Another Confirmation That Testosterone Can Treat Prostate Cancer

[Ras]

"A man with advanced prostate cancer is believed to be cured after doctors 'shocked' his tumour to death with huge amounts of testosterone."

"One individual whose PSA levels dropped to zero after three months and shows no remaining trace of the disease after 22 cycles of treatment appears to be cured, said the researchers."

The Telegraph

 

[ecstatichamster]

honestly, although interesting, this is probably nonsense. There is no study, no paper, just PR.

 

[Dante]

"A man with advanced prostate cancer is believed to be cured after doctors 'shocked' his tumour to death with huge amounts of testosterone."

"One individual whose PSA levels dropped to zero after three months and shows no remaining trace of the disease after 22 cycles of treatment appears to be cured, said the researchers."

The Telegraph

It's Bipolar androgen therapy. You deprive the body out of androgen for a month and then give testosterone therapy on the 28th day. This is completely different from claiming that Regular T injection treats prostate cancer. I think Koveras posted a paper related to this if i remember correctly.
However i found something in the comment section interesting . I am copy pasting it.
"The mechanism why this works is actually known to many doctors.

Excess testosterone in the male body gets changed into estradiol via the aromatase enzyme.

Estrogen therapy has also been known to subdue prostate cancer in Male-to-Female transgender patients, in fact prostate cancer is rare in older MtF transgender women who have been taking estradiol all their lives since they transitioned from formerly being men.
We could just give estrogen injections as a direct treatment for prostate cancer, but not very many cis-gender men want to grow breasts and feminize the appearance of their faces
-- W.Carlton, MD (endocrinologist)"

^^ is it true what the doc says ^^

 

[bdawg]

Abstract here:

Rapid cycling high dose testosterone (Bipolar Androgen Therapy) as therapy for men with metastatic castrate-resistant prostate cancer (mCRPC)

 

[aquaman]

Cancer "paradox": Testosterone Inhibits Prostate Cancer

Think this is what Haidut posted in jan 2015

 

[johnwester130]

I thought every 18 year old had trouble urinating and hair loss though ?

 

[haidut]

So, this is what the medical industry has gotten to. After its therapies on androgen deprivation failed, and then an androgen paradoxically treats the very condition it is supposed to cause what does a cunning pharma exec or clueless doctor do? Claim that the androgen converts into estrogen and this is how it treats the condition. First of all, giving high dose T injections raises BOTH estrogen and T. Anybody who claims giving T will do nothing but raise estrogen needs to re-attend medical school. Second, giving T injections raises T a lot more then it raises estrogen. Third, it raises DHT a lot more than it raises estrogen. Remember, DHT is the "evil" guy in prostate cancer. So any increase of DHT (and T) should have led to rapid progression but instead it put these men into remission. And if estrogen was truly the beneficial hormone why not simply give high dose oral DHEA, which is probably the most effective oral estrogen precursor!? Oh, wait, it was tried and actually made the cancer worse. Wow, how sick the medical industry has become. It will do anything but face the idiocy in its own thinking.
Oh, and last but not least - the direct estrogen therapy has been tried many times before. You know what it does - it kills the person by stroke or heart attack, so that the death can be attributed to other causes and estrogen is in the clear and can continue to be prescribed for cancer.
Anyways, here is yet another study showing that aggressive prostate cancer is due to a "new" type of estrogen receptor and that prostate cancer cells express aromatase more than any other enzyme, including 5-AR.
http://www.fasebj.org/cgi/content/meeting_abstract/20/4/A221-b
"...Prostate cancer is the second leading cause of cancer mortality in American males. Although early diagnosis and treatment have been proven to be efficacious, a significant portion of these tumors metastasize to remote sites resulting in death. While the role of androgens in prostate cancer progression has been well characterized the role of estrogens is still unclear. Prostate cancer cells express aromatase (CYP19) which converts androstenedione to estradiol, thus providing a rationale for estrogen playing a role in prostate cancer biology. Previous studies have focused on the classical estrogen receptors (

and ß) in prostate cancer growth and metastases. Recently a novel membrane bound G-protein coupled estrogen receptor, GPR30, has been identified and shown to regulate rapid intracellular signaling events in breast cancer cells. The purpose of this study was to determine if GPR30 is expressed in prostate cancer cell lines that exhibit differing degrees of invasiveness. Prostate cancer cells LnCap, PC-3 and DU-145 were grown in serum supplemented media, harvested and analyzed by western blot with an antibody directed GPR30. Our results demonstrate that the invasive cell lines PC-3 and DU-145 express GPR30 while less invasive LnCap cells showed no expression. This study is the first to demonstrate that GPR30 is expressed in aggressive prostate cancer cell lines. The role of GPR30 in the regulation of prostate cancer growth remains to be determined. Interestingly, GPR30 has two splice variant sites that may have functional significance in the differing reports on the action of estrogens in prostate cancer. In conclusion, GPR30 may represent a new therapeutic target in aggressive prostate cancers."

