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WHO CAN POST A SCIENTIFIC EXPLANATION TO NO DECA & FINASTERIDE MIXES??
- Thread starter imortal
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Generic MALE
New member
I think the story behind this idea is that aromatase converts testosterone into dihydrotest(DHT) and converts nandrolone into dihydronan(DHN). DHT is a more androgenic compound so makes it more likely to grow your prostate into a pumpkin and make your hair rain off your head like autumn leaves. However DHN is a less androgenic compound so it is a milder substance than nandrolone. Finesteride prevents aromatase from converting test and nan to the dihydro form - which is good in the case of testo if you want to prevent androgenic sides, but bad in the case of nan.
Of course some feel DHT is not so bad - it gives good strength and while the evidence indicates it does cause hair loss on the head and hair sprouting everywhere else, it may not have as much effect on the prostate as once thought. Some feel estrogen may be of greater harm to the prostate. In fact DHT may help by downregulating estrogen receptors :
Scientific journal : Biol Reprod. 2004 Feb;70(2):297-302. Epub 2003 Oct 01.
Title of article : Attenuation of estrogenic effects by dihydrotestosterone in the pig uterus is associated with downregulation of the estrogen receptors.
Researchers : Cardenas H, Pope WF.
Department of Animal Sciences, The Ohio State University, Columbus, Ohio 43210, USA. [email protected]
Androgens are known to attenuate some effects of estradiol-17beta (E) in the uterus. The objectives of the present experiment were to determine effects of 5alpha-dihydrotestosterone (DHT) on estrogenic actions in the pig uterus and its associations with changes in expression of the estrogen receptor (ER) alpha and ERbeta. Postpubertal gilts (120-130 kg of body weight; n = 16) were ovariectomized, and 3-4 weeks later received once-a-day injections (i.m.) of one of the following treatments during four consecutive days: 1) vehicle (corn oil), 2) E (250 microg), 3) E (250 microg) plus 1 mg DHT, or 4) E (250 microg) plus 10 mg DHT. Uterine tissues were collected 24 h after the last treatment. Gilts receiving E or E plus 1 mg DHT had greater uterine wet weight, uterine horn diameter, luminal epithelium thickness, and endometrial gland diameter compared with gilts treated with vehicle or E plus 10 mg DHT. Gilts receiving E or E plus 1 mg DHT were not different in these characteristics. Relative amounts of mRNAs in the endometrium for the cell proliferation marker histone H2a and the E-inducible protein complement component C3 increased in gilts treated with E compared with gilts treated with vehicle. E-induced increases in histone H2a and C3 mRNAs were not altered by cotreatment with E plus 1 mg DHT but were inhibited by E plus 10 mg DHT. Androgen receptor (AR) mRNA in the endometrium increased by treatment with E. Cotreatment of gilts with E and DHT did not alter the E-induced AR mRNA increase. Gilts treated with E plus 10 mg DHT had lesser amounts of immunoreactive ERalpha in cell nuclei of the myometrium and endometrial stroma and a tendency for a decrease in luminal epithelium compared with gilts treated with E. Amounts of immunoreactive ERalpha in glandular epithelium were not influenced by the treatments. Relative amounts of ERalpha and ERbeta mRNAs decreased in the endometrium of gilts treated with E plus 10 mg DHT compared with gilts treated with E. Downregulation of the ERs, particularly ERalpha in the myometrium and endometrial stroma, might be a relevant mechanism in the antagonism of estrogenic effects by DHT in the pig uterus.
Of course some feel DHT is not so bad - it gives good strength and while the evidence indicates it does cause hair loss on the head and hair sprouting everywhere else, it may not have as much effect on the prostate as once thought. Some feel estrogen may be of greater harm to the prostate. In fact DHT may help by downregulating estrogen receptors :
Scientific journal : Biol Reprod. 2004 Feb;70(2):297-302. Epub 2003 Oct 01.
Title of article : Attenuation of estrogenic effects by dihydrotestosterone in the pig uterus is associated with downregulation of the estrogen receptors.
Researchers : Cardenas H, Pope WF.
