Search

Parent engagement is an important aspect of parenting during childhood. However, little is known about the unique longitudinal associations of mother and father engagement with adolescents' externalizing and internalizing problem behaviors. This study uses Future of Families and Child Wellbeing Study data to examine the potential direct and indirect associations of parent engagement at age 9 on adolescent externalizing and internalizing behaviors at age 15. The analytic sample size is 1349, and at age 9, the mean age of children was 9.40 years (SD = 0.37). Forty-eight percent of children were female and 68% of them were from the married families. The results show that while controlling for mother engagement, higher father engagement at age 9 was directly associated with fewer adolescent internalizing behaviors, only among adolescent boys and in married families. In addition, among adolescent boys, father engagement had an indirect association with externalizing behaviors through father-child closeness. Mother engagement, however, is only found to have an indirect association with adolescents' externalizing and internalizing behaviors through maternal hostility (while controlling for father engagement). The results for mother engagement held for boys and in married families only. The findings indicate that both mother and father engagement during childhood is important and helpful to prevent adolescent problem behaviors directly or indirectly via parent-child relationship., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Studies that distinguish parental monitoring (parent-driven behaviors) from parental knowledge often fail to find protective effects of monitoring on adolescent behavior problems. To answer whether parental monitoring is more strongly associated with adolescent behavior problems among adolescents who may need it most, this study applied group-based trajectory modeling to change in early- to mid-adolescent aggressive behavior problems and examined associations between parental monitoring with different subgroups. Three latent groups of adolescents were found: Low Aggression, Medium-Increasing Aggression, and High-Increasing Aggression. Results show that more maternal and paternal monitoring were associated with fewer adolescent aggressive behavior problems only for adolescents in the High-Increasing Group. This result suggests that parental monitoring is a protective factor against adolescent aggressive behavior problems for subgroups of adolescents who may need it most and less impactful for other adolescents., Competing Interests: Declaration of Interest Statement: We have no known conflict of interest to disclose.

To understand whose parenting (mothers vs. fathers) and which type of parenting (warmth vs. hostility) is more important in predicting adolescent aggression, this study applied dominance analysis to evaluate the relative importance of four different parenting dimensions (maternal hostility, paternal hostility, maternal warmth, and paternal warmth). Four waves of adolescent-reported longitudinal data from the PROSPER project ( N = 626, 52% adolescent girls, 89% White rural, age 12 to 15) were used to investigate longitudinal change in the relative importance of these dimensions over time. Findings reveal that at most ages, maternal hostility was relatively more important than both paternal hostility and maternal warmth in predicting adolescent aggression among adolescent girls and boys. However, paternal parenting was more important for boys at specific ages. Findings are discussed in terms of implications for interventions and further research on parenting. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

This study using PROSPER data ( N = 977, age 11.5 to age 15) investigated the longitudinal within-family associations between parent-reported parental monitoring and adolescent aggression. Importantly, this study is the first one to examine parent gender and adolescent gender differences on these within-family associations. Results differed between mothers and fathers. There was a negative, bidirectional within-family association between maternal monitoring and adolescent aggression, such that more maternal monitoring than usual was associated with fewer adolescent aggressive behavior problems than usual within the same family, and vice versa. In contrast, during mid-adolescence, a positive, bidirectional within-family association between paternal monitoring and adolescent males' aggression was found, such that more paternal monitoring than usual was related to more adolescent males' aggression than usual within the same family, and vice versa. Practical implications on intervention strategies are discussed., Competing Interests: We have no known conflict of interest to disclose.

Differential susceptibility theory stipulates that individuals vary in their susceptibility to environmental effects, often implying that the same individuals differ in the same way in their susceptibility to different environmental exposures. The latter point is addressed herein by evaluating the extent to which early-life harshness and unpredictability affect mother's psychological well-being and parenting, as well as their adolescent's life-history strategy, as reflected in number of sexual partners by age 15 years, drawing on data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development. Results indicated that mothers whose well-being and parenting proved more susceptible to harshness also proved somewhat more susceptible to environmental unpredictability, with the same being true of adolescent sexual behavior. Nevertheless, findings caution against overgeneralizing sample-level findings to all individuals.