Regardless of how much these goons deny that T (and DHT) was the direct therapeutic agent, the cat is out of the bag. So, it does not really matter if the official "mechanism of action" is claimed to be estrogen through aromatization of T, lives will be saved regardless. Finally, if there is ANY benefit in estrogen therapy it is because it actually...wait for it...increased DHT in humans with prostate cancer.
The mechanism of action of estrogen in castration-resistant prostate cancer: clues from hormone levels. - PubMed - NCBI
"...CONCLUSION: Androgens decline in response to estrogen therapy. A decline in DHEA-S and a rise in DHT are both associated with a decline in PSA while patients receive estrogen therapy."

 

[johnwester130]

but finasteride does work for some people , about 25% success rate.

 

[haidut]

but finasteride does work for some people , about 25% success rate.

How do you define working? And did you know that after the initial improvement, it can trigger the aggressive form of prostate cancer that usually kills the person within 6 months?

 

[Dante]

but finasteride does work for some people , about 25% success rate.

fin protects against low grade cancer (you are more likely to die by other means than from those types of cancer) but paradoxically causes high grade deadly ones. Apparently one DHT metabolite- 3-beta diol which protects against high grade prostate cancer is increased locally in bald scalp. There is a med hypothesis on pubmed that says premature MPB happens to protect against prostate cancer (that means even some MDs acknowledge that DHT protects against prostate cancer). So, finasteride by blocking the 5AR opens up an another pandora box (fin stops hair loss though , there is no contention there but no one should take it for chemoprevention).

 

[Dante]

So, this is what the medical industry has gotten to. After its therapies on androgen deprivation failed, and then an androgen paradoxically treats the very condition it is supposed to cause what does a cunning pharma exec or clueless doctor do? Claim that the androgen converts into estrogen and this is how it treats the condition. First of all, giving high dose T injections raises BOTH estrogen and T. Anybody who claims giving T will do nothing but raise estrogen needs to re-attend medical school. Second, giving T injections raises T a lot more then it raises estrogen. Third, it raises DHT a lot more than it raises estrogen. Remember, DHT is the "evil" guy in prostate cancer. So any increase of DHT (and T) should have led to rapid progression but instead it put these men into remission. And if estrogen was truly the beneficial hormone why not simply give high dose oral DHEA, which is probably the most effective oral estrogen precursor!? Oh, wait, it was tried and actually made the cancer worse. Wow, how sick the medical industry has become. It will do anything but face the idiocy in its own thinking.
Oh, and last but not least - the direct estrogen therapy has been tried many times before. You know what it does - it kills the person by stroke or heart attack, so that the death can be attributed to other causes and estrogen is in the clear and can continue to be prescribed for cancer.
Anyways, here is yet another study showing that aggressive prostate cancer is due to a "new" type of estrogen receptor and that prostate cancer cells express aromatase more than any other enzyme, including 5-AR.
GPR30: A novel estrogen receptor expressed in aggressive prostate cancer -- Maier et al. 20 (4): A221 -- The FASEB Journal
"...Prostate cancer is the second leading cause of cancer mortality in American males. Although early diagnosis and treatment have been proven to be efficacious, a significant portion of these tumors metastasize to remote sites resulting in death. While the role of androgens in prostate cancer progression has been well characterized the role of estrogens is still unclear. Prostate cancer cells express aromatase (CYP19) which converts androstenedione to estradiol, thus providing a rationale for estrogen playing a role in prostate cancer biology. Previous studies have focused on the classical estrogen receptors (

and ß) in prostate cancer growth and metastases. Recently a novel membrane bound G-protein coupled estrogen receptor, GPR30, has been identified and shown to regulate rapid intracellular signaling events in breast cancer cells. The purpose of this study was to determine if GPR30 is expressed in prostate cancer cell lines that exhibit differing degrees of invasiveness. Prostate cancer cells LnCap, PC-3 and DU-145 were grown in serum supplemented media, harvested and analyzed by western blot with an antibody directed GPR30. Our results demonstrate that the invasive cell lines PC-3 and DU-145 express GPR30 while less invasive LnCap cells showed no expression. This study is the first to demonstrate that GPR30 is expressed in aggressive prostate cancer cell lines. The role of GPR30 in the regulation of prostate cancer growth remains to be determined. Interestingly, GPR30 has two splice variant sites that may have functional significance in the differing reports on the action of estrogens in prostate cancer. In conclusion, GPR30 may represent a new therapeutic target in aggressive prostate cancers."

