Purpose
To explore and validate the factor structure of the Pittsburgh Sleep Quality Index (PSQI) in young collegiate adults.MethodsSix hundred university students were initially contacted and invited to participate in a survey of their sleep experience and history. Of this preliminary sample 418 of the students (age = 20.92 ± 1.81 years, BMI = 23.30 ± 2.57 kg/m2) fulfilled the screening criteria and ultimately completed the Pittsburgh Sleep Quality Index (PSQI), a self-report survey of respondents’ sleep habits and sleep quality. The students were enrolled in various undergraduate and postgraduate programs at Jamia Millia Islamia, New Delhi, India. Exploratory factor analysis (EFA) investigated the latent factor structure of the scale. Confirmatory factor analysis evaluated both of the models found by EFA.
ResultsThe Kaiser’s criteria, the Scree test, and the cumulative variance rule revealed that a 2-factor model accounted for most of the variability in the data. However, a follow up Parallel Analysis found a 1-factor model. The high correlation coefficient (r = 0.91) between the two factors of the 2-factor model and almost similar values of the fit indices supports the inference that the PSQI is a unidimensional scale.ConclusionsThe findings validate the 1-factor model of the PSQI in young collegiate adults.
The possible therapeutic role of melatonin in the pathophysiology of coronary artery disorder (CAD) is increasingly being recognized. In humans, exogenous melatonin has been shown to decrease nocturnal hypertension, improve systolic and diastolic blood pressure, reduce the pulsatility index in the internal carotid artery, decrease platelet aggregation, and reduce serum catecholamine levels. Low circulating levels of melatonin are reported in individuals with CAD, arterial hypertension, and congestive heart failure. This review assesses current literature on the cardiovascular effects of melatonin in humans. It can be concluded that melatonin deserves to be considered in clinical trials evaluating novel therapeutic interventions for cardiovascular disorders.
Background/Aims: Psychological conditions are increasingly linked with cardiovascular disorders. We aimed to examine the association between psychological distress and hypertension. Methods: We used data from the National Health Interview Survey for 2004-2013. Hypertension was self-reported and the 6-item Kessler Psychological Distress Scale was used to assess psychological distress (a score ≥13 indicated distress). We used a logistic regression model to test the assumption that hypertension was associated with psychological distress. Results: Among the study participants completing the survey (n = 288,784), 51% were female; the overall mean age (±SEM) was 35.3 ± 0.02 years and the mean body mass index was 27.5 ± 0.01. In the entire sample, the prevalence of psychological distress was 3.2%. The adjusted odds of reporting hypertension in psychologically distressed individuals was 1.53 (95% CI = 1.31-1.80, p = 0.01). Conclusion: The findings suggest that psychological distress is associated with higher odds of hypertension after adjusting for other risk factors for high blood pressure. Further studies are needed to confirm these findings and to elucidate the mechanisms by which stress increases hypertension risk.
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