I saw an old friend yesterday, He told me he had low grade Gleason 6 PCa, 2 cores with 10%, He told me he was on active surveillance. He told Me he was on vitamin D, 10,000 iu and Vitamin C , then He told me he was doing something controversial , since he was low energy he was taking testosterone supplements apparently with his Drs. knowledge. Has anyone heard of giving T to Men with active PCa cells even if they are low grade 10% cores. I have heard of Dr Bob Leibowitz giving T to men after therapy with complete response with no active cells left, but never with a man with active cancer on active surveillance. I told him I thought he was playing with fire, any thoughts?

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  • When I was diagnosed, I noted that my urologist was in no way interested in my testosterone [T]. As with many others, I assumed that, since ADT was used as treatment, T must be driving my cancer. Perhaps my T was too high?

    In fact, as I discovered when plowing through the papers on PubMed, cases as a whole have lower T than matched controls, & lower T within cases is associated with poorer prognosis.

    Men start to see a decline in T starting in their early 30's, at a rate of 1-2% per year. Is it a coincidence that PCa emerges just as the T decline becomes significant?

    It is accepted that T does not cause PCa. Interestingly, at diagnosis, the androgen receptor [AR] is usually normal (ADT changes that big time). While AR is needed for PCa growth, the existence of normal AR & normal T does not cause out of control growth.

    I have written elsewhere on the intracrine nature of prostatic growth. When T is converted to DHT in the cell, where is the growth brake? It doesn't come from outside. The enzyme for DHT clearance is generated, & one of the DHT metabolites is 3beta-Adiol:

    "... a steroid which does not bind AR, but interact with the estrogen receptor beta (ERbeta). 3beta-Adiol inhibits cell migration of PC through the activation of the ERbeta signalling" [1]


    ERbeta opposes growth. Thus, under normal conditions, growth inhibition depends on a metabolite of DHT - the very hormone that is viewed as being particularly dangerous.

    If AR is typically normal in untreated men, what is abnormal in PCa cells? Epithelial cells normally have ERbeta, but little or no ERalpha (which is found in stromal cells). As PCa progresses, the amount of ERbeta diminishes & growth-promoting ERalpha emerges. When ERbeta disappears, so does the growth brake, & it is probably worthwhile to begin using Avodart, to inhibit the conversion of T to DHT.

    For men with GS=3+3 on active surveillance, T & DHT levels are typically ignored. A man might be borderling hypogonadal (<350 ng/dL), 650 or 950 ng/dL, & it's all the same to the doctor. But I think it might be very important.

    In a paper [2] from March, involving "220 patients who underwent radical prostatectomy (RP)":

    "Preoperative PSA/FT index ratio is an independent strong factor which directly associates with aggressive features of pathology PCA; moreover, it might express prognostic potential for clustering the patient population in risk classes."

    "FT" is free T. Total T [TT] "correlated to FT", as might be expected, but individuals can have high SHBG levels which can reduce FT. FT is normally 1-2% TT.

    The PSA/FT index being a risk factor means that FT is inversely associated with risk. Lets use two examples:

    a) a hypogonadal man (300 ng/dL) with < 1% FT, i.e. FT < 3.0 ng/dL

    b) a man with middling normal T (600 ng/dL) & 1.5% FT, i.e. FT = 9.0 ng/dL

    In terms of risk associated with a particular PSA, (a) has triple the risk of (b).

    I believe that there is a window of opportunity to improve the situation by increasing T.

    In a paper [3] from last month:

    "Both testosterone deficiency (TD) and prostate cancer (CaP) have increasing prevalence with age. However, because of the relationship between CaP and androgen receptor activation, testosterone therapy (TT) among patients with known CaP has been approached with caution."

    "We identified a cohort of 82 hypogonadal men with CaP who were treated with TT. These included 50 men treated with Radiation Therapy (XRT), 22 with Radical Prostatectomy (RP), 8 managed with Active Surveillance (AS), 1 with Cryotherapy and 1 with High-Intensity Focused Ultrasound. We monitored prostate specific antigen (PSA), testosterone, hemoglobin, biochemical recurrence (BCR) and PSA Velocity (PSAV)."

    "... median follow up was 41 months. We found an increase in both testosterone ... and PSA ... levels in the entire cohort. PSA increased in the AS patients, however no patients were upgraded to higher Gleason Score on subsequent biopsies, and none have yet gone on to definitive treatment. We did not have any cases of BCR amongst RP patients, but 3 XRT patients (6%) experienced BCR."

    "... our study supports the hypothesis that TT may be oncologically safe in hypogonadal men following definitive treatment or active surveillance for CaP"


    [1] cancerres.aacrjournals.org/...

    [2] ncbi.nlm.nih.gov/pubmed/270...

    [3] ncbi.nlm.nih.gov/pubmed/271...

  • Johns Hopkins has been doing trials with high dose T in treating prostate cancer. My onc had considered trying it, but we opted to stick the standard of care and official clinical trial options because of the proximity of my mets to the spine.

  • Probably related to Denmeade's work:




  • T rub, I was told was at least masking (falsely lowering) my PSA test. I think this is way wrong.

  • I hear that they used to do supraphysiological (I prefer hyperphysiological - sounds cooler) amounts of testosterone, and some are trying it again now. I like the idea myself. It's called BAT. see: medscape.com/viewarticle/85...

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