| 1. |
- Alaie, Iman, et al.
(författare)
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Adolescent depression, early psychiatric comorbidities, and adulthood welfare burden : a 25-year longitudinal cohort study
- 2021
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Ingår i: Social Psychiatry and Psychiatric Epidemiology. - : Springer. - 0933-7954 .- 1433-9285. ; 56:11, s. 1993-2004
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Depression at all ages is recognized as a global public health concern, but less is known about the welfare burden following early-life depression. This study aimed to (1) estimate the magnitude of associations between depression in adolescence and social transfer payments in adulthood; and (2) address the impact of major comorbid psychopathology on these associations.METHODS: This is a longitudinal cohort study of 539 participants assessed at age 16-17 using structured diagnostic interviews. An ongoing 25-year follow-up linked the cohort (n = 321 depressed; n = 218 nondepressed) to nationwide population-based registries. Outcomes included consecutive annual data on social transfer payments due to unemployment, work disability, and public assistance, spanning from age 18 to 40. Parameter estimations used the generalized estimating equations approach.RESULTS: Adolescent depression was associated with all forms of social transfer payments. The estimated overall payment per person and year was 938 USD (95% CI 551-1326) over and above the amount received by nondepressed controls. Persistent depressive disorder was associated with higher recipiency across all outcomes, whereas the pattern of findings was less clear for subthreshold and episodic major depression. Moreover, depressed adolescents presenting with comorbid anxiety and disruptive behavior disorders evidenced particularly high recipiency, exceeding the nondepressed controls with an estimated 1753 USD (95% CI 887-2620).CONCLUSION: Adolescent depression is associated with considerable public expenditures across early-to-middle adulthood, especially for those exposed to chronic/persistent depression and psychiatric comorbidities. This finding suggests that the clinical heterogeneity of early-life depression needs to be considered from a longer-term societal perspective.
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| 2. |
- Alaie, Iman, et al.
(författare)
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Parent-youth conflict as a predictor of depression in adulthood : a 15-year follow-up of a community-based cohort
- 2020
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Ingår i: European Child and Adolescent Psychiatry. - : Springer Science and Business Media LLC. - 1018-8827 .- 1435-165X. ; 29:4, s. 527-536
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Tidskriftsartikel (refereegranskat)abstract
- Experiencing conflictual relations with one's parents while growing up has been linked to onset, recurrence, and worse treatment outcome of adolescent depression. While this suggests that significant problems in the parent-youth relationship make depressive disorders more relentless, it is not clear whether this effect lasts into adulthood. Our aim was to examine if major and minor conflict with parents while growing up predicts depression in adulthood in youth with and without a history of depression. We utilized data from the Uppsala Longitudinal Adolescent Depression Study. This community-based cohort was assessed with structured diagnostic interviews both at age 16-17 and at follow-up 15 years later. The analyses included 382 individuals (227 with a history of child or adolescent depression; 155 peers without such a history). Binary logistic regression was used, adjusting for sex, disruptive behavior disorders, and additional family-related adversities. Among individuals with adolescent depression, major conflict with parents was strongly associated with adult depression (adjusted OR 2.28, 95% CI 1.07-4.87). While major conflict with parents was rare among non-depressed controls, a non-significant association of similar magnitude was still observed. Minor conflict, on the other hand, was not significantly associated with adult depression. Overall, conflict with parents did not predict adult anxiety disorders, substance use, suicidal behavior, somatoform disorders, or psychotic disorders. In conclusion, major parent-youth conflict during upbringing seems to be linked with an increased risk of depression in adulthood. These findings underscore the need to consider contextual/familial factors in the prevention and clinical management of early-life depression.
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| 3. |
- Alm, Susanne, et al.
(författare)
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Poor family relationships in adolescence as a risk factor of in-patient somatic care across the life course : Findings from a 1953 cohort
- 2021
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Ingår i: SSM - Population Health. - : Elsevier. - 2352-8273. ; 14
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Tidskriftsartikel (refereegranskat)abstract
- Background: Prior research has shown that poor family relations during upbringing have long-term detrimental effects on mental health. Few previous studies have, however, focused on somatic health outcomes and studies rarely cover the life span until retirement age. The aims of the current study were, firstly, to examine the association between poor family relationships in adolescence and in-patient somatic care across the life course whilst adjusting for confounders at baseline and concurrent psychiatric in-patient care; and secondly, to compare the risks of somatic and psychiatric in-patient care across the life course.Methods: Prospective data from the Stockholm Birth Cohort study were used, with 2636 participants born in 1953 who were followed up until 2016. Information on family relationships was collected from the participants' mothers in 1968. Annual information on in-patient somatic and psychiatric care was retrieved from official register data from 1969 to 2016.Results: Poisson regressions showed that poor family relationships in adolescence were associated with an increased risk of in-patient somatic care in mid- and especially in late adulthood (ages 44-53 and 54-63 years), even when controlling for the co-occurrence of psychiatric illness and a range of childhood conditions. No statistically significant association was observed in early adulthood (ages 16-43 years), when controlling for confounders. These findings are in sharp contrast to the analyses of inpatient psychiatric care, according to which the association with poor family relations was strongest in early adulthood and thereafter attenuated across the life course.Conclusion: Poor family relationships in adolescence are associated with an increased risk of severe consequences for somatic health lasting to late adulthood even when controlling for confounders including in-patient psychiatric care, emphasising the potentially important role of early interventions.