Regardless of how much these goons deny that T (and DHT) was the direct therapeutic agent, the cat is out of the bag. So, it does not really matter if the official "mechanism of action" is claimed to be estrogen through aromatization of T, lives will be saved regardless. Finally, if there is ANY benefit in estrogen therapy it is because it actually...wait for it...increased DHT in humans with prostate cancer.
The mechanism of action of estrogen in castration-resistant prostate cancer: clues from hormone levels. - PubMed - NCBI
"...CONCLUSION: Androgens decline in response to estrogen therapy. A decline in DHEA-S and a rise in DHT are both associated with a decline in PSA while patients receive estrogen therapy."

Why is DHT increasing when exogenous estrogen would suppress testosterone and other androgens?
Some doubts: - Reanalysis PCPT trial by some scientists convey that the increase in high grade gleason score was due to fin's effect on prostate volume and due to better detection.
Finasteride unlikely to induce high grade prostate cancers (Journal of NCI)
Quoting from the study -
"Detection of high-grade cancers in the placebo group increased as the prostate size decreased. They found that prostate size in the finasteride group was 25 percent smaller than in the placebo group. Therefore, when the prostate size was taken into consideration, there was not a statistically significant difference between the prevalence of high-grade prostate cancer in the two groups."
"In a second study, M. Scott Lucia, M.D., of the University of Colorado Health Sciences Center in Denver and colleagues investigated whether finasteride changes the appearance of tumor tissue so that lower-grade tumors are diagnosed as high-grade. The researchers examined surgically-removed prostates and high-grade prostate cancer biopsies from men treated with finasteride and a placebo for signs that finasteride affected prostate size, tumor size, or disease stage"
"Although the evidence does not exclude the possibility that finasteride may have induced high-grade prostate cancer in some men, the analysis of prostatectomies from the PCPT does indicate that the relative increase in high-grade tumors in the finasteride group is less than originally believed. This evidence further suggests that increased detection ...may have contributed to the finasteride-associated increase in high-grade disease"

The utility of 5-alpha reductase inhibitors in the prevention and diagnosis of prostate cancer. - PubMed - NCBI
"The original PCPT data revealed that finasteride reduced the risk of prostate cancer by approximately 25% in comparison with placebo. However, patients who received finasteride had a greater incidence of high-grade tumors, which prohibited acceptance of finasteride as a chemopreventive agent by most urologists. Recent updates of the PCPT findings confirmed that finasteride reduces the risk of clinically significant prostate cancer, including high-grade tumors, primarily due to its effects on improving the performance characteristics of prostate-specific antigen and prostate biopsy. There was no increase in high-grade prostate cancer. Rather, there was improved detection of high-grade prostate cancer due to decreased prostate volume."

THEIR WORDS NOT MINE.

 

[LeeLemonoil]

Striking growth-inhibitory effects of minocycline on human prostate cancer cell lines. - PubMed - NCBI

This is a new study demonstrating Minocycline to have
Striking growth-inhibitory effects of minocycline on human prostate cancer cell lines

The main author of the study is actualy looking into neuroprotective effects of Minocyclin and Retinoic acid in several mdisorders but came up with that result in prostate cancer as well and recommends clinical trials.
Apparently they found a mechanism that Minocyclin prevents "breaking down" of Retinoic acid in various tissues, by that enbaling RA to exert protective effects - I assume there is some
sort of Homoeostatsis at play, because supplemented high doses of RA in acne patientes often has detrimental effects on mental healt.
Either way, given the connection betwenn Minocycline and Vitamin K, and also the importance of Vitamin A and K in androgen metbabolism, it seems an interesting find.

