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Vadlin, S., Åslund, C. & Nillson, K. W. (2018). A longitudinal study of the individual- and group-level problematic gaming and associations with problem gambling among Swedish adolescents. Brain and Behavior, 8(4), Article ID e00949.
Open this publication in new window or tab >>A longitudinal study of the individual- and group-level problematic gaming and associations with problem gambling among Swedish adolescents
2018 (English)In: Brain and Behavior, ISSN 2162-3279, E-ISSN 2162-3279, Vol. 8, no 4, article id e00949Article in journal (Refereed) Published
Abstract [en]

Aim:  The aims of the present study were to investigate the long-term stability of problematic gaming among adolescents and whether problematic gaming at wave 1 (W1) was associated with problem gambling at wave 2 (W2), three years later.

Methods:  Data from the SALVe cohort, including adolescents in Västmanland born in 1997 and 1999, were accessed and analyzed in two waves W2, N = 1576; 914 (58%) girls). At W1 the adolescents were 13 and 15 years old, and at W2 they were 16 and 18 years old. Adolescents self-rated on the Gaming Addiction Identification Test (GAIT), Problem Gambling Severity Index (PGSI), and gambling frequencies. Stability of gaming was determined using Gamma correlation, Spearman’s rho, and McNemar. Logistic regression analysis and General linear model (GLM) analysis were performed and adjusted for sex, age, and ethnicity, frequency of gambling activities and gaming time at W1, with PGSI as the dependent variable, and GAIT as the independent variable, to investigate associations between problematic gaming and problem gambling.

Results:  Problematic gaming was relative stable over time, g = 0.739, P £ 0.001, r = 0.555, P £ 0.001, and McNemar P £ 0.001. Furthermore, problematic gaming at W1 increased the probability of having problem gambling three years later, logistic regression OR = 1.886 (95% CI 1.125-3.161), P = 0.016, GLM F = 10.588, h2 = 0.007, P = 0.001.  

Conclusions: Problematic gaming seems to be relatively stable over time. Although associations between problematic gaming and later problem gambling were found, the low explained variance indicate that problematic gaming in an unlikely predictor for problem gambling within this sample.

Keywords
Adolescence, behavioral addiction, comorbidity, gaming problems, gambling problems
National Category
Substance Abuse Psychology
Research subject
Psychiatry
Identifiers
urn:nbn:se:uu:diva-352513 (URN)10.1002/brb3.949 (DOI)000429700300014 ()
Projects
SALVe Cohort
Funder
Fredrik och Ingrid Thurings StiftelseForte, Swedish Research Council for Health, Working Life and Welfare, 2015-00897Åke Wiberg Foundation, M15-0239
Available from: 2018-06-05 Created: 2018-06-05 Last updated: 2018-06-08Bibliographically approved
Larm, P., Åslund, C., Raninen, J. & Nilsson, K. W. (2018). Adolescent non-drinkers: Who are they? Social relations, school performance, lifestyle factors and health behaviours. Drug and Alcohol Review, 37(S1), S67-S75
Open this publication in new window or tab >>Adolescent non-drinkers: Who are they? Social relations, school performance, lifestyle factors and health behaviours
2018 (English)In: Drug and Alcohol Review, ISSN 0959-5236, E-ISSN 1465-3362, Vol. 37, no S1, p. S67-S75Article in journal (Refereed) Published
Abstract [en]

Introduction and Aims

Traditionally, non-drinking adults or young adults have been associated with health deficits rather than health benefits. However, as the proportion of Swedish non-drinking adolescents has doubled since 2000, their health profiles are of interest. The aim of the present study is to examine whether social relations, school characteristics, lifestyle factors or health behaviours distinguish adolescent non-drinkers from adolescent drinkers, and if their health profiles have changed from 2004 to 2012.

Design and Methods

Data from the Survey of Adolescent Life in Vestmanland, a health survey biennially distributed to all 9th graders (15-16years) in a medium-sized Swedish county, was used. In total, 2872 students in 2004 and 2045 students in 2012 were included.

