I had my testosterone level checked. It currently is 12.3 ng/ml or 42.65 nmol/L or 1230 ng/dL. So its way too high. I am asymptomatic.
Currently I am on hormone therapy with 50mg Bicalutamide per day and 20 mg Tamoxifen. Plus 850 mg Metformin.
Any suggestions what is causing this testosterone level and what I should do?
Do you have results from earlier tests?
What is the reference range for the lab?
You say 1230 ng/dL is way too high. What were you expecting from the test?
-Patrick
Patrick,
beginning of last year I had a testosterone level of 593 ng/dL without ADT which I considered normal. The lab specifies that 193 to 740 ng/dL would be a normal range. That made me think 1.230 ng/dL is too high. However, I just did some reading and sometimes a level up to 1.200 ng/dl is considered normal. So I do not know what's right.
Beginning of January 2019 I had 960 ng/dL and now 1.230 ng/dL.
Bicalutamide can increase the testosterone level but tamoxifen is supposed to lower it.
I have no explanation for the current level. I just want a normal level which does not cause problems.
I don't think that high-normal T will be a problem. In T replacement therapies there is a possibilty that the red blood cell count will be above the normal range (Polycythemia). I have been up around your number due to T injections & my RBC has always been in the middle of the normal range. I believe that TRT docs go by hematocrit tests. But elevation seems to be an age-related problem.
From a PCa perspective, I doubt that it matters whether you are at 600 or 1,200 ng/dL. You are way above Morgentaler's saturation point in either case.
As Nalakrats says - you should look at free T. But typically, as T rises SHBG falls. Odd, but true.
-Patrick
Your testosterone level is high because of the kind of hormone therapy you are using. Bicalutamide prevents testosterone from being used by cells, so it accumulates in the serum. If you want to lower your serum testosterone level, you have to use a GnRH agonist or antagonist. The effect of tamoxifen is comparatively very small on T levels - it acts as a mild estrogenic in lowering T levels.
Thank you very much for the information provided! I will ask my doctor why his lab specifies the range as 193 to 740 ng/dL and not 300 to 1200 ng/dL as other labs do. I also will get the SHBG (sex hormone-binding globulin) and Albumin values determined and see if the free testosterone is in the normal range. If this is the case, I guess I do not need to worry about the testosterone level.
so what is its true level, 12,42, or 1230?
My standard total testosterone level is: "12.3 ng/ml or 42.65 nmol/L or 1230 ng/dL". This is the same value in different units. There are different units used for testosterone levels, so I provided the most common ones. I thought readers would be familiar with different units and wanted to make it easy for them.
I just went to MD Anderson for a full evaluation and second opinion. I'm a Gleason 9 stage IV. No mets anywhere except the lymph system1. My testosterone was 38 and should be less than 20. I had the RP on 10/5/18 with PE and pneumonia complications. MD found a lymph node that needs a biopsy. Back to the testrone level, the MO at MD said the lymph node could be causing the up tick in psa and adding Casadex or one of the other ones to the Lupron will help bring down the testosterone levels. Talk to your MO and ask about it.
My URO was also convinced that Casodex will lower the testosterone level. I did not agree. Your MO at MD should have said that adding Casodex to Lupron will lower the PSA value, it will not lower the testosterone level. Instead, Casodex works by blocking the androgen receptor of the tumor cell, the target of testosterone.
I was told the same as GP24 by several doctors. Casodex blocks T to the cells but does not stop the body from making T. There have been clinical studies that have shown that PCa grows the fastest in low T environment and the slowest in a high T environment. That is, if the T is not being blocked to the cells altogether by Casodex or if the body is prevented from making T entirely by Lupron).
Do the Supra levels of T quoted in the BAT tests show corresponding high levels of free T?
From what I understand, T acts in a biphasic manner, with the upper range phase the least understood in its interactions and role vis-à-vis pca
I have never seen even a hypothetical model that explains its interactions, so all they seem to have are observations of clinical results, for a certain population
Perhaps dr Friedman? could be asked to comment on his views , given his book got quite deep into the theory-he might, at least , provide the beginning of a trail to follow
just saw this:
Back to Clinical Trials
From the Desk of Evan Yu: “Is Testosterone Such a Bad Thing for Prostate Cancer? Rationale for Using Supraphysiologic Testosterone to Treat Castration-Resistant Prostate Cancer.”
