To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The public health burden of alcohol is unevenly distributed across the life course, with levels of use, abuse, and dependence increasing across adolescence and peaking in early adulthood. Here, we leverage this temporal patterning to search for common genetic variants predicting developmental trajectories of alcohol consumption. Comparable psychiatric evaluations measuring alcohol consumption were collected in three longitudinal community samples (N = 2,126, obs = 12,166). Consumption-repeated measurements spanning adolescence and early adulthood were analyzed using linear mixed models, estimating individual consumption trajectories, which were then tested for association with Illumina 660W-Quad genotype data (866,099 SNPs after imputation and QC). Association results were combined across samples using standard meta-analysis methods. Four meta-analysis associations satisfied our pre-determined genome-wide significance criterion (FDR < 0.1) and six others met our ‘suggestive’ criterion (FDR <0.2). Genome-wide significant associations were highly biological plausible, including associations within GABA transporter 1, SLC6A1 (solute carrier family 6, member 1), and exonic hits in LOC100129340 (mitofusin-1-like). Pathway analyses elaborated single marker results, indicating significant enriched associations to intuitive biological mechanisms, including neurotransmission, xenobiotic pharmacodynamics, and nuclear hormone receptors (NHR). These findings underscore the value of combining longitudinal behavioral data and genome-wide genotype information in order to study developmental patterns and improve statistical power in genomic studies.
Previous studies have emphasized the importance of rater issues in studying the etiology of variation in internalizing and externalizing problems in children. Earlier results indicate only moderate agreement between parents, and assume that parents assess a specific aspect of their child's behavior. In comparable samples of younger children, additive genetic effects are the main factor explaining individual differences in both internalizing and externalizing behavior. It is unknown whether this pattern of rater influences and variance decomposition will be consistent in older children. Child Behavior Checklists (Achenbach, 1991), completed by both parents, were collected in a sample of 2956 Dutch 10-year-old twin pairs. The etiology of individual differences in internalizing and externalizing syndromes was examined using a model that corrected for possible rater bias, rater-specific effects and unreliability. The best fitting model suggested that disagreement between the parents is not merely the result of unreliability and/or rater bias, but each parent also provides specific information from his/her own perspective on the child's behavior. Significant influences of additive genetic, shared environmental and unique environmental factors were found for internalizing and externalizing syndromes.
The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course.
The last decades have shown a rapid increase in nonresponse rates. For this reason it is important to study nonresponse and think about it critically. In this article we investigated whether nonresponse affected estimates of the levels of adjustment problems in children and the correlations between these outcomes. The nonresponse was caused by parents who refused permission to interview their children at school, parents who did not return a questionnaire, teachers who did not complete the questionnaire, and parents who refused to participate in an in-depth study, with nonresponse rates of 9%, 69%, 25%, and 46% respectively. The sample consisted of 1282 children aged 4–5 years and the dependent measures were peer-rated sociometric status, self-rated wellbeing at school, and teacher-rated behaviour problems. Despite considerable nonresponse in some conditions our results showed hardly any evidence for bias. This suggested that bias cannot simply be inferred from the amount of nonresponse and that standard rules such as ‘‘nonresponse rates higher than 50% are not acceptable’’ lack a scientific basis. Instead, we argue that to assess nonresponse bias the specific conditions and analyses of the study will need to be considered and special measures may be required.
We examined differences between school classes with
respect to three aspects of psychosocial
adjustment at school, namely the extent that children in the class liked
to play with each
other, the number of teacher-reported behaviour problems, and children's
feelings of well-being at school. The sample consisted of 1282 4- to 5-year-olds from 94
school classes and
51 schools, but due to nonresponse actual sample sizes were somewhat smaller
analyses. Multilevel analyses showed that on average 87% of the variance
was at the child
level, 11% at the class level, and 3% at the school level. This indicated
that a non-negligible
amount of variance could not be accounted for by factors at the child level.
variance was mainly associated with differences between classes instead
between schools. A set of variables that pertained to sociodemographic
schools, school facilities, organisational aspects of classrooms, and the
teacher did not
provide an adequate explanation for the differences in adjustment levels.
In contrast to these
traditional variables, social network indices yielded substantial correlations,
consistent trends across the different adjustment measures, and fulfilled
requirement that to explain differences between school classes the predictor
themselves should differ for classes within the same school. These results
aspects of the interpersonal relations of children in the classroom such
integration, and the amount of contact could be determinants of differences
classes in psychosocial adjustment.
Email your librarian or administrator to recommend adding this to your organisation's collection.