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| 4. |
- Bohman, Hannes, 1965-
(författare)
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Poor family reletionships as a risk factor off in-patient care across the life course : A prospective cohort study
- 2020
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Ingår i: Scandinavian Journal of Public Health. - Stockholm : SAGE Publications. - 1403-4948 .- 1651-1905. ; 48:7, s. 726-732
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Tidskriftsartikel (refereegranskat)abstract
- Background: Previous research has shown that poor family relations in childhood are associated with adverse mental health in adulthood. Yet, few studies have followed the offspring until late adulthood, and very few have had access to register-based data on hospitalisation due to psychiatric illness. The aim of this study was to examine the association between poor family relations in adolescence and the likelihood of in-patient psychiatric care across the life course up until age 55. Methods: Data were derived from the Stockholm Birth Cohort study, with information on 2638 individuals born in 1953. Information on family relations was based on interviews with the participants' mothers in 1968. Information on in-patient psychiatric treatment was derived from administrative registers from 1969 to 2008. Binary logistic regression was used. Results: Poor family relations in adolescence were associated with an increased risk of later in-patient treatment for a psychiatric diagnosis, even when adjusting for other adverse conditions in childhood. Further analyses showed that poor family relations in adolescence were a statistically significant predictor of in-patient psychiatric care up until age 36-45, but that the strength of the association attenuated over time. Conclusions: Poor family relationships during upbringing can have serious negative mental-health consequences that persist into mid-adulthood. However, the effect of poor family relations seems to abate with age. The findings point to the importance of effective interventions in families experiencing poor relationships.
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| 5. |
- Bohman, Hannes, 1965-, et al.
(författare)
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Preclinical atherosclerosis in adolescents with psychotic or bipolar disorders investigated with carotid high-frequency ultrasound.
- 2020
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Ingår i: Brain and Behavior. - : Wiley. - 2162-3279 .- 2162-3279. ; 10:12
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Early-onset psychosis (EOP) and bipolar disorder (EOBP) (at <18 years of age), are associated with an increased future risk of cardiovascular disease (CVD) and premature death. Yet it is unknown whether the arteries show visible signs of atherosclerosis in EOP and EOBP. This study investigated whether having EOP or EOBP was associated with detectable signs of preclinical atherosclerosis.METHOD: By using 22 MHz high-frequency ultrasound, different layers of the arterial wall of the left common carotid artery (LCCA) were assessed in 77 individuals with EOP (n = 25), EOBP (n = 22), and in age-matched healthy controls (n = 30). Conventional CVD confounders were included in the analyses.RESULTS: Adolescents with EOP and EOBP, compared to controls, had a significantly thicker LCCA intima thickness (0.132 vs. 0.095 mm, p < .001) and intima/media ratio (0.24 vs. 0.17 p < .001). There was a nonsignificant intima difference between EOP and EOBP. Conventional CVD risk factors did not explain the association between EOP/EOBP and intima thickness. In the group of EOP/EOBP, there was a significant correlation between the dose of current antipsychotic medication and intima thickness; however, the correlation was attenuated to a nonsignificant level when adjusted for global function.CONCLUSIONS: Adolescents with EOP or EOBP had an increased LCCA intima thickness, interpreted as a sign of preclinical atherosclerosis. Global function of the disorders was the strongest determinant of intima thickness. The findings, if replicated, might have implications for long-term treatment of EOP and EOBP in order to reduce a future risk of CVD.
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| 6. |
- Engen, Kristine, et al.
(författare)
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Autoantibodies to the N-Methyl-D-Aspartate Receptor in Adolescents With Early Onset Psychosis and Healthy Controls
- 2020
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Ingår i: Frontiers in Psychiatry. - : Frontiers Media SA. - 1664-0640. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- Background Autoantibodies to theN-methyl-D-aspartate receptor (NMDAR-Abs) in autoimmune encephalitis have been associated with prominent psychiatric symptoms. The aims of the present study are to identify the prevalence of NMDAR-Abs in adolescents with early onset psychosis disorders (EOP) and healthy controls (HC) and examine its clinical significance. Method Plasma samples were acquired from 46 adolescent EOP patients and 69 age- and sex matched HC, and assessed for the presence of immunoglobulin G NMDAR-Abs. All participants underwent psychiatric evaluation, neurological examination and head magnetic resonance imaging. Results NMDAR-Abs were detected in three of 46 (6.5%) EOP patients and in two of 69 (2.9%) HC. One NMDAR-Abs EOP patient presented with unusual psychopathology and minor T1 weighted lesions of vasculopathological origin located bi-frontally and in the basal ganglia, and had a recent diagnosis of a separate autoimmune disease. One NMDAR-Ab HC displayed a T2 weighted FLAIR hyperintensity lesion in the left frontal lobe. The remaining three NMDAR-Ab participants were two EOP patients without neurological or radiological findings, and one HC without any clinical findings. Conclusions We report that a small number of EOP patients and HC have NMDAR-Abs with a similar frequency in both groups. The presence of the antibodies was not associated with any distinctive clinical or radiological features. Detection of the antibodies had no diagnostic implication, and a positive NMDAR antibody test must be carefully interpreted and reviewed within the individual clinical context.
