In their now classic article on father absence and reproductive strategy, Draper and Harpending (1982)
proposed that individuals have evolved to be sensitive to specific features of their early childhood environments, and that girls whose early family experiences are characterized by father absence and discordant male–female relationships will tend to perceive that male parental investment is not crucial to reproduction and will develop in a manner that accelerates onset of sexual activity and reproduction without careful choice of mates. Belsky et al. (1991)
proposed several extensions to Draper and Harpending's original theory, including the addition of early pubertal timing as a component of the accelerated reproductive strategy, a shift in emphasis from the social address of father absence to more dynamic family processes, and the expansion from a more delimited father-based model to a more general family ecology model.
The central and most intriguing hypothesis proposed by Belsky et al. (1991)
—that quality of early family relationships influences timing of pubertal development in adolescence—received reasonable support from this study. As predicted only by the theory and no other formulation of socialization processes, more time spent by the father in child care, greater supportiveness in the parental dyad, more father–daughter affectionate–positivity, and more mother–daughter affectionate–positivity each predicted later pubertal timing by daughters in seventh grade. These relations emerged (a) even though there was an 8-year time period between measurements (prekindergarten assessment of quality of family relationships vs. seventh-grade assessment of daughters' puberty), (b) even though the correlations were across independent data sources (interview reports and behavioral observations of family relationships vs. daughters' self-reported pubertal timing), and (c) whether quality of family relationships was assessed indirectly through mother-based interviewer reports or directly through home observations. The results of the present study generally support and extend past longitudinal research linking quality of family relationships to timing of pubertal maturation in girls (Ellis & Garber, in press
; Graber et al., 1995
; Moffitt et al., 1992
; Steinberg, 1988
; Wierson et al., 1993
An important limitation of the present study was that it was not genetically informative. The evolutionary models of pubertal timing presented in this article rest on the concept of conditional
reproductive strategies; that is, they emphasize environmentally triggered processes that shunt individuals toward given reproductive strategies. An alternative explanation, however, is that individual differences in pubertal timing and associated characteristics represent alternative
reproductive strategies, which result from genetic differences. Consider this possibility: Girls who mature earlier tend to exhibit earlier onset of sexual activity (e.g., Bingham, Miller, & Adams, 1990
; Helm & Lidegaard, 1990
; Phinney, Jensen, Olsen, & Cundick, 1990
) and earlier age of first marriage and first birth (Manlove, 1997
; Udry, 1979
; Udry & Cliquet, 1982
), which in turn are associated with increased probability of divorce and lower quality paternal investment. This covariation may occur because early pubertal timing results in precocious sexual and, reproductive behavior (cf. Caspi & Moffitt, 1991
) or because pubertal, sexual, and reproductive timing are genetically correlated traits. Because mothers who are early maturers tend to have daughters who are early maturers (Brooks-Gunn & Warren, 1988
; Garn, 1980
), the correlation between quality of paternal investment and timing of pubertal maturation in girls may be spurious; that is, it may simply be due to genetic transmission of pubertal timing and associated characteristics (Kim & Smith, 1998
; Surbey, 1990
On the basis of the present study, we cannot rule out this alternative explanation. It is worth noting, however, that previous studies that have controlled for either mothers' timing of pubertal maturation (Graber et al., 1995
) or mothers' age at first childbirth (Ellis & Garber, in press
) have still found significant associations between quality of family relationships and timing of daughters' puberty. Nevertheless, our study would have provided a better test of Belsky et al.'s (1991)
conditional adaptation model if it had controlled for parents' pubertal timing. Unfortunately, relevant data on parental puberty were not collected.