Recent developments in the application life history theory to human development indicate two fundamental dimension of the early environment - harshness and unpredictability - are key regulators life history strategies. Few studies have examined the manner with which these dimensions influence development, though age at menarche (AAM) and age at first sexual intercourse have been proposed as possible mechanisms among women. Data from the Avon Longitudinal Study of Parents and Children ( N = 3,645) were used to examine direct and indirect effects of harshness (financial difficulties) and unpredictability (paternal transitions) on lifetime and past year sexual partners during adolescence and young adulthood. Genetic confounding was addressed using an AAM polygenic score (PGS) and potential gene-by-environment interactions were also evaluated using the PGS. Path model results showed only harshness was directly related to AAM. Harshness, unpredictability, and AAM were indirectly related to lifetime and past year sexual partner number via age at first sexual intercourse. The PGS did not account for any of the associations and no significant interactions were detected. Implications of these results for developmental models derived from life history theory are discussed as well as the role of PGSs in gene-environment interplay research.

Father absence has a small but robust association with earlier age at menarche (AAM), likely reflecting both genetic confounding and an environmental influence on life history strategy development. Studies that have attempted to disambiguate genetic versus environmental contributions to this association have shown conflicting findings, though genomic-based studies have begun to establish the role of gene-environment interplay in the father absence/AAM literature. The purpose of this study was to replicate and extend prior genomic work using the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective longitudinal cohort study (N = 2,685), by (a) testing if an AAM polygenic score (PGS) could account for the father absence/AAM association, (b) replicating G×E research on lin-28 homolog B (LIN28B) variation and father absence, and (c) testing the G×E hypothesis using the PGS. Results showed that the PGS could not explain the father absence/AAM association and there was no interaction between father absence and the PGS. Findings using LIN28B largely replicated prior work that showed LIN28B variants predicted later AAM in father-present girls, but this AAM-delaying effect was absent or reversed in father-absent girls. Findings are discussed in terms genetic confounding, the unique biological role of LIN28B, and using PGSs for G×E tests.

Little is known about the developmental course of informant discrepancies in adolescent aggressive behavior problems, though whether aggression increases or decreases over time depends on reporter. Evaluating discrepancies longitudinally can uncover patterns of agreement/disagreement between reporters across time and determine contexts that give rise to these differences. This study addresses longitudinal informant discrepancies by examining parent-report and adolescent report of adolescent aggressive behavior problems over time and further investigates possible contextual factors related to the longitudinal discrepancy. Five-waves (from age 11.5 to 15) of multi-informant data from the PROSPER project (N = 977; 52% female; 87% Caucasian) were used to test longitudinal change in informant discrepancies between mother-, father-, and adolescent-reported aggressive behavior problems. Results showed that parents reported more aggression than their adolescents at age 11.5 and that the discrepancy at first converged over time before diverging. By age 15, adolescents reported more aggression than their parents. Parental hostility, family status, and adolescent gender predicted change in informant discrepancies. Practical and developmental implications are discussed for assessing and determining accurate change in adolescent aggressive behavior problems., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The most extensively studied influence on adolescent conduct problem behaviors is peers, and the literature points to genetics as one source of individual differences in peer influence. The purpose of this study was to test the hypothesis that an environmental sensitivity genetic index comprised of DRD4, 5-HTTLPR, and GABRA2 variation would moderate the association between peer and adolescent conduct problems. Latent growth modeling was applied to PROSPER project longitudinal data from adolescents and their peers. Results showed the hypothesis was supported; adolescents with more copies of putative sensitivity alleles were more strongly influenced by their peers. The interaction form was consistent with differential susceptibility in follow-up analyses. Strengths and weaknesses of genetic aggregates for sensitivity research are discussed., (© 2020 Society for Research on Adolescence.)

