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Please post a response! Is anyone afraid of the long term damage from juice? Or death
- Thread starter jc3899
- Start date
Scott Steinner
New member
Re: quote; "if i lose 2-3 years off my life, oh well. its the worst years, the ones at th
I did a print of his info!
Jeff_rys said:
I did a print of his info!
Thanx guys. COX-2 also plays a role in arthritisis. Drugs like celebrex are COX-2 inhibitors. I did not know it had a role in cancer, interesting. Again, I do not believe that androgens create cancer, but what they may be able to do is make a tiny island of cancerous cells into something alot worse - a full fledged tumor. Think about estrogen's role in breast cancer. Estrogen inhibition with tamoxifin and arimidex, the whole reason why those drugs were created, can slow the growth of breast cancers and can prevent a reoccurance after tumor removal or mastecomy. I think medical science will prove that prostate cancer is not much of a different animal in reaction to androgens as breast cancer is in reaction to estrogens. But much like Arnold's heart vavle androgens don't create the problem but may definately aggrivate a non-problem into something more serious. If you have a genetic predisposition to prostate cancer I would certainly be careful at any rate.
Mark,
Agreed. Those predisposed should stay away from androgens. I think that in terms of androgens causing cancer, they dont, but they make a bad situation worse (cause cancer to grow).
I know of people who have had prostate cancer for years and years that hasnt grown due anti-androgen therapy, similar to treatment of metastatic breast cancer with anti-estrogenic compounds.
Not only are COX-2 enzymes used for arthritis, they are good to use if you have the FAP gene (Familial Adenomatous Polyposis) to prevent colon cancer which you would be likley to get. 400mg twice a day of celexicob has been shown to reduce colon pollups in FAP humans up to 30%.
COX-2 is becoming a big area of study in cancer treatment (almost all cancers it plays a role in except cancers of the lymphatic system).
Agreed. Those predisposed should stay away from androgens. I think that in terms of androgens causing cancer, they dont, but they make a bad situation worse (cause cancer to grow).
I know of people who have had prostate cancer for years and years that hasnt grown due anti-androgen therapy, similar to treatment of metastatic breast cancer with anti-estrogenic compounds.
Not only are COX-2 enzymes used for arthritis, they are good to use if you have the FAP gene (Familial Adenomatous Polyposis) to prevent colon cancer which you would be likley to get. 400mg twice a day of celexicob has been shown to reduce colon pollups in FAP humans up to 30%.
COX-2 is becoming a big area of study in cancer treatment (almost all cancers it plays a role in except cancers of the lymphatic system).
I think medical science will not prove that. In fact they have already proved that to be false. There is no correlation between androgens and prostate cancer.
What the Published Literature Says about Testosterone and Prostate Cancer
Studies Indicating That Testosterone Does Not Cause Prostate Cancer
Study 1: " This nested case-control study was based on the cohort of men who donated blood to the Janus serum bank at Oslo University Hospital between 1973 and 1994. Cancer incidence was ascertained through linkage with the Norwegian Cancer Registry. The study included sera from 59 men who developed prostate cancer subsequent to blood donation and 180 men who were free of any diagnosed cancer in 1994 and were of similar age and had similar blood storage time. Neither testosterone, DHT, nor the ratio testosterone
HT was associated with risk of developing prostate cancer. These results showed no association, positive or negative, between androgens measured in serum and the subsequent risk of developing prostate cancer."
Cancer Epidemiology Biomarkers Prev. (1997 Nov: 6(11):967-9
Study conducted at: Department of Community Medicine and General Practice, University Medical Center, Trondheim, Norway. lars.vatten@ medisin.ntnu.no
Study 2:" We conducted a nested case-control study in a cohort of 6860 Japanese-American men examined from 1971 to 1975. At the time of examination, a single blood specimen was obtained, and the serum was frozen. After a surveillance period of more than 20 years, 141 tissue-confirmed incident cases of prostate cancer were identified, and their stored sera and those of 141 matched controls were assayed for total testosterone, free testosterone, dihydrotestosterone, 3-alpha-androstanediol glucuronide, androsterone glucuronide, and androstenedione. The findings of this study indicate that none of these androgens is strongly associated with prostate cancer risk."
Cancer Epidemiol. Biomarkers Prev. (1996 Aug; 5(8):621-5)
Study conducted at: Japan-Hawaii Cancer Study, Kuakini Medical Center, Honolulu 96817, USA.