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| 7. |
- Gurholt, Tiril P., et al.
(författare)
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Intracranial and subcortical volumes in adolescents with early‐onset psychosis : A multisite mega‐analysis from the ENIGMA consortium
- 2020
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Ingår i: Human Brain Mapping. - Stockholm : Wiley. - 1065-9471 .- 1097-0193. ; 43:1, s. 373-384
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Tidskriftsartikel (refereegranskat)abstract
- Early-onset psychosis disorders are serious mental disorders arising before the age of 18 years. Here, we investigate the largest neuroimaging dataset, to date, of patients with early-onset psychosis and healthy controls for differences in intracranial and subcortical brain volumes. The sample included 263 patients with early-onset psychosis (mean age: 16.4 ± 1.4 years, mean illness duration: 1.5 ± 1.4 years, 39.2% female) and 359 healthy controls (mean age: 15.9 ± 1.7 years, 45.4% female) with magnetic resonance imaging data, pooled from 11 clinical cohorts. Patients were diagnosed with early-onset schizophrenia (n = 183), affective psychosis (n = 39), or other psychotic disorders (n = 41). We used linear mixed-effects models to investigate differences in intracranial and subcortical volumes across the patient sample, diagnostic subgroup and antipsychotic medication, relative to controls. We observed significantly lower intracranial (Cohen's d = −0.39) and hippocampal (d = −0.25) volumes, and higher caudate (d = 0.25) and pallidum (d = 0.24) volumes in patients relative to controls. Intracranial volume was lower in both early-onset schizophrenia (d = −0.34) and affective psychosis (d = −0.42), and early-onset schizophrenia showed lower hippocampal (d = −0.24) and higher pallidum (d = 0.29) volumes. Patients who were currently treated with antipsychotic medication (n = 193) had significantly lower intracranial volume (d = −0.42). The findings demonstrate a similar pattern of brain alterations in early-onset psychosis as previously reported in adult psychosis, but with notably low intracranial volume. The low intracranial volume suggests disrupted neurodevelopment in adolescent early-onset psychosis.
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| 8. |
- Lundberg, Mathias, et al.
(författare)
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Clozapine protects adult neural stem cells from ketamine-induced cell death in correlation with decreased apoptosis and autophagy
- 2020
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Ingår i: Bioscience Reports. - : Portland Press Ltd.. - 0144-8463 .- 1573-4935. ; 40:1
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Tidskriftsartikel (refereegranskat)abstract
- Adult neurogenesis, the production of newborn neurons from neural stem cells (NSCs) has been suggested to be decreased in patients with schizophrenia. A similar finding was observed in an animal model of schizophrenia, as indicated by decreased bromodeoxyuridine (BrdU) labelling cells in response to a non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist. The antipsychotic drug clozapine was shown to counteract the observed decrease in BrdU-labelled cells in hippocampal dentate gyrus (DG). However, phenotypic determination by immunohistochemistry analysis could not reveal whether BrdU-positive cells were indeed NSCs. Using a previously established cell model for analysing NSC protection in vitro, we investigated a protective effect of clozapine on NSCs.Primary NSCs were isolated from the mouse subventricular zone (SVZ), we show that clozapine had a NSC protective activity alone, as evident by employing an ATP cell viability assay. In contrast, haloperidol did not show any NSC protective properties. Subsequently, cells were exposed to the non-competitive NMDA-receptor antagonist ketamine. Clozapine, but not haloperidol, had a NSC protective/anti-apoptotic activity against ketamine-induced cytotoxicity. The observed NSC protective activity of clozapine was associated with increased expression of the anti-apoptotic marker Bcl-2, decreased expression of the pro-apoptotic cleaved form of caspase-3 and associated with decreased expression of the autophagosome marker 1A/1B-light chain 3 (LC3-II).Collectively, our findings suggest that clozapine may have a protective/anti-apoptotic effect on NSCs, supporting previous in vivo observations, indicating a neurogenesis-promoting activity for clozapine. If the data are further confirmed in vivo, the results may encourage an expanded use of clozapine to restore impaired neurogenesis in schizophrenia.
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