I have a piece in the NYT Sunday Review on the neurological problems sometimes associated with celiac disease. So, in case it’s not clear: The piece does not argue that gluten causes autism or mental illness. Rather, it points out that some cases of undiagnosed celiac can resemble these disorders.
As for the possible link with schizophrenia — still quite hypothetical — but here’s some additional info:
As I alluded to, the supposed celiac-schizophrenia connection isn’t new. It dates to the mid 20th century when F. C. Dohan proposed a link based on a supposed decline in schizophrenia diagnoses when wheat became scarce during WWII.
The idea has been argued about ever since, with some evidence suggesting gluten avoidance could improve symptoms, and other studies showing no response to a gluten-free diet. And that’s where the hypothesis was — in limbo — when the Johns Hopkins University group began looking at the question again in the past 10 years.
First, in 2004, they found an association with celiac and schizophrenia in Denmark.
That find was immediately questioned partly on the basis that celiac disease might have been under diagnosed in the general population, artificially producing the threefold increased risk of celiac among patients with schizophrenia.
A different group later showed a 55 percent increased risk of psychosis among people with celiac.
And the Johns Hopkins group also later found a higher risk of autoimmune disease in the family of people with schizophrenia, and among schizophrenics themselves.
Of course, recent GWAS studies on schizophrenia keep turning up genes involved in immunity.
Now, I should note that gluten-free trials have been tested before in schizophrenia. Some saw improvements. Others didn’t. That means, essentially, that it hasn’t been shown to convincingly work at all.
But no one has targeted just that group with the gluten-related antibodies– the very group that might respond. That subgroup hadn’t been identified until the 2011 study mentioned in the piece (a find replicated here, by the way).
So we’ll see what happens with Deanna Kelly’s study.
Meanwhile, here’s another major caveat: Those antigliadin antibodies may not be directed at gliadin at all.
If, as Armin Alaedini’s study suggests, gliadin happens to mimic proteins in our neuronal synapses, then it’s possible that what we interpret as anti-gliadin antibodies are really the result of some primary problem in the brain (or wherever else those proteins occur), and the antibodies are produced in response to that problem. That goes for autism and bipolar disorder as well, two other disorders where anti-gliadin antibodies have also shown up.
Some evidence supports this counterfactual. It comes from brain disorders associated with genetic mutations, such as Huntington’s disease or genetic ataxias. Khalaf Bushara has shown that those anti-gliadin antibodies are also over represented in people with both disorders.
That is, disorders of the brain known to be caused by genetic mutations somehow lead to what looks like gluten sensitivity.
Now, pure speculation, but it could also be that, because we have an extensive nervous system in the gut, anything that affects the head brain, be it genetic or environmental, also causes problems in the gut brain, leading to a barrier defect and an increased propensity to an adverse reaction to gluten.
Which brings us back to square one. Complete uncertainty.
In the meantime, a nice randomized and controlled study from Finland showing objective improvements in some measures of gut health, as well as a decline in the celiac-associated endomysial antibodies, in patients who went on a gluten-free diet for a year. They also felt better. These patients didn’t actually have overt celiac disease, just the associated antibodies.
Sort of supports the idea of a spectrum of gluten-related disorders that aren’t celiac.