The Woolley and Shaw1 hypothesis, expounded in 1954, that serotonin may be causally related to schizophrenia has had an impact upon psychiatry. Since that time a body of evidence has been amassed directed at proving or disproving the hypothesis, evidence at times contradictory. The general approach has been comparisons of schizophrenic and normal populations with respect to the urinary excretion of endogenously produced 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin, endogenous blood serotonin levels and the ability to metabolize exogenously administered tryptophan, a precursor of serotonin, and serotonin.
The 2-dimensional paper chromatographic technique was used by several laboratories to quantitate the excretion of urinary 5--HIAA with contradictory results. Feldstein,2 Curzon,3 Buscaino,4 Sano,5,6 and their coworkers have reported that there is no difference in the endogenous output of 5-HIAA between acute and chronic schizophrenic patients and normal