Browsing by Subject "MAJOR DEPRESSION"

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  • Wesolowska, Karolina; Elovainio, Marko; Hintsa, Taina; Jokela, Markus; Pulkki-Raback, Laura; Lipsanen, Jari; Juonala, Markus; Raitakari, Olli; Keltikangas-Jarvinen, Liisa (2018)
    Objective: Depressive symptoms have been associated with Type 2 diabetes, but the temporal direction of this association and the underlying mechanisms remain unclear. The present study examined a potential bidirectional association between depressive symptoms and glucose levels in women and men, and the factors mediating this association. Method: The participants were from the Cardiovascular Risk in Young Finns Study, a prospective, population-based, cohort study (N = 2,534). Depressive symptoms were assessed using a modified Beck Depression Inventory. Fasting glucose was measured concurrently with depressive symptoms. To analyze the data, a multiple-group cross-lagged analysis and parallel multiple mediation in structural equation modeling were used. Results: Depressive symptoms in 2001 were positively associated with glucose levels in 2012 in women (beta = .07, p = .023) but not in men (beta = -.03, p = .45). This sex difference was statistically significant (p = .042). Glucose levels in 2001 did not predict depressive symptoms in 2012 in either women or men (ps = .96). Changes in body mass index, high-sensitivity C-reactive protein, alcohol consumption, or tobacco or cigarette smoking did not mediate the observed association (ps > .05). Conclusions: The results showed a positive association between depressive symptoms and glucose levels in women but not in men. The direction of this relationship seems to be from depressive symptoms to glucose levels rather than the reverse. Changes in body fat, inflammation, alcohol consumption, or tobacco or cigarette smoking may not play a mediating role in this observed association.
  • Mohammad, H.; Marchisella, F.; Ortega-Martinez, S.; Hollos, P.; Eerola, K.; Komulainen, E.; Kulesskaya, N.; Freemantle, E.; Fagerholm, V.; Savontous, E.; Rauvala, H.; Peterson, B. D.; van Praag, H.; Coffey, E. T. (2018)
    Promoting adult hippocampal neurogenesis is expected to induce neuroplastic changes that improve mood and alleviate anxiety. However, the underlying mechanisms remain largely unknown and the hypothesis itself is controversial. Here we show that mice lacking Jnk1, or c-Jun N-terminal kinase (JNK) inhibitor-treated mice, display increased neurogenesis in adult hippocampus characterized by enhanced cell proliferation and survival, and increased maturation in the ventral region. Correspondingly, anxiety behaviour is reduced in a battery of tests, except when neurogenesis is prevented by AraC treatment. Using engineered retroviruses, we show that exclusive inhibition of JNK in adult-born granule cells alleviates anxiety and reduces depressive-like behaviour. These data validate the neurogenesis hypothesis of anxiety. Moreover, they establish a causal role for JNK in the hippocampal neurogenic niche and anxiety behaviour, and advocate targeting of JNK as an avenue for novel therapies against affective disorders.
  • Madsen, I. E. H.; Nyberg, S. T.; Hanson, L. L. Magnusson; Ferrie, J. E.; Ahola, K.; Alfredsson, L.; Batty, G. D.; Bjorner, J. B.; Borritz, M.; Burr, H.; Chastang, J. -F.; de Graaf, R.; Dragano, N.; Hamer, M.; Jokela, M.; Knutsson, A.; Koskenvuo, M.; Koskinen, A.; Leineweber, C.; Niedhammer, I.; Nielsen, M. L.; Nordin, M.; Oksanen, T.; Pejtersen, J. H.; Pentti, J.; Plaisier, I.; Salo, P.; Singh-Manoux, A.; Suominen, S.; ten Have, M.; Theorell, T.; Toppinen-Tanner, S.; Vahtera, J.; Vaananen, A.; Westerholm, P. J. M.; Westerlund, H.; Fransson, E. I.; Heikkila, K.; Virtanen, M.; Rugulies, R.; Kivimaki, M.; IPD Work Consortium (2017)
    Background. Adverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression. Method. We identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol. Results. We included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47-2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04-1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94-1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81-1.32). Conclusions. Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.
