Wheat’s long shadow: does anyone escape its effects?
In part 1 we looked at Coeliac Disease (CD) which affects 1% of the population worldwide, but forms only the tip of the gluten iceberg. In part 2 we looked at the latest research on Non Coeliac Gluten Sensitivity (NCGS) which affects 6% of the population. In part 3 we look at ten areas of research that illustrate how gluten’s long shadow affects the lives of the remaining 93%.
This post includes some of the most up-to-date studies on the health effects of gluten and wheat outside of coeliac disease. Many of these were published just this year, yet you are unlikely to have heard about them on any other blog, let alone in the mass media.
Much of what has been learned about gluten’s effects at the cellular level comes from 20 years of intensive research into coeliac disease. To researchers surprise, many of those mechanisms appeared to be active in healthy individuals, leading to speculation that wheat could be involved in other diseases, beyond coeliac. In the last three years, with the recognition of the new clinical entity Non Coeliac Gluten Sensitivity, the wheat cat is well and truly out of the coeliac bag.
Alongside an understanding of gluten’s biochemical effects in non-coeliacs, reports are accumulating of the successful use of gluten-free diets in an extremely diverse range of conditions, showing that gluten’s long shadow extends well beyond gut diseases. This conclusion from a recent review paper summarising our current understanding of how just one gluten protein – gliadin – affects intestinal cells says it all:
In conclusion, gliadin (from gluten) and its undigested peptides have biological effects not only in cells and the intestinal mucosa of patients with celiac disease but also in normal subjects or in different diseases. How these effects can affect the health of non-celiac subjects will be the object of future research. – Maria Barone et al, International journal of molecular sciences (2014)
As this quote indicates, research into gluten’s health effects in non-coeliacs is currently in its infancy; Indeed it is considered to be at least twenty years behind that of coeliac disease. The purpose of this post is to bring together some of the early evidence demonstrating gluten’s involvement in an extraordinary range of disease processes.
Evidence in this post is drawn from
- Identified biochemical effects of gluten/wheat/grain components that have been shown to affect non coeliacs
- The bidirectional link between coeliac disease and a host of other diseases
- Controlled studies showing benefits of a gluten-free diet across a wide range of diseases
- Early studies into effects of wheat/gluten/grains on healthy individuals, and finally,
- Personal clinical experience – I have had many patients whose health problems have benefited from a grain-free diet when nothing else has worked
An important point to keep in mind as you read what follows is that for most people, the effects of grains do not necessarily manifest as a recognised gluten disorder, but nevertheless may be causing them problems that neither they nor their doctors would associate with the grains in their diet. The only way an individual will discover if they would be better off on a grain-free diet is by trialling it properly for at least six weeks, and preferably three months. The proof of the pudding will be in the (not) eating! If you are thinking ‘but I don’t have any health problems!’ please read post 1, in which I describe a study where relatives of coeliac patients were placed on a gluten-free diet and experienced improvements in symptoms that they had previously been unaware of. The only way to know if grains are adversely affecting your health is to strictly eliminate them from your diet for three months.
So lets get stuck in with a graphical overview of plausible mechanisms by which wheat may exert adverse health effect in non-coeliac conditions…
Fig 1. Components in wheat contributing to clinical symptoms among non coeliacs – Aziz et al. The spectrum of noncoeliac gluten sensitivity. Nat. Rev. Gastroenterol. Hepatol. (Jun 2015)
Don’t worry if that’s too much to make sense of right now – the key points to appreciate are: (i) it’s more than just the gluten in wheat that exert negative health effects, and (ii) these mechanisms are at work in healthy individuals, not just coeliacs.
Ten reasons to avoid wheat
1. No one can digest gluten
Gluten is a complex protein that gives dough its elasticity. It is made of many different protein molecules that are still being enumerated. They are classed into groups, known as gliadins, glutenins, albumins and globulins. Each fraction has its story to tell, but the gliadins are notable for their central role in coeliac disease.