Guided by paternal investment theory (PIT), the current research examines the effects of fathers on daughters' expectations for men in adulthood, and the role of these expectations in mediating women's short-term (casual or uncommitted) sexual behavior. Using a genetically informed differential sibling-exposure design (N = 223 sister pairs from divorced/separated families), we found that developmental exposure to low-quality paternal behavior (but not paternal absence per se) predicted adult women's expectations for men as partners. For older sisters, who spent much of their childhoods living with their fathers, lower-quality paternal behavior predicted lower expectations for male investment in their relationships as adults. Moreover, lower expectations for men as partners predicted higher numbers of sexual partners (past and anticipated) among these women. By contrast, for younger sisters, who spent relatively little time coresiding with their fathers, no such effects of quality of paternal behavior were observed. The current work provides evidence that exposure to low-quality paternal behavior during development may help calibrate daughters' expectations for the behavior of male relationship partners, and these expectations may shape their sexual behavior in adulthood. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Better integrating human developmental factors in genomic research is part of a set of next steps for testing gene-by-environment interaction hypotheses. This study adds to this work by extending prior research using time-varying effect modeling (TVEM) to evaluate the longitudinal associations between the PROSPER preventive intervention delivery system, a GABRA2 haplotype linked to alcohol use, and their interaction on adolescent delinquency. Logistic and Poisson analyses on eight waves of data spanning ages 11 to 19 (60% female, 90% Caucasian) showed the intervention reduced delinquency from ages 13 to 16. Moreover, interaction analysis revealed that the effect of the multicomponent intervention was significantly greater for T-allele carriers of the GABRA2 SNP rs279845, but only during the 13 to 16 age period. The results are discussed in terms of adolescent delinquency normativeness, implications for preventive intervention research, and the utility of incorporating development in GxE research.

To illuminate which features of an unpredictable environment early in life best forecast adolescent and adult functioning, data from two longitudinal studies were examined. After decomposing a composite unpredictability construct found to predict later development, results of both studies revealed that paternal transitions predicted outcomes more consistently and strongly than did residential or occupational changes across the first 5 years of a child's life. These results derive from analyses of the NICHD Study of Early Child Care and Youth Development, which included diverse families from 10 different sites in the United States, and from the Minnesota Longitudinal Study of Risk and Adaptation, whose participants came from one site, were disproportionately economically disadvantaged, and were enrolled 15 years earlier than the NICHD Study sample. The finding that results from both studies are consistent with evolutionary, life history thinking regarding the importance of males in children's lives makes this general, cross-study replication noteworthy.

Data from the in-school sample of the PROSPER preventive intervention dissemination trial were used to investigate associations between alcohol dehydrogenase genes and alcohol use across adolescence, and whether substance misuse interventions in the 6th and 7th grades (targeting parenting, family functioning, social norms, youth decision making, and peer group affiliations) modified associations between these genes and adolescent use. Primary analyses were run on a sample of 1,885 individuals and included three steps. First, we estimated unconditional growth curve models with separate slopes for alcohol use from 6th to 9th grade and from 9th to 12th grade, as well as the intercept at Grade 9. Second, we used intervention condition and three alcohol dehydrogenase genes, 1B (ADH1B), 1C (ADH1C), and 4 (ADH4) to predict variance in slopes and intercept. Third, we examined whether genetic influences on model slopes and intercepts were moderated by intervention condition. The results indicated that the increase in alcohol use was greater in early adolescence than in middle adolescence; two of the genes, ADH1B and ADH1C, significantly predicted early adolescent slope and Grade 9 intercept, and associations between ADH1C and both early adolescent slope and intercept were significantly different across control and intervention conditions.

