1. Objectifs

Intentions :
«The present study aimed to document longitudinal contributions between AS [anxiety symptoms] and DS [depressive symptoms], and their genetic/environmental underpinnings from ages 6 to 12 years.» (p. 105)

Questions/Hypothèses :
«We predicted that AS and DS would share genetic and unique environmental factors but no shared environment factors at each time point and that they would both be moderately and increasingly stable through elementary school years. We also predicted both a positive contribution from previous AS to subsequent DS and previous DS to subsequent AS contributions through genetic and unique environmental influences.» (p. 113)

2. Méthode

Échantillon/Matériau :
«Data come from a longitudinal twin study of child development, the Quebec Newborn Twin Study (QNTS; Boivin et al. 2012), which conducted quasi-annual assessments on a range of individual, social, family, and school characteristics in 1324 twins (662 families). Parents of all twins born in the Greater Montreal area between April 1995 and December 1998 were identified through birth records and invited by letter or phone to participate. Among the 989 families contacted, 662 agreed to participate.» (p. 107)

Instruments :
Questionnaire

Type de traitement des données :
Analyse statistique

3. Résumé

«Results [showed] substantial discontinuity in AS and DS during middle childhood, especially in early AS. Previous time points accounted for, at best, 14% and 20% respectively of subsequent DS and AS. Though AS and DS were moderately heritable at onset, there was substantial genetic and unique environmental innovation at each time point while shared environment factors were negligible. As predicted, their etiological features substantially overlapped at onset as did their genetic innovations at subsequent time points. Yet, AS and DS also showed distinct etiological features throughout this period. More importantly, their developmental patterns were different: DS were moderately stable through both genetic and unique environmental influences that span across adjacent time points, whereas AS were mainly predicted by previous DS and their shared etiological features in the early half of middle childhood. Thereafter, AS became stable mainly through genetic factors that span the later years. Finally, and partly in line with our hypothesis, results indicated the presence of temporal sequences between AS and DS up to age 10 years, whereby previous DS increased subsequent AS throughout this period through common genes and unique experiences, and previous levels of AS marginally contributed to subsequent levels of DS from age 7 years onward, only through common genes.» (p. 113)