Prostate Restored
Prostate Restored
Photo: Amar Preciado
Black males had higher concentrations of total, free, and bioavailable testosterone compared to white males. When stratified by age, black males had significantly higher total (P < 0.01) and free testosterone (P < 0.01) compared to white males aged 20–39 years.
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Read More »Using a large nationally representative sample from the NHANES, we found that black and white males had different age-related patterns of testosterone. These results suggest that the magnitude of age-related declines in testosterone differs between black and white males. Notably, these findings may have implications for PCa racial disparities. As we described previously, each individual may have his own threshold of testosterone for prostatic carcinogenesis, which may be associated with his baseline or peak testosterone levels. If the baseline testosterone level is high, the threshold may be relatively higher as the normal prostate is acclimated to a high-testosterone level. If this is true, the relatively higher testosterone levels among young adult black males (20–30 years old) may indicate that they also have relatively higher thresholds compared to white males. We also found that black males experienced a more dramatic age-related change in testosterone levels than white males. These results suggest that testosterone levels more frequently fall below the necessary threshold in black males, which may eventually lead to the development of PCa and help explain racial disparities in PCa. However, this hypothesis warrants further investigation. In addition, the magnitude of age-related testosterone declines could also help explain inconsistent findings regarding the relationship between testosterone and PCa. The prevailing wisdom that high-testosterone levels are a risk factor for PCa is not supported by extensive evidence [23]. In fact, recent studies refute this notion. First, it is inconsistent with the age-related pattern of PCa risk. Although males exhibit their peak levels of testosterone between the ages of 20 and 30 years, this is not the highest risk period for the development of PCa; indeed, approximately 90 % of PCa cases are diagnosed after the age of 60 years old when testosterone levels have already declined to relatively low levels. Moreover, recent studies have shown that low testosterone is associated with an increased risk of PCa on biopsy, high Gleason scores, seminal vesicle invasion, and biochemical recurrence [24]. Thus, comparing testosterone levels measured at a single point in time, as most previous studies have done, is not adequate for an investigation into the relationship between testosterone and PCa. We theorize that PCa patients can have relatively higher or lower testosterone at the time of diagnosis, as levels at a single point in time are irrelevant to the genesis of PCa; however, the magnitude of age-related declines in testosterone levels is significant. These assumptions allow us to explain the inconsistent findings regarding the relationship between testosterone and PCa. For example, men who have high levels of testosterone at young ages may have levels that remain relatively high at the time of PCa diagnosis even after a significant fall in testosterone with aging. On the other hand, men who exhibit low levels of testosterone at a young age may have even lower testosterone levels at the time of PCa diagnosis. If a study includes both groups, then it is plausible that testosterone levels at diagnosis will not be associated with PCa; this helps to explain the null associations found in a recent collaborative analysis of 18 prospective studies [20]. Therefore, the inconsistent findings from previous studies may be attributable to the focus on testosterone levels measured at a single point in time as opposed to the magnitude of age-related declines in testosterone [18–24, 30, 31]. As we used cross-sectional data for this study, we were not able to investigate the difference in lifetime testosterone variations between PCa cases and controls. However, recent studies in PCa patients have found that lower testosterone is associated with advanced pathologic stage, high Gleason score, and biochemical recurrence after radical prostatectomy [32]. If it is true that men diagnosed with PCa and controls have similar levels of testosterone and/or that men who eventually develop PCa have higher testosterone levels at a young age, then it is also likely that men with PCa experience more significant declines in testosterone throughout a lifetime. Furthermore, studies have reported higher PCa prevalence in hypogonadal men [21, 23], further supporting the hypothesis that a significant decline in testosterone may be related to the development of PCa. These findings may have implications for hormone replacement therapy as well. Due to individual hormonal variations, patients may require different therapeutic amounts. Personalized medication may improve the outcome of hormone replacement therapy.
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Read More »Several aspects of our study merit further discussion. First, the NHANES data provided us with a unique opportunity to study racial disparities in age-related variations of testosterone in a large nationally representative sample. However, given the cross-sectional design of the NHANES, we cannot assess differences in an individual’s hormonal trajectory over a lifetime by race. Trends in testosterone levels may be affected by potential period or cohort effects; moreover, the trend in racial differences might also be partially explained by temporal changes. Although we were able to adjust for many potential confounders in this study, residual confounders (e.g., puberty status, which was not available in the data) may be possible. Finally, as our data were drawn from participants free of PCa, we could not directly investigate the magnitude of testosterone decline among patients with PCa or whether different hormonal profiles and trajectories over a lifetime resulted in PCa. Future studies will include a cohort design and long-term follow-up to further examine this hypothesis.
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