Many of you clearly enjoyed the last issue’s overview of the Gluten Summit judging by your comments, thank you. If you have been on the edge of your seat waiting for the speaker mini-series to start, you’re in luck.
Obviously, the speakers had a lot more than this to say – and you can listen to their interviews in full using the links I gave you in the above article. For the mini-series, I have tried to tease out what I thought was the essence of their thinking and pull out any nuggets that have the potential to really help us in our day to day gluten lives. Hope you find it useful, and will forgive me for paraphrasing, otherwise I’d have bored you silly with direct quotes.
Let’s start with the first speaker at the conference and, surprisingly, the one with the most stridently-put views; he got quite animated!
Dr Michael Marsh, Gastroenterologist, Coeliac/Gluten Specialist
Dr Marsh invented the Marsh coeliac scoring system in 1992 but now says coeliac disease (CD) is not a disease of the small intestine and looking at villi changes is too narrow a focus diagnostically. He feels there is too much emphasis on his own Marsh stage 4 and calls for clinicians to take much more notice of the earlier Marsh 0-3 stages as we know, without doubt, that people can get symptoms, nutritional deficiencies, especially of iron and bone minerals, and even lymphomas way before stage 4.
He got quite angry about it all, actually, and says the literature already shows the development of related illnesses far earlier than stage 4 and not recommending a gluten free diet in suspect cases, even in the absence of current test parameters, has no medical, moral or probably legal defence. Ooer. Strong words.
He thinks that gluten illness has changed dramatically in his lifetime and this may be to do with environmental shifts and the effect those are having on our genetic expression. Many more people are gluten sensitive without villi involvement and this is hardly surprising to him since we have eaten it as humans now for more than 10,000 years and still have not evolved an enzyme to digest it effectively. No human can actually digest gluten; it is just that some people can cope and never have a problem, others can cope for a time and a smaller number of genetic gluten sensitives don’t cope at all.
Diagnostically, he feels we should not be waiting for end-stage damage markers like villi changes and antibodies and to do so is letting patients down. He wants to see more emphasis on discovering ways to monitor mucosal morphology (physical) changes and levels of the T lymphocyte cells known to signal early problems. He recommends not relying on the presence of DQ2/DQ8 genes for diagnosis of CD but advises regular monitoring as the genes can be triggered at any time. To ignore their presence is wrong.
Treatment-wise, he is not impressed with the idea of vaccines and recommends a gluten free diet, especially if blood antibodies are found – even a single one eg. a gliadin antibody. If blood tests are negative and the person feels better off gluten, he recommends a gluten free diet, not waiting for the genes to trigger or for enough damage to be done to show up on current tests.
Key Practical Message:
Don’t wait for the damage and a Stage 4 problem. If you find an antibody or feel better off gluten, even if everything else is negative, follow a gluten free diet.
And that’s from the so-called ‘Godfather of Coeliac Disease’…
Professor Alessio Fasano, Gastroenterologist and Research Scientist
Fasano first broke the story about CD being much more common than previously thought – 1 in 133 in 2003. He discovered the gluten/zonulin connection in 2000 and set up the first US Coeliac Center in 1996.
In essence, he believes that there is a kind of gluten ‘triad’ required to develop a gluten-related disorder. You need:
- the right DQ genes (he believes DQ2 and DQ8 but I and others believe other DQ genes are also involved – especially DQ1, more on this later in the series)
- an environmental trigger (in this case, gluten) and
- a breach of the body barriers (hyper-permeability).
In terms of pathology, he thinks there are two different processes going on in CD and NCGS, but there is much debate about this still.
His belief is that non-coeliac gluten sensitivity (NCGS) is an innate first immune response problem, which is inflammatory in nature. That inflammation then goes on to cause the symptoms and damage as in pain, migraine, chronic fatigue etc. He believes CD is a second (humoral) immune response and involves an auto-immune attack on the villi.
I think that is right to a point, but we will cover Prof. Vojdani’s immunology explanation of what happens later in this series and views of other scientists, including Prof. Hadjivassiliou’s, who has found auto-immune reactions, eg. GAD antibodies (Glutamic Acid Decarboxylase antibodies found high in Type 1 diabetes, stiff person syndrome and some neuro diseases) are rife in NCGSs. My own view is that Prof. Vojdani is probably closest to what’s going on – a gluten related disorder starts as an inflammatory response and CD is just one of the auto-immune reactions that can follow, but then so is auto-immune thyroiditis etc.
Either way, you have to lower inflammation if you don’t want things to develop any further. And, he adds, that it makes no difference to treatment – it is the same for both: a gluten free diet acting as the removal of the key trigger. Personally, my view differs again here (in case this helps you): there is a difference beyond the diet if the auto-immunity process has been triggered.
He passionately argued that we have massively underestimated the role of the body barriers and the microbiome (the gut environment). The microbiome is inherently linked to our human genome and affects hugely how our own genes are expressed and triggered, how we control immunity and keep the barriers intact.
In fact, he and many of the speakers, asked the fascinating rhetorical question as to just which genome is in charge? The microbiome has zillions more genes than the human genome does and many experts are starting to believe that we have become the strongest species on the planet purely because of the symbiotic genome relationship we have as hosts for the bacterial colony. It is postulated that the environmental changes of the last few decades have had a deleterious effect on the microbiome and the triggering of the various genes involved in common diseases. This is a massive topic but I mention it here as I found it quite a plausible way of thinking about why we are developing such loss of tolerance to foodstuffs, chemicals and the like.
He explained (as did others in the Summit) that no-one can break gluten down and it breaches everyone’s gut barrier because of the effect it has on the zonulin which controls the tight junctions, the gate-keepers, if you like, of the body barriers. Most of us have immune systems that can cope but some genetically-susceptible people can’t. A lot of us probably lose the battle over time, which rather partly explains why we merrily munch gluten for years and then suddenly develop a problem.
The barrier function loss, he feels, is down to the changes in the microbiome and the biggest factors in those changes are the food we eat, antibiotics and toxin exposure. We can have many years of oral tolerance and then a sudden loss, whereas we used to think gluten illness was from birth. We now know that was wrong.
He agrees with Prof. Vojdani that once the genes have been triggered, there is no undoing that and gluten exposure must be avoided otherwise you will re-trigger the underlying pathology of inflammation or auto-immunity, depending on which pathway your body has gone with. This was not an easy thing to hear. Happily others have a more positive view and feel that if we can correct the barriers and the microbiome, we are in with a chance of changing the genetic expression.
Key Practical Message:
In his view, diagnostics for gluten related disorders (GRDs) should involve looking for the gluten genes, toxicity levels, the state of the microbiome (gut flora), the known coeliac antibodies, inflammation markers and barrier breakdown, notably the zonulin antibodies. Treatment must involve – as a minimum - repair of the barrier, avoidance of the trigger (gluten, here) and re-setting the microbiome. For symptoms, you need to lower inflammation. The microbiome is the key for him.
Useful stuff, I hope. In fact, we will return to Prof. Fasano again at the end of this series because he has just been involved in another conference I have summarised where he was man enough to say he was wrong about coeliac disease for many years and strongly resisted the notion of gluten related disorders. He now believes it is a spectrum disorder, certainly not just coeliac disease, and is trying to convince other sceptics. Nice turnaround, Professor F!
Hope you found those illuminating. Two more in the next issue…
To read the introduction to the Gluten Summit, see here. Catch up with the mini-series 1, 2, 3, 4 and 5. And to read the conclusion see here
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