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  • JAMA Psychiatry April 1, 2014

    Figure 1: Distribution of Rates of Drug Abuse in Peers

    Rates were assessed at the proband age of 15 years across 7738 Small Areas for Market Statistics in Sweden.
  • JAMA Psychiatry April 1, 2014

    Figure 4: Results From the Linear Hazard Model With the Main Effects of Genetic Risk, Peer Deviance, and Their Interaction

    We examined 5 levels of genetic risk from categories outlined in Table 3: low (no affected relative), moderate (only mother affected), moderately high (all siblings affected), high (father and 50% of siblings affected), and very high (monozygotic co-twin affected). The excess numbers of new drug abuse cases per 10 000 person-years for those with low genetic risk raised in a Small Area for Market Statistics with 0% vs 15% rates of drug abuse in peers were 8.0 and 36.1, respectively, for a difference of 28.1. For those at moderate, moderately high, high, and very high genetic risk, the figures were 21.5 and 59.7 for a difference of 38.2; 34.5 and 82.4 for a difference of 47.9; 51.2 and 111.6 for a difference of 60.4; and 74.8 and 152.8 for a difference of 78.0, respectively.
  • Peer Deviance, Parental Divorce, and Genetic Risk in the Prediction of Drug Abuse in a Nationwide Swedish Sample: Evidence of Environment-Environment and Gene-Environment Interaction

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    JAMA Psychiatry. 2014; 71(4):439-445. doi: 10.1001/jamapsychiatry.2013.4166

    Kendler and coauthors examine how strongly peer deviance increases the risk of drug abuse.

  • JAMA Psychiatry April 1, 2014

    Figure 3: Results From the Linear Hazard Model

    Results include main effects of divorce, peer deviance, and their interaction, as well as the genetic risk score. The excess numbers of new drug abuse cases per 10 000 person-years for those with no parental loss raised in a Small Area for Market Statistics with 0% vs 15% rates of drug abuse in peers were 0 and 35.7, respectively, for a difference of 35.7. For those with parental loss, the figures were 4.4 and 51.2, respectively, for a difference of 46.8.
  • JAMA Psychiatry August 1, 2013

    Figure 2: Response to Reward Anticipation and Feedback in the Ventral Striatum (VS) in Adolescents With Prenatal Exposure to Maternal Cigarette Smoking and Their Nonexposed Peers

    A, Response of the VS in all participants to anticipation of any reward vs no reward. The display is set to threshold t = 4.88 (P < .05, familywise error [FWE] corrected with ≥25 contiguous voxels). B, Differences between nonexposed and exposed adolescents in signal change in the left and right VS to anticipation. Error bars indicate SEM. *P < .01. C, Response of the VS in all participants to feedback of win vs no win. The display is set to threshold t = 4.88 (P < .05, FWE corrected with ≥25 contiguous voxels). D, Differences between nonexposed and exposed adolescents in signal change in left and right VS to feedback. Error bars indicate SEM.
  • Altered Reward Processing in Adolescents With Prenatal Exposure to Maternal Cigarette Smoking

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    JAMA Psychiatry. 2013; 70(8):847-856. doi: 10.1001/jamapsychiatry.2013.44

    Müller et al assess whether adolescents with prenatal exposure to maternal cigarette smoking differ from their nonexposed peers in the response of the ventral striatum to the anticipation or the receipt of a reward.

  • Adult Psychiatric Outcomes of Bullying and Being Bullied by Peers in Childhood and Adolescence

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    JAMA Psychiatry. 2013; 70(4):419-426. doi: 10.1001/jamapsychiatry.2013.504
    In a prospective, population-based study of 1420 participants who had being bullied and bullying assessed 4 to 6 times between the ages of 9 and 16 years, Copeland and coauthors test whether bullying and/or being bullied in childhood predicts psychiatric problems and suicidality in young adulthood after accounting for childhood psychiatric problems and family hardships.
  • JAMA Psychiatry June 1, 2009

    Figure 1: Environmental Adversity and Increasing Genetic Risk for Externalizing Disorders

    Externalizing (EXT) disorders composite. Full model of moderation of the genetic and environmental influences on EXT as a function of different levels of antisocial peers. A indicates additive genetic effects; C, shared environmental effects; and E, nonshared environmental effects. The parameters a21, c21, and e21 include genetic and environmental influences that overlap between antisocial peers and EXT (ie, can be used to derive the genetic and environmental covariance), whereas a22, c22, and e22 are genetic and environmental influences unique to EXT. Antisocial peers can moderate the common variance with EXT or the unique variance of EXT. The β levels indicate the direction (+ or −) and magnitude of any moderation effects on the paths from the ACE effects to EXT, whereas M indicates the level of the moderator (ie, the number of antisocial peers).
  • Mental Health of College Students and Their Non–College-Attending Peers: Results From the National Epidemiologic Study on Alcohol and Related Conditions

