Not a survivor (yet) but seeking advice

Cushions,

You are correct, the original Higgins study was done on castration rather than managing T levels. Dr. Abraham Morgentaler study on testosterone provided a series of reports from oncologists because it contradicted their opinions on hormonal treatments. However, Morgentaler fidings related to the risk of having PCa when T is low than when it is high. His "low level" in terms of total T in circulation does not correspond to the levels considered and recommended by the Endocrine Society. In other words, these opinions on testosterone levels have no meaning when trying to classify a cancer as aggressive or indolent. It may be influential when considering the progression of the disease.

All the doctors involved in PCa rsearches agree that androgens (T in male) is what drives prostate cancer to survive and proliferate. But it is not clear if exogenous testosterone (injected) is as well involved in disease progression as it is endogenous testosterone. Zero T (castration) surely will turn PCa indolent and this bandit will try all means to survive to the extent of starting to produce its own androgens (Darwin principle on survival of the species).

Your T is low but above the normal low limit, which level has been fixed in basis on several health factors and symptoms. If for any reason you are pondering T injections to get you out of menopause-like symptoms I would suggest you to consider estrogen patches more than TRT if PCa is diagnosed.

Try all means to get a copy of the MRI report. We can help you to understand the results.

VG

hewhositsoncushions said:

@Will and RobLee

@Will and RobLee

Sorry to hear about your challenges. I hope you kep on fighting! I am as confused as you are about all this

Hi VG

This is a fascinating topic - I am not sure I am reading the same as you about T driving proliferation of PCa. Quite a lot of the more recent studies appear to show no correlation and some people argue that even very low levels of T are enough to feed PCa anyway and that high(er) T ay be of more benefit fighting cancer and for general health and longivety. I think there was something about the difference between feeding and starving. Once I get the tests done I am going to engage with my GP, T specialist and urologist to see what is best to do but I do need something to get my balls back out of wifey's purse

http://www.cancernetwork.com/oncology-journal/new-concepts-regarding-testosterone-and-prostate-cancer-breath-fresh-air was the report that summarised this.

Also https://www.sciencedaily.com/releases/2016/06/160621112103.htm.

Caveat emptor, big pharma

Not sure about gels - I have lurked on various T forums and they seem to have a lot of side effects whilst being less effective.

Will keep you posted!

In the diagnosis of virtually every man here, T-levels were irrelevant to their discussions.  Later, with metastatic disease or during HT, it does become relevant.

Anyone knows of any good Experienced Robotic Prostate surgeon at Kaiser Southern California ? Or how to check for one from Kaiser list ? Does Kaiser let us check the back ground and credentials of their surgeons ?

Thank You so much for any comment

Cushions,

I would very much appreciate if you dedicate time in “exploring” the intrigues of the Testosterone in regards to the values of T in PCa therapies, and post your findings. Not many here know the details or have enter into such theme exactly because of the lack of existing evidence to point to the contrary of what is informed by our oncologists.

In fact, my above post resumes to what is known at the moment. The Resolution 8 set by Dr. Luiz Torres in the link you provide, identifies these facts and ends by saying “…Although large, long-term studies are lacking, the available evidence does not support increased PCa risk with T therapy ….”. In other words doesn’t support either way. The study of the 1966 Nobel Prize winner Dr. Charles Huggins regarding hormone dependent cancers is still the only valid evidence.

By experience, I had low levels of testosterone (close to yours) in 2000 (50 years old) but such did not affect my drive for sex (very active always ready for the fight) nor my fitness. The bandit was there too producing a substantial amount of PSA serum of 22.4 ng/ml (at PCa diagnosis). When recurrence was verified after radiotherapy in 2008, I engaged in researches on hormonal therapies. I read many clinical papers on drugs and on their effects on Pca. Chemical castration (T lower than 30 ng/dL) drove the PSA to undetectable levels and these climb out of undetectable as soon as my testosterone increased surpassing the 50 ng/dL (clinical castration level). From there T climbed to a maximum of 450 and then plateaued at the 300 range. The PSA also plateaued at the 1.5 ng/ml level.
I wonder if any additional climbing of my endogenous testosterone would influence the bandit and make the PSA to climb further too.

