TreasureVibe
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OVERVIEW
Over 80% of patients with prostate cancer respond to androgen deprivation using drugs or surgery that marked reduce male sex hormone (testosterone) and related androgen levels from the body. Anti-androgens are a class of drugs that specifically block the entry of testosterone into cells of the body, thus preventing its biological effects. Examples of such drugs that are available on the U.S. market include flutamide (Eulexin®), bicalutamide (Casodex®) and nilutamide (Nilandron™). Cyproterone (Androcur) is another anti-androgen that is not available in the U.S.
In approximately 50% of patients whose cancer has started to grow again despite treatment that includes an antiandrogen, the cancer has been noted to regress by simply stopping the anti-androgen. This unusual response is referred to as the Anti-Androgen Withdrawal Response (AAWR). Scientists theorize that prostate cancer cells exposed to antiandrogens for a prolonged time may mutate (undergo genetic change) that paradoxically causes the anti-androgen to stimulate cancer growth.
Although more research is needed, we believe a trial of stopping the anti-androgen for a period of time is warranted in order to determine whether or not an AAWR may occur before considering other types of treatment. A review of the scientific studies that support this treatment approach follows below:
The anti-androgen withdrawal response (AAWR) may be seen, in up to 50% of patients who have PSA relapse while receiving androgen blockade. An AAWR response usually lasts 6 to 8 months, but for some patients, may last as long as 2 years.
Source: " AAWR" THE ANTI-ANDROGEN WITHDRAWAL RESPONSE
A R T I C L E
=============================
"...simultaneous treatment of intact...rats with testosterone and estradiol-17beta for 16 weeks consistenly induced a putative precancerous lesion, termed dysplasia, in the dorsolateral prostate of all animals. Since treatment of rats with androgen alone did not elicit the same response, we concluded that estrogen played a critical role in the genesis of this proliferative lesion." Shuk-mei Ho and M. Yu, in "Selective increase in type II estrogen-binding sites in the dysplastic dorsolateral prostates of Noble rats," Cancer Research 53, 528-532, 1993.
Source: Ray Peat article on Prostate Cancer
Over 80% of patients with prostate cancer respond to androgen deprivation using drugs or surgery that marked reduce male sex hormone (testosterone) and related androgen levels from the body. Anti-androgens are a class of drugs that specifically block the entry of testosterone into cells of the body, thus preventing its biological effects. Examples of such drugs that are available on the U.S. market include flutamide (Eulexin®), bicalutamide (Casodex®) and nilutamide (Nilandron™). Cyproterone (Androcur) is another anti-androgen that is not available in the U.S.
In approximately 50% of patients whose cancer has started to grow again despite treatment that includes an antiandrogen, the cancer has been noted to regress by simply stopping the anti-androgen. This unusual response is referred to as the Anti-Androgen Withdrawal Response (AAWR). Scientists theorize that prostate cancer cells exposed to antiandrogens for a prolonged time may mutate (undergo genetic change) that paradoxically causes the anti-androgen to stimulate cancer growth.
Although more research is needed, we believe a trial of stopping the anti-androgen for a period of time is warranted in order to determine whether or not an AAWR may occur before considering other types of treatment. A review of the scientific studies that support this treatment approach follows below:
The anti-androgen withdrawal response (AAWR) may be seen, in up to 50% of patients who have PSA relapse while receiving androgen blockade. An AAWR response usually lasts 6 to 8 months, but for some patients, may last as long as 2 years.
Source: " AAWR" THE ANTI-ANDROGEN WITHDRAWAL RESPONSE
A R T I C L E
=============================
"...simultaneous treatment of intact...rats with testosterone and estradiol-17beta for 16 weeks consistenly induced a putative precancerous lesion, termed dysplasia, in the dorsolateral prostate of all animals. Since treatment of rats with androgen alone did not elicit the same response, we concluded that estrogen played a critical role in the genesis of this proliferative lesion." Shuk-mei Ho and M. Yu, in "Selective increase in type II estrogen-binding sites in the dysplastic dorsolateral prostates of Noble rats," Cancer Research 53, 528-532, 1993.
Source: Ray Peat article on Prostate Cancer