AS & prostate cancer

[jamotech]

As we all know prostate cancer is the most hereditary cancer for men, and both of my grandfathers have had it. Im sure a lot of you have a similar situation, my question is will as now cause prostate cancer later. Im almost guaranteed to get it someday, will as promote the cancer or does it just cause some damage to the prostate.

[Alex Cross]

Well... Um I have been on AR for some time, i was due for a name change....

Anyways, stuff like this can be debated over and over again. In all honesty, I dont think anyone here is really qualified to answer it. Most of the peeps on here, albeit knowledgable, are fairly young. It seems all the different Doctors have a different say on AS and their long term effects...But I see it like this. We all know this shit isnt good for you, regardless. But I think if youre already predisposed to something -heart disease, prostate cancer, male pattern baldness- you should think long and hard before you do anything.... Don't get me wrong, I am not in the clear, but I can never tell anyone that i didnt know! Good luck and study up.


A/C

[Rickson]

I think prostate problems are more a result of DHT and estrogen but when it comes to cancer the study below indicates indicates low free test may be a contributor to the severity of the disease.



Is low serum free testosterone a marker for high grade prostate cancer?

Hoffman MA, DeWolf WC, Morgentaler A.
Division of Urology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

PURPOSE: The association of free and total testosterone with prostate cancer is incompletely understood. We investigated the relationship of serum free and total testosterone to the clinical and pathological characteristics of prostate cancer. MATERIALS AND METHODS: We retrospectively reviewed the clinical records of 117 consecutive patients treated by 1 physician and diagnosed with prostate cancer at our medical center between 1994 and 1997. Low free and total testosterone levels were defined as 1.5 or less and 300 ng./dl., respectively. RESULTS: After evaluating all 117 patients we noted no correlation of free and total testosterone with prostate specific antigen, patient age, prostatic volume, percent of positive biopsies, biopsy Gleason score or clinical stage. However, in patients with low versus normal free testosterone there were an increased mean percent of biopsies that showed cancer (43% versus 22%, p = 0.013) and an increased incidence of a biopsy Gleason score of 8 or greater (7 of 64 versus 0 of 48, p = 0.025). Of the 117 patients 57 underwent radical retropubic prostatectomy. In those with low versus normal free testosterone an increased mean percent of biopsies demonstrated cancer (47% versus 28%, p = 0.018). Pathological evaluation revealed stage pT2ab, pT2c, pT3 and pT4 disease, respectively, in 31%, 64%, 8% and 0% of patients with low and in 40%, 40.6%, 12.5% and 6.2% in those with normal free testosterone (p>0.05). CONCLUSIONS: In our study patients with prostate cancer and low free testosterone had more extensive disease. In addition, all men with a biopsy Gleason score of 8 or greater had low serum free testosterone. This finding suggests that low serum free testosterone may be a marker for more aggressive disease.

PMID: 10687985 [PubMed - indexed for MEDLINE]
Drugs Aging 1999 Aug;15(2):131-42 Related Articles, Books, LinkOut


LOW TEST LEVELS NOT HIGH

[Rickson]

Here are some enlargement treatments but not cancer treatments.


Prevention and Treatment of Benign Prostate Enlargement
Enlargement of the prostate gland occurs in most men with advancing age and is accompanied by reduced urinary flow and increased residual urine volume. Hormonal imbalances have previously been blamed for age related prostate disorders, but other factors have been identified as causes of the benign proliferation of prostate cells (BPH) and accompanying urinary impairment caused by this condition. Men with severe BPH often use a combination of saw palmetto and pygeum to improve urine flow and bladder voiding. These men usually wake up less frequently at night to urinate.

Published scientific literature, along with ten years of reports from members of the Life Extension Foundation, show that saw palmetto extract is effective in alleviating symptoms of BPH in most men. Pygeum extract has been shown to specifically inhibit prostate cell proliferation by blocking the binding of dihydrotestosterone (DHT) and other growth factors to prostate cell membranes. Pygeum has anti-edema effects that shrink the prostate gland significantly. Recent studies show it also inhibits the proliferation of prostate cells, by interfering with the activity of the enzyme kinase C that is needed by all rapidly growing benign and malignant cells.

