scholarly journals Childhood Trauma and Trajectories of Depressive Symptoms Across Adolescence

Author(s):  
Alex S. F. Kwong ◽  
Jennifer M. Maddalena ◽  
Jazz Croft ◽  
Jon Heron ◽  
George Leckie

AbstractBackgroundGrowth curve modelling such as trajectory analysis is useful for examining the longitudinal nature of depressive symptoms, their antecedents and later consequences. However, issues in interpretation associated with this methodology could hinder the translation from results to policy changes and interventions. The aim of this article is to provide a “model interpretation framework” for highlighting growth curve results in a more interpretable manner. Here we demonstrate the association between childhood trauma and trajectories of depressive symptoms. Childhood trauma has been shown to a be strong predictor for later depression, but less is known how childhood trauma has an effect throughout adolescence and young adulthood. Identifying when childhood trauma (and its severity) is likely to have its greatest impact on depression is important for determining the timing of interventions for depression.MethodsWe used data on over 6,500 individuals from the Avon Longitudinal Study of Parents and Children (ALSPAC) to estimate trajectories of depressive symptoms between the ages of 11 and 24. Depressive symptoms were measured using the short mood and feelings questionnaire (SMFQ) across 9 occasions. Childhood trauma was assessed between the ages of 5 and 10 years old, and we estimated population averaged multilevel growth curves of depressive symptoms for exposure to trauma (yes vs no) and then in a separate model, the number of trauma types reported such as inter-personal violence or neglect (coded as 0, 1, 2, 3+). We then calculated what the depressive symptoms scores would be ages 12, 14, 16, 18, 20, 22, 24, between these varying trajectories.ResultsReported exposure to childhood trauma was associated with less favourable trajectories of depressive symptoms across adolescence, mainly characterised by exposed individuals having worse depressive symptoms at age 16. There was an exposure-response relationship between the number of childhood traumas and trajectories of depressive symptoms.Individuals exposed to 3 or more types of trauma had substantially steeper and less favourable trajectories of depressive symptoms: becoming worse at a more rapid rate until the age of 18. By age 18, individuals that reported the greatest exposure to trauma (3+ types of trauma) had 14% more depressive symptoms compared to non-exposed participants.LimitationsThis study was subject to attrition, particularly towards the latter ages of the SMFQ.ConclusionChildhood trauma is strongly associated with less favourable trajectories of depressive symptoms across adolescence. Individuals exposed to multiple types of inter-personal violence or neglect are at the greatest risk of worsening depressive symptoms throughout adolescence and young adulthood. Individuals exposed to traumatic experiences in childhood should be identified as at high risk of depression and other adverse outcomes as early trauma may disrupt social development and have lasting consequences on mental health outcomes.The model interpretation framework presented here may be more interpretable for researchers, clinicians and policy makers as it allows comparisons of depression across multiple stages of development to highlight when the effects of depression are greatest.

Author(s):  
Alex S. F. Kwong ◽  
Tim T. Morris ◽  
Rebecca M. Pearson ◽  
Nicholas J. Timpson ◽  
Frances Rice ◽  
...  

AbstractAdolescence marks a period where depression will commonly onset and previous research using twin studies has suggested that genetic influences play a role in how depression develops and changes across adolescence. Recent genome-wide association studies have also shown that common genetic variants – which can be combined into a polygenic risk score (PRS) – are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine the association between a PRS for depressive symptoms and depressive symptoms across adolescence and young adulthood, and how polygenic risk is associated with changes in depressive symptoms using two methods: cross-sectional analysis and multilevel growth curve modelling to examine the rate of change over time. Using data from over 6000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) we examined associations between genetic liability to depressive symptoms (PRS for depressive symptoms) and self-reported depressive symptoms (short mood and feelings questionnaire over 9 occasions from 10-24 years). We examined cross-sectional associations at each age and longitudinal trajectories of depressive symptoms in a repeated measures framework using growth curve analysis. The PRS was associated with depressive symptoms throughout adolescence and young adulthood in cross-sectional and growth curve analyses, though associations were stronger in the latter analyses. Growth curve analyses also provided additional insights, demonstrating that individuals with a higher PRS had steeper trajectories of depressive symptoms across adolescence with a greater increasing rate of change. These results show that common genetics variants as indexed by a PRS for depressive symptoms influence both the severity and rate of change in adolescent depressive symptoms. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights into the factors that influence the onset and persistence of adolescent depression.


