Testosterone cured prostate cancer

[thebigbus]

I've lost 3 people in my family to prostate cancer any tips on how to avoid it?

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I hate to hear that. The only real "lifestyle" variant I've seen that may POSSIBLY be related is obesity and/or high sat fat diet. But some studies show opposite.

So anyone with family history needs to be screened earlier than most, with both rectal exam and PSA. Otherwise just live as "healthy" a lifestyle as you can. Obviously anabolics aren't super healthy, but as far as prostate cancer risk I think they are low on the list as long as estradiol isn't constantly high.

 

[Dezzy]

I hate to hear that. The only real "lifestyle" variant I've seen that may POSSIBLY be related is obesity and/or high sat fat diet. But some studies show opposite.

So anyone with family history needs to be screened earlier than most, with both rectal exam and PSA. Otherwise just live as "healthy" a lifestyle as you can. Obviously anabolics aren't super healthy, but as far as prostate cancer risk I think they are low on the list as long as estradiol isn't constantly high.

Ok thanks. How early? My family members got it in their early 50's. I've changed my diet. Trying to get lots of veggies, I cut out red meat drastically.

How do you feed about finasteride? I've been taking a low dose for years now.

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[alfresco]

I've lost 3 people in my family to prostate cancer any tips on how to avoid it?

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To the best of my knowledge, there is nothing you can do avoid it. No pills, no magic potions, no injections,
no prayers, no diet or lifestyle will provide you protection against prostate cancer. It is a fantasy, a folly to
believe otherwise.

The best you can do is have your prostate checked at least 2X per year. And remember, no matter what
anybody tells you, testosterone does not cause prostate cancer. But . . . if you do have it, testosterone
feeds it. It acts like a ‘fertilizer.’

Having recently lost my father to stage 5 prostate cancer, and my grandfather to prostate long ago
(not to mention three cousins who caught it early) I have taken a keen interest in the subject and do
what I recommend above. Thankfully, my PSA has not budged from 0.7 for as long as I can remember.
I still have another year of having my prostate checked 2 – 3X per year, I am 62 now. After that, 1X
per year. Because after the age of 63, statistically your odds of getting prostate cancer become the
same as the general population, but until that time they are greater do to it ‘running in the family.’

And if you live long enough, you will get prostate cancer. Literally every male does. You might not die
from it (slow growing), but you will die with it. No escaping that. Ask any reputable oncologist or urologist.

 

[BBB]

I've lost 3 people in my family to prostate cancer any tips on how to avoid it?

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Control estrogen. See below.

The role of estrogen dominance provides a more probable hypothesis. Estrogen dominance is the only known cause of endometrial (uterine) cancer. The prostate is the male equivalent of the uterus; they both developed from the same embryonic cells. They both contain the oncogene, Bcl-2, and the cancer-protective gene. And it has been shown that estradiol "turns on" p53 which blocks Bcl-2 in both breast cells and prostate cells. This suggests that if the ration of testosterone to estradiol in men changes so that the estradiol effect becomes dominant, prostate cancer cells develop. Recent studies find that this correlation is fact.

 

[BBB]

Although I am not a doctor, I have studied this issue extensively. From what I understand, DHT will cause PSA to increase to the point of saturation and then stabilize. Testosterone has not affect on the prostate except for it's ability to convert to both DHT and estrogen. Estrogen is the primary cause of uterine cancers in females and prostate cancer in men.

I have tried fen. It causes my preexisting gyno to flare even at very low doses.

 

[BBB]

Circulating Estradiol, But Not Testosterone, Is a Significant Predictor of High-Grade Prostate Cancer in Patients Undergoing Radical Prostatectomy

BACKGROUND: The objective of this study was to assess the association between preoperative circulating levels of 17b-estradiol (E2) and high-grade prostate cancer (HGPCa) (Gleason grade _4 þ 3) at the time patients underwent radical retropubic prostatectomy (RRP). METHODS: Serum total testosterone (tT), sex hormone-binding globulin (SHBG), and E2 levels were measured the day before surgery (8-10 AM) in a cohort of 655 consecutive Caucasian-
European patients who underwent RRP at a single institution. Logistic regression models were used to test the association between predictors (including age, body mass index, prostate-specific antigen [PSA], clinical tumor classification, biopsy Gleason sum, tT, SHBG, and E2) and HGPCa. Serum E2 was included in the model as both a continuous variable and a categorized variable (according to the most informative cutoff: 50 pg/mL). RESULTS: Pathologic
HGPCa was identified in 156 patients (23.8%). Patients with HGPCa had significantly higher PSA, clinical tumor classification, and biopsy Gleason sum than those without HGPCa (all P < .001). No other significant differences were observed between groups. At univariate analysis, continuously coded E2 was not associated significantly with HGPCa (odds ratio [OR], 1.009; P ¼ .25), whereas patients with E2 levels _50 pg/mL had a 3.24-fold increased risk of HGPCa
(P < .001). At multivariate analysis, E2 was associated significantly with HGPCa both as a continuous predictor (OR, 1.02; P ¼ .04) and as a categorical predictor (OR, 3.94; P < .001) after accounting for other variables. Conversely, tT and SHBG levels were not associated significantly with HGPCa. CONCLUSIONS: E2 was associated significantly with pathologic HGPCa, whereas SHBG and tT failed to demonstrate any association.

 

[BBB]

Estrogen and Prostate Cancer
The role that estrogen plays in malignant prostate disease is contradictory and complex. Some studies indicate that estrogen and its toxic metabolites are a cause of prostate cancer.15, 16 Yet once prostate cancer develops, certain estrogen compounds demonstrate anticancer effects.
This paradox can be explained by the mechanisms that estradiol (and its toxic metabolites) uses to damage prostate cell DNA, 17 causing gene mutations that result in the loss of cell growth regulatory control, i.e. cancer. Interestingly, once a prostate tumor manifests, estrogen may exert anti-tumor effects, though cancer cells eventually become resistant to estrogen drugs and then even use endogenous estrogen to fuel their growth.
The fact that estrogen may temporarily exert anti-tumor effects in certain types of prostate cancer cells does not diminish the argument that estrogen may have contributed to the initiation of the same cancer. For example, in a study published two years ago, researchers discovered that when “estradiol is added to testosterone treatment of rats, prostate cancer incidence is markedly increased and even a short course of estrogen treatment results in a high incidence of prostate cancer.” These scientists hypothesize that metabolites of estrogens can be converted to reactive intermediates that can adduct to DNA and cause generation of reactive oxygen species; thus, estradiol is a weak DNA-damaging carcinogen that causes DNA damage to prostate cell genes.18 This kind of damage to DNA regulatory genes is what initiates prostate cancer.
Many published studies, however, show no association between high blood estradiol levels and diagnosed prostate cancers.19 One reason there are not more diagnosed prostate cancers in men with high estrogen may be that the high estradiol level that initiated DNA damage then serves to keep prostate cancer temporarily under control once it develops.