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marylin monroe
Showing posts with label celiac. Show all posts
Showing posts with label celiac. Show all posts

Gluten Free, But not Suitable For Celiacs: Milk, Chocolate, Corn, Instant Coffee and 20 Other Foods & Food Ingredients That Could Cross-React With Gluten Anti-Bodies

Unless you got the right, i.e. breast milk as a baby and have rendered your gut "gluten proof" - being breast fed, when you are first exposed (or being exposed later in life) has after all been suggested as a protective factor (Farrell. 2005)
This is not going to be a long post; and still, at least for some of you it is going to be an important post. A post that may have the potential to change your life for the better or for the worse depending on whether you actually suffer from gluten-intolerance or have simply been bamboozeled by the "gluten is the devil" messages that are plastered all over the Internet these days.

Actually, I would hope that you belong to neither of the groups and can thus simply ignore this post. For the unfortunate rest, I have prepared a mini-summary of the results of a recent study from the Immunosciences Lab in Los Angeles (Vojdani. 2013)

Milk and cornflakes - a killer combo

A couple of recent studies, as well as reports from patients all of which clearly suggested that "being gluten free" does not equal "being symptom free" had spiked the researchers interest. Was it possible that the persistent symptoms were brought about by cross-reactions between the anti-bodies that would usually attach to the gluten proteins to trigger an immune reaction and other molecules? Molecules from such innocent foods, as dairy, chocolate, and even coffee!?
Suggested read: "Leaky Gut & Gluten Belly: Bacterial Firebugs Translocate from Your Gut to Your Ever-Growing Visceral Fat Depots" | read more
"[W]hen histological response was assessed in celiac patients after 6 months of following a GFD [gluten free diet], complete normalization and reconstruction of villous architecture was observed only in 8% of individuals, while 65% of these patients were in remission and 27% did not respond to GFD and had no observable change in their clinical symptoms (Lanzini. 2009).

The lack of improvement in histopathology and clinical symptomatology in a subgroup of patients on a GFD may be associated with dietary non-ad-herence or cross-reactive epitopes triggering a state of heightened immunological reactivity in gluten-sensitive individuals (Hadjivassiliou. 1997)." (Vojdani. 2013)
The hypothesis certainly isn't totally odd. Kristjansson et al. were for example able to show that 50% of their celiac patients experienced a significant mucosal inflammatory response similar to that elicited by gluten, when they were exposed to cow’s milk protein. Of the 15 healthy controls in their study, however, not a single one showed the slightest signs of auto-immune related inflammatory processes (Kristjansson. 2007).

So is this "real" celiac disease?

It should be obvious though that the corresponding "cross reactive" agents do not induce celiac disease (which is per definition an auto-immune disease that's triggered by the reaction to gliadin). They are however well able to alter the intestinal barrier integrity - a symptom that is also one of the key feature of the early stages of celiac disease.
Figure 1: Reaction of affinity-purified α-gliadin 33-mer polyclonal antibodies to gliadin and different food antigens; data in large figure relative to control, data in small inset relative to a-gliadin (Vodjdan. 2013)
If full remission of celiac disease cannot be achieved even on gluten-free diet, the underlying reason may thus well be the presence of peptides and antigens that (cross-)react with the same anti-bodies the body of celiac patients produces against the α-gliadin 33-mer peptide aka gliadin. Scientists even speculate that the co-exposition to these agents could eventually lead to the establishment of "new" auto-immune diseases and food allergies and some argue that the ever-increasing spectrum of allergies is partly a result of untreated autoimmune reactions which are then "spreading" to other previously well-tolerated foods and food ingredients.

Suggested read: "Beyond Celiac: Study Sheds New Light on Obesogenic Effects of Gluten - Are PPARs & Bacteria Both Involved?" | read more
The problem seems real, if you're really gluten intolerant: With milk, all sorts of dairy products (including whey), instant coffee (but not espresso; see small inset), avenin containing oat products (unfortunately, I cannot tell you how you can recognize the "unproblematic" oats at the super market, but if you google "avenin-free oats" you will see a couple of products and stories pop up; Comino. 2011) and corn having a significant potential for cross-reactivity, it appears almost reasonable that some people come back from their visit with a mostly self-proclaimed expert in all things celiac with an endless list of items they are not supposed to eat and a tiny 5-item list of foods they are supposed to live on for the rest of their lives.

