To determine if patients with chronic hyperserotoninaemia from the carcinoid syndrome have increased basal adrenocortical function, I have determined the urinary free Cortisol excretion of seventeen patients with carcinoid tumours and the carcinoid syndrome, twelve patients with carcinoid tumours without the carcinoid syndrome and seventeen normal subjects. There was no significant difference in the urinary free Cortisol excretion of the patients with carcinoid tumours and the carcinoid syndrome (133±20±0 nmoles/24 h), patients with carcinoid tumours without the carcinoid syndrome (115±29 nmoles/24 h) and the normal subjects (96 ±r 9 nmoles/24 h). There was no correlation between the urinary free Cortisol secretion and urinary 5‐hydroxyindoleacetic acid or serum serotonin concentration in the patients with the carcinoid syndrome. There was a suggestion that patients with 5‐hydroxytryptophan (5‐HTP) secreting carcinoid tumours had higher urinary free Cortisol excretion than patients with predominantly serotonin (5‐HT) secreting carcinoid tumours. This may be due to the fact that the non‐polar 5‐HTP molecule penetrates the blood‐brain barrier more effectively than the polar 5‐HT molecule. 5‐HTP is then converted to 5‐HT within the brain. None of the twenty‐nine patients with carcinoid tumours had clinical or laboratory evidence of the ectopic ACTH syndrome.