Science of Gluten Free
Author: Dr. Alan Barclay
Gluten and wheat free foods, meals and diets are increasingly popular. People are avoiding gluten due to serious health conditions like coeliac disease, dermatitis herpetiformis, wheat allergy or non-coeliac gluten sensitivity, or simply due to personal food preferences. Whatever the reason, it’s important that the gluten/wheat free diet is nutritionally adequate, culturally appropriate, enjoyable and affordable, in order for people to achieve and maintain their optimal nutritional status.
Gluten is the protein complex that is formed when wheat flour is physically manipulated with water. It is comprised of two protein fractions (gliadin and glutenin) in approximately equal amounts. Gliadins and glutenins are unusually rich in the amino acids proline and glutamine, and are not completely digestible by human small intestinal digestive enzymes 1.
Rye, barley and oats contain similar alcohol-soluble protein fractions (secalins, hordeins and avenins, respectively) known as prolamins (rich in proline and glutamine)2. Therefore, the word “gluten” is used to describe collectively, the grain storage proteins from wheat, rye, triticale (a hybrid of wheat and rye), barley and oats 3.
The gastro-intestinal digestion of gliadins and related proteins (secalins, hordeins and avenins) results in the formation of relatively large peptides, because of the large amount of proline residues in the sequence of these proteins, that blocks the cleavage of the polypeptide sequence by gastrointestinal enzymes at positions immediately next to proline. The size of the digested peptides, along with the position of the digested peptides, and the position of the glutamine residues in the primary structure of the peptides, is thought to play a pivotal role in their activity in coeliac disease and related conditions 4.
Coeliac disease, or gluten-sensitive enteropathy, is an immune-mediated small intestinal enteropathy that is triggered by exposure to “gluten” in genetically predisposed individuals 5. It is characterized by a specific genotype (human leucocyte antigen (HLA)-DQ2 and HLA-DQ8 genes) and auto-antibodies (anti-tissue transglutaminase and anti-endomysial) 6.
In Australia, the most recent estimated prevalence of coeliac disease is 1.2% in adult men (1 in 86) and 1.9% in adult women (1 in 52) 7.
Coeliac disease can develop at any age and is more frequently diagnosed in females than males with a ratio between 1.5 and 2 but this gender imbalance may decrease with age 5.
A high prevalence (10%) among first-degree relatives of people with coeliac disease and a greater concordance rate in monozygotic twins (∼75%) than in dizygotic twins indicates the important role of genetics in the diseases development 5.
Finally, people with type 1 diabetes are at much greater risk of developing coeliac disease than those without the condition. The most recent estimates based on duodenal biopsy suggest that 3.5% of children with type 1 diabetes also have coeliac disease, with again a higher prevalence in females than males (4.3 vs. 2.7%)8.
Development of Coeliac Disease
Genetic predisposition and “gluten” (gliadin/secalin/hordein) consumption are both necessary, but not sufficient, for the development of coeliac disease, because not everyone with the genetic predisposition develops the condition. Other environmental factors are therefore important in coeliac disease development. Gastrointestinal infections, pharmaceuticals, interferon α, surgery, imbalance of the intestinal microbiota and infant feeding practices have all been implicated as trigger factors in susceptible individuals, but more research is needed 5;9.
The final product of the partial digestion of “gluten” in the gastrointestinal tract is a mix of peptides that can trigger physiological responses in genetically susceptible people, including increased intestinal permeability, and innate and adaptive immune responses, that closely resemble those activated by the exposure to gastrointestinal pathogens (e.g., bacteria, fungi, viruses, etc...) 6.
“Gluten” can cause an immediate and transient increase in intestinal permeability. This permeating effect is secondary to the binding of specific undigestible gliadin/secalin/hordein fragments to the CXCR3 chemokine receptor in small intestinal cells, with subsequent release of zonulin, a modulator of intercellular tight junctions, which increases small intestinal permeability 6.
