[More treatment but no less depression. An uncomfortable paradox]. / Meer behandeling, maar niet minder depressie; een ongemakkelijke paradox.

BACKGROUND: Treatments for depression have improved, and their availability has markedly increased since the 1980s. Mysteriously, the prevalence of depression in the general population has not decreased. This ‘treatment-prevalence paradox’ (TPP) raises fundamental questions about the diagnosis and treatment of depression. AIM: To clarify the TPP. METHOD: We discuss seven explanations for the TPP, based on an integrative narrative review. RESULTS: The first two explanations assume that improved and more widely available treatments did reduce the prevalence, but that the reduction has been offset by an increase in: 1. misdiagnosing distress as depression, yielding more ‘false positive’ diagnoses; or 2. an actual increase in the incidence of first episodes. The remaining five explanations assume prevalence did not decrease, but suggest that 3. acute phase treatments and 4. relapse prevention are less efficacious than believed; 5. trial efficacy doesn’t generalize to real-world settings; 6. expansion of treatment was not optimally targeted at recurrent-chronic cases which account for most prevalence; and 7. treatments have sometimes counterproductive effects. CONCLUSION: Our analysis suggest that there is little evidence that false positives or first incidence have increased as a result of error or fact but rather strong evidence that (a) the published literature overestimates treatment efficacy, that (b) treatments are considerably less effective as deployed in ‘real world’ settings, and (c) that treatment impact differs substantially for chronic-recurrent cases relative to non-recurrent cases. Collectively, these three explanations probably account for most of the paradox. Further exploration of counterproductive effects of treatment is critical. Significant prevalence reduction requires not only better treatment but foremost long-term structurally funded prevention targeting powerful determinants.

[Antidepressants are frequently prescribed but still critized; a perspective on causes and solutions]. / Antidepressiva: al decennia voor­geschreven én toch nog steeds bekritiseerd; een perspectief op oorzaken en oplossingen.

BACKGROUND: From around 1980, antidepressants (ad) have increasingly been prescribed, for longer periods of time, especially selective serotonin reuptake inhibitors (ssris). Paradoxically, their effectiveness is still doubted, especially outside the psychiatric profession.
AIM: To explain increase and offer a perspective on causes and solutions, and to indicate how to reach consensus.
METHOD: Position paper with critical analysis and synthesis of relevant literature.
RESULTS: The rise in AD prescriptions results from: 1. increased safety and ease of prescribing, 2. increased presentation and recognition of depression in primary care, 3. extension of indication criteria, 4. effective marketing strategies, and 5. effectiveness in acute phase (aad) and of relapse/recurrence prevention in continuation/maintenance phases (coad).Critics point to: 1. low added value of aad relative to placebo, 2. many drop-outs and non-responders, 3. relapse/recurrence prevention with coad works only for responders to aad, 4. relapse/recurrence after AD discontinuation often involves withdrawal symptoms, and 5. publication bias, selective reporting, selective patient selection, and suboptimal blinding, resulting in overestimated effectiveness and underestimated disadvantages.Factors that keep fueling the controversy are: 1. critics stress the net effectiveness of AD whereas proponents point at gross effectiveness which includes spontaneous recovery and placebo effect; 2. persistence of distrust in industry-funded rcts; 3. ideological positions, reinforced by conflicts of interest and selective citations; 4. lack of rcts with relevant long-term outcome measurements.
CONCLUSION: Although consensus is difficult to achieve given the ideological component, there are options. Three factors are critically important: confer to establish which data convince the opposition, response prediction (what works for whom), and rcts with long-term functional outcomes.

Beyond not bad or just okay: social predictors of young adults' wellbeing and functioning (a TRAILS study).

