Gluten, Casein And The Child With Autism
Current research shows that many cases of autism result from an immune-system dysfunction that affects the body's ability to break down certain proteins which in turn affects the developing brains of some children, causing autistic behaviors.
Gluten-Casein Free Diet - A Ray Of Hope?
These proteins are transported to the brain where they bind to receptors causing an effect that our research indicates is manifested in the symptoms of autism.
Gluten-free diet as an intervention for autism and associated spectrum disorders: preliminary findings
The opioid-excess hypothesis of autism suggests that autism is the consequence of the incomplete breakdown and excessive absorption of peptides with opioid activity (derived from foods which contain gluten and casein), causing disruption to biochemical and neuroregulatory processes. Biochemical evidence has indicated the presence of increased levels of peptides in the urine of people with autism, and previous behavioural studies have demonstrated a connection between the long term exclusion of gluten and casein from the diet and improvements in the behaviour of some children with autism. The introduction of a gluten-free diet to children with autism and associated spectrum disorders (n = 22) was monitored over a 5 month period using a battery of parental and teacher interview/questionnaire sessions, observation reports, psychometric tests and urinary profiling. Results suggested that participants on a gluten-free diet showed an improvement on a number of behavioural measures. However there was no significant decrease in specific urinary compounds excreted when compared with controls and a gluten challenge group.
Paul Whiteley et al
Sporadic cerebellar ataxia associated with gluten sensitivity
A total of 104 patients with sporadic cerebellar ataxia were tested for antigliadin and antiendomysium antibodies. Twelve individuals (11.5%) with gluten sensitivity underwent duodenal biopsy and extensive clinical, electrophysiological, neuropsychological, radiological and laboratory investigations including human leucocyte antigen (HLA) typing. Two patients showed typical changes of gluten-sensitive enteropathy with crypt hyperplasia and mucosal flattening. In five patients, the intraepithelial lymphocyte count was elevated. Sporadic ataxia with gluten sensitivity was found to be tightly linked to the HLA DQB1*0201 haplotype (70%). Neurological symptoms were not related to hypovitaminosis or inflammatory CSF changes. The clinical syndrome was dominated by progressive cerebellar ataxia with ataxia of stance and gait (100%), dysarthria (100%) and limb ataxia (97%). Oculomotor abnormalities were gaze-evoked nystagmus (66.7%), spontaneous nystagmus (33.3%), saccade slowing (25%) and upward gaze palsy (16.7%). Extracerebellar features also included deep sensory loss (58.3%), bladder dysfunction (33.3%) and reduced ankle reflexes (33.3%). In accordance with clinical findings, electrophysiological investigations revealed prominent axonal neuropathy with reduced amplitudes (50%) and abnormal evoked potentials (58.3%). On neuropsychological testing, patients presented with moderate verbal memory and executive dysfunction. All patients had evidence of cerebellar atrophy on MRI. We conclude that sporadic ataxia may be associated with positive antibodies against gliadin. Nevertheless, mucosal pathology does not represent an obligatory condition of ataxia with gluten sensitivity. The fact that the disease is strongly associated with the same HLA haplotypes found in coeliac disease not only demonstrates coeliac disease and ataxia with gluten sensitivity to be part of the same disease entity but supports the hypothesis of an immunological pathogenesis of cerebellar degeneration.
K. Burk et al