It’s important to note that this process takes place in everyone who ingests “gluten”. For the majority of people, these events do not lead to any abnormal consequences. However, in genetically predisposed individuals, these same events can lead to an inflammatory process when the immune system mistakenly identifies “gluten” as a pathogen once it enters the lamina propria of the small intestine 6.
Additionally, there is evidence that during the acute phase of coeliac disease, “gluten” can also cross the intestinal barrier through the transcellular pathway via transferrin receptor CD71, once tolerance to “gluten” has been lost 6.
Innate immune response
Innate immunity plays a critical role in initiating coeliac disease and possibly non-coeliac gluten sensitivity (see page 11). Cytokines such as interleukin (IL) 15 and interferon alfa can prime the innate immune response by polarizing dendritic cells and intraepithelial lymphocyte function. These intestinal mucosal events, along with the breach of the epithelial barrier, function secondary to the gliadin/secalin/hordein-mediated zonulin release, lead to the passage of undigested peptides from the gut lumen to the lamina propria of the small intestine. Once gliadin crosses the epithelial barrier, neutrophil recruitment through IL8 production, or a direct neutrophil chemoattractant effect, causes a loss of tolerance to “gluten” in genetically susceptible individuals 6.
Adaptive immune response
The adaptive immune response is the consequence of a highly specific interplay between selected “gluten” peptides and major histocompatibility complex class II HLA-DQ2/8–restricted T-cell antigens, and also plays a role in coeliac disease pathogenesis. The contact of CD4+ T cells in the lamina propria of the small intestine with “gluten” induces their activation and proliferation, leading to production of proinflammatory cytokines, metalloproteases, and keratinocyte growth factor, which induces cryptal hyperplasia and villous blunting secondary to intestinal epithelial cell death induced by intraepithelial lymphocytes. Coeliac disease crypt hyperplasia has been hypothesized to be the consequence of an imbalance between continuous tissue damage due to the mucosal autoimmune insult described above, and the inability of the stem cells to compensate 6.
What about oats?
The prolamin fraction in oats (avenins) is slightly different from the prolamin fractions in wheat, rye, triticale and barley, and it only comprises a small proportion of oats total protein content 2. However, in Australia, oats are frequently grown, stored or processed with other “gluten” containing grains including wheat, rye, triticale or barley and therefore typically contain “gluten” via contamination. Oats grown and processed without contamination, or even cleaned of contaminating grains, are available commercially in many parts of the world, but they are rare in Australia 2.
Under Australia’s current Food Standards Code, companies are not permitted to make gluten free claims on oats, or oat-based products, regardless of their source 10.
Recent Australian research suggests that the avenin protein from oats can stimulate intestinal gluten-reactive T cells in 8% of people with coeliac disease consuming 100 g (1 ¼ Cup) of un-contaminated oats per day. However, it’s thought that the amount of oats commonly consumed are insufficient to cause clinical relapse in most people with coeliac disease 11. In support of this, a recent systematic review and meta-analysis of randomised controlled trials determined that un-contaminated oats are tolerated by the majority of people with coeliac disease 2.
Oats may increase the nutritional value, and improve the palatability, texture, and fibre content of “gluten” free diets. Some people may therefore want to include them in their “gluten” free diet. Undertaking a gastroscopy and small bowel biopsy before and after 3 months of regular uncontaminated oat consumption is the simplest way of determining if a person with coeliac disease can safely consume oats 3.
Symptoms of Coeliac Disease
Symptoms of classic coeliac disease include malabsorption dominated by diarrhoea, steatorrhoea, weight loss and/or failure to thrive. However, newly diagnosed people with coeliac disease can present with a wide range of symptoms and signs, including anaemia, vague abdominal symptoms (often similar to irritable bowel syndrome (IBS)), neuropathy, ataxia, depression, short stature, osteomalacia and osteoporosis, adverse pregnancy outcomes and lymphoma (Table 1)5.
Table 1: symptoms of coeliac disease 5;6.
