# Peer Victimization in Childhood and Timing of Substance Use Initiation: Evidence from a Twin Study

## TL;DR

This study examines how childhood peer victimization relates to when teens start using substances, using a twin sample to explore genetic and environmental influences.

## Contribution

The study is the first to investigate genetic and environmental contributions to the link between childhood victimization and substance use initiation.

## Key findings

- Most associations between victimization and substance use initiation were not statistically significant after correction for multiple testing.
- Genetic and nonshared environmental factors influenced verbal and physical victimization, while shared and nonshared factors influenced relational victimization.
- Sex differences were found in the genetic and environmental contributions to the timing of alcohol and marijuana use initiation.

## Abstract

Previous studies robustly link childhood peer victimization experience to the timing of substance use initiation. However, no study has investigated the contributions of genetic and environmental factors to this link. The current study focused on a sample of 779 twin pairs followed from age 9–10 to 19–20, which is racially/ethnically and socioeconomically representative of the greater Los Angeles area. The aims were to investigate (1) the associations between childhood victimization, including physical (e.g., kicking, pushing), verbal (e.g., taunting), and relational victimization (e.g., spreading rumors), and timing of substance use initiation, and (2) the contributions of genetic/environmental factors to these associations. Multinomial logistic regressions revealed several small associations, but none of these survived corrections for multiple testing. Univariate genetic models suggested genetic (A) and nonshared environmental influences (E) on verbal victimization (VA = .43, VE = .57), shared environmental (C) and nonshared environmental factors on relational victimization (VC = .22, VE = .78), and ambiguous familial influences and E on physical victimization (VA = .34, VE = .66; VC = .26, VE = .74). Timing of cigarette initiation were explained by A, C, and E (VA = .48, VC = .31, VE = .21). Quantitative sex differences in contributions of A, C, and E were detected for alcohol (VAM = .90, VEM = .10; VCF = .86, VEF = .14) and marijuana initiation (VAM = .89, VEM = .11; VCF = .79, VEF = .21); however, A could be dropped for females and C could be dropped for males across both variables. Multivariate twin analyses were not feasible, due to the low cross-trait correlations. These findings call into question the robustness of links between self-reported victimization in childhood and prospectively measured timing of substance initiation across adolescence.

The online version contains supplementary material available at 10.1007/s10519-025-10222-4.