Results

Non-drinkers were distinguished from drinkers in both 2004 and 2012 by elevated parental supervision, a lower rate of school truancy and lower rates of cannabis use, use of other illicit drugs, daily smoking and lower scores on antisocial behaviour, but more problems of getting new friends. No differences between 2004 and 2012 were found.

Discussion and Conclusions

Non-drinkers presented more adaptive and healthier behaviours than their drinking peers, but it is difficult to determine whether their health benefits were related to their improved alcohol status or to the more general trend towards adaptation that occurred from 2004 to 2012 among adolescents.

Place, publisher, year, edition, pages
WILEY, 2018
Keywords
adolescence, alcohol, non-drinkers, health
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:uu:diva-356810 (URN)10.1111/dar.12640 (DOI)000431986800009 ()29218748 (PubMedID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2015-00857Forte, Swedish Research Council for Health, Working Life and Welfare, 2015-00897Forte, Swedish Research Council for Health, Working Life and WelfareThe Swedish Brain Foundation
Available from: 2018-08-16 Created: 2018-08-16 Last updated: 2018-08-16Bibliographically approved
Bendre, M., Comasco, E., Checknita, D., Tiihonen, J., Hodgins, S. & Nillson, K. W. (2018). Associations Between MAOA-uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males. Alcoholism: Clinical and Experimental Research, 42(3), 508-519
Open this publication in new window or tab >>Associations Between MAOA-uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males
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2018 (English)In: Alcoholism: Clinical and Experimental Research, ISSN 0145-6008, E-ISSN 1530-0277, Vol. 42, no 3, p. 508-519Article in journal (Refereed) Published
Abstract [en]

Background

Epigenetic mechanisms are candidate moderators of the effect of maltreatment on brain and behavior. Interactions between maltreatment and the monoamine oxidase A upstream variable number tandem repeat genotype (MAOA-uVNTR) are associated with alcohol-related problems. However, presently it is not known whether DNA methylation moderates this association. The study focused on 53 young adult males and aimed to determine whether MAOA methylation moderated the association of alcohol-related problems with the interaction of MAOA-uVNTR and maltreatment, and whether alcohol consumption moderated the association of MAOA methylation with the interaction of MAOA-uVNTR and maltreatment.

Methods

MAOA-uVNTR genotypes with 3 and > 3 repeats were categorized as short (S) and long (L), respectively. Data on maltreatment were obtained retrospectively, using self-reported questionnaires. DNA methylation of 16 candidate CpGs within part of the MAOA first exon and intron was assessed and grouped based on principal component analyses. Alcohol-related problems were assessed using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol consumption was measured using AUDIT-C. Moderation effects were assessed and probed using the moderated moderation model and Johnson-Neyman's method, respectively.

Results

Carriers of the S allele, who experienced maltreatment and displayed lower Component 1 (mean of CpGs 13-16 in the first intron) MAOA methylation levels, reported higher AUDIT score in contrast to L-allele carriers. Carriers of the S allele, who reported higher AUDIT-C score and experienced maltreatment, displayed lower Component 3 (mean of CpGs 2-6 in the first exon) MAOA methylation levels than L-allele carriers.

Conclusions

Intronic methylation moderated the association of alcohol-related problems with the interaction of MAOA-uVNTR and maltreatment. Alcohol consumption moderated the association of exonic methylation with the interaction of MAOA-uVNTR and maltreatment. These results suggest that epigenetic factors as well as genotype and maltreatment play a role in the development of alcohol misuse among young adult males.

