Pregnant women have an increased risk of experiencing restless legs syndrome (RLS). Aim of this study was to elucidate the relationship between pregnancy-related hormonal and metabolic changes and RLS symptomatology.Blood measurements and overnight polysomnography were performed during the third trimester of pregnancy and again 3 months after delivery. We investigated blood hormonal levels (estradiol, prolactin, progesterone, testosterone, follicle-stimulating hormone [FSH], luteinizing hormone [LH], iron, ferritin, hemoglobin) and polysomnographic sleep parameters. Subjective sleep quality and RLS symptoms were evaluated using the Pittsburgh Sleep Quality Index (PSQI) and the International RLS study group (IRLSSG) rating scale.Sleep laboratory.Ten pregnant women fulfilling the IRLSSG criteria for RLS diagnosis and 9 pregnant healthy controls underwent the protocol.N/A.Women with RLS showed higher levels of estradiol during pregnancy compared to controls (34,211 +/- 6397 pg/mL vs. 25,475 +/- 7990 pg/mL, P<0.05). Patients also showed more periodic limb movements (PLMs) before and after delivery, particularly during sleep stage 1 and wakefulness (P<0.05). PLMs decreased postpartum in subjects with RLS only (P<0.05); sleep efficiency increased in women without RLS and remained unchanged in patients (P<0.05). No significant differences were found between groups before or after delivery in plasma concentrations of prolactin, progesterone, testosterone, FSH, LH, iron, ferritin or hemoglobin.RLS in pregnant women goes along with transiently increased estradiol levels and PLM indices suggesting that estrogens play a pathophysiological role for triggering RLS symptoms during pregnancy.
The mechanisms underlying weight gain induced by psychopharmacological agents are poorly understood. Because the recently discovered enteric hormone, ghrelin, stimulates food intake, we hypothesized that increases in circulating ghrelin levels might mediate the weight gain caused by certain antidepressants and atypical antipsychotic drugs. Fifty-two patients receiving psychopharmacological treatments were included in the study: 16 patients received antidepressants that are not known to induce weight gain, and 13 patients received mirtazapine or trimipramine, which are antidepressants known to lead to weight gain; 6 patients received clozapine and olanzapine, which have the highest liability among the antipsychotics to cause weight gain, and 17 patients received other antipsychotics. Fasting venous blood samples for the measurement of ghrelin were drawn in the morning between 06:00 and 08:00 a.m. in the second week of treatment. Although psychopharmacological treatment induced significant weight changes in the expected directions (most prominent in the clozapine or olanzapine treatment group), ghrelin levels did not differ significantly between groups. Psychotropic drugs with different propensities to induce body weight gain are associated with similar concentrations of plasma ghrelin in psychiatric patients after a short period of treatment.
Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been shown to promote slow-wave sleep (SWS, non-REM sleep stages 3 and 4). Plasma levels of ghrelin are dependent on food intake and increase in sleeping subjects during the early part of the night. It is unknown whether sleep itself affects ghrelin levels or whether circadian networks are involved. Therefore, we studied the effect of sleep deprivation on nocturnal ghrelin secretion. In healthy male volunteers, plasma levels of ghrelin, cortisol, and human growth hormone (hGH) were measured during two experimental sessions of 24 h each: once when the subjects were allowed to sleep between 2300 and 0700 and once when they were kept awake throughout the night. During sleep, ghrelin levels increased during the early part of the night and decreased in the morning. This nocturnal increase was blunted during sleep deprivation, and ghrelin levels increased only slightly until the early morning. Ghrelin secretion during the first hours of sleep correlated positively with peak hGH concentrations. We conclude that the nocturnal increase in ghrelin levels is more likely to be caused by sleep-associated processes than by circadian influences. During the first hours of sleep, ghrelin might promote sleep-associated hGH secretion and contribute to the promotion of SWS.
Introduction: It is well established that the regulation of sleep, wakefulness and circadian rhythmicity are tightly coupled to neuroendocrine networks, the regulation of feeding and metabolism. Ghrelin is a recently discovered orexigenic peptide which promotes NREM sleep in humans. Plasma ghrelin levels increase between meals, but also in subjects fasted over night during the early morning hours. It is unknown so far if sleep itself affects ghrelin levels or whether circadian networks are involved. Methods: Nine healthy male volunteers (age 28±1.22 years, BMI 22.8±1.79) took part in the present study after written informed consent had been obtained. The study protocol had been approved by an independent Ethics Committee. Each subject, in a randomized order, underwent twice a 24-hour protocol starting at 07.30h. Subjects remained throughout in a semi-recumbent position in a clinical sleep research center. Illumination was below 100 lux. Standardized breakfast, lunch and dinner were served at fixed time points (07.30, 12.00, 19.00h). Water was available ad libitum. After dinner, until the next morning, no food was available. During one of the 24-hour protocols subjects slept between 2300 and 0700 hours, whereas during the other protocol they were kept awake by social interaction throughout the night. Polygraphic recordings of EEG, EOG and EMG were performed continuously. Blood samples were collected by a through-the-wall technique and assayed for ghrelin levels hourly in duplicate using a commercially available radioimmunoassay (Phoenix Pharmaceuticals, CA, U.S.A.). Data were analyzed statistically by analysis of variance (general linear model, GLM incorporated in SPSS) with condition as between-subject factor and time as within-subject factor. Results: In the sleep condition subjects showed a normal nocturnal sleep between 2300 and 0700 hours. Throughout the day and during the sleep deprivation schedule no major lapses into sleep (>5min) occurred. Ghrelin plasma levels showed the established relationship to meals, i.e. levels increased prior to every meal and sharply declined thereafter. During sleep ghrelin levels displayed an initial increase followed by a decline towards morning awakening. In contrast, during the sleep deprivation condition ghrelin levels increased steadily to a plateau and did not decrease prior to breakfast again. Conclusion: We conclude that an early increase of ghrelin levels during sleep and a decline in the morning hours are related to sleep itself, because overnight wakefulness coincides with steadily increasing ghrelin levels.
Ghrelin, an endogenous ligand for the growth hormone secretagogues, has been shown to influence many processes including appetite and sleep regulation. Recently, steroid hormones has been discussed to effect plasma hormone levels of ghrelin in humans and in rats. We measured plasma ghrelin levels under different hormone constellations: three times during the menstrual cycle (menses, late follicular and mid luteal phase), during pregnancy (third trimester) and 3 month after delivery during the lactation period. Blood samples were taken in the morning at 8 a. m. before breakfast. Results show significantly higher plasma ghrelin levels postpartal during the lactation period compared to pregnancy. No difference was found between pregnancy and controls (measurements across the menstrual cycle). These results show that ghrelin levels differ at different hormonal states in women. The underlying meachanisms are still to be elucidated.
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)
