Early-maturing girls are at risk for negative health outcomes, including emotional and substance use problems, early sexual debut, and, later in life, breast and other reproductive cancers.1–3
The impact of this developmental period on short and long-term health trajectories is substantial and spans a broad range of physical and mental health issues. This is particularly alarming given evidence that girls in the U.S. now enter puberty earlier than in the past.4
Environmental conditions, particularly those in the family domain, influence girls’ timing of puberty.5
Specifically, the absence of a biologically-related father has been shown to accelerate reproductive development. Evolutionary life history theory,6–8
which posits that humans have evolved to display adaptive plasticity in response to contextual circumstances, provides a theoretical foundation for how human biology responds to environmental conditions. Two decades ago, Belsky, Steinberg and Draper9
extended this theory to familial conditions and sexual maturation. These researchers posited that, during human evolutionary history, when girls encountered familial conditions that were unfavorable for survival (e.g., insecure and unsupportive family relationships), it was adaptive to become reproductively mature earlier. Since then, numerous empirical studies have confirmed that father absence predicts earlier maturation.10–13
Girls in father-absent homes are about twice as likely to experience menarche prior to age 12y. Mother absence does not appear to influence pubertal timing.10
Animal models illustrate biophysiological mechanisms through which parent-child processes affect maturation of the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-adrenal axes (HPA). In rodents, physical and social environments produce alterations in parent-offspring interactions, which in turn calibrate the development of stress- and steroid-responsive neural circuits and associated reproductive strategies, including pubertal timing and hormone profiles.14 15
Ecological stress causes low-quality parental care, which predicts a faster reproductive strategy in offspring.
A major gap in the epidemiological literature is that most studies focus on menarche, which occurs relatively late in puberty, or overall sexual development without distinguishing between onset of breast (thelarche) and pubic hair (pubarche) development. This is problematic given that these pubertal events represent observable markers of underlying hormones that are dependent on the maturation of unique endocrine axes (HPG, HPA), which may play differential roles in the etiology of health outcomes, such as breast cancer.
Another significant gap is that studies rarely examine mechanisms through which father absence may influence puberty. Although the most commonly suggested determinant of early puberty is overweight,16
only two known studies have examined weight in the pathway between father absence and puberty.10 17
Neither found mediating effects; however, one was retrospective10
and both focused on menarche. A related prospective study examining family adversity, but not father absence, found associations with BMI and pubertal timing, but BMI was not a mediator.18
However, elevated cumulative risk in a child’s home is strongly associated with heightened cardiovascular and neuroendocrine problems, including increased body fat deposition and allostatic load.19
A possible mechanism is that father absence signals other stressors in the home that influence BMI and subsequently impact puberty. Given that father absence is not considered modifiable, the study of BMI may yield one potential intervention target.
We utilized data from a prospective study of ethnically-diverse girls to test whether father absence predicts pubertal markers that occur prior to menarche (i.e., thelarche, pubarche). The activation of the gonadal axis is linked to fat deposition, therefore, we predicted that BMI would mediate the effect of father absence on thelarche, but not pubarche. We expected father absence to directly influence pubarche, which would lend mechanistic support to the hormonal stress response related to the development of the adrenal axis.
We also examined differences across income and ethnicity. Given that cumulative stress may augment pubertal acceleration, we hypothesized that girls growing up in lower-income families would be at greatest risk for experiencing early puberty as a result of father absence. Conversely, we anticipated that girls in higher-income father-absent families would be buffered from pubertal acceleration given greater access to resources. Potential cultural differences across ethnic groups (e.g., access to kinship networks and alternative caregivers) might also modify the effect of father absence on puberty. African American families historically have stronger extended familial networks to support child rearing compared to Caucasians.20
We predicted that African American girls growing up in father-absent homes may be less prone to accelerated puberty given availability of alternative caregiver support.