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Abstract Background Adolescence is a critical developmental period regarding exposure to substances. Therefore, it is important to be able to identify those adolescents who are most vulnerable to substance abuse in the (near) future. The JOiN study was specifically designed to examine two endophenotypes of adolescent substance use in a normal risk (NR) and high risk (HR) sample of adolescents: (1) behavioural disinhibition, and (2) individual differences in stress sensitivity. Methods The NR adolescents were part of a longitudinal general population study at the Erasmus Medical Center in Rotterdam, the Netherlands of children and adolescents initially aged 6 to 18 years old. Three assessment waves have been nearly completed, and data are available of N = 711 participants for stress sensitivity measures, and of a subsample of N = 110 for electroencephalography (EEG) measures. Added to this study, HR adolescents who had at least one parent with a substance use disorder and who were treated by an outpatient clinic of a primary addiction care provider were approached via their parent(s). In total, N = 83 adolescents formed this HR sample. NR and HR adolescents participated in standardized stress procedure and EEG procedures in our laboratory. Questionnaires were filled out on background variables, behavioural and emotional problems, and substance use, and a diagnostic interview was conducted with adolescents and parents to assess psychopathology symptoms. DNA was collected through saliva or blood samples. Discussion The design of the JOiN study is optimal for examining the predictive role of endophenotypes of adolescent substance use. The combination of different methods, i.e. stress physiology, electrophysiology, genetics, and questionnaire data from several informants on a range of behaviours and environmental factors enables the investigation of the multifactorial nature of adolescent substance use.

Abstract Background In 1992 a cargo aircraft crashed into a residential area of Amsterdam. A troublesome aftermath followed, with rumors on potential toxic exposures and health consequences. Health concerns remained even though no excess morbidity was predicted in retrospective risk evaluations. This study aimed to assess to what extent the rescue workers attribute long-term physical complaints to this disaster, including its aftermath, and to examine associations between such attribution and types of exposure and background variables. Methods Historic cohort study that collected questionnaire data on occupational disaster exposure, attribution of physical complaints, and background variables on average 8.5 years post-disaster. For the present study the workers who were exposed to the disaster were selected from the historic cohort, i.e. the professional firefighters (n = 334), police officers (n = 834), and accident and wreckage investigators (n = 241) who performed disaster-related tasks. Results Across the three occupational groups, a consistent percentage (ranging from 43% to 49%) of exposed workers with long-term physical complaints attributed these to the disaster, including its aftermath. Those with more physical complaints attributed these to a stronger degree. Multivariate logistic regression analyses showed that attribution was significantly more often reported by firefighters who rescued people, and by police officers who reported the identification and recovery of or search for victims and human remains, clean-up, or security and surveillance of the disaster area; who witnessed the immediate disaster scene; who had a close one affected by the disaster; and who perceived the disaster as the worst thing that ever happened to them. Age, sex and educational level were not significantly associated with attribution. Conclusion This study provides further cross-sectional evidence for the role of causal attribution in post-disaster subjective physical health problems. After on average 8.5 years, almost a third (32%) of all the exposed workers, and almost half (45%) of the exposed workers with physical complaints, attributed these complaints to the disaster, including its aftermath. The similarity of the results across the occupational groups suggests a general rather than an occupation-specific attribution process. Longitudinal studies are needed to determine whether causal disaster attribution leads to persistence of post-disaster complaints and health care utilization.

Abstract Background In 1992, a cargo aircraft crashed into apartment buildings in Amsterdam, killing 43 victims and destroying 266 apartments. In the aftermath there were speculations about the cause of the crash, potential exposures to hazardous materials due to the disaster and the health consequences. Starting in 2000, the Epidemiological Study Air Disaster in Amsterdam (ESADA) aimed to assess the long-term health effects of occupational exposure to this disaster on professional assistance workers. Methods/Design Epidemiological study among all the exposed professional fire-fighters and police officers who performed disaster-related task(s), and hangar workers who sorted the wreckage of the aircraft, as well as reference groups of their non-exposed colleagues who did not perform any disaster-related tasks. The study took place, on average, 8.5 years after the disaster. Questionnaires were used to assess details on occupational exposure to the disaster. Health measures comprised laboratory assessments in urine, blood and saliva, as well as self-reported current health measures, including health-related quality of life, and various physical and psychological symptoms. Discussion In this paper we describe and discuss the design of the ESADA. The ESADA will provide additional scientific knowledge on the long-term health effects of technological disasters on professional workers.

