READ: Part 1 and Part 2
A curious aspect of non-coeliac gluten sensitivity (NCGS) is that this syndrome is usually acquired after childhood. It is odd because statistically, adults have a smaller percentage of allergy sufferers than children – one presumes childhood allergens are better tolerated as one grows older and develops a more rounded (or stronger) immune system.
It might be suggested that NCGS is akin to lactose intolerance, which develops after the body stops producing the enzyme lactase. The difference is the human body is innately unable to produce the enzymes to digest many complex carbohydrates at any age – it needs bacteria in the human gastrointestinal microbiota (HGM) to do this, and one supposes adults have a larger range of bacterial fauna than children.
To be clear, humans do produce enzymes to digest some common carbohydrates, especially starches (made up of amylose and amylopectin) and sugars – but most other carbohydrates need digestive help from the HGM. This is why FODMAPs may be allergens behind NCGS if the HGM is defective in some way. FODMAP stands for Fermentable, Oligo-, Di-, Mono-saccharides And Polyols, and are varieties of carbohydrates which humans cannot digest natively via enzymes – and they are often found in food where gluten is present, and also in foods where there is no gluten.
Old wheat vs new wheat?
As modern wheat is a hybrid derived from various grasses, it is worth determining if some change in wheat genes is a cause of NCGS. This was investigated by the University of Reading in 2017. Analysis of various ancient strains established differences in various compounds compared to modern wheat, in particular carotenoid lutein, a colourant mostly bred out of modern wheat (as people prefer white wheat flour). There were also minor differences in plant phytochemicals and dietary fibre content. Curiously, the profiles of FODMAPs are remarkably similar in both ancient and modern wheats. So if FODMAPs are a root cause of NCGS, then people have been suffering for thousands of years.
One mildly interesting outcome is there seems a lesser reaction to FODMAPs from a strain of khorasan wheat called kamut (also known as “mummy wheat” as it allegedly came from wheat grains found in Egyptian tombs). Symptoms of NCGS and irritable bowel syndrome (IBS) appear to be reduced with kamut wheat, and analysis of faecal samples suggested that kamut wheat has a different impact on HGM than normal bread wheat. However, the studies were on small groups and therefore not conclusive – also complicating matters is the fact that nutrition profiles of kamut grown in various countries have wide differences which may or may not be significant.
Gluten, FODMAPs and baking
Next was a look into the impact of modern processing of wheat flour, especially in commercial bakeries and food processing plants. Research in 2015 in Britain suggests that bread gluten becomes less digestible after baking (possibly due to structural changes) – in particular, baked gluten is even more indigestible in people deficient in producing the enzyme amylase (used for digesting amylose).
Furthermore, a 2014 Flinders University study researched the impact of baking on two major prebiotics in bread wheat flour: arabinoxylans (AX) and fructans – prebiotics are non-digestible food compounds which feed the HGM, and are also FODMAPs.
The study found slight variations in AX content after various stages of baking – which implies AX is not hugely affected by processing. More interesting is the impact on fructans; in particular, the use of yeast to ferment and leaven bread flour before baking can reduce fructan content in bread by 60% (though it is important to also note the baseline content and types of fructans vary widely depending on the source of the flour).
This is significant because most commercial bakeries do not proof (ferment with yeast) breads as it takes too long – instead they often use chemicals (eg. sodium bicarbonate, sodium aluminium phosphate, etc) to raise bread quickly in commercial ovens, and therefore the fructan content is significantly higher than for leavened breads.
Fructans are oligosaccharides (complex sugars consisting of polymers or chains of fructose-based molecules). There are several categories of fructans, delineated by different hydroxyl (radical –OH) bonds in their structure and the most well-known types are inulin and levan. They are interesting because a 2017 study at Oslo University claimed that fructans is a possible cause of NCGS. Although the study was small, it was a well-done double-blind exercise, though it is odd that the test fructans (inulin derived from chicory roots) are also sold as prebiotics to promote HGM health.
