GLUTEN-FREE DI­ETS AND SKIN

A CAUSE AND EF­FECT RE­LA­TION­SHIP

Alternative Medicine - - News - BY ALAN M. DAT­TNER, MD

Gluten-free has be­come a trend in the food world, but why? Alan M. Dat­tner, MD, ex­plains some of the ben­e­fits of cut­ting gluten out of your diet

Gluten has long been known to trig­ger a very spe­cific skin con­di­tion known as Der­mati­tis her­peti­formis. There is now doc­u­mented ev­i­dence that it can cause other kinds of rashes in the skin, even in pa­tients with­out celiac dis­ease.

Gluten’s dis­rup­tion of nor­mal gut- and skin-bar­rier func­tion causes leak­age of in­testi­nal mol­e­cules into the blood and lym­phat­ics and can lead to var­i­ous al­ler­gic and au­toim­mune con­di­tions that may in­volve the skin. Der­mati­tis her­peti­formis (DH) is char­ac­ter­ized by ex­treme itch­ing with groups of small blis­ters, es­pe­cially on the ex­trem­i­ties. Ex­am­in­ing the skin be­side the blis­ters through biopsy reveals the ap­pear­ance of sep­a­ra­tion be­tween the cells in the up­per layer of the skin, lead­ing to the blis­ter for­ma­tion. Fur­ther­more, stain­ing tech­niques for ex­am­in­ing ad­ja­cent skin show pres­ence of the an­ti­body “Im­munoglob­u­lin A” (IgA), along the junc­tion be­tween the epi­der­mis and the der­mis lay­ers. It has been sus­pected that the an­ti­body plays some part in the sep­a­ra­tion of the cells that oc­curs. IgA plays an im­por­tant role in bar­rier func­tion in the gas­troin­testi­nal tract.

The con­di­tion has of­ten been suc­cess­fully treated by strict avoid­ance of gluten. Stud­ies in Eng­land showed gluten avoid­ance to be an ef­fec­tive treat­ment as early as the 1970s, while stud­ies in the US at that time dis­agreed. It is pos­si­ble that both de­fects in US la­bel­ing laws and poor ad­her­ence to care in avoid­ing gluten con­tam­i­na­tion of food-re­lated ma­chin­ery

Der­mati­tis her­peti­formis has of­ten been suc­cess­fully treated by strict avoid­ance of gluten.

led to this prob­lem. More re­cent stud­ies show strict gluten avoid­ance treats the dis­ease.

A re­cent ar­ti­cle by Veron­ica Bon­ci­olini de­scribed a pre­dom­i­nantly fe­male group of 17 non­celiac pa­tients with var­i­ous rashes that were not DH, but still as­so­ci­ated with gluten in­take. Re­mov­ing gluten from their di­ets re­sulted in res­o­lu­tion of their rashes. The itch­ing oc­curred over as­pects of their ex­trem­i­ties that af­fected straight­en­ing and had an ap­pear­ance vaguely like eczema, pso­ri­a­sis, or DH. How­ever, test­ing did not re­veal the IgA de­po­si­tion that is char­ac­ter­is­tic of DH.

This leaves the largest and most poorly de­fined cat­e­gory of skin dis­ease as­so­ci­ated with gluten. Alessio Fasano, MD, has writ­ten ex­ten­sively on the re­la­tion­ship be­tween gluten and dis­rup­tion of the in­testi­nal bar­rier and the sub­se­quent leak­age of in­testi­nal anti­gens, lead­ing to de­vel­op­ment of au­toim­mune con­di­tions of var­i­ous sorts. He has iden­ti­fied a pro­tein mol­e­cule known as “zonulin” that is el­e­vated af­ter gluten con­sump­tion and other stresses. It is re­spon­si­ble for dis­rupt­ing the tight junc­tions be­tween cells lead­ing to in­train­testi­nal sub­stances leak­ing out.