  • Toffol, Elena; Kalleinen, Nea; Haukka, Jari; Vakkuri, Olli; Partonen, Timo; Polo-Kantola, Paivi (2014)
  • Lisboa, S. F.; Issy, A. C.; Biojone, C.; Montezuma, K.; Fattori, V.; Del-Bel, E. A.; Guimaraes, F. S.; Cunha, F. Q.; Verri, W. A.; Joca, S. R. L. (2018)
    Preclinical and clinical evidence suggests pro-inflammatory cytokines might play an important role in the neurobiology of schizophrenia and stress-related psychiatric disorders. Interleukin-18 (IL-18) is a member of the IL-1 family of cytokines and it is widely expressed in brain regions involved in emotional regulation. Since IL-18 involvement in the neurobiology of mental illnesses, including schizophrenia, remains unknown, this work aimed at investigating the behavior of IL-18 null mice (KO) in different preclinical models: 1. the prepulse inhibition test (PPI), which provides an operational measure of sensorimotor gating and schizophrenic-like phenotypes; 2. amphetamine-induced hyperlocomotion, a model predictive of antipsychotic activity; 3. resident intruder test, a model predictive of aggressive behavior. Furthermore, the animals were submitted to models used to assess depressive- and anxiety-like behavior. IL-18KO mice showed impaired baseline PPI response, which was attenuated by D-amphetamine at a dose that did not modify PPI response in wild-type (WT) mice, suggesting a hypodopaminergic prefrontal cortex function in those mice. D-Amphetamine, however, induced hyperlocomotion in IL-18KO mice compared to their WT counterparts, suggesting hyperdopaminergic activity in the midbrain. Moreover, IL-18KO mice presented increased basal levels of IL-1 beta levels in the hippocampus and TNF-alpha in the prefrontal cortex, suggesting an overcompensation of IL-18 absence by increased levels of other proinflammatory cytokines. Although no alteration was observed in the forced swimming or in the elevated plus maze tests in naive IL-18KO mice, these mice presented anxiogenic-like behavior after exposure to repeated forced swimming stress. In conclusion, deletion of the IL-18 gene resembled features similar to symptoms observed in schizophrenia (positive and cognitive symptoms, aggressive behavior), in addition to increased susceptibility to stress. The IL-18KO model, therefore, could provide new insights into how changes in brain immunological homeostasis induce behavioral changes related to psychiatric disorders, such as schizophrenia.
  • Sandman, Nils; Valli, Katja; Kronholm, Erkki; Vartiainen, Erkki; Laatikainen, Tiina; Paunio, Tiina (2017)
    Nightmares are intensive dreams with negative emotional tone. Frequent nightmares can pose a serious clinical problem and in 2001, Tanskanen et al. found that nightmares increase the risk of suicide. However, the dataset used by these authors included war veterans in whom nightmare frequency -and possibly also suicide risk -is elevated. Therefore, re-examination of the association between nightmares and suicide in these data is warranted. We investigated the relationship between nightmares and suicide both in the general population and war veterans in Finnish National FINRISK Study from the years 1972 to 2012, a dataset overlapping with the one used in the study by Tanskanen et al. Our data comprise 71,068 participants of whom 3139 are war veterans. Participants were followed from their survey participation until the end of 2014 or death. Suicides (N = 398) were identified from the National Causes of Death Register. Frequent nightmares increase the risk of suicide: The result of Tanskanen et al. holds even when war experiences are controlled for. Actually nightmares are not significantly associated with suicides among war veterans. These results support the role of nightmares as an independent risk factor for suicide instead of just being proxy for history of traumatic experiences.
  • Neyazi, Alexandra; Theilmann, Wiebke; Brandt, C; Rantamäki, Tomi Pentti Johannes; Matsui, Nobuaki; Rhein, M; Kornhuber, J; Bajbouj, M; Sperling, W; Bleich, S; Frieling, H; Löscher, W (2018)
    Although electroconvulsive therapy (ECT) is among the most effective treatment options for pharmacoresistant major depressive disorder (MDD), some patients still remain refractory to standard ECT practise. Thus, there is a need for markers reliably predicting ECT non/response. In our study, we have taken a novel translational approach for discovering potential biomarkers for the prediction of ECT response. Our hypothesis was that the promoter methylation of p11, a multifunctional protein involved in both depressive-like states and antidepressant treatment responses, is differently regulated in ECT responders vs. nonresponders and thus be a putative biomarker of ECT response. The chronic mild stress model of MDD was adapted with the aim to obtain rats that are resistant to conventional antidepressant drugs (citalopram). Subsequently, electroconvulsive stimulation (ECS) was used to select responders and nonresponders, and compare p11 expression and promoter methylation. In the rat experiments we found that the gene promoter methylation and expression of p11 significantly correlate with the antidepressant effect of ECS. Next, we investigated the predictive properties of p11 promoter methylation in two clinical cohorts of patients with pharmacoresistant MDD. In a proof-of-concept clinical trial in 11 patients with refractory MDD, higher p11 promoter methylation was found in responders to ECT. This finding was replicated in an independent sample of 65 patients with pharmacoresistant MDD. This translational study successfully validated the first biomarker reliably predicting the responsiveness to ECT. Prescreening of this biomarker could help to identify patients eligible for first-line ECT treatment and also help to develop novel antidepressant treatment procedures for depressed patients resistant to all currently approved antidepressant treatments.
