Contrary to accepted wisdom. It has been long assumed that testosterone
stimulates the growth of prostate cancer; just like estrogen does for breast
cancer. It is standard procedure
to proscribe a drug that blocks testosterone (pharmaceutical castration), the equivalent
is done to women with breast cancer. Both
assumptions about hormones are false. Will it stimulate the progression
of pre-cancerous microscopic tumors into cancer? This study addresses that
question and answers it in the negative. Testosterone does not accelerate
transformation of these pre-cancerous tumors into cancer, though low testosterone
does. The study below is of
the serum levels of testosterone related androgens and their metabolites. The
serum levels of those with
prostate cancer and those without were essentially the same. More recent studies show a positive effect of
testosterone as to prevent and slowing the progression of prostate cancer. The Bottom section has links to those
articles, and a like set on estrogen and breast cancer—jk.
Endogenous sex hormones and prostate cancer: a quantitative
review of prospective studies
Eaton NE, Reeves GK, Appleby PN, Key TJ.
Imperial Cancer Research Fund, Cancer Epidemiology
Unit, Radcliffe Infirmary, Oxford, UK.
This paper presents a quantitative review of
the data from eight prospective epidemiologieal studies, comparing mean serum concentrations of sex hormones in men who subsequently
developed prostate cancer with those in men who remained cancer free. The hormones reviewed have been postulated to be involved
in the aetiology of prostate cancer: androgens and their metabolites testosterone (T), non- SHBG-bound testosterone (non-SHBG-bound
T), di-hydrotestosterone (DHT), androstanediol glucuronide (A-diol-g), androstenedione (A-dione), dehydroepiandrosterone sulphate
(DHEAS), sex hormone binding globulin (SHBG), the oestrogens, oestrone and oestradiol, luteinizing hormone (LH) and prolactin.
The ratio of the mean hormone concentration in prostate cancer cases to that of controls (and its 95% confidence interval (CI)) was calculated for each study, and the results summarized by calculating the weighted
average of the log ratios. No differences in the average concentrations of the hormones were found between prostate
cancer cases and controls, with the possible exception of A-diol-g which exhibited a 5% higher mean serum concentration among cases relative to controls (ratio 1.05, 95% CI 1.00-1.11), based on 644
cases and 1048 controls. These data suggest that there are no large differences in circulating hormones
between men who subsequently go on to develop prostate cancer and those who remain free of the disease. Further
research is needed to substantiate the small difference found in A-diol-g concentrations between prostate cancer cases and