Although more than 80% of men report improvement after using saw palmetto and/or pygeum extracts, some prostate enlargement often remains that continues to interfere with urinary flow and bladder evacuation. Urtica dioica, an herbal extract of nettle root that has been used in Germany for more than a decade to treat BPH, has been shown to reduce symptoms by 86% after 3 months of use. Learning of these studies, researchers at St. Luke’s/Roosevelt Hospital in New York conducted a study to discover the mechanism by which standardized nettle root extract relieves the symptoms of BPH. In their study, published in 1995, these scientists showed Urtica dioica inhibits the binding of a testosterone -related protein to receptor sites on prostate cell membranes. In January 1998, the Foundation made nettle root extract available in one formula combined with saw palmetto and pygeum. Saw palmetto, pygeum and Urtica dioica are approved drugs in Germany for the treatment of BPH.

Saw palmetto has been shown to work by inhibiting the enzyme (5-alpha reductase) in the prostate gland that converts testosterone to DHT. New studies show saw palmetto also reduces smooth muscle contraction, relaxing the bladder and sphincter muscles that cause urinary urgency. Super Saw Palmetto contains the highly effective super-critical extract from saw palmetto.

[Rickson]

Here's some more abstracts that have to do with tumor growth based on the influence of androgens.

A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy.
Cancer Res 2001 Jun 1;61(11):4315-9 (ISSN: 0008-5472)
Gregory CW; He B; Johnson RT; Ford OH; Mohler JL; French FS; Wilson EM [Find other articles with these Authors]
Laboratory for Reproductive Biology, Department of Pediatrics, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.
The development and growth of prostate cancer depends on the androgen receptor and its high-affinity binding of dihydrotestosterone, which derives from testosterone . Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. A critical question is whether the androgen receptor mediates recurrent tumor growth after androgen deprivation therapy. Here we report that a majority of recurrent prostate cancers express high levels of the androgen receptor and two nuclear receptor coactivators, transcriptional intermediary factor 2 and @#%$ receptor coactivator 1. Overexpression of these coactivators increases androgen receptor transactivation at physiological concentrations of adrenal androgen. Furthermore, we provide a molecular basis for this activation and suggest a general mechanism for recurrent prostate cancer growth.

Androgen receptor expression in prostate cancer lymph node metastases is predictive of outcome after surgery.
J Urol 1999 Apr;161(4):1233-7 (ISSN: 0022-5347)
Sweat SD; Pacelli A; Bergstralh EJ; Slezak JM; Cheng L; Bostwick DG [Find other articles with these Authors]
Department of Laboratory Medicine and Pathology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
PURPOSE: Androgens mediate the growth of prostate cancer cells. The predictive value of androgen receptor immunostaining in patient outcome is controversial. We studied the expression of androgen receptors in a large series of patients with node positive cancer, and correlated the results with clinical progression and survival. MATERIALS AND METHODS: We evaluated 197 patients with a mean age of 65.5 years who had node positive adenocarcinoma, and who underwent bilateral pelvic lymphadenectomy and/or radical prostatectomy at our clinic between 1987 and 1992. Mean followup was 6.3 years. Immunohistochemical studies were performed using an antihuman androgen receptor monoclonal antibody. In each case 100 nuclei were counted from 3 separate areas (total 300 nuclei per diagnostic category) of benign epithelium, cancer and lymph node metastases. Mean androgen receptor expression was determined from the mean of the individual cases. The intensity of immunoreactivity was evaluated on a scale of 0-no staining to 3-strong staining. We assessed the correlation of androgen receptor immunoreactivity, deoxyribonucleic acid ploidy, Gleason score and preoperative serum prostate specific antigen (PSA) with clinical progression, all cause survival and cancer specific survival using the Cox proportional hazards model. Clinical progression was defined as a positive bone scan. RESULTS: There was heterogeneous staining in the majority of cells in benign and malignant prostatic epithelium. The mean number of immunoreactive nuclei was similar in all groups (56, 53 and 56% of benign epithelium, cancer and lymph node metastases, respectively). Pairwise comparisons revealed that the only significant difference was between benign epithelium and cancer (p = 0.001) with greater immunoreactivity in benign epithelium. Intensity was lower in benign epithelium than in cancer and lymph nodes (p <0.05). Androgen receptor expression in lymph node metastases was associated with all cause and cancer specific survival on univariate analysis (p = 0.03 and 0.04, respectively). The 7-year cause specific survival was 98, 94 and 86% in patients with 51 to 69, less than 50 and greater than 70% androgen receptor expression in lymph node metastases, respectively (p <0.05). The association of androgen receptor expression in lymph node metastases was significant on multivariate analysis for cancer specific survival (p = 0.021) but not all cause survival (p = 0.16) after controlling for Gleason score, deoxyribonucleic acid ploidy and preoperative PSA. Androgen receptor immunoreactivity in lymph nodes was not a significant univariate or multivariate predictor of clinical progression, while androgen receptor expression in the primary cancer was not predictive of clinical progression or survival (p >0.05). CONCLUSIONS: Androgen receptor expression was similar in benign epithelium, primary cancer and lymph node metastases with approximately half of the epithelial cell nuclei staining. Androgen receptor immunoreactivity in lymph node metastases was predictive of cancer specific but not all cause survival in univariate and multivariate models. Gleason score was the strongest predictor of all cause survival in this cohort of patients. Our results indicate that it may be clinically useful to determine lymph node androgen receptor expression in men with advanced prostate cancer when combined with Gleason score and PSA.