BACKGROUND: Various childhood social experiences have been reported to predict adult outcomes. However, it is unclear how different social contexts may influence each other's effects in the long run. This study examined the joint contribution of adolescent family and peer experiences to young adult wellbeing and functioning. METHODS: Participants came from the TRacking Adolescents' Individual Lives Survey (TRAILS) study (n = 2230). We measured family and peer relations at ages 11 and 16 (i.e. family functioning, perceived parenting, peer status, peer relationship quality), and functioning as the combination of subjective wellbeing, physical and mental health, and socio-academic functioning at age 22. Using structural equation modelling, overall functioning was indicated by two latent variables for positive and negative functioning. Positive, negative and overall functioning at young adulthood were regressed on adolescent family experiences, peer experiences and interactions between the two. RESULTS: Family experiences during early and mid-adolescence were most predictive for later functioning; peer experiences did not independently predict functioning. Interactions between family and peer experiences showed that both protective and risk factors can have context-dependent effects, being exacerbated or overshadowed by negative experiences or buffered by positive experiences in other contexts. Overall the effect sizes were modest at best. CONCLUSIONS: Adolescent family relations as well as the interplay with peer experiences predict young adult functioning. This emphasizes the importance of considering the relative effects of one context in relation to the other.

The association between executive functioning and psychopathology: general or specific?

BACKGROUND: We modeled both psychopathology and executive function (EF) as bi-factor models to study if EF impairments are transdiagnostic or relate to individual syndromes, and concurrently, if such associations are with general EF or specific EF impairments. METHODS: Data were obtained from the Tracking Adolescents' Individual Lives Survey (TRAILS; N = 2230). Psychopathology was assessed with parent-report questionnaires at ages 11, 14, 16, and 19, and EF with tasks from the Amsterdam Neuropsychological Tasks program at ages 11 and 19. Bi-factor models were fitted to the data using confirmatory factor analysis. Correlations were estimated to study the associations between general or specific components of both psychopathology and EF. RESULTS: A bi-factor model with a general psychopathology factor, alongside internalizing (INT), externalizing, attention deficit/hyperactivity (ADHD), and autism spectrum (ASD) problem domains, and a bi-factor model with a general EF factor, alongside specific EFs were adequately fitting measurement models. The best-fitting model between EF and psychopathology showed substantial associations of specific EFs with the general psychopathology factor, in addition to distinct patterns of association with ASD, ADHD, and INT problems. CONCLUSIONS: By studying very diverse psychopathology domains simultaneously, we show how EF impairments cross diagnostic boundaries. In addition to this generic relation, ADHD, ASD, and INT symptomatology show separable profiles of EF impairments. Thus, inconsistent findings in the literature may be explained by substantial transdiagnostic EF impairments. Whether general EF or specific EFs are related to psychopathology needs to be further studied, as differences in fit between these models were small.

Functional outcomes of child and adolescent mental disorders. Current disorder most important but psychiatric history matters as well.

BACKGROUND: Various sources indicate that mental disorders are the leading contributor to the burden of disease among youth. An important determinant of functioning is current mental health status. This study investigated whether psychiatric history has additional predictive power when predicting individual differences in functional outcomes. METHOD: We used data from the Dutch TRAILS study in which 1778 youths were followed from pre-adolescence into young adulthood (retention 80%). Of those, 1584 youths were successfully interviewed, at age 19, using the World Health Organization Composite International Diagnostic Interview (CIDI 3.0) to assess current and past CIDI-DSM-IV mental disorders. Four outcome domains were assessed at the same time: economic (e.g. academic achievement, social benefits, financial difficulties), social (early motherhood, interpersonal conflicts, antisocial behavior), psychological (e.g. suicidality, subjective well-being, loneliness), and health behavior (e.g. smoking, problematic alcohol, cannabis use). RESULTS: Out of the 19 outcomes, 14 were predicted by both current and past disorders, three only by past disorders (receiving social benefits, psychiatric hospitalization, adolescent motherhood), and two only by current disorder (absenteeism, obesity). Which type of disorders was most important depended on the outcome. Adjusted for current disorder, past internalizing disorders predicted in particular psychological outcomes while externalizing disorders predicted in particular health behavior outcomes. Economic and social outcomes were predicted by a history of co-morbidity of internalizing and externalizing disorder. The risk of problematic cannabis use and alcohol consumption dropped with a history of internalizing disorder. CONCLUSION: To understand current functioning, it is necessary to examine both current and past psychiatric status.