Common symptoms in children
- Diarrhoea or constipation
- Abdominal distention, pain and flatulence
- Large, bulky, foul stools
- Nausea and vomiting
- Mouth ulcers
- Rash (e.g., eczema or dermatitis herpetiformis)
- Poor weight gain and retarded growth in younger children
- Weight loss in older children
- Delayed puberty
- Chronic anaemia
- Lactose intolerance
- In children with type 1 diabetes, difficulty in managing blood glucose levels, which may lead to hypoglycaemia or hyperglycaemia
Common symptoms in adults
- Diarrhoea - This may begin at any age and often persists for many years
- It may first appear after other illnesses such as bacterial or viral gastroenteritis, or abdominal operations
- Constipation - some people experience this more often than diarrhoea
- Flatulence, abdominal distention/bloating, and cramping
- Nausea and vomiting
- Gastrointestinal reflux
- Lactose intolerance
- Unexplained weight loss
- Anaemia - iron or folic acid deficiency are the most common. The anaemia will either not respond to appropriate treatment or will recur after treatment
- Fatigue and lethargy
- In people with type 1 diabetes, difficulty in managing blood glucose levels, which may lead to hypoglycaemia or hyperglycaemia
Less common symptoms in adults
- Vitamin B12, A, D, E and/or K deficiency
- Low blood calcium levels with muscle spasms
- Easy bruising of the skin – due to the vitamin deficiencies
- Unusual skin rashes such as Dermatitis Herpetiformis
- Ulcerations and/or swelling of the mouth and tongue
- Miscarriages and infertility in women
It is important to note that sometimes there are no obvious symptoms of coeliac disease. This is particularly the case in people with Type 1 diabetes, where 85% of people with coeliac disease are asymptomatic 12.
Diagnosis of coeliac disease requires duodenal biopsy when the person has been consuming a “gluten”-containing diet for several months, and for the vast majority of adults, also positive serology. For a definite diagnosis, villous atrophy is required. However, lesser degrees of damage (≥25 intraepithelial lymphocytes (IELs) but no villous atrophy) combined with positive serology (IgA-endomysium antigen (EMA), tissue transglutaminase (TTG) or IgG-deamidated gliadin peptides (DGP)) may also represent coeliac disease (“probable coeliac disease”), and in these circumstances, a trial with a “gluten” free diet may be considered to further support the diagnosis of coeliac disease. HLA status may also aid diagnosis 5.
It’s important to note that biopsy remains essential for the diagnosis of adult coeliac disease and cannot be replaced by serology 5.
Morbidity and mortality associated with coeliac disease
Systematic reviews of observational studies suggest that people with coeliac disease are at slightly increased risk (11%) of developing cardiovascular disease (e.g., coronary heart disease), and in particular stroke 13;14. It is thought that individuals with coeliac disease have chronic low-level inflammation, which can drive atherosclerosis and vascular damage. Gluten free diets are typically low in dietary fibre, certain vitamins and minerals and can have a higher glycemic index and be high in saturated fat, increasing the risk of cardiovascular diseases 15;16.
A number of studies have examined mortality in people with undiagnosed coeliac disease. Some demonstrate increased mortality, while others don’t. A recent meta-analysis suggested that the overall malignancy risk in people with diagnosed coeliac disease is not elevated, compared with the risk in general population–based controls. However, individual cancers, such as lymphoproliferative cancer and gastrointestinal cancers, may still be positively associated with coeliac disease 6.
Prevention of Coeliac Disease
Additional environmental risk factors, such as the way in which “gluten” is introduced into the diet, have also been proposed as triggers for coeliac disease in susceptible individuals 9;17. Both prolonged breast feeding and “gluten” introduction during an optimal “window” period (4-6 months), in which the infant’s immune system is more likely to adapt to food antigens, have until recently been assumed as protective factors for the development of the condition 9.
