I know this is a long ass article but maybe itll provide some info hopefuly
Despite this prevailing point of view that anabolic steroids cause prostate cancer, in my experience, the opposite is true and testosterone is necessary for optimal prostate health. So let us review the original data that lead to the conclusion anabolic steroids increase prostate cancer growth to hopefully perform future actions that do not leave patients without the care they need.
Common Sense
Even before examining the medical research, general observations lead me to a conclusion that testosterone or anabolic steroids are not “bad” for prostate health. Just comparing disease occurrences and the basic physiology of man throughout adulthood may provide evidence that elevated anabolic steroid levels do not cause prostate problems, and that the reverse is true. Young men between the ages of 18 to 30 years old typically have the highest levels of anabolic steroids among adult men (Leifke, Gorenoi et al. 2000). Yet, men under 30 years old also have the lowest prevalence of prostate problems, including prostate cancer. On the other hand, prostate cancer is more common in the elderly (Merrill 2001). Accordingly, the hormonal milieu of the aging male, which is marked by steady declines in circulating anabolic steroids, seems to be more problematic for prostate health (Gordon, Gray et al. 1989). Other researchers have recognized the relationship that prostate cancer is more prevalent in people who have falling levels of anabolic steroids (Morgentaler 2006). Published in the New England Journal of Medicine, “…it should be recognized that prostate cancer becomes more prevalent exactly at the time of a man’s life when testosterone levels decline” (Rhoden and Morgentaler 2004). Thus, common sense would support a relationship that too little anabolic steroids or other differences between young and elderly men besides elevated anabolic steroid levels are related to prostate cancer development.
In the Beginning
The conception of the belief that anabolicsteroids cause prostate cancer to grow all boils down to the original experiments by Huggins and Hodges in 1941. Huggins and Hodges claimed that prostate cancer was hormonally responsive by reporting marked reductions in testosterone (from castration or estrogen treatment) inhibited metastatic prostate cancer. In addition, the administration of exogenous testosterone caused prostate cancer to further activate (Huggins and Hodges 1941). These concepts still seem to be applicable today, but must remain in context. Huggins’ and Hodges’ experiments showed the suppression of prostate cancer from hormone restrictions were similar in magnitude to the increase of prostate reactivation with testosteronere introduction. Even though the authors claimed their experiments provided evidence for this concept, the case results did not demonstrate anabolic steroid or testosterone administration causes prostate cancer (without previous restriction) to grow in any person with prostate cancer. It is only when a person’s endocrine homeostasis is first reduced to subphysiological low levels that the administration of testosterone and restoration of these levels may affect the prostate. Yet, Huggins and Hodges took their findings out of context, and the rest of the world followed suit. They claimed testosterone or anabolic steroid administration caused prostate cancer to grow, no matter the previous endocrine status of the patient. This erroneous extrapolation of their concept was treated as if it were part of a “Ten Commandments” of medicine.
Unfortunately, their experiments had many shortcomings to develop any prevailing medical theories or concepts in regard to anabolic steroid administration on previously untreated prostate cancer. First, the population size was extremely small. Only three men with prostate cancer were involved in the exogenous testosterone experiment. Second, not all of the data was provided. Although three men were involved in the experiment, only results for two men were reported. Third, there was more than one scientific variable at a time being evaluated. Exogenous testosterone administration was not the only scientific variable present in the test subjects. One of the two men with reported results had been castrated. Fourth,the objective marker used in the experiment did not have a control or behave uniquely with the variable. In the remaining noncastrated man with prostate cancer, acid phosphatase levels elevated during 18 days of exogenous testosterone injections, but varied extensively before and after the injections. The same peak level of acid phosphatase during testosterone administration was observed in this individual again three weeks after discontinuing testosterone treatment. Hence, in this one patient, testosterone injections did not cause a unique change in acid phosphatase levels. The original allegation that anabolic steroids cause prostate cancer to grow was therefore based on erratic acid phosphatase levels in a single individual.
