Abstract
BackgroundSince the landmark study conducted by Huggins and Hodges in 1941, a failure to distinguish between the role of testosterone in prostate cancer development and progression has led to the prevailing opinion that high levels of testosterone increase the risk of prostate cancer. To date, this claim remains unproven.Presentation of the hypothesisWe present a novel dynamic mode of the relationship between testosterone and prostate cancer by hypothesizing that the magnitude of age-related declines in testosterone, rather than a static level of testosterone measured at a single point, may trigger and promote the development of prostate cancer.Testing the hypothesisAlthough not easily testable currently, prospective cohort studies with population-representative samples and repeated measurements of testosterone or retrospective cohorts with stored blood samples from different ages are warranted in future to test the hypothesis.Implications of the hypothesisOur dynamic model can satisfactorily explain the observed age patterns of prostate cancer incidence, the apparent conflicts in epidemiological findings on testosterone and risk of prostate cancer, racial disparities in prostate cancer incidence, risk factors associated with prostate cancer, and the role of testosterone in prostate cancer progression. Our dynamic model may also have implications for testosterone replacement therapy.
Highlights
Since the landmark study conducted by Huggins and Hodges in 1941, a failure to distinguish between the role of testosterone in prostate cancer development and progression has led to the prevailing opinion that high levels of testosterone increase the risk of prostate cancer
Based on evidence from published studies, we propose a dynamic model as a theoretical framework to understand the relationship between testosterone and the development of Prostate cancer (PCa)
Presentation of the hypothesis Two key components are included in our dynamic model: the magnitude of the age-related declines in testosterone and the individual-based threshold level of testosterone to maintain the normal function of prostate gland
Summary
Prostate cancer (PCa) is the most common cancer and the second leading cause of cancer mortality among American men. Based on evidence from published studies, we propose a dynamic model as a theoretical framework to understand the relationship between testosterone and the development of PCa. As an illustration, we propose a dynamic model to interpret and improve our understanding of the following: the observed age patterns of PCa, the inconsistent findings from published studies, the racial disparities in PCa incidence, the risk and protective factors for PCa, the role of testosterone in PCa growth and the use of androgen replacement therapy as primary prevention of PCa. Presentation of the hypothesis Two key components are included in our dynamic model: the magnitude of the age-related declines in testosterone and the individual-based threshold level of testosterone to maintain the normal function of prostate gland. The relative differences of testosterone levels between young adulthood and old age (e.g. 65 years old) may provide some clues about the threshold level as most of prostate cancer occurs in old age
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