Functional analysis of androgen receptor N-terminal and ligand binding domain interacting coregulators in prostate cancer.
J Formos Med Assoc (China 2000 Dec;99(12):885-94 (ISSN: 0929-6646)
Yeh S; Sampson ER; Lee DK; Kim E; Hsu CL; Chen YL; Chang HC; Altuwaijri S; Huang KE; Chang C [Find other articles with these Authors]
George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, Radiation Oncology, and Cancer Center, University of Rochester, Rochester, NY 14642, USA.
Several new androgen receptor (AR) coregulators, including ARA70, ARA55, ARA54, ARA160 and ARA24, associated with the N-terminal or the ligand-binding domain (LBD) of AR, have been identified by our group. We first identified the AR-LBD coregulators ARA70, ARA55, and ARA54. Our previous reports suggest that ARA70 can enhance the androgenic activity of 17 beta-estradiol (E2) and antiandrogens toward AR. It is of interest to compare and determine if the specificity of sex hormones and antiandrogens can be modulated by different coregulators. Our results indicate that, ARA70 is the best coregulator for increasing the androgenic activity of E2. Only ARA70 and ARA55 were able to significantly increase the androgenic activity of hydroxyflutamide, the active metabolite of a widely-used antiandrogen for the treatment of prostate cancer. Furthermore, our results suggest that among the LBD coregulators, ARA70 has a relatively high specificity for AR in the human prostate cancer cell line DU145. Together, our data suggest that the androgenic activity of some sex hormones and antiandrogens can be modulated by selective AR coactivators. In addition to the AR-LBD associated proteins, ARA24 and ARA160 have been identified as AR coregulators, interacting with the AR N-terminal instead of the LBD. Functional analysis revealed that the AR N-terminal coregulator ARA160 could cooperate with the AR LBD-associated coregulator ARA70. Our data indicate that ARA24 could also interact with AR, and that this binding is decreased by an expanding poly-glutamine (Q) length within AR. The length of the poly-Q stretch in the AR N-terminal domain is inversely correlated with the transcriptional activity of AR. Our data suggest that optimal AR transactivation may require interaction of AR with AR coregulators. The identification of factors or peptides that can interrupt androgen-mediated AR-ARA interactions may be useful in the development of better antiandrogens for treating androgen-related diseases, such as prostate cancer.

[Rickson]

Allelic variants of aromatase and the androgen and estrogen receptors: toward a multigenic model of prostate cancer risk.

Modugno F, Weissfeld JL, Trump DL, Zmuda JM, Shea P, Cauley JA, Ferrell RE.
Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA. [email protected]

