New study below [1].
Elizabeth Platz [Johns Hopkins] has been involved in many interesting (to me) PCa studies over the past 3 decades. Including this one.
It is an estradiol-selenium study using NHANES III data (National Health and Nutrition Examination Survey), but the context is the possible link to PCa risk. (It is a joint Swiss-UK-US study.)
Alas, I'm unable to copy-paste from the full text [1], but it's refreshing to read about "growing evidence for a role of estrogen in" PCa. & "the progressive emergence of the ERalpha during ... progression". etc.
As I have mentioned elsewhere, the U.S. population, in general, enjoys sufficient levels of selenium because domestic wheat is largely grown in selenium-rich soil. So, deficiency would not be common in the NHANES population.
A number of observational studies have associated PCa incidence risk with selenium deficiency, with no benefit from higher levels once adequacy has been attained. So I was somewhat bemused that the researchers thought it worthwhile to examine estradiol [E2] at increasing levels of selenium in this well-nourished population.
"We calculated age/race-ethnicity-adjusted and multivariable-adjusted geometric mean serum concentrations of total and estimated free testosterone and estradiol, androstanediol glucuronide (AAG), and sex hormone binding globulin (SHBG) and compared them across quartiles of serum selenium. Results: Adjusting for age, race/ethnicity, smoking status, serum cotinine, household income, physical activity, alcohol consumption and percent body fat, mean total estradiol (e.g. Q1:38.00 pg/mL ... vs Q4:35.29 pg/mL ...) and free estradiol [e.g.Q1: 0.96 pg/mL ... vs Q4: 0.90 ...] concentrations decreased over quartiles of selenium."
"No associations were observed for the other sex steroid hormones studied."
"Our findings suggests that a possible mechanism by which selenium may be protective for prostate cancer is related to estrogen."
If so, IMO, "protective" relates to progression rather than incidence.
...
In 2016, the same Van Hemelrijck (UK), Rohrmann (Switzerland) & Platz (US) were involved in another NHANES analysis [2]. This time "Pre‐diabetes and serum sex steroid hormones".
Not a PCa study, but worth thinking about, IMO.
A puzzle: why do diabetics get more cancer of every type - except PCa, where they get less?
My view: the non-diabetic PCa population tends to be pre-diabetic (most pre-diabetics never become diabetic). Pre-diabetics produce more insulin. Diabetics have "solved" the insulin problem by burning out their pancreatic beta cells. It isn't that diabetics have less PCa, but that pre-diabetics have more. Again, IMO.
Not only do pre-diabetics have elevated insulin - a recognized PCa growth factor - but they tend to have more symptoms of the metabolic syndrome. & I believe an unfavorable estrogen:testosterone [E2:T] ratio.
The study found less T in pre-diabetics, but also slightly less E2. It did not calculate E2:T, so I did. The T units are ng/mL & the E2 are pg/mL, but a crude division, for comparison, gives E2:T = 7.008 for pre-diabetics versus 6.147. i.e. more estrogen-dominant.
"Several studies demonstrate a link between diabetes and sex steroid hormones, but the link with pre‐diabetes remains elusive. In this study, we hypothesize that pre‐diabetes, which is characterised by having impaired fasting glucose and/or impaired glucose tolerance and/or impaired HbA1C, may influence circulating sex steroid hormone concentrations in men."
"Our findings suggest that men with pre‐diabetes have lower circulating total testosterone and SHBG and higher free estradiol levels."
-Patrick