A recent systematic review of 14 observational studies (9 prospective) and 2 intervention studies has challenged these assumptions 9. Nine of the 16 studies examined the effect of breast feeding at the time of “gluten” introduction on later development of coeliac disease. Two retrospective studies found a preventive effect of being breast fed at the first ingestion of “gluten” during the introduction of solid foods. However, none of the six prospective studies found a protective effect. The prospective studies were the most recent, had the highest quality scores, and included children with a common genetic background predisposing them to coeliac disease or type 1 diabetes or were DQ2/8+ positive children 9. Eight of the 11 studies (9 prospective) investigating the timing of “gluten” introduction did not find any relationship between the age of the children at this stage and development of coeliac disease, either 9.
Breast milk may independently prevent gastrointestinal infections, which are thought to be one of the triggering factors for coeliac disease, by modulating the intestinal microbiota, increasing the number of bifidobacteria, and boosting the mechanisms of oral tolerance by means of several immunomodulatory molecules, offering a high biological plausibility to the interpretation of a protective effect against immune-mediated diseases such as coeliac disease. However, 10 of the 16 studies (2 clinical trials and 8 prospective studies) investigating the effect of breast feeding on the risk of coeliac disease concluded that the duration of breast feeding did not show a preventive effect on the development of coeliac disease. These studies were also the most recent and had the highest quality scores 9.
There is therefore at present no evidence for an optimal breastfeeding duration or the effects of avoiding early (<4 months of age) or late (≥6 or even at 12 months) “gluten” introduction in children at risk of coeliac disease. Accordingly, no specific general recommendations about “gluten” introduction or optimal breastfeeding duration can be presently provided in order to prevent coeliac disease 9.
It is important to note that none of the studies included in this systematic review compared the effect of different amounts of “gluten” given to children during weaning on the risk of coeliac disease 9. More research is therefore needed.
Even in the absence of evidence of the protective effect of breast feeding, it must be emphasised that breast feeding is best whenever possible for all infants, including those at genetic risk of coeliac disease, for its many, well-documented benefits, including its unique role in maternal–infant bonding 9.
Management of Coeliac Disease
Currently, the only available treatment for coeliac disease is lifelong adherence to a “gluten” free diet 15. As noted previously, while not technically correct, the word “gluten” is used to describe not only wheat-based proteins (gliadins), but also those from barley (hordeins) and rye (secalins), cereal hybrids such as triticale, and for some people, oats 2;5;11.
Therefore, a gluten free diet means life-long avoidance of all “gluten”-containing grains, and products that contain ingredients made from these grains. This includes most breads, pastas, some breakfast cereals, most biscuits, cakes, scones, pizza and pies as well as many other processed foods.
Corn (maize), rice, sago, tapioca, buckwheat, potato flour, soy flour and arrowroot, and products that are made from these foods, are all “gluten” free. Fresh fruit, vegetables, meat (except most processed meats), chicken, fish and milk and most other dairy foods are also all “gluten” free.
Even in the absence of evidence of the protective effect of breast feeding, it must be emphasised that breast feeding is best whenever possible for all infants, including those at genetic risk of coeliac disease, for its many, well-documented benefits, including its unique role in maternal–infant bonding 9.
Gluten free and food labelling
As currently defined by the Australia and New Zealand Food Standard Code, “a gluten free food should contain no detectable gluten; and no oats or their products; or cereals containing gluten that have been malted, or their products”. Foods that have “gluten free” claims on their labels can therefore be safely consumed by people with coeliac disease 10.
Foods without “gluten free” claims may or may not contain gluten. To determine whether they do or not, people with coeliac disease should be advised to check the ingredient list. Australia’s Food Standards Code requires that all ingredients derived from wheat, rye, oats, and barley must be declared on the food label 10. For example, a thickener derived from wheat would appear on the labels as “thickener 1442 (wheat)”. Importantly, ingredients where the grain is not specifically identified after the additive name or number are from a “gluten free” grain.