  • Liskola, Krista; Raaska, Hanna; Lapinleimu, Helena; Elovainio, Marko (2018)
    Parental depressive symptoms have shown to be associated with offspring depression but much of the research has been focused on maternal depression. The aim of our study was to investigate the extent to which depressive symptoms of both parents associate with offspring depressive symptoms and whether social factors mediate these associations using data from adopted children with no shared genetic background. Data were derived from the Finnish Adoption survey study (a subsample of adopted children aged between 9 and 12years, n=548). Parental depressive symptoms were measured using short version of the General Health Questionnaire and Children's Depression Inventory (CDI) was used to measure depressive symptoms in adoptees. Paternal depressive symptoms were related to the total CDI (B=0.33, p=0.05) and two dimensions of offspring depressive symptoms: negative mood (B=0.10, p=0.03) and interpersonal problems (B=0.06, p=0.009). These associations remained significant even when adjusted for child's age and gender, age at adoption, type of placement before adoption, continent of birth and adoptive family's SES. No associations were found between maternal and any dimensions of offspring depressive symptoms. No information about the mental health of biological parents was available. We interpret the results as demonstrating that intergenerational transmission of depressive symptoms is not solely related to shared genes. Also, the results highlight the association of paternal depression with offspring depressive symptoms.
  • Berg, Noora; Kiviruusu, Olli; Karvonen, Sakari; Rahkonen, Ossi; Huurre, Taina (2017)
    Poor childhood family conditions have a long-term effect on adult mental health, but the mechanisms behind this association are unclear. Our aim was to study the pathways from problematic family relationships in adolescence to midlife psychological distress via disadvantages in early adulthood. Participants of a Finnish cohort study at the age of 16 years old in 1983 were followed up at ages 22, 32 and 42 years old (N = 1334). Problems in family relationships were measured with poor relationship with mother and father, lack of parental support in adolescent's individuation process and poor home atmosphere, and mental health was assessed using Kessler's Psychological Distress Scale (K10). We analyzed the indirect effects of adolescent family relations on mental health at age 42 years old via various disadvantages (somatic and psychological symptoms, relationship/marital status, low education/unemployment and heavy drinking) at ages 22 and 32 years old. Problematic adolescent family relationships were associated with midlife psychological distress in women (0.19; 95% CI 0.11, 0.26) and men (0.13; 95% CI 0.04, 0.21). However, after adjustment for adolescent psychological symptoms, the association was only significant for women (0.12; 95% CI 0.04, 0.20). Poor family relationships were associated with various disadvantages in early adulthood. The association from poor family relationships (16 years old) to psychological distress (42 years old) was in part mediated via psychological symptoms in women (0.03; 95% CI 0.01, 0.04) and men (0.02; 95% CI 0.00, 0.04) and in women also via heavy drinking in early adulthood (0.02; 95% CI 0.00, 0.03). Adolescent family relationships have a role in determining adult mental health. Targeted support addressing psychological well-being and hazardous drinking for adolescents with problematic family relationships might prevent disadvantages in early adulthood, and further prevent poor midlife mental health.