Study 3: " Prostate cancer was identified in 14% (11/77) of the entire group and in 10 men (29%) aged 60 years or older. The median age for men with cancer was 64 years. No significant differences were noted between the cancer and benign groups with regard to PSA level, PSA density, prostate volume, total testosterone level, or free testosterone level. A high prevalence of biopsy-detectable prostate cancer was identified in men with low total or free testosterone levels despite normal PSA levels and results of digital rectal examination. These data suggest that (1) digital rectal examination and PSA levels are insensitive indicators of prostate cancer in men with low total or free testosterone levels, and (2) PSA levels may be altered by naturally occurring reductions in serum androgen levels."
Journal of the American Medical Association (JAMA) 1996 Dec.18;276(23):1904-6
Study conducted at: Division of Urology, Beth Israel Hospital, Harvard Medical School, Boston, Mass. 02215.
Study 4: " We conducted a prospective nested case-control study to evaluate the relationships of serum androgens and estrogens to prostate cancer using serum collected at baseline for the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. None of the individual androgens or estrogens was significantly related to prostate cancer. These results do not support a strong relationship of serum androgens and estrogens with prostate cancer in smokers."
Cancer Epidemiology and Biomarkers Prev. (1998 Dec;7(12):1069-74)
Study conducted at: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892-7374. jd7g@ nih.gov
Study 5: "We report a nested case-control study of serum biomarkers of 5 alpha-reductase activity and the incidence of prostate cancer. From a cohort of more than 125,000 members of the Kaiser Permanente Medical Care Program who underwent multiphasic health examinations during 1964-1971, we selected 106 incident prostate cancer cases. A control was pair matched to each case on age, date of serum sampling, and clinic location. The adjusted odds ratios and 95% confidence intervals for a one quartile score increase were 1.00 for total testosterone (1.00 = no increased risk), 1.14 for free testosterone, 1.13 for androsterone glucuronide, and 1.16 for 3 alpha-diol G."
Cancer Epidemiology Biomarkers Prev. (1997 Jan;6(1):21-4 )
Study conducted at: Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill 27599-7400.
Study 6: "Serum samples were obtained from 6860 men during their study examination from 1971 to 1975. After a surveillance period of about 14 years, 98 incident cases of prostate cancer were identified. Their stored sera and that of 98 matched controls from the study population were tested for the following: testosterone, dihydrotestosterone, estrone, estradiol, and sex hormone globulin. There was a suggestion that serum dihydrotestosterone levels were lower and the testosterone/dihydrotestosterone ratios were higher in the prostate cancer cases compared with their controls. However, none of these associations or that of the other hormones was strongly significant."
Cancer Research (1988 June 15;48(12):3515-7)
Study conducted at: Japan-Hawaii Cancer Study, Kuakini Medical Center, Honolulu 96817.
Study 7: " A case-control study of prostatic cancer was carried out to examine the association between selected physical characteristics and factors related to sexual development and behaviour and the risk for this disease. The levels of testosterone (T), dihydrotestosterone, salivary testosterone and T/SHBG (sex hormone binding globulin) did not vary with age. Older men had higher oestradiol (estrogen) levels. Further, little association between hormone levels and risk factors was found, except for married subjects having increased serum androgens and heavy subjects having decreased serum androgens (not significant)."
European Journal of Cancer Prev., (1992 April;1(3):239-45 )
Study conducted at: Department of Urology, Erasmus University Rotterdam, The Netherlands.
Study 8: "A population-based nested case-control study was conducted to determine the relation of prediagnostic serum levels of testosterone, dihydrotestosterone, prolactin, follicle-stimulating hormone, luteinizing hormone, estrone, and estradiol to the risk of subsequent prostate cancer. Serum specimens of study subjects were available from a blood collection campaign in Washington County, Maryland, in 1974. There were no significant differences in levels of these hormones between cases and controls, although elevated levels of luteinizing hormone and of testosterone:dihydrotestosterone ratios were associated with mild increased risks of prostate cancer."
Cancer Epidemiology Biomarkers Prev. (1993 Jan-Feb;2(1):27-32 )
Study conducted at: National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland 20892.