Experimental research designs are needed to test for the causal influence of family relationships on pubertal timing. Forgatch (1991)
and Kellam and Rebok (1992)
have suggested that randomized, longitudinally designed prevention trials can be used to test the causal status of parenting practices. In the case of pubertal timing, the prevention trials should begin prior to the onset of puberty (no later than the 2nd grade), should target dysfunctional families, and should focus on improving the positive quality of family relationships and paternal investment. Given a successful preventive intervention, the conditional adaptation model predicts that girls in the experimental condition will experience later pubertal timing than girls in the control condition. Such a preventive intervention study is currently underway (Ellis, Dodge, McFadyen-Ketchum, & The Conduct Problems Prevention Research Group, 1999
). Without such experimental data, however, one must be cautious about attributing causal status to the observed relations between family environment and pubertal timing. With this limitation in mind, we now turn to implications of the present findings.
The Social Address of Father Absence Versus the Dimensional Quality of Father–Daughter Relationships
Whereas Draper and Harpending (1982
focused largely on the social address of father absence, Belsky et al. (1991)
emphasized the role of more dynamic family processes, especially parent–child processes, in the development of female reproductive strategies. An implication of Belsky et al.'s model is that not only in father-absent homes, but also in dysfunctional father-present homes, girls should experience relatively early pubertal timing. The present study provides support for this approach. Consistent with past research (e.g., Ellis & Garber, in press
; Moffitt et al., 1992
; Surbey, 1990
), girls who were raised in single-mother homes tended to experience earlier pubertal timing than girls who were raised in two-parent homes. Extending past research, among girls who were raised in two-parent homes, variations in the dimensional quality of father–daughter relationships were associated with individual differences in pubertal timing. Two sets of results converged on this conclusion. First, greater father–daughter affectionate–positivity during the prekindergarten observations was associated with later pubertal timing in daughters. All of the father–daughter behavioral observations were made in father-present homes. Second, within father–present homes, more time spent by fathers in child care during the first 5 years of their daughters' lives was associated with later pubertal timing. This relation held even in the subset of families in which the fathers had been present in the home throughout their daughters' entire childhood. In sum, father-effects on daughters' pubertal timing clearly involved more than just father-absent effects. These data highlight the dimensional quality of father–daughter relationships as a possible influence on the timing of daughters' pubertal development.
Positive Versus Negative Dimensions of Early Family Relationships
Belsky et al. (1991)
conceptualized negative–coercive family relationships and positive–harmonious family relationships as opposite sides of the same coin. Whereas negative–coercive relationships were hypothesized to provoke earlier pubertal timing, positive–harmonious family relationships were hypothesized to promote later pubertal timing. The present data suggest that this theorizing was partially correct and partially incorrect. Factor analyses of both the interview and behavioral-observation data indicated that positive and negative family relationships were distinct but correlated dimensions of family environment. These dimensions differed in their relation to daughters' pubertal timing. As predicted by Belsky et al., higher levels of positive family relationships predicted significantly later pubertal timing by daughters. This finding replicated across both the interviewer ratings and behavioral observation ratings of positive family relationships. In contrast, variations in levels of negative family relationships were not associated with pubertal timing. This null finding was contrary to Belsky et al.'s theory. Taken together, these data indicate that it was levels of positive investment and support in family relationships, rather than levels of conflict and coercion in these relationships, that accounted for the relations with daughters
' pubertal timing
A possible interpretation of the null relations found in our study between negative family relationships and daughters' pubertal timing is that the measures of negative family relationships were poorly indexed. This interpretation is unlikely, however, because the measures of negative family relationships generally showed good internal consistency, reliability across raters, and reliability across independent data sources (i.e., behavioral observation vs. interviewer reports). Further, other analyses have shown that the present measures of negative family relationships are good long-term predictors of child adjustment (Dodge, Pettit, & Bates, 1994
; McFadyen-Ketchum, Bates, Dodge, & Pettit, 1996
; Pettit, Bates, & Dodge, 1997
Why did the predicted relation between negative–coercive family relationships in early childhood and subsequent pubertal timing fail to emerge? There are theoretical grounds for calling the prediction into question, Drawing on life history theory, MacDonald (1997)
and Miller (1994)
argued that in K-selected species (those characterized by high-investment, low-fertility reproductive strategies, such as those of humans) there should be a negative correlation between stress levels and speed of sexual maturation, rather than a positive correlation. Both of these theorists suggested that from an evolutionary perspective, it makes more sense in the face of physical or psychological stress for individuals to delay maturation and reproductive viability until predictably better times.5
Consistent with this perspective, Susman and colleagues (Susman, Dorn, & Chrousos, 1991
; Susman et al., 1985
) have hypothesized that stressful environments tend to delay pubertal onset by increasing levels of stress-related hormones from the adrenal axis. Increases in adrenal hormones have an inhibitor effect on sex steroid levels, resulting in delay of pubertal development.
