Broadly speaking, lifetime exposure to testosterone is reflected in the incidence of prostate cancer, with the world’s highest incidences being among African-American men (Brawley & Kramer, 1996). It was once thought that lower incidences prevail among Black West Indians and sub-Saharan Africans, but this apparent exception is now ascribed to underreporting (Glover et al., 1998; Ogunbiyi & Shittu, 1999; Osegbe, 1997).
This picture has been confirmed by a recent American study:
From the 1970s to the current statistical analysis of the National Cancer Institute Surveillance, Epidemiology, and End Results program African-American men have continued to have a significant higher incidence and mortality rate than European-American men. Autopsy studies show a similar prevalence of early small subclinical prostate cancers but a higher prevalence of high grade prostatic intraepithelial neoplasia.
Clinical studies show a similarity in prostate cancer outcome when pathological stage is organ confined but a worse outcome when disease is locally advanced and metastatic in African-American vs European-American men. There is increasing genetic evidence that suggest that prostate cancer in African-American vs European-American men may be more aggressive, especially in young men.
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).:
Black men in the United Kingdom have substantially greater risk of developing prostate cancer compared with White men, although this risk is lower than that of Black men in the United States. The similar rates in Black Caribbean and Black African men suggest a common genetic aetiology, although migration may be associated with an increased risk attributable to a gene–environment interaction” (Ben-Shlomo et al 2008).
We are only just beginning to identify the actual genes that account for the White/Black difference in prostate cancer risk. The most recent study was Benson 2014.
With respect to the Black/White difference in testosterone level, African Americans have a clear testosterone advantage over Euro-Americans only from puberty to about 24 years of age. This advantage then shrinks and eventually disappears at some point during the 30s. The pattern then seems to reverse at older ages (Ellis & Nyborg 1992; Gapstur et al. 2002; Nyborg 1994, pp. 111-113; Ross et al. 1986; Ross et al. 1992; Tsai et al. 2006; Winters et al. 2001).
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.
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.
More seriously however, she used serum samples that the National Center for Health Statistics had earlier collected as part of its Third National Health and Nutrition Examination Survey (NHANES III). Only 1,479 samples were still available out of an initial total of 1,998, i.e., one quarter were missing. An earlier study had used the same serum bank for research on a sexually transmitted disease: Herpes Simplex virus type 2 (HSV-2).
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.
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