This study investigated the oxytocin receptor (OXTR) gene's moderation of associations between exposure to a substance misuse intervention, average peer substance use, and adolescents' own alcohol use during the 9th-grade. OXTR genetic risk was measured using five single nucleotide polymorphisms (SNPs), and peer substance use was based on youths' nominated closest friends' own reports of alcohol, cigarette, and marijuana use, based on data from the PROSPER project. Regression models revealed several findings. First, low OXTR risk was linked to affiliating with friends who reported less substance use in the intervention condition but not the control condition. Second, affiliating with high substance-using friends predicted youth alcohol risk regardless of OXTR risk or intervention condition. Third, although high OXTR risk youth in the intervention condition who associated with low substance-using friends reported somewhat higher alcohol use than comparable youth in the control group, the absolute level of alcohol use among these youth was still among the lowest in the sample.

Preventive intervention effects on adolescent alcohol misuse may differ based on genotypes in gene-by-intervention (G x I) interactions, and these G x I interactions may vary as a function of age. The current study uses a novel statistical method, time-varying effect modeling (TVEM), to test an age-varying interaction between a single nucleotide polymorphism in the GABRA2 gene (rs279845) and a preventive intervention in predicting alcohol misuse in a longitudinal study of adolescents (ages 11-20). The preventive intervention was PROSPER, a community-based system for delivery of family and school programs selected from a menu of evidence-based interventions. TVEM results revealed a significant age-varying GABRA2 x intervention interaction from ages 12 to 18, with the peak effect size seen around age 13 (IRR = 0.50). The intervention significantly reduced alcohol misuse for adolescents with the GABRA2 TT genotype from ages 12.5 to 17 but did not reduce alcohol use for adolescents with the GABRA2 A allele at any age. Differences in intervention effects by GABRA2 genotype were most pronounced from ages 13 to 16-a period when drinking is associated with increased risk for alcohol use disorder. Our findings provide additional evidence that intervention effects on adolescent alcohol misuse may differ by genotype, and provide novel evidence that the interaction between GABRA2 and intervention effects on alcohol use may vary with age. Implications for interventions targeting adolescent alcohol misuse are discussed.

This study addresses replication in candidate gene × environment interaction (cG×E) research by investigating if the key findings from Brody, Beach, Philibert, Chen, and Murry (2009) can be detected using data (N = 1,809) from the PROSPER substance use preventive intervention delivery system. Parallel to Brody et al., this study tested the hypotheses that substance misuse initiation would increase faster from age 11 to age 14 and be higher at age 14 among: (a) 5-HTTLPR short carrier adolescents versus long homozygotes, (b) control versus intervention adolescents, and (c) 5-HTTLPR short carriers in the control condition versus all other participants. The hypotheses were generally supported and results were consistent with Brody et al.'s cG×I finding. Results are discussed in light of replication issues in cG×E research and implications for intervention., (© 2016 The Authors. Child Development © 2016 Society for Research in Child Development, Inc.)

Girls who receive higher quality fathering engage in less risky sexual behavior (RSB) than their peers. Previous research identifies higher levels of parental monitoring/knowledge and reduced affiliation with deviant peers as potential mediators of this observed fathering effect. Although paternal investment theory posits a causal effect of fathers on daughters' RSB, and on the intervening processes that mediate this effect, these relations could arise from genetic or environmental confounds. To address this limitation, we employed the genetically- and environmentally controlled differential sibling-exposure design (N = 101 sister pairs; ages 18-36), which retrospectively examines the effects of differential sibling exposure to family disruption/father absence and quality of fathering. Consistent with a causal explanation, differences between older and younger sisters in the effects of fathering quality on parental monitoring and peer RSB were greatest in biologically disrupted families when there was a large age gap between the sisters (thus maximizing differential exposure to fathers), with greater exposure within families to higher quality fathering increasing parental monitoring and reducing affiliation with sexually promiscuous peers. No such differences were found between older and younger sisters in families with little or no differential exposure to fathers (e.g., biologically intact families) or in response to differences in mothering quality. Taken together, these findings suggest that higher quality fathering may decrease daughters' engagement in RSB by increasing the amount of parental monitoring that they receive and decreasing their affiliation with peers who promote RSB. (PsycINFO Database Record, ((c) 2017 APA, all rights reserved).)

