I haven’t completely discredited the notion that Rushton and Lynn may be correct on this variable, but I’m highly skeptical. Hormonal data doesn’t show it. Hormones like IGF-1 and androgen don’t show the differences between races that would lead you to believe that Rushton’s Rule applies here.
PP is at it again, citing the same studies, not providing primary sources, and not addressing what I say to him about hormones in regards to penis size. Hormones affect the body in different ways, and different races have different levels of hormones. This is what I will discuss today.
Insulin-like growth factor 1 (IGF-1) is a hormone that, as it’s name implies, is structurally similar to the hormone insulin. IGF-1 is “partly responsible for systemic GH activities although it possesses a wide number of own properties (anabolic, antioxidant, anti-inflammatory and cytoprotective actions).” Laron and Klinger (1998) showed that children with Laron syndrome who stopped receiving IGF-1 injections showed reductions in penile and testicular size and they returned to pretreatment serum levels. This shows the effects of IGF-1 on sexual organ size.
Knowing this about IGF-1, for Rushton’s theory to be plausible, Blacks would have higher levels, Asians the lowest, and whites in the middle, skewing towards Asians. Platz et al (1999) investigated whether there were racial differences in circulating IGF-1 and insulin-like growth factor-binding protein 3 (IGFBP-3). IGFBP-3 binds IGF-1 and 2, with a dysregulation of IGFBP-3 correlating with cancer. IGFBP-3 is the main transporter of IGF-1 and 2 in the blood stream. The researchers tested men whose self-described ancestry (we know that self-describer ancestry is a great proxy for race, having a 99.86 percent success rate) African American (63) a random sample of Asians and Caucasians (75 respectively) aged 45 to 78 years old. Caucasians had the highest levels of IGF-1 (224 ng/ml), Asians (208 ng/ml), and African Americans (205 ng/ml). The IGF-1:IGFBP-3 ratio was greatest in Caucasians and lowest in Asians. This study was carried out to see if IGF-1 had an effect on prostate cancer. The 13 percent difference in IGFBP-3 between blacks and whites may account for the higher levels of prostate cancer, as IGFBP-3 can control IGF-1 bioavailabilty.
PP also cites Ross et al (1986) showing that blacks have “19 percent higher testosterone”, attempting to use this as evidence for the theory in favor of an inverse relationship between brain size and penis size. He seems to think that total testosterone matters, when what matters is free testosterone.It’s also 15 percent circulating testosterone, 13 percent free testosterone in that one study. Free testosterone is biologically active, and is able to exert its effect by passing through a cell and activating its receptor. Speaking of free testosterone, in this meta-analysis of 23 studies on black-white differences in testosterone, Richard et al (2014) showed a 2.5 to 4.9 percent difference in free testosterone and concluded that that difference was not enough to account for the racial disparity in prostate cancer. So it’s either black Americans have lower levels of IGFBP-3 or diet/environmental factors that cause this racial disparity in prostate cancer, not testosterone.
Rohrmann et al (2007) showed that testosterone differences between blacks (n=363) and whites (n=674) did not noticeably differ (5.29 ng/ml and 5.11 ng/ml respectively). Mexican Americans (n=376) , on the other hand, showed a higher average rate (5.48 ng/ml) over both cohorts. Blacks had higher levels of estradiol than whites (40.80 pg/nl and 35.46 pg/nl respectively). Blacks also had a higher level of sex hormone-binding globulin (SHGB) (36.49 nmol/liter) than whites (34.91 nmol/liter) and Mexican Americans (34.91 nmol/liter). That may account for some of the racial disparity in prostate cancer, but it’s not testosterone (which shows that ‘higher levels of testosterone’ as PP says, isn’t proof of any racial differences in penis size).
The Kinsey data is nonrepresentative and nonrandom. We have comparative sizes for certain ethnies, and the only statistical difference is between Nigerians and Koreans and Czechs. Rushton and Boegart didn’t mention that blacks danced less than white college students, blacks are more prudish regarding nudity, more likely to have a prostitute as a sexual partner and less likely to want large families (Weizmann et al, 1990). A study on certain CAG repeats shows that Africans cluster with East Asians on two measures, contradicting Lynn’s hypothesis. French Army Surgeon, lol (see Weizman et al 1990 from above):
This work is filled with internal contradictions. For example, an average African Negro penis is said to be 7 3/4 to 8 inches long on p. 56, while on p. 242 it is stated that it “generally exceeds” 9 inches. Similarly, while the French Army surgeon announces on p. 56 that he once discovered a 12-inch penis, an organ of that size becomes “far from rare” on p. 243. As one might presume from such a work, there is no indication of the statistical procedures used to compute averages, what terms such as “often” mean, how subjects were selected, how measurements were made, what the sample sizes were, etc.
I think I’ve shown that there are no “””racial””” differences in size with the Veale et al 2014 study and the Orakwe and Ebuh (2007) study. As far as I see, two statistical differences exist between Nigerians and Koreans and Czechs. But there’s not enough “””quality data””” to say “this race bigger than that race”. To believe there are racial differences in penis size or that there is even an inverse relationship between penis size and brain size takes a huge leap of faith to believe.
There are, without a doubt, average differences in a lot of things between races; hormones being one of them. Any differences between races in IGF-1 have no effect on penis size (IGF-1 is, however, one reason why black girls reach menarche at a younger age than white girls. Will write more on that in the future.). Africans were more similar to Asians that Caucasians on two of the five androgen indicators that Dutton (2015) tested. The Kinsey data is nonrepresentative and nonrandom and that is what PP continuously references. I’m highly skeptical leading towards no based on my knowledge of hormones and how they work in the human body. Testosterone does not explain any racial differences in penis size, and does not explain any differences in prostate cancer acquisition (though, other hormones do).