What is not reasonable, however, is that this is the case for more and more people who are basically asymptomatic... well, aside from their "inability to lose weight" that is obviously not related to their "inability to exercise" and their "inability to stop watching TV and browsing the Internet for easy quick-fix solutions to obesity problems", but most obviously be brought about by gluten intolerance ;-(

References:
  • Comino I, Real A, de Lorenzo L, Cornell H, López-Casado MÁ, Barro F, Lorite P, Torres MI, Cebolla A, Sousa C. Diversity in oat potential immunogenicity: basis for the selection of oat varieties with no toxicity in coeliac disease. Gut. 2011 Jul;60(7):915-22.
  • Hadjivassiliou M, Chattopadhyay AK, Davies-Jones GA, Gibson A, Grünewald RA, Lobo AJ. Neuromuscular disorder as a presenting feature of coeliac disease. J Neurol Neurosurg Psychiatry. 1997 Dec;63(6):770-5.
  • Kristjánsson G, Venge P, Hällgren R. Mucosal reactivity to cow's milk protein in coeliac disease. Clin Exp Immunol. 2007 Mar;147(3):449-55.
  • Lanzini A, Lanzarotto F, Villanacci V, Mora A, Bertolazzi S, Turini D, Carella G, Malagoli A, Ferrante G, Cesana BM, Ricci C. Complete recovery of intestinal mucosa occurs very rarely in adult coeliac patients despite adherence to gluten-free diet. Aliment Pharmacol Ther. 2009 Jun 15;29(12):1299-308. 
  • Vojdani A, Tarash I. Cross-reaction between gliadin and different food and tissue antigens. Food and Nutrition. 2013; 4:20-32.

Study Says: Wheat Belly is All in Australians' Head. And in Fact, the Peer-Reviewed Scientific Evidence for Non-Celiac Gluten-Sensitivity is Scarce, But Probably Not Non-Existent

From a paper in the Journal of Cereal Science: Histological structure of wheat grain showing bioactive components which are related to the fiber fraction of wheat and are present in whole meal but absent in refined flour. (Brouns. 2013).
A recent study from the CSIRO Food Futures National Research Flagship and the University of Adelaide says: The data indicate that many adult Australians are consciously avoiding consumption of wheat foods, predominantly without any formal diagnosis. Reported symptoms suggest a physiological but not allergenic basis to this behavior.

Can this be? Can your "gluten intolerance" really be in your head? Certainly it can, it's what scientists call a nocebo effect: A situation, where a harmless substance taken by a patient is associated with harmful effects due to negative expectations or the psychological condition of the patient.

But wheat is no harmless substance, right?

Certainly not. At least not for those people who suffer from celiac disease. As far as the ever-spreading gluten-intolerance is concerned, though, more and more scientists voice concerns over the ever-increasing number of self-diagnosed gluten-intolerant individuals strike one food item after the other from their already short list of "gluten kosher" foods.
Social influences on Australian "wheat avoiders" (Golley. 2014)
Surprisingly, it's not the Internet that makes people go gluten-free. That's at least what the "wheat avoiders" in Sinead Golley's study claim. For them individuals in their surrounding had a much greater impact on their decision to go gluten free. It's their naturopath, their alternative medicine practicioner, friends, family and, surprisingly, even the doctor. And that in spite of the fact real illnesses (from asthma to IBS) were rare among the "wheat avoiders". Non-wheat food intolerances and allergies, on the other hand, were significantly more prevalent among the wheat avoiders than among their wheat eating (generally healthies) peers.
In an enlightening paper with the telling title "But we're not hypochondriacs: The changing shape of gluten-free dieting and the contested illness experience" in Social Science & Medicine, Lauren Renée Moore wrote only a couple of months ago:
"[T]his research suggests that self-ascriptive looping results in a greatly expanded illness prototype, and that gluten-free individuals promote a broadened illness prototype and self-diagnosis to their friends and families. Some work to promote the diet further. As a result, self-ascriptive looping can function as one vector in the diet's growing popularity." (Moore. 2014).
The so-called looping effect describes how categories are continually redefined as the people within them change. The group of "gluten intolerant" individuals, once only celiacs, has thus over time transformed into an amalgam with celiac patients on the one end and real hypochondriacs on the other end of the extreme. And they all have one thing in common. For each of them, his or hear gluten intolerance is absolutely real.

