1100 words

Back in 2016 I wrote about racial differences in menarche and how there is good evidence that leptin is a strong candidate for the cause in my article Leptin and its Role in the Sexual Maturity of Black Girls (disregard the just-so stories). Black girls are more likely to hit puberty at a younger age than white girls. Why? One reason may be that leptin may play a role in the accelerated growth and maturation of black girls, since there was a positive relationship between leptin concentration and obesity in black girls (Wagner and Heyward, 2000). When girls start to develop at younger and younger ages, a phrase you hear often is “It’s the chemicals in the food” in regard to, for example, early breast development on a young, pre-teen girl.

Black girls are more likely to be obese than white girls (Freedman et al, 2000) and it is thought that body fat permits the effects of earlier menarche due to leptin being released from the adipocyte (fat cell) (Salsberry, Reagen, and Pajer, 2010). Freedman et al (2000) showed that black girls experienced menarche 3 months earlier than white girls on average, while over a 20 year period the median age decreased by 9.5 months. There is also evidence of earlier thelarche (breast development) in black girls, which was mediated by gonadotropin (Cabrera et al, 2014). Wong et al (1998) found that circulating serum leptin levels were correlated with earlier menarche in black girls which was related to body fatness and age but lessened after fat mass, maturation and physical fitness. There is a ton of evidence that exists that body fatness is related to obesity and, as I said above, the mechanism is probably fat cells releasing leptin, permitting earlier menarche (see Kaplowitz, 2008). Higher levels of body fat cause earlier menarche; earlier menarche does not cause higher levels of body fat. The evidence is there that leptin indeed plays the permissive role to allow a girl to enter into puberty earlier, and that this is how and why black girls enter menarche earlier than white girls.

So when fat mass increases, so does leptin; when leptin increases, girls have puberty at an earlier age (Apter, 2009). Black girls have higher levels of circulating leptin than white girls (Ambrosious et al, 1998). So knowing the relationship between leptin and obesity and how fat cells release leptin into the body permissing earlier puberty, we can confidently say that leptin is a major cause of earlier pubertal development in black girls. Total body fat correlates with fasted leptin (Ebenibo et al, 2018).

Siervogel et al (2003) write:

A negative relationship between age at menarche, BMI and body fatness in girls has been shown [63, 64, 65]. It is still unclear, however, whether increased early childhood adiposity induces an earlier onset of puberty, if rapid maturation and early puberty induce an increase in body fat later in life, or whether both of these phenomena occur.

The average age of menarche in black girls was 12 years of age whereas for white girls it was 12.5 (Regan et al, 2013). Since we now know the causes of earlier menarche, we can talk about ultimate causation.

Since menarche is correlated with obesity and circulating leptin levels, then food quality would be an easy culprit to look at.

Deardorff et al (2014) write:

Three sets of findings stood out. One, grandmother’s lower education was related to later menarche for Black girls. Two, mother’s unmarried status (at birth and age 7) was associated with earlier menarche for Hispanics and Whites, but not for Blacks. Three, family income at child’s birth was related to earlier menarche for Blacks and Hispanics, but not Whites.

Lower family income at birth was associated with earlier menarche for Blacks (and to some extent for Hispanics), but not for white girls.

Deardorff et al’s (2014) study suggests that social determinants of health can be intervened upon and differences in pubertal timing can be ameliorated since they are driven by social factors.

Black children have higher levels of insulino-glucose ratios than white children, even after adjusting for confounds (Wong et al, 1999). There were similar findings when comparing normal-weight black and white girls matched for age, bone age, weight, and BMI. Black girls also had higher levels of insulin than white girls. Black girls grow faster than white girls beginning at 2 years of age, with the cause hypothesized to be “higher serum insulin concentrations in healthy African American girls suppress the hepatic production of IGFBP-1, which results in higher circulating concentrations of free IGF-I, contributing to the accelerated growth observed in African American girls compared with their white counterparts” (Wong et al, 1999: 297).

Wong et al (1999) found that black girls were older and more sexually mature than white girls according to the Tanner stages of development (using pubic hair as a measure). Even after adjusting for age, black girls were still more sexually mature, heavier, and had higher levels of fat-free mass. Both serum insulin levels and serum concentrations of IGF-1 were significantly higher in black girls compared to white girls. Even after they controlled for differences in pubic hair development and fat mass, the differences in IGF-1 and IGFBP-1 remained significant. So black girls in this study had higher levels of IGF-1 and insulin than white girls.

This is significant because higher levels of IGF-1 at age 8 are associated with earlier menarche in girls (Thankamoney et al, 2012). Earlier menarche is related to higher levels of adiposity, as noted above, and the mechanism for earlier menarche is fat cells releasing insulin which has a permissive effect on menarche. Further, there is evidence that lower levels of circulating growth hormones are related to delayed menarche (Circo, 2014).

IGF-1 is a protein “coded for” by the IGF-1 gene (Hoppener et al, 1985). IGF-1 is molecularly similar to insulin (Laron, 2001). This makes sense. Body fat cannot be stored unless insulin is high; since they are molecularly similar, they both cause growth, albeit in different ways.

In conclusion, there is strong evidence that body fatness is related to earlier menarche, with the mechanism being fat cells releasing leptin which has a permissive effect on pubertal development. Further evidence indicates that circulating hormones like insulin and IGF-1 also have permissive effects on pubertal development. Black girls are more likely to be obese than white girls. Black girls are more likely to have higher levels of circulating hormones like IGF-1 and insulin than white girls. Thus, a cause—a major cause in my opinion—for earlier menarche in black girls compared to white girls is higher levels of body fat and higher levels of circulating hormones like IGF-1 and insulin which have a permissive effect on menarche.