Fig 2. Both gliadins and glutenins are now considered as triggers of coeliac disease. Albumins include the amylase trypsin inhibitors which have been shown to drive intestinal inflammation (see 3 below). The albumins and globulins are both linked to allergic reactions. Wheat globulins appear to be involved in the development of Type 1 diabetes.
Few people are aware that gluten is an intrinsically indigestible protein. Whilst most other proteins in the human diet are efficiently broken down into their constituent amino acids by our digestive system – a bit like how a shredding machine reduces paper to confetti, we simply do not have enzymes capable of cleaving the glutamine and prolein-rich sections of gluten. The partially digested residues of gluten are more like screwed up balls of paper – far too large to be properly absorbed. This exposes our small intestines to large undigested fragments known as gluten peptides. Unlike amino-acids, these have the capacity to set up an immune reaction, increase gut permeability and trigger cell proliferation.
Here is one well studied fragment, alpha-gliadin, that is responsible for many, but not all, of gluten’s toxic effects:
This inability of our digestive system to deal with gluten is a demonstration of evolutionary-medicine: we simply are not adapted to these ‘novel’ foods which have only been in the human diet in significant quantities for 5000 years – a mere blink of the eye in evolutionary terms.
2. Gliadin increases gut permeability in everyone
A key feature of coeliac disease is a ‘leaky gut’. Before autoimmunity can start, dietary antigens need to get through the gut lining and stimulate the immune system. This mechanism appears to be behind many, if not all, autoimmune diseases (such as type 1 diabetes [ref]). Gliadin (the chief immune reactive peptide fraction of gluten) is implicated in coeliac disease as it stimulates the enterocytes (gut lining cells) to release zonulin – a compound that opens the tight junctions between the enterocytes, allowing substances to bypass the gut lining – making it ‘leaky’. This allows the passage of incompletely digested proteins and gut bacteria into the blood, which can set up immune reactions. If there are similarities between these proteins and human tissue ‘cross reactivity’ can occur, leading the immune system to attack its own tissue, causing autoimmunity or even cancer.
The whole process is explained in the following rather technical paper, the title of which tells you most of what you need to know for this post: “Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer” Alessio Fasano, Physiological Reviews (January 2011)
Fig 4. Changes in permeability of intestinal biopsies following exposure to gliadin. The highest level of induced permeability (the lowest curve, orange) was amongst people with active coeliac disease (ACD), followed by gluten sensitive (GS). Gliadin even caused increased permeability in healthy controls (NC). Least affected were recovering coeliacs (RCD) as they were the only ones on a strict gluten-free diet!
In one of their most recently published paper, Fasano’s team show that gliadin increases gut permeability in active coeliacs, recovering coeliacs, NCGS as well as healthy controls – i.e. everyone!
Interestingly, the NCGS and active coeliacs showed the greatest reaction to gluten exposure, suggesting, perhaps, that increased gut permeability is the common factor in both conditions. Confusingly, this is in contraditction to earlier work that found reduced permeability in NCGS.
Even more surprising was the finding that recovering coeliacs had the lowest reaction to gliadin exposure – lower even than healthy controls. Why? Probably because they were the only group that had been on a strict long-term gluten-free diet.
This study provides clear evidence that everyone is affected by gluten, even if they have no symptoms, unless that is, they are on a strict gluten-free diet.
Another aspect of gluten’s effects was reported a 2011 study by Jana Cinova’s team, from the Department of Immunology at the Academy of Sciences of the Czech Republic. They found that gliadin leads to a reduction in the number of mucus producing goblet cells in the intestine wall, however, the effect was modified by the kinds of gut bacteria present.
Researchers exposed the digestive tract of mice to gliadin, with or without various gut bacteria. As you can see in the graph opposite, gliadin reduced the percentage of mucus producing goblet cells in the epithelium, from 55% to 35%.
