Previous research has demonstrated that exposure to family disruption/father absence (due to parental relationship dissolution) is a significant risk factor for early pubertal development in daughters. Moreover, the earlier in life that this exposure occurs, the greater the risk of these outcomes for girls. Two opposing classes of explanation have been proposed for this reliable finding. First, evolutionary-based developmental experience models have proposed that father absence may actually cause early pubertal development in daughters through mechanisms that remain to be elucidated. Second, this association may arise from either a genetic or a family-wide environmental confound. To discriminate between these two competing classes of explanation (i.e., causal vs. noncausal), a retrospective study employing a community sample of full biological sister pairs was conducted in New Zealand. This study examined menarchael age in (a) a primary group comprising age-discrepant biologically disrupted/father absent sister pairs (n = 68), and (b) a matched control group comprising age-discrepant biologically intact/father present sister pairs (n = 93). According to the causation model, if greater exposure to family disruption/father absence causes earlier pubertal development in girls, then in families in which (a) full biological sisters are discrepant in age, and (b) the younger sister has experienced more prolonged father absence than has her older sister, younger sisters should be at greater risk for earlier pubertal development. By contrast, if a genetic or family-wide environmental confound explains this association, full biological sisters should not systematically differ in pubertal timing as a function of birth order, even if they have experienced different amounts of father absence. The unique contribution of the current study to this area of inquiry is its employment of a differential sibling exposure design to test the explanatory value of the two opposing classes of explanation (i.e., causal versus noncausal). This genetically and environmentally controlled sibling design was utilised (a) to test the central hypothesis that the birth order/age discrepancy (older versus younger) between sisters would interact with family type (biologically disrupted vs. biologically intact) to predict the size of sibling differences in menarcheal age, and (b) to test for potential moderating effects of paternal dysfunction. Consistent with evolutionary causal models, the current sibling comparison study revealed that within biologically disrupted/father-absent families, younger sisters (who had more prolonged exposure to father absence) had earlier menarcheal ages than did their older sisters. The current study was therefore not only able to distinguish between the two competing classes of explanations, but its findings plausibly supported a causal rather than a noncausal explanation for the association between father absence and earlier pubertal timing in girls. Moreover, it revealed that this association is more nuanced than previously thought, because the accelerating effect of family disruption/father absence on daughters’ menarcheal timing was moderated by fathers’ functioning in the family. The current study has eight important limitations that can be used to direct future research. These limitations are detailed along with proffered suggestions (where applicable) for addressing them in future studies. Possible mediating mechanisms for the earlier menarcheal timing found in daughters from biologically disrupted/father absent families are also proposed. Finally, the implications of the current study’s findings for both parents and daughters in biologically disrupted/father absent families are discussed.