Keywords
Alcohol, DNA Methylation, Gene by Environment, MAOA-, uVNTR, Maltreatment
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-351264 (URN)10.1111/acer.13578 (DOI)000426489600005 ()29222910 (PubMedID)
Funder
Swedish Research Council, VR: 2015-00495
Available from: 2018-06-11 Created: 2018-06-11 Last updated: 2018-06-11Bibliographically approved
Checknita, D., Ekström, T. J., Comasco, E., Nilsson, K. W., Tiihonen, J. & Hodgins, S. (2018). Associations of monoamine oxidase A gene first exon methylation with sexual abuse and current depression in women. Journal of neural transmission, 125(7), 1053-1064
Open this publication in new window or tab >>Associations of monoamine oxidase A gene first exon methylation with sexual abuse and current depression in women
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2018 (English)In: Journal of neural transmission, ISSN 0300-9564, E-ISSN 1435-1463, Vol. 125, no 7, p. 1053-1064Article in journal (Refereed) Published
Abstract [en]

Childhood physical abuse (PA) and sexual abuse (SA) interact with monoamine oxidase A (MAOA) gene polymorphism to modify risk for mental disorders. In addition, PA and SA may alter gene activity through epigenetic mechanisms such as DNA methylation, thereby further modifying risk for disorders. We investigated whether methylation in a region spanning the MAOA first exon and part of the first intron was associated with PA and/or SA, MAOA genotype, alcohol dependence, drug dependence, depression disorders, anxiety disorders, and conduct disorder. 114 Swedish women completed standardized diagnostic interviews and questionnaires to report PA and SA, and provided saliva samples for DNA extraction. DNA was genotyped for MAOA-uVNTR polymorphisms, and methylation of a MAOA region of interest (chrX: 43,515,544-43,515,991) was measured. SA, not PA, was associated with hypermethylation of the MAOA first exon relative to no-abuse, and the association was robust to adjustment for psychoactive medication, alcohol and drug dependence, and current substance use. SA and MAOA-uVNTR genotype, but not their interaction, was associated with MAOA methylation. SA associated with all measured mental disorders. Hypermethylation of MAOA first exon mediated the association of SA with current depression, and both methylation levels and SA independently predicted lifetime depression. Much remains to be learned about the independent effects of SA and MAOA-uVNTR genotypes on methylation of the MAOA first exon.

Place, publisher, year, edition, pages
SPRINGER WIEN, 2018
Keywords
Child abuse, Depression, Epigenetics, Gene-environment interaction methylation, Women
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-358274 (URN)10.1007/s00702-018-1875-3 (DOI)000435405600006 ()29600412 (PubMedID)
Funder
Forte, Swedish Research Council for Health, Working Life and WelfareStockholm County CouncilThe Karolinska Institutet's Research Foundation
Available from: 2018-08-30 Created: 2018-08-30 Last updated: 2018-08-30Bibliographically approved
Culverhouse, R. C., Saccone, N. L., Horton, A. C., Ma, Y., Anstey, K. J., Banaschewski, T., . . . Bierut, L. J. (2018). Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression. Molecular Psychiatry, 23(1), 133-142
Open this publication in new window or tab >>Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression
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2018 (English)In: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 23, no 1, p. 133-142Article in journal (Refereed) Published
Abstract [en]

The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.

National Category
Occupational Health and Environmental Health Psychiatry Neurology Neurosciences Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-346381 (URN)10.1038/mp.2017.44 (DOI)000423441000016 ()28373689 (PubMedID)
Funder
Wellcome trust, 102215/2/13/2German Research Foundation (DFG), LA 733/2-1; DA1151/5-1NIH (National Institute of Health), R01 AA07065; NIH R01; HD042157-01A1; MH081802; 1RC2 MH089951; 1RC2 MH089995EU, European Research Council, EU-FP7HEALTH-F2-2008-222963Åke Wiberg Foundation, M15-0239European Science Foundation (ESF)
Available from: 2018-03-23 Created: 2018-03-23 Last updated: 2018-03-23Bibliographically approved
Pettersson, R., Söderström, S. & Nilsson, K. W. (2018). Diagnosing ADHD in Adults: An Examination of the Discriminative Validity of Neuropsychological Tests and Diagnostic Assessment Instruments. Journal of Attention Disorders, 22(11), 1019-1031
Open this publication in new window or tab >>Diagnosing ADHD in Adults: An Examination of the Discriminative Validity of Neuropsychological Tests and Diagnostic Assessment Instruments
2018 (English)In: Journal of Attention Disorders, ISSN 1087-0547, E-ISSN 1557-1246, Vol. 22, no 11, p. 1019-1031Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: The objective of this study is to investigate the discriminative validity of neuropsychological tests and diagnostic assessment instruments in diagnosing adult ADHD in a clinical psychiatric population.