However, in the presence of pro-biotic ‘good bacteria’ (Bifidobacterium bifidum) these harmful effects of gliadin on goblet cells were significantly reduced. Pathogenic gut bacteria such as Shigella and E. coli on the other hand, magnified the damage induced by gliadin (the two bars at the bottom of Fig 5.)
These data suggest that the health of an individual’s gut microbiome may determine how ‘toxic’ wheat is for them, and go some way to explaining the apparent increase in gluten-related disorders over the last thirty years, coinciding as it has with an increased use of antibiotics, caesarian births, and reduced contact with soil organisms in modern living – all of which contribute to gut dysbiosis (i.e. disordered gut microbes). There is also the possibility that for otherwise healthy individuals, a change in their gut flora due to infection, antibiotics or diet could precipitate gluten sensitivity.
Other ways in which gliadin affects intestinal cells of coeliacs and non-coeliacs alike, include:
- Changes to the shape and structure of enterocytes and fibroblasts
- Changes in permeability
- Changes in the movement and structure of dendritic cells
- Deregulation of NF-κB-related gene expression
- Increasing inflammatory markers such as IL-15
“In the general issue of food and tissue inflammation, gliadin and its undigested peptides plays a leading role.” – Maria Barone et al, International journal of molecular sciences (2014)
3. Wheat amylase trypsin inhibitors drive intestinal inflammation
Apart from gliadin, wheat proteins contain albumins, one subset of which includes the amylase trypsin inhibitors. These proteins – part of wheat’s natural pesticide armoury – had previously only been linked to wheat allergies like baker’s asthma and exercise induced wheat anaphylaxis, affecting approximately 0.2% of the population (a mere 14 million people worldwide!) However, in 2012 Detlef Schuppan’s group published evidence that amylase trypsin inhibitors in wheat can drive intestinal inflammation via the innate immune system, activating monocytes, macrophages and dendritic cells. This contrasts with coeliac disease where it is primarily the adaptive immune system that causes the inflammatory damage.
Consequently, wheat amylase trypsin inhibitors are now suspected of fueling inflammation and immune reactions in several intestinal and non-intestinal immune disorders, in coeliacs and non-coeliacs:
“ATIs represent up to 4% of total wheat protein and are highly resistant to intestinal [digestion]. In line with their dose-dependent function as co-stimulatory molecules in adaptive immunity of celiac disease, they appear to play a role in promoting other immune-mediated diseases within and outside the GI tract. Thus, ATIs may be prime candidates of severe forms of non-celiac gluten (wheat) sensitivity.” – Schuppan & Zevallos, Digestive diseases (2015)
4. Fructans in wheat can cause bloating, intestinal discomfort and diarrhoea
Fructans are oligosaccharides – chains of sugar molecules resistant to digestion, found in high levels in wheat, barley and rye. When these simple carbohydrates reach the colon they can be rapidly fermented by bacteria. As well as pain from the gas that is produced these molecules have an osmotic effect pulling water into the bowel causing diarrhoea. A study in Gastroenterology in 2013 found that 37 IBS patients placed on a diet low in these poorly digested carbohydrates (FODMAPs) improved markedly and did not relapse when purified gluten was added to their diets.
An initial interpretation of these results was that NCGS might not be caused by gluten but by FODMAPS. Studies since, however, have shown that gluten is a factor in many cases of NCGS [ref]. Furthermore, many of the participants in the 2013 study reverted to a gluten-free diet even when the results were explained to them, suggesting that avoiding gluten-containing foods had an even better effect on their symptoms than simply avoiding fructans. A further point to consider before dismissing a specific problem with grains is that fructans are high in onions and other vegetables, yet most NCGS sufferers find their symptoms improve on a gluten-free diet without avoiding these other sources of FODMAPs.
Either way, the fructans in wheat are yet another reason to give it second thoughts, especially if you suffer gastro-intestinal symptoms like bloating, IBS, constipation or diarrhoea.