Department of Animal Sciences, The Ohio State University, Columbus, Ohio 43210, USA. [email protected]
Androgens are known to attenuate some effects of estradiol-17beta (E) in the uterus. The objectives of the present experiment were to determine effects of 5alpha-dihydrotestosterone (DHT) on estrogenic actions in the pig uterus and its associations with changes in expression of the estrogen receptor (ER) alpha and ERbeta. Postpubertal gilts (120-130 kg of body weight; n = 16) were ovariectomized, and 3-4 weeks later received once-a-day injections (i.m.) of one of the following treatments during four consecutive days: 1) vehicle (corn oil), 2) E (250 microg), 3) E (250 microg) plus 1 mg DHT, or 4) E (250 microg) plus 10 mg DHT. Uterine tissues were collected 24 h after the last treatment. Gilts receiving E or E plus 1 mg DHT had greater uterine wet weight, uterine horn diameter, luminal epithelium thickness, and endometrial gland diameter compared with gilts treated with vehicle or E plus 10 mg DHT. Gilts receiving E or E plus 1 mg DHT were not different in these characteristics. Relative amounts of mRNAs in the endometrium for the cell proliferation marker histone H2a and the E-inducible protein complement component C3 increased in gilts treated with E compared with gilts treated with vehicle. E-induced increases in histone H2a and C3 mRNAs were not altered by cotreatment with E plus 1 mg DHT but were inhibited by E plus 10 mg DHT. Androgen receptor (AR) mRNA in the endometrium increased by treatment with E. Cotreatment of gilts with E and DHT did not alter the E-induced AR mRNA increase. Gilts treated with E plus 10 mg DHT had lesser amounts of immunoreactive ERalpha in cell nuclei of the myometrium and endometrial stroma and a tendency for a decrease in luminal epithelium compared with gilts treated with E. Amounts of immunoreactive ERalpha in glandular epithelium were not influenced by the treatments. Relative amounts of ERalpha and ERbeta mRNAs decreased in the endometrium of gilts treated with E plus 10 mg DHT compared with gilts treated with E. Downregulation of the ERs, particularly ERalpha in the myometrium and endometrial stroma, might be a relevant mechanism in the antagonism of estrogenic effects by DHT in the pig uterus.
Generic MALE
New member
This is a bit of psuedo science but screw taking finesteride
===================
In 1941 Huggins showed that castration slowed progression of prostate cancer.
The cancer benefit was assumed to be due to testosterone reduction. Since that time, physicians have focused their treatment of prostate cancer on suppression of testosterone production.
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 plus 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 no survival 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. Why has it taken this long to find that this form of androgen blockade has no benefit in treating metastatic prostate cancer?
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 choose testosterone as the probable 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 age when prostate cancer is least likely? Why does prostate cancer occur so often in aging men?
In test mammals, pre-treatment with testosterone prevents successful transplantation of prostate cancer cells. Testosterone given to test mammals after successful transplantation of prostate cancer tissue will slow tumor growth.
In men, the incidence of prostate cancer and prostate hypertrophy correlates better with low testosterone levels, rather than with higher levels. It is time for a new hypothesis.
Consider the changes in testicular hormone production as men age. Estradiol gradually rises while progesterone and testosterone levels decline. Since progesterone is a potent inhibitor of 5 - reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT), any decline in progesterone increases the conversion of testosterone to DHT.
Testosterone is a direct antagonist of estradiol (and DHT isn’t). The result is estrogen dominance. Could estrogen be the major 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 similar 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 tests show the following:
(1) estradiol increases Bcl-2 product that leads to cell proliferation and delay in apoptosis, both of which increase cancer risk;
(2) progesterone suppresses Bcl-2 action and increases p53 product that slows cell proliferation and restores proper apoptosis, both of which decrease cancer risk; and
(3) insulin increases cancer cell growth.
It should be recalled that male estradiol serum levels are equivalent to or greater than that of postmenopausal females. In addition to testicular estradiol, estrogen is produced in body fat in both men and women by conversion (aromatization) of androstenedione to estrone.
About 50% of circulating estrone is converted to estradiol by the liver and intestinal cells. Estradiol effects such as breast growth, however, are suppressed (antagonized) by the male’s greater production of testosterone.
As noted above, 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 but also by its increased conversion to DHT, while estradiol levels persist. Just as estradiol is an endometrial carcinogen, so also is estradiol a likely prostate carcinogen in aging males.
In this regard, nutrients are also important. Zinc, for example, inhibits aromatization of androgens into estradiol. Prostaglandin balance modulates inflammation.