 

[haidut]

Why is DHT increasing when exogenous estrogen would suppress testosterone and other androgens?
Some doubts: - Reanalysis PCPT trial by some scientists convey that the increase in high grade gleason score was due to fin's effect on prostate volume and due to better detection.
Finasteride unlikely to induce high grade prostate cancers (Journal of NCI)
Quoting from the study -
"Detection of high-grade cancers in the placebo group increased as the prostate size decreased. They found that prostate size in the finasteride group was 25 percent smaller than in the placebo group. Therefore, when the prostate size was taken into consideration, there was not a statistically significant difference between the prevalence of high-grade prostate cancer in the two groups."
"In a second study, M. Scott Lucia, M.D., of the University of Colorado Health Sciences Center in Denver and colleagues investigated whether finasteride changes the appearance of tumor tissue so that lower-grade tumors are diagnosed as high-grade. The researchers examined surgically-removed prostates and high-grade prostate cancer biopsies from men treated with finasteride and a placebo for signs that finasteride affected prostate size, tumor size, or disease stage"
"Although the evidence does not exclude the possibility that finasteride may have induced high-grade prostate cancer in some men, the analysis of prostatectomies from the PCPT does indicate that the relative increase in high-grade tumors in the finasteride group is less than originally believed. This evidence further suggests that increased detection ...may have contributed to the finasteride-associated increase in high-grade disease"

The utility of 5-alpha reductase inhibitors in the prevention and diagnosis of prostate cancer. - PubMed - NCBI
"The original PCPT data revealed that finasteride reduced the risk of prostate cancer by approximately 25% in comparison with placebo. However, patients who received finasteride had a greater incidence of high-grade tumors, which prohibited acceptance of finasteride as a chemopreventive agent by most urologists. Recent updates of the PCPT findings confirmed that finasteride reduces the risk of clinically significant prostate cancer, including high-grade tumors, primarily due to its effects on improving the performance characteristics of prostate-specific antigen and prostate biopsy. There was no increase in high-grade prostate cancer. Rather, there was improved detection of high-grade prostate cancer due to decreased prostate volume."

THEIR WORDS NOT MINE.

I am not denying that finasteride can have some benefit for prostate cancer. It is known to raise both serum T and serum progesterone. Both of these would help treat the prostate cancer, so initially it may have beneficial effects. However, inhibiting 5-AR leads to elevations of ACTH and cortisol, as well as inhibition of bile acid synthesis. I is well known in medical circles that both ACTH and cortisol stimulate tumor growth, and the inhibition of bile acid synthesis downregulates metabolism as I posted in a few other threads. So, the long term cumulative effect of finasteride is increase in cortisol and prolactin, and eventually estrogen (due to increased T levels and lack of DHT to oppose estrogen) combined with downregulated metabolism. Not a good situation for any cancer patient to be in.
Anyways, I think we are close to finding out what is the real cause of prostate cancer. Some of these men that got the huge doses of testosterone will probably ask for an AI to control gyno and such. If they don't get it from their doctor they will buy it themselves. The doctor in the interview even said that men do not like the feminizing symptoms, which estrogen therapy (and high dose T) will cause. So, if some of these men end up getting an AI + T therapy for whatever reason and there is still clinically relevant benefit for their prostate cancer, then it becomes hard to defend the "DHT is evil" motto.

 

[Dante]

@haidut , Do you think that the reanalysis of PCPT trial data is to somewhere exonerate finasteride when more high gleason score PCs were found in the finasteride group. There have been some studies showing DHT metabolites like 3 beta diol show anti-proliferative activity but the official explanation seems to be better detection. Read the second study linked before.
It goes on to say that finasteride also decreases high gleason score cancer. There was no increase in high-grade prostate cancer. Rather, there was improved detection of high-grade prostate cancer due to decreased prostate volume.
HOW CAN DECREASED PROSTATE VOLUME LEAD TO IMPROVED DETECTION OF HIGH-GRADE PROSTATE CANCER ?

 

[haidut]

@haidut , Do you think that the reanalysis of PCPT trial data is to somewhere exonerate finasteride when more high gleason score PCs were found in the finasteride group. There have been some studies showing DHT metabolites like 3 beta diol show anti-proliferative activity but the official explanation seems to be better detection. Read the second study linked before.
It goes on to say that finasteride also decreases high gleason score cancer. There was no increase in high-grade prostate cancer. Rather, there was improved detection of high-grade prostate cancer due to decreased prostate volume.
HOW CAN DECREASED PROSTATE VOLUME LEAD TO IMPROVED DETECTION OF HIGH-GRADE PROSTATE CANCER ?

Yeah, that confused me too. I have to read the full study to see how can a lower volume lead to better detection when it should be the other way around. Also, I think there is more than one study that showed finsateride to increase high-grade prostate cancer. I will dig them up and post here.