5. Modern wheat is more allergenic
Cardiologist William Davis in his book Wheat Belly posited, somewhat controversially, that modern wheat has become more toxic due to intensive breeding. Initially scoffed at, this concept is now taken seriously by some researchers who have put the hypothesis to the test. The first randomised controlled trial comparing ancient vs modern wheat in patients with irritable bowel syndrome (IBS) found that symptoms were significantly worse when on modern wheat (read our report here).
More recently a detailed and comprehensive study has been undertaken of the effects of ancient and modern wheat strains on immune cell (cytokine) reactivity in NCGS compared to healthy controls. Key results are summarised in Fig 6.
Fig 6. CXCL10 secretion by cultured PBMC stimulated with different wheat protein extracts. PBMC obtained from healthy donors (A) or from NCGS patients (B) were stimulated for 24 h with total wheat protein extracts from different wheat cultivars. After Valerii , June 2015
As you can see, compared to rice, all wheat strains caused raised cytokine responses in both healthy and NCGS, but the response was far greater in the NCGS group, and stronger for modern, compared to ancient strains. Whilst this may go someway to explaining the increased incidence of NCGS and coeliac in recent years, it would be a mistake to think that gluten problems will be resolved by switching to ancient wheat varieties as the response may be reduced, but not eliminated. In the case of coeliac disease, ancient and modern varieties have been shown to be just as damaging. [ref]
“Our findings provide further evidence for the need for a strict gluten-free diet in coeliac patients, including avoidance of ancient strains of wheat.”
– Šuligoj T et al, Clinical nutrition (2013)
Rice, which was used as a control in the above study, is one of the least reactive and least problematic grains. For people struggling to adapt to a grain-free diet, rice in moderation can often be safely consumed. That said, I have had patients – especially those with severe gastrointestinal symptoms such as ulcerative colitis and Crohn’s that cannot even tolerate rice. Another problem with eating large quantities of rice is that it is often high in arsenic, and has actually led to poisoning in at least one case of coeliac disease. [ref] Issues around the grains that are typically used in gluten-free foods will be the subject of another post, but suffice it to say, I recommend a fully grain-free paleo type diet for maximum health benefits.
6 Modern wheat is less nutritious
Whilst becoming more antigenic in the last half century, wheat has simultaneously become depleted of minerals. The graphs above show wheat yields and mineral content between 1880 and 2000. With the development of dwarf wheat varieties and artificial fertilisers in the 1950’s, yields doubled (top two graphs), however, starting from the same time, we see levels of zinc and copper in wheat decline by half whilst iron and magnesium fall by 25%. (graphs c to f)
7. Phytates in grains reduce absorption of essential minerals
Fig 7. Increase in iron absorption when phytic acid is removed from the grain
Soy, maize and many other seeds, nuts and grains, but especially wheat contain phytate – also known as phytic acid – a recognised anti-nutrient. Phytic acid is a phosphorous storage compound found in seeds, primarily in the bran; hence levels are higher in whole wheat rather than than white flour products.
Phytate binds to iron, zinc, calcium and magnesium in the digestive tract making these minerals far less available for absorption. Indeed phytate can bind minerals from other foods eaten concurrently, potentially leading to mineral deficiencies. Figure 7 shows the increase in iron absorption when phytic acid is removed from various grains. As usual wheat is the worst offender.
In countries with a high dependence on grains, especially where grain based porridges are used through the critical period of child weaning, dietary phytates cause widespread mineral deficiencies – a direct indication of their suboptimal nutritional quality.
