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I enjoy reading what other bloggers write about testosterone and its supposed link to crime, aggression, and prostate cancer; I used to believe some of the things they did, since I didn’t have a good understanding of the hormone nor its production in the body. However, once you understand how its produced in the body, then what others say about it will seem like bullshit—because it is. I’ve recently read a few articles on testosterone from the HBD-blog-o-sphere and, of course, they have a lot of misconceptions in them—some even using studies I have used myself on this blog to prove my point that testosterone does not cause crime!! Now, I know that most people don’t read studies that are linked, so they would take what it says on face value because, why not, there’s a cite so what he’s saying must be true, right? Wrong. I will begin with reviewing an article by someone at The Alternative Hypothesis and then review one article from Robert Lindsay on testosterone.
The Alternative Hypothesis
Faulk has great stuff here, but the one who wrote this article, Testosterone, Race, and Crime, 1) doesn’t know what he’s talking about and 2) clearly didn’t read the papers he cited. Read this article, you’ll see him make bold claims using studies I have used for my own arguments that testosterone doesn’t cause crime! Let’s take a look.
One factor which explains part of why Blacks have higher than average crime rates is testosterone. Testosterone is known to cause aggression, and Blacks are known to at once have more of it and, for genetic reasons, to be more sensitive to its effects.
- No it doesn’t.
- “Testosterone is known to cause aggression“, but that’s the thing: it’s only known that it ’causes’ aggression, it really doesn’t.
- Evidence is mixed on blacks being “… for genetic reasons … more sensitive to its effects” (Update on Androgen Receptor gene—Race/History/Evolution Notes).
Testosterone activity has been linked many times to aggression and crime. Meta-analyses show that testosterone is correlated with aggression among humans and non human animals (Book, Starzyk, and Quinsey, 2001).
Why doesn’t he say what the correlation is? It’s .14 and this study, while Archer, Graham-Kevan and Davies, (2005) reanalyzed the studies used in the previous analysis and found the correlation to be .08. This is a dishonest statement.
Women who suffer from a disease known as congenital adrenal hyperplasia are exposed to abnormally high amounts of testosterone and are abnormally aggressive.
Abnormal levels of androgens in the womb for girls with CAH are associated with aggression, while boys with and without CAH are similar in aggression/activity level (Pasterski et al, 2008), yet black women, for instance, don’t have higher levels of testosterone than white women (Mazur, 2016). CAH is just girls showing masculinized behavior; testosterone doesn’t cause the aggression (See Archer, Graham-Kevan and Davies, 2005)
Actually, no. Supraphysiological levels of testosterone administered to men (200 and 600 mg weekly) did not increase aggression or anger (Batrinos, 2012).
Finally, people in prison have higher than average rates of testosterone (Dabbs et al., 2005).
Dabbs et al don’t untangle correlation from causation. Environmental factors can explain higher testosterone levels (Mazur, 2016) in inmates, and even then, some studies show socially dominant and aggressive men have the same levels of testosterone (Ehrenkraz, Bliss, and Sheard, 1974).
Thus, testosterone seems to cause both aggression and crime.
No, it doesn’t.
Furthermore, of the studies I could find on testosterone in Africans, they have lower levels than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006) so, along with the studies and articles cited on testosterone, aggression, and crime, that’s another huge blow to the testosterone/crime/aggression hypothesis.
Richard et al. (2014) meta-analyzed data from 14 separate studies and found that Blacks have higher levels of free floating testosterone in their blood than Whites do.
They showed that blacks had 2.5 to 4.9 percent higher testosterone than whites, which could not explain the higher prostate cancer incidence (which meta-analyses call in to question; Sridhar et al 2010; Zagars et al 1998). That moderate amount would not be enough to cause differences in aggression either.
Exacerbating this problem even further is the fact that Blacks are more likely than Whites to have low repeat versions of the androgen receptor gene. The androgen reception (AR) gene codes for a receptor by the same name which reacts to androgenic hormones such as testosterone. This receptor is a key part of the mechanism by which testosterone has its effects throughout the body and brain.
The rest of the article talks about CAG repeats and aggressive/criminal behavior, but it seems that whites have fewer CAG repeats than blacks.
