I didn’t catch that Zonulin wave that hit Australian integrative health practitioners a few years back. I think it might have been after Dr. Frassano himself, made an appearance at one of our big conferences. Like the true bloody sceptic I am, I stayed dry on the shore. In fact, I chucked my board in my panel van and drove straight for the library to do some research. Yep…boy do I know how to have fun in the sun 😎 But I am really glad I did.
While I am forever grateful to researchers like Frassano and so many others, who pioneer new perspectives, if not paradigms, in health, I also know that research is a long, long, long road and sometimes we get a little over-excited trying to ‘catch that wave’ too early.
This was especially the case with Zonulin testing.
When I finally left the library about a year later in 2017, I flagged my concerns. As always, my stand was
subtle: Mind the Gap with Zonulin Testing. This was my Update in Under 30 offering, encouraging us all to think about this test more critically and make a balanced review of the evidence both for and against it, as a marker of increased intestinal permeability, especially in comparison with the Lactulose Mannitol Test, considered the gold standard of IP assessment.
I also flagged that not every individual has the capacity to make Zonulin no matter how ‘gappy their guts is’…and this was something most struggled to comprehend or accept. But guess what? This fact has now gone mainstream along with even more concerns regarding the inaccuracy of commercial Zonulin testing.
“Three genetic polymorphisms in human haptoglobin expression, Hp1-1, Hp2-1, and Hp2-2, are determined by the HP1 and HP2 alleles harboured by chromosome 16q22. As zonulin is the precursor to haptoglobin-2, individuals who bear the heterozygous Hp2-1 or homozygous Hp2-2 polymorphism are zonulin-producers whereas those with the homozygous Hp1-1 polymorphism are unable to produce zonulin.” But wait, Ajamian et al 2019 has so much more in store for any remaining believers. “In conclusion, the current commercial zonulin ELISA assays investigated in this study detect different proteins, neither of which was zonulin.” Yes, that’s what they found. Two different big commercial kit assays – one from China, one from Germany…neither actually measured zonulin. I am passionate about CAM and passionate about testing…but cautious & concerned about the CAM-Sham that does get peddled to us at times, under the guise of ‘cutting edge functional testing’. Another name for that..unfounded, not yet validated, waste of money and source of possible misdirection for the practitioner. It’s tough talkin’ Tuesday…just sayin’ 🙄
Need some more help to Mind the Gap with Zonulin Testing?
Following the important discovery of the role of intestinal Zonulin in the pathophysiology of coeliac disease our fascination with measuring zonulin in non-coeliac patients suspected of ‘leaky gut’, has moved faster than the facts. It’s time to critically reassess what value, if any, there is in testing serum Zonulin – which patients and when? Let’s talk about its false positives (flagging a IP problem when there isn’t one) and negatives (failing to flag a problem when there is one) and how it compares with the gold standard for detecting increased intestinal permeability, in our patients.
Kupfernickel. It’s the original German name for Nickel and it literally translates to ‘Copper Nickel’ which inferred it to be the ‘Devil’s Copper’. There’s an interesting story behind this of course and lo and behold the explanation (as is often the case with minerals and metals) is revealed by looking at where Nickel sits in the periodic table. Haven’t heard me rave on before about how all the key nutritional relationships are illustrated in that cornerstone of chemistry?? Where have you been?! Nickel is a transition metal and that tells us many things – including that its key relationships and interactions are likely to be with Iron, Cobalt, Zinc and Copper. And guess what? It’s all true. Still, I’ve had another Nickel-centric chemistry lesson of late because I actually had not the slightest appreciation of how noxious this can make it for us humans.
It started with one patient then, as is always the way, I’ve had about 3 in the past few months: predominantly women, some with ‘known’ nickel allergies, in the form of jewellery-related dermatitis and sometimes not, many with significant gut disturbance (IBS like, non-infectious gastritis) and most with early or advanced autoimmunity.
And the vast amount of scientific literature on the prevalence of Ni allergy (conservative figures suggest 15% population with a very high female:male) and its capacity to go beyond the ‘cosmetic’ and trigger gross immunological aberrations in Th1 cells, well, the case for Noxious Nickel is one of those things that once you see it, you can’t ‘unsee’, ever. Think if you or your patients have never had an issue with wearing cheap jewellery we can rule this one out? Think again. While the jewellery reaction might be the helpful clue in some patients, there are also 3 other ways that the old Kupfernickel may be undermining your health. And yes! The fact that contact dermatitis to nickel-containing silver jewellery is such a common issue tells us straight up, that its absorbed via our skin, think: watches, mobile phones, e-cigarettes, hair clips, and…yes I am having another crack at these again…tattoos! We also inhale and consume it via a wide variety of food and drink we consume. Oh and did I mention dental interventions, yet? 👀 Sheesh….