Dysregulated physiological stress reactivity has been suggested to impact the development of children and adolescents with important health consequences throughout the life span. Both environmental adversity and genetic predispositions can lead to physiological imbalances in stress systems, which in turn lead to developmental differences. We investigated genetic and environmental contributions to autonomic nervous system reactivity to a psychosocial stressor. Furthermore, we tested whether these effects were consistent with the differential susceptibility framework. Composite measures of adverse life events combined with socioeconomic status were constructed. Effects of these adversity scores in interaction with a polygenic score summarizing six genetic variants, which were hypothesized to work as susceptibility factors, were tested on autonomic nervous system measures as indexed by heart rate and heart rate variability. Results showed that carriers of more genetic variants and exposed to high adversity manifested enhanced heart rate variability reactivity to a psychosocial stressor compared to carriers of fewer genetic variants. Conversely, the stress procedure elicited a more moderate response in these individuals compared to carriers of fewer variants when adversity was low. [ABSTRACT FROM AUTHOR]

Background Socioeconomically disadvantaged children often have psychosocial problems. This study examined the mediating role of maternal depressive symptoms during pregnancy, infancy and early childhood in the association between maternal education, as indicator of socioeconomic status (SES), and child's psychosocial problems. Methods Included were 3410 children from the Amsterdam Born Children and their Development (ABCD) study. To assess the child's psychosocial problems at age 5–6 years, mothers and teachers completed the Strengths and Difficulties Questionnaire (SDQ). Maternal depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale and the Depressive Anxiety and Stress Scale 21. Mediation analysis was performed to calculate the direct effect of maternal education on SDQ score and indirect effects through maternal depressive symptoms. Results The mean mother-reported SDQ total score was significantly higher (P < 0.001) for children of low-educated mothers (6.74 ± 4.41) compared with children of highly educated mothers (4.47 ± 3.73). Levels of maternal depressive symptoms were also higher in low-educated mothers during pregnancy, infancy and early childhood. Maternal depressive symptoms explained 27.5% of the association between maternal education and mother-reported SDQ scores and 22.9% for combined mother/teacher SDQ scores. Maternal depressive symptoms during pregnancy had the strongest indirect effect. Conclusion Maternal depressive symptoms during pregnancy mediate the association between low maternal education and child's psychosocial problems. Early recognition and treatment of maternal depressive symptoms is important to prevent psychosocial problems in children, especially in those with low education. [ABSTRACT FROM AUTHOR]

There is substantial evidence for the assumption that particularly heavy cannabis usett is associated with a variety of psychopathologic conditions. Little is known about the relationship between cannabis and anxiety. Prior studies have concluded that cannabis use alone is not sufficient for the development of long-term anxiety, and it has been suggested that cannabis is simply a risk factor that operates in conjunction with other risk factors. One such risk factor may be an individuals' genetic vulnerability. The present study examines the relationship between cannabis use and symptoms of anxiety by taking a developmental molecular-genetic perspective with a focus on a polymorphism involved in the regulation of serotonin. Specifically, we concentrated on changes in cannabis use and symptoms of anxiety over time and differences herein for individuals with and without the short allele of the 5-HTTLPR genotype. Data were from 1424 adolescents over a period of 5 years. We used different statistical analyses to test co-development of cannabis use and symptoms of anxiety throughout adolescence and the possible role of the 5-HTTLPR genotype in this process. Results from different analyses showed that cannabis use is associated with an increase in symptoms of anxiety, but only in carriers of the short allele of the 5-HTTLPR genotype, not in non-carriers. The findings of the present study show first evidence that the links between cannabis use and symptoms of anxiety are conditional on the individuals' genetic make-up. [ABSTRACT FROM AUTHOR]

Background: We examined the longitudinal associations of autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal (HPA) axis rest and reactivity measures with anxiety and depressive symptoms at one-year follow-up in children with anxiety disorders.Methods: In a clinical sample of 152 children with a primary DSM-IV anxiety disorder, aged 8 to 12 years, anxiety and depressive symptoms were assessed with the Multidimensional Anxiety Scale for Children and the Children's Depression Inventory at pre-treatment baseline and one year later, after treatment with cognitive behavioral therapy. At baseline, children participated in a 70min stress task. Salivary cortisol was measured directly prior to and 20min post stress task. Skin conductance level (SCL), heart rate and high frequency heart rate variability (HRV) were continuously measured during rest and the stress task. To investigate if rest or reactivity measures predicted anxiety and depressive symptoms at one year follow-up, linear regression analyses were conducted for rest and reactivity measures of SCL, heart rate, HRV and cortisol separately.Results: Higher SCL reactivity predicted less decrease of anxiety symptoms at one-year follow-up. Cortisol reactivity showed a weak association with depressive symptoms at one-year follow-up: lower cortisol reactivity predicted less decrease in depressive symptoms.Limitations: Only self-reported anxiety and depressive symptoms were used. However, all predictors were objective biological measures, hence there is no risk of shared method variance bias.Conclusions: These findings suggest that pre-treatment HPA and ANS responsiveness to stress are predictive biomarkers for a lack of symptom improvement in children with a clinical anxiety disorder. [ABSTRACT FROM AUTHOR]