Published 08 February 2019
We have known for decades that androgen deprivation offers remarkable efficacy and palliation for men with advanced prostate cancer. Yet, soon after Charles Huggins Nobel Prize-winning discovery, many case series started emerging, describing paradoxical benefits of testosterone supplementation for patients with prostate cancer.1,2 These clinical observations seem so counterintuitive given that androgen deprivation therapy is the hallmark of treatment for advanced prostate cancer. Yet, there may be supportive biological rationale to this surprising observation.
It is well known that prostate cancer cells adapt to a low androgen environment by upregulation of the androgen receptor.3,4 It is possible that adaptive autoregulation of the androgen receptor may sensitize prostate cancer cells to supraphysiologic androgen-induced cell death. This theory has been supported by multiple pre-clinical studies with prostate cancer cell lines and xenografts, as supraphysiologic androgen administration inhibits cell growth.5-7 For tumors harboring androgen receptor splice variants, such as the constitutively active ARv7, these truncated androgen receptors may confer resistance to androgen receptor targeted therapies, like abiraterone acetate or enzalutamide.8 In certain androgen receptor variant xenograft models, direct androgen receptor inhibition does not affect xenograft growth, yet exogenous testosterone induces tumor regression.9 This functional result seemed to be mediated by testosterone-induced rapid downregulation of both full-length androgen receptor and ARv7 expression.
Other pre-clinical work has found that in high androgen receptor expressing cell lines, rapid transition from a castrate to a high androgen environment can induce double-strand DNA breaks, likely mediated by the enzyme, topoisomerase IIB (TOP2B).10-12 This rapid cycling seems to lead to tangling of DNA as androgen receptor-mediated transcription proceeds. TOP2B induces transient double-strand DNA breaks to relieve these knots, before repairing them. Hence, it is not surprising to observe synergistic effects when DNA damaging dose of radiation is applied in conjunction with supraphysiologic testosterone, in vivo.13
As these pre-clinical studies have generated interesting hypotheses and moved into early clinical trials, approaches to avoid prostate cancer cell adaptation to either very low or very high androgen levels have led to use of intermittent high-dose testosterone therapy, termed Bipolar Androgen Therapy (BAT). This clinical approach conforms with pre-clinical observations that supraphysiologic testosterone-induced double-strand DNA breaks and apoptosis are transient. Hence, rapid cycling of high-dose testosterone could result in repeated rounds of DNA damage and enhanced antitumor effects.
An early pilot study combined BAT with etoposide to potentially synergize with TOP2B effects.12 In this early trial, 7/14 (50%) patients had a significant PSA decline from baseline. Soft tissue tumor shrinkage was also observed. Preliminary data from the phase II RESTORE trial, where patients progressing on enzalutamide were administered BAT (n=30), have shown 9/30 (30%) of patients to have ≥50% PSA decline from baseline.14 Additionally, clinical/radiographic progression-free survival of 8.6 months was observed. These early trials have also shown BAT to be well tolerated, and there are anecdotes of some patients reporting increased energy, vigor and a sense of well being. The TRANSFORMER trial is a recently accrued trial, randomizing patients with metastatic castration-resistant prostate cancer who previously progressed on abiraterone acetate to BAT vs. enzalutamide (NCT02286921). We eagerly await results from this trial.
As one considers the sum of the clinical data in this arena, it is important to recognize that these more contemporary trials with supraphysiologic testosterone therapy in metastatic castration-resistant prostate cancer are distinct from some earlier attempts. There have been a couple of clinical trials that have used exogenous testosterone therapy to achieve up to physiologic androgen levels.15,16 These trials saw no objective responses and only 1 patient had a ≥50% PSA decline from baseline. It is felt that there is a major functional difference on prostate cancer between eugonadal and supraphysiologic testosterone levels in this patient population.
anti androgren monotherapy and testosterone levels
Decreasing testosterone level
High testosterone treatment
testosterone level.