So while we all accept humans have zero requirement for Nickel, it’s in us all the time and the question is (always) how each individual inner chemistry lab (!) is interacting with it and to what extent this may explain some pretty potent health problems, from GIT disturbance to Hashimotos and from skin conditions and alopecia to CFS & Fibromyalgia-like conditions.
My latest Update in Under 30: How Noxious is Nickel – highlights the fundamentals of Nickel in terms of our sources of exposure and who is most susceptible and just how this can play out as a driver of disease. Next month we move onto our testing options, drilling down into the myriad signs & symptoms and how to effectively manage the patient dancing with the Devil’s Copper. This one has been a real ‘sleeper’ for me, but it’s time to wake the beast for us all 👀
While nickel sits benignly among its mineral mates in the transition metals of the periodic table, it is a metal that humans are constantly exposed to yet have no need for. What could possibly go wrong? Well, a lot it seems. Nickel is the most prevalent metal allergen worldwide and beyond this there is strong evidence of its potential to trigger autoimmunity, major endocrine pathology and a raft of GIT problems that masquerade as other conditions like IBS & NCGS. This episode captures the dance we all do with the ‘Devil’s Copper’ and why some of our patients are likely to end up with a bigger dose and a much bigger disease picture as a result of noxious nickel.
Hear all about it by listening to my latest Update in Under 30:
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.
Histamine, Oxalates & Nickel…any of which may be at fault when your patient reports they experience adverse reactions from eating them. The same can be said for legumes, with a few extra contenders thrown in like oligosaccharides for those farty on FODMAPs. Additionally, in either case, there could be a bona fide allergy (IgE) or an intolerance (IgG) at play. Tricky, right?
I hear from practitioners often, though, that their interpretation of food reactions like these are at risk of being 1 dimensional, like a food word association game: tomato = histamine; legumes = FODMAPS; gluten = NCGS.
The labyrinth of possible pathways for food reactions is just that, a labyrinth!! So, we have to always be on our toes and try and approach each case methodologically.
I outlined how to approach this in clinic in A Guide to Investigating Food Reactions, released earlier this year. We cover a lot in this 2hr recording, but let’s face it, it’s an area that needs yet more time and a field that we never stop learning in. Next week, as part of our UU30 series on Getting to the Guts of Joint Pain, we need to take a little scenic detour along Oxalate Boulevard! Keep your eyes open peeps, because our very own food prescriptions tend to be full of them!! Not naming any names….berries, green smoothies, sweet potato &…
Need to catch up on investigating adverse food reactions??
Elimination of suspected food 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 adverse food reactions landscape.
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?
Watch the gap! You know I love a good diagnostic test probably (way!) more than the next person but I am slow to come around when there’s suddenly a ‘new-kid-on-the-block’ that every functional testing company wants to offer you. This is how I felt about serum zonulin testing as marker of intestinal permeability too. In spite of Fasano’s important work, identifying this molecule and its role in the reversible opening of tight junctions in the small intestine – I didn’t embrace the test. Why not? Didn’t I love Fasano’s ability to add this piece to the jigsaw that had been missing til now? Well I did. Does that make it an accurate and reliable marker of intestinal permeability in every client with any kind of digestive issue…? Well heck no! That’s not how science works friends and I suspect we may have really jumped the gun a little on this one. (more…)
Back a few weeks ago I had the pleasure of presenting at the Integria Symposium and the even greater pleasure of listening to some of the fabulous speakers …you see I’ve heard my stuff before! 😉 The ‘Mosaic of Autoimmunity’ was delivered by the very funny and knowledgeable Professor Yehuda Shoenfeld, who reiterated the sequence of events now well recognised to precede and precipitate autoimmunity: genetic susceptibility + endocrine context + environmental trigger –>autoimmunity.
