Circadian rhythms of melatonin and cortisol in manifest Huntington's disease and in acute cortical ischemic stroke.

Recent studies indicate disruptions to the circadian system in brain injury and neurodegeneration. The results, however, are often not consistent and limited by measurement of only one circadian marker and by infrequent sampling rates. In this study, we examined diurnal rhythmicity in different stages of Huntington (HD) disease and in patients with acute moderate ischemic stroke (AIS) outside the retinohypothalamic pathway by evaluating serum concentrations of melatonin and cortisol at twelve timepoints. All study participants were subjected to the same study protocol of 12-hour light/dark cycle and controlled room conditions. Using cosinor analysis of data and comparing the results with the controls we found melatonin phase delay with lowered amplitude and mesor in stage III HD patients. These changes coexisted with phase advanced rhythm and elevated values of mesor and amplitude for cortisol. Early and mid-stages of HD showed only a phase advance in cortisol secretion. In AIS the circadian rhythm of serum melatonin was sustained without any phase shift and exhibited more flattened profile (lowered mesor and amplitude values), while advanced rhythm with higher mesor for cortisol was present. In conclusion, 1) abnormal pattern of melatonin release in the late stages of HD and in moderate AIS occurs in conjunction with phase-advanced rhythm of cortisol; 2) changes observed in late stages of HD are similar to those that occur with ageing; 3) brain regions other than the presumptive retinopineal neural pathway may play an important role in the pineal production of melatonin in humans; 4) lesion in extrahypothalamic region is related to the strong adrenal stimulation in response to AIS.

Gender-related effect of cold water swimming on the seasonal changes in lipid profile, ApoB/ApoA-I ratio, and homocysteine concentration in cold water swimmers.

It has been proposed that regular cold swimming is associated with health benefits. However, the effect of cold adaptation on particular cardiovascular risk factors, within a single swimming season, remains unknown. Our aim was to evaluate the impact of cold water swimming on the seasonal changes in lipid profile and on apolipoprotein and homocysteine concentration in 34 cold water swimmers (CWS) aged 48 - 68 years. Blood samples were collected at the beginning (October), the middle (January), and the end (April) of the swimming season. Body mass (BM), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TG), ApoB/ApoA-I ratio, and homocysteine concentrations were evaluated. In October, female CWS showed lower BM (P = 0.01), TG concentrations (P = 0.03), and ApoB/ApoA-I ratios (P = 0.008), and higher HDL (P = 0.01) than in men. Similar trends in BM (P = 0.002), HDL (P = 0.0006), and ApoB/ApoA-I ratio (P = 0.01) were seen in January, and for BM (P = 0.002), TG (P = 0.005), HDL (P = 0.003), and ApoB/ApoA-I (P = 0.01) in April. A decrease in TG concentration between January and April (P = 0.05), lower homocysteine concentration between October and January (P = 0.01), and between October and April (P = 0.001) were documented in CWS. A strong drop in homocysteine concentration was observed in female versus male CWS (P = 0.001 versus P = 0.032), particularly between October and April in women (P = 0.001) and October and January in men (P = 0.05). The ApoB/ApoA-I ratio in female CWS decreased over the season (P = 0.02), particularly between October and January (P = 0.05), and a trend toward the TG concentration to reduce over the swimming season was also observed in female CWS. No beneficial changes were noticed in the control group over the season. Our results suggest that the favorable effect of cold swimming on the cardiovascular risk factors may be gender-dependent; further studies are thus needed to draw a precise conclusion.