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. 2006 Aug;63(8):890-6.
doi: 10.1001/archpsyc.63.8.890.

Timing of menarche and the origins of conduct disorder

S Alexandra Burt  1 , Matt McGue, Janeen A DeMarte, Robert F Krueger, William G Iacono
Affiliations

Timing of menarche and the origins of conduct disorder

S Alexandra Burt et al. Arch Gen Psychiatry. 2006 Aug.

Abstract

Context: Precocious onset of menses (ie, age < or =11 years) has repeatedly been identified as a risk factor for higher rates of delinquency or conduct disorder (CD) in girls. Although this association is often conceptualized as environmentally mediated (via processes such as affiliation of early-menstruating youth with older, more deviant peers), such conclusions are premature as biological and genetic explanations have yet to be fully considered.

Objective: To uncover the origins of the association between CD and timing of menarche.

Design, setting, and participants: The sample consisted of a population-based birth cohort of 708 mid-adolescent female twins assessed as part of the ongoing Minnesota Twin Family Study. We conducted 2 sets of analyses: standard bivariate analyses to uncover possible common genes and moderator analyses to evaluate possible moderation of genetic influences on CD by timing of menarche.

Main outcome measures: Conduct disorder was assessed via individual semistructured interviews with mothers and adolescents. Menarcheal status and age at menarche were assessed via the Pubertal Development Scale.

Results: The results argued against common genetic influences but did provide evidence of etiological moderation of CD by timing of menarche. The heritability of CD was strongest (67%) in girls with average timing of menarche (ie, age 12-13 years) and substantially weaker (8%) in those with early onset. Those with late initiation of menses (ie, age >13 years) similarly exhibited weaker genetic influences (29%). Shared environmental influences showed the opposite pattern, as they were far stronger for those with precocious and delayed onset vs those with average onset.

Conclusions: Our findings provide indirect support for psychosocial interpretations of the impact of precocious menarche and, to a lesser extent, delayed menarche on CD development. Further, they lend support to the notion that in some cases, genetic influences on psychopathology may be strongest in the "average, expectable" environment.

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Figures

Figure 1
Figure 1
Standardized path estimates of the additive genetic (A), shared environmental (C), and nonshared environmental (E) contributions to the variance within and covariance between conduct disorder (CD) and timing of menarche. Path coefficients were squared to index the percentage of variance accounted for (these percentages are indicated below their respective phenotypes, followed by their 95% confidence intervals in parentheses). Genetic and environmental correlations are indicated via the double-headed arrows in the upper portion of the diagram. Confidence intervals that do not overlap with 0 indicate statistical significance at P<.05.
Figure 2
Figure 2
Standardized genetic (A), shared environmental (C), and nonshared environmental (E) variance contributions to conduct disorder by timing of menarche.
See this image and copyright information in PMC

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