  • Ribeiro, Deidiane Elisa; Casarotto, Plinio C.; Staquini, Laura; Pinto e Silva, Maria Augusta; Biojone, Caroline; Wegener, Gregers; Joca, Samia (2019)
    Purinergic receptors, especially P2RX, are associated to the severity of symptoms in patients suffering from depressive and bipolar disorders, and genetic deletion or pharmacological blockade of P2RX7 induces antidepressant-like effect in preclinical models. However, there is scarce evidence about the alterations in P2RX7 or P2RX4 levels and in behavioral consequences induced by previous exposure to stress, a major risk factor for depression in humans. In the present study, we evaluated the effect of imipramine (IMI) on P2RX7 and P2RX4 levels in dorsal and ventral hippocampus as well as in the frontal cortex of rats submitted to the pretest session of learned helplessness (LH) paradigm. Repeated, but not acute administration of IMI (15 mg/kg ip) reduced the levels of both P2RX7 and P2RX4 in the ventral, but not in dorsal hippocampus or frontal cortex. In addition, we tested the effect of P2RX7/ P2RX4 antagonist brilliant blue G (BBG: 25 or 50 mg/kg ip) on the LH paradigm. We observed that repeated (7 days) but not acute (1 day) treatment with BBG (50 mg) reduced the number of failures to escape the shocks in the test session, a parameter mimicked by the same regimen of IMI treatment. Taken together, our data indicates that pharmacological blockade or decrease in the expression of P2RX7 is associated to the antidepressant-like behavior observed in the LH paradigm after repeated drug administration.
  • Riihimaki, K.; Vuorilehto, M.; Jylhä, P.; Isometsa, E. (2016)
    Background: Response styles theory of depression postulates that rumination is a central factor in occurrence, severity and maintaining of depression. High neuroticism has been associated with tendency to ruminate. We investigated associations of response styles and neuroticism with severity and chronicity of depression in a primary care cohort study. Methods: In the Vantaa Primary Care Depression Study, a stratified random sample of 1119 adult patients was screened for depression using the Prime-MD. Depressive and comorbid psychiatric disorders were diagnosed using SCID-I/P and SCID-II interviews. Of the 137 patients with depressive disorders, 82% completed the prospective five-year follow-up with a graphic life chart enabling evaluation of the longitudinal course of episodes. Neuroticism was measured with the Eysenck Personality Inventory (EPI-Q). Response styles were investigated at five years using the Response Styles Questionnaire (RSQ-43). Results: At five years, rumination correlated significantly with scores of Hamilton Depression Rating Scale (r = 0.54), Beck Depression Inventory (r = 0.61), Beck Anxiety Inventory (r = 0.50), Beck Hopelessness Scale (r = 0.51) and Neuroticism (r = 0.58). Rumination correlated also with proportion of follow-up time spent depressed (r = 0.38). In multivariate regression, high rumination was significantly predicted by current depressive symptoms and neuroticism, but not by anxiety symptoms or preceding duration of depressive episodes. Conclusions: Among primary care patients with depression, rumination correlated with current severity of depressive symptoms, but the association with preceding episode duration remained uncertain. The association between neuroticism and rumination was strong. The findings are consistent with rumination as a state-related phenomenon, which is also strongly intertwined with traits predisposing to depression. (C) 2015 Elsevier Masson SAS. All rights reserved.
  • Pelkonen, Mirjami; Marttunen, Mauri; Aro, Hillevi (2003)
    Background: Few longitudinal studies have attempted to identify risk factors in mid-adolescence for subsequent depression in young adulthood. Mid-adolescence is a critical developmental phase for studying vulnerability to depression due to high incidence and prevalence of depression. Methods: In a longitudinal study, following an urban Finnish community cohort (761 males and 887 females) from age 16, mid-adolescent risk factors for depression at age 22 years were studied. Data were collected by a questionnaire at school at age 16, and by a postal questionnaire at age 22. Results: Of the females 116 (13%) and of the males 69 (9%) had depression (S-BDI) in young adulthood. In multivariate analyses baseline depressive symptoms, low self-esteem, dissatisfaction with academic achievement, problems with the law, poor atmosphere at home and having no close friends predicted subsequent depression. Risk factors for males included more 'externalizing' aspects, for females more 'internalizing' factors. Conclusions: Mid-adolescence is an important age to study risk for depression, and self-reported perceptions of psychosocial well-being have predictive value. Preventive efforts can be selectively targeted at adolescents who have been exposed to identifiable risk factors. (C) 2002 Elsevier B.V. All rights reserved.