PURPOSE: The purpose of this study was to determine whether polymorphisms in the CAG repeat in exon 1 of the androgen receptor (AR), two intronic restriction sites in the estrogen receptor (ESR1 XbaI and ESR1 PvuII), and an Arg264Cy5 substitution in the aromatase gene (CYP19) contribute to prostate cancer risk. EXPERIMENTAL DESIGN: A case-control study was performed with 88 Caucasian prostate cancer patients and 241 Caucasian male controls. Logistic regression models were used to assess individual and joint contributions of genotypes to prostate cancer risk. RESULTS: For single polymorphisms, only the AR repeat number was significantly related to increased prostate cancer risk [age- and body mass index (BMI)-adjusted odds ratio (OR), 1.14; 95% confidence interval (CI), 1.04-1.25], suggesting a 14% increase in risk for each missing CAG repeat. When subjects were classified as either long (> or =23 AR CAG repeats) or short (<23 repeats) carriers, a significant increase in risk was also observed (age- and BMI-adjusted OR, 1.75; 95% CI, 1.05-2.95; P = 0.04). The aromatase C/T was associated with an increase in risk of borderline significance (age- and BMI-adjusted OR, 2.50; 95% CI, 0.99-6.28). When examining the effects of two polymorphisms on prostate cancer risk, homozygosity for the ESR1 XbaI restriction site together with a longer AR was more frequent among controls (32%) than cases (18%; age- and BMI-adjusted OR, 0.39; 95% CI, 0.19-0.78). The aromatase C/C genotype together with a longer AR was also more frequent among controls (55%) than cases (41%; age- and BMI-adjusted OR, 0.51; 95% CI, 0.30-0.89). CONCLUSIONS: Estrogen and aromatase may play a role in prostate cancer. A multigenic model of prostate cancer susceptibility is also supported.

[Rickson]

Progesterone receptor expression in human prostate cancer: correlation with tumor progression.

Bonkhoff H, Fixemer T, Hunsicker I, Remberger K.
Institute of Pathology, University of the Saarland, Homburg/Saar, Germany. [email protected]

[Rickson]

Dr. John Lee, a Norwegian practicing in California, has written the following for treatment of Prostate Cancer.

Prostate Cancer and Testosterone

In 1941, Dr. Huggins showed that castration slowed the progression of prostate cancer. The cancer benefit was assumed to be due to testosterone reduction. Since that time, physicians have relied on suppression of testosterone production in their treatment of the disease. However, the benefit does not last and eventually prostate cancer progresses, presumably a result of an androgen-insensitive state of the cancer cells. Despite this fact, metastatic prostate cancer patients continue to be treated with androgen blockade. Castration and/or synthetic analogs of gonadotropin releasing hormone (e.g. Lupron) eliminate testicular testosterone but do not diminish androgens of adrenal origin. Total androgen blockade can be achieved by a combination of castration or gonadotropin-releasing hormone with an anti-androgen that blocks cell nucleus uptake of all androgens. One such anti-androgen drug is flutamide. A recent (8 Oct 1998 NEJM) study reported that, in patients with metastatic prostate cancer, the combination of orchiectomy plus flutamide conferred nosurvival advantage over orchiectomy alone. In fact, the only observed effect of flutamide was a reduction in quality of life, particularly more diarrhea and worse emotional functioning. Brain cells, as we know need some testosterone.


This finding raises several interesting points. One is that medicine has made no real progress in treating prostate cancer by androgen reduction since 1941. Second, flutamide has been under study since at least 1989, and recommended for prostate cancer treatment for over five years. Conventional medicine claims superiority over alternative practice by reason of being "evidence based." Why did it take five years for conventional medicine to discover that it had embraced a worthless drug? Perhaps this recent study will stimulate a re-examination of the conventional hypothesis concerning the role of testicular hormones.


Orchiectomy removes not only testicular testosterone production but also its production of estradiol. Why chose testosterone as the cause of prostate cancer? Is it not clear that the time of life when testosterone is at its highest level (around age 18) is the same time of life when prostate cancer is least likely? Why does prostate cancer occur so often in aging men? Testosterone supplementation prevents survival of prostate cancer cells transplanted to test mammals. Testosterone given to test mammals after transplantation of prostate cancer tissue will slow tumor growth. In prostate cancer cell culture, testosterone kills the cancer cells. It is time for a new hypothesis.


Consider three changes in testicular hormone production as men age. Progesterone production falls and since progesterone is a potent inhibitor of 5 alpha-reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT), this decline of progesterone causes increased testosterone conversion to DHT. Since testosterone is a direct antagonist of estradiol (and DHT isn't), relative estradiol effect increases. Could this be the cause of prostate cancer?