Adherence to the gluten free diet
Research shows that daily intakes of <10 mg of “gluten” have no effect on small intestinal mucosal histology, whereas observable alterations develop at 100 mg / day and definite alterations are caused by a daily intake of ≥ 500 mg / day. Therefore, at present, a safe limit of “gluten” consumption could be set at between 10 and 100 mg of “gluten” per day for most adults with coeliac disease 5
Adherence to a “gluten” free diet helps reverse intestinal damage (57–76% of people), normalise nutrient absorption and relieve symptoms, and also reduces the risk of serious future complications, including osteoporosis, malignancy and fertility difficulties 5.
However, there is evidence to suggest that adherence to a “gluten” free diet is generally poor 18, but highly variable among different age and ethnic groups, ranging from 42% to 91% 19. Unsurprisingly, individuals with ongoing symptoms are more likely to adhere to a “gluten” free diet than those without any obvious symptoms.
Research investigating adherence to the “gluten” free diet have indicated that many people do not intentionally follow a “gluten” free diet 19. Poor adherence is associated with lower education levels, perceived ability to maintain a “gluten” free diet and low availability of “gluten”-free foods. There is a paucity of research, particularly in Australia, comprehensively investigating the effect of food cost on adherence 19.
However, a recent Australian study evaluated the cost of two healthy food baskets. These were designated the Healthy Food Basket (HFB) and the “gluten”-free Healthy Food Basket. Baskets were priced at five locations in Southern NSW and costs as a proportion of the Equivalised Household Disposable Income and average weekly earnings for welfare recipients were calculated. The “gluten” free HFB was significantly more expensive than one with “gluten”-containing equivalents for all four family types studied. The “gluten” free HFB was between 5.8% and 16.7% more expensive than the regular HFB. The “gluten” free diet was considered unaffordable for the majority of family types studied (nuclear, single-parent and single young male family types) and for most family types receiving welfare payments in Australia 19.
Nutritional status of people with Coeliac Disease
When first diagnosed, up to 28% of children with coeliac disease have a nutritional deficiency, including iron (28- 50%), folate (14%), vitamin B12 (1%), and/or vitamin D (27%) deficiency. Adults diagnosed with coeliac disease are also likely to have a nutritional deficiency, including iron (32%), folate (20%), B12 (19%), and/or zinc (67%) deficiency 6;15.
Indeed, the most common extra-intestinal manifestation of coeliac disease at the time of diagnosis is iron deficiency anaemia which is mainly due to malabsorption 15. Malabsorption and inflammation caused by coeliac disease also contribute to a low bone mineral density 15. People with coeliac disease have a risk for bone fractures 40% higher than people without coeliac disease 15.
Finally, up to 22% of people with coeliac disease have neurologic symptoms, psychiatric symptoms, or both. The aetiology may at least in part be attributable to nutritional deficiencies such as vitamin B12 and folate deficiency. Peripheral neuropathy is also relatively common - in one study, neuropathy was diagnosed in 0.7% of people with coeliac disease, compared with 0.3% of controls 6.
A number of studies in Australia and overseas have investigated the nutritional adequacy of “gluten” free foods and diets 15;20. The most common dietary issue is inadequate fibre intake, due to the avoidance of “gluten”-containing grains 15. Not only are “gluten”-free grain alternatives usually lower in fibre, they also contain less magnesium and folate compared to “gluten”-containing equivalents 15.
Additionally, people appear to focus more on the “gluten” content of their diets than their overall nutritional quality. Systematic reviews of the dietary quality of “gluten” free diets have determined that they have a higher saturated and hydrogenated fat content and a higher glycemic index and glycemic load 15, potentially increasing the risk of cardiovascular disease.
In Australia, analysis of 7-day food records of people described as adherent to a “gluten” free diet determined that fibre intake was inadequate for all except experienced men. More than one in 10 of both newly-diagnosed and experienced women had inadequate thiamin, folate, vitamin A, magnesium, calcium and iron intakes. More than one in 10 newly-diagnosed men had inadequate thiamin, folate, magnesium, calcium and zinc intakes. The frequency of inadequacies was similar pre- and post-diagnosis, except for thiamin and vitamin A, where inadequacies were more common after “gluten” free diet implementation. Inadequacies of folate, calcium, iron and zinc also occurred more frequently than in the general Australian population 20.