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    Arch Gen Psychiatry. 2008; 65(12):1429-1437. doi: 10.1001/archpsyc.65.12.1429
  • JAMA Psychiatry November 3, 2008

    Figure 1: Amygdala and Ventrolateral Prefrontal Cortex Function During Anticipated Peer Evaluation in Pediatric Social Anxiety

    The chat room paradigm consisted of 2 visits to the laboratory. A, Approximately 2 weeks before the scan, participants rated how interested they were in chatting online with peers based on photographs. A median split divided the ratings into low and high peer-desirability groups. Participants were told that the same peers would learn how they had been rated and rate the participants' photographs in a similar fashion. B, During the second visit participants were scanned while reviewing previously judged photographs and rated how interested they thought each peer would be in chatting online with them.
  • JAMA Psychiatry November 3, 2008

    Figure 2: Amygdala and Ventrolateral Prefrontal Cortex Function During Anticipated Peer Evaluation in Pediatric Social Anxiety

    A, A significant group difference in right amygdala activity is illustrated on high-resolution images from a representative subject. Bilateral amygdala activation was greater in patients vs controls when appraising expected peer evaluation by low- vs high-desirability peers (P < .005). After correcting for multiple comparisons in the amygdala regions (P < .05), the maximum intensity value for the cluster encompassing the left amygdala was t = 3.62 (x = −23, y = 3, z = −20) and for the right amygdala was t = 3.53 (x = 27, y = −3, z = −21). B, Group × peer desirability interaction effects on the event-elicited percentage of signal change in the left (F1,26 = 13.26; P = .001) and right amygdala (F1,26 = 12.91; P = .001). Data were collected at functional magnetic resonance imaging scan during appraisal of expected peer evaluation, converted to percentage of signal change using voxelwise time series mean as a baseline, and averaged within each functionally defined amygdala region of interest.
  • Amygdala and Ventrolateral Prefrontal Cortex Function During Anticipated Peer Evaluation in Pediatric Social Anxiety

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    Arch Gen Psychiatry. 2008; 65(11):1303-1312. doi: 10.1001/archpsyc.65.11.1303
  • Creating a Social World: A Developmental Twin Study of Peer-Group Deviance

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    Arch Gen Psychiatry. 2007; 64(8):958-965. doi: 10.1001/archpsyc.64.8.958
  • JAMA Psychiatry August 1, 2007

    Figure 1: Creating a Social World: A Developmental Twin Study of Peer-Group Deviance

    Unstandardized additive genetic (A), shared or common environmental (C), and individual-specific environmental (E) variance for peer-group deviance across 5 time periods estimated from our best-fit growth curve model.
  • JAMA Psychiatry August 1, 2007

    Figure 2: Creating a Social World: A Developmental Twin Study of Peer-Group Deviance

    Standardized additive genetic (A), shared or common environmental (C), and individual-specific environmental (E) variance for peer-group deviance across 5 time periods estimated from our best-fit growth curve model. The standardized additive genetic effects equal the heritability.
  • JAMA Psychiatry August 1, 2007

    Figure 3: Creating a Social World: A Developmental Twin Study of Peer-Group Deviance

    Parameter estimates from the biometrical latent growth curve analysis were used to construct expected growth curve patterns for hypothetical individuals with different underlying liabilities with respect to genetic (A), shared or common environmental (C), and individual-specific environmental (E) variance for peer-group deviance. The mean curve was constructed by setting the deviation for each of these latent constructs at 0, while the upper and lower curves, respectively, were constructed by setting the deviations for A, C, and E at 1.96 or − 1.96 while holding the others at 0, thus providing 97.5% and 2.5% percentiles for expected variation due to each of these sources of variance.
  • Prediction of Early-Onset Deviant Peer Group Affiliation: A 12-Year Longitudinal Study

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    Arch Gen Psychiatry. 2006; 63(5):562-568. doi: 10.1001/archpsyc.63.5.562
  • JAMA Psychiatry May 1, 2006

    Figure 1Prediction of Early-Onset Deviant Peer Group Affiliation: A 12-Year Longitudinal Study

    Developmental trajectories of deviant peer group affiliation throughout adolescence. Adapted from Lacourse et al.
  • JAMA Psychiatry May 1, 2006

    Figure 2Prediction of Early-Onset Deviant Peer Group Affiliation: A 12-Year Longitudinal Study

    Proportion of boys in kindergarten behavioral profiles who followed an early or middle adolescence deviant peer group trajectory.
  • JAMA Psychiatry May 1, 2006

    Figure 3Prediction of Early-Onset Deviant Peer Group Affiliation: A 12-Year Longitudinal Study

    Proportions of boys in kindergarten behavioral profiles, with and without family adversity, who followed an early or middle adolescence deviant peer group trajectory.