Embryology teaches us that the prostate is the male equivalent of the female uterus. They differentiate from the same embryonic cells and they share many of the same genes such as the oncogene, Bcl-2, and the cancer protector gene, p53. It is, therefore, no surprise that the hormonal relationships in endometrial cancer will be the SAME in prostate cancer. Researchers TS Wiley and Prof. Bent Formby, using prostate cancer cell cultures, have clarified much of the relationships between hormones, gene effects, and prostate cancer cell growth. Their in vitro test show the following:


Estradiol increases Bcl-2 product that leads to cell proliferation and delay in apoptosis, both of which increase cancer risk. Progesterone suppresses Bcl-2 action and increases p53 product that slows cell proliferation and restores proper apoptosis, both of which decrease cancer risk. Testosterone (but not the DHT) stops cancer cell growth. Insulin increases cancer cell growth.

It should be recalled that adult male's estradiol levels are equivalent to or greater than that of post menopausal females. Estradiol's effects, however, are suppressed (antagonized) by the male's greater production of testosterone. As noted above, progesterone is a potent inhibitor of 5 alpha-reductase and, as males age, the decline of progesterone increases the conversion rate of testosterone to DHT. Thus, in aging males, testosterone levels fall not only because of less production of but also by its increased conversion to DHT. In this situation, estradiol effect rises. Just as estradiol is a known endometrial carcinogen, so also is estradiol a likely prostate cancer carcinogen in aging males.


Lastly, it is recognized that chronic inflammation may also be carcinogenic. It is wise therefore, to maintain one's intake of anti-oxidants such as vitamin C, selenium, and the fat soluble anti-oxidant vitamins, A, E, D, and K.


It is time to revamp the prostate cancer hypothesis. Orchiectomy provided a prostate cancer benefit not because it removed testicular testosterone but it lowered estradiol levels. The course of prostate cancer growth is not a linear progression of cancer cells multiplying from one rogue cell; it is due to continued change of normal prostate cells to cancer cells because of the continued presence of an underlying metabolic imbalance. The most likely underlying metabolic imbalance in all hormone dependent cancers is estrogen dominance (too much estrogen). Prevent the estrogen dominance and you will prevent the cancer. If the cancer is already underway, correcting the estrogen dominance will slow the cancer growth and prolong life.


In the case of prostate cancer, the new treatment plan would include the following:


1. Diet should avoid sugar, refined starches, and other glycemic (insulin-raising) foods as well as high estrogen foods such as feedlot meat and milk.


2. Maintain a good intake of anti-oxidants.


3. Monitor saliva hormone levels of progesterone and testosterone in males over 50.


4. Supplement progesterone and testosterone by transdermal cream to maintain saliva levels consistent with that of healthy mature males. When supplemented in this manner, the doses required are quite small: I suspect that appropriate doses will be in the range of 8-10 mg/day of progesterone and 2-3 mg/day of testosterone.


From my clinical experience, it would not surprise that exercise and an active sex life are also protective factors against prostate cancer.


Male castration's prostate cancer benefit stemmed from estradiol reduction, not testosterone reduction. Given the choice, I would choose testosterone and progesterone supplementation over castration.


John Lee, M.D.


January 1999

Three other books of note to buy are:


What Your Doctor May Not Tell You About Menopause by John Lee, M.D.

Our Stolen Future by Theo Colborn

Healthy Living in a Toxic World by Cynthia Fincher, Ph.D.

[TNT]

This is prostate brain. This is your prostate on test . . . Wait, I digress.

Quite simply, heridity increases your risk for prostate cancer, but will not cause it per se, nor will the use of test or other AS kick you into prostate cancer unless you are personally predisposed to it. Even then, it may contribute, but will not directly cause cancer or BPE (benign prostate enlargement).

There are two simple tests to determine whether one may have BPE or prostate cancer. The most basic - and most important - is the Digital Rectal Exam (DRE). Yes, the finger. And if you're a guy who has hang-up's about a physician sticking his or her finger up your butt, get over it - it may save your life. In fact, if you have regular physical examinations and your doctor does not stick his or her finger up your butt, find a new doctor. Seriously.

The second test, generally recommended for men who are over 50 (over 40 if there is a family history of prostate cancer) is the Prostate Specific Antigen (PSA), a simple blood test.

For what it's worth, my father was diagnosed with prostate cancer ten years ago, and it was found thanks to the good ol' finger up the butt followed up by a confirming high PSA. He underwent radiation, and is alive and well today - and with a normal PSA for the past several years. (There are now many more alternatives to radiation which are less radical.)

