High Testosterone and Prostate Cancer Risk

By doctor Francesco Casillo

Note from the author. The author does not promote the use of any kind of doping substances (moreover, prohibited by Italian law in sports). In this sense, the sections concerning the effects of testosterone and anabolic steroids are only informative. of a scientific nature (amply confirmed by bibliographical references).

The use of testosterone is accompanied by a series of side effects, some potential (alopecia, gynecomastia, acne etc.), as they depend on the individual response to the male steroid, and others certain (feedback long negative on the pituitary and ultralong on the hypothalamus and consequent testicular atrophy).

Another potential postponed side effect of testosterone use is prostate cancer.
The association between testosterone and prostate cancer is accepted as a scientific fact and as such permeates and forges the "established" knowledge in this regard in the medical field and in the scientific community. This is mainly due to the fact that scientific publications often cover character of "omnipotence"; in order not to allow publications based on untrue facts, a system of peer reviewing (peer review) used by leading scientific journals. According to this criterion, an article or publication to have scientific value, and therefore to be the subject of scientific publication, must pass the suitability analysis performed by experts in the field. And therefore, the assumption that associates testosterone and prostate cancer finds validation according to a scientific publication.
The publications from which this knowledge derives primarily are the work of Huggins and Hodges "Studies in prostatic cancer, I: The effect of castration, of estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate", published in 1941, and the Review by Huggins of 1967.
In Review in 1967, men with overt prostate cancer were subjected to three different types of therapeutic interventions: castration, estrogen therapy (aimed at inducing feedback negative on the hypotolamus-pituitary-gonadal axis) and testosterone administration. The result of the study (which later became a publication and, consequently, a "scientific assumption" still accepted by many professionals today) concludes that testosterone suppression induces regression in cancer at prostate where, on the other hand, exogenous administration of testosterone determines its evolution.
Instead, in the 1941 study, testosterone propionate was administered and as a result the acid phosphatase levels were increased. Acid phosphatase is an enzyme produced by the prostate. The highest levels of acid phosphatase are present in cases of metastatic prostate cancer. Hence the fact that the risk of prostate cancer is higher according to their incremental level and that, therefore, the risk factor is the stimulus that favors the incremental levels - in this case testosterone.
It is true that once a study is published it is "gospel" but ... until the contrary is proven! With the advent of medicine anti-aging and the incremental demand for testosterone replacement therapy (again at a medical level and in a curative function), authoritative voices have brought to light evidence in radical contrast to the long-held belief that associated testosterone and prostate cancer. The most persuasive is represented by Review by surgeon Abraham Morgentaler (Harvard School professor) published in the ""European Urology" and entitled "Testosterone and prostate cancer: an historical perspective on a modern myth" .
Following the review of the Huggins and Hodges study, Dr. Morgentaler pointed out that the claim that the suppression of testosterone production induced the regression of prostate cancer lacked tangible evidence to attribute to testosterone the role of carcinogenic promoter, making the duo "testosterone-prostate cancer" a duo. In fact, in the 1941 study, only 3 individuals with prostate cancer were given testosterone propionate (to see its effect on the pre-existing tumor). 3 subjects included in the study - and one of the two was already castrated, therefore exogenous administration no longer represented the surplus hormonal at physiological-endogenous levels (a situation that made him an inappropriate subject for the study).
No studies of imaging or biopsies to objectify tumor growth in response to testosterone therapy. Acid phosphatase levels were only observed (increased on day 18 of therapy but with fluctuations both before and after treatment). The highest levels were found 3 weeks after the interruption of hormone therapy, a time interval in which blood testosterone levels, in all probability, could be low for two reasons: the short half-life of the ester used (propionate), the suppression of endogenous testosterone levels induced by hormone therapy.
It is surprising how much this assertion - relating to the connection between testosterone and prostate cancer - has enjoyed strong credit in the scientific community and has also persisted over the years, in the face of such weak evidence to support it. On this basis, if the study in question had been published in our day, in all likelihood it would not have surpassed the standard from peer review for its scientific publication.
The documented facts show completely conflicting results at the publication of Huggins and Hodges. Here are some of them:

serum testosterone levels peak in late adolescence and around the age of 20, whereas prostate cancer occurs primarily in individuals over the age of sixty and only rarely in individuals under the age of forty;
the chance of finding prostate cancer increases over the years, as we age, and testosterone levels decrease during the process of aging ;
the incidence of prostate cancer has increased over the past 36 years and this has happened in conjunction with a decline in serum testosterone levels; - men with low serum testosterone values are more likely to be diagnosed with prostate cancer;
men with prostate cancer and low testosterone have the worst tumors and have poor healing abilities;
testosterone replacement therapy did not record increases in cancer evolution in men with benign prostatic hyperplasia or high-grade precancerous lesions of the prostate;
studies e review they have not yet been able to consistently and consistently prove that testosterone causes prostate cancer. Indeed, elevated levels of testosterone and adrenal androgens have been associated with a reduced risk of aggressive prostate cancer;
Prostate cancer has been reported in male transsexual individuals who underwent surgery (castration) to become women, continuing on estrogen therapy, six or more years after undergoing the surgery;
testosterone levels in the prostate do not match blood levels. When blood levels are low, prostatic ones remain high; but when the serum values increase the prostatic levels do not increase to the same extent;
testosterone can prevent or delay the onset of prostate cancer.