Monika Raniti

Early physiological markers of cardiovascular risk in community based adolescents with a depressive disorder

BACKGROUND Depression is recognised as an independent cardiovascular risk factor in adults. Identifying this relationship early on in life is potentially important for the prevention of cardiovascular disease (CVD). This study investigated whether clinical depression is associated with multiple physiological markers of CVD risk in adolescents from the general community. METHODS Participants aged 12-18 years were recruited from the general community and screened for depressive symptoms. Individuals with high and low depressive symptoms were administered a diagnostic interview. Fifty participants, 25 with a current depressive episode and 25 matched healthy controls, subsequently completed cardiovascular assessments. Variables assessed were automatic brachial and continuous beat-to-beat finger arterial blood pressure, heart rate, vascular functioning by pulse amplitude tonometry following reactive hyperaemia and pulse transit time (PTT) at rest. Blood samples were collected to measure cholesterol, glucose and glycohaemoglobin levels and an index of cumulative risk of traditional cardiovascular risk factors was calculated. RESULTS Depressed adolescents had a significantly lower reactive hyperaemia index and shorter PTT, suggesting deterioration in vascular integrity and structure. Higher fasting glucose and triglyceride levels were also observed in the depressed group, who also had higher cumulative risk scores indicative of increased engagement in unhealthy behaviours and higher probability of advanced atherosclerotic lesions. LIMITATIONS The sample size and number of males who completed all cardiovascular measures was small. CONCLUSIONS Clinically depressed adolescents had poorer vascular functioning and increased CVD risk compared to controls, highlighting the need for early identification and intervention for the prevention of CVD in depressed youth.

Sleep Duration and Sleep Quality: Associations with Depressive Symptoms Across Adolescence

This study explored whether short sleep duration and sleep quality mediate the relationship between age and depressive symptoms. For comparison, we also explored whether depressive symptoms mediate the relationship between age and short sleep duration and sleep quality. The sample comprised 741 adolescents (63.5% female, mean age 15.78 years, range 11.92–19.67 years) in grades 7–12 from 11 secondary schools in metropolitan Melbourne, Australia. Students completed the Pittsburgh Sleep Quality Index (PSQI) and Center for Epidemiologic Studies Depression Scale (CES-D). Path analyses suggested that short sleep duration significantly mediated the relationship between age and depressive symptoms. Poor sleep quality also significantly mediated this relationship when sleep quality was defined by subjective judgement, but not sleep disturbance, sleep efficiency, or sleep onset latency. Depressive symptoms significantly mediated the relationship between age and short sleep duration and sleep quality (subjective judgement, sleep disturbance, sleep efficiency, and sleep onset latency). These findings suggest that the population-wide increase in depressive symptoms across adolescence is partially mediated by sleep-related developmental changes. They also highlight the importance of examining specific sleep problems when investigating the relationship between sleep and mood in this age group.

Nocturnal indicators of increased cardiovascular risk in depressed adolescent girls.

Depression is an independent risk factor for cardiovascular disease in adults, and recent literature suggests preclinical signs of cardiovascular risk are also present in depressed adolescents. No study has examined the effect of clinical depression on cardiovascular factors during sleep. This study examined the relationship between clinical depression and nocturnal indicators of cardiovascular risk in depressed adolescent girls from the general community (13–18 years old; 11 clinically depressed, eight healthy control). Continuous beat‐to‐beat finger arterial blood pressure and heart rate were monitored via Portapres and electrocardiogram, respectively. Cardiovascular data were averaged over each hour for the first 6 h of sleep, as well as in 2‐min epochs of stable sleep that were then averaged within sleep stages. Data were also averaged across 2‐min epochs of pre‐sleep wakefulness and the first 5 min of continuous non‐rapid eye movement sleep to investigate the blood pressure dipping response over the sleep‐onset period. Compared with controls, depressed adolescents displayed a similar but significantly elevated blood pressure profile across sleep. Depressed adolescents had significantly higher systolic and diastolic blood pressure and mean arterial pressures across the entire night (P < 0.01), as well as during all sleep stages (P < 0.001). Depressed adolescents also had higher blood pressure across the sleep‐onset period, but the groups did not differ in the rate of decline across the period. Higher blood pressure during sleep in depressed adolescent females suggests that depression has a significant association with cardiovascular functioning during sleep in adolescent females, which may increase risk for future cardiovascular pathology.

Factor structure and psychometric properties of the Pittsburgh Sleep Quality Index in community-based adolescents

Study Objectives The Pittsburgh Sleep Quality Index (PSQI) is a widely used self-report questionnaire that assesses general sleep quality. This study aimed to validate the single-factor scoring structure and related psychometric properties in the English language version of the PSQI in community-based adolescents. Methods Participants were 889 (352 males, 39.6%) students (age M = 15.71 ± 1.57; 12.08-18.92 years) recruited from 14 Australian secondary schools. Participants completed the PSQI, Center for Epidemiological Studies-Depression (CES-D) scale, and Spence Childrens Anxiety Scale (SCAS). Exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) of PSQI component scores were performed on two independent random half-samples (i.e. cross-validation approach). The internal consistency of PSQI components and convergent validity of the PSQI global score with CES-D and SCAS total scores were also assessed. Results EFA yielded a single-factor model. CFA of the single-factor model in a separate sample yielded acceptable model fit to the data after important relationships were modeled. Namely, modification indices suggested improved model fit by correlating residual scores of PSQI components of sleep duration and sleep efficiency, and sleep efficiency and sleep latency. Internal consistency was acceptable (Cronbachs α = 0.73). The PSQI global score had moderate-to-large positive correlations with CES-D (r = 0.58) and SCAS (r = 0.45) total scores, demonstrating good convergent validity with emotional problems as predicted. Conclusions The findings validate the single-factor scoring structure of the PSQI in an adolescent sample and highlight important covariation between poor sleep duration, efficiency, and latency in this age group. Further validation studies are required to determine an appropriate PSQI clinical cut-off score for adolescents.