Neuroticism's prospective association with mental disorders halves after adjustment for baseline symptoms and psychiatric history, but the adjusted association hardly decays with time: a meta-analysis on 59 longitudinal/prospective studies with 443 313 participants.

BACKGROUND: This meta-analysis seeks to quantify the prospective association between neuroticism and the common mental disorders (CMDs, including anxiety, depression, and substance abuse) as well as thought disorders (psychosis/schizophrenia) and non-specific mental distress. Data on the degree of confounding of the prospective association of neuroticism by baseline symptoms and psychiatric history, and the rate of decay of neuroticism's effect over time, can inform theories about the structure of psychopathology and role of neuroticism, in particular the vulnerability theory. METHOD: This meta-analysis included 59 longitudinal/prospective studies with 443 313 participants. RESULTS: The results showed large unadjusted prospective associations between neuroticism and symptoms/diagnosis of anxiety, depression, and non-specific mental distress (d = 0.50-0.70). Adjustment for baseline symptoms and psychiatric history reduced the associations by half (d = 0.10-0.40). Unadjusted prospective associations for substance abuse and thought disorders/symptoms were considerably weaker (d = 0.03-0.20), but were not attenuated by adjustment for baseline problems. Unadjusted prospective associations were four times larger over short (<4 year) than long (⩾4 years) follow-up intervals, suggesting a substantial decay of the association with increasing time intervals. Adjusted effects, however, were only slightly larger over short v. long time intervals. This indicates that confounding by baseline symptoms and psychiatric history masks the long-term stability of the neuroticism vulnerability effect. CONCLUSION: High neuroticism indexes a risk constellation that exists prior to the development and onset of any CMD. The adjusted prospective neuroticism effect remains robust and hardly decays with time. Our results underscore the need to focus on the mechanisms underlying this prospective association.

Predicting mental disorders from hypothalamic-pituitary-adrenal axis functioning: a 3-year follow-up in the TRAILS study.

BACKGROUND: Hypothalamic-pituitary-adrenal axis functioning, with cortisol as its major output hormone, has been presumed to play a key role in the development of psychopathology. Predicting affective disorders from diurnal cortisol levels has been inconclusive, whereas the predictive value of stress-induced cortisol concentrations has not been studied before. The aim of this study was to predict mental disorders over a 3-year follow-up from awakening and stress-induced cortisol concentrations. METHOD: Data were used from 561 TRAILS (TRacking Adolescents' Individual Lives Survey) participants, a prospective cohort study of Dutch adolescents. Saliva samples were collected at awakening and half an hour later and during a social stress test at age 16. Mental disorders were assessed 3 years later with the Composite International Diagnostic Interview (CIDI). RESULTS: A lower cortisol awakening response (CAR) marginally significantly predicted new disorders [odds ratio (OR) 0.77, p = 0.06]. A flat recovery slope predicted disorders with a first onset after the experimental session (OR 1.27, p = 0.04). Recovery revealed smaller, non-significant ORs when predicting new onset affective or anxiety disorders, major depressive disorder, or dependence disorders in three separate models, corrected for all other new onsets. CONCLUSIONS: Our results suggest that delayed recovery and possibly reduced CAR are indicators of a more general risk status and may be part of a common pathway to psychopathology. Delayed recovery suggests that individuals at risk for mental disorders perceived the social stress test as less controllable and less predictable.

Mental health in Dutch adolescents: a TRAILS report on prevalence, severity, age of onset, continuity and co-morbidity of DSM disorders.

