IN 1963 Coppen and Shaw1 investigated mineral metabolism in melancholia. Thirteen patients recovering after electroshock therapy showed no increase in their total body potassium (40K). In 1966, however, the same authors stated these results showed that during depression there was a relative deficiency of TBK. Also, the concentration of intracellular potassium was low when compared to values obtained from normal subjects.2 In view of the lack of change during depression and recovery, they also suggested that these patients, even when well, suffered from potassium deficiency.
On the basis of increased residual sodium and decreased intracellular potassium in depression, Coppen and Shaw, estimating from the Nernst equation, stated that depressed patients would have a mean action potential 7 mv below the mean for normal individuals. They also reported that the antidepressant effect of tryptophan is enhanced by potassium and carbohydrate supplements.3