When the word 'gluten’ is mentioned, you can be sure that there will be controversy. Some consider it the source of all diseases and misfortunes, others eat steaks made out of pure gluten and do just fine. In such polarized subjects, the truth usually lies somewhere in the middle. The aim of this text is not to prove whether gluten is healthy or not, because in my opinion the only answer to this question is 'it depends’. What does it depend on? For example, whether an autoimmune disease such as psoriasis is present.

What happens in our body when we eat gluten?

Gluten is a mixture of two proteins called gliadin and glutenin. They give wheat products their characteristic elasticity and texture that is pleasant to chew. In addition to wheat, gluten can also be found in rye, barley and oat products. However, for the purposes of this text, we will focus on wheat gluten, because it causes the most problems and controversies.

Digestion of gluten begins in the stomach, where gluten is broken down into gliadin and glutenin via pepsin (a digestive enzyme) and then travel through the digestive system to the small intestine. This is where the problem with gliadin, which gluten owes its bad reputation, comes into play.

Gliadin is not completely digested and absorbed. Instead, it binds to a receptor on the surface of enterocytes – the cells, which line the inner surface of the gut. This in turn leads to the release of zonulin, a protein which can control intestinal permeability. When zonulin is released, tight junctions disassemble, and thus increased intestinal permeability occurs. It is worth remembering that the intestines are never completely sealed – otherwise it would be impossible to absorb nutrients. However, the problem arises when, as a result of significant leakage, the intestinal barrier does not retain substances that should not enter the bloodstream – such as bacteria and their products and food particles. This leads to the development of local and systemic inflammation, which in itself can damage the intestinal barrier – and a vicious circle continues (1,2,3).

Release of zonuline from enterocytes leads to increased intestinal permeability due to disassembling of tight junctions.

It all sounds concerning, but it is important to remember that there are many factors that increase the permeability of the gut and do not necessarily lead to serious problems. Examples of such factors are stress, the use of painkillers, pregnancy and even… physical activity (4). Short-term increase in intestinal permeability in healthy people does not have to have serious consequences. However, the situation becomes more complicated when we are dealing with chronically increased intestinal permeability. This is what happens in autoimmune diseases – psoriasis, celiac disease, type 1 diabetes and Hashimoto’s disease. In these diseases, the additional increase in gut permeability due to gluten consumption may become a problem.

Gluten and psoriasis

In the past few years, the topic of intestinal permeability in people with psoriasis has become the subject of many studies. The results indicate that significantly increased intestinal permeability is observed in people with psoriasis (5,6,7,8,9). What’s more, numerous studies show that eliminating gluten from the diet leads to an improvement in skin symptoms in many – perhaps even all – people with psoriasis (10). In one study, 1,206 people with psoriasis were asked whether food had an effect on their symptoms. As many as 54% of respondents answered that the elimination of gluten led to a significant improvement in skin symptoms of psoriasis (11). Obviously, such subjective observations cannot prove a causal relationship between gluten consumption and the occurrence of psoriasis symptoms. In my opinion, however, it is worth listening to patients – their observations are often of great value, especially if placed in a broader clinical context.

It is also important to mention celiac disease, an autoimmune disease in which gluten consumption leads to the damage of intestinal villi (the main villian here is our good friend gliadin). A meta-analysis of 18 studies found a double risk of developing celiac disease in people with psoriasis compared to healthy people. The same increase in risk of developing psoriasis was also observed in people with celiac disease (12). One of the reasons for the increased risk is that both diseases share the same genetic predisposition to develop immune disorders. Patients with psoriasis also more often have antibodies to gliadin (IgA-AGA), which indicate an immunological reaction to the presence of this protein (13, 14). Moreover, in case of people diagnosed with celiac disease, following a gluten-free diet reduces the intensity of psoriasis symptoms (15). There is also limited evidence that a higher gluten intake may increase the risk of developing psoriasis (16).

