High dose testosterone replacement therapy results in increased circulating IGF-1 and IGFBP-3 levels. Results from a recent paper support a role for androgens in the regulation of the insulin-like growth factor system in human males.
In our study we observed that higher dosages of T were administered to some of our patients than was reported in the literature. This dosage pattern was mainly related to age and comorbidities.
The average age at diagnosis was 68 years, with a large variation between different regions in the USA. The average age of diagnosis differed significantly according to race (65 yr in White Americans vs 69 yr in Black American), socioeconomic class (64 yr in low-socioeconomic status vs 71 yr in high-socioeconomic status), and geographic region (69 yr in Midland, Michigan). These data imply that prostate cancer incidence varies significantly across racial, socioeconomic, geographic regions, and even among specific areas within these regions.
High dose testosterone therapy should be considered based on the risks of testosterone therapy and aging. Older men who received higher doses showed an increased rates of fatal and non-fatal cardiovascular events compared to those treated with lower doses. Risk factors for cardiovascular mortality were statistically significant only among men receiving high doses of testosterone.
High doses of testosterone increase prostate volume, but they do not affect PSA, DRE, or MPS in men with a normal prostate. There was no difference in prostate volume between the groups. Recent findings suggest that high dosage of testosterone should be reconsidered before using it routinely for treatment.
Although it was hypothesized that genetic factors account for about 20% of prostate cancer, we found that the HER2/neu gene is not involved in prostate cancer development. Rather, other genes are more likely to be responsible for prostate cancer.
Recent findings suggest that there are multiple genetic predispositions for familial PCa. This finding underlines the need for prospective studies that will identify genes and/or environmental conditions that contribute to familial PCa.
The mortality rate for PCa was not significantly different between whites and blacks, but Blacks displayed more aggressive features, including a higher prevalence of lymph node metastasis. These data suggest that Blacks are at high risk for treatment failure following surgery, because of poorer prognosis factors when compared with Whites.
Although the understanding of PCa biology remains incomplete, it is clear that PCa is a heterogeneous group of different diseases, including clinically indolent yet biologically aggressive forms of prostate cancer.
Neither the biological nor the clinical responses were superior to those obtained using low dose estrogen alone. In our experience, high dose testosterone, either alone or combined with estrogens, seems to be less effective than low doses in achieving durable biochemical remission. This effect is probably related to the fact that only a small percentage of the patients showed a complete response to treatment.
In this population-based study of [prostate cancer](https://www.withpower.com/clinical-trials/prostate-cancer), we found no evidence that prostate cancer was spreading faster than any other type of cancer. Thus, while prostate cancer is an aggressive disease, it appears to be just as likely to spread quickly as other forms of cancer.