  • Fisher, Miranda L.; Loukola, Anu; Kaprio, Jaakko; Turner, Jill R. (ACADEMIC PRESS INC ELSEVIER SCIENCE, 2015)
    International Review of Neurobiology
    Smoking is currently the leading cause of preventable death in the United States and is responsible for over four million deaths annually worldwide. Therefore, there is a vast clinical unmet need with regards to therapeutics targeting smoking cessation. This is even more apparent when examining smokers co-morbid with psychiatric illness, as rates of smoking in this population are similar to 4 x higher than in the general population. Examining common genetic and molecular signaling pathways impinging upon both smoking behavior and psychiatric illness will lead to a better understanding of co-morbid disorders and potential development of novel therapeutics. Studies have implicated the Neuregulin Signaling Pathway in the pathophysiology of a number of psychiatric illnesses. Additionally, recent studies have also shown an association between the Neuregulin Signaling Pathway and smoking behaviors. This review outlines basic mechanisms of the Neuregulin Signaling Pathway and how it may be exploited for precision medicine approaches in treating nicotine dependence and mental illness.
  • Kraus, Christoph; Castrén, Eero; Kasper, Siegfried; Lanzenberger, Rupert (2017)
    Serotonin modulates neuroplasticity, especially during early life, and dysfunctions in both systems likewise contribute to pathophysiology of depression. Recent findings demonstrate that serotonin reuptake inhibitors trigger reactivation of juvenile-like neuroplasticity. How these findings translate to clinical antidepressant treatment in major depressive disorder remains unclear. With this review, we link preclinical with clinical work on serotonin and neuroplasticity to bring two pathophysiologic models in clinical depression closer together. Dysfunctional developmental plasticity impacts on later-life cognitive and emotional functions, changes of synaptic serotonin levels and receptor levels are coupled with altered synaptic plasticity and neurogenesis. Structural magnetic resonance imaging in patients reveals disease-state-specific reductions of gray matter, a marker of neuroplasticity, and reversibility upon selective serotonin reuptake inhibitor treatment. Translational evidence from magnetic resonance imaging in animals support that reduced densities and sizes of neurons and reduced hippocampal volumes in depressive patients could be attributable to changes of serotonergic neuroplasticity. Since ketamine, physical exercise or learning enhance neuroplasticity, combinatory paradigms with selective serotonin reuptake inhibitors could enhance clinical treatment of depression. (C) 2017 Elsevier Ltd. All rights reserved.
  • Santangeli, Olena; Porkka-Heiskanen, Tarja; Virkkala, Jussi; Castaneda, Anu E.; Marttunen, Mauri; Paunio, Tiina; Urrila, Anna S. (2017)
    Objective: Adolescence is a vulnerable period of life that is characterized by increasing incidence of depression. Sleep disturbance is one of the diagnostic symptoms of depressive disorder. Adolescence is also characterized by dramatic maturational changes in sleep and its regulation. The goal of this study was to assess sleep macroarchitecture and slow-wave activity (SWA) in depressed adolescent boys. Methods: Eight non-medicated adolescent boys meeting the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria for depressive disorder and 10 age-matched healthy controls (average age 16.0 years) underwent polysomnography in their home environment for two consecutive nights. Sleep macroarchitecture, SWA, and SWA dissipation were assessed in all subjects. Results: Depressed boys showed a flattened pattern of SWA dissipation through the night. SWA power was lower during the first non-rapid eye movement (NREM) episode in the frontal derivation and higher during the third NREM episode in the central derivation in the group of depressed boys as compared to healthy boys. The SWA dissipation pattern correlated with the severity of depressive symptoms, and the correlation was strongest in the frontal derivation. In addition, total sleep time was shorter in patients as compared to the control group, but no other differences were found in the macroarchitecture of sleep. Conclusion: Depression in adolescent boys is characterized by more evenly distributed SWA through the night as compared to healthy subjects, and we showed for the first time that this pattern of SWA distribution is associated with severity of depressive symptoms. These findings suggest that homeostatic regulation of sleep may be impaired in adolescent depression. (C) 2017 Elsevier B.V. All rights reserved.
