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? i have a family history of prostate cancer. is proviron bad for the prostate?
is proviron bad for the prostate
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perfectspecimen
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what can i substitue for my post cycle regimine?
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FreakMonster
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There is no evidence in the medical literature that Proviron increases the risk of prostate cancer. Please post 1 study to back this up.
Benign prostate hypertrophy (enlarged prostate) and the related conditions such as prostate cancer:
Recent evidence shows that estrogen too is a mediator in the development of this condition, which would lead us to draw the conclusion that a purely androgenic compound, lest taken with a highly aromatizing substance, has considerably less risk for aggravating such a condition than DHT formed by testosterone. The side-effects of DHT are largely exaggerated. But that doesn't mean they just went away because I said so, extreme caution needs to be exercised by individuals at risk for prostate problems.
So basically excess DHT is not just to blame for Prostate Cancer. DHT, Estrogen and Cortisol all play a role in causing Prostate cancer.
Most likely, it's a synergism between DHT and estradiol that most effectively promotes growth of tumor cell in prostate.
DHT, by itself, will only make your penis grow...
Here is a study showing how Estradiol is heavily implicated to Prostate Cancer:
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]
BACKGROUND: The recent discovery of the classical estrogen receptor alpha (ERalpha) in metastatic and recurrent prostatic adenocarcinoma suggests that estrogens are implicated in prostate cancer progression. METHODS: To get more insight into estrogen signaling in prostate cancer tissue, the current study has examined the immunoprofile of the estrogen-inducible progesterone receptor (PR), and evaluated its relation to ERalpha gene expression. RESULTS: In primary tumors, the PR was detectable in 36% of primary Gleason grade 3 (5 of 14 cases), 33% of primary Gleason grade 4 (5 of 15 cases), and in 58% of primary Gleason grade 5 tumors (7 of 12 cases). None of the 41 primary tumors investigated revealed significant PR expression in more than 50% of tumor cells. Conversely, moderate to strong receptor expression was observed in 60% of metastatic lesions (9 of 15 cases), and in 54% of androgen-insensitive tumors (38 of 71 cases). Irrespective of grades and stages, the presence of the PR was invariably associated with high steady state levels of ERalpha mRNA, whereas the ERalpha protein was undetectable by immunohistochemistry (IHC) in a significant number of cases (58 of 97 cases). CONCLUSIONS: The progressive emergence of the PR during tumor progression obviously reflects the ability of metastatic and androgen-insensitive tumors to use estrogens through a ERalpha-mediated pathway. The present data provide a theoretical background for studying the efficiency of antiestrogens and antigestagens in the medical treatment of advanced prostate cancer. Copyright 2001 Wiley-Liss, Inc.
Benign prostate hypertrophy (enlarged prostate) and the related conditions such as prostate cancer:
Recent evidence shows that estrogen too is a mediator in the development of this condition, which would lead us to draw the conclusion that a purely androgenic compound, lest taken with a highly aromatizing substance, has considerably less risk for aggravating such a condition than DHT formed by testosterone. The side-effects of DHT are largely exaggerated. But that doesn't mean they just went away because I said so, extreme caution needs to be exercised by individuals at risk for prostate problems.
So basically excess DHT is not just to blame for Prostate Cancer. DHT, Estrogen and Cortisol all play a role in causing Prostate cancer.
Most likely, it's a synergism between DHT and estradiol that most effectively promotes growth of tumor cell in prostate.
DHT, by itself, will only make your penis grow...