This one is much more basic, and tiring to rebut but I’ll do it anyway. Lindsay has a whole slew of articles on testosterone on his blog that show he doesn’t understand the hormone, but I’ll just talk about this one for now: Black Males and Testosterone: Evolution and Perspectives.
It was also confirmed by a recent British study (prostate cancer rates are somewhat lower in Black British men because a higher proportion of them have one White parent)
Jones and Chinegwundoh (2014) write: “Caution should be taken prior to the interpretation of these results due to a paucity of research in this area, limited accurate ethnicity data, and lack of age-specific standardisation for comparison. Cultural attitudes towards prostate cancer and health care in general may have a significant impact on these figures, combined with other clinico-pathological associations.”
This finding suggests that the factor(s) responsible for the difference in rates occurs, or first occurs, early in life. Black males are exposed to higher testosterone levels from the very start.
In a study of women in early pregnancy, Ross found that testosterone levels were 50% higher in Black women than in White women (MacIntosh 1997).
I used to believe this, but it’s much more nuanced than that. Black women don’t have higher levels of testosterone than white women (Mazur, 2016; and even then Lindsay fails to point out that this was pregnant women).
According to Ross, his findings are “very consistent with the role of androgens in prostate carcinogenesis and in explaining the racial/ethnic variations in risk” (MacIntosh 1997).
Testosterone has been hypothesized to play a role in the etiology of prostate cancer, because testosterone and its metabolite, dihydrotestosterone, are the principal trophic hormones that regulate growth and function of epithelial prostate tissue.
Testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Diet explains any risk that may be there (Hayes et al, 1999; Gupta et al, 2009; Kheirandish and Chinegwundoh, 2011; Williams et al, 2012; Gathirua-Mingwai and Zhang, 2014). However in a small population-based study on blacks and whites from South Carolina, Sanderson et al (2017) “did not find marked differences in lifestyle factors associated with prostate cancer by race.”
Regular exercise, however, can decrease PCa incidence in black men (Moore et al, 2010). A lot of differences can be—albeit, not too largely— ameliorated by environmental interventions such as dieting and exercising.
Many studies have shown that young Black men have higher testosterone than young White men (Ellis & Nyborg 1992; Ross et al. 1992; Tsai et al. 2006).
Ellis and Nyborg (1992) found 3 percent difference. Ross et al (1992) have the same problem as Ross et al (1986), which used University students (~50) for their sample. They’re not representative of the population. Ross et al (1992) also write:
Samples were also collected between 1000 h and 1500 h to avoid confounding
by any diurnal variation in testosterone concentrations.
Testosterone levels should be measured near to 8 am. This has the same time variation too, so I don’t take this study seriously due to that confound. Assays were collected “between” the hours of 10 am and 3 pm, which means it was whenever convenient for the student. No controls on activities, nor attempting to assay at 8 am. People of any racial group could have gone at whatever time in that 5 hour time period and skew the results. Assaying “between” those times completely defeats the purpose of the study.
This advantage [the so-called testosterone advantage] then shrinks and eventually disappears at some point during the 30s (Gapstur et al., 2002).
This makes it very difficult if not impossible to explain differing behavioral variables, including higher rates of crime and aggression, in Black males over the age of 33 on the basis of elevated testosterone levels.
See above where I talk about crime/testosterone/aggression.
Critics say that more recent studies done since the early 2000’s have shown no differences between Black and White testosterone levels. Perhaps they are referring to recent studies that show lower testosterone levels in adult Blacks than in adult Whites. This was the conclusion of one recent study (Alvergne et al. 2009) which found lower T levels in Senegalese men than in Western men. But these Senegalese men were 38.3 years old on average.
Alvergne, Fauri, and Raymond (2009) show that the differences are due to environmental factors:
This study investigated the relationship between mens’ salivary T and the trade-off between mating and parenting efforts in a polygynous population of agriculturists from rural Senegal. The men’s reproductive trade-offs were evaluated by recording (1) their pair-bonding/fatherhood status and (2) their behavioral profile in the allocation of parental care and their marital status (i.e. monogamously married; polygynously married).
They also controlled for age, so his statement “But these Senegalese men were 38.3 years old on average” is useless.
These critics may also be referring to various studies by Sabine Rohrmann which show no significance difference in T levels between Black and White Americans. Age is poorly controlled for in her studies.
