Father Absence, Body Mass Index, and Pubertal Timing in Girls: Differential Effects by Family Income and Ethnicity

Division of Community Health and Human Development, School of Public Health, University of California-Berkeley, CA 94720, USA.
Journal of Adolescent Health (Impact Factor: 3.61). 05/2011; 48(5):441-7. DOI: 10.1016/j.jadohealth.2010.07.032
Source: PubMed


Numerous studies show associations between father absence and girls' early puberty. However, most research has been retrospective, focused on menarche, and failed to consider body mass index (BMI), ethnicity, and income in the analyses. This study resolves these scientific gaps.
This was a prospective study of 444 girls aged 6-8 years and their caregivers (96% mothers). Data were collected annually in clinic, including weight, height, and Tanner stage for breast and pubic hair. Caregivers reported on father absence and demographics. This report focuses on the assessment of father absence at baseline and 2 years of follow-up for pubertal outcomes. Cox proportional hazards regression models were used to test whether father absence at baseline predicted pubertal onset by follow-up visit 2. BMI was assumed to be in the causal pathway. Differences by ethnicity and income were examined.
Income and ethnicity moderated associations between father absence and pubertal onset when adjusting for BMI. Father absence predicted earlier onset of breast development only in higher-income families and onset of pubic hair development only in higher-income African Americans families. BMI was not related to father absence and therefore was not in the causal pathway.
Among girls from higher-income families, father absence was linked to earlier puberty. This was particularly true for African Americans in terms of pubic hair development. These effects are not explained by body weight. Future research is needed to identify social and biophysiological mechanisms through which father absence, ethnicity, and income affect the pubertal onset.

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Available from: Louise Greenspan, May 08, 2014
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    • "estradiol levels and gray matter density in girls we can only speculate. Possible candidates for this environmental source are nutrition, as body mass index has been shown to advance the start of puberty (Wagner et al. 2012), or father absence, the effect of which is moderated by ethnicity and income (Deardorff et al. 2011). Although the evidence for a shared genetic background for pubertal brain development and pubertal hormones is limited in our cohort, there are certainly genes that influence both processes. "
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    ABSTRACT: Puberty is characterized by major changes in hormone levels and structural changes in the brain. To what extent these changes are associated and to what extent genes or environmental influences drive such an association is not clear. We acquired circulating levels of luteinizing hormone, follicle stimulating hormone (FSH), estradiol and testosterone and magnetic resonance images of the brain from 190 twins at age 9 [9.2 (0.11) years; 99 females/91 males]. This protocol was repeated at age 12 [12.1 (0.26) years] in 125 of these children (59 females/66 males). Using voxel-based morphometry, we tested whether circulating hormone levels are associated with grey matter density in boys and girls in a longitudinal, genetically informative design. In girls, changes in FSH level between the age of 9 and 12 positively associated with changes in grey matter density in areas covering the left hippocampus, left (pre)frontal areas, right cerebellum, and left anterior cingulate and precuneus. This association was mainly driven by environmental factors unique to the individual (i.e. the non-shared environment). In 12-year-old girls, a higher level of circulating estradiol levels was associated with lower grey matter density in frontal and parietal areas. This association was driven by environmental factors shared among the members of a twin pair. These findings show a pattern of physical and brain development going hand in hand. Electronic supplementary material The online version of this article (doi:10.1007/s10519-015-9708-8) contains supplementary material, which is available to authorized users.
    Full-text · Article · Feb 2015 · Behavior Genetics
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    • "The mechanisms stimulating this response include father absence, and family aggression and stress, a process Ellis (2004) referred to as ''psychosocial acceleration theory;'' the role of father absence he called ''paternal investment theory.'' Researchers evaluating this theory have found correlations between father absence and MT (Chisolm et al. 2005; Deardorff et al. 2011; Doughty and Rodgers 2000; Hoier 2003; Mustanski et al. 2004; Rowe 2002; see Brooks-Gunn 1988 for an exception). "
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    ABSTRACT: A powerful longitudinal data source, the National Longitudinal Survey of Youth Children data, allows measurement of behavior problems (BP) within a developmental perspective linking them to menarcheal timing (MT). In a preliminary analysis, we evaluate the bivariate relationships between BP measured at different developmental periods and the timing of menarche. Correlations were not consistent with any correlational/causal relationship between BP and MT. In the major part of our study, MT was used to moderate the developmental trajectory of BP, within a genetically-informed design. Girls reaching menarche early had behavior problem variance accounted for by the shared environment; those reaching menarche with average/late timing had behavior problem differences accounted for by genetic variance. Our findings match previous empirical results in important ways, and also extend those results. A theoretical interpretation is offered in relation to a theory linking genetic/shared environmental variance to flexibility and choices available within the family in relation to BP.
    Full-text · Article · Sep 2014 · Behavior Genetics
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    • "However, in this study, absence of the biological father was not associated with early menarche. The current findings are congruent with those of Ellis [36,37], in that the impact of early father absence on early menarche does not exist independent of other moderating factors in the environment. At the same time, the finding that sexual abuse prior to menarche is the strongest predictor of early menarche may implicate a related pathway. "
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    ABSTRACT: Background Epidemiological evidence suggests that early menarche, defined as onset of menses at age 11 or earlier, has increased in prevalence in recent birth cohorts and is associated with multiple poor medical and mental health outcomes in adulthood. There is evidence that childhood adversities occurring prior to menarche contribute to early menarche. Methods Data collected in face-to-face interviews with a nationally representative sample of women age 18 and over (N = 3288), as part of the National Comorbidity Survey-Replication, were analyzed. Associations between pre-menarchal childhood adversities and menarche at age 11 or earlier were estimated in discrete time survival models with statistical adjustment for age at interview, ethnicity, and body mass index. Adversities investigated included physical abuse, sexual abuse, neglect, biological father absence from the home, other parent loss, parent mental illness, parent substance abuse, parent criminality, inter-parental violence, serious physical illness in childhood, and family economic adversity. Results Mean age at menarche varied across decadal birth cohorts (χ2₍₄₎ = 21.41, p < .001) ranging from a high of 12.9 years in the oldest cohort (age 59 or older at the time of interview) to a low of 12.4 in the second youngest cohort (age 28-37). Childhood adversities were also more common in younger than older cohorts. Of the 11 childhood adversities, 5 were associated with menarche at age 11 or earlier, with OR of 1.3 or greater. Each of these five adversities is associated with a 26% increase in the odds of early menarche (OR = 1.26, 95% CI 1.14-1.39). The relationship between childhood sexual abuse and early menarche was sustained after adjustment for co-occurring adversities. (OR = 1.77, 95% CI 1.21-2.6). Conclusions Evidence from this study is consistent with hypothesized physiological effects of early childhood family environment on endocrine development. Childhood sexual abuse is the adversity most strongly associated with early menarche. However, because of the complex way that childhood adversities cluster within families, the more generalized influence of highly dysfunctional family environments cannot be ruled out.
    Full-text · Article · Jul 2014 · International Journal of Pediatric Endocrinology
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