 

[Koveras]

So, this is what the medical industry has gotten to. After its therapies on androgen deprivation failed, and then an androgen paradoxically treats the very condition it is supposed to cause what does a cunning pharma exec or clueless doctor do? Claim that the androgen converts into estrogen and this is how it treats the condition. First of all, giving high dose T injections raises BOTH estrogen and T. Anybody who claims giving T will do nothing but raise estrogen needs to re-attend medical school. Second, giving T injections raises T a lot more then it raises estrogen. Third, it raises DHT a lot more than it raises estrogen. Remember, DHT is the "evil" guy in prostate cancer. So any increase of DHT (and T) should have led to rapid progression but instead it put these men into remission. And if estrogen was truly the beneficial hormone why not simply give high dose oral DHEA, which is probably the most effective oral estrogen precursor!? Oh, wait, it was tried and actually made the cancer worse. Wow, how sick the medical industry has become. It will do anything but face the idiocy in its own thinking.
Oh, and last but not least - the direct estrogen therapy has been tried many times before. You know what it does - it kills the person by stroke or heart attack, so that the death can be attributed to other causes and estrogen is in the clear and can continue to be prescribed for cancer.
Anyways, here is yet another study showing that aggressive prostate cancer is due to a "new" type of estrogen receptor and that prostate cancer cells express aromatase more than any other enzyme, including 5-AR.
GPR30: A novel estrogen receptor expressed in aggressive prostate cancer -- Maier et al. 20 (4): A221 -- The FASEB Journal
"...Prostate cancer is the second leading cause of cancer mortality in American males. Although early diagnosis and treatment have been proven to be efficacious, a significant portion of these tumors metastasize to remote sites resulting in death. While the role of androgens in prostate cancer progression has been well characterized the role of estrogens is still unclear. Prostate cancer cells express aromatase (CYP19) which converts androstenedione to estradiol, thus providing a rationale for estrogen playing a role in prostate cancer biology. Previous studies have focused on the classical estrogen receptors (

and ß) in prostate cancer growth and metastases. Recently a novel membrane bound G-protein coupled estrogen receptor, GPR30, has been identified and shown to regulate rapid intracellular signaling events in breast cancer cells. The purpose of this study was to determine if GPR30 is expressed in prostate cancer cell lines that exhibit differing degrees of invasiveness. Prostate cancer cells LnCap, PC-3 and DU-145 were grown in serum supplemented media, harvested and analyzed by western blot with an antibody directed GPR30. Our results demonstrate that the invasive cell lines PC-3 and DU-145 express GPR30 while less invasive LnCap cells showed no expression. This study is the first to demonstrate that GPR30 is expressed in aggressive prostate cancer cell lines. The role of GPR30 in the regulation of prostate cancer growth remains to be determined. Interestingly, GPR30 has two splice variant sites that may have functional significance in the differing reports on the action of estrogens in prostate cancer. In conclusion, GPR30 may represent a new therapeutic target in aggressive prostate cancers."

Regardless of how much these goons deny that T (and DHT) was the direct therapeutic agent, the cat is out of the bag. So, it does not really matter if the official "mechanism of action" is claimed to be estrogen through aromatization of T, lives will be saved regardless. Finally, if there is ANY benefit in estrogen therapy it is because it actually...wait for it...increased DHT in humans with prostate cancer.
The mechanism of action of estrogen in castration-resistant prostate cancer: clues from hormone levels. - PubMed - NCBI
"...CONCLUSION: Androgens decline in response to estrogen therapy. A decline in DHEA-S and a rise in DHT are both associated with a decline in PSA while patients receive estrogen therapy."

Further information against estrogen - hypoxia-inducible factor (HIF) promotes cancer, estrogen promotes HIF

The HIF/PHF8/AR axis promotes prostate cancer progression. - PubMed - NCBI

Estrogen stabilizes hypoxia-inducible factor 1α through G protein-coupled estrogen receptor 1 in eutopic endometrium of endometriosis. - PubMed - NCBI

 

[TreasureVibe]