That is one study out of many that I reference. Rohrmann et al (2007) controlled for age. I like how he literally only says “age is poorly controlled for in her studies“, because she did control for age.
That study found that more than 25% of the samples for adults between 30 and 39 years were positive for HSV-2. It is likely that those positive samples had been set aside, thus depleting the serum bank of male donors who were not only more polygamous but also more likely to have high T levels. This sample bias was probably worse for African American participants than for Euro-American participants.
Why would they use diseased samples? Do you even think?
Young Black males have higher levels of active testosterone than European and Asian males. Asian levels are about the same as Whites, but a study in Japan with young Japanese men suggested that the Japanese had lower activity of 5-alpha reductase than did U.S. Whites and Blacks (Ross et al 1992). This enzyme metabolizes testosterone into dihydrotestosterone, or DHT, which is at least eight to 10 times more potent than testosterone. So effectively, Asians have the lower testosterone levels than Blacks and Whites. In addition, androgen receptor sensitivity is highest in Black men, intermediate in Whites and lowest in Asians.
Ethnicmuse also showed that, contrary to popular belief, Asians have higher levels of testosterone than Africans who have higher levels of testosterone than Caucasians in his meta-analysis. (Here is his data.)
Let us look at one study (Ross et al 1986) to see what the findings of a typical study looking for testosterone differences between races shows us. This study gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in Blacks were 19% higher than in Whites, and free testosterone levels were 21% higher. Both these differences were statistically significant.
Assay times between 10 am and 3 pm, unrepresentative sample of college men, didn’t have control for waist circumference. Horribly study.
A 15% difference in circulating testosterone levels could readily explain a twofold difference in prostate cancer risk.
No, it wouldn’t (if it were true).
Higher testosterone levels are linked to violent behavior.
Causation not untangled.
Studies suggest that high testosterone lowers IQ (Ostatnikova et al 2007). Other findings suggest that increased androgen receptor sensitivity and higher sperm counts (markers for increased testosterone) are negatively correlated with intelligence when measured by speed of neuronal transmission and hence general intelligence (g) in a trade-off fashion (Manning 2007).
Who cares about correlations? Causes matter more. High testosterone doesn’t lower IQ. Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut.
Racial differences in testosterone don’t exist/are extremely small in magnitude (as I’ve covered countless times). The one article from TAH literally misrepresents studies/leaves out important figures in the testosterone differences between the two races to push a certain agenda. Though if you read the studies you see something completely different. It’s the same with Lindsay. He misunderstood a few studies to push his agenda about testosterone and crime and prostate cancer. They’re both wrong, though.
Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut. People read and write about things they don’t understand, which is the cause of these misconceptions with the hormone, as well as, of course, misinterpreting studies. Learn about the hormone and you won’t fear it. It doesn’t cause crime, prostate cancer nor aggression; these people who write these articles have one idea in their head and they just go for it. They don’t understand the intricacies of the endocrine system and how sensitive it is to environmental influence. I will cover more articles that others have written on testosterone and aggression to point out what they got wrong.
Misinformation about testosterone and strength in regards to race is rampant in the HBD-o-sphere. One of the most oft-repeated phrases is that “Blacks have higher levels of testosterone than whites”, even after controlling for numerous confounds. However, the people who believe this literally only cite one singular study with 50 blacks and 50 whites. Looking at more robust data with higher ns shows a completely different story. Tonight I will, again, go through the race/testosterone conundrum (again).
Type I fibers fire first when heavy lifting. Whites have more type I fibers. Powerlifters and Olympic lifters have a greater amount type IIa fibers, with fewer type IIx fibers (like whites). This explains why blacks are hardly represented in powerlifting and strongman competitions.
Somatype, too, also plays a role. Whites are more endo than blacks who are more meso. Endomorphic individuals are stronger, on average, than mesomorphic and ectomorphic individuals.
Blacks have narrower hips and pelves. This morphological trait further explains why blacks dominate sports. Some people may attempt to pick out one variable that I speak about (fiber type, morphology, somatype, fat mass, etc) and attempt to disprove it, thinking that disproving that variable will discredit my whole argument. However, fiber typing is set by the second trimester, with no change in fiber type from age 6 to adulthood (Bell et al, 1980).
