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This is the study that many have used to discredit psa velocity, but that is cherry picking the authors conclusions.  The authors did find an association with a positive psa velocity and + prostate biopsy.  Not useless, but useful in the right context.

Review of PSA doubling time (PSADT) and PSA velocity in the aid in therapy of prostate cancer.

Good article.  This article (case series) found that 40% of the men included had no increase in PSA with Testosterone.  One point on the Testosterone dosage is that they used androgen, which is an overdose of Testosterone.  That gives 60% that the PSA did increase.  These men had higher PSA to begin with which leads to the suggestion that the prostate cells were abnormal.  Those men that had a prostatectomy were more likely to have little if any increase in PSA.  This study did use a the 5 alpha reductase inhibitor dutasteride.

DIM, from cruciferous veggies often used to aid estrogen metabolism, is found to decrease PSA transcription and function as an androgen receptor antagonist in prostate cancer cell lines.

IL‐6 increases PSA and androgen receptor expression through a STAT3‐dependent pathway in the absence of androgen in LNCaP cells. Our results agreed with those of an earlier study that indicated that IL‐6 induced expression of the androgen receptor, which up‐regulated PSA promoter activity in the androgen‐independent pathway. Moreover, curcumin blocked stimulation of IL‐6 on the androgen receptor, which attenuated PSA gene expression in a ligand‐independent manner.

Testosterone therapy post brachytherapy radiation found to have no recurrence and/or documented cancer progression in follow up out to 9 years.  Not all the men included in this study had none detectable psa levels.  PSA levels were all less than 1 ng/ml; 74.2% were none detectable, but 22% were detectable up to 0.5 ng/ml.  One of the patients had a transient rise in psa, but no recurrence or cancer progression was noted, and therapy was continued.

Nice review of the mixed data on Testosterone and Prostate disease. It is clear that Testosterone does not precipitate prostate cancer.  The intraprostatic hormone milieu likely is different than that present in the serum.  No surprise there.  5alpha reductase decreases prostate volume, PSA, and low-grade prostate cancer, but actually increases aggressive prostate cancer. Supraphysiologic doping in young men associated with no increase in prostate disease. PSA no longer to be followed in men < 55.  Mortality rate not changed.  PSA change of 1.4 ng/ml is appropriate for additional prostate evaluation.  Testosterone therapy on average increased 0.5 ng/ml. Still, no mention of aromatase activity in this article.  Why is it that hormone sensitive disease in men is only with regards to androgens and women estrogen.

Study finds negligible effect of Testosterone therapy (4.8 mg) on PSA.  The study consisted of several phases, the longest being 6 years.  However, each phase the parcipitants significantly declined.  The long held belief that Testosterone and DHT promote an increase in PSA is just not supported in the science.  In fact, aromatase knockout mice don't develop prostate cancer, only BPH.

Taxanes associated with PSA flare. The authors concluded that the flar within 12 weeks of therapy was not associated with any change in outcomes and could be ignored. The Taxanes as a whole group appears to be associated with this PSA flare pheonomenon.

GC-MAF levels exist in inverse relationship to nagalase.  In this study of men with prostate cancer, weekly GCMAF injections reduced Nagalase activity to levels found in healthy controls suggesting tumor free. The dose was 100 ng/week. Nagalase is a protein that suppresses GC-MAF production and thus is immunosuppressive.

PSA increased more in men with prostate cancer compared to no disease in men on finasteride therapy. This supports the idea that finasteride has a greater PSA reduction in benign prostate disease compared to prostate cancer.

Great confusion exists in the medical profession about Testosterone and PSA and the health of the prostate. The conversion of Estrogen, whether E2 or E1, and other variables are responsible for increases in PSA while on Testosterone therapy. This study points out that Estradiol in men stimulates cell line growth of prostate cancer. In contrast, Epitestosterone, an androgen metabolite, has antiandrogen, inhibits this estrogen activity. Epitestosterone exists in an inverse relationship to Estradiol and IGF-1.

Study looked at aromatase activity in androgen production in older men.  The study found that aromatase inhibition with arimidex increased Testosterone production.  PSA was also monitored and PSA increased in the smaller dose group versus the high dose group.

bipolar androgen therapy proposed as a mechanism to restore AR sensitivity in those men with castration resistant prostate cancer.  This was a very small pilot study.  The effects on PSA were limited in effect as all men eventually developed PSA increase

Corticoidsteroid found to be associated with docetaxol associated PSA flare.

larger study post radical prostatectomy for prostate cancer finds that no increase in PSA with Testosterone therapy in men with non-detectable PSA levels.  F/u was 13 months.

Good review of data on Testosterone therapy and prostate cancer risk: the take home is there is no increased risk.  Also, included is a discussion of the prostate saturation theory.

Case study shows increased PSA with testosterone replacement.  This study reveals the effect of excessive testosterone therapy.  The twice weekly injections of androgen therapy is excessive and likely was driving aromatase activity and thus inflammation.

Finasteride more likely to lower PSA associated with benign prostate conditions compared to cancer of prostate.

Study finds little link to Testosterone replacement therapy to elevation in PSA in "healthy" men.  All the members of this study had negative prostate biopsies prior to therapy.