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Georges Copinschi and Eve Van Cauter

With the noticeable exception of gonadotrophins secretion in post-menopausal women, most modifications of pituitary secretion observed in aging are associated with alterations of circadian rhythmicity, which is centrally generated by a pacemaker located in the suprachiasmatic nuclei of the hypothalamus, and of sleep, another centrally controlled process. In animals and humans, these nuclei present a number of agerelated morphological and neurochemical alterations (1). While circadian rhythmicity persists in healthy elderly subjects, many 24-h rhythms are dampened and/or advanced in old age. The tendency for earlier sleep onset, a more fragmented and more shallow sleep period and earlier morning awakenings is representative of these alterations (2). Several hormonal rhythms that are modulated by the circadian clock have been shown to be of lower amplitude and/or phase advanced, including those of cortisol, melatonin and thyroidstimulating hormone (TSH) (3). In addition, several studies also suggest a shortening of the endogenous circadian period (3–5).

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Eve Van Cauter and Kristen L Knutson

Sleep is an important modulator of neuroendocrine function and glucose metabolism in children as well as in adults. In recent years, sleep curtailment has become a hallmark of modern society with both children and adults having shorter bedtimes than a few decades ago. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity. There is rapidly accumulating evidence from both laboratory and epidemiological studies to indicate that chronic partial sleep loss may increase the risk of obesity and weight gain. The present article reviews laboratory evidence indicating that sleep curtailment in young adults results in a constellation of metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, elevated sympathovagal balance, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. We also review cross-sectional epidemiological studies associating short sleep with increased body mass index and prospective epidemiological studies that have shown an increased risk of weight gain and obesity in children and young adults who are short sleepers. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity.

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Lisa L Morselli, Arlet Nedeltcheva, Rachel Leproult, Karine Spiegel, Enio Martino, Jean-Jacques Legros, Roy E Weiss, Jean Mockel, Eve Van Cauter, and Georges Copinschi


We previously reported that adult patients with GH deficiency (GHD) due to a confirmed or likely pituitary defect, compared with healthy controls individually matched for age, gender, and BMI, have more slow-wave sleep (SWS) and higher delta activity (a marker of SWS intensity). Here, we examined the impact of recombinant human GH (rhGH) therapy, compared with placebo, on objective sleep quality in a subset of patients from the same cohort.


Single-blind, randomized, crossover design study.


Fourteen patients with untreated GHD of confirmed or likely pituitary origin, aged 22–74 years, participated in the study. Patients with associated hormonal deficiencies were on appropriate replacement therapy. Polygraphic sleep recordings, with bedtimes individually tailored to habitual sleep times, were performed after 4 months on rhGH or placebo.


Valid data were obtained in 13 patients. At the end of the rhGH treatment period, patients had a shorter sleep period time than at the end of the placebo period (479±11 vs 431±19 min respectively; P=0.005), primarily due to an earlier wake-up time, and a decrease in the intensity of SWS (delta activity) (559±125 vs 794±219 μV2 respectively; P=0.048).


Four months of rhGH replacement therapy partly reversed sleep disturbances previously observed in untreated patients. The decrease in delta activity associated with rhGH treatment adds further evidence to the hypothesis that the excess of high-intensity SWS observed in untreated pituitary GHD patients is likely to result from overactivity of the hypothalamic GHRH system due to the lack of negative feedback inhibition by GH.