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Hub AI
Chemical castration AI simulator
(@Chemical castration_simulator)
Hub AI
Chemical castration AI simulator
(@Chemical castration_simulator)
Chemical castration
Chemical castration is castration via anaphrodisiac drugs, whether to reduce libido and sexual activity, to treat cancer, or otherwise. Unlike surgical castration, where the gonads are removed through an incision in the body, chemical castration does not remove organs and is not a form of sterilization.
Chemical castration is generally reversible when treatment is discontinued, although permanent effects in body chemistry can sometimes be seen, as in the case of bone density loss increasing with length of use of depot medroxyprogesterone acetate (DMPA). In men, chemical castration reduces sex drive and the capacity for sexual arousal, side effects of some drugs may include depression, suicidal ideation, hot flashes, anemia, infertility, increase in body fat and higher risks of cardiovascular diseases and osteoporosis. In women, chemical castration acts by decreasing testosterone levels in order to lower their sex drive, side effects include the deflation of breast glands, expansion of the size of the nipple and shrinking of bone mass.
In some jurisdictions, chemical castration has been used to reduce the libido of sexual offenders. The effectiveness of chemical castration in decreasing recidivism among sex offenders is controversial.
When used on males, these drugs can reduce sex drive, sexual fantasies, and capacity for sexual arousal. Life-threatening side effects are rare, but some users show increases in body fat and reduced bone density, which increase long-term risk of cardiovascular disease and osteoporosis, respectively. Males may also experience gynecomastia (development of larger-than-normal mammary glands in males); full development is less common unless chemical castration is combined with feminizing oestrogen therapy.
Some drugs, such as medroxyprogesterone acetate, cyproterone acetate, and LHRH agonists can decrease serum testosterone and estradiol in the body, thus impairing the metabolism of glucose and lipid. These drugs can also cause depression, hot flashes, infertility, and anemia, aside from cardiovascular diseases and osteoporosis. The risk of side effects caused by chemical castration drugs can increase depending on the length of time under which they are administered. A 2004 study in which eleven men were chemically castrated ended with one committing suicide after one year of treatment; in another 2020 study, increases in suicidal ideations was reported by 8% of its treatment group, which led to the hospitalization of two of the 25 subjects who had been administered degarelix.
When used on females, the effects are similar, though there is little research about chemically lowering female's sex drive or female-specific anaphrodisiacs, since most research focuses on the opposite, but anti-androgenic hormone regimens would lower testosterone in females which can impact sex drive or sexual response. These drugs also deflate the breast glands and expand the size of the nipple. Also seen is a sudden shrinking in bone mass and discoloration of the lips, reduced body hair, and muscle mass.
The first use of chemical castration occurred in 1944, when diethylstilbestrol was used with the purpose of lowering men's testosterone. The antipsychotic agent benperidol was sometimes used to decrease sexual urges in people who displayed what was thought of as inappropriate sexual behavior, and as likewise given by depot injection, though benperidol does not affect testosterone and is therefore not a castration agent. Chemical castration was often seen as an easier alternative to life imprisonment or the death penalty because it allowed the release of the convicted.