2006 ◽  
Vol 189 (5) ◽  
pp. 422-427 ◽  
Author(s):  
Jennifer Y. F. Lau ◽  
Thalia C. Eley

BackgroundDepression rises markedly in adolescence, a time when increased and new genetic influences have been reported.AimsTo examine ‘new’ and ‘stable’ genetic and environmental factors on depressive symptoms in adolescence and young adulthood.MethodA questionnaire survey investigated a sample of twin and sibling pairs at three time points over an approximately 3-year period. Over 1800 twin and sibling pairs reported depressive symptoms at the three time points. Data were analysed using multivariate genetic models.ResultsDepressive symptoms at all time points were moderately heritable with substantial non-shared environmental contributions. Wave I genetic factors accounted for continuity of symptoms at waves 2 and 3. ‘New’ genetic effects at wave 2 also influenced wave 3 symptoms. New non-shared environmental influences emerged at each time point.ConclusionsNew genetic and environmental influences may explain age-related increases in depression across development.


2018 ◽  
Vol 54 (5) ◽  
pp. 950-962 ◽  
Author(s):  
Lotte van Doeselaar ◽  
Theo A. Klimstra ◽  
Jaap J. A. Denissen ◽  
Susan Branje ◽  
Wim Meeus

2016 ◽  
Vol 183 (4) ◽  
pp. 269-276 ◽  
Author(s):  
Shakira F. Suglia ◽  
Ryan T. Demmer ◽  
Richa Wahi ◽  
Katherine M. Keyes ◽  
Karestan C. Koenen

2021 ◽  
Author(s):  
Iryna Culpin ◽  
Hein Heuvelman ◽  
Dheeraj Rai ◽  
Rebecca M Pearson ◽  
Carol Joinson ◽  
...  

Background: High prevalence of parental separation and resulting biological father absence raises important questions regarding its impact on offspring mental health across the life course. However, few studies have examined prospective associations between biological father absence in childhood and risk of offspring depression and depressive symptoms trajectories across adolescence and young adulthood. We specifically examined whether these relationships vary by sex and the timing of exposure to father absence (early or middle childhood). Methods: This study is based on up to 8,409 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Participants provided self-reports of depression (Clinical Interview Schedule-Revised) at age 24 years and depressive symptoms (Short Mood and Feelings Questionnaire) between the ages of 10 and 24 years. Biological father absence in childhood was assessed through maternal questionnaires at regular intervals from birth to 10 years. We used logistic regression to examine the association between biological father absence and depression/depressive symptoms at age 24. We estimated the association between biological father absence and trajectories of depressive symptoms using multilevel growth-curve modelling. Results: Early but not middle childhood father absence was strongly associated with increased odds of offspring depression and greater depressive symptoms at age 24 years. Early childhood father absence was associated with higher trajectories of depressive symptoms during adolescence and early adulthood compared with father presence. Differences in the level of depressive symptoms between middle childhood father absent and father present groups narrowed into early adulthood. Girls whose father was absent in early childhood, compared with present, manifested higher levels of depressive symptoms throughout adolescence, but this difference narrowed by early adulthood. In contrast, boys who experienced father absence in early childhood had similar trajectories of depressive symptoms compared to the father present group but experienced a steep increase in early adulthood. Girls whose fathers were absent in middle childhood manifested higher trajectories across middle adolescence into young adulthood compared to the father present group. Conclusions: We found evidence that father absence in childhood is persistently associated with offspring depression in adolescence and early adulthood and that this relationship varies by sex and timing of father's departure. Further research is needed to examine whether this relationship is causal and to identify mechanisms that could inform preventative interventions to reduce the risk of depression in children who experience father absence.


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