Study 9: " The possible relationship between changes in peripheral hormone levels and the occurrence of prostatic pathology was studied in a case-control study, involving estimation of various plasma hormones in 368 Dutch and 258 Japanese men, who were grouped as controls and patients with benign prostatic hyperplasia, focal prostatic carcinoma, or clinically evident prostatic carcinoma. There were no significant differences in plasma androgen levels between Japanese or Dutch prostate cancer cases and their respective control subgroups. These findings do not support a correlation between the lower plasma testosterone levels and a lower incidence of prostate cancer in the Japanese men. Furthermore, no significant differences were found between salivary levels of testosterone or the ratio between testosterone and SHBG in the various Dutch subgroups. In Japanese benign prostatic hyperplasia patients, the testosterone to SHBG ratio was significantly increased. In conclusion, the results of this retrospective, cross-sectional study do not indicate that hormonal levels play a primary role in the origin or promotion of prostatic abnormalities."
Cancer Research (1991 July 1; 51(13):3445-50)
What the Published Literature Says about Testosterone and Prostate Cancer
Studies Indicating That Testosterone Does Not Cause Prostate Cancer
Study 1: " This nested case-control study was based on the cohort of men who donated blood to the Janus serum bank at Oslo University Hospital between 1973 and 1994. Cancer incidence was ascertained through linkage with the Norwegian Cancer Registry. The study included sera from 59 men who developed prostate cancer subsequent to blood donation and 180 men who were free of any diagnosed cancer in 1994 and were of similar age and had similar blood storage time. Neither testosterone, DHT, nor the ratio testosterone
HT was associated with risk of developing prostate cancer. These results showed no association, positive or negative, between androgens measured in serum and the subsequent risk of developing prostate cancer." Cancer Epidemiology Biomarkers Prev. (1997 Nov: 6(11):967-9
Study conducted at: Department of Community Medicine and General Practice, University Medical Center, Trondheim, Norway. lars.vatten@ medisin.ntnu.no
Study 2:" We conducted a nested case-control study in a cohort of 6860 Japanese-American men examined from 1971 to 1975. At the time of examination, a single blood specimen was obtained, and the serum was frozen. After a surveillance period of more than 20 years, 141 tissue-confirmed incident cases of prostate cancer were identified, and their stored sera and those of 141 matched controls were assayed for total testosterone, free testosterone, dihydrotestosterone, 3-alpha-androstanediol glucuronide, androsterone glucuronide, and androstenedione. The findings of this study indicate that none of these androgens is strongly associated with prostate cancer risk."
Cancer Epidemiol. Biomarkers Prev. (1996 Aug; 5(8):621-5)
Study conducted at: Japan-Hawaii Cancer Study, Kuakini Medical Center, Honolulu 96817, USA.
Study 3: " Prostate cancer was identified in 14% (11/77) of the entire group and in 10 men (29%) aged 60 years or older. The median age for men with cancer was 64 years. No significant differences were noted between the cancer and benign groups with regard to PSA level, PSA density, prostate volume, total testosterone level, or free testosterone level. A high prevalence of biopsy-detectable prostate cancer was identified in men with low total or free testosterone levels despite normal PSA levels and results of digital rectal examination. These data suggest that (1) digital rectal examination and PSA levels are insensitive indicators of prostate cancer in men with low total or free testosterone levels, and (2) PSA levels may be altered by naturally occurring reductions in serum androgen levels."
Journal of the American Medical Association (JAMA) 1996 Dec.18;276(23):1904-6
Study conducted at: Division of Urology, Beth Israel Hospital, Harvard Medical School, Boston, Mass. 02215.
Study 4: " We conducted a prospective nested case-control study to evaluate the relationships of serum androgens and estrogens to prostate cancer using serum collected at baseline for the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. None of the individual androgens or estrogens was significantly related to prostate cancer. These results do not support a strong relationship of serum androgens and estrogens with prostate cancer in smokers."
Cancer Epidemiology and Biomarkers Prev. (1998 Dec;7(12):1069-74)
Study conducted at: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892-7374. jd7g@ nih.gov
Study 5: "We report a nested case-control study of serum biomarkers of 5 alpha-reductase activity and the incidence of prostate cancer. From a cohort of more than 125,000 members of the Kaiser Permanente Medical Care Program who underwent multiphasic health examinations during 1964-1971, we selected 106 incident prostate cancer cases. A control was pair matched to each case on age, date of serum sampling, and clinic location. The adjusted odds ratios and 95% confidence intervals for a one quartile score increase were 1.00 for total testosterone (1.00 = no increased risk), 1.14 for free testosterone, 1.13 for androsterone glucuronide, and 1.16 for 3 alpha-diol G."
