Testosterone?

doinalright said...
Before my surgery I would get erect just thinking about anything sexual but now I do not think about sex at all.

Sounds like me too.. Except I've been on T-meds for almost two years and no real improvement in that department.

Not sure about getting a test injection. The typical gels that are used take a while to build up your T number. You might also need to wait another year for the T meds...

With all the "T" supplement and drug ads on TV and in magazines, it's easy to see a huge conflict building between maintaining testosterone levels into late middle-age and beyond and the number of men being diagnosed with prostate cancer...

It's almost comical listening to the warnings that accompany these ads while smiling, happy people frolic in the video portion of the ad...

Hi doinalright,
Testosterone replacement therapy (TRT) is being accepted as a QOL issue in patients treated for PCa. It is not a simple issue. Here are some thoughts:

The cause of prostate cancer has never been determined. In simpler words, no one knows what starts the cancer process in the prostate gland. There are hypothesis. On one side, some say that in aggressive cancer when a diagnosis is made, a number of men have LOWER levels of testosterone. On another side, some point out that men with high testosterone are at increased risk to develop prostate cancer. So, who is right?

The answer is no one knows with a high degree of certainty.What it is known is that in the presence of prostate cancer, androgens (testosterone and its metabolites) drive the growth of cancer cells. How do they know this? They know it by the response that cancer patients demonstrate when treated with androgen deprivation therapies. This response it directly proportional to the state of the patient’s tumor load at the time of the diagnosis. In general the response is poor in widely disseminated disease and better in earlier stages of the disease. As a matter of fact, in extremely disseminated PCa, there is short or no response to androgen deprivation.

Prostate cells are predominantly androgen dependent, but in the prostate gland there is a number of androgen independent cells that we are born with. This is one reason why androgen deprivation as a therapy is never “curative”. Prostate cancer is therefore highly androgen dependent in its initial stages and typically responds well when androgen deprivation is initiated at that stage. In time and through a variable progression rate, cancer cells learn how to survive by using different mechanisms. There is a natural process to insure their survival by which androgen dependent cancer cells tend to become androgen independent.

Prostate cells have in their surface chemical entities that behave as doors to other chemical entities. These are known as the androgen receptors (AR) and like a lock and key only accept other chemical entities that “fit”. These receptors are the way that these cells multiply, grow and die. There tends to be an equilibrium as new cells are born and others die in a process to maintain a balance of the physical conditions of the prostate gland.

In normal conditions, these androgen receptors(AR) are charged with the way the prostate gland maintains itself. They(the ARs) preferentially link to a very potent metabolite of testosterone known as dihydrotestosterone (DHT). When these two chemical entities link (the AR and DHT) they form a complex that then is able to move to the cell’s nucleus and start a process known as cell cycle or cell division (by which the cell splits into two “daughter” cells). This is a normal process (homeostasis) triggered to maintain a balance within (in this case) the prostate gland.

In the carcinogenic process of the prostate, the normal proliferation rate of the cells tends to be slow or close to that of normal cells. This can change as DNA changes accumulate and the normal character of the cells change. In time and through a process of dedifferentiation cancer cells try to survive by acquiring a very different character. The cancer cells can learn how to survive by using other chemical entities than androgens. It is known that the AR can link to growth factors such as epidermal growth factor (EGF), vascular endothelial growth factor (VEGF) and many others to regulate cell-cycle, cell death and differentiation outcomes. In short, these growth factors are one way for cancer cells to acquire androgen-independence.

This is a complex process. Difficult to define precisely because of number of the different possible pathways and receptors involved. Normal prostate cells and prostate cancer cells also exhibits estrogen receptors. The mostly express is estrogen receptor Beta (ERb)and some do express estrogen receptor Alpha (ERa). These can drive prostate cancer growth in the presence of estradiol (estradiol is derived from testosterone by an aromatization conversion). This is why testosterone replacement therapy (TRT) in patients who have been treated for PCa needs to be instituted with caution to monitor metabolic products and avoid any of them to drive cancer progression.

Many men, otherwise healthy, with low testosterone resort to supplementation with testosterone without understanding that the addition of this external source of testosterone will eventually reduce his normal source of internal testosterone production. This is a “for life commitment”, as with time it will cause testicular atrophy and lower endogenous testosterone production.

In men with who have been treated for prostate cancer it is important to control the metabolic products of testosterone. It is also of extreme importance to differentiate patients that have no prostate gland (surgically removed) from those that have been treated with radiation. Given the complexity of possible receptors involved, men need to be treated by physicians that closely monitor the metabolic products of testosterone. Mainly dihydrotestosterone (DHT and estradiol (E2). To add testosterone without monitoring these is risky. PSA by necessity needs to be monitored closely to prevent unrecognized progression.

In summary, testosterone replacement therapy (TRT) might be an important addition to improve QOL in PCa patients. It is important to understand the details and the necessary commitment to undergo this therapy. Physicians that understand the process are an important requirement. Finding one might not be easy. As one who did it, proceed with caution.

RalphV

Interesting supposition, that an average guy with no issues would have any reason to run a very expensive test just for fun.

I had never had a T level test, didn't need it. My GP did run one after my PCa diagnosis, since I had blown out my deductible and out of pocket, but I never noticed it on the piles of paperwork.

Back to today. I'm 4 months into a Lupron vacation, and my T is higher than it was before surgery. But I still don't notice the hot girls in the "correct" way. I suspect there is much more involved than T level.