(THE STAR/ASIA NEWS NETWORK) - The story begins with a personal (and unscientific) anecdote about gluten.
Several years ago, in Taipei, Taiwan, I was convulsed with severe abdominal cramps after several days of eating (too much of) the delicious steamed wheat-flour buns and wheat noodles there.
As I have had previously issues with commercial breads, I suspected a link to gluten and a quick switch to eating rice-based foods resolved the problem, seemingly confirming the suspicions.
So I cut down on all gluten for a while after Taiwan – which was a pretty flawed decision and the reasons why will be clear later.
What is gluten?
Since you have probably heard a lot about it, let us examine what gluten actually is.
The word is derived from the Latin word for glue and gluten is basically an agglomeration of grain-based proteins called glutelins and prolamins. These proteins can stretch and remain springy even under high cooking temperatures, conferring that lovely chewy texture to breads and other baked foods.
Wheat prolamins are known as gliadins, soy prolamins are glycinins, barley has hordeins and other grains have different prolamins – wheat gliadins are water-soluble and are the molecules most associated with gluten sensitivity, though there likely sensitivities also to other prolamins and glutelins as well.
A genetic condition known as coeliac disease (CD) is typified mostly by severe intolerance to gliadins in wheat gluten, with a variety of symptoms such as chronic diarrhoea, abdominal distension, fatigue, intestinal pain, hypoproteinemia (low blood protein) and so on.
There is also non-classic CD, which has indeterminate symptoms such as chronic migraine, infertility, teeth enamel defects and depression; and a variant called asymptomatic CD, where no obvious symptoms are evident even though sufferers have characteristic intestinal lesions.
All proteins are made up of linked chains of amino acids – therefore, CD is a genetically-based autoimmune response triggered by certain amino acid chains in wheat gliadin (and probably other gluten proteins).
Due to the wide range of symptoms associated with CD, a firm diagnosis is not really possible without a serological (blood serum) test to detect the gene-based markers behind CD.
If you are interested, markers assessed for diagnosing CD include anti-tissue transglutaminase immunoglobulins (in particular IgA) and, in borderline assessments, secondary tests may be required to confirm presence of CD-related anti-endomysium antibodies, IgA-transglutaminase 2 (TG2) and/or positive IgG-deamidated gliadin peptides.
An intriguing 2017 paper indicated that CD can be caused by certain human reovirus strains, particularly one called Type 1 Lang (T1L), which is known to infect intestines and disrupt their functions.
In experiments, healthy mice infected by these reovirus strains developed CD.
However, there are no human epidemiology studies linking T1L to CD, so this remains an interesting theory.
A reovirus is based exclusively on ribonucleic acid (RNA) while a virus can have both deoxyribonucleic acid (DNA) and RNA as its infection vectors.
Consumption of gluten-free foods
Statistically, CD affects around 1 per cent of the population in most developed nations. Yet the gluten-free food business in the United States grew by 136 per cent from 2013 to 2015 and is currently estimated to be worth more than US$17 billion (S$22.7 billion) annually.
More than 18 per cent of Americans now consume gluten-free food (30 per cent would also prefer it if they can) and, judging from the numerous gluten-free items in local supermarkets, Europeans are catching up fast.
One reason for the huge growth in gluten-free was that initial research supported the idea that non-CD gluten sensitivity (NCGS) is a real condition – and people with NCGS can recover from gastrointestinal issues by avoiding gluten.
A classic 2011 paper from Monash University determined that foods containing dietary gluten caused gastrointestinal distress in non-CD subjects.
To be fair, the researchers were themselves not wholly convinced by the result and they repeated the study in 2013, after enhancing the methodology and monitoring more food compounds.
With the more rigorous study, the team could find no link between gluten and gastrointestinal problems, but they did establish a link between NCGS and a class of food compounds called FODMAPs (acronym for fermentable, oligo-, di-, mono-saccharides and polyols).
Needless to say, FODMAPs are usually present in foods that contain gluten – a detailed analysis follows later.
The revised study also identified that some people were sensitive to foods which have no gluten or FODMAPs – and which may be attributable to other allergies such as nut and lactose intolerance.
So if gluten is not the real gastrointestinal culprit, then why is a large percentage of the developed world going gluten-free?
It is partly because gluten-free became a fad, heavily promoted by countless “alternative health/medicine/cure” websites, magazines, videos and books.
It is also highly probable people are ascribing other allergic reactions to gluten.
Gluten-free is also lumped in with general but technically vague trends such as “healthy living” and “better eating/living”.
A pretty complex subject
To reflect the complexity of the subject, gluten is possibly not off the hook entirely, according to some recent hypotheses – one claim is that NCGS may be due to metabolites (or intermediate digestion products) created during the processing of gluten by the digestive system.
Other research also linked NCGS with other afflictions such as postural tachycardia syndrome (abnormal heart rate/blood flow issues caused by changes in posture) and Histamine Intolerance, though, again, it is not conclusive whether gluten is the sole culprit and not FODMAPs or other food compounds. And as mentioned, it is entirely feasible that other allergic reactions may be classed incorrectly as NCGS.
Another possible factor is the complexity of the genes in bread wheat – the biggest source of gluten and FODMAPs in human diets.
The original wheat (Triticum dicoccoides) grown around 10,000 years ago was crossed with Aegilops tauschii (goat grass) about 8,000 years ago to improve yields and hardiness. Hybridisation continued until variants called Triticum aestivum were developed to suit modern farming environments.
Bread wheat is therefore a complex hybrid, with 17 billion base-pairs of DNA (compared with only three billion for humans), derived from 42 chromosomes (compared with 46 for humans).
There is a lot of duplication of DNA pairs in wheat (80 per cent is repeated), which makes it difficult to establish which genes are relevant to human digestive systems in any part of the wheat genome. It may be one DNA pair, many DNA pairs, certain permutations of genes or all three – we do not know for certain which combinations of wheat genes trigger negative reactions in humans.
Regardless of all the above, NCGS remains mostly a self-diagnosed syndrome and is seldom based on medical assessments.
Gluten-free is now therefore mostly a lifestyle choice and not conclusively linked to any real gastrointestinal issues to do with gluten itself – unless, of course, you actually have CD.
It is similar to fat-free foods, where some people choose to ingest sugar-laden foods textured by synthetic emulsifiers, conditioners and additives, just to avoid the natural fats in, for example, yogurt.
As with many “lifestyle choices”, the food industry is delighted to offer another range of premium-priced consumables.
Love of cake
After the unnerving episode in Taiwan, I was fearful of gluten for some time – but eventually my fondness of baking cakes helped overcome reservations. And I found, as before I went to Taiwan, that I had no discernible problems with wheat flour.
But the old digestive problems with industrial breads persisted – a condition common to many people choosing to go gluten-free.
Since wheat flour is involved in all cases, what might be the problem issue?
Frankly, there is no single definitive answer – human digestive systems are too complicated for that, especially its obscure, largely unexplored and often perplexing interactions with modern food ingredients and additives.
So on offer instead next is a summary of an investigation into reactions such as NCGS along with some plausible explanations as to why people may be affected by dietary issues – and I hope that you will find it as interesting as I did researching it.
If nothing else, the next part should be a surprising insight into why humans evolved to have such negative reactions in the first place, how human immune systems work in conjunction with bacteria in the human gastrointestinal microbiota and a strange observation about most research into food.