Clinicians know that overwhelmingly women dominate when it comes to autoimmune disease epidemiology and most understand that this is a consequence of oestrogen’s immunostimulatory effects. Professor Shoenfeld, described the female, or E2 dominant, immune system as being ‘super charged’ and that increased rates of autoimmune diseases were a reflection of this. Sometimes practitioners do initially great work with a/immune clients – clearing up the diet & gut, ensuring vitamin D adequacy etc and then get ‘stuck’ or plateau with antibody levels that ‘won’t budge’. Going back and checking the hormonal contribution in the case is often indicated. If the patient has an unhealthy E2 dominance and /or impaired detoxification and clearance of this hormone then working on this aspect often kickstarts the next stage of improvement.
A new thing to me (I know I’m a bit slow sometimes 🙁 ) was his mention of the potential link also with high prolactin (PRL). The literature on this is extensive and hyperprolactinemia (HPRL), even just mild elevations, have been correlated with a very long list of both systemic and organ specific diseases including: (more…)
As we head rapidly towards the change over of our calendars we would like to offer you a special on the very best educational recordings from 2014 – buy 2 CDs before Jan 31st and receive one complimentary Premium Audio Recording of your choice OR purchase 4 CDs and receive a 3 month Premium Audio subscription for free.
It’s been a busy year during which Rachel has delivered 7 very successful new seminars in the area of mental health and beyond, most notably fortifying her role as a leader in the field of diagnostics and pathology interpretation. This has included collaborations with ACNEM, Biomedica, Health Masters Live, MINDD and Nutrition Care, however, each recording is classic Rachel – full of fresh perspectives on diagnosis & treatment, colourful analogies & humour. In case you missed some of these this year or want a copy for keeps – here’s a quick summary of the 2014 recordings included in this end of year offer: (more…)
In the Byron shire we have a fabulous local comedian called Mandy Nolan who makes a lot of fun of the health and food fads that regularly sweep this area and one of her favourite catch-cries is “I’m gluten intolerant-intolerant, if I meet another person who tells me they’re gluten intolerant I’m going to scream!” Although I take genuine gluten reactions very seriously I do get where she’s coming from and it stems primarily from pervasive misunderstandings & misuse of terms in the community. The problems with this are multiple: firstly those people who are walking around with an exaggerated sense of their problem will unnecessarily limit their diet (and perhaps the diets of their loved ones) at significant financial, nutritional & even psychological cost and then we have people who have the most extreme gluten reactions not receiving the serious attention that they absolutely need in all sorts of settings like restaurants, childcare centres and schools…because seemingly everyone has some sort of ‘gluten issue’ & therefore it has become dangerously ‘normalised’.
So let’s just recap the possibilities and try to clear the confusion. When people walk through our door and tell us they ‘can’t eat bread’ or ‘pasta makes them bloat’ or ‘I don’t think wheat agrees with me’, that’s where our work just begins in terms of needing to clarify what the nature of their reaction is. Putting them immediately on a gluten free diet is a mistake because it doesn’t tell us which one of the below issues is at play and therefore fails to give us clear guidance about what is an appropriate course of treatment & dietary intervention.
- Coeliac disease – while there are a multitude of testing options for CD the first place to start is the genotype. If you don’t have the gene it is extremely unlikely that you have CD. If you have the gene then there’s about a 1/3 chance you might & specific tailored antibody testing or jejunal investigations are necessary.
- A genuine wheat allergy (not CD) is rare but is more common in infants & toddlers. It can be diagnosed by blood antibody tests (IgE RAST) or skin prick testing (SPT) for wheat
- Non-coeliac disease gluten sensitivity – may not involve the immune system at all, however, raised anti-gliadin antibodies are frequently seen in these patients
- FODMAPS – is not an allergy but a type of intolerance due to impaired digestion of the fructans found in wheat. We must rule this out as a possible explanation for someone’s reaction and I would start with a good checklist of other FODMAP foods to check tolerance e.g. soy, dairy, increased fruit intake and check for other conditions that can lead to this via disruption or destruction of the small intestinal brush border
- Carbohydrate digestion issues other than (or in addition to) FODMAPs i.e. underfunctioning of the pancreas
- Red herring! And don’t forget this old pearl… it could of course be a total red herring. Perhaps the reaction is due to another component in bread (yeasts, preservatives etc.), or the other foods they always eat with the pasta (tomato etc.) or their general poor diet quality and speed of eating, lack of relaxation around meals etc. etc.
My one exception would be in children diagnosed on the spectrum for autism. I think going gluten free where possible is appropriate from the get-go in ASD. For everyone else, a correct diagnosis is the essential first step to effective & proportionate treatment so keep your wits about you my fabulous fellow diet detectives!