Context: It has been suggested that radiation-induced growth hormone neurosecretory dysfunction exists in children; however, the pathophysiology is poorly understood and it is unknown if such a phenomenon exists in adult life. Study subjects: 24-hour spontaneous GH secretion was studied by 20 min sampling both in the fed state (n=16; 6 women) and the last 24 hours of 33-hour fast (n=10; 3 women) in adult cancer survivors of normal GH status defined by two GH provocative tests, 13.1 ± 1.6 (range 3-28) yr after cranial irradiation (18-40Gy) for non-pituitary brain tumors (n=12) or leukemia (n=4) in comparison with 30 (9 women) age-, and BMI-matched normal controls (fasting, 11 men and 3 women). Results: Using previously published diagnostic thresholds, all patients had stimulated peak GH responses in the normal range to both, the insulin tolerance test and the combined GHRH plus arginine stimulation test, as well as normal individual mean profile GH levels during the fed and fasting states. However, gender specific comparisons revealed marked reduction (by 40%) in the overall peak GH responses to both provocative tests but similar GH secretory profiles; no differences were seen in the pulsatile attributes of GH secretion (cluster analysis) or the profile absolute and mean GH levels in the fed state or when the h-p axis was stimulated by fasting. Conclusions: Radiation-induced GHNSD either does not exist or is a very rare phenomenon in irradiated adult cancer survivors. The normality of physiological GH secretion in the context of reduced maximum somatotroph reserve suggests compensatory overdrive of the partially damaged somatotroph axis and constitutes a relative argument against somatotroph dysfunction being explained purely by hypothalamic damage with secondary atrophy due to GHRH deficiency. It is therefore possible that radiation in doses less than 40Gy causes dual damage to both the pituitary and the hypothalamus.