Obsessive-compulsive disorder: a neuronal membrane phospholipid hypothesis and concomitant therapeutic strategy

Abstract

Obsessive-compulsive disorder (OCD) is briefly characterized and several of the hypothesized neuroanatomical and neurochemical substrates of this etiologically heterogeneous syndrome are indicated as well as similarities among OCD, schizophrenia and bipolar disorder. A neuronal membrane phospholipid hypothesis is proposed for OCD analogous to those developed for schizophrenia by Horrobin et al. and for bipolar disorder by Stoll et al. Essential fatty acid (EFA) dietary supplementation has shown some efficacy in treating schizophrenia and bipolar disorder patients and should also be considered for OCD. Supporting this, a case report is presented of a subject with OCD who developed comorbid paresthesia, for whose latter condition a regimen of ibuprofen was instituted. Thirteen weeks thereafter subject’s OCD symptomatology had declined by 40% (YBOC scale) from baseline. Inasmuch as ibuprofen and numerous other non-steroidal anti-inflammatory drugs (NSAIDS) block brain neuronal prostaglandin synthase (several also inhibiting phospholipases A2and C), thereby reducing catabolism of neuronal membrane arachidonic acid, the ibuprofen apparently increased the integrity of subject’s neuronal membranes, as would likely also be the case with EFA dietary supplementation. This OCD NSAID-EFA therapy concept should be further tested by seeking other OCD subjects, especially from arthritis and rheumatism practices (where NSAIDS are routinely employed) and medical record data banks, as OCD has an estimated worldwide population lifetime prevalence of 1% to 3% and at least a subset of OCD patients might possibly benefit.