Here is a study showing how Estradiol is heavily implicated to Prostate Cancer:
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]
BACKGROUND: The recent discovery of the classical estrogen receptor alpha (ERalpha) in metastatic and recurrent prostatic adenocarcinoma suggests that estrogens are implicated in prostate cancer progression. METHODS: To get more insight into estrogen signaling in prostate cancer tissue, the current study has examined the immunoprofile of the estrogen-inducible progesterone receptor (PR), and evaluated its relation to ERalpha gene expression. RESULTS: In primary tumors, the PR was detectable in 36% of primary Gleason grade 3 (5 of 14 cases), 33% of primary Gleason grade 4 (5 of 15 cases), and in 58% of primary Gleason grade 5 tumors (7 of 12 cases). None of the 41 primary tumors investigated revealed significant PR expression in more than 50% of tumor cells. Conversely, moderate to strong receptor expression was observed in 60% of metastatic lesions (9 of 15 cases), and in 54% of androgen-insensitive tumors (38 of 71 cases). Irrespective of grades and stages, the presence of the PR was invariably associated with high steady state levels of ERalpha mRNA, whereas the ERalpha protein was undetectable by immunohistochemistry (IHC) in a significant number of cases (58 of 97 cases). CONCLUSIONS: The progressive emergence of the PR during tumor progression obviously reflects the ability of metastatic and androgen-insensitive tumors to use estrogens through a ERalpha-mediated pathway. The present data provide a theoretical background for studying the efficiency of antiestrogens and antigestagens in the medical treatment of advanced prostate cancer. Copyright 2001 Wiley-Liss, Inc.
FreakMonster
New member
Here is another great read on why DHT is not the only culprit in Prostate Cancer:
DHT, estrogen, and the prostate
When it comes to sex hormones, few things are as misunderstood by the general consumer as the relationship of the prostate to DHT. The inaccurate and overly simplistic attitude that DHT is responsible for prostate hypertrophy, and even prostate cancer predominates amongst most people.
The real situation is, of course, much more complex. One must understand that there are marked differences between healthy prostate growth (developmental growth), prostate growth due to BPH, and cancerous prostate growth.
The first period of prostate growth, deemed developmental growth, is connected to puberty and the testicular secretion of androgens. This takes the prostate from its prepubertal dormancy to the normal sized, healthy, and functional prostate gland of an adult. During the early and mid adult years the prostate stays at this stage, despite the constant high levels of androgens in the body. However, if androgens are blocked in the body then the adult prostate will shrink in size. This can occur by castration, or even by blockade of 5-AR (recall that DHT is the active androgen in the prostate).
Later in life, there is often a second stage of growth. This growth is deemed benign prostate hypertrophy (BPH) and this growth occurs in a wholly different hormonal environment than that of developmental growth. Evidence is mounting that the existence of a high estrogen / androgen ratio – a condition common in older men – is highly correlated to the development of BPH.
Experimental studies have shown the inability of androgens with saturated A rings (DHT related) to induce an initial condition of prostate hypertrophy. These compounds are non-aromatizable. Aromatizable androgens on the other hand, such as testosterone or androstenedione can induce hyperplasic modifications of the prostate of monkeys, but these effects are reversed by the addition of an aromatase inhibitor.
So apparently, estrogen is a causative factor in BPH or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen.
None of this may come as news to many of you, but I bet that very few of you know that DHT can actually be used to treat BPH!! How can it do that? It basically does this by replacing the testosterone in the body, which then has the effect of reducing the amount of estrogen in the body. As I started to explain before, DHT is a strong androgen that will signal the pituitary to decrease the production of gonadotropins. The decrease in gonadotropins will then cause less testosterone to be produced which will in turn cause the estrogen levels to drop. The resulting change in the hormonal milieu (high DHT, low estrogen) then apparently results in a regression of BPH.
The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:
"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.
Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01)."
This kind of flies in the face of the traditional thinking concerning BPH now doesn’t it?
Conclusion
People have a natural tendency to classify things as either good or bad, with no gray areas. DHT (like estrogen) has recently been on everyone’s bad list, and is often considered to be a hormone that serves no function in the body except to cause harm. As you can see, this view is far from the truth. In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that really don’t need it should be reconsidered. So give DHT a break. I now pronounce June "DHT Appreciation Month". Thank you.