BACKGROUND: With psychopathology rising during adolescence and evidence suggesting that adult mental health burden is often due to disorders beginning in youth, it is important to investigate the epidemiology of adolescent mental disorders. METHOD: We analysed data gathered at ages 11 (baseline) and 19 years from the population-based Dutch TRacking Adolescents' Individual Lives Survey (TRAILS) study. At baseline we administered the Achenbach measures (Child Behavior Checklist, Youth Self-Report) and at age 19 years the World Health Organization's Composite International Diagnostic Interview version 3.0 (CIDI 3.0) to 1584 youths. RESULTS: Lifetime, 12-month and 30-day prevalences of any CIDI-DSM-IV disorder were 45, 31 and 15%, respectively. Half were severe. Anxiety disorders were the most common but the least severe whereas mood and behaviour disorders were less prevalent but more severe. Disorders persisted, mostly by recurrence in mood disorders and chronicity in anxiety disorders. Median onset age varied substantially across disorders. Having one disorder increased subjects' risk of developing another disorder. We found substantial homotypic and heterotypic continuity. Baseline problems predicted the development of diagnosable disorders in adolescence. Non-intact families and low maternal education predicted externalizing disorders. Most morbidity concentrated in 5-10% of the sample, experiencing 34-55% of all severe lifetime disorders. CONCLUSIONS: At late adolescence, 22% of youths have experienced a severe episode and 23% only mild episodes. This psychopathology is rather persistent, mostly due to recurrence, showing both monotypic and heterotypic continuity, with family context affecting particularly externalizing disorders. High problem levels at age 11 years are modest precursors of incident adolescent disorders. The burden of mental illness concentrates in 5-10% of the adolescent population.

Does neuroticism make you old? Prospective associations between neuroticism and leukocyte telomere length.

BACKGROUND: Telomere attrition, causing accelerated aging, might be one of the mechanisms through which neuroticism leads to somatic disease and increased all-cause mortality. In the current study we investigated whether neuroticism is prospectively associated with shorter telomere length (TL), a biological marker of aging. METHOD: Participants were 3432 adults (mean age 52.9 years, range 32-79). Data were collected at baseline (T1) and at two follow-up visits after 4 years (T2) and 6 years (T3). Neuroticism was assessed using the 12-item neuroticism scale of the Revised Eysenck Personality Questionnaire (EPQ-R) at T2 and T3. TL was measured by a monochrome multiplex quantitative polymerase chain reaction (PCR) assay at T1, T2 and T3. A linear mixed model was used to assess whether neuroticism could predict TL prospectively after adjusting for age, sex, body mass index (BMI), frequency of sports, smoking status, presence of chronic diseases and level of education. RESULTS: Neuroticism was a significant negative predictor of TL at follow-up (B = -0.004, p = 0.044) after adjusting for sex, age, baseline TL and various biological and lifestyle factors. CONCLUSIONS: High neuroticism is significantly and prospectively associated with telomere attrition independent of lifestyle and other risk factors.

Psychopathology and academic performance, social well-being, and social preference at school: the TRAILS study.

Psychopathology during adolescence has been associated with poor academic performance, low social well-being, and low social preference by peers at school. However, previous research has not accounted for comorbid psychopathology, informant-specific associations between psychopathology and functioning, and gender and age differences. This study addresses these limitations by examining adolescents' psychopathology and functioning at school, reported by child, parent, teacher, and peers during primary and secondary school in a large Dutch longitudinal cohort study (N = 2230). Teacher reports of psychopathology, especially regarding attention problems and withdrawn/depressed problems, followed by parent reports regarding hyperactivity, were most strongly associated with academic performance. The same held for social preference which was associated with teacher and parent ratings of withdrawn/depressed problems and hyperactivity. In contrast, social well-being was best predicted by child reports (at primary school) of affective problems. In girls, the association between ADHD problems and poor academic performance was stronger than in boys and conduct problems were more often associated with poor school functioning in general. These findings can help identify adolescents at risk for poor functioning and design interventions that effectively reduce or prevent poor school functioning.

Reciprocal effects of stable and temporary components of neuroticism and affective disorders: results of a longitudinal cohort study.