Moreover, increased intestinal permeability is closely related to the malfunctioning of the gut microbiome. Dysbiosis of the intestinal microflora is currently considered one of the hallmarks of psoriasis (17,18,19) and deserves a separate post.

So, a gluten-free diet for everyone with psoriasis?

There is no doubt that in people with psoriasis who have severe digestive symptoms, testing for celiac disease should be performed. This includes total level of IgA antibodies, tTG IgA, and small intestine biopsy. In case of diagnosed celiac disease, following a gluten-free diet is unavoidable. It is worth remembering that in addition to celiac disease, there is also a non-celiac hypersensitivity to gluten. People with this hypersensitivity often have anti-gliadin antibodies (AGA IgA or IgG), which are no longer used in the diagnosis of celiac disease. However, these antibodies are not found in all people with gluten sensitivity. Thus, the best way to determine the effect of gluten on the symptoms of psoriasis is to temporarily eliminate (for 4-6 weeks) and then reintroduce gluten-containing products into the diet. It is advisable to consult a dietitian to make sure that elimination and provocation are being carried out correctly.

If your skin symptoms worsen after re-introducing gluten, it is a good idea to go gluten-free for a longer period of time. Here it may also be helpful to consult a dietitian, as gluten-free diets can pose problems when it comes to diet composition and choosing gluten-free alternatives.

In my opinion, elimination and re-introduction of gluten should be performed in every person suffering from psoriasis. This is the only way to clearly answer the question of whether gluten is harmful in this particular case or not. In many people, the reaction will depend on the amount of gluten consumed and its source (wheat gluten most often causes reactions). The reactions themselves can also vary in intensity, the area on which they occur, and the systems they affect. Therefore, it is not possible to create universal recommendations for patients with psoriasis – solutions must be highly individualized. It is definitely worth spending some time and energy on observing your body, because in some patients, the elimination of gluten can lead to a significant improvement in psoriasis symptoms or even remission of the disease.

Finally, a bit of controversy. Considering all the currently available evidence, I personally advise against consuming meat substitutes made from pure gluten (seitan) in people with psoriasis. Consuming such large doses of gluten in a condensed form is not a good idea, especially since the vast majority of these products are highly processed and contain large amounts of salt and oils. Adding these meat substitutes to your diet is a kind of gluten supplementation, which in light of this article seems highly unreasonable in case of an autoimmune disease.