Prior research indicates that being reared in stressful environments is associated with earlier onset of menarche in girls. In this research, we examined (a) whether these effects are driven by exposure to certain dimensions of stress (harshness or unpredictability) during the first 5 years of life and (b) whether the negative effects of stress on the timing of menarche are buffered by secure infant-mother attachment. Results revealed that (a) exposure to greater harshness (but not unpredictability) during the first 5 years of life predicted earlier menarche and (b) secure infant-mother attachment buffered girls from this effect of harsh environments. By connecting attachment research to its evolutionary foundations, these results illuminate how environmental stressors and relationships early in life jointly affect pubertal timing., (© The Author(s) 2016.)

Introduction: Prevention intervention programs reduce substance use, including smoking, but not all individuals respond. We tested whether response to a substance use prevention/intervention program varies based upon a set of five markers (rs16969968, rs1948, rs578776, rs588765, and rs684513) within the cluster of nicotinic acetylcholine receptor subunit genes (CHRNA5/A3/B4)., Methods: Participants (N = 424) were randomly assigned to either control condition, or a family-based intervention in grade 6 and a school-based drug preventive intervention in grade 7. Smoking in the past month was assessed in grades 9-12 using a four-point scale (0 = never smoked, 1 = smoked but not in last month, 2 = one or a few times, 3 = about once a week or more)., Results: There was a main effect of both the intervention (b = -0.24, P < .05) and genotype at rs16969968 (b = 0.14, P < .05) on high school smoking. Using dummy coding to allow for nonlinear effects, individuals with the A/A genotype smoked more often than those with G/G (b = 0.33, P < .05). A genotype × intervention effect was found with reduced smoking among those with A/A and G/A genotypes to levels similar to those with the G/G genotype (G/G vs. A/A: b = -0.67, P < .05; A/G vs. A/A: b = -0.61, P < .05; G/G vs. A/G ns). Results were nonsignificant for the other four markers., Conclusions: Preventive interventions can reduce the genetic risk for smoking from rs16969968., (© The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Although peer pressure can influence adolescents' alcohol use, individual susceptibility to these pressures varies across individuals. The dopamine receptor D4 gene (DRD4) is a potential candidate gene that may influence adolescents' susceptibility to their peer environment due to the role dopamine plays in reward sensation during social interaction. We hypothesized that DRD4 genotype status would moderate the impact of 7th-grade antisocial peer pressure on 12th-grade lifetime alcohol use (n = 414; 58.7% female; 92.8% White). The results revealed significant main effects for antisocial peer pressure, but no main effects for DRD4 genotype on lifetime alcohol use. Adolescent DRD4 genotype moderated the association between peer pressure and lifetime alcohol use. For individuals who carried at least one copy of the DRD4 7-repeat allele (7+), antisocial peer pressure was associated with increased lifetime alcohol use. These findings indicate that genetic sensitivity to peer pressure confers increased alcohol use in late adolescence.

Several studies have established that child interparental conflict evaluations link parent relationship functioning and adolescent adjustment. Using differential susceptibility theory and its vantage sensitivity complement as their framework, the authors examined differences between adolescents who vary in the DRD4 7 repeat genotype (i.e. 7+ vs. 7-) in how both interparental conflict and positivity affect adolescents' evaluations of interparental conflict (i.e., threat appraisals) and how these evaluations affect internalizing problems. Results from longitudinal multiple-group path models using PROSPER data ( N = 452) supported the hypothesis that threat appraisals for 7+ adolescents would be more affected by perceptions of interparental positivity compared to 7- adolescents; however, threat appraisals for 7+ adolescents were also less affected by interparental conflict. Among 7- adolescents, interparental conflict perceptions were associated with higher threat appraisals, and no association was found for perceptions of positivity. For adolescents of both genotypes, higher threat was associated with greater internalizing problems.

