Cereal Grain Proteins
Gluten and the Brain
We believe that food allergy is a common cause of mental illness. Allergy to proteins from cows milk, hens eggs and wheat are the three most common problems. One idea is that antibodies generated by gluten proteins can attack the brain. This immune mistake is generally known as molecular mimicry. A second idea is that gluten proteins or peptides generated from them during digestion can act directly on the brain. A third idea is that your brain is affected by immune responses in other parts of your body. All immune activity sends signals to the brain to change behavior and to recruit a range of defensive responses.
Disturbances to brain function vary from routine effects such as sleepiness, fogginess, and brief episodes of confusion to symptoms of major mental or neurological illness. For example, people with celiac disease suffer for many years before the diagnosis is made. They often state that they never feel well. Most of these patients will report episodes of fatigue with cognitive dysfunction; difficulty concentrating, mental "fogginess", recent memory dropouts. They complain of mood liability and are often tearful and irritable. They return to normal when they no longer eat problem foods.
We have recognized that Gluten-related diseases involve the absorption of complete proteins such as gliadin or its peptide-fragments. Anti-protein antibodies circulate in the blood and form immune-complexes, combining antibody with food protein. Immune complexes 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. 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 proteins as a set of triggering antigens. Many years ago, Dohan advocated a gluten-schizophrenia link. He 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 ideas was 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 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.
Some Examples of Gluten caused Brain Disease
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.
Neurological diseases associated with celiac disease
Hagen_EM; Gjerde_IO; Vedeler_C; Hovdenak_N
Tidsskr Nor Laegeforen, 2000 00, 120: 4, 439-42 J. Neurol Sci 1982 Jan;53(1):9-22
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.
Degeneration of the central nervous system associated with celiac disease.
Kinney HC, Burger PC, Hurwitz BJ, Hijmans JC, Grant JP. Eur Neurol
Coeliac disease presenting with neurological disorders.
Luostarinen L, Pirttila T, Collin P. Neuropathol Appl Neurobiol 2000
The neurology and neuropathology of coeliac disease. Wills AJ.
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.
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