You are correct. The ones patronizing the above Resolutions are all tainted by the big pharmas (refer to Potential Competing Interests in the same article). We can expect a number of newer TRT drugs on sale pretty soon.

Best,

VGama

I, of course do not know your age but, I was 61 when I was diagnosed.  I, like you no doubt, was given a short list of treatment possibilities from surgery to "wait and watch".  I wanted no part of having this disease in me and immediately opted for the surgery.  There is a scale (sorry but I can't remember the name) that runs from 1 to 10 With 10 being the worst.  Post op biopsy showed mine to be a 9.  They also removed lymph glands in the area just as a precaution.  Seven years cancer free and counting.  Be sure to share your concerns with your family and cancer survivors when possible.  Oh, and be sure to pray!

hewhositsoncushions said:

Quick update

Had TRUS biopsy on Monday after all the toing and froing to ensure informed consent.

Procedure not as grim as made out (was making Carry on Doctor jokes throughout) but side effects a bit.... lets just say I know how women feel wrt TOTM now!

Results discussion due in a few days.

Scan showed prostate was normal size and seond DRE fine.

I asked about penis shortening after RP and the consutant said that was not really an issue. Hmmmm....

Don't believe him.  That's what one urologist said to me.  He actually said the penis does not get shorter and technically he is/was correct.  But although this may an issue for the urologists, it definitely is for all of the men who have had surgery and have been willing to admit to it.

It is physiologically IMPOSSIBLE for the penis NOT to appear shorter following surgery.  The degree of shortening in appearance will vary but will generally be around 1" of flaccid length because that's about the diameter of the prostate, which they always say is about the size of a walnut but the size of walnuts varies.

The prostate is positioned between the top of the penis and the bottom of the bladder.  There are urinary sphincters located at each end which if damaged or weakened by surgery is at least one reason why men always experience incontinence following surgery -- usually temporarily until sphincter strength recovers but sometimes permanently.

In any event, when you take the prostate out by means of surgery, a gap is created and the top of the penis has to be connected to the bottom of the bladder to fill the space causing the shortened appearance of the penis.

That is a fact.  Whether this an "issue" for the man concerned depends on the man but there is no doubt that, although technically your **** will not BE shorter than it was before surgery, it will defintely "appear" shorter after surgery than it did before.

That mattered A LOT to me because my equipment when flaccid was/is not that long to begin with.  Every inch (or fraction thereof) counted to me and it was one (of many reasons) why I chose to avoid surgery.

Cushions,

ASAP cells can go either way, benign or cancerous. It depends if other cell structures (in benign environment) are missing. Some pathologists are suspicious on these atypical acinar proliferations found in biopsies because of the high percentage (40%) of ASAP cases that turn into positive cases after repeating the boring at close tissue. In fact one core (⌀ 1 mm x 2 cm) draws only about 1/800th of the gland. It easily can miss cancer.

 I would appreciate if you share the complete report of the pathologist: How many cores/needles were taken? Did they find hyperplasia or calculi that could justify the high level of PSA? In which region did the ASAP exist?

Can you substantiate on the urologist's opinion That "... anything serious would have been picked up by now". What kind of image (color doppler ?) was used or data that leads him to state the above?

I hope this suspicious is found to be benign.

VG

So far you have not been diagnosed with Pca. Even if such becomes the case you have time to educate on the details and then decide on what to do next. PCa takes a sluggish pace to develop and progress to affect the holder. Other similar bandits, like breast cancer, are much faster and risky. Everybody gets nervous in front of the doctor when cancer is the subject. In any case one does not need to decided in just one visit. Listen and take notes, and then schedule the next appointment in a way that you have time to digest what was told.

Now it is time to relax and enjoy life as usual.

Best,

VG