“Even though iron and zinc are present in significant amounts in the plant-based diets typically consumed in developing countries, their bioavailability is low due to high levels of absorption inhibitors such as phytate. “- Troesch B et al. Food Nutr Bull. (Jun 2013)
However, even in Europe, mineral deficiencies are prevalent amongst weaning children with one study finding that across 11 European countries the prevalence of iron deficiency at 12 months was 7.2% [ref]. A Danish study [ref] found that iron status from 6 to 9 months was:
- Positively associated with meat and fish intake
- Negatively associated with cows milk and bread intake
Finally, reductions in calcium absorption may be an important contributing factor in the development of osteoporosis in postmenopausal women. In Japan, the chief source of phytate in this age group is soy. A study published in January 2015 in the International Journal of Molecular Sciences investigated the role of phytate in age related osteoporosis, using phytate-removed soy which prevented osteoporosis in a rat model. [ref]
Whilst phytate can have positive effects on gut microbiota similar benefits can be maintained by increasing vegetable consumption – a far better fibre source with fewer down sides than grains can provide.
8. Lectins in wheat germ inhibits gut cell repair
Lectins are a class of protein present in many foods, some of which are toxic to humans. They are found in particularly high levels in black beans, soybeans, kidney beans, and whole grains [ref]. Wheat contains a lectin called wheat-germ agglutinin (WGA), which is present in whole wheat or whole meal products. Whilst most people know that if you do not cook kidney beans thoroughly you can expect to get severe gastrointestinal pain, most people are unaware of any such requirement for wheat germ. One reason for this is that WGA’s effects are far more subtle, so sprinkling wheat germ on one’s muesli is unlikely to produce the extreme reaction associated with raw kidney beans.
The second reason is that most wheat products commonly consumed have been cooked, deactivating most of the WGA. Because of this some authors claim that WGA represents a negligible risks, but there are reasons to question this assumption, not least of which is that many people have antibodies to WGA. This would not be possible if dietary WGA was 100% destroyed by cooking. Furthermore, the world experts on non coeliac gluten sensitivity do not rule it out as shown in figure 1.
So what does this wheat lectin do? WGA binds to the surface of a range of cells in the digestive tract. In fact it is one of the most potent lectins in this respect: “Compared to other plant lectins, WGA binds to intestinal cell lines of human origin, human colonocytes, and prostate cancer cells at the highest rate” [ref]. Studies in the last 30 years have shown that its ingestion causes increased permeability and changes to the structure of villi in the gut lining [ref]. Prior to the identification of gliadin as the causative factor in coeliac disease WGA was considered a potential candidate.
Whilst WGA might not be the primary cause of coelaic disease it is most certainly not out of the frame of gluten-related damage. In 2007, an elegant study showed that WGA has a direct effect on the cellular repair mechanism of gut lining cells, reducing protective mucous production, and increasing cell death. [ref] This finding has implications for all of us, whether we are coeliac, NCGS or not. Furthermore, although only ~0.1% of WGA gets through the intestinal barrier, it has been shown that even at nano-molar concentrations it is inflammatory:
“At nanomolar concentrations WGA stimulates the synthesis of pro-inflammatory cytokines and thus the biological activity of WGA should be reconsidered by taking into account the effects of WGA on the immune system at the gastrointestinal interface. These results shed new light onto the molecular mechanisms underlying the onset of gastrointestinal disorders observed in vivo upon dietary intake of wheat-based foods.” – Chiara Dalla Pellegrina et al. Toxicology and applied pharmacology (2009)
9. IgE reactions to cereal grains
IgE reactions are associated with allergic asthma, sinusitis, allergic rhinitis, food allergies, some chronic urticaria and atopic dermatitis (eczema).
Allergic reactions to wheat have been known about for many years, and in adults include Baker’s asthma, exercise induced wheat allergy and wheat anaphylaxis (as serious as peanut allergy). These affect a relatively small, though not insignificant, number of people (0.2%). However, among infants and children the prevalence is between 0.4% and 1%. Symptoms can range from immediate type anaphylaxis, urticaria, vomiting or wheezing or worsening of eczema after ingestion of wheat-containing products. Most children outgrow the disease by school age, or in their teens.
