Psychiatric manifestations of gluten sensitivity/celiac disease and why it is important to psychiatric providers
The spectrum of gluten sensitivity to celiac disease is caused by a molecule contained in wheat, rye, barley and through cross-contamination on oats. These disorders are commonly associated with the gut but current research suggests they may be more likely to manifest as psychiatric conditions. These include but are not limited to schizophrenia, depression, attention deficit, and autism spectrum. Celiac disease is up to 25% more prevalent in people with psychiatric disorders [i]. People suffering from these conditions often initially present to psychiatric providers. Therefore, psychiatric nurse practitioners should have a basic understanding of celiac/gluten sensitivity to assist with early detection and diagnosis.
Gliadin, the offending protein in gluten, causes a breakdown of the protective cells of the gut. This occurs in all people, regardless of celiac status, and can lead to increased gut permeability [ii]. Essential this process allows dangerous macromolecules into the gut and eventually into the blood stream[iii]. This stimulates an inflammatory reaction that has been found to have an effect on neuronal Purkinje cells, cortical neurons and the brain stem[iv] [v]. There is evidence to suggest a gluten free diet causes a regression of the inflamatory assult as well as a lessening of psychiatric symptoms in celiac patients.
What does this mean to psychiatric practitioners? Undrstanding that there is a connection between psychiatric disorders and celiac is essential in managing our client’s overall health. A history of familial food sensitivities and GI disorders is often common in psychiatiric, gluten sensitive patients. If this connection exists testing can be helpful in making a diagnosis. If caught early the prognosis is good and the client can be managed with a combination of a gluten free diet and psychotropic medication. A full recovery from psychiatric symptoms has been noted in several studies but the diet complexity and lifstyle changes warrent a referal to a nutritionist.
For more information or complete list of references please contact pikec@uw.edu
[v] Boscolo, S. et al. (2007) Gluten ataxia: passive transfer in a mouse model. Ann N Y Acad Sci, 1107, 319-28.
Tests | CD/GS | Sensitivity | Specificity | Notes |
tTG-IgA (TG2) | CD | 95% | 90% | If positive it is villous atrophy highly likely but a negative does not rule out CD or GS |
IgA-AGA | GS | 53-100% | 65-100% | Can positive with extra-intestinal symptoms, a negative does not rule out CD/GS |
IgG-AGA | GS | 57-100% | 42-100% | Can positive with extra-intestinal symptoms, a negative does not rule out CD/GS False positive in Crone’s, wheat protein allergy, and with recent diarrhea |
Anti-deaminated gliadin-IgA/IgG | CD | 90&92% Respectively | 98&75% Respectively | Shows CD before intestinal damage occurs |
Total IgA | CD/GS | No Data | No Data | IgA deficiency can cause all AGA tests to show false negative |
TG6 | GS | No Data | No Data | Associated with neurological symptoms Not readily available yet |
Genetic | CD/GS | % in CD | % in GS | Notes |
HLA-DQ8 | CD/GS | 95% | 50% | 30% of the general population will have this halotype, Helps with inconclusive serology |
HLA-DQ2 | CD/GS | 5% | 9% | Helps with inconclusive serology |
HLA-DQ1 | GS | 0 | 1% | Helps with inconclusive serology |
Biopsy results | Increased intraepithelial lymphocytes | Crypt Hyperplasia | Villous Atrophy | Notes |
Marsh Grade I | Present | Not present | Not Present | Found in pre-celiac and GS |
Marsh II | Present | Present | Not Present / Partial | Pre-Celiac/CD |
Marsh Grade III | Present | Present | Total | Celiac Disease |