Interest in adult growth hormone replacement has increased since identification of the associated vascular morbidity and mortality. Although total cholesterol and low density lipoprotein reduction and high density lipoprotein increases are anticipated, reports are conflicting and there is no uniformity in lipoprotein(a) changes. In 1990 we commenced an open trial of therapy with human recombinant GH and now have results to 36 months for 21 patients. Deficiency status was confirmed by insulin stress test with flat GH response < 2.0 ng/ml, mean insulin-like growth factor-I value 122 ng/ml (+/- 69 SD). Lipoprotein(a) was measured by monoclonal assay. Lipid analysis yields two subgroups: baseline cholesterol levels of greater or less than 6.22 mmol/l, with hypercholesterolaemic patients showing an enhanced hypolipaemic response. ANOVA was utilized, with 95% confidence limits. The most significant changes are of reductions in cholesterol and low density lipoprotein; the rate of change is greatest at 6 and 12 months but not sustained to 36 months. High density lipoprotein rises as expected, not to full significance. Lipoprotein(a) levels rose significantly in six patients of the cohort, and the increase was sustained over 36 months.

The concentration of melatonin was determined, using a sensitive and reliable radioimmunoassay, in plasma samples obtained at 20 min intervals during a 12 hr period (from 20.00 to 8.00) from six normal men. Polygraphic sleep recording was simultaneously performed. Each subject was studied twice at a 1 week interval. For each session, the plasma melatonin profile showed an episodic secretion: a mean frequency of 4.5 peaks and 4.0 troughs per night in the first study and a mean frequency of 4.0 peaks and 3.5 troughs in the second study. The two nocturnal melatonin profiles obtained from each subject were very similar. However, considerable interindividual variation was found (areas under the curve [AUC] from 15.3 to 125 pg X hr/ml). No relationship could be obtained between AUC and body weight. Apparent melatonin half-life calculated from the semilogarithmic plots of the melatonin pattern was 57 +/- 34 min. Chi-square testing revealed that the nocturnal pattern of melatonin levels was not related to sleep stages. Our data do not favor a direct relationship between melatonin secretion and the sleep-waking cycle in humans.

hGRF (iv 50 \ g=m\ g) was administered to 6 normal young adult males at 09.00 and 20.00 h on different days. Nocturnal GH secretion was monitored during polygraphic sleep recordings on both control nights and nights following hGRF administration. Sleep-related GH secretion and sleep parameters were not affected by diurnal hGRF administration.The close association in adult man between the occurrence of the initial episode of slow-wave sleep (SWS) and the highest peak of plasma GH concen¬ tration in a 24-h period led to the concept of sleep-related GH secretion (Takahashi et al. 1968; Sassin et al. 1969), submitted to control mecha¬ nisms probably different from those involved in day-time secretion and in pharmacologically indu¬ ced secretion (Mendelson et al. 1979). It has been reported that in man administration of GH subsequently can blunt the secretory re¬ sponse to pharmacological stimulation of GH secretion (Hagen et al. 1972) as well as sleeprelated GH secretion (Mendelson et al. 1983). This negative feedback appears, then, to be exerted at some common point of the pathways involved in the secretory mechanisms. Administration of GH in animals (Stern et al. 1975 ; Drucker-Collin et al. 1975 ; Stern & Morgane 1977) results in some changes in sleep stages with increased REM sleep and decreased SWS. In man, acute administration of GH (5 U) is followed by a decrease in SWS and an increment in REM sleep (Mendelson et al. 1980; Mendelson 1982), whereas iterative administration has no significant effect on sleep (Mendelson et al. 1983).Synthetic human growth hormone-releasing fac¬ tor (hGRF) powerfully stimulates GH release in normal young adult men (Thorner et al. 1983;Rosenthal et al. 1983;Gelato et al. 1984;Sassolas et al. 1984). This study was undertaken in order to determine whether a GH-rise, induced during day¬ time by hGRF administration, would exert an effect on the sleep-related GH secretion and on sleep stages. Materials and MethodsSix normal young men (22-26 years of age) taking no medication, within 10% of their ideal body weights, were enrolled for this study. They had given written informed consent. Protocol had been approved by our institutional Ethics Committee.The subjects were admitted to the Centre de Médecine Nucléaire (Lyon) for two trial periods at intervals of 1 week. The first period included a first control night

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