It is commonly believed that blacks have higher levels of testosterone than whites. However, this claim is literally based off of one study (Ross et al, 1986) when other studies have shown low to no difference in T levels (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Richard et al 2014). People who still push the “blacks-have-higher-T-card” in the face of this evidence are, clearly, ideologues who want to cushion their beliefs when presented with contradictory evidence (Nyhan and Reifler, 2010).
‘Honor Culture’ and testosterone
In all of my articles on this subject, I have stated—extensively—that testosterone is mediated by the environment. That is, certain social situations can increase testosterone. This is a viewpoint that I’ve emphatically stated. I came across a paper while back that talks about a sociological perspective (I have huge problems with social ‘science’, [more on that soon] but this study was very well done) in regards to the testosterone difference between blacks and whites.
Some people when they read this, however, may go immediately to the part of the paper that says what they want it to say without fully assessing the paper. In this section, I will explain the paper and how it confirms my assertions/arguments.
Mazur (2016) begins the paper talking about ‘honor culture‘, which is a culture where people avoid intentionally offending others while also maintaining a status for not backing down from a confrontation. This theory was proposed by Richard Nisbett in 1993 to explain why the South had higher rates of violence—particularly the Scotch-Irish.
However parsimonious the theory may sound, despite its outstanding explanatory power, it doesn’t hold while analyzing white male homicides in the South. It also doesn’t hold analyzing within-county homicide rates either, since apparently poverty better explains higher homicide rates.
But let’s assume it’s true for blacks. Let’s assume the contention to be true that there is an ‘honor culture’ that people take part in.
Young black men with no education had higher levels of testosterone than educated whites and blacks. Looking at this at face value—literally going right to the section of the paper that says that poor blacks had higher testosterone, nearly 100 ng/ml higher than the mean testosterone of whites. As Mazur (2016) notes, this contradicts his earlier 2009 study in which he found no difference in testosterone between the races.
Note the low testosterone for both races at age 20-29—ranging from about 515 to 425—why such low testosterone levels for young men? Anyway, the cause for the higher levels is due to the type of honor culture that blacks participate in, according to Mazur (which is consistent with the data showing that testosterone rises during conflict/aggressive situations).
Mazur cites Elijah Anderson, saying that most youths have a “code of the streets” they take part in, which have to do with interpersonal communication such as “gait and verbal expressions” to deter aggressive behavior.
Testosterone is not a causal variable in regards to violent behavior. But it does rise during conflicts with others, watching a favorite sports team, asserting dominance, and even how you carry yourself (especially your posture). Since low-class blacks participate in these types of behaviors, then they would have higher levels of testosterone due to needing to “keep their status.”
When testosterone rises in these situations, it increases the response threat in mens’ brains, most notably showing increased activity in the amygdala. Further, dominant behavior and posture also increase testosterone levels. Putting this all together, since blacks with only a high school education have higher testosterone levels and are more likely to participate in honor culture compared to whites and blacks with higher educational achievement, then they would have higher testosterone levels than whites and blacks with a high school education who do not participate in honor culture.
Further, as contrary to what I have written in the past (and have since rescinded), there is no indication of higher testosterone levels in black women with low education. It seems this ‘honor culture’ effect on testosterone only holds for black men with only a high school education.
Mazur’s (2016) most significant finding was that black men aged 20-29 with only a high school education had 91 ng/ml higher testosterone than whites. Among older and/or educated men, testosterone did not vary. This indicates that since they have attained higher levels of educational success, there is no need to participate in ‘honor culture’.
This is yet further evidence for my assertion that environmental variables such as posture, dominance, and aggressive behavior raise testosterone levels.
The honor culture hypothesis is found to hold in Brazil in a comparative study of 160 inmates and non-inmates (De Souza et al, 2016). As Mazur (2016) notes, the honor culture hypothesis could explain the high murder rate for black Americans—the need to ‘keep their status’. It’s important to note that this increase in testosterone was not noticed in teenage or female blacks (because they don’t participate in honor culture).
There is a perfectly good environmental—not genetic—reason for this increase in testosterone in young blacks with only a high school education. Now that we know this, back to race and strength.
