Opiates and opioid peptides have been shown to stimulate the release of Growth hormone (GH) in the rat and naloxone was reported to block this response (Kato et al., 1978; Bruni et al., 1977). Studies in man, however, failed to demonstrate any changes of GH release to administration of opiates (Morley et al., 1980). Moreover, GH levels stimulated by arginine, sleep, exercise, L-dopa and hypoglycaemia are modestly or not at all inhibited by naloxone (Morley 1981; Grossman & Rees, 1983), suggesting that opioids are not important modulators of GH secretion in man. We have recently demonstrated a significant rise of GH following naloxone administration in young Tourette's syndrome (TS) subjects aged 6-12 years (Sandyk & Barnford, in press, a). We have extended our study to evaluate the effects of acute naloxone challenge on GH release in an older group of TS-patients and in a small group of non-TS disease controls (6 narcoleptics). Following an overnight fast, naloxone (1.2 mg I.M.) was administered at 12:00 p.m. to six unmedicated TS patients aged 16-68 years (5 males, 1 female). Blood levels of GH were drawn 30 minutes after naloxone administration. Basal levels were drawn just prior to the naloxone challenge. Results are given in Table 1. While in the young TS patients, acute naloxone challenge produced a significant rise in plasma GH levels (Sandyk & Bamford, in press, a), in the adult group, naloxone produced suppression of GH plasma levels in 4 patients within 30 minutes of administration. The control group did not show any response to naloxone which is consistent with the reported norm (Grossman & Rees, 1983). These findings (1) suggest alterations in opioid control of GH release in TS that are maturation-related, and (2) complement many other clinical physiological and biochemical phenomena in TS that are also maturation-related. A variety of studies have demonstrated the absence of any direct effect of the opioids on pituitary GH release (Wehrenberg et