Candidate Gene × Environment (cGxE) interaction research holds promise for helping us understand for whom and why environments matter for families and development. In their commentary on our target article (G. L. Schlomer, G. M. Fosco, H. H. Cleveland, D. J. Vandenbergh, & M. E. Feinberg, 2015), J. E. Salvatore and D. M. Dick (2015) present their view of the current state and future of cGxE research and frame the debate regarding its merits for advancing knowledge of gene-environment interplay. In this reply, we discuss points of agreement and departure and provide a list of 5 domains by which the quality of cGxE research should be evaluated. Our hope is that researchers will use this list as a guide for their own work.

Aggression-related problems such as assault and homicide among adolescents and young adults exact considerable social and economic costs. Although progress has been made, additional research is needed to help combat this persistent problem. Several lines of research indicate that parental hostility is an especially potent predictor of adolescent aggression, although most longitudinal research has focused on clarifying the direction of effects. In this study, we used longitudinal data from the PROSPER project (N = 580; 54.8% female), a primarily rural Caucasian preventative intervention sample, to examine developmental change in early- to mid-adolescent aggressive behavior problems (age 11-16 years). In addition, we examined maternal hostility as a predictor of developmental change in aggression and the PROSPER preventative intervention, designed to reduce substance use and aggression, as a potential influence on this association. Lastly, several studies indicate that variation in the DRD4 7-repeat gene moderates both parenting and intervention influences on externalizing behavior. Accordingly, we examined the potential moderating role of DRD4. As hypothesized, there was a significant maternal hostility by intervention interaction indicating that the intervention reduced the negative impact of maternal hostility on adolescent change in aggressive behavior problems. DRD4 7-repeat status (7+ vs. 7-) further conditioned this association whereby control group 7+ adolescents with hostile mothers showed increasing aggressive behavior problems. In contrast, aggression decreased for 7+ adolescents with similarly hostile mothers in the intervention. Implications for prevention are discussed as well as current perspectives in candidate gene-by-environment interaction research.

Data drawn from the in-home subsample of the PROSPER intervention dissemination trial were used to investigate the moderation of intervention effects on underage alcohol use by maternal involvement and candidate genes. The primary gene examined was dopamine receptor D4 (DRD4). Variation in this gene and maternal involvement were hypothesized to moderate the influence of intervention status on alcohol use. The PROSPER data used were drawn from 28 communities randomly assigned to intervention or comparison conditions. Participating youth were assessed in five in-home interviews from sixth to ninth grades. A main effect of sixth-grade pretest maternal involvement on ninth-grade alcohol use was found. Neither intervention status nor DRD4 variation was unconditionally linked to ninth-grade drinking. However, moderation analyses revealed a significant three-way interaction among DRD4 status, maternal involvement, and intervention condition. Follow-up analyses revealed that prevention reduced drinking risk, but only for youth with at least one DRD4 seven-repeat allele who reported average or greater pretest levels of maternal involvement. To determine if this conditional pattern was limited to the DRD4 gene, we repeated analyses using the serotonin transporter linked polymorphic region site near the serotonin transporter gene. The results for this supplemental analysis revealed a significant three-way interaction similar but not identical to that found for DRD4.