Mazur (2009) found that black men in the age range of 20-69, they averaged .39 ng/ml higher testosterone than whites, which is partly explained by lower marriage rates and low adiposity. White men are more likely to be obese than black men, since black men with more African ancestry are less likely to be obese. When controlling for BMI, blacks are found to have 2.5-4.9 percent more testosterone than whites (Gapstur et al, 2002, Rohrmann et al, 2007, Richard et al, 2014). There is little evidence for the assertion that blacks have higher levels of testosterone without environmental triggers.
Blacks between the age of 12 and 15 average lower levels of testosterone than whites. However, after the age of 15, “testosterone levels increase rapidly” with blacks having higher peak levels than whites (seen in table 2 below). After adjusting for the usual confounds (BMI, smoking, age, physical activity, and waist circumference), blacks still had higher levels of testosterone—which is attributed to higher levels of lean mass.
As seen above in table 2 from Hu et al (2014), the difference in total testosterone between blacks and whites aged 20-39 was 6.29 ng/ml and 5.04 ng/ml respectively, with free testosterone for whites being 11.50 and 13.56 for blacks and finally bioavailable testosterone for whites and blacks aged 20-39 was 281.23 and 327.18 ng/ml respectively. These small differences in testosterone cannot account for racial disparities in violence nor prostate cancer—since there is no relationship between prostate cancer and testosterone (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).
In regards to Africans, the best studies I can find comparing some African countries with the West study salivary testosterone. However, there is a direct correlation between salivary testosterone and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burrin, 1987). Of the studies I could find, Kenyan pastoralists called the Ariaal have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Campbell, Gray, and Ellison, 2006) while men in Zimbabwe had levels “much lower” compared to Western populations (Lukas, Campbell, and Ellison, 2004). Lastly, among men aged 15 to 30, salivary testosterone levels in an American sample was 335 pmol//l compared to 286 pmol/l in men from the Congo (Elisson et al, 2002). Even certain African populations don’t have higher testosterone levels than Western peoples.
The meme that blacks have higher rates of testosterone in comparison to whites needs to be put to rest. This is only seen in blacks who participate in ‘honor culture’, which is an environmental variable. This is in contrast to people who believe that it is genetic in nature—environmental variables can and do drive hormones. Mazur (2016) is proof of that. Mazur (2016) also shows that the honor culture hypothesis doesn’t hold for teens or black males—so they don’t have elevated levels of testosterone. Certain studies of African populations, however, do not show higher levels of testosterone than Western populations.
Looking at the complete literature—rather than a select few studies— we can see that testosterone levels between white and black Americans are not as high as is commonly stated (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Further, even if blacks did have higher levels of testosterone than whites—across the board (sans honor culture), it still wouldn’t explain higher rates of black violence when compared to whites, nor would it explain higher prostate cancer rates (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).
Only blacks with low educational achievement have higher levels of testosterone—which, even then is not enough to explain higher rates of violence or prostate cancer acquisition. Other factors explain the higher murder rate (i.e., honor culture, which increases testosterone, the environmental trigger matters first and foremost) and violent crime that blacks commit. But attempting to explain it with 30-year-old studies (Ross et al, 1986) and studies that show that environmental factors increase testosterone (Mazur, 2016) don’t lend credence to that hypothesis.
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I showed in part I, that the oft-cited reason for racial differences in prostate cancer acquisition and mortality are not due to higher levels of circulating testosterone when comparing blacks to whites (Richard et al, 2014). I posited (and provided sufficient evidence) that the disparity could come down to differences in vitamin D between the races. Black Americans are far removed from their ancestral environment, living in a cooler area. Their pigmentation reduces vitamin D production in the skin, since blacks need a lot more sunlight to synthesize the hormone than whites do, and the main culprit is the environment: not getting enough sunlight (Harris, 2006). I will provide further evidence for the theory.
The etiology of prostate cancer is not known (ACA, 2016; Bashir, 2015). The cause for the disparity in racial differences in prostate cancer may possibly come down to circulating vitamin D levels, with sunlight playing a large role in the variance. Racial differences in prostate cancer were larger in areas with less sunshine (Taksler et al, 2013). However, it is not known whether getting more sunlight (though the problem would still be getting enough in places with low levels of sunlight) or supplementing with vitamin D will help close the gap. Vitamin D is relevant for lethal prostate cancer (Shui et al 2012), whereas Li et al (2007) showed that supplementing with higher rates of vitamin D, especially during the winter months, may be particularly beneficial to men with low levels of circulating vitamin D. A study on veterans showed that men who had prostate cancer AND the lowest levels of vitamin D were more likely to die than veterans who had higher levels of the hormone (Der et al, 2014). Murphy et al (2014) showed in a biopsy, that in black Americans, low levels of vitamin D were associated with increased the odds of prostate cancer acquisition during the biopsy.
