1050 words

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.

Scott McGreal writes:

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