Tobacco-related behaviors and the underlying addiction to nicotine are complex tangles of genetic and environmental factors. Efforts to understand the genetic component of these traits have identified sites in the genome (single nucleotide polymorphisms, or SNPs) that might account for some part of the role of genetics in nicotine addiction. Encouragingly, some of these candidate SNPs remain significant in meta-analyses. However, genetic associations cannot be fully assessed, regardless of statistical significance, without an understanding of the functional consequences of the alleles present at these SNPs. The proper experimental test for allelic function can be very difficult to define, representing a roadblock in translating genetic results into treatment to prevent smoking and other nicotine-related behaviors. This roadblock can be navigated in part with a new web-based tool, the Encyclopedia of DNA Elements (ENCODE). ENCODE is a compilation of searchable data on several types of biochemical functions or "marks" across the genome. These data can be queried for the co-localization of a candidate SNP and a biochemical mark. The presence of a SNP within a marked region of DNA enables the generation of better-informed hypotheses to test possible functional roles of alleles at a candidate SNP. Two examples of such co-localizations are presented. One example reveals ENCODE's ability to relate a candidate SNP's function with a gene very far from the physical location of the SNP. The second example reveals a new potential function of the SNP, rs4105144, that has been genetically associated with the number of cigarettes smoked per day. Details for accessing the ENCODE data for this SNP are provided to serve as a tutorial. By serving as a bridge between genetic associations and biochemical function, ENCODE has the power to propel progress in untangling the genetic aspects of nicotine addiction - a major public health concern., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Drawing on the evolutionary terminal investment hypothesis and Trivers' (1974) parent-offspring conflict theory, we advance and evaluate a mediational model specifying why and how maternal age, via mating effort and parental investment, affects mother-child conflict. Data from a longitudinal study of 757 families indicate that (a) older maternal age predicts lower mating effort during the child's first 5 years of life, and (b) thereby, higher maternal investment in middle childhood when the child is around 10 years old. (c) Higher maternal investment, in turn, forecasts less child-perceived mother-child conflict in adolescence (age 15). These results proved robust against theoretically relevant covariates (family resources, parity, maternal education, and maternal personality characteristics) and in the context of an autoregressive model. Study limitations are noted and results are discussed in terms of the unique contributions of an evolutionary perspective to the determinants-of-parenting literature., (PsycINFO Database Record (c) 2012 APA, all rights reserved.)

The current study tested sex-specific pathways to early puberty, sexual debut, and sexual risk taking, as specified by an integrated evolutionary-developmental model of adolescent sexual development and behavior. In a prospective study of 238 adolescents (n = 129 girls and n = 109 boys) followed from approximately 12-18 years of age, we tested for longitudinal relations between ecological stressors, family relationships, pubertal maturation, self-perceived mate value, and sexual risk taking in both boys and girls. Consistent with the theory, (a) higher levels of familial and ecological stress predicted earlier sexual debut and greater sexual risk taking; (b) pubertal maturation partially mediated these relations among girls but not among boys; (c) father absence had unique effects on female sexual outcomes but not on male sexual outcomes; (d) higher self-perceived mate value directly predicted earlier sexual debut and, through it, greater sexual risk taking; and (e) relations between pubertal maturation and early sexual debut were partially mediated by higher self-perceived mate value in boys but not in girls. Discussion focuses on the contribution of an integrated evolutionary-developmental theory to the adolescent sexual health literature.

Drawing on life history theory, Ellis and associates' (2009) recent across- and within-species analysis of ecological effects on reproductive development highlighted two fundamental dimensions of environmental variation and influence: harshness and unpredictability. To evaluate the unique contributions of these factors, the authors of present article examined data from a national sample 1364 mothers and their children participating in the NICHD Study of Early Child Care and Youth Development. Harshness was operationalized as income-to-needs ratio in the first 5 years of life; unpredictability was indexed by residential changes, paternal transitions, and parental job changes during this same period. Here the proposition was tested that these factors not only uniquely predict accelerated life-history strategy, operationalized in terms of sexual behavior at age 15, but that such effects are mediated by change over the early-childhood years in maternal depression and, thereby, observed maternal sensitivity in the early-elementary-school years. Structural equation modeling provided empirical support for Ellis et al.'s (2009) theorizing, calling attention once again to the contribution of evolutionary analysis to understanding contemporary human parenting and development. Implications of the findings for intervention are discussed.

Girls receiving lower quality paternal investment tend to engage in more risky sexual behavior (RSB) than peers. Whereas paternal investment theory posits that this effect is causal, it could arise from environmental or genetic confounds. To distinguish between these competing explanations, the current authors employed a genetically and environmentally controlled sibling design (N = 101 sister pairs; ages 18-36), which retrospectively examined the effects of differential sibling exposure to family disruption/father absence and quality of fathering. Consistent with a causal explanation, differences between older and younger sisters in the effects of quality of fathering on RSB were greatest in biologically disrupted families when there was a large age gap between the sisters (thus maximizing differential exposure to fathers), with greater exposure within families to higher quality fathering serving as a protective factor against RSB. Further, variation around the lower end of fathering quality appeared to have the most influence on RSB. In contrast, differential sibling exposure to family disruption/father absence (irrespective of quality of fathering) was not associated with RSB. The differential sibling-exposure design affords a new quasi-experimental method for evaluating the causal effects of fathers within families.

