When asked by her grandmother what she would like for dinner, my 6 year old answers “Anything with Gluten”
She is living in a gluten free home. Rice cakes, rice, rice bread, rice milk. It’s all a compromise. Gone is the brain pleasure of gliadin triggering the gliamorphine receptors giving us a white bread high. Also gone is the fat belly’s bloated farting constipated achy tired family. (Well some of us are free of this unpleasantness)
So is it a fad? or is there scientific evidence behind gluten intolerance..
Lets take a look at the symptoms of Coeliac disease/ Gluten Sensitivity (non-caeliac gluten sensitivity or NCGS is where blood tests or biopsy are negative for coeliac disease but the symptoms are still present)
Gastrointestinal pain and discomfort
constipation and/or diarrhoea
even.. neuropsychiatric disorders such as autism and schizophrenia
These reported signs and symptoms occur after ingestion of foods containing gluten and ameliorate within days or weeks of eliminating gluten from the diet.
$2.5 billion USD was spent in 2010 on gluten free products. This spending makes big business, government and the media sit up and take notice.
Gluten is the main structural protein in wheat (with equivalent toxic proteins found in rye and barley) These toxic protein fractions of gluten include gliadins and glutenins.
With NY Best sellers like Wheat Belly and Grain Brain, the experts may still be deliberating, but the patients are voting with their purchases and eating choices.
Gluten sensitivity is now estimated to be affecting not 3% but up to 30% of the population!. Gluten free eating is expensive and difficult. But when you experience a life with the symptoms of gluten sensitivity, and the subsequent ‘recovery’ and wonderful effects of removing this toxin – there is no need for any expert to confirm what is a very clear and real improvement to health and quality of life.
It is important to further understand the difference between irritable bowel syndrome and wheat allergy. I find those who tolerate rye are sufferers of wheat which is another story.
“There is a kind of chronic indigestion which is met with in persons of all ages, yet is especially apt to affect children between one and five years old. Signs of the disease are yielded by the faeces; being loose, not formed, but not watery; more bulky than the food taken would seem to account for; pale in colour, as if devoid of bile; yeasty, frothy, an appearance probably due to fermentation; stinking, stench often very great, the food having undergone putrefaction rather than concoction……….
“But if the patient can be cured at all, it must be by means of diet.”
•Dr Samuel Gee 1888
For those wanting more: Heres the techy bit
Testing for Gluten Sensitivity – discuss this with your doctor….
The difficulty is proving the positive changes are significant and not due to the very powerful placebo effect. The concern is placing unnecessary restrictions and increased financial strain on families if there is no real medical need.
Lets look at diagnosis and categories. There are three main types of Gluten disorders:
1. Allergic – Wheat allergy – this is like a typical bee sting or peanut allergy. It occurs minutes to hours after exposure. This is the least common and can lead to severe illness and death. So blood testing is the suggested – IgE antibodies (anti wheat, rye barley and anti-alpha-amylase igE in serum) 1.
2. Autoimmune – True Coeliac disease, includes dermatitis heretiformic, and gluten ataxia. First described in ancient Greece where Aretaeus named it “koiliakos’ meaning ‘suffering in the bowels’. 17 Centuaries later “Some patients have appeared to derive considerable advantage from living almost entirely upon rice..” Dr Matthew Baillie 1800’s (2)
Blood measurement of IgA antibodies to transglutaminase (anti-tTG) is recommended for initial testing for Coeliac Disease while IgA anti endomysial antibodies is considered as a confirmatory test. Histological findings of a small bowel biopsy remain the gold standard of diagnosis for Coeliac Disease (3)
During the 1970s, Coeliac Disease was considered a rare disorder affecting 1:1000 (0.1%) individuals predominantly of European origin (5) We now know that Coeliac Disease occurs in both adults and children at rates approaching 1% of the population. (6)
75% of individuals with Coeliac Disease remain undiagnosed. The rate of diagnosis is increasing (7) A negative test result for serology or small bowel biopsy does not preclude Coeliac Disease development at a later stage.
Is Genotyping – Gene Testing useful to predict future development? 99% of patients with Coeliac Disease carry one or both the genes. HLA DQ2 or DQ8 halotypes have an excellent negative predictive value – so these are good for a ‘once and for all’ exclusion test. If you don’t have any you can be reassured. (8)
Gluten challenge: How much?
For patients with positive gene tests ( HLA DQ2 or DQ8 halotypes), who wish to proceed with a formal diagnostic process, a gluten challenge is required. Four slices of bread for an adult and two or more slices of bread for a child consumed for six weeks is considered enough to produce the serological and histological evidence required for a diagnosis of Coeliac Disease (9)
3. Possible Immune Mediated – Gluten Sensitivity
Thought due to the steady modification of wheat, and pre-treatment of flours.
Some individuals who experience distress when eating gluten-containing products and show improvement when eating gluten-free may have Gluten Sensitivity instead of Coesliac Disease. Gluten Sensitivity is a condition distinct from Coeliac Disease and is not accompanied by the concurrence of anti-tTG autoantibodies or other autoimmune comorbidities (10)
There are no blood or genetic tests to confirm gluten sensitivity. This is a clinical diagnosis, with a symptomatic patient doing an elimination test then reintroduction to prove the symptoms.
There is a life threatening immediate wheat allergy – IgE blood tests can detect this.
Coeliac Disease is a genetically predetermined, but environmentally triggered autoimmune disease diagnosed by Blood anti –TTG and confirmed with Anti-endomysial Antibodies. This is then confirmed with a biopsy of the bowel during gastroscopy. This can be false if not exposed to gluten at the time, if symptoms continue exposure and retest are necessary. Gene testing can rule out, but is not very accurate at ruling in Coeliac disease. 1% of the population or 200,000 Australians are Coeliac, but 75% of Coeliacs are undiagnosed.
Gluten sensitivity is on the rise, maybe due to changes to wheat and flour treatment. There is no testing it is a clinical diagnosis. Elimination of all wheat rye barley and oats, and processed gluten containing products, is the treatment.
1. Catassi C, Bai JC, Bonaz B, et al. Non-celiac gluten sensitivity: the new frontier of gluten related disorders. Nutrients 2013;5(10):3839-3853.
2. Biersiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind,randomised, placebo controlled trial. Am J Gastroenterol 2011;106(3):508-514.
3. Dr Joanna Harnett PhD
4. Dr Matthew Baille 1888
5. Ludvigsson, Brandt et al. 2009.
6. Walker and Murray 2011.
7. Lohi, Mustalahti et al. 2007 Accomando and Cataldo 2004; Lohi, Mustalahti et al. 2007; Lohi 2010
9. West, Logan et al 2003
10. Anderson 2008–(Tye-Din and Anderson 2008; Kneepkens and von Blomberg
11. Gibson, Shepherd et al. 2012
12. Sapone 2010
ACNEM (Australian college of nutritional and environmental medicine) –
Gastrointestinal Disorders Protocol.
nbDr Stephano Guandialini in 1980’s refined the diagnosis, now The Marsh Classification recognises increased intraepithelial lymphocytes and crypt hyperplasia with intact villi as part of gluten enteropathy spectrum, while some individuals have more subtle abnormalities identified only on electron microscopy. The histological diagnosis of Coeliac Disease no longer requires small intestine villous atrophy (4)
Classic food allergy affecting the skin, gastrointestinal tract or respiratory tract. (This category includes Occupational Asthma (Bakers asthma), rhinitis and contact urticaria.) IgE antibodies play a central role in the pathogenesis of these diseases. Skin prick testing is less effective due to cross reactivity with grass pollens (PPV less than 75%)