African-American/white differences in the age of menarche: Accounting for the difference

Abstract

Lifetime health disparity between African-American and white females begins with lower birthweight and higher rates of childhood overweight. In adolescence, African-American girls experience earlier menarche. Understanding the origins of these health disparities is a national priority. There is growing literature suggesting that the life course health development model is a useful framework for studying disparities. The purpose of this study was to quantify the influence of explanatory factors from key developmental stages on the age of menarche and to determine how much of the overall race difference in age of menarche they could explain. The factors were maternal age of menarche, birthweight, poverty during early childhood (age 0 through 5 years), and child BMI z-scores at 6 years. The sample, drawn from the US National Longitudinal Surveys of Youth Child–Mother file, consisted of 2337 girls born between 1978 and 1998. Mean age of menarche in months was 144 for African-American girls and 150 for whites.

An instrumental variable approach was used to estimate a causal effect of child BMI z-score on age of menarche. The instrumental variables were pre-pregnancy BMI, high gestational weight gain and smoking during pregnancy. We found strong effects of maternal age of menarche, birthweight, and child BMI z-score (−5.23, 95% CI [−7.35,−3.12]) for both African-Americans and whites. Age of menarche declined with increases in exposure to poverty during early childhood for whites. There was no effect of poverty for African-Americans. We used Oaxaca decomposition techniques to determine how much of the overall race difference in age of menarche was attributable to race differences in observable factors and how much was due to race dependent responses. The African-American/white difference in childhood BMI explained about 18% of the overall difference in age of menarche and birthweight differences explained another 11%.

Introduction

African-American females are less healthy than whites throughout their lives. As neonates they have lower birthweight (Blumenshine, Egerter, Barclay, Cubbin, & Braveman, 2010; Whitehead & Helms, 2010); in childhood they are more likely to be obese (Ogden et al., 2006); and in adulthood they experience higher rates of chronic diseases such as cardiovascular disease and depression (Baker, Buchanan, & Spencer, 2010). Understanding the origins and pathways of these health disparities is a high national priority and there is a growing literature suggesting that a life course health development model is a useful framework for studying disparities (Braveman & Barclay, 2009; Halfon & Hochstein, 2002; Lu & Halfon, 2003). Within the life course model, health development is seen as the result of biological processes unfolding during defined developmental stages, interacting with physical, social, economic, and psychological environments. Health disparities are thought to originate in exposures to disadvantage at critical developmental stages and/or because of compounding and cumulative effects with continual exposure to disadvantage. This framework has the benefit of being able to consider proximal factors as well as distal risks from previous development stages. In this study, we were interested in understanding the racial difference in age of menarche as a function of factors from developmental periods (i.e., intrauterine, early childhood, middle childhood, adolescence) known to be associated with age of menarche and to have significant variation across racial group.

Contemporary African-American girls experience a younger age of menarche than do their white counterparts (Huang, Biro, & Dorn, 2009), a finding replicated in several large population studies. For example, the Pediatric Research in Office Settings data revealed that mean age of menarche was 12.2 years for African-American girls compared to 12.9 years for whites (Herman-Giddens et al., 1997); the National Health and Nutrition Examination Survey (NHANES III) data indicated mean ages of 12.1 and 12.7 years for the two groups respectively (Wu, Mendola, & Buck, 2002); and the Bogalusa Heart Study reported mean age of 12.1 years for African-American girls and 12.5 years for whites (Freedman et al., 2002). Although the race differences in age of menarche were statistically significant in all studies, its explanation remains elusive.

