GH and its regulation and action were studied in 17 adult patients with severe protein–calorie malnutrition (PCM) in a Calcutta hospital. Patients were selected for the severity of their malnutrition and for absence of other diseases. After 2–4 months of refeeding there was complete recovery, and control studies were performed. Serum GH was very high in PCM and was suppressed only minimally by glucose infusion. After the first ½ hr of the iv glucose tolerance test GH rose well above basal levels. GH responses to infusions of arginine and mixed amino acids, respectively, were clearly intact and greater than normal in magnitude. During refeeding GH fell promptly to normal, and results of studies after refeeding were similar to experience in normal subjects. Substantial arginine-induced increases in GH in 3 PCM patients were accompanied by increases in plasma levels of most amino acids and increased negative amino acid balance across the forearm tissues. It appears that PCM produces an increased hypothalamic “set,” resulting in high basal GH levels and augmented GH response to various metabolic stimuli, and that this is readily reversed with refeeding. Acute increases in GH do not produce any rapidly discernible anabolic effect on amino acid balance in peripheral tissues. Hence, the physiologic significance of elevated GH in PCM remains uncertain.