Tissues subjected to chronic inflammation are more likely to develop cancer. Prostaglandin balance is influenced by protein intake and by omega-3 and omega-6 fatty acids in diet. (Read The Anti-Aging Zone, by Barry Sears PhD., and Fats that Heal, Fats that Kill, by Udo Erasmus, alive books, Burnaby, BC, Canada).
Antioxidants also are important in suppressing inflammation. 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 because it lowered estradiol levels.
The course of prostate cancer growth, like breast cancer growth, is not due to a linear progression of cancer cells multiplying from one rogue cell; it is due to a continued underlying metabolic imbalance that continually changes normal cells into cancer cells.
The two most important factors in the underlying metabolic imbalance prostate (and all hormone-dependent cancers) are estrogen dominance and nutritional imbalance. Prevent these two factors 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 sugars, refined starches, and other glycemic (insulin-raising) foods as well as high estrogen food such as feedlot meat and milk.
2. Learn to eat a diet that promotes a healthy prostaglandin balance.
3. Maintain a good intake of antioxidants and zinc.
4. Monitor saliva hormone levels of progesterone and testosterone in males > 50.
5. 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 6-8 mg/day of progesterone and 1-2 mg/day of testosterone.
From my clinical experience, it would not surprise me that exercise and an active sexual 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 R. Lee, MD
July 1999
===================
In 1941 Huggins showed that castration slowed progression of prostate cancer.
The cancer benefit was assumed to be due to testosterone reduction. Since that time, physicians have focused their treatment of prostate cancer on suppression of testosterone production.
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 plus 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 no survival 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. Why has it taken this long to find that this form of androgen blockade has no benefit in treating metastatic prostate cancer?
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 choose testosterone as the probable 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 age when prostate cancer is least likely? Why does prostate cancer occur so often in aging men?
In test mammals, pre-treatment with testosterone prevents successful transplantation of prostate cancer cells. Testosterone given to test mammals after successful transplantation of prostate cancer tissue will slow tumor growth.
In men, the incidence of prostate cancer and prostate hypertrophy correlates better with low testosterone levels, rather than with higher levels. It is time for a new hypothesis.
Consider the changes in testicular hormone production as men age. Estradiol gradually rises while progesterone and testosterone levels decline. Since progesterone is a potent inhibitor of 5 - reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT), any decline in progesterone increases the conversion of testosterone to DHT.
Testosterone is a direct antagonist of estradiol (and DHT isn’t). The result is estrogen dominance. Could estrogen be the major 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 similar 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 tests show the following:
(1) estradiol increases Bcl-2 product that leads to cell proliferation and delay in apoptosis, both of which increase cancer risk;
(2) progesterone suppresses Bcl-2 action and increases p53 product that slows cell proliferation and restores proper apoptosis, both of which decrease cancer risk; and
(3) insulin increases cancer cell growth.
It should be recalled that male estradiol serum levels are equivalent to or greater than that of postmenopausal females. In addition to testicular estradiol, estrogen is produced in body fat in both men and women by conversion (aromatization) of androstenedione to estrone.
About 50% of circulating estrone is converted to estradiol by the liver and intestinal cells. Estradiol effects such as breast growth, however, are suppressed (antagonized) by the male’s greater production of testosterone.
As noted above, 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 but also by its increased conversion to DHT, while estradiol levels persist. Just as estradiol is an endometrial carcinogen, so also is estradiol a likely prostate carcinogen in aging males.
In this regard, nutrients are also important. Zinc, for example, inhibits aromatization of androgens into estradiol. Prostaglandin balance modulates inflammation.
Tissues subjected to chronic inflammation are more likely to develop cancer. Prostaglandin balance is influenced by protein intake and by omega-3 and omega-6 fatty acids in diet. (Read The Anti-Aging Zone, by Barry Sears PhD., and Fats that Heal, Fats that Kill, by Udo Erasmus, alive books, Burnaby, BC, Canada).
Antioxidants also are important in suppressing inflammation. 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 because it lowered estradiol levels.
The course of prostate cancer growth, like breast cancer growth, is not due to a linear progression of cancer cells multiplying from one rogue cell; it is due to a continued underlying metabolic imbalance that continually changes normal cells into cancer cells.