Dermatitis herpetiformis is the cutaneous manifestation of coeliac disease caused by dietary exposure to “gluten”. It is characterised clinically by herpetiform clusters of intensely itchy urticated papules and small blisters distributed on the extensor aspects of the elbows and knees and over the buttocks and on the scalp. Although it may occur at any age after weaning, it most frequently develops in the 20’s and 30’s. Unlike coeliac disease, males are twice as likely to develop the condition than females. Like coeliac disease, dermatitis herpetiformis is a lifelong condition, with varying periods of activity, most likely due to varying degrees of dietary adherence 5.
Less than 10% of people with dermatitis herpetiformis have symptoms or signs of malabsorption but most have some evidence of coeliac disease that responds to a “gluten” free diet and relapses on “gluten” challenge. People with dermatitis herpetiformis present with their skin manifestations and are not usually troubled by the underlying small bowel problem at the time of presentation. However, abnormality of the small intestinal mucosa with either total or subtotal villous atrophy is found in approximately 70% of patients with dermatitis herpetiformis and a further 25% have normal villous architecture with increased intraepithelial lymphocytes 5.
Like people with coeliac disease, people with dermatitis herpetiformis have an increased risk of developing lymphomas but this seems to be confined to those with severe gut involvement. Similarly, the risk declines with time on a strict “gluten” free diet 5.
Current management of dermatitis herpetiformis is the same as that for people with coeliac disease – life-long adherence to a “gluten” free diet.
Wheat allergy, the third “gluten”-related disorder, is defined as an adverse type-2 helper T-cell immunologic reaction to wheat proteins and typically presents soon after wheat ingestion, with signs of anaphylaxis such as swelling or itching of the mouth, throat, and skin; nasal congestion; watery eyes; and difficulty breathing. Like all allergies, wheat allergy is more common in children, with reported prevalence between 2 - 9% in children and 0.5 - 3% in adults 6.
The reaction to wheat is mediated by T-cell activation in the gastrointestinal mucosa. In classic wheat allergy, it is the cross-linking of immunoglobulin (Ig)E by repeat sequences in “gluten” peptides (for example, serine-glutamine-glutamine -glutamine-(glutamine-)proline-proline-phenylalanine) that triggers the release of chemical mediators, such as histamine, from basophils and mast cells 1. Adverse reactions can also be non-IgE mediated, or a combination of both IgE and non-IgE 21;22.
Diagnosis is based on clinical history, skin prick test, specific IgE dosage, and oral challenge. A “gluten” free diet improves or eliminates symptoms. Non-IgE-mediated wheat allergy has a wide range of systemic or gastrointestinal symptoms and can be diagnosed by a double-blind placebo-controlled challenge. There are no biochemical or serologic markers and intestinal mucosa shows architectural normality except for an increased number of eosinophils. Pathogenic mechanisms are not known, and clinical response to a wheat free diet is essential to confirm diagnosis 1;22.
Different peptides of wheat than those involved in coeliac disease are implicated 22, but like people with coeliac disease, to be safe, all wheat products and ingredients should be avoided. Unlike people with coeliac disease, rye, barley and oats, and ingredients made from these grains, can be included in the diet of people with wheat allergy.
Non-coeliac gluten sensitivity
In addition to coeliac disease, dermatitis herpetiformis and wheat allergy, some people react to “gluten” in ways in which neither allergic nor autoimmune mechanisms are involved. These people are generally described as having non-coeliac gluten sensitivity 1. The prevalence of non-coeliac gluten sensitivity in Australia is unknown owing to the lack of validated biomarkers, but globally, it is thought to be more common than coeliac disease with an estimated 3-5% of the population affected 6;23.