METHOD: Of 108 patients, 60 were diagnosed with ADHD. The Diagnostic Interview for ADHD in adults (DIVA 2.0) and Adult ADHD Self-Report Scale (ASRS) v.1.1 together with eight neuropsychological tests were investigated.

RESULTS: All instruments showed poor discriminative ability except for the DIVA, which showed a relatively good ability to discriminate between the groups (sensitivity = 90.0; specificity = 72.9). A logistic regression analysis model with the DIVA and measures of inattention, impulsivity, and activity from continuous performance tests (CPTs) showed a sensitivity of 90.0 and a specificity of 83.3.

CONCLUSION: Neuropsychological tests have a poor ability to discriminate between patients diagnosed with ADHD and patients not diagnosed with ADHD, but variables from CPT tests can contribute to increasing the specificity by 10% if used in combination with the DIVA.

National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-281763 (URN)10.1177/1087054715618788 (DOI)000441402600001 ()26681530 (PubMedID)
Funder
The Swedish Brain Foundation
Available from: 2016-03-30 Created: 2016-03-30 Last updated: 2018-10-23Bibliographically approved
Torres Soler, C., Olofsdotter, S., Vadlin, S., Ramklint, M., Nilsson, K. W. & Sonnby, K. (2018). Diagnostic accuracy of the Montgomery-Åsberg Depression Rating Scale parent report among adolescent psychiatric outpatients. Nordic Journal of Psychiatry, 72(3), 184-190
Open this publication in new window or tab >>Diagnostic accuracy of the Montgomery-Åsberg Depression Rating Scale parent report among adolescent psychiatric outpatients
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2018 (English)In: Nordic Journal of Psychiatry, ISSN 0803-9488, E-ISSN 1502-4725, Vol. 72, no 3, p. 184-190Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The diagnostic accuracy of the parent report of the Montgomery-Åsberg Depression Rating Scale (MADRS-P) for the screening of major depressive disorder (MDD) in adolescents has not been evaluated.

AIM: The aim was to explore the psychometric properties and diagnostic accuracy of the MADRS-P in general child and adolescent psychiatric outpatient services in Sweden.

METHOD: The study was a validation and a diagnostic accuracy study. Consecutive adolescent psychiatric patients (n = 101, 45 males, mean age 15 years) were assessed with a diagnostic interview, the Kiddie Schedule of Affective Disorders and Schizophrenia for School-Age Children - Present and Lifetime version (K-SADS-PL), as a reference test. Thereafter, their parents reported on the MADRS-P. Both categorical MDD diagnoses and dimensional MDD symptom severity scores were obtained from the K-SADS-PL.

RESULTS: The internal consistency of the MADRS-P, measured with Cronbach's alpha, was 0.846. The concurrent validity, assessed by Spearman's rho as a correlation between the K-SADS MDD symptom severity score and the MADRS-P score, was 0.580. The area under the curve in a receiver operating characteristic analysis for all participants was 0.786 (95% confidence interval 0.694-0.877, p < .001). At a cut-off of 10, sensitivity was 0.86, specificity 0.54, positive predictive value 0.59 and negative predictive value 0.84.

CONCLUSIONS: The parent-rated MADRS-P showed similar psychometric properties as previously shown for the self-rated MADRS-S in adults. Although the MADRS-P has acceptable diagnostic accuracy for screening for MDD in adolescents in a general psychiatric setting, it cannot be used alone for diagnosing MDD.

