A possible link between beta -carboline metabolism and infantile autism

Benzodiazepine receptors and abnormal hepatic metabolism have been suggested to participate in several neuropsychiatric disorders including autism. Neuropsychoactive beta-carboline alkaloids as the potent ligands for benzodiazepine receptors are endogenously produced and exogenously supplied much more than benzodiazepines. 1-Methyl-1,2,3,4-tetrahydro-beta-carboline, a predominant alkaloid in humans and foodstuffs, is metabolically hydroxylated in liver. Although its in vivo levels show no difference between autistic and healthy children, the metabolic 6-hydroxylation is significantly decreased in autistic subjects. Therefore, it could be hypothesized that the reduced hepatic metabolism of 1-methyl-1,2,3, 4-tetrahydro-beta-carboline to 6-hydroxyl metabolite may be linked to the pathogenesis of infantile autism as suggested for autistic occurrence to involve the pathology similar to hepatic encephalopathy.