The mechanism underlying increased tryptaminuria after alcohol ingestion

It is demonstrated that the increased tryptaminuria which follows alcohol ingestion can be abolished by the concurrent ingestion of alkali even when the amount of alkali consumed is insufficient to increase urinary pH to 6.5 (above which pH a fall in urinary tryptamine may be anticipated, from previous studies, to occur). It is suggested that this increased tryptaminuria is largely if not wholly dependent on the metabolic acidosis induced by alcohol which the concurrent ingestion of alkali abolishes.