Place, publisher, year, edition, pages
Taylor & Francis Group, 2018
Keywords
Depression, adolescents, parents, questionnaire, validation study
National Category
Clinical Medicine
Research subject
Psychiatry
Identifiers
urn:nbn:se:uu:diva-342265 (URN)10.1080/08039488.2017.1414873 (DOI)000424948600005 ()29258381 (PubMedID)
Available from: 2018-02-19 Created: 2018-02-19 Last updated: 2018-04-10Bibliographically approved
Olofsdotter, S., Åslund, C., Furmark, T., Comasco, E. & Nilson, K. W. (2018). Differential susceptibility effects of oxytocin gene (OXT)polymorphisms and perceived parenting on social anxiety among adolescents. Development and psychopathology (Print), 30(2), 449-459
Open this publication in new window or tab >>Differential susceptibility effects of oxytocin gene (OXT)polymorphisms and perceived parenting on social anxiety among adolescents
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2018 (English)In: Development and psychopathology (Print), ISSN 0954-5794, E-ISSN 1469-2198, Vol. 30, no 2, p. 449-459Article in journal (Refereed) Published
Abstract [en]

Social anxiety is one of the most commonly reported mental health problems among adolescents, and it has been suggested that parenting style influences an adolescent's level of anxiety. A context-dependent effect of oxytocin on human social behavior has been proposed; however, research on the oxytocin gene (OXT) has mostly been reported without considering contextual factors. This study investigated the interactions between parenting style and polymorphic variations in the OXT gene in association with social anxiety symptoms in a community sample of adolescents (n = 1,359). Two single nucleotide polymorphisms linked to OXT, rs4813625 and rs2770378, were genotyped. Social anxiety and perceived parenting style were assessed by behavioral questionnaires. In interaction models adjusted for sex, significant interaction effects with parenting style were observed for both variants in relation to social anxiety. The nature of the interactions was in line with the differential susceptibility framework for rs4813625, whereas for rs2770378 the results indicated a diathesis–stress type of interaction. The findings may be interpreted from the perspective of the social salience hypothesis of oxytocin, with rs4813625 affecting social anxiety levels along a perceived unsafe–safe social context dimension.

Place, publisher, year, edition, pages
New York: , 2018
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-323574 (URN)10.1017/S0954579417000967 (DOI)
Funder
Fredrik och Ingrid Thurings StiftelseThe Swedish Brain Foundation, F02015-0315Forte, Swedish Research Council for Health, Working Life and Welfare, FORTE 2015-00897Åke Wiberg Foundation, MI5-0239Swedish Research Council, VR 2015-00495EU, FP7, Seventh Framework Programme, INCA 600398
Available from: 2017-06-08 Created: 2017-06-08 Last updated: 2018-07-31Bibliographically approved
Nilsson, K. W., Åslund, C., Comasco, E. & Oreland, L. (2018). Gene-environment interaction of monoamine oxidase A in relation to antisocial behaviour: current and future directions.. Journal of neural transmission, 125(11), 1601-1626
Open this publication in new window or tab >>Gene-environment interaction of monoamine oxidase A in relation to antisocial behaviour: current and future directions.
2018 (English)In: Journal of neural transmission, ISSN 0300-9564, E-ISSN 1435-1463, Vol. 125, no 11, p. 1601-1626Article, review/survey (Refereed) Published
Abstract [en]