Parental deployment during military conflicts has the potential to impact child adjustment. As increased numbers of military Service members have children, it is critical to understand the association between military deployment and child adjustment. In order to resolve inconsistencies in the existing literature, we performed a meta-analytic review of 16 studies that report associations of military deployment with internalizing, externalizing, and academic adjustment among children. Results indicate a small association between deployment and poorer adjustment. This association varied across several features of the studies. Age moderation was such that the associations are strongest in middle childhood and weakest during adolescence. The method that adjustment was assessed also moderated this association, such that maladjustment was evident primarily with parents' reports. Study design also moderated associations, such that comparisons to civilian controls indicated associations with maladjustment, whereas comparisons to nondeployed military and prepost comparisons did not. These findings summarize the existing quantitative literature to indicate that parental deployment has a negligible association with child maladjustment and provide a foundation for future research.

Decades of research demonstrate that conflict shapes and permeates a broad range of family processes. In the current article, we argue that greater insight, integration of knowledge, and empirical achievement in the study of family conflict can be realized by utilizing a powerful theory from evolutionary biology that is barely known within psychology: parent-offspring conflict theory (POCT). In the current article, we articulate POCT for psychological scientists, extend its scope by connecting it to the broader framework of life history theory, and draw out its implications for understanding conflict within human families. We specifically apply POCT to 2 instances of early mother-offspring interaction (prenatal conflict and weaning conflict); discuss the effects of genetic relatedness on behavioral conflict between parents, children, and their siblings; review the emerging literature on parent-offspring conflict over the choice of mates and spouses; and examine parent-offspring conflict from the perspective of imprinted genes. This review demonstrates the utility of POCT, not only for explaining what is known about conflict within families but also for generating novel hypotheses, suggesting new lines of research, and moving us toward the "big picture" by integrating across biological and psychological domains of knowledge.

This article urges counseling psychology researchers to recognize and report how missing data are handled, because consumers of research cannot accurately interpret findings without knowing the amount and pattern of missing data or the strategies that were used to handle those data. Patterns of missing data are reviewed, and some of the common strategies for dealing with them are described. The authors provide an illustration in which data were simulated and evaluate 3 methods of handling missing data: mean substitution, multiple imputation, and full information maximum likelihood. Results suggest that mean substitution is a poor method for handling missing data, whereas both multiple imputation and full information maximum likelihood are recommended alternatives to this approach. The authors suggest that researchers fully consider and report the amount and pattern of missing data and the strategy for handling those data in counseling psychology research and that editors advise researchers of this expectation.

The current paper synthesizes theory and data from the field of life history (LH) evolution to advance a new developmental theory of variation in human LH strategies. The theory posits that clusters of correlated LH traits (e.g., timing of puberty, age at sexual debut and first birth, parental investment strategies) lie on a slow-to-fast continuum; that harshness (externally caused levels of morbidity-mortality) and unpredictability (spatial-temporal variation in harshness) are the most fundamental environmental influences on the evolution and development of LH strategies; and that these influences depend on population densities and related levels of intraspecific competition and resource scarcity, on age schedules of mortality, on the sensitivity of morbidity-mortality to the organism's resource-allocation decisions, and on the extent to which environmental fluctuations affect individuals versus populations over short versus long timescales. These interrelated factors operate at evolutionary and developmental levels and should be distinguished because they exert distinctive effects on LH traits and are hierarchically operative in terms of primacy of influence. Although converging lines of evidence support core assumptions of the theory, many questions remain unanswered. This review demonstrates the value of applying a multilevel evolutionary-developmental approach to the analysis of a central feature of human phenotypic variation: LH strategy.