Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanistic theoretical model with no systematic review protocol or original human trial data.
PubMed 18838208 · doi:10.1016/j.eururo.2008.09.024
What was done
The authors conducted a narrative literature review of publications from 1941 to 2008 evaluating the experimental and clinical effects of androgen concentration manipulation on prostate growth across cell lines, animal models, and human studies.
What was found
The abstract reports no numerical values or quantitative effect sizes. It describes a non-linear relationship where prostate growth is sensitive to variations in androgen concentrations at very low levels (such as during castration or androgen administration to castrated men) but becomes insensitive at higher concentrations once maximal androgen-receptor binding is reached well below the physiologic range.
Why it matters
This review proposes the "Saturation Model," offering a biological rationale that reconciles the effectiveness of androgen deprivation therapy with the lack of accelerated prostate cancer growth seen with testosterone therapy in eugonadal men.
Limits
The abstract outlines a narrative rather than a systematic review and does not state quantitative inclusion criteria, quality appraisal methods, or the total number of studies analyzed. Findings rely on synthesized mechanistic and observational literature rather than direct prospective trial data.
Cited by
- supports According to the androgen saturation model, increasing testosterone from hypogonadal to eugonadal levels (around 300+ ng/dL) stimulates prostate growth and increases PSA, but prostate androgen receptors saturate and further increases in testosterone do not dose-dependently increase prostate size.