For those who have been diagnosed with prostate cancer, it can kill you - unless you have been diagnosed early, in which case it is almost curable. (Well-known patients who were not diagnosed or treated early and died of prostate cancer include Frank Zappa and Muppets founder Jim Hensen. Hensen, however, was a Christian Scientist who refused medical treatment for his cancer.)

Testosterone and some other AS are known to have a negative effect on the prostate, and this can occur whether you are predisposed to prostate cancer or not. I have used mucho test, and because of my dad's history, I get a PSA done every six months. Thus far, I have seen no increase in my PSA levels, nor has their been any change or irregularity in my annual exam (which includes a DRE).

So, will the use of AS foster prostate cancer? Probably not, at least in most people. But the old expression holds that if it only happens 1% of 1% of the time and it happens to you, then to you the incidence has become 100%. Thus, if you are using AS, simply do the right thing and have the DRE and PSA done on a regular basis.

[jamotech]

Originally posted by Rickson
Dr. John Lee, a Norwegian practicing in California, has written the following for treatment of Prostate Cancer.

Prostate Cancer and Testosterone

In 1941, Dr. Huggins showed that castration slowed the progression of prostate cancer. The cancer benefit was assumed to be due to testosterone reduction. Since that time, physicians have relied on suppression of testosterone production in their treatment of the disease. However, the benefit does not last and eventually prostate cancer progresses, presumably a result of an androgen-insensitive state of the cancer cells. Despite this fact, metastatic prostate cancer patients continue to be treated with androgen blockade. Castration and/or synthetic analogs of gonadotropin releasing hormone (e.g. Lupron) eliminate testicular testosterone but do not diminish androgens of adrenal origin. Total androgen blockade can be achieved by a combination of castration or gonadotropin-releasing hormone with an anti-androgen that blocks cell nucleus uptake of all androgens. One such anti-androgen drug is flutamide. A recent (8 Oct 1998 NEJM) study reported that, in patients with metastatic prostate cancer, the combination of orchiectomy plus flutamide conferred nosurvival advantage over orchiectomy alone. In fact, the only observed effect of flutamide was a reduction in quality of life, particularly more diarrhea and worse emotional functioning. Brain cells, as we know need some testosterone.


This finding raises several interesting points. One is that medicine has made no real progress in treating prostate cancer by androgen reduction since 1941. Second, flutamide has been under study since at least 1989, and recommended for prostate cancer treatment for over five years. Conventional medicine claims superiority over alternative practice by reason of being "evidence based." Why did it take five years for conventional medicine to discover that it had embraced a worthless drug? Perhaps this recent study will stimulate a re-examination of the conventional hypothesis concerning the role of testicular hormones.


Orchiectomy removes not only testicular testosterone production but also its production of estradiol. Why chose testosterone as the cause of prostate cancer? Is it not clear that the time of life when testosterone is at its highest level (around age 18) is the same time of life when prostate cancer is least likely? Why does prostate cancer occur so often in aging men? Testosterone supplementation prevents survival of prostate cancer cells transplanted to test mammals. Testosterone given to test mammals after transplantation of prostate cancer tissue will slow tumor growth. In prostate cancer cell culture, testosterone kills the cancer cells. It is time for a new hypothesis.


Consider three changes in testicular hormone production as men age. Progesterone production falls and since progesterone is a potent inhibitor of 5 alpha-reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT), this decline of progesterone causes increased testosterone conversion to DHT. Since testosterone is a direct antagonist of estradiol (and DHT isn't), relative estradiol effect increases. Could this be the cause of prostate cancer?


Embryology teaches us that the prostate is the male equivalent of the female uterus. They differentiate from the same embryonic cells and they share many of the same genes such as the oncogene, Bcl-2, and the cancer protector gene, p53. It is, therefore, no surprise that the hormonal relationships in endometrial cancer will be the SAME in prostate cancer. Researchers TS Wiley and Prof. Bent Formby, using prostate cancer cell cultures, have clarified much of the relationships between hormones, gene effects, and prostate cancer cell growth. Their in vitro test show the following:


Estradiol increases Bcl-2 product that leads to cell proliferation and delay in apoptosis, both of which increase cancer risk. Progesterone suppresses Bcl-2 action and increases p53 product that slows cell proliferation and restores proper apoptosis, both of which decrease cancer risk. Testosterone (but not the DHT) stops cancer cell growth. Insulin increases cancer cell growth.