This leak­age is now pop­u­larly known as leaky gut and can al­low poorly di­gested food or other in­testi­nal contents to reach the lym­phatic tis­sue sur­round­ing the small in­testines, lead­ing to sen­si­ti­za­tion. It can also lead to such mol­e­cules es­cap­ing via the blood stream and be­ing dis­persed to var­i­ous parts of the body in­clud­ing the skin, sweat glands, and se­ba­ceous glands. If there is sen­si­ti­za­tion to th­ese mol­e­cules, a cross-re­ac­tive at­tack by lym­pho­cytes can in­duce an in­flam­ma­tory at­tack, lead­ing to a skin dis­or­der if the tar­get is lo­cated in the skin. Other prob­lem­atic sub­stances such as en­do­tox­ins from gut bac­te­ria can also es­cape and cre­ate their own havoc as tar­gets in the skin.

My own stud­ies at the der­ma­tol­ogy branch of the NIH in the late 1970s were on what is known as cross-re­ac­tive recog­ni­tion by white cells of the im­mune sys­tem known as lym­pho­cytes. We found that sen­si­tiz­ing im­mune cells to a chem­i­cal or bacterial sub­stance caused a cross-re­ac­tive at­tack against sim­i­lar sub­stances. We can trans­pose that to say be­com­ing sen­si­tive to the wrong food al­ler­gen might cause an at­tack to a spe­cific sim­i­lar-ap­pear­ing tar­get in your skin, lead­ing to a rash or au­toim­mune prob­lem. Other stud­ies show that gluten ex­po­sure does not lead to rashes for peo­ple on el­e­men­tal di­ets (which would be de­void of rec­og­niz­able al­ler­gens to es­cape), sug­gest­ing that the gluten in th­ese cases is dis­rupt­ing the bar­rier and lead­ing to es­cape of in­flam­ma­tion­caus­ing sub­stances.

Fur­ther sup­port of the role of gluten in skin dis­or­ders comes from anec­do­tal re­ports of celiac dis­ease as­so­ci­ated with other skin con­di­tions. The im­pli­ca­tion again is that in­creased in­testi­nal per­me­abil­ity from gluten is as­so­ci­ated with pen­e­tra­tion of mol­e­cules that lead to au­toim­mune re­ac­tions. One ex­ten­sive study showed that pa­tients with pso­ri­a­sis have more than twice the chance of hav­ing celiac dis­ease as matched con­trol sub­jects, and al­most two-and-a-half times the chance of hav­ing antigliadin an­ti­bod­ies. A com­bi­na­tion of study re­sults showed in­creased an­ti­bod­ies to gliadin, a pro­tein in gluten in 14 per­cent of pso­ri­a­sis pa­tients vs 5 per­cent of matched nor­mal sub­jects. Many of those with such an­ti­bod­ies did not have biopsy ev­i­dence of celiac dis­ease, sug­gest­ing that pso­ri­a­sis was as­so­ci­ated with gluten sen­si­tiv­ity it­self. A small clin­i­cal trial showed de­creased ac­tiv­ity scores with gluten elim­i­na­tion in pso­ri­a­sis pa­tients, and 3 case re­ports showed res­o­lu­tion of pso­ri­a­sis with gluten elim­i­na­tion.

Stud­ies of pa­tients with skin-in­volv­ing au­toim­mune con­nec­tivetis­sue dis­eases such as sys­temic scle­ro­sis, lu­pus, and Sjo­gren’s dis­ease showed in­creased lev­els of an­ti­bod­ies di­rected against gluten. There have been re­ports of pa­tients with both celiac dis­ease and lu­pus. There is also a re­port of a pa­tient with celiac dis­ease and Lichen scle­ro­sis, an­other dis­or­der likely to have au­toim­mune causes. This sup­ports Fasano’s ob­ser­va­tions about au­toim­mune dis­or­ders be­ing re­lated to gluten sen­si­tiv­ity. The greater im­pli­ca­tion of all of th­ese stud­ies and Fasano’s sug­ges­tion of the re­la­tion­ship be­tween gluten and leaky gut is that there is a sig­nif­i­cant sub­set of all of those peo­ple with in­flam­ma­tory skin dis­or­ders of un­known cause who are ei­ther sen­si­tive to gluten, or who ex­pe­ri­ence in­testi­nal bar­rier dis­rup­tion from it, lead­ing to leak­age of gut al­ler­gens into the blood and lym­phat­ics, and set­ting off in­flam­ma­tory con­di­tions in the skin. There are other sub­stances that can cause this leak­age, so gluten is not the only cul­prit here, but it is an im­por­tant one to con­sider when search­ing for the un­der­ly­ing causes of a skin dis­or­der.

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