Timing of Menarche and the Origins of Conduct Disorder

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Utilizing data from the ongoing Minnesota Twin Family Study, Burt and colleagues examined possible common genes and the moderation of genetic influences on the association of menarche timing on conduct disorder (CD). The sample comprised 708 mid-adolescent female twins identified by birth records in Minnesota: 436 monozygotic (identical) twins, and 272 dizygotic (fraternal) twins ranging in age from 13.6 to 16.9 years (mean = 14.8 years) at their first 3-year follow-up visit, as well as their mothers. A count of conduct disorder symptoms was obtained by trained interviewers employing a maternal-report and self-report standardized psychiatric interview for children and adolescents. Mothers and twins were interviewed by separate interviewers and reported on symptom presence in the last 3 years. Only symptoms judged to be clinically significant in both severity and frequency were considered present, and a symptom was considered present if it was endorsed by either the mother or the child. Onset of menses data, assessed with the teen self-report Pubertal Development Scale, was available for 688 of the girls. Participants who had begun menstruating (n = 644) were split into 3 categories: those with early menarche (ie, onset at age ≤11 years; 20% of the sample), those with an average timing of menarche (ie, onset at age 12-13 years; 62% of the sample), and those with delayed onset of menses (ie, age >13 years; 12% of the sample). Girls who had yet to begin menstruating (44 girls; 6% of the sample) were added to the delayed group. Two sets of structural equation statistical analyses were conducted: (1) a bivariate model to determine whether CD symptoms and timing of menarche covaried as a function of genetic influences, and (2) biometric moderator analyses to evaluate whether and how timing of menarche impacted the etiology of CD.

Comparing girls with 3 or more symptoms of CD (the number required for diagnosis) across timing of menarche status, those with early menarche were 1.29 times as likely to have CD as those with an average timing of menarche. Including girls with 2 or more symptoms of CD, those with early menarche were 1.67 times as likely to have probable CD as those with an average timing of menarche, and 2.38 times as likely as those with late menarche. Timing of menarche was unrelated to childhood-onset CD (ie, defined as lifetime occurrence of CD by age 11 years), indicating that relatively early-onset menarche is specific to adolescent-onset CD. The bivariate model indicated that the genetic contributions to CD did not overlap with those for timing of menarche (r genetic = –0.06; not significant). In contrast, the shared environmental correlation was estimated at 1.0 and accounted for roughly 95% of the covariance between CD and timing of menarche. In analyzing the moderator model, it was found that genetic influences on CD were strongest (67%) for girls with an average age at menarche and were significantly smaller for girls with early or late initiation of menses; particularly low for those with early initiation (8%). Non-shared environmental influences appeared strongest for early-maturing girls as compared with on-time- or late-maturing girls.

Supporting psychosocial interpretations of the association between pubertal status and conduct problems, the authors concluded a largely environmental mediation of CD for girls with relatively early menarche and, to a lesser extent, delayed menarche. They also drew attention to a conceptualization of gene-environment interplay related to the “average, expectable” environment. In this case, genetic influences are thought to be most strongly expressed under normal to optimal environmental conditions rather than at the extremes.

Burt SA, McGue M, DeMarte JA, Krueger RF, Iacono WG. Timing of menarche and the origins of conduct disorder. Arch Gen Psychiatry. 2006;63:890-6.

Editor’s Comment

I have long been intrigued by the reported link between father abandonment and daughters’ early menarche.1 This phenomenon of accelerated maturation appears to also extend to boys.2 In the case of girls, it had been suggested3 (with another study failing to confirm4) that a single common gene (the X-linked androgen receptor gene passed from fathers to their daughters) has effects on multiple traits, in this case contributing to early pubertal timing as well as a tendency toward conduct problems. Instead, the present study suggests that unspecified environmental factors mediate the association between relatively early-onset menarche and conduct disorder symptoms.

The authors pointed out a number of limitations of their study. For instance, the study was not longitudinal and, therefore, it cannot be assumed that the behavior symptoms reported in the interviews persist to later ages. In addition, the findings may not be generalizable to boys; and the study relies on the critiqued “equal environments assumption” (ie, that monozygotic and dizygotic twins experience equally-correlated environments) for interpretation of results. To this list I would add further limitations such as the study was conducted in a largely (98%) White sample and that menarche, rather than publicly visible cues of pubertal onset (ie, breast development) were employed as the index of pubertal status. Understandably, recall of age at breast development is less reliable than that of age at first menses. However, it is likely that breast development and associated changes in body composition form the perceptual stimulus placing early maturing girls at heightened risk for conduct problems. Further, the average age of breast development is significantly lower among African-American girls than White girls.5 For these reasons, it seems important that future studies which examine the association between puberty and problem behavior consider a possibly more relevant pubertal index, and that the study be conducted in a racially heterogeneous sample.

Finally, lest readers come away from reading this article concerned that CD among girls with relatively early menarche is a high likelihood outcome, the authors noted that the rates of CD should be considered upper estimates of the possible disorder prevalences, as duration of symptom requirements were omitted.

David E. Sandberg, PhD

References - (linked to Pubmed Links)

  1. Belsky J, Steinberg L, Draper P. Childhood experience, interpersonal development, and reproductive strategy: and evolutionary theory of socialization. Child Dev. 1991;62:647-70.
  2. Mustanski BS, Viken RJ, Kaprio J, Pulkkinen L, Rose RJ. Genetic and environmental influences on pubertal development: longitudinal data from Finnish twins at ages 11 and 14. Dev Psychol. 2004;40:1188-98.
  3. Comings DE, Muhleman D, Johnson JP, MacMurray JP. Parent-daughter transmission of the androgen receptor gene as an explanation of the effect of father absence on age of menarche. Child Dev. 2002;73:1046-51.
  4. Jorm AF, Christensen H, Rodgers B, Jacomb PA, Easteal S. Association of adverse childhood experiences, age of menarche, and adult reproductive behavior: does the androgen receptor gene play a role? Am J Med Genet B Neuropsychiatr Genet. 2004;125:105-11.
  5. Herman-Giddens ME, Slora EJ, Wasserman RC, et al. Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network. Pediatrics. 1997;99:505-12.

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