The two most important factors in the underlying metabolic imbalance prostate (and all hormone-dependent cancers) are estrogen dominance and nutritional imbalance. Prevent these two factors 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 sugars, refined starches, and other glycemic (insulin-raising) foods as well as high estrogen food such as feedlot meat and milk.
2. Learn to eat a diet that promotes a healthy prostaglandin balance.
3. Maintain a good intake of antioxidants and zinc.
4. Monitor saliva hormone levels of progesterone and testosterone in males > 50.
5. 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 6-8 mg/day of progesterone and 1-2 mg/day of testosterone.
From my clinical experience, it would not surprise me that exercise and an active sexual 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 R. Lee, MD
July 1999
Generic MALE
New member
If you are worried about the effects of DHT, on prostate, maybe you should consider tamoxifen. Taking tamox does not block the conversion of testo to DHT, ...and DHT downregulates estrogen receptors, and may protect against cancer. Then use nizoral 2% for blocking DHT in your hair.
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Prostate. 1998 Sep 15;37(1):51-9.
Prostate cancer cell growth inhibition by tamoxifen is associated with inhibition of protein kinase C and induction of p21(waf1/cip1).
Rohlff C, Blagosklonny MV, Kyle E, Kesari A, Kim IY, Zelner DJ, Hakim F, Trepel J, Bergan RC.
Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
BACKGROUND: Inhibition of protein kinase C (PKC) and modulation of transforming growth factor-beta (TGF-beta) are both associated with tamoxifen treatment, and both appear to be important in the regulation of prostate cancer cell growth. Investigations were performed which sought to measure the efficacy, and to elucidate the mechanism of growth inhibition by tamoxifen, in hormone-refractory prostate cancer. METHODS: Growth assays were performed on PC3, PC3-M, and DU145 prostate cancer cells. TGF-beta was measured by ELISA; p21(waf1/cip1) and retinoblastoma (Rb) protein levels were measured by Western blot; PKC activity was measured by kinase assay; and effects upon cell cycle were measured by flow cytometric analysis. RESULTS: IC50s for growth inhibition ranged from 5.5-10 microM, and were not affected by estrogen. Tamoxifen-mediated growth inhibition was not associated with induction of TGF-beta. However, tamoxifen treatment was associated with inhibition of PKC, which was followed by induction of p21(waf1/cip1), Rb dephosphorylation, and G1/S phase cell cycle arrest. Similar effects were observed with the known PKC inhibitor, Ro31-8220. CONCLUSIONS: These data suggest that micromolar concentrations of tamoxifen inhibit prostate cancer cell growth by inhibition of PKC, resulting in induction of the p21(waf1/cip1) protein.
/////////////////
Prostate. 1998 Sep 15;37(1):51-9.
Prostate cancer cell growth inhibition by tamoxifen is associated with inhibition of protein kinase C and induction of p21(waf1/cip1).
Rohlff C, Blagosklonny MV, Kyle E, Kesari A, Kim IY, Zelner DJ, Hakim F, Trepel J, Bergan RC.
Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
BACKGROUND: Inhibition of protein kinase C (PKC) and modulation of transforming growth factor-beta (TGF-beta) are both associated with tamoxifen treatment, and both appear to be important in the regulation of prostate cancer cell growth. Investigations were performed which sought to measure the efficacy, and to elucidate the mechanism of growth inhibition by tamoxifen, in hormone-refractory prostate cancer. METHODS: Growth assays were performed on PC3, PC3-M, and DU145 prostate cancer cells. TGF-beta was measured by ELISA; p21(waf1/cip1) and retinoblastoma (Rb) protein levels were measured by Western blot; PKC activity was measured by kinase assay; and effects upon cell cycle were measured by flow cytometric analysis. RESULTS: IC50s for growth inhibition ranged from 5.5-10 microM, and were not affected by estrogen. Tamoxifen-mediated growth inhibition was not associated with induction of TGF-beta. However, tamoxifen treatment was associated with inhibition of PKC, which was followed by induction of p21(waf1/cip1), Rb dephosphorylation, and G1/S phase cell cycle arrest. Similar effects were observed with the known PKC inhibitor, Ro31-8220. CONCLUSIONS: These data suggest that micromolar concentrations of tamoxifen inhibit prostate cancer cell growth by inhibition of PKC, resulting in induction of the p21(waf1/cip1) protein.