Just this month a study comparing IgE responses in allergic and non-allergic children found that both groups formed IgE antibodies to multiple components of ingested wheat [ref].
Varjonen E et al published a paper in Clinical and Experimental Allergy in 1995, in which they report administering skin prick allergy tests to 34 children with severe atopic dermatitis. 33 were positive for wheat, 18 reacted to oats and 16 to rice, maize, millet and buckwheat. Further, they found that gliadin only produced skin prick reactions in those children that also had a reaction to oral gluten challenge. This shows that there are IgE cereal allergens beyond gluten and the gluten containing grains. (We will look at the problems with grains other than wheat in a future post)
Many people are allergic to grass pollen – evident as hayfever in the summer. Should we be surprised that they are also allergic to the grasses (cereal grains) that they eat?
10. Gluten in diverse diseases
Fig 8. Increased incidence of various diseases and coeliac disease. (compiled from Luddvigson, 2006,2007, 2011 and Olen 2008)
Coeliac’s are at an increased risk of many other diseases subsequently, and conversely, many of those diseases, when diagnosed first, indicate a higher risk of developing coeliac disease after.
A good example of this is tuberculosis (TB), where coeliacs have a threefold higher risk of contracting TB and six times the risk of death from TB. Conversely, those who have previously had TB are at a 2.5 times risk of subsequently being diagnosed with coeliac disease. [ref]
This bi-directional relationship suggests that gluten containing grains may contribute to the initiation of a wide range of diseases possibly even in those who do not go on to develop coeliac.
One example is iron deficiency anemia which was found to be present in approximately half of undiagnosed coeliacs identified by screening. Conversely studies screening patients suffereing with iron deficiency anemia consistently find 5-6% have celiac disease. [ref] Some of these bidirectional risks are summarised in the Fig 8. (click to enlarge)
Research in this potentially vast field is currently in its infancy, but already some findings are coming to light:
- IgA nephropathy (IgAN) – in a paper published in March this year, gluten was found to accelerate IgA nephropathy in a rodent model, and a gluten free diet prevented disease progression. The authors state: “Our results indicate that an early treatment with gluten-free diet in patients with sera positive for IgA AGA [Anti gliadin antibodies] and without renal function decline may represent a safe and simple approach for the prevention of IgAN progression.”[ref]
- Schizophrenia, bipolar and ASD – there is a marked increase in gluten and casein antibodies in sufferers of these conditions. Whether these have a causative or subsequent relationship is not known, but in some studies a gluten-free diet has had dramatic effects with partial or complete reversal of neurological symptoms (see below). Also: see our post Gluten and Schizophrenia – does it all start in the womb?
- Type 1 diabetes – there is a clear link between type 1 diabetes (T1D) and coeliac disease. Where both occur it is usual for T1D to be diagnosed first – “probably due to the diabetes-protective effect of a gluten-free diet”. However, gluten-induced inflammation has been identified in T1D individuals without the genetic risk for coeliac disease, suggesting “a direct, diabetes-specific effect of gluten.”
Current studies suggest “that gluten, and perhaps other wheat proteins, influence the development of type 1 diabetes.”[ref] Indeed, the two animal models for studying type 1 diabetes, (the non-obese-diabetic (NOD) mouse and the diabetes-prone BioBreeding (BBdp) rat) spontaneously develop the disease on a normal wheat based diet, but have a lower incidence and the disease takes longer to manifest, when fed a gluten-free diet. One research team stated: “In studies of [these] rats… wheat gluten was the most potent diabetes-inducing protein source.” [ref] Indeed, they went on to identify a wheat globulin with an amino acid sequence identical to a protein in pancreatic islet cells, and identified pancreatic auto-antibodies for that wheat protein in type 1 diabetics, but not in healthy controls.
