Individuals with gluten sensitivity (whereby gluten consumption activates symptoms identical to celiac disease, but without having the related intestinal damage) are usually told that the condition is “all in the mind.” But a new research may turn this understanding on its head, after discovering a biological clarification for gluten sensitivity.
In a research presented in the journal Gut, investigators led by Columbia University Medical Center (CUMC) recommend gluten sensitivity may occur as an outcome of a weakened intestinal barrier, which activates an inflammatory immune reaction when gluten is consumed.
Proteins identified in wheat, rye, barley, and triticale all come under the gluten category. They are existing in a wide range of foods, mainly breads, cereals, and pasta.
It is approximated that about 1 in 141 Individuals in America have celiac disease – an autoimmune disorder in which the immune system strikes the small intestine in reaction to gluten consumption, causing symptoms like as bloating, constipation, chronic diarrhea, stomach pain, vomiting, and chronic fatigue.
Approximately 18 million people in America, however, are thought to experience identical symptoms in reaction to gluten consumption, but they do not have the intestinal damage that occurs with celiac disease, nor do they have the associated tissue transglutaminase (tTG) antibodies.
This condition is recognized as gluten sensitivity, non-celiac gluten sensitivity, or non-celiac wheat sensitivity. It is described by the Celiac Disease Foundation as “a problem with symptoms similar to those of celiac disease that enhance when gluten is removed from the diet.”
Finding the causes of gluten sensitivity
Gluten sensitivity has long baffled scientists, who have been incapable to determine the actual mechanisms of the disorder.
This has led to some investigators indicating that gluten sensitivity is not a real condition, and that symptoms that occur in reaction to gluten among individuals without celiac disease are psychological.
However, the new research – led by Armin Alaedini – seems to have recognized a biological explanation for gluten sensitivity, offering a proof that the disorder is not all in the mind.
The new study engaged 80 people with non-celiac gluten sensitivity, 40 people with celiac disease, and 40 healthy people.
The people with non-celiac gluten sensitivity all revealed experiencing gastrointestinal symptoms after taking foods that contains gluten, such as wheat, barley, and rye, the team reports; such symptoms vanished when gluten-containing foods were taken out for a period of 6 months, and they came back when reintroduced.
The investigators took blood samples from all 3 groups, which they used to determine markers of immune system activity.
Study reveals symptoms of gluten sensitivity ‘are not imagined’
In the blood samples of individuals with celiac disease, the investigators identified no markers of enhanced innate immune system activity, regardless of this group experiencing considerable intestinal damage.
This indicates that the intestinal immune reaction in individuals with celiac disease has the capability to neutralize microbes that travel via the damaged intestinal barrier, the team states, which stops an inflammatory reaction from taking place.
For people with non-celiac gluten sensitivity, on the other hand, it was a different story; the investigators identified that, while they did not possess the cytotoxic T cells identified in individuals with celiac disease, they did have a marker of intestinal cell damage, together with markers of acute systemic immune activity.
With respect to the authors, this discovery signifies that sufferers with non-celiac gluten sensitivity have a weakened abdominal barrier as an outcome of intestinal cell damage, which activates inflammatory immune activity in reaction to gluten.
In addition, the investigators identified that markers of intestinal cell damage and immune system activity among the people with non celiac gluten sensitivity stabilized when they refrained from consuming gluten-containing foods for 6 months, further supporting their theory.
Study co-author Dr. Peter H. Green says:
“Our research shows that the symptoms claimed by people with this condition are not dreamed of, as some individuals have suggested. It shows that there is a biological base for these symptoms in a significant number of these sufferers.”
The team recommends it may one day be feasible to use such markers to diagnose non-celiac gluten sensitivity; at present, no diagnostic tests for the problem exist. The markers could also be utilized to monitor sufferers’ response to therapy.
Another co-author of the study Dr. Umberto Volta says:
“These outcomes shift the paradigm in our recognition and knowing of non-celiac wheat sensitivity and will likely have significant effects for diagnosis and treatment.”
“Taking into consideration the large number of individuals affected by the problem and its considerable negative health effect on sufferers, this is an essential area of study that deserves considerably more attention and funding.”