BACKGROUND: Cross-sectional studies show that neuroticism is strongly associated with affective disorders. We investigated whether neuroticism and affective disorders mutually reinforce each other over time, setting off a potential downward spiral. METHOD: A total of 2981 adults aged 18-65 years, consisting of healthy controls, persons with a prior history of affective disorders and persons with a current affective disorder were assessed at baseline (T1) and 2 (T2) and 4 years (T3) later. At each wave, affective disorders according to DSM-IV criteria were assessed with the Composite Interview Diagnostic Instrument (CIDI) version 2.1 and neuroticism with the Neuroticism-Extraversion-Openness Five Factor Inventory (NEO-FFI). RESULTS: Using structural equation models the association of distress disorders (i.e. dysthymia, depressive disorder, generalized anxiety disorder) and fear disorders (i.e. social anxiety disorder, panic disorder, agoraphobia without panic) with neuroticism could be attributed to three components: (a) a strong correlation of the stable components of distress and fear disorders with the stable trait component of neuroticism; (b) a modest contemporaneous association of change in distress and fear disorders with change in neuroticism; (c) a small to modest delayed effect of change in distress and fear disorders on change in neuroticism. Moreover, neuroticism scores in participants newly affected at T2 but remitted at T3 did not differ from their pre-morbid scores at T1. CONCLUSIONS: Our results do not support a positive feedback cycle of changes in psychopathology and changes in neuroticism. In the context of a relative stability of neuroticism and affective disorders, only modest contemporaneous and small to modest delayed effects of psychopathology on neuroticism were observed.

Effects of structural and dynamic family characteristics on the development of depressive and aggressive problems during adolescence. The TRAILS study.

Both structural (i.e., SES, familial psychopathology, family composition) and dynamic (i.e., parental warmth and rejection) family characteristics have been associated with aggressive and depressive problem development. However, it is unclear to what extent (changes in) dynamic family characteristics have an independent effect on problem development while accounting for stable family characteristics and comorbid problem development. This issue was addressed by studying problem development in a large community sample (N = 2,230; age 10-20) of adolescents using Linear Mixed models. Paternal and maternal warmth and rejection were assessed via the Egna Minnen Beträffande Uppfostran for Children (EMBU-C). Aggressive and depressive problems were assessed via subscales of the Youth/Adult Self-Report. Results showed that dynamic family characteristics independently affected the development of aggressive problems. Moreover, maternal rejection in preadolescence and increases in paternal rejection were associated with aggressive problems, whereas decreases in maternal rejection were associated with decreases in depressive problems over time. Paternal and maternal warmth in preadolescence was associated with fewer depressive problems during adolescence. Moreover, increases in paternal warmth were associated with fewer depressive problems over time. Aggressive problems were a stable predictor of depressive problems over time. Finally, those who increased in depressive problems became more aggressive during adolescence, whereas those who decreased in depressive problems became also less aggressive. Besides the effect of comorbid problems, problem development is to a large extent due to dynamic family characteristics, and in particular to changes in parental rejection, which leaves much room for parenting-based interventions.

Physical activity and onset of depression in adolescents: a prospective study in the general population cohort TRAILS.

Although it has often been suggested that physical activity and depression are intertwined, only few studies have investigated whether specific aspects of physical activity predict the incidence of major depression in adolescents from the general population. Therefore the aim of this study was to investigate the effects of nature, frequency, duration and intensity of physical activity during early adolescence on the onset of a major depressive episode in early adulthood. In a population sample of adolescents (N = 1396), various aspects of physical activity were assessed at early adolescence (mean age 13.02, SD = 0.61). Major depressive episode onset was assessed using the Composite International Diagnostic Interview. A Cox regression model was performed to investigate whether physical activity characteristics and their interactions with gender predicted a major depressive episode onset up until mean age 18.5 (SD = 0.61). The individual characteristics of physical activity (nature, frequency, duration and intensity) or their interactions with gender did not predict a major depressive episode onset (p values >0.05). So far, there is no prospective evidence that physical activity protects against the development of adolescent depressive episodes in either boys or girls.