- IgA deficiency – is the commonest human immunodeficiency, is 10–15 times more common in patients with coeliac disease with a prevalence that may reach 3% [ref]
Interestingly, gluten’s role in IgA nephropathy and schizophrenia both involved alterations in immune complex formation (part of the antigen-antibody system). In the case of schizopheria, this occurs in-utero whilst the baby is developing, in the case of IgA nephropathy it appears to happen early in the development of the disease. In both cases the implication is that initiation of a gluten-free diet would be better earlier. At present there is no way of identifying who would benefit from early gluten withdrawal, and in most cases once symptoms appear significant damage has already been done.
Fortunately, as gluten-free foods, recipes and internet support-sites have increased many more people are trying gluten free diets for themselves. And despite skepticism from some authors who see the popular faddy side of the diet’s rise, many researchers now acknowledge the very real benefits for some patients:
“A lot of people spontaneously adopt a gluten free diet, solving their intestinal and extra-intestinal symptoms such as diarrhea, abdominal discomfort or pain, bloating, flatulence and headache, lethargy, attention-deficit/hyperactivity disorder, ataxia or recurrent oral ulceration.” – Veronica Bonciolini, University of Florence, (2015)
Now research beyond the coeliac population is under way, gluten-free diets are being found to benefit patients with many conditions. Examples of improvement or remission in humans (as opposed to animal models) include:
Inflammatory bowel disease (IBD) – not to be confused with IBS – includes ulcerative colitis and Crohn’s disease – both severe chronic autoimmune diseases of the small and large bowel. The prevalence of IBD in Europe is approximately 0.8% (6 million people) and increasing over time [ref]. In a paper published last year, a survey of 1647 IBD patients found that nearly a fifth had tried a gluten-free diet, two thirds of whom experienced improvement in symptoms. The improvements in symptoms they reported are shown in Fig 9. [ref]
Fig 9. Reported improvement in symptoms among IBD sufferers during self imposed gluten-free diet.
Gluten and the skin
Fig 10. Dermatitis herpetiformis is a gluten-induced autoimmune skin disease, often referred to as coeliac of the skin.
Almost everyone has heard of coeliac disease, and an increasing number have heard of non coeliac gluten sensitivity, but much less well known, is dermatitis herpetiformis, an autoimmune skin condition induced by gluten for which the only treatment is life-long adherence to a gluten-free diet. It is often referred to as ‘coeliac of the skin’. [Fig 10]
Interestingly, patients with dermatitis herpetiformis who have been on long term gluten-free diets to resolve their symptoms are found to have decreased incidents of heart disease [ref] and overall mortality [ref, ref] compared to healthy (gluten consuming) controls. This is despite the increased incidence of cancers and type 1 diabetes similar to that observed in coeliac disease.
I can see a couple of possible explanations for this. (i) that the genes that predispose an individual to dermatitis herpetiformis also confer some positive health benefit (ii) that gluten-free diets are healthier overall, reducing heart disease and all cause mortality in everyone.
I think hypothesis (i) is unlikely as the genetic risk factors for coeliac and dermatitis herpetiformis have been well studied, and no such benefit has been reported to my knowledge. Hypothesis (ii) is more likely to my mind, but would be undocumented for different reasons. To identify the benefits of gluten-free diets you would need a large enough population of otherwise healthy people on a long-term gluten-free diet. No such population exists. We are left then with the question of why this reduced mortality is not seen in coeliac patients – and I would suggest this is because coeliac disease, being of the gut rather than the skin, has life-long effects on digestion. i.e. in coeliac the long term harm masks the added benefits of a gluten-free diet.
Cutaneous Gluten Sensitivity – a new clinical entity
A paper from The University of Florence, published last month in the prestigious journal Nutrients, has begun to outline a new clinical entity they are calling cutaneous gluten sensitivity (CGS). They examined the skin lesions of 17 diagnosed non-coeliac gluten sensitive patients before and after the adoption of a gluten free diet. Initially their rashes were severely itchy, similar to psoriasis, eczema or dermatitis herpetiformis. Most of them had suffered with these symptoms for many years. Once they adopted a gluten-free diet the skin lesions resolved or significantly improved in a month or so.
