In a collaboration between the Weill Medical College of Cornell, the Sheppard Pratt Health System in Baltimore and the Hopkins Medical Center, researchers have found that schizophrenic patients have an immune intolerance to gluten. This finding leads to a paradox that could be the next key in solving the mystery of schizophrenia.
Schizophrenia is a mental disorder characterized by abnormalities in perception or awareness of reality. These distortions may affect all five senses but are mostly present in the form of hallucinations, which the movie A Beautiful Mind made famous. Other symptoms of the disease are paranoia, bizarre delusions, incoherent speech and social dysfunction.
Even more troubling, the onset of the disease is late (typically occurring in young adulthood), and sometimes goes unnoticed in medical diagnoses. In sum, schizophrenia affects one percent of the entire world's population and treatments still remain remedial, even in today's advancing scientific world.
For these reasons, this study, led by Diana Samaroo of Weill Medical College, is particularly important because it suggests a very interesting link between schizophrenia and a composite of the proteins gliadin and glutenin, called gluten.
Gluten is found in many foods, including bread, pasta and other wheat products. People who have celiac disease are unable to process or tolerate gluten. If left untreated, the disease can inflict damage on the small intestine's ability to absorb nutrients.
Although scientists have been linking celiac disease with schizophrenia for several years, these findings imply that patients with celiac disease have a different immunological reaction to gluten compared to schizophrenics. In other words, both groups of people cannot tolerate gluten, but this intolerance plays out in different ways.
People with celiac disease have characteristically high concentrations of antibodies against gliadin, deamidated gliadin (lacking a nitrogen-oxygen group) and the TG2 protein, which amplifies the body's immune response to gliadin. The body sees the gliadin and TG2 molecules as a threat to the body, and uses antibodies like molecular red flags to bind and mark them for destruction.
However, for the schizophrenics in the study, antibody concentrations against deamidated gliadin and TG2 were significantly lower than levels in people with celiac disease. This indicates that the majority of schizophrenics with gluten-intolerance actually do not have celiac disease.
But because anti-gliadin antibodies were at elevated levels, researchers suspect that these are the antibodies that have a role in schizophrenia.
Antibodies to proteins have been known to cross-react with certain "self" antigens, where an antibody intended for a certain target also happens to react with the body's own tissues, eliciting disease. These self-attacking antibodies are also known as "auto-antibodies."
Furthermore, antibodies can play a role in disease by activating the secretion of various inflammatory molecules that affect the function of other cells, which could have a role in neurodevelopment defects, including those seen in schizophrenia. For all these reasons, the anti-gliadin antibodies that do not illicit celiac disease in schizophrenics need further analysis.
Analyzing the body's heightened immune response to gluten could reveal valuable insight into the mechanisms behind the development of schizophrenia independent of celiac disease.
Samaroo's study provides an intriguing difference between two different ailments, which has the potential to lead us to a new awareness of a relatively misunderstood disease.