Since the pioneering finding of Caspi and co-workers in 2002 that exposure to childhood maltreatment predicted later antisocial behaviour (ASB) in male carriers of the low-activity MAOA-uVNTR allele, frequent replication studies have been published. Two meta-analyses, one in 2006 and the other in 2014, confirmed the original findings by Caspi and co-workers. In the present paper, we review the literature, note some methodological aspects of candidate gene–environment interaction (cG×E) studies and suggest some future directions. Our conclusions are as follows. (1) The direction of the effect in a cG×E model may differ according to the positive and negative environmental background of the population. (2) There is a predictor-intersection problem such that when measuring one type of maltreatment in a person, other kinds of maltreatment often co-occur. Other forms of abuse are implicitly considered in statistical models; therefore, it is difficult to draw conclusions about the effects of timing and the severity of different forms of stressful life events in relation to ASB. (3) There is also an outcome-intersection problem because of the major intersection of ASB and other forms of mental health problems. It is likely that the G×E with MAOA is related to a common unmeasured factor. (4) For the G×E model, in which the effect of the gene on the outcome variable is dependent on other predictor variables, theoretically, hypothesis-driven statistical modelling is needed.

Keywords
Antisocial personality disorder, Brunner syndrome, Conduct disorder, Genetic association studies, Genetic susceptibility, Gene–environment interaction, Juvenile delinquency, Monoamine oxidase A, Review
National Category
Psychiatry
Identifiers
urn:nbn:se:uu:diva-368637 (URN)10.1007/s00702-018-1892-2 (DOI)000449118500007 ()29881923 (PubMedID)
Funder
The Swedish Brain FoundationForte, Swedish Research Council for Health, Working Life and Welfare, 2015-00897Fredrik och Ingrid Thurings StiftelseStiftelsen Söderström - Königska sjukhemmet, SLS-559921; SLS-655791; SLS-745221Swedish Research Council, VR: 2015-00495EU, FP7, Seventh Framework Programme, INCA 600398Science for Life Laboratory - a national resource center for high-throughput molecular bioscience
Available from: 2018-12-06 Created: 2018-12-06 Last updated: 2019-01-08Bibliographically approved
Åslund, C. & Nilsson, K. W. (2018). Individual biological sensitivity to environmental influences: testing the differential susceptibility properties of the 5HTTLPR polymorphism in relation to depressive symptoms and delinquency in two adolescent general samples. Journal of neural transmission, 125(6), 977-993
Open this publication in new window or tab >>Individual biological sensitivity to environmental influences: testing the differential susceptibility properties of the 5HTTLPR polymorphism in relation to depressive symptoms and delinquency in two adolescent general samples
2018 (English)In: Journal of neural transmission, ISSN 0300-9564, E-ISSN 1435-1463, Vol. 125, no 6, p. 977-993Article in journal (Refereed) Published
Abstract [en]

The gene-environment interaction research field in psychiatry has traditionally been dominated by the diathesis-stress framework, where certain genotypes are assumed to confer increased risk for adverse outcomes in a stressful environment. In later years, theories of differential susceptibility, or biological sensitivity, suggest that candidate genes that interact with environmental events do not exclusively confer a risk for behavioural or psychiatric disorders but rather seem to alter the sensitivity to both positive and negative environmental influences. The present study investigates the susceptibility properties of the serotonin transporter-linked polymorphic region (5HTTLPR) in relation to depressive symptoms and delinquency in two separate adolescent community samples: n = 1457, collected in 2006; and n = 191, collected in 2001. Two-, three-, and four-way interactions between the 5HTTLPR, positive and negative family environment, and sex were found in relation to both depressive symptoms and delinquency. However, the susceptibility properties of the 5HTTLPR were distinctly less pronounced in relation to depressive symptoms. If the assumption that the 5HTTLPR induces differential susceptibility to both positive and negative environmental influences is correct, the previous failures to measure and control for positive environmental factors might be a possible explanation for former inconsistent findings within the research field.

Keywords
Antisocial behaviour, Depression, Emotion regulation, Gene-environment interaction, Human, SERT, SLC6A4
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-357554 (URN)10.1007/s00702-018-1854-8 (DOI)000433116200010 ()29427067 (PubMedID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2015-00897Forte, Swedish Research Council for Health, Working Life and Welfare
Available from: 2018-08-17 Created: 2018-08-17 Last updated: 2018-08-17Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-8853-2508

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