The principles of the scientific method declare when scientific hypotheses, like anabolic steroids cause prostate cancer to grow, are tested and proven with experimentation, the experiments should be reproducible by someone else with the same results to form a scientific theory. Otherwise, if different results are achieved in the same types of experiments, reconciliation of methods should occur or new scientific hypotheses should be generated to explain all observations. In the case anabolic steroids cause prostate cancer to grow, further experiments near that time period with exogenous testosterone in untreated (meaning without anabolic steroid restriction by castration or estrogen therapy) men with prostate cancer failed to produce similar results of rapidly stimulating prostate cancer (Brendler, Chase et al. 1950;Trunnell and Duffy 1950; Pearson 1957; Prout and Brewer 1967). Some of these additional experiments even involved men with advanced disease, and some actually show anabolic steroid treatment may be beneficial for patients with prostate cancer.Since the data from these studies did not support the prevailing Huggins’ and Hodges’ conclusion that anabolic steroids cause prostate cancer to grow, a new or altered hypothesis should have been formed according to the principles of the scientific method. Dr. Pearson recognized that his and others’ data did not coincide with Huggins’ and Hodges’ hypothesis, and he specifically requested new hypotheses be considered to explain everyone’s experimental observations.Dr. Pearson wrote, “These observations invite the development of new concepts to explain the response of these prostatic cancers to alterations in the endocrine environment” (Pearson 1957). Instead, these studies were ignored, interpreted with a preconceived notion or forgotten by the medical community. The historical foundation of medical data has been filtered to justify a predetermined conclusion, rather than analyzing all of the data to arrive at a more correct theory that is consistent with all observed effects anabolic steroids have on prostate cancer.
Prostate and Steroid Current Evidence-Based Concept Review
Eunuchs, hypogonadal and growth hormone-deficient men develop prostate glands that are smaller in size.
Hypogonadal men receiving anabolic steroid therapy experience prostate growth to a volume similar to what would be expected from their eugonadal counterparts. Then their prostate size is sustained. Growth hormone-deficient men who are treated with growth hormone to normalize their levels also experience prostate growth to a volume similar to the expected volume of men without growth hormone dysfunction. The prostate growth reaches a plateau, like in anabolic steroid treatments.
PSA levels change accordingly in hypogonadal men receiving anabolic steroid treatments with an initial modest rise followed by a sustained plateau. In addition, anabolic steroid treatments may result in minor changes in urological flow parameters.
PSA levels in young men (less than 40 years of age) are unresponsive to anabolic steroid treatments, even at supraphysiological levels.
No evidence exists that demonstrates normal levels of testosterone promote the development of cancer of the prostate.
No evidence exists that shows administration of anabolic steroids enhances a preexisting prostatic malignancy in men who are not at castrate levels of hormones.
Current evidence does not support the view that anabolic steroid treatments administered to hypogonadal elderly men have a causal relationship with prostate cancer.
The published conclusions of studies from respectable establishments that review the data regarding steroids and prostate cancer all have the same theme. Dr. Morgentaler of Harvard Medical School published in a peer-reviewed medical journal, “This historical perspective reveals that there is notnow--nor has there ever been--a scientific basis for the belief that testosterone causes prostate cancer to grow” (Morgentaler 2006). Other authors have similar findings. Dr. Morley wrote in a medical journal from the Mayo Clinic, “There is no clinical evidence that the risk of either prostate cancer or benign prostate hyperplasia increases with testosterone replacement therapy” (Morley 2000). Dr. Morales from the Department of Urology at Queen’s University acknowledges that testosterone has been used for 70 years and that “no evidence exists that appropriate androgen administration with knowledgeable monitoring carries significant or potentially serious adverse effects on the prostate gland” (Morales 2005). These medical journal research reviews unanimously agree that testosterone does not cause prostate cancer.
For a more detailed and inclusive review of the available literature, please see my book, Demystifying Steroids. A copy is available to purchase at Invalid Link Removed or a PDF download at shop.personalcatalyst.net.