In view of the way this illness prototype or rather its contemporary realization is constantly changing it's no wonder that it has lost all resemblance to what doctors call "gluten intolerance". The logical consequence: Patients feel misunderstood and blame their "doctors for their failure to correctly diagnose the problem." (Moore. 2014)

The illness is real, and so are the risks

In the end, it's thus not a question of who's wrong and who's right. For the "patients" who have now become their own doctors their illness is absolutely real. The previously asked question, whether wheat is a harmless substance or not is thus no longer practically relevant for them and they are willing to pay the price - literally that is by paying significantly more money for (oftentimes) nutritiously inferior foods from the "gluten-free" industry (Hallert. 1998; Long. 2010).
Figure 1: 0.548% of the US citizens are "gluten-free" spec. middle-aged + older women are jumping aboard - for what? Well the only potentially health-relevant differences between wheat eaters and non-wheat eaters are lower TSH (thyroid gaspadel) and higher HDL values - and no one knows if those weren't present before going gluten-free (DiGiacomo. 2013)
Money is yet not the only concern researchers have with the increased trend towards gluten-free "elimination diets". Many of them warn that this trend entails a significant risk for the self-diagnosed gluten intolerant individual, who may not just be risking his health by consuming unnecessarily restrictive diets with potentially serious dietary imbalances, but could also be overlooking a much more serious health issue that's the actual cause of their symptoms (Monsbakken. 2006; Teufel. 2007) - or as Golley apptly puts it: The most serious risk is the delay in diagnosis and treatment of potentially serious underlying medical condition, due to self-diagnosis of symptoms as due to a food intolerance.

What about the physiological side?

As the previous remarks have shown, there is little doubt that the contemporary trend towards "gluten-free" diets is a socio-psychological phenomonen that's not (yet?) rooted in conclusive scientific evidence that would point towards general detrimental effects of wheat consumption on non-celiac human beings (Brouns. 2013).
Table 1: Trends in publication on celiac disease (CD) and non-celiac gluten sensitivity (NCGS) during the last decades (Catassi. 2013). It's not as if researchers were not interested in non-celiac-gluten-sensitivity (NCGS).
And still, there is a significant difference between the absence of conclusive evidence and the claim that "no data justifies a negative opinion about whole-wheat products in a healthy population" you will find in Brouns', Buuls' & Shewry's unquestionable not exactly impartial review of the literature in the Journal of Cereal Science (Brouns. 2013). If you look closely and without the wheat-colored glasses the National Association of Wheat Growers may have sponsored, you will find a handful of studies which do suggest that the consumption of high amounts of wheat and gluten has general detrimental effects on our health:
  • Wheat amylase trypsin inhibitors may drive intestinal inflammation via activation of toll-like receptor 4 -- Yvonne Junker et al. report in a 2012 paper that the natural α-amylase/trypsin inhibitors in wheat "may fuel inflammation and immune reactions in other intestinal and non-intestinal immune disorders." (Junker. 2012).
  • Auto-immune reactions could be triggered without the expression of T-cell specific antigens -- Using recent evidence from celiac patients as an example, Ludvig M. Sollid & Bana Jabri argue that the constant exposure to certain immuno-modulating substances such as gluten, could be exogenous factors which "might be identified as drivers of autoimmune processes, in particular when evidence for T cells with specificity for self antigens driving the disease is lacking." (Sollid. 2013)
  • Low-fermentable, poorly-absorbed, short-chain carbohydrates could contribute to symptoms (at least those related to IBS) experienced by non-celiac-gluten-sensitivity patients -- With the low-fermentable, poorly-absorbed, short-chain carbohydrates, i.e. fermentable oligo-, di-, and mono-saccharides and polyols, aka FODMAPs an international group of scientists suspects another of the blogosphere's usual suspects may be to blame.

