1200 words

There are differences between the races in regards to sexual maturity. I’ve recently discovered that leptin plays a role in black female teenagers and how they reach puberty earlier than that of white women. This is one out of many variables that prove Rushton’s three-way rule; that the races all differ on certain variables, on average.

Buried in the middle of this article on black and white differences in body composition, it is observed that the mean concentration of leptin was significantly greater in black girls than that of white girls. The authors conclude that leptin may play an important role in the accelerated growth and sexual maturation of black girls:

In one study, the mean leptin concentration was significantly (P < 0.01) higher in 57 black girls (15.0 ± 10.1 μg/L) than in 79 white girls (8.4 ± 11.1 μg/L) aged 8–17 y (58). The authors concluded that this difference might play an important role in the accelerated growth and sexual maturation of black girls. Likewise, Nicklas et al (57) reported a strong correlation between leptin and %BF for both black (r = 0.71, P < 0.0001) and white (r = 0.61, P < 0.001) obese postmenopausal women, but a significant racial difference in leptin concentration (36.0 ± 4.8 compared with 45.8 ± 3.5 μg/L; P < 0.05), respectively. Additionally, leptin correlated with resting energy expenditure in black women (r = 0.58, P < 0.001) but not in white women (r = 0.08).

Also noticed, was that leptin correlated with REE (resting energy expenditure) in black women but not in white women.

Wong et al (1998), state that because African-American girls tend to be heavier and mature faster than white girls, then there must be a leptin difference between the 2 groups. He measured serum leptin concentrations in 12 hour fasted blood samples of 57 black and 79 white girls. Body comp was measured by x-ray absorptiometry, sexual maturity by doctor examination and physical fitness by treadmill testing. What was found was the serum leptin levels were positively correlated with body fat, maturation and insulin were higher in the black girls after controlling for age. Differences remained, but lessened, after controlling for differences in fat mass, maturation, and physical fitness. This is more proof that leptin is a cause for the role in earlier sexual maturity in black girls.

Kaplowitz (2008) observed in his paper Link Between Body Fat and the Timing of Puberty that several studies have shown that the increase in earlier sexual maturation may indeed be linked to the obesity epidemic which started to rise around 50 to 60 years ago when fat was demonized as “being the cause for fat gain”, all the while carbs were championed as a better macro over fat. Of course, we now know that’s not true, but the implications of this lie that we’ve been told are now coming out in the light 50 years later.

Kaplowitz states that the evidence currently out points to obesity being a cause for earlier puberty in girls, rather than earlier puberty causing an increase in body fat (hmmm.. where have I heard confusing one cause for another before? Oh yeah, the IQ/obesity cause).Many studies have come out that show, in both rats and humans, that leptin may be the critical link between body fat and earlier puberty. Both mice and humans who were deficient in leptin both failed to reach puberty unless leptin was administered. Though he says that leptin may end up playing a permissive, rather than a critical metabolic signal that initiates puberty. But with the data of black girls having higher leptin levels, leptin being correlated highly with body fat, and both being highly correlated with increased sexual maturation show the reason why black girls are a) more sexually active at a younger age and b) why black girls mature faster than white girls. He finally concludes that it makes evolutionary sense that body fat and reproduction in girls evolved as a mechanism to ensure that pregnancy won’t occur unless adequate levels of body fat are had.

This is yet more biological evidence for physiological differences between the races.

When fat mass increases, so do leptin levels. When leptin levels increase, puberty happens earlier. Black girls have higher rates of  leptin, which correlates highly with body fat and sexual maturity, so it’s no surprise that we see these factors here.

What are evolutionary causes for this? Well, seeing Africa’s life expectancy, the rate of parasitic load as well as disease in Africa, and Rushton’s r/K Life History Theory, which states that those more r selected will have more children and show less care for them whereas those more k selected will have less progeny, but show more care, we can easily see how such a mechanism evolved. With IQ being highly correlated with life expectancy (at .95), we can see part of the reason why, for instance, black women evolved to have higher rates of 2 egg twinning in comparison to whites (16 per 1000 for blacks, 8 per 1000 for whites and 4 per 1000 for Orientals). To quote Rushton from Race, Evolution, and Behavior:

Black women, compared to white women, average a shorter period of ovulation and produce more eggs per ovulation in addition to all the other characteristics in Table 1.1. As mentioned, the rate of dizygotic twinning, a direct index of egg production, is less than 4 per 1,000 births among Mongoloids, 8 per 1,000 among Caucasoids, and 16 or greater per 1,000 among Negroids. (pg. 6)

This is a clear evolutionary strategy. Have more children where it’s less hospitable and there is a higher mortality rate, especially for young children and have fewer children where it is more stable and less environmental dangers are around.

Even more evidence to bolster my claim is how 82 percent of black women are overweight or obese (Ogden et al, 2014). Genes related to obesity have also been found in African-Americans, as well as European-Americans, which also bolster the claim seeing as the genes were found to do the same things in both populations. To quote myself from the above article:

In a study published back in 2013, researchers were looking for obesity genes in African Americans. The study, which involved more than 70,000 men and women of African descent, they were able to identify 3 SNPs that were associated with obesity and BMI in the sample population. What was also found, was that those same genetic sequences also heighten rates of obesity in peoples with no African ancestry, all of the genetic variants associated with obesity were also found in European populations. The same genes found in African populations did the same in European populations, and vice versa.

To quote the paper:

We provide evidence for a shared genetic influence on BMI across populations, as we found directionally consistent associations with the majority of known BMI risk variants. This observation suggests that bioloically functional alleles are ancient and probably arose before migrations out of Africa. In addition, we were able to refine the window of association of some of the previously established BMI loci, which may eventually help identify the biologically functional variant(s).

BMI is also between .75 and .82 heritable. These factors show yet another cause for black women’s high obesity rates, of course with eating garbage food all of the time, but I’m talking about evolutionary reasons.

There are reasons why black girls mature faster than white girls, it’s because of leptin, which precedes an increase in body fat to prepare for eventual menstruation and higher body fat helps to protect the baby in vitro. R/K Life History Theory then shows the evolutionary reasons why earlier sexual maturity happens for black girls over white girls: lower life expectancy.