Disability mediates the impact of common conditions on perceived health.

BACKGROUND: We examined the extent to which disability mediates the observed associations of common mental and physical conditions with perceived health. METHODS AND FINDINGS: WHO World Mental Health (WMH) Surveys carried out in 22 countries worldwide (n = 51,344 respondents, 72.0% response rate). We assessed nine common mental conditions with the WHO Composite International Diagnostic Interview (CIDI), and ten chronic physical with a checklist. A visual analog scale (VAS) score (0, worst to 100, best) measured perceived health in the previous 30 days. Disability was assessed using a modified WHO Disability Assessment Schedule (WHODAS), including: cognition, mobility, self-care, getting along, role functioning (life activities), family burden, stigma, and discrimination. Path analysis was used to estimate total effects of conditions on perceived health VAS and their separate direct and indirect (through the WHODAS dimensions) effects. Twelve-month prevalence was 14.4% for any mental and 51.4% for any physical condition. 31.7% of respondents reported difficulties in role functioning, 11.4% in mobility, 8.3% in stigma, 8.1% in family burden and 6.9% in cognition. Other difficulties were much less common. Mean VAS score was 81.0 (SD = 0.1). Decrements in VAS scores were highest for neurological conditions (9.8), depression (8.2) and bipolar disorder (8.1). Across conditions, 36.8% (IQR: 31.2-51.5%) of the total decrement in perceived health associated with the condition were mediated by WHODAS disabilities (significant for 17 of 19 conditions). Role functioning was the dominant mediator for both mental and physical conditions. Stigma and family burden were also important mediators for mental conditions, and mobility for physical conditions. CONCLUSIONS: More than a third of the decrement in perceived health associated with common conditions is mediated by disability. Although the decrement is similar for physical and mental conditions, the pattern of mediation is different. Research is needed on the benefits for perceived health of targeted interventions aimed at particular disability dimensions.

Negative and positive life events are associated with small but lasting change in neuroticism.

BACKGROUND: High neuroticism is prospectively associated with psychopathology and physical health. However, within-subject changes in neuroticism due to life experiences (LEs) or state effects of current psychopathology are largely unexplored. In this 2-year follow-up study, four hypotheses were tested: (1) positive LEs (PLEs) decrease and negative LEs (NLEs) increase neuroticism; (2) LE-driven change in neuroticism is partly long-lasting; and (3) partly independent of LE-driven changes in anxiety/depression; and (4) childhood adversity (before age 16 years) moderates the influence of NLEs/PLEs on neuroticism scores in adult life. METHOD: Data came from the Netherlands Study of Depression and Anxiety [NESDA, n = 2981, mean age 41.99 years (s.d. = 13.08), 66.6% women]. At follow-up (T2) we assessed PLEs/NLEs with the List of Threatening Experiences (LTE) over the prior 24 months and categorized them over recent and distant PLE/NLE measures (1-3 and 4-24 months prior to T2 respectively) to distinguish distant NLE/PLE-driven change in trait neuroticism (using the Dutch version of the Neuroticism-Extroversion-Openness Five Factor Inventory, NEO-FFI) from state deviations due to changes in symptoms of depression (self-rated version of the 30-item Inventory of Depressive Symptomatology, IDS-SR30) and anxiety (Beck Anxiety Inventory, BAI). RESULTS: Distant NLEs were associated with higher and distant PLEs with lower neuroticism scores. The effects of distant LEs were weak but long-lasting, especially for distant PLEs. Distant NLE-driven change in neuroticism was associated with change in symptoms of anxiety/depression whereas the effect of distant PLEs on neuroticism was independent of any such changes. Childhood adversity weakened the impact of distant NLEs but enhanced the impact of distant PLEs on neuroticism. CONCLUSIONS: Distant PLEs are associated with small but long-lasting decreases in neuroticism regardless of changes in symptom levels of anxiety/depression. Long-lasting increases in neuroticism associated with distant NLEs are mediated by anxiety/depression.