Black Americans are significantly more likely than European Americans to suffer from and die from prostate cancer (Hardiman et al, 2016). A difference of over 8,000 genes were found to be expressed differently. Blacks also have higher rates of prostate tumors and higher grade tumors than do European men. The racial disparity in prostate cancer mirrors circulating levels of vitamin D in the blood between the races (Nelson et 2016). Prostate cells become less sensitive to vitamin D through loss of receptors or signaling molecules “that mediate vitamin D’s actions, or through changes in metabolic enzymes that synthesize or degrade vitamin D compounds” (Peehl and Feldman, 2013). Hardiman et al (2016) showed that there were over 3,000 genes that differed between blacks and whites. Due to the fact that blacks are living outside of their ancestral climes, this is a large mediator of the prostate cancer gap. Vitamin D deficiency can also explain a large variation of the black-white prostate cancer gap (Grant and Peiris 2011).
Along with direct measurement of circulating vitamin D in the bloodstream, we also have correlates. Hypertension is correlated with prostate cancer: blacks have higher rates of hypertension; obesity further exacerbates the problem. Blacks males are more likely to be obese (though barely, which is where the other environmental factors come in). Men suffering from two or more health problems linked to metabolic syndrome are more likely to get prostate cancer. Blacks are more likely to get metabolic syndrome.
Clearly, a large portion of the variation in prostate cancer acquisition and mortality can be attributed to environmental factors (vitamin D intake specifically). We can also look to East Asia and their increasing rates of prostate cancer as well (Chen et al, 2014; Zhu et al, 2014). There are no genetic changes in the past ten years to account for this, so the only culprit is diet. Our Americanized diets have been making it to East Asia recently and it’s having a negative effect on them. China’s obesity rate is dramatically increasing, along with their rates of prostate cancer acquisition. It seems that the Western diet could also play a part in racial differences in prostate cancer acquisition.
To be fair the non-significance of this result might be attributable to the small number (only four) of African nations in the analysis. A number of previous studies have actually found that people of African descent on average do have shorter CAG repeats than other peoples (Ackerman et al., 2012; Esteban et al., 2005; Kittles et al., 2001; Lange et al., 2008). However, whether this actually indicates anything about the life history strategy of different populations remains questionable. The two other androgen indicators for which African data was available follow a completely different pattern. For androgenic hair, Caucasians have the highest rate, followed by Asians, then Africans. For prostate cancer, Caucasians have the highest rate, followed by Asians and Africans, who do not significantly differ.
The difference comes down, mostly in my opinion, due to diet. You can see this by looking at rates of prostate cancer in populations that have adopted, or are current adopting our Western diet.
There is a good chance that environmental factors explain a large part of the variance in prostate cancer acquisition and mortality. I, of course, do not deny intrinsic genetic explanations or other hormonal imbalances, however this is the best explanation I’ve come across. The fact that sunlight dictates prostate cancer acquisition is a huge tell and should be further researched.
I used to be a proponent of the testosterone theory, however, Richard et al (2014) shows a 2.5 to 4.9 percent difference in free testosterone between blacks and whites, which they conclude, does not explain the disparity between the races. Hormones do matter, and hormones can and do vary individually and by group, which are mediated by diet. Once we find out which foods either hurt or help prostate cancer growth, then we can have better treatments for this disease for men of all races.
There are numerous ways in which prostate cancer can be mitigated, with diet obviously playing a large factor (Son, Aronson, and Litwin, 2005; Lin, 2015; Nelson, Demarzo, and Yegnasubramanian, 2014). Future studies researching the racial disparities in prostate cancer should take into account UV radiation from the sun, circulating vitamin D in the blood, and diet amongst a myriad of other variables (these three just stand out to me). Moreover, large-scalre cohorts should be undertaken to see what effects diet can have on the mortality of those suffering from prostate cancer, as possibly supplementing vitamin D to attempt to fight the disease
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).