    Figure 2: A low FODMAP diet will progressively reduce the symptoms of NCGS (Biesiekierski. 2013)
    The data from a 7-day low FODMAP study does actually appear to support a relevant interaction of FODMAPs and gluten sensitivity (Biesiekierski. 2013).

    The results do yet require experimental verification and further research should try to reveal the underlying mechanism which could explain the reduction in gluten sensitivity in response to the low FODMAP diet, will yet have to be elucidated - an involvement of the gut microbiome, by the way, is not impossible.
The interaction with non-fermentable short-chain carbohydrates and the influence of the gut microbiome are also two key points in Aziz' and Sanders' recent editorial "Patients Who Avoid Wheat and Gluten: Is That Health or Lifestyle?", in which they emphasize the role of excessive fermentation from small intestinal bacterial overgrowth in the etiology of what many people think was "gluten intolerance". Whether "SIBO" (small intestinal bacterial overgrowth) and "gluten intolerance" are co-incidental or whether one is actually responsible for the other will yet have to be determined in future studies. Studies of which the data in Table 1 suggests that they will be done, as the relative research interest in non-celiac gluten sensitivity is continuously growing.
Bottom line: In the end, it may not even be important if non-celiac gluten sensitivity is a real or a social-psychological epidemic. If you are "infected" and avoiding gluten-containing foods and or non-fermentable short-chain carbohydrates helps you, do it! As long as you keep an eye on your micronutrient intake and don't live off ready-made processed gluten-free junk, it's probably not going to harm you - physiologically that is.
It's not always easy to be "gluten-free", even for animals (Gulls Comic)
As far as to the psychological side effects are concerned, I am yet not sure, whether the constant (perceived) need to double check each and every product level is not going to drive one or another of the mostly already OCD-ridden anti-wheat-warriors to insanity.
Reference:
  • Biesiekierski, Jessica R., et al. "No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates." Gastroenterology 145.2 (2013): 320-328.
  • Brouns, Fred JPH, Vincent J. van Buul, and Peter R. Shewry. "Does wheat make us fat and sick?." Journal of Cereal Science 58.2 (2013): 209-215.
  • Catassi, Carlo, et al. "Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders." Nutrients 5.10 (2013): 3839-3853.
  • DiGiacomo, Daniel V., et al. "Prevalence of gluten-free diet adherence among individuals without celiac disease in the USA: results from the Continuous National Health and Nutrition Examination Survey 2009-2010." Scandinavian journal of gastroenterology 48.8 (2013): 921-925.
  • Golley,  Sinéad  et al. "Motivations for avoiding wheat consumption in Australia: results from a population survey." Public Health Nutrition (2014). First view available on CJO2014. 
  • Hallert, C., et al. "Quality of life of adult coeliac patients treated for 10 years." Scandinavian journal of gastroenterology 33.9 (1998): 933-938. 
  • Junker, Yvonne, et al. "Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4." The Journal of experimental medicine 209.13 (2012): 2395-2408.
  • Long, K. H., et al. "The economics of coeliac disease: a population‐based study." Alimentary pharmacology & therapeutics 32.2 (2010): 261-269.
  • Moore, Lauren Renée. "“But We’re Not Hypochondriacs”: The Changing Shape of Gluten-Free Dieting and the Contested Illness Experience." Social Science & Medicine (2014).
  • Monsbakken, K. W., P. O. Vandvik, and P. G. Farup. "Perceived food intolerance in subjects with irritable bowel syndrome–etiology, prevalence and consequences." European journal of clinical nutrition 60.5 (2006): 667-672. 
  • Sollid, Ludvig M., and Bana Jabri. "Triggers and drivers of autoimmunity: lessons from coeliac disease." Nature Reviews Immunology 13.4 (2013): 294-302.
  • Teufel, Martin, et al. "Psychological burden of food allergy." World Journal of Gastroenterology 13.25 (2007): 3456.