Cancer Epidemiology Biomarkers Prev. (1997 Jan;6(1):21-4 )
Study conducted at: Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill 27599-7400.
Study 6: "Serum samples were obtained from 6860 men during their study examination from 1971 to 1975. After a surveillance period of about 14 years, 98 incident cases of prostate cancer were identified. Their stored sera and that of 98 matched controls from the study population were tested for the following: testosterone, dihydrotestosterone, estrone, estradiol, and sex hormone globulin. There was a suggestion that serum dihydrotestosterone levels were lower and the testosterone/dihydrotestosterone ratios were higher in the prostate cancer cases compared with their controls. However, none of these associations or that of the other hormones was strongly significant."
Cancer Research (1988 June 15;48(12):3515-7)
Study conducted at: Japan-Hawaii Cancer Study, Kuakini Medical Center, Honolulu 96817.
Study 7: " A case-control study of prostatic cancer was carried out to examine the association between selected physical characteristics and factors related to sexual development and behaviour and the risk for this disease. The levels of testosterone (T), dihydrotestosterone, salivary testosterone and T/SHBG (sex hormone binding globulin) did not vary with age. Older men had higher oestradiol (estrogen) levels. Further, little association between hormone levels and risk factors was found, except for married subjects having increased serum androgens and heavy subjects having decreased serum androgens (not significant)."
European Journal of Cancer Prev., (1992 April;1(3):239-45 )
Study conducted at: Department of Urology, Erasmus University Rotterdam, The Netherlands.
Study 8: "A population-based nested case-control study was conducted to determine the relation of prediagnostic serum levels of testosterone, dihydrotestosterone, prolactin, follicle-stimulating hormone, luteinizing hormone, estrone, and estradiol to the risk of subsequent prostate cancer. Serum specimens of study subjects were available from a blood collection campaign in Washington County, Maryland, in 1974. There were no significant differences in levels of these hormones between cases and controls, although elevated levels of luteinizing hormone and of testosterone:dihydrotestosterone ratios were associated with mild increased risks of prostate cancer."
Cancer Epidemiology Biomarkers Prev. (1993 Jan-Feb;2(1):27-32 )
Study conducted at: National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland 20892.
Study 9: " The possible relationship between changes in peripheral hormone levels and the occurrence of prostatic pathology was studied in a case-control study, involving estimation of various plasma hormones in 368 Dutch and 258 Japanese men, who were grouped as controls and patients with benign prostatic hyperplasia, focal prostatic carcinoma, or clinically evident prostatic carcinoma. There were no significant differences in plasma androgen levels between Japanese or Dutch prostate cancer cases and their respective control subgroups. These findings do not support a correlation between the lower plasma testosterone levels and a lower incidence of prostate cancer in the Japanese men. Furthermore, no significant differences were found between salivary levels of testosterone or the ratio between testosterone and SHBG in the various Dutch subgroups. In Japanese benign prostatic hyperplasia patients, the testosterone to SHBG ratio was significantly increased. In conclusion, the results of this retrospective, cross-sectional study do not indicate that hormonal levels play a primary role in the origin or promotion of prostatic abnormalities."
Cancer Research (1991 July 1; 51(13):3445-50)
M
manny78
Guest
MUSTANG_18 said:
agree, just dont try to be a hardcore wannabe. If you know your limits you should be ok
Ulter,
As i stated above, i dont think that androgens CAUSE cancer, but fuel it, like estrogen does breat cancer. That is why hormone therapy is so effective in treating prostate cancer. Androgens cause prostate hypertrophy that is benign and im thinking the same for malignant tissue. Most of studies look like they state that androgens wont cause mutation that lead to a carcinogenic tumor.
As i stated above, i dont think that androgens CAUSE cancer, but fuel it, like estrogen does breat cancer. That is why hormone therapy is so effective in treating prostate cancer. Androgens cause prostate hypertrophy that is benign and im thinking the same for malignant tissue. Most of studies look like they state that androgens wont cause mutation that lead to a carcinogenic tumor.
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