The clinical symptoms of non-coeliac gluten sensitivity begin after the ingestion of “gluten” containing grains and grain products. Symptoms improve or disappear with withdrawal of these grains and grain products from the diet, and symptoms reappear after “gluten” challenge, usually within hours or days. The clinical gastrointestinal presentation of non-coeliac gluten sensitivity is characterized by abdominal pain, bloating, bowel irregularity (diarrhea, constipation, or both), while extra intestinal manifestations include “foggy brain,” which is described as slowed thinking, memory disturbance, or reduced level of alertness, along with headache, joint and muscle pain, fatigue, depression, leg or arm numbness, dermatitis (eczema or skin rash), and anaemia 6.
No specific biomarkers have yet been identified and validated for non-coeliac gluten sensitivity. Since similar symptoms also can be seen with coeliac disease and, to a lesser extent, with wheat allergy, these conditions need to be preliminarily excluded with serologic and histologic evidence to focus on the suspicion of non-coeliac gluten sensitivity. In a clinical setting, clinicians/dietitians may suggest a blinded gluten challenge during which a person is given approximately 8 g of gluten (corresponding to approximately 2 slices of bread) or placebo (e.g., 2 slices of gluten free bread) for 1 week each, separated by at least a 1-week “gluten”-free washout period. Symptoms should be monitored throughout the challenge using a diary 6.
The pathophysiology of non-coeliac gluten sensitivity remains largely undetermined. In addition to “gluten”, α-amylase/trypsin inhibitors in “gluten”-containing grains are hypothesised to play a key role. A recent study found that people with non-coeliac gluten sensitivity have a significant reduction in T-regulatory cell markers compared with controls and people with coeliac disease, and an increase in the α and β classes of intraepithelial lymphocytes, with no increase in adaptive immunity related gut mucosal gene expression. These findings suggest an important role of the intestinal innate immune system in the pathogenesis of non-coeliac gluten sensitivity without an adaptive immune response. This hypothesis is also supported by the lack of villous enteropathy in non-coeliac gluten sensitivity, a feature detected in coeliac disease as a sign of HLA-driven adaptive immune response 6.
Like coeliac disease, the current recommendation for non-coeliac gluten sensitivity is adherence to a “gluten” free diet 6.
Gluten Free meals
Eating plays an integral role in everyday life for most people. In fact, it is considered to be the most social of human activities. Food helps form individual, group, religious, ethnic and national identities and serves numerous physical, emotional and communicative functions, besides providing adequate nutrition 18.
In the United Kingdom, 68% of people with coeliac disease state that the “gluten” free diet reduces their enjoyment of food, and 54% say they participate in enjoyable activities less often, particularly going out for a meal. In Canada, 60% of participants have difficulty finding “gluten” free foods, 48% avoid restaurants and 25% avoid travelling 18.
In most countries, high-quality “gluten” free products are available in supermarkets or in special health food stores and on the internet, but the cost of “gluten”-free food is significantly greater than the equivalent “gluten”-containing foods 5;18-20.
Established in 2017, The Gluten Free Meal Co has developed a delicious range of “gluten” free meals, desserts and party foods suitable for people with coeliac disease, dermatitis herpetiformis, wheat allergy or non-coeliac gluten sensitivity. They are affordable, and can be enjoyed at home, at parties, in the office or when travelling (if a microwave oven is available).
Coeliac Australia is a national federated not-for-profit body comprising five state organisations supporting people with coeliac disease, dermatitis herpetiformis and those medically diagnosed as requiring a “gluten” free diet.
Advice and information is given on the “gluten” free diet, ingredients and additives, where to buy food, recipes and cooking, eating out, overseas travel, educational material, as well as research information. Seminars, information sessions, cooking demonstrations, dinners, picnics etc, are also organised. A full-colour quarterly magazine produced by Coeliac Australia to provide the latest information including ingredients, foods available, upcoming events and recipes (with carbohydrate exchanges for those with diabetes).
Suite 1, 41-45 Pacific Highway,
Waitara, NSW, 2077
Coeliac Australia has a professional membership program for Australian Health Professionals in all States and Territories:
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