I read his book and he states that the aromatization of testosterone into estradiol causes PCa. He bases some of his conclusions on Lebowitz Triple Androgen Blockade..if you combine the theories of Friedman...Leibowitz...BAT...a protocol to control PCa and prevent CRPC would be: 12 months of Lupron + Casodex + Avodart + Arimidex followed by 3 month cycles of High Dose Testosterone (1500 -2000 ng/dl) + Avodart + Arimidex...then a 3 month cycle of Lupron + Avodart + Arimidex and keep repeating the alternating 3 month cycles
I don't want to get into a debate about this, and I confess that I haven't studied Edward Friedman's original papers. But all of the data from the PATCH clinical trial in the UK show that estradiol does NOT causes prostate cancer. That study is in phase III with about 1200 patients in the trial so far. The PATCH data show that parenteral estradiol is as good as the LHRH drugs in controlling PCa. Furthermore there are a lot of male to-female transsexuals, who go on androgen blocking drugs and high dose estrogen. The incidence of prostate cancer in those individuals is incredibly rare.
As long as the PCa is hormonally sensitive, estradiol can limit the risk of PCa and can control PSA. The situation, however, is different when the cancer is castrate resistant. In that situation just about any steroid can become an activating ligand.
If anyone is really interest in this, they can back channel me for citation.
No it does not show that....controlling PCa is not the same as what causes PCa...PCa needs Testosterone but they have proven Testosterone does not cause PCa...applying an estrogen patch could lower Testosterone probably works along the lines of DES...Edwards shows that intercellular levels of estradiol and it effects on ER Alpha and ER Beta and raising levels of BCL-2 causes PCa.
Optimal levels of estradiol [E2] for male health are somewhere in the 20-30 pg/mL range (according to an analysis of studies that LEF did.)
In a 2005 paper [1]:
"Phase II study of transdermal estradiol in androgen-independent prostate carcinoma"
"The mean ... serum estradiol level increased from 17.2 pg.mL (range, 14.8–19.6 pg/mL) to 460.7 pg/mL (range, 334.6–586.7 pg/mL)."
That's a crazy-high level, of course, &, one might anticipate, not without consequences. But E2 at those levels cannot drive PCa. That's because E2-induce growth needs lowish levels of T, & such E2 levels castrate a man.
I don't know what the target T is for male to female transsexuals, but at very low levels the risk of PCa should be reduced.
Only one case but I used estrogen patches to drop my T to castrate levels. I've done far better than Mayo docs predicted (their predictions involved using Lupron, chemo, and radiation). PSA was zero throughout the 6 months of estrogen ADT. I did use zytiga though. I think that might have helped. T was undetectable and E2 was on the low side for SPE - 100 to 200. (SPE -> supraphysiological estrogen)
Control and initiate are two different things. It is my opinion that E2 initiates it but needs some T to facilitate its dirty work.
As an aside, SOC docs don't seem well versed in basic human biology. I asked FOUR different SOC docs about using estrogen patches to drop T (including a nationally known one at Mayo). All FOUR said it wouldn't work. I reviewed my high school biology and went for it. Some of the docs I've talked to since then are quite sharp. Maybe I just phrased my questions poorly or maybe they didn't want to tell me that Lupron wasn't the only option for me.
Interesting post Gus. I've been reading Dr John Lee's book Hormone Balance for Men and again it points to increased levels of estradiol as a cause. Both men and women are constantly exposed to xenoestrogens through food, water and different chemicals from skincare, plastic packaging, pesticides and cleaning products. I also think it is our exposure to these which increase oestrogen dominance and our risk of cancer rather than excessive testosterone. The body can convert testosterone to oestrogen if it wants to. Surely having healthy levels of testosterone cannot be the cause but preventing it from converting to an oestrogen.
I'm trying to find the answers for my Dad. After androgen deprivation therapy he's struggling with insomnia, hot flashes, an increased belly, fatty liver and fatigue. Sounds like he has too much oestrogen and not enough testosterone to balance it out. Also the liver is vital in eliminating oestrogen metabolites so it's a vicious circle.
I wonder if aiding the body in reducing oestrogen dominance is key. Supplements like DIM found in small amounts naturally in vegetables such as broccoli are useful however I don't know about giving this to a former cancer patient.
the estradiol theory makes a lot of sense....why do men who have low T get more aggressive PCa then men with high T...for years scientists have said all the phyto-estrogens and even estrogen like substances in pesticides which get into the food supply is the major cause of both prostate and breast cancer.
Leibowitz says it's because low T (anything below about 400 in his experience) is stressing our PC tumors enough that they complete the adaptation pretty quickly once drugs drive our T toward castrate levels. In the men he selects for high T treatment, he likes to keep their T well over a thousand -- some of his men are in the low thousands and thriving for many years.
Thank you all you who understand this stuff. I'm Gleason 9, stage pt3b at post RP pathology at age 69. Now Age 73. After coming off 13 months of HT in Nov. 2016, my RO has had me on avodart, finasteride, cabergoline , metformin and he likes that I'm also on Crestor and celecoxib for cholesterol and arthritis. I'm also on cymbalta for anxiety and pain. I've had rising PSA after RP, SRT and RT to pelvic nodes. While on Lupron, bicalutamide and avodart I was undetectable. PSA is rising again but appears to have hit a plateau lately at 1.3 my highest level since dx. My prolactin is very low but I have fatty liver. No SEs now except hot flashes occasionally during the day. Have not decided on next steps. Waiting for next monthly PSA. If it gets to 2.0 we're thinking of axumin scan. All ultrasound, CT and bone density scans have been negative since RT to pelvic nodes.
Thoughts???
Ed is a cool guy. I have been reading his posts for over ten years. Always interesting.
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