So, this is what the medical industry has gotten to. After its therapies on androgen deprivation failed, and then an androgen paradoxically treats the very condition it is supposed to cause what does a cunning pharma exec or clueless doctor do? Claim that the androgen converts into estrogen and this is how it treats the condition. First of all, giving high dose T injections raises BOTH estrogen and T. Anybody who claims giving T will do nothing but raise estrogen needs to re-attend medical school. Second, giving T injections raises T a lot more then it raises estrogen. Third, it raises DHT a lot more than it raises estrogen. Remember, DHT is the "evil" guy in prostate cancer. So any increase of DHT (and T) should have led to rapid progression but instead it put these men into remission. And if estrogen was truly the beneficial hormone why not simply give high dose oral DHEA, which is probably the most effective oral estrogen precursor!? Oh, wait, it was tried and actually made the cancer worse. Wow, how sick the medical industry has become. It will do anything but face the idiocy in its own thinking.
Oh, and last but not least - the direct estrogen therapy has been tried many times before. You know what it does - it kills the person by stroke or heart attack, so that the death can be attributed to other causes and estrogen is in the clear and can continue to be prescribed for cancer.
Anyways, here is yet another study showing that aggressive prostate cancer is due to a "new" type of estrogen receptor and that prostate cancer cells express aromatase more than any other enzyme, including 5-AR.
http://www.fasebj.org/cgi/content/meeting_abstract/20/4/A221-b
"...Prostate cancer is the second leading cause of cancer mortality in American males. Although early diagnosis and treatment have been proven to be efficacious, a significant portion of these tumors metastasize to remote sites resulting in death. While the role of androgens in prostate cancer progression has been well characterized the role of estrogens is still unclear. Prostate cancer cells express aromatase (CYP19) which converts androstenedione to estradiol, thus providing a rationale for estrogen playing a role in prostate cancer biology. Previous studies have focused on the classical estrogen receptors (

and ß) in prostate cancer growth and metastases. Recently a novel membrane bound G-protein coupled estrogen receptor, GPR30, has been identified and shown to regulate rapid intracellular signaling events in breast cancer cells. The purpose of this study was to determine if GPR30 is expressed in prostate cancer cell lines that exhibit differing degrees of invasiveness. Prostate cancer cells LnCap, PC-3 and DU-145 were grown in serum supplemented media, harvested and analyzed by western blot with an antibody directed GPR30. Our results demonstrate that the invasive cell lines PC-3 and DU-145 express GPR30 while less invasive LnCap cells showed no expression. This study is the first to demonstrate that GPR30 is expressed in aggressive prostate cancer cell lines. The role of GPR30 in the regulation of prostate cancer growth remains to be determined. Interestingly, GPR30 has two splice variant sites that may have functional significance in the differing reports on the action of estrogens in prostate cancer. In conclusion, GPR30 may represent a new therapeutic target in aggressive prostate cancers."

Regardless of how much these goons deny that T (and DHT) was the direct therapeutic agent, the cat is out of the bag. So, it does not really matter if the official "mechanism of action" is claimed to be estrogen through aromatization of T, lives will be saved regardless. Finally, if there is ANY benefit in estrogen therapy it is because it actually...wait for it...increased DHT in humans with prostate cancer.
The mechanism of action of estrogen in castration-resistant prostate cancer: clues from hormone levels. - PubMed - NCBI
"...CONCLUSION: Androgens decline in response to estrogen therapy. A decline in DHEA-S and a rise in DHT are both associated with a decline in PSA while patients receive estrogen therapy."

So far studying it, I also come to the conclusion that estrogen and aromatase both can play a significant role in the development of prostate cancer and perhaps BPH too. I find it weird how I cannot find any study about the use of aromatase inhibitors for prostate cancer.

 

[haidut]

So far studying it, I also come to the conclusion that estrogen and aromatase both can play a significant role in the development of prostate cancer and perhaps BPH too. I find it weird how I cannot find any study about the use of aromatase inhibitors for prostate cancer.

The reason you can't find studies on it is that AI are known to raise T/DHT so it directly contradicts the mainstream theory and will not be tried as if it worked it would pretty much kill that theory. Also, estrogen is currently used as actual "therapy" for prostate cancer in the forms of injections and that is also incompatible with the idea of lowering estrogen being therapeutic.

 

[TreasureVibe]

The reason you can't find studies on it is that AI are known to raise T/DHT so it directly contradicts the mainstream theory and will not be tried as if it worked it would pretty much kill that theory. Also, estrogen is currently used as actual "therapy" for prostate cancer in the forms of injections and that is also incompatible with the idea of lowering estrogen being therapeutic.

What could be a reason for extreme high levels of PSA in men? (in the thousands for example)

 

[haidut]

What could be a reason for extreme high levels of PSA in men? (in the thousands for example)

Probably estrogen.
Test For Estrogenic Activity And Prostate Cancer
Test For Estrogenic Activity And Prostate Cancer