In their conclusion the authors suggest that anyone presenting with gastrointestinal disorders and a severe skin itch should “adopt a gluten-free diet for at least three months assessing any positive effects.”
As a herbalist, this is no surprise to me, as part of the herbalist perspective has always been that the gut and skin are a clinical continuum, and when treating skin conditions I always look to treat any underlying gut pathology.
Neurological and psychotic disorders
Fig 11. An example of gluten ataxia, a condition in which coordination and movement become increasingly disrupted. It is shocking that such a condition can be caused and maintained by such a common food as wheat.
Whilst neurological symptoms have always been part of the picture of coeliac disease, it was only in 1996 that researchers identified gluten as a causative factor in a majority of sporadic ataxias – a condition in which coordination and movement become increasingly impaired. [Fig 11]
Marios Hadjivassiliou, a consultant gastro-enterologist at The Royal Hallamshire Hospital, Sheffield, UK, discovered and named gluten ataxia. His team found gluten to be the single biggest cause of sporadic idiopathic ataxia.
In his 2003 paper in the BMJ, he describes how these patients were significantly more likely to test positive for antigliadin antibodies (AGA) than patients whose ataxia could be explained by other causes such as brain injury or stroke. Unlike coeliac disease, gluten ataxia patients rarely exhibit gastrointestinal symptoms. The main treatment is a life long gluten-free diet. Recovery depends on how far the disease has progressed. It appears that the anti-gliadin antibodies cross-react with Purkinje cells in the brain – if the damage has gone too far it cannot be fully reversed.
Other neurological conditions
In the following video Professor Alessio Fassano discusses the possible link between gluten and schizophrenia and autism – just two aspects of gluten-related neurological conditions
Whilst Coeliac disease and Non Coeliac Gluten Sensitivity are widely recognised as including a range of neurological symptoms from depression to gluten ataxia and encephalopathies [ref], there is increasing evidence that gluten’s effects on the brain extend beyond these two groups. Whilst the link between gluten and psychosis remains controversial there is increasing evidence that a sub-set of patients are indeed gluten sensitive and benefit from a gluten-free diet. Some recent papers investigating gluten-related psychoses are illuminating:
The papers above are mostly looking at a gluten-free diet after psychotic symptoms have already manifested. However, if gluten is responsible for the development of these diseases then a gluten-free diet before symptom manifestation would be infinitely preferable!
The early detection of cases of gluten sensitivity with neurological manifestations and subsequent treatment with the gluten-free diet could provide remarkable benefits to the patients. – Hernandez-Lahoz C et al. Rev Neurol. (Sep 2011)
In some cases this early intervention may extend back to the diet of the mother. (See our article Gluten and Schizophrenia – does it all start in the womb?)
So there you have it: You don’t have to be coeliac or even diagnosed with non coeliac gluten sensitivity for wheat to have a negative impact on your health. Although our understanding of how gluten affects health outside coeliac disease is still in its infancy, an increasing number of conditions are being linked to its consumption. Furthermore, the list of conditions that respond to a gluten-free diet is growing.
If you want to find out if a gluten-free diet can improve your health the only way is to do it properly. That means at least six weeks, and prefereably three months, being 100% scrupulous. During that time instead of switching to ‘gluten-free’ substitute foods (bread, biscuits, cakes etc), try a paleo diet based around real foods that are naturally gluten free – fish, meat, vegetables, nuts and fruit. You can include dairy if you tolerate it well. There are plenty of recipes on this blog to help you make the change. If you need further support get in touch or come to one of my public talks. If you wish to see me as a patient I will provide on-going support and a personalised diet, supplements and herbal medication as indicated in your particular case,
Then let me know how you are getting on!