When test subjects did not know what they were eating, 22% reported intestinal issues with gluten while 46% reported the LEAST problems when ingesting gluten. With fructans, 41% recorded issues, almost double the number for subjects troubled by gluten. Moreover, the study suggested that issues with fructans may be dose-dependent – doubling the amount of fructans normally eaten provoked negative reactions which were absent with less consumption.
There are some considerations. The fructans used in the study were derived from chicory roots – which are different from fructans in wheat and other foods. The same fructans used are also sold commercially as prebiotic supplements to promote HGM health – presumably there are not many people reacting negatively to such supplements or else it would not be a business.
The gluten is based on the 19 most allergenic gliadins (out of around 890 types of known gliadins) – these proteins are 33-mer peptides, and as such not all the gliadins in a normal diet are covered.
It should therefore be noted that not all combinations of fructan and gluten compounds in normal diets were tested.
As an aside, durum wheat (found in good spaghetti and pasta) lacks the gene to produce 33-mer peptides so if you have a reaction to bread wheats, you might try eating some pasta instead to see if it helps.
In 1965, Bronstein’s research into the digestion of wheat gliadins indicated the resulting acidic peptides are a cause of coeliac disease (CD) as sufferers lack an enzyme to digest such peptides, which then circulate around the digestive tract. In response, the body produces antibodies to counter these peptides which are perceived as foreign pathogens. Later in 2000, Fassano showed that intestines also increase production of zonulin in such situations – this protein loosens the tight cellular linkages in the intestines, causing “leaky gut syndrome” where digestive substances permeate into the blood stream, provoking more severe reactions.
Then a 2015 US paper researched the effect of pre-digested wheat gliadins on intestinal tissues extracted from people with CD, NCGS and controls with no gluten sensitivity. The outcome was sobering – ALL tissue samples demonstrated increased permeability reactions to pre-digested gliadins. In addition, it was found that the controls produced significantly more of a protein called cytokine IL-10, which is an anti-inflammatory factor.
It should be noted that tests on tissue extracts with chemically pre-digested gliadins may not accurately reflect conditions in the body. Or it can be suggested gliadins in wheat gluten consistently provoke intestinal inflammatory issues and people who produce enough cytokine IL-10 do not feel the effects of such inflammation.
The probability that humans are reacting to chemical food additives used in modern processed foods also cannot be ignored. This is a long complex subject, covered in the six-part series, “How to count on food”.
If you’re not confused by now, you’re not paying attention
A summary is now in order.
Gluten (especially wheat gliadins) and FODMAPs are broad, complex groups of food substances which vary widely in quantity and types. Due to idiosyncratic differences in humans, it is difficult to pin-point exactly which compound or combinations in one or both groups cause NCGS.
FODMAPs are indigestible food compounds which need the HGM to help with digestion. As they can promote fermentation in the gut, some FODMAPs are associated with gas and distended bellies. They are not necessarily bad – but they do need a compatible, robust HGM to process them.
Ironically, a lot of commercial gluten-free food is bulked up with FODMAPs and often contain industrially-processed oils and added sugars – in short, gluten-free foods are not always inherently healthy.
Fructans are fructose-based FODMAPs which can trigger NCGS, though the reasons why are not known – maybe it is related to HGM. Fructan content varies widely by source and also by certain food processing steps, such as yeast fermentation.
Gliadins in bread wheat gluten, particularly 33-mer peptides, have been linked with intestinal permeability.
Food additives can trigger NCGS, though relevant impact analysis data is currently not available due to the wide range of additives in modern food processing.
Back to Taiwan
Based on the above, my incident in Taiwan in Part 1 of this series was likely due to over-consuming wheat flour in noodles and buns, pushing gliadin and FODMAP consumption past levels which overwhelmed the body’s anti-inflammatory response.
The same issue may apply for commercial breads using unleavened dough with high fructan content and textured with industrial additives.
Subjectively, although problems develop after consuming certain compounds (eg. gliadins, FODMAPs, additives) past a tolerance threshold, it does not mean I have NCGS – in the same way getting drunk does not mean an alcohol allergy.
So if you still consider NCGS a problem issue, you now have all the (currently known) facts before deciding to pay premium prices for gluten-free foods.