  • Urrila, Anna S.; Karlsson, Linnea; Kiviruusu, Olli; Pankakoski, Maiju; Pelkonen, Mirjami; Strandholm, Thea; Marttunen, Mauri; Adolescent Depression Study Grp (2014)
  • Levola, Jonna; Pitkanen, Tuuli; Kampman, Olli; Aalto, Mauri (2018)
    To compare the associations of alcohol-related variables with Quality of Life (QoL) in depressed and non-depressed individuals of the general population. This cross-sectional study utilized data from the FINRISK 2007 general population survey. A subsample (n = 4020) was invited to participate in an interview concerning alcohol use. Of them, 2215 (1028 men, 1187 women; response rate 55.1%) were included in the analyses. Bivariate associations between mean weekly alcohol consumption, frequency of binge drinking, Alcohol Use Disorders Identification Test (AUDIT)-score and QoL were analysed according to categorization into depressed and non-depressed using the Beck Depression Inventory, Short Form. Linear regression models were calculated in order to determine the associations of the alcohol variables and QoL after adjusting for socio-demographic variables as well as somatic and mental illness. Depressed individuals had lower mean QoL and higher AUDIT-scores than non-depressed respondents. Bivariate correlations showed that mean weekly alcohol consumption, frequency of binge drinking and AUDIT-scores were statistically significantly associated with impaired QoL in depressed individuals. Abstinence was not associated with QoL. After adjustment for covariates, frequency of binge drinking and AUDIT-score were statistically significantly associated with QoL in depressed individuals and AUDIT-score in the non-depressed group. When analysing all respondents regardless of depression, both AUDIT-score and binge drinking were associated with QoL. Of the alcohol-related variables, binge drinking and alcohol problems indicated by AUDIT-score contributed to impaired QoL in depressed individuals and both should be assessed as part of the clinical management of depression.
  • Saarinen, Aino; Hintsanen, Mirka; Hakulinen, Christian; Pulkki-Råback, Laura; Lehtimäki, Terho; Raitakari, Olli; Keltikangas-Järvinen, Liisa (2018)
    Background: The aim of this study was to examine longitudinally in the general population (a) whether depressive symptoms co-occur with paranoid ideation from late adolescence to middle age (b) whether depressive subsymptoms are differently linked with paranoid ideation (c) whether depressive symptoms are associated with state-level or trait-level paranoid ideation. Methods: Altogether 2109 subjects of the Young Finns study completed the Paranoid Ideation Scale of the Symptom Checklist-90 Revised and a modified version of the Beck Depression Inventory in 1992, 1997, 2001, 2007, and 2012, and the Beck Depression Inventory-II in 2007, 2011, and 2012. Results: Higher self-rated depressive symptoms were associated with the course of more severe paranoid ideation over age, especially in late adolescence and early adulthood. Regarding depressive subsymptoms, the associations of negative attitude and performance difficulties with paranoid ideation were evident over age, whereas the influence of somatic symptoms (such as changes in sleep and appetite) was not significant until after early adulthood. Additionally, depressive symptoms were more evidently associated with the development of traitthan state-level paranoid ideation. Limitations: Our study mostly captured mild depressive and paranoid symptoms. The results cannot be directly generalized to clinical populations. Conclusions: Depressive symptoms were associated with the course of paranoid ideation from late adolescence to middle age. Patients with paranoid ideation might merit from evaluation of potential depressive symptoms, especially in late adolescence and early adulthood. Among patients with co-occurring depressive symptoms and paranoid ideation, there may be a substantial need for neurocognitive rehabilitation and community-based treatments.
  • Elovainio, Marko; Vahtera, Jussi; Pentti, Jaana; Hakulinen, Christian; Pulkki-Råback, Laura; Lipsanen, Jari; Virtanen, Marianna; Keltikangas-Järvinen, Liisa; Kivimäki, Mika; Kähönen, Mika; Viikari, Jorma; Lehtimäki, Terho; Raitakari, Olli (2020)
    The association between socioeconomic disadvantage and increased risk of depressive symptoms in adulthood is well established. We tested 1) the contribution of early exposure to neighborhood socioeconomic disadvantage to later depressive symptoms throughout life, 2) the persistence of the potential association between early exposure and depressive symptoms, and 3) the contributions of other known risk factors to the association. Data were collected from the Young Finns Study, a prospective, population-based 32-year follow-up study that included participants aged 3-18 years at baseline in 1980. Participants were followed up with repeated measurements of depressive symptoms between 1992 and 2012 (n = 2,788) and linked to national grid data on neighborhood disadvantage via residential addresses. We examined the associations in mixed models separately for the 5-, 10-, 15-, and 20-year follow-ups. Living in a disadvantaged neighborhood during childhood and adolescence was associated with a higher level of depressive symptoms in adulthood during all follow-up periods (beta = 0.07, P = 0.001) than living in a nondisadvantaged area. Individual adulthood socioeconomic status mediated the associations. These findings suggest that living in a socioeconomically disadvantaged area during childhood and adolescence has a long-lasting negative association with mental health irrespective of family-related risks, partially due to socioeconomic adversity later in life.