Belsky's Family Ecology Model Versus a More Specific Father-Effects Model
Draper and Harpending's (1982
original theory of the development of reproductive strategies focused on fathers' role in the family. Belsky et al.'s (1991)
theory of the development of reproductive strategies expanded this father-based model into a more general family ecology model. This family ecology model subsumed all of the predictions of a more limited father-effects model of pubertal timing (i.e., that father–daughter and father–mother relationships will influence puberty) and added to it new predictions (i.e., that mother–daughter relationships will influence pubertal timing and that proximal family relationships will mediate the link between contextual family stressors and puberty).
Although our study supports Belsky et al.'s (1991)
focus on dynamic family processes and novel conceptualization of pubertal timing as an outcome of these processes, we found relatively little support for Belsky et al.'s shift to a general family ecology framework. A more limited father-effects model appears to provide a better fit to the data. As predicted by both the family ecology and father-effects models, the quality of fathers' early investment in the family emerged as a consistent predictor of daughters' pubertal timing, Beyond these father effects, however, the additional predictions of the family ecology model were not consistently supported. There are two sets of results that are relevant to this issue. First, of the contextual family stressors used in the present study (low SES, family life stressors, and single-parent status), only single-parent status (i.e., father absence) was associated with earlier pubertal timing in daughters. This association, of course, is consistent with a father-effects model. Second, father-effects emerged more strongly than mother effects. The direct comparison of mother- and father-effects on daughters' pubertal timing was conducted on the behavioral observation subsample. Consistent with the family ecology model, both mother–daughter affectionate–positivity and father–daughter affectionate–positivity were associated with later pubertal timing in daughters. However, only father–daughter affectionate–positivity made a unique contribution to the prediction of daughters' puberty (after controlling for the quality of mother–daughter relationships). Further, beyond mother–daughter affectionate–positivity, all of the other predictor variables in the study that were significantly correlated with pubertal timing were markers of fathers' investment in the family (i.e., father absence, time spent by the father in child care, supportiveness in the parental dyad, and father–daughter affectionate–positivity).
In total, the present data suggest that the quality of fathers' investment in the family is the most important feature of the proximal family environment relative to daughters' pubertal timing
. This conclusion is consistent with Surbey's (1990)
finding that girls who grew up in father-absent homes, but not in mother-absent homes, experienced earlier menarche than girls who grew up with both parents present. The primacy of father effects is notable, given that quality of mothering is generally more closely associated with child outcomes than is quality of fathering (Rothbaum & Weisz, 1994
Although the zero-order correlations presented in highlight the relation between positive paternal investment and daughters' pubertal timing, the second multiple regression presented in suggests that paternal investment per se (whether positive or negative) may account for the relations with daughters' pubertal timing. When father–daughter affectionate–positivity and father–daughter coercive control were entered simultaneously on Step 1 of the regression, each accounted for unique variance in daughters' pubertal timing. Most striking, not only did more father–daughter affectionate–positivity predict later pubertal timing in daughters (after controlling for father–daughter coercive control), but also more father–daughter coercive control predicted later pubertal timing in daughters (after controlling for father–daughter affectionate–positivity). Because the measures of both affectionate–positivity and coercive control were sensitive to frequency of father–daughter interactions, it may be that more father–daughter interaction or involvement per se delays pubertal maturation in daughters.