Bibliography

  1. Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Ann N Y Acad Sci. 2012 Jul;1258(1):25-33.
  2. Sturgeon, C., & Fasano, A. (2016). Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases. Tissue barriers, 4(4), e1251384.
  3. Barbaro, M. R., Cremon, C., Morselli-Labate, A. M., Di Sabatino, A., Giuffrida, P., Corazza, G. R., Di Stefano, M., Caio, G., Latella, G., Ciacci, C., Fuschi, D., Mastroroberto, M., Bellacosa, L., Stanghellini, V., Volta, U., & Barbara, G. (2020). Serum zonulin and its diagnostic performance in non-coeliac gluten sensitivity. Gut, 69(11), 1966–1974.
  4. Camilleri M. Leaky gut: mechanisms, measurement and clinical implications in humans. Gut. 2019 Aug;68(8):1516-1526. doi: 10.1136/gutjnl-2019-318427. Epub 2019 May 10.
  5. Richetta, A. G., Grassi, S., Moliterni, E., Chello, C., Calvieri, C., Carnevale, R., Peruzzi, M., Violi, F., & Calvieri, S. (2020). Increased intestinal barrier permeability in patients with moderate to severe plaque-type psoriasis. The Journal of dermatology, 47(10)
  6. Sikora, M., Chrabąszcz, M., Maciejewski, C., Zaremba, M., Waśkiel, A., Olszewska, M., & Rudnicka, L. (2018). Intestinal barrier integrity in patients with plaque psoriasis. The Journal of dermatology, 45(12), 1468–1470.
  7. Sikora, M., Chrabąszcz, M., Waśkiel-Burnat, A., Rakowska, A., Olszewska, M., & Rudnicka, L. (2019). Claudin-3 – a new intestinal integrity marker in patients with psoriasis: association with disease severity. Journal of the European Academy of Dermatology and Venereology : JEADV, 33(10), 1907–1912.
  8. Sikora, M., Stec, A., Chrabaszcz, M., Giebultowicz, J., Samborowska, E., Jazwiec, R., Dadlez, M., Olszewska, M., & Rudnicka, L. (2021). Clinical Implications of Intestinal Barrier Damage in Psoriasis. Journal of inflammation research, 14, 237–243.
  9. Haidmayer, A., Bosch, P., Lackner, A., D’Orazio, M., Fessler, J., & Stradner, M. H. (2020). Effects of Probiotic Strains on Disease Activity and Enteric Permeability in Psoriatic Arthritis-A Pilot Open-Label Study. Nutrients, 12(8), 2337.
  10. Kanda, N., Hoashi, T., & Saeki, H. (2020). Nutrition and Psoriasis. International journal of molecular sciences, 21(15), 5405.
  11. Afifi, L., Danesh, M.J., Lee, K.M. et al. Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey. Dermatol Ther (Heidelb) 7, 227–242 (2017).
  12. Acharya, P., & Mathur, M. (2020). Association between psoriasis and celiac disease: A systematic review and meta-analysis. Journal of the American Academy of Dermatology, 82(6), 1376–1385.
  13. Passali, M., Josefsen, K., Frederiksen, J. L., & Antvorskov, J. C. (2020). Current Evidence on the Efficacy of Gluten-Free Diets in Multiple Sclerosis, Psoriasis, Type 1 Diabetes and Autoimmune Thyroid Diseases. Nutrients, 12(8), 2316.
  14. Bhatia BK, Millsop JW, Debbaneh M, Koo J, Linos E, Liao W. Diet and psoriasis, part II: celiac disease and role of a gluten-free diet. J Am Acad Dermatol. 2014 Aug;71(2):350-8.
  15. De Bastiani, R., Gabrielli, M., Lora, L., Napoli, L., Tosetti, C., Pirrotta, E., Ubaldi, E., Bertolusso, L., Zamparella, M., De Polo, M., Nebiacolombo, C., Bortot, M., Mancuso, M., Bacchin, P., Marsala, V., Pinna, R., Tursi, A., Benedetto, E., Cuffari, A., Pati, A., … Gasbarrini, A. (2015). Association between coeliac disease and psoriasis: Italian primary care multicentre study. Dermatology (Basel, Switzerland), 230(2), 156–160.
  16. Drucker, A. M., Qureshi, A. A., Thompson, J. M., Li, T., & Cho, E. (2020). Gluten intake and risk of psoriasis, psoriatic arthritis, and atopic dermatitis among United States women. Journal of the American Academy of Dermatology, 82(3), 661–665.
  17. Buhaș, M. C., Gavrilaș, L. I., Candrea, R., Cătinean, A., Mocan, A., Miere, D., & Tătaru, A. (2022). Gut Microbiota in Psoriasis. Nutrients, 14(14), 2970.
  18. Kierasińska, M., & Donskow-Łysoniewska, K. (2021). Both the microbiome and the macrobiome can influence immune responsiveness in psoriasis. Central-European journal of immunology, 46(4), 502–508.
  19. Olejniczak-Staruch, I., Ciążyńska, M., Sobolewska-Sztychny, D., Narbutt, J., Skibińska, M., & Lesiak, A. (2021). Alterations of the Skin and Gut Microbiome in Psoriasis and Psoriatic Arthritis. International journal of molecular sciences, 22(8), 3998.

Dodaj komentarz

Twój adres e-mail nie zostanie opublikowany. Wymagane pola są oznaczone *