We have recognized that Gluten-related diseases involve the absorption of complete proteins such as gliadin or its peptide-fragments. Anti-protein antibodies circulating in the blood  and immune-complexes, combining antibody with  food protein,   provoke the release of mediators which may cause multiple disturbances in all body systems and  tissue damage. These circulating problems  influence brain function in a variety of undesirable ways.

A family history of psychiatric problems is more common in patients with celiac disease. Celiac disease is genetically determined involving two or more concurrent genes. The genes involved are part of the immune-recognition complex, which determine the "Self" identity markers, protecting one's own cells from attack by the immune system. Celiac patients have an increased frequency of the serum histocomptability antigens (self-markers) of the HLA-B8 and HLA-Dw3 types. This genetic marker may indicate a predisposition for bowel absorption abnormalities or immunologic propensities that result, not only in celiac disease itself, but other contingent abnormalities as well.

Schizophrenia has been associated with gluten intolerance. The diagnosis, schizophrenia, describes a variety of differing individuals who belong to complex group of brain-disordered people often with a chronic or relapsing disease that leads to dementia. The schizophrenic process distorts sensing, feeling, remembering, deciding, and acting. It is unlikely that schizophrenia is a single disease with a single cause. 

The milder, but similar brain dysfunctions observed  with gluten allergy suggests that food allergy may play a role in schizophrenia, with gluten as a  set of triggering antigens. Dr. F.C.Dohan  consistently advocated a gluten-schizophrenia link. (Dohan FC Cereals and Schizophrenia: Data and hypothesis. 1966 Acta Psychiatr. Scand 42:125-42 and Dohan FC More on Celiac Disease as a model for schizophrenia. 1983 Biol. Psychiatry 18:561-4)

Dohan stated:

" Many diseases are caused by genetically-deficient utilization of specific food substances. Perhaps the best studied example is phenyketonuria... far more common disorders, for example, atherosclerosis, and coronary heart disease, are strongly suspected of being due to genetically defective utilization of certain food constituents. " Similarly, considerable evidence indicates that the major cause of schizophrenia is the inborn inability to process certain digestion products of some food proteins, especially cereal grain glutens..."

Among Dr. Dohan's interesting an relevant recommendations is the idea of a "Gluten tolerance test". Such a test has not yet been developed, but is the sort of evaluation method that NP advocates in general. A gluten tolerance test could be initiated with routine evaluations before and after ingestion of grain foods. More sophisticated versions would measure gluten proteins and derived peptides in the blood, and would track the path of these molecules into organs, especially the brain. Finally the impact of these molecules would be evaluated by monitoring the function of the target organ in real time. I have been eager to do real-time monitoring of brain activity, topologically-computed in gluten-sensitive patients. These patients report changes in their energy, mood, cognitive abilities and emotions which no researcher to date has documented objectively. The problem of adverse brain effects of molecules derived from food is a major under-recognized phenomenon of nutrition and molecular pathophysiology. Research in the next 10-20 years will, I am convinced, reveal a great deal about the extent, mechanisms, and importance of this consequence of eating problematic foods to our mental status.

Recommendations: The Alpha Nutrition Program is gluten-free and is recommended as the diet revision strategy for anyone with diagnosed celiac disease, or any person with symptoms suggestive of gluten allergy.

Gluten-Free Diet in Patients with Gluten Sensitivity and Cerebellar Ataxia

sponsored by National Institute of Neurological Disorders and Stroke (NINDS)

Study Details:  In many patients with cerebellar ataxia, the etiology is unknown. Sensitivity to gluten (wheat protein) has been suggested as a cause for cerebellar ataxia even in the absence of malabsorption symptoms or intestinal pathology. However, the prevalence of gluten sensitivity in patients presenting with cerebellar ataxia is unknown and the effect of gluten-free diet on gluten sensitivity-associated cerebellar ataxia has not been systematically studied.  The aim of this project is: 1) To identify gluten sensitive cerebellar ataxia patients attending the Human Motor Control Clinic at the NIH using tests for celiac disease antibodies as a screening method. 2) To conduct open-label controlled clinical trial to assess the efficacy of gluten-free diet in the patients identified using a detailed cerebellar ataxia scale as an objective clinical measure.

Abstract   During the period from May 1997 to October 1998, eight patients with coeliac disease or dermatitis herpetiformis and neurological disorders were admitted to the Department of Neurology, University Hospital of Bergen. The most frequent conditions were polyneuropathy (seven patients) and spinocerebellar ataxia (three patients). Other conditions were lower motor neuron disease, myelopathy, epilepsy and encephalopathy. The patients used various degrees of gluten-free diet at the time of admission. It remains unclear whether there is a shared common pathogenetic mechanism or the neurological disorder is a complication to the coeliac disease. Both vitamin depletion and immunological mechanisms may cause neurological disorder. Neurological manifestations may occur before the gastrointestinal symptoms. With reference to our patients and available literature we discuss prevalence, clinical picture, pathogenesis, treatment and prognosis. Neurologists, gastroenterologists and general practitioners should be aware that coeliac disease can cause neurological diseases, especially polyneuropathy, cerebellar ataxia and encephalopathy.

 J. Neurol Sci 1982 Jan;53(1):9-22        

Degeneration of the central nervous system associated with celiac disease.

Kinney HC, Burger PC, Hurwitz BJ, Hijmans JC, Grant JP.

The following report describes a 57-year-old man with celiac disease who developed a progressive and fatal neurologic disorder despite intensive medical and nutritional care. The clinical and pathological CNS findings in this patient are compared with those of 9 previously reported patients with well documented celiac disease in whom a progressive CNS disorder was carefully studied both pre-and postmortem. An entity of CNS degeneration associated with celiac disease appears to emerge from the study of these 10 cases. This disorder affects predominantly the cerebellum, deep gray masses, certain brain stem nuclei, and spinal cord; its cause and pathogenesis are unknown.

Eur Neurol 1999;42(3):132-5

Coeliac disease presenting with neurological disorders.

Luostarinen L, Pirttila T, Collin P.

Department of Neurology, Tampere University Hospital, Kuopio, Finland. marrku.lostarinen@netlife.fi

It is well known that coeliac disease may be associated with various neurological manifestations. We have had a high index of suspicion of coeliac disease during recent years in our neurological clinic. As a result 10 (7%) out of 144 of our new coeliac patients were detected because of neurological symptoms. The most common neurological manifestations were neuropathy, memory impairment and cerebellar ataxia. In these patient groups screening for coeliac disease with serological antibody tests helps to find patients who may suffer from this disease.

Neuropathol Appl Neurobiol 2000 Dec;26(6):493-6

The neurology and neuropathology of coeliac disease.

Wills AJ.

Department of Neurology, University Hospital Nottingham, UK. ade@wills99.swinternet.co.uk

A number of neurological syndromes have been described in association with coeliac disease. These include disorders of the central nervous system encompassing epilepsy, myoclonus, ataxia, internuclear opthalmoplegia, multifocal leukoencephalopathy and dementia.

Most of these associated conditions show a poor response to gluten restriction. Peripheral neuropathies, of axonal and demyelinating types, have also been reported and may respond to elimination of gluten from the diet. The mechanism underlying these processes remains obscure but may be immunological or related to trace vitamin deficiencies. Controversially, it has also been claimed that occult coeliac disease accounts for a substantial proportion of patients with neurological dysfunction of unknown cause. Some authorities recommend that cryptogenic ataxias and neuropathies should be routinely screened for the presence of gluten-sensitivity but this remains contentious and has not been universally accepted. This review will attempt to review the clinical and pathological findings in this condition and speculate on pathogenesis and directions for future research.