Onset of Impaired Sleep and Cardiovascular Disease Risk Factors: A Longitudinal Study

STUDY OBJECTIVES: Impaired sleep has been linked to increased risk of cardiovascular disease (CVD), but the underlying mechanisms are still unsettled. We sought to determine how onset of impaired sleep affects the risk of established physiological CVD risk factors (i.e., hypertension, diabetes, and dyslipidemia). METHODS: In a longitudinal cohort study with 3 survey waves (2000, 2004, 2008) from the Finnish Public Sector study we used repeated information on sleep duration and disturbances to determine onset of impaired sleep. Information on development of CVD risk factors, as indicated by initiation of medication for hypertension, diabetes, and dyslipidemia was derived from electronic medical records within 8 years of follow-up. Data on 45,647 participants was structured as two data-cycles to examine the effect of change in sleep (between two waves) on incident CVD events. We applied strict inclusion and exclusion criteria to determine temporality between changes in sleep and the outcomes. RESULTS: While we did not find consistent effects of onset of short or long sleep, we found onset of disturbed sleep to predict subsequent risk of hypertension (hazard ratio = 1.22, 95% CI: 1.04–1.44) and dyslipidemia (HR = 1.17, 95% CI: 1.07–1.29) in fully adjusted analyses. CONCLUSIONS: Results suggest that onset of sleep disturbances rather than short or long sleep mark an increase in physiological risk factors, which may partly explain the higher risk of CVD observed among impaired sleepers

Pre-treatment of blood samples reveal normal blood hypocretin/orexin signal in narcolepsy type 1

The hypocretin/orexin system regulates arousal through central nervous system mechanisms and plays an important role in sleep, wakefulness and energy homeostasis. It is unclear whether hypocretin peptides are also present in blood due to difficulties in measuring reliable and reproducible levels of the peptides in blood samples. Lack of hypocretin signalling causes the sleep disorder narcolepsy type 1, and low concentration of cerebrospinal fluid hypocretin-l/oreadn-A peptide is a hallmark of the disease. This measurement has high diagnostic value, but performing a lumbar puncture is not without discomfort and possible complications for the patient. A blood-based test to assess hypocretin-1 deficiency would therefore be of obvious benefit. We here demonstrate that heating plasma or scrum samples to 65 degrees C for 30 min at pH 8 significantly increases hypocretin-1 immunoreactivity enabling stable and reproducible measurement of hypocretin-1 in blood samples. Specificity of the signal was verified by high-performance liquid chromatography and by measuring blood samples from mice lacking hypocretin. Unspecific background signal in the assay was high. Using our method, we show that hypocretin-1 immunoreactivity in blood samples from narcolepsy type 1 patients does not differ from the levels detected in control samples. The data presented here suggest that hypocretin-1 is present in the blood stream in the low picograms per millilitres range and that peripheral hypocretin-1 concentrations are unchanged in narcolepsy type 1