Research has traced differences in age of menarche to early compromise in the intrauterine environment. Size at birth, whether measured by birthweight, weight for gestational age, or a combination of birthweight and birth length, has been used as a summary measure of the quality of the intrauterine environment. There is no consensus in the literature about the effect of birth size on age of menarche. However, it does appear to be sensitive to controls for growth in infancy and childhood. Adair (2001) reported that long and light infants had earlier menarche and the effect was more pronounced controlling for post natal growth in infancy. Tam, de Zegher, Garnett, Baur, and Cowell (2006) found that long and light infants had an earlier menarche, but only after controlling for adiposity at age 8 years. Sloboda, Hart, Doherty, Pennell, and Hickey (2007) found independent effects of low birthweight and weight gain through age 8 years, with earliest menarche occurring in girls with low birthweight and high BMI. In contrast, Terry, Ferris, Tehranifar, Wei, and Flom (2009) found that a higher birthweight was associated with an earlier age of menarche, but only after controlling for weight gain until age 7 years. dos Santos Silva et al. (2002) found that higher birthweight was associated with lower age of menarche after controlling for growth in infancy, but the effect disappeared when controls for growth through age 7 were added. Direct comparison of these studies is difficult as there was variation in the study populations, in the growth measures, and the analytic approaches.

Stress levels related to factors in the child's early environment, including material resources, environmental toxins, harsh/positive parenting styles, and family structure, have been linked to age of menarche (Belsky, Steinberg, Houts, & Halpern-Felsher, 2010; Hulanicka, Gronkiewicz, & Koniarek, 2001). Exposures to nicotine in utero and during childhood have been associated with later age of menarche (Ferris, Flom, Tehranifar, Mayne, & Terry, 2010; Windham, Zhang, Longnecker, & Klebanoff, 2008). It is widely acknowledged that African-American families experience increased material hardship and levels of stress (Logan, 2002), thereby introducing a mechanism through which possible race differences in the age of menarche may originate. Lower economic status at age 7 and declining economic status between birth and age 7 have been associated with a younger age of menarche in a racially mixed population (James-Todd, Tehranifar, Rich-Edwards, Titievsky, & Terry, 2010). However, others have reported different race effects of exposure to poverty on age of menarche. Compared to girls of the same race above the poverty line, African-American girls living in poverty had later menarche whereas white girls living in poverty had earlier menarche (Braithwaite et al., 2009).

A girl's BMI has been the most widely researched factor in understanding race differences in age of menarche. Overweight is currently accepted as the primary explanation for differences in age of menarche across all races (Anderson, Dallal, & Must, 2003) and in particular the African-American/white difference (Freedman et al., 2002). Increased adiposity has been linked to early menarche, with numerous mechanisms hypothesized to be in play. Frisch and McArthur (1974) hypothesized that a minimum weight or body fat percent was required for menarche. Current theories focus on hormonal mechanisms that may be altered in girls with higher BMIs, including the influence of leptin activation on the gonadotropin-releasing hormone pulse generator, but definitive paths are not known and considerable research is ongoing. Furthermore, because the obesity epidemic has disproportionately impacted African-American girls (Strauss & Pollack, 2001) many have inferred that the earlier age of menarche experienced by African-American girls is due to increased BMI (Kaplowitz, 2006; Lee et al., 2007; Wang, 2002).

Only a few studies have explicitly explored the reasons for the African-American/white difference in age of menarche and the results are far from conclusive. Kaplowitz, Slora, Wasserman, Pedlow, and Herman-Giddens (2001) found an association between increased weight and earlier puberty for both white and African-American girls, but the effect was stronger for whites, leading them to conclude that other factors, perhaps genetics or environmental factors, may also be operating. Anderson et al. (2003) concluded that increased BMI leads to earlier menarche, but that race differences in age of menarche cannot be explained entirely by race differences in BMI.

While this substantial body of work highlights key factors associated with age of menarche, there remain gaps in our knowledge. First, prior approaches using standard methods like OLS may have resulted in biased estimates of the effects of child BMI because BMI and age of menarche are likely to be influenced by some of the same unobserved factors. The second gap is linked to understanding the racial difference in age of menarche. Few studies have explicitly examined why racial differences in age of menarche occur. The purpose of this study was to identify and quantify the influence of explanatory factors from key developmental stages on the age of menarche. This study is novel in the sense that we use an instrumental variable (IV) approach, i.e., two-stage least squares, to overcome the problem of endogenous child BMI and to obtain causal effects of the explanatory factors on age of menarche. The study also assesses the extent to which each explanatory factor contributes to the race difference in age of menarche by implementing a Blinder–Oaxaca decomposition analysis.