ABSTRACT
Psychotic disorders often run a chronic course and are associated with a considerable emotional and social impact for patients and their relatives. Therefore, early recognition, combined with the possibility of preventive intervention, is urgently warranted since the duration of untreated psychosis (DUP) significantly determines the further course of the disease. In addition to established diagnostic tools, neurobiological factors in the development of schizophrenic psychoses are increasingly being investigated. It is shown that numerous molecular alterations already exist before the clinical onset of the disease. As schizophrenic psychoses are not elicited by a single mutation in the deoxyribonucleic acid (DNA) sequence, epigenetics likely constitute the missing link between environmental influences and disease development and could potentially serve as a biomarker. The results from transcriptomic and proteomic studies point to a dysregulated immune system, likely evoked by epigenetic alterations. Despite the increasing knowledge of the neurobiological mechanisms involved in the development of psychotic disorders, further research efforts with large population-based study designs are needed to identify suitable biomarkers. In conclusion, a combination of blood examinations, functional imaging techniques, electroencephalography (EEG) investigations and polygenic risk scores should be considered as the basis for predicting how subjects will transition into manifest psychosis.
ABSTRACT
According to epidemiological studies, insomnia is associated with cardiovascular mortality. However, it is yet to be determined whether this link is mediated by known cardiovascular risk factors. The current study aimed at investigating the association between primary insomnia, defined as subjectively reported sleep disturbance in the absence of any other pathology or substance intake, and alterations in polysomnographically determined nocturnal heart rate (HR) and heart rate variability (HRV). A total of 4,581 nocturnal short-term electrocardiographic recordings (5 min each) from 104 participants (58 with primary insomnia, 46 healthy controls) were evaluated for HR as well as for time and frequency domain measures of HRV. In the primary insomnia group, we found a lower wake-to-sleep HR reduction and a lower standard deviation of RR intervals (SDNN) compared to healthy controls. However, between-group differences in resting HR were not found, and previous results of an increase in sympathovagal balance and a decrease in parasympathetic nocturnal activity in objectively determined insomnia could not be confirmed in our sample of self-report insomnia patients. When restricting our analyses to insomnia patients with objectively determined short sleep duration, we found reduced parasympathetic activity as indicated by decreased high frequency power of HRV, as well as decreased root mean square of successive RRI differences (RMSSD) and percentage of successive RRIs that differ by more than 50 ms (pNN50) values. A lower wake-to-sleep HR reduction and alterations in HRV variables might, at least partially, mediate the increased rates of cardiovascular morbidity and mortality observed in insomnia patients.