Plasticity genes do not modify associations between physical activity and depressive symptoms.

OBJECTIVE: Physical activity is inversely associated with depression in adolescents, but the overall associations are fairly weak, suggesting individual differences in the strength of the associations. The aim of this study was to investigate whether plasticity genes modify the reciprocal prospective associations between physical activity and depressive symptoms found previously. METHODS: In a prospective population-based study (N = 1,196), physical activity and depressive symptoms were assessed three times, around the ages of 11, 13.5, and 16. Structural Equation Modeling was used to examine reciprocal effects of physical activity and depressive symptoms over time. The plasticity genes examined were 5-HTTLPR, DRD2, DRD4, MAOA, TPH1, 5-HTR2A, COMT, and BDNF. A cumulative gene plasticity index consisting of three groups (low, intermediate, and high) according to the number of plasticity alleles carried by the adolescents was created. Using a multigroup approach, we examined whether the associations between physical activity and depressive symptoms differed between the three cumulative plasticity groups, as well as between the individual polymorphisms. RESULTS: We found significant cross-sectional and cross-lagged paths from physical activity to depressive symptoms and vice versa. Neither the cumulative plasticity index nor the individual polymorphisms modified the strengths of these associations. CONCLUSION: Associations between adolescents' physical activity and depressive symptoms are not modified by plasticity genes.

An increase in depressive symptoms after myocardial infarction predicts new cardiac events irrespective of depressive symptoms before myocardial infarction.

BACKGROUND: Depression after myocardial infarction (MI) is associated with poor cardiovascular prognosis. There is some evidence that specifically depressive episodes that develop after the acute event are associated with poor cardiovascular prognosis. The aim of the present study was to evaluate whether an increase in the number of depressive symptoms after MI is associated with new cardiac events. METHOD: In 442 depressed and 325 non-depressed MI patients the Composite International Diagnostic Interview interview to assess post-MI depression was extended to evaluate the presence of the ICD-10 depressive symptoms just before and after the MI. The effect of an increase in number of depressive symptoms during the year following MI on new cardiac events up to 2.5 years post-MI was assessed with Cox regression analyses. RESULTS: Each additional increase of one symptom was significantly associated with a 15% increased risk of new cardiac events, and this was stronger for non-depressed than for depressed patients. This association was independent of baseline cardiac disease severity. There was no interaction with the number of depressive symptoms pre-MI. CONCLUSIONS: Our findings suggest that an increase in depressive symptoms after MI irrespective of the state of depression pre-MI explains why post-MI depression is associated with poor cardiovascular prognosis. Also increases in depressive symptoms after MI resulting in subthreshold depression should be evaluated as a prognostic marker. Whether potential mechanisms such as cardiac disease severity or inflammation underlie the association remains to be clarified.

[Symptoms of anxiety in adolescents. Findings from the TRAILS-study]. / Angstsymptomen bij adolescenten; bevindingen uit de TRAILS-studie.

BACKGROUND: The Dutch TRAILS-study focuses on development from early adolescence into adulthood. An important aspect of this development is the development of anxiety. Hitherto little has been known about typical development of symptoms of anxiety during adolescence. AIM: To describe both the normative development of anxiety during adolescence, and the risk indicators for high levels of anxiety in adolescents. METHOD: Studies were embedded in trails, a large cohort study that followed children from the age of 10 to adulthood. RESULTS: Our results showed that, on average, levels of anxiety decrease in early adolescence and subsequently increase in middle or late adolescence, depending on the subtype of anxiety involved. Child-, parent- and peer-factors at age 10-12 years were related to higher subsequent anxiety levels. Some factors, such as the style of upbringing, were related to higher anxiety levels solely in early adolescence, whereas other factors such as being bullied by peers were related to continuing higher anxiety levels throughout adolescence, irrespective of later victimisation. CONCLUSION: Our study should, we hope, lead to a better understanding of the normative development of anxiety in the general adolescent population.