”
To be clear, while these increased rates are TERRIBLE and unacceptable in the context of the ‘set and forget’ prescribing that seems it be rife in most countries, they still only effect a small % of patients e.g. approx 5% of patients had adverse renal effects on PPIs Vs 1% on the older generation H2 blockers for reflux but it’s yet another reason (like we needed more?!) to think twice before our patients are initiated on these meds, which are presented to patients as being benign. Typically with drug development, the older drugs in a class are superseded by newer ones that are ‘cleaner’, and therefore more effective with less adverse effects but this is one situation where if one of my patients really did need a med, I would say out with the new and in with the old!
One scenario where PPIs in combo with multiple antibiotics get routinely rolled out is of course H.pylori infections. But does this make sense??
For a bacteria identified just a few decades ago as being a cause of chronic gastritis, atrophic gastritis and gastric carcinoma, the escalation of number of antibiotics used to eradicate it (4 at last count + PPI) has been nothing short of breathtaking. A management approach more consistent with both integrative medicine and with an improved understanding of the delicate microbiome focuses on changing the gastric environment to ‘remove the welcome mat’. What do we know about how to do this successfully? It turns out…quite a lot. You can find out here with our previous UU30: H.pylori- Eradicate or Rehabilitate?
While we’re on the topic…I tend to think, that as good as we are at asking a lot about a patient’s health, we can always do better. One of the classic pitfalls for practitioners is having to rely so much on patient self-reporting: Is your period heavy,moderate or light?; How would you rate your appetite?; Do you suffer from excess flatulence? When our patients answer these questions, who are they able to compare their own experiences with? Or do they only compare them with themselves at another time in their life, e.g. my periods are heavier/lighter than they were before? Either way, this may lead to unintentionally misleading information from our patients, producing erroneous conclusions for us as clinicians. Do you suffer from excess flatulence? Well do they?? How exactly would most of us know?! Unless we can define what ‘normal’ looks like…?
(But as many as 22 times a day – that’s almost one on the hour)
That’s the average number of ‘pop offs’, ‘air biscuits’, ‘bench-warmers’, ‘fluffs’, or whatever you want to call them, healthy humans do per day as cited in this great evidence based & entertaining article. Funnily enough I had exactly the same lecturing experience as the author: performing a snap poll on my students, asking for averages…and can I just say almost everyone was clearly under-reporting!! But the point is clear. How can our patients accurately rate the magnitude, severity or normality V abnormality of their bowels, menses, appetite, pain threshold etc – unless we provide some goalposts? And are we, in fact being lead to believe there is a problem when perhaps there isn’t? That certainly has been the conclusion of several studies into the matter of self-reported excessive flatulence. Hippocrates himself put in a good word for bottom trumpeting, saying “passing gas is necessary to well-being” and as a recent article in the Harvard Health Letter reads, “A little bit of extra flatulence, could be an indication that you’re eating the way you should!” Here here!
But my favourite quote from this article has to be about the high tech solutions on offer – for those who do accurately fall into the excessive category:
“Such as carbon fiber odor-eating underwear (cost: $65), which were put to the test in an American Journal of Gastroenterology study that included such gems as “Utilising gas-tight Mylar pantaloons, the ability of a charcoal lined cushion to adsorb sulphur-containing gases instilled at the anus of eight subjects was assessed.” Assessed, that is, by a panel of fart-sniffing judges. And the name of the charcoal lined cushion? The “Toot Trapper.”
How different that scene in Bridge Jones’ Diary would have been had these been her undergarment of choice instead of the control briefs!
Of course, if there is associated pain or an odour (which the article discusses as well) that makes the family dog leave the room…well, that’s another matter…;)
Is Glutamine your go-to prescription for patients with gut problems? Do you look for good levels of it when you’re choosing your gut repair formulas? Most of us do this because we’ve heard that a deficiency negatively impacts the gut tight junctions , villi structure and immunity etc. but how long has it been since you’ve reviewed the latest human studies on the digestive effects of Glutamine supplementation? The time is now. This previous UU30 installment cuts to the chase on the big research findings that warrant our urgent attention and necessitate big adjustments in how we use glutamine for guts.
Oral sex. There I said it. Last month when I talked about Helicobacter pylori and where people might ‘catch’ this – if they didn’t inherit the little critter from their mum or family as an infant – we thankfully were able to rule out kissing as a source of transmission between couples P.H.E.W…but I sort of got shy (Who, you, Rachel?!!) and danced a little bit around the question of whether other forms of sexual contact represent a possible route of exposure (pardon the pun). Until a lovely colleague after listening to Blowing the lid on H.pylori-who gets it & why – said, ‘Now seriously Rach, are you trying to say, oral sex may be an issue?’ Well…ahem…maybe. You see, remember what I said about candida being a vector for H.pylori and therefore H.pylori being present in the vaginas of women who have this bacteria residing in their stomachs. Ok…enough of that now I am blushing..but if you want to read more on this grab this article in BMJ from 2000 by Eslick who discusses (and seems a little too interested in, can I just say), the risks of H.pylori transmission via a myriad of sexual activities.
A month has passed since that last UU30 edition and it’s time for another instalment. This month, I’ve taken the giant leap forward many of you requested, into the fascinating realm of how best to manage H.pylori positive patients, in whom this bacteria really does constitute a pathogen.
Do we just try with multiple relentless antimicrobials to blast holes in this critter, a lot like the conventional approach…which, thanks to its significant capacity for developing resistance, is like aiming at a constantly moving target,…or…?
I’ve got a very different suggestion and approach. Increasingly we realise that the GIT microbiome is a vulnerable & dynamic balancing act and as a result, when treating patients with confirmed parasites, or worms or potentially (but not always) pathogenic bacteria such as H.pylori, most of us are doing much less ‘weeding’, less ‘eradicating’ and definitely less ‘shooting at things only to hit others’, these days. Instead we think about how we can best change the environment. So, what is it about someone’s stomach that opens the door to H. pylori and lets it in, and then perpetually ‘feeds’ it to ensure it stays longer and wreaks some real havoc, we identify & treat what about this over-friendly stomach is amenable to rehabilitation? As it turns out…that’s a lot.
And surely if add to our antimicrobials a larger focus on rejuvenating the gastric environment of H.pylori patients, to control the growth and activity of this bacteria, and in some cases even kick it out of the big brother house altogether…the chances of relapse and reinfection (a big one in this condition) will be dramatically less..not to mention the broader benefits on the greater GIT function, now the stomach has been remediated.
Or you could just keep trying to hit the moving bulls-eye?
For a bacteria identified just a few decades ago as being a cause of chronic gastritis, atrophic gastritis and gastric carcinoma, the escalation of number of antibiotics used to eradicate it (4 at last count + PPI) has been nothing short of breathtaking. A management approach more consistent with both integrative medicine and with an improved understanding of the delicate microbiome includes a bigger focus on changing the gastric environment to ‘remove the welcome mat’. What do we know about how to do this successfully? It turns out…quite a lot.
Hear all about it by listening by my latest Update in Under 30: H.pylori – Eradicate or Rehabilitate? 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.
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…)