It should be recalled that adult male's estradiol levels are equivalent to or greater than that of post menopausal females. Estradiol's effects, however, are suppressed (antagonized) by the male's greater production of testosterone. As noted above, progesterone is a potent inhibitor of 5 alpha-reductase and, as males age, the decline of progesterone increases the conversion rate of testosterone to DHT. Thus, in aging males, testosterone levels fall not only because of less production of but also by its increased conversion to DHT. In this situation, estradiol effect rises. Just as estradiol is a known endometrial carcinogen, so also is estradiol a likely prostate cancer carcinogen in aging males.


Lastly, it is recognized that chronic inflammation may also be carcinogenic. It is wise therefore, to maintain one's intake of anti-oxidants such as vitamin C, selenium, and the fat soluble anti-oxidant vitamins, A, E, D, and K.


It is time to revamp the prostate cancer hypothesis. Orchiectomy provided a prostate cancer benefit not because it removed testicular testosterone but it lowered estradiol levels. The course of prostate cancer growth is not a linear progression of cancer cells multiplying from one rogue cell; it is due to continued change of normal prostate cells to cancer cells because of the continued presence of an underlying metabolic imbalance. The most likely underlying metabolic imbalance in all hormone dependent cancers is estrogen dominance (too much estrogen). Prevent the estrogen dominance and you will prevent the cancer. If the cancer is already underway, correcting the estrogen dominance will slow the cancer growth and prolong life.


In the case of prostate cancer, the new treatment plan would include the following:


1. Diet should avoid sugar, refined starches, and other glycemic (insulin-raising) foods as well as high estrogen foods such as feedlot meat and milk.


2. Maintain a good intake of anti-oxidants.


3. Monitor saliva hormone levels of progesterone and testosterone in males over 50.


4. Supplement progesterone and testosterone by transdermal cream to maintain saliva levels consistent with that of healthy mature males. When supplemented in this manner, the doses required are quite small: I suspect that appropriate doses will be in the range of 8-10 mg/day of progesterone and 2-3 mg/day of testosterone.


From my clinical experience, it would not surprise that exercise and an active sex life are also protective factors against prostate cancer.


Male castration's prostate cancer benefit stemmed from estradiol reduction, not testosterone reduction. Given the choice, I would choose testosterone and progesterone supplementation over castration.


John Lee, M.D.


January 1999

Three other books of note to buy are:


What Your Doctor May Not Tell You About Menopause by John Lee, M.D.

Our Stolen Future by Theo Colborn

Healthy Living in a Toxic World by Cynthia Fincher, Ph.D.

I found this one to be the most interesting/understandable and it seems to coincide with your first post- that low test levels could be contributing to prosate cancer because with low test levels youll naturally have higher estradoil levels. It seems from the last study its not the lack of test its the estradoil levels that are higher due to low test levels. Thanks Rickson for taking the time to post the studies, dont ever let anyone tell you that youre not thorough!

[jamotech]

Originally posted by TNT


For what it's worth, my father was diagnosed with prostate cancer ten years ago, and it was found thanks to the good ol' finger up the butt followed up by a confirming high PSA. He underwent radiation, and is alive and well today - and with a normal PSA for the past several years. (There are now many more alternatives to radiation which are less radical.)

Testosterone and some other AS are known to have a negative effect on the prostate, and this can occur whether you are predisposed to prostate cancer or not. I have used mucho test, and because of my dad's history, I get a PSA done every six months. Thus far, I have seen no increase in my PSA levels, nor has their been any change or irregularity in my annual exam (which includes a DRE).

So, will the use of AS foster prostate cancer? Probably not, at least in most people. But the old expression holds that if it only happens 1% of 1% of the time and it happens to you, then to you the incidence has become 100%. Thus, if you are using AS, simply do the right thing and have the DRE and PSA done on a regular basis.

Glad to hear your dad caught it in time, and that is the trick. One of my grandfathers caught it in time and was fine after treatment, the other unfortunately didnt catch soon enough and was just told that the cancer has spread to his bones(I guess this news sparked my question). At what age TNT did you start getting tested, im 25, would it be unnecessary to start getting "probed" now, I hope so. My father started when he was 35, am I too paranoid at this age?