In all regions of the world and across all social and economic systems, mothers invest more time and energy in the direct care of children than do fathers (reviewed in Geary, 1998). Although mothers (and sometimes their female kin) form the primary foundation of parental care in all societies, the contribution of fathers to the family is—and presumably always has been—widely variable (see Draper & Harpending, 1982
; Geary, 1998). Within and across cultures, some men tend to form transient relationships with female partners and contribute relatively little to the care and provisioning of children, whereas other men tend to form long-term relationships with female partners and make considerable investment in children. Over the course of human evolution, this variability in male reproductive strategies must have afforded young girls with important cues to the reproductive opportunities and constraints they were likely to encounter later in life. Drawing on this logic, Draper and Harpending (1982
posited that girls have evolved to experience early socialization with their “antennae” tuned to the father's role in the family (both in terms of father–mother and father–daughter relationships) and that different paternal roles bias girls toward the acquisition of different reproductive strategies. The present data showing an association between early paternal investment and subsequent timing of puberty in daughters is consistent with this theorizing.
Although the present data highlight the role of positive family relationships and paternal investment in the regulation of daughters' reproductive development, they do not directly shed light on the psychological mechanisms and processes that mediate the relation between early family relationships and adolescent pubertal timing. As discussed earlier, one possibility is that the relation is spurious—the result of genetic transmission of pubertal timing and associated reproductive behaviors. Another possibility, consistent with Belsky et al. (1991)
, is that stress is the causal mechanism but that it is the particular kind of stress associated with either low levels of positive family relationships, a lack of paternal investment, or both that provokes earlier puberty. Future research could address this issue by collecting both behavioral data on family relationships and physiological data on daughters' stress responses (see Flinn & England, 1995
, for the use of this methodology).
A third possibility is that exposure to unrelated adult males is the causal mechanism (Ellis & Garber, in press
; Surbey, 1990
), Research on a variety of mammalian species (e.g., mice, cows, pigs, tamarins) indicates that exposure to pheromones produced by unrelated adult male conspecifics accelerates female pubertal development (Izard, 1990
; Sanders & Reinisch, 1990
; Ziegler, Snowdon, & Uno, 1990
). Consistent with findings from this animal research, Ellis and Garber's (in press)
findings indicated that years of exposure to unrelated father figures (stepfathers and mothers' boyfriends), rather than years of biological father absence, best accounted for earlier pubertal timing in girls. It may be that girls from paternally deprived homes are more likely to become exposed to the pheromones of stepfathers and other unrelated adult males, which in turn accelerates pubertal development. Unfortunately, the present study did not include enough information on daughters' exposure to unrelated males to test for its effects.
Another possible mechanism is inhibition of pubertal development through pheromonal exposure to the biological father (Hoogland, 1982
; Surbey, 1990
). There is some evidence in the animal research literature that the presence of closely related adult males inhibits reproductive maturation in females (and may function as an incest avoidance mechanism). In prairie dogs, for example, first ovulation is delayed in females who remain in contact with their biological fathers (Hoogland, 1982
). In the present study, among the subset of girls who had lived with their biological fathers throughout their lives (and thus were not exposed to stepfathers), more time spent by the father in child care during the girls' first 5 years of life was associated with later pubertal timing in seventh grade. Further, as discussed above, more father–daughter interaction or involvement per se was associated with later pubertal maturation. These data are consistent with the hypothesis that increased pheromonal exposure to biological fathers inhibits sexual maturation. However, it is also likely that girls who have high-investing fathers in the home tend to begin sex and dating at a later age (e.g., Flinn, 1988
; Hetherington, 1972
) and thus have less pheromonal exposure to male dating partners in early adolescence.
In closing, we would like to comment on the possible clinical implications of this work, As noted earlier, both father absence and early pubertal timing have been implicated as risk factors for female sexual promiscuity and teenage pregnancy, A father-based model of female reproductive development suggests that early pubertal maturation, risky sexual behavior, and early age of first birth are all components of an integrated reproductive strategy that derives, in part, from low paternal investment. The present data highlight the importance of early paternal involvement in the development of “healthy” reproductive functioning in daughters. At the same time, one should not interpret these data as suggesting that any adult male involvement is beneficial, as other research suggests that the presence of unrelated father figures may actually accelerate pubertal maturation in girls (Ellis & Garber, in press