DHT, estrogen, and the prostate
When it comes to sex hormones, few things are as misunderstood by the general consumer as the relationship of the prostate to DHT. The inaccurate and overly simplistic attitude that DHT is responsible for prostate hypertrophy, and even prostate cancer predominates amongst most people.
The real situation is, of course, much more complex. One must understand that there are marked differences between healthy prostate growth (developmental growth), prostate growth due to BPH, and cancerous prostate growth.
The first period of prostate growth, deemed developmental growth, is connected to puberty and the testicular secretion of androgens. This takes the prostate from its prepubertal dormancy to the normal sized, healthy, and functional prostate gland of an adult. During the early and mid adult years the prostate stays at this stage, despite the constant high levels of androgens in the body. However, if androgens are blocked in the body then the adult prostate will shrink in size. This can occur by castration, or even by blockade of 5-AR (recall that DHT is the active androgen in the prostate).
Later in life, there is often a second stage of growth. This growth is deemed benign prostate hypertrophy (BPH) and this growth occurs in a wholly different hormonal environment than that of developmental growth. Evidence is mounting that the existence of a high estrogen / androgen ratio – a condition common in older men – is highly correlated to the development of BPH.
Experimental studies have shown the inability of androgens with saturated A rings (DHT related) to induce an initial condition of prostate hypertrophy. These compounds are non-aromatizable. Aromatizable androgens on the other hand, such as testosterone or androstenedione can induce hyperplasic modifications of the prostate of monkeys, but these effects are reversed by the addition of an aromatase inhibitor.
So apparently, estrogen is a causative factor in BPH or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen.
None of this may come as news to many of you, but I bet that very few of you know that DHT can actually be used to treat BPH!! How can it do that? It basically does this by replacing the testosterone in the body, which then has the effect of reducing the amount of estrogen in the body. As I started to explain before, DHT is a strong androgen that will signal the pituitary to decrease the production of gonadotropins. The decrease in gonadotropins will then cause less testosterone to be produced which will in turn cause the estrogen levels to drop. The resulting change in the hormonal milieu (high DHT, low estrogen) then apparently results in a regression of BPH.
The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:
"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.
Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01)."
This kind of flies in the face of the traditional thinking concerning BPH now doesn’t it?
Conclusion
People have a natural tendency to classify things as either good or bad, with no gray areas. DHT (like estrogen) has recently been on everyone’s bad list, and is often considered to be a hormone that serves no function in the body except to cause harm. As you can see, this view is far from the truth. In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that really don’t need it should be reconsidered. So give DHT a break. I now pronounce June "DHT Appreciation Month". Thank you.
FreakMonster
New member
Here is one showing that actually giving older men pure DHT increased their strength and did not harm their prostates
: J Clin Endocrinol Metab 2001 Sep;86(9):4078-88
A double-blind, placebo-controlled, randomized clinical trial of transdermal dihydrotestosterone gel on muscular strength, mobility, and quality of life in older men with partial androgen deficiency.
Ly LP, Jimenez M, Zhuang TN, Celermajer DS, Conway AJ, Handelsman DJ.
Department of Andrology, Concord Hospital, Concord, New South Wales 2139, Australia.
The efficacy and safety of androgen supplementation in older men remains controversial. Despite biochemical evidence of partial androgen deficiency in older men, controlled studies using T demonstrate equivocal benefits. Furthermore, the importance of aromatization and 5alpha reduction in androgen actions among older men remains unclear. Dihydrotestosterone is the highest potency natural androgen with the additional features that it is neither aromatizable nor susceptible to potency amplification by 5alpha reduction. Therefore, the effects of dihydrotestosterone may differ from those of T in older men. This study evaluated the efficacy and safety of 3 months treatment with transdermal dihydrotestosterone gel on muscle strength, mobility, and quality of life in ambulant, community-dwelling men aged 60 yr or older. Eligible men (plasma T < or =15 nmol/liter) were randomized to undergo daily dermal application of 70 mg dihydrotestosterone gel (n = 18) or vehicle (n = 19) and were studied before, monthly during, and 1 month after treatment. Among 33 (17 dihydrotestosterone, 16 placebo) men completing the study with a high degree of compliance, dihydrotestosterone had significant effects on circulating hormones (increased dihydrotestosterone; decreased total and free testosterone, LH, and FSH; unchanged SHBG and estradiol), lipid profiles (decreased total and low-density lipoprotein cholesterols; unchanged high-density lipoprotein cholesterol and triglycerides), hematopoiesis (increased hemoglobin, hematocrit, and red cell counts), and body composition (decreased skinfold thickness and fat mass; unchanged lean mass and waist to hip ratio). Muscle strength measured by isokinetic peak torque was increased in flexion of the dominant knee but not in knee extension or shoulder contraction, nor was there any significant change in gait, balance, or mobility tests, in cognitive function, or in quality of life scales. Dihydrotestosterone treatment had no adverse effects on prostate (unchanged prostate volumes and prostate-specific antigen) and cardiovascular (no adverse change in vascular reactivity or lipids) safety markers. We conclude that 3 months treatment with transdermal dihydrotestosterone gel demonstrates expected androgenic effects, short-term safety, and limited improvement in lower limb muscle strength but no change in physical functioning or cognitive function.
Publication Types:
Clinical Trial
Evaluation Studies
Randomized Controlled Trial
: J Clin Endocrinol Metab 2001 Sep;86(9):4078-88
A double-blind, placebo-controlled, randomized clinical trial of transdermal dihydrotestosterone gel on muscular strength, mobility, and quality of life in older men with partial androgen deficiency.
Ly LP, Jimenez M, Zhuang TN, Celermajer DS, Conway AJ, Handelsman DJ.
Department of Andrology, Concord Hospital, Concord, New South Wales 2139, Australia.
The efficacy and safety of androgen supplementation in older men remains controversial. Despite biochemical evidence of partial androgen deficiency in older men, controlled studies using T demonstrate equivocal benefits. Furthermore, the importance of aromatization and 5alpha reduction in androgen actions among older men remains unclear. Dihydrotestosterone is the highest potency natural androgen with the additional features that it is neither aromatizable nor susceptible to potency amplification by 5alpha reduction. Therefore, the effects of dihydrotestosterone may differ from those of T in older men. This study evaluated the efficacy and safety of 3 months treatment with transdermal dihydrotestosterone gel on muscle strength, mobility, and quality of life in ambulant, community-dwelling men aged 60 yr or older. Eligible men (plasma T < or =15 nmol/liter) were randomized to undergo daily dermal application of 70 mg dihydrotestosterone gel (n = 18) or vehicle (n = 19) and were studied before, monthly during, and 1 month after treatment. Among 33 (17 dihydrotestosterone, 16 placebo) men completing the study with a high degree of compliance, dihydrotestosterone had significant effects on circulating hormones (increased dihydrotestosterone; decreased total and free testosterone, LH, and FSH; unchanged SHBG and estradiol), lipid profiles (decreased total and low-density lipoprotein cholesterols; unchanged high-density lipoprotein cholesterol and triglycerides), hematopoiesis (increased hemoglobin, hematocrit, and red cell counts), and body composition (decreased skinfold thickness and fat mass; unchanged lean mass and waist to hip ratio). Muscle strength measured by isokinetic peak torque was increased in flexion of the dominant knee but not in knee extension or shoulder contraction, nor was there any significant change in gait, balance, or mobility tests, in cognitive function, or in quality of life scales. Dihydrotestosterone treatment had no adverse effects on prostate (unchanged prostate volumes and prostate-specific antigen) and cardiovascular (no adverse change in vascular reactivity or lipids) safety markers. We conclude that 3 months treatment with transdermal dihydrotestosterone gel demonstrates expected androgenic effects, short-term safety, and limited improvement in lower limb muscle strength but no change in physical functioning or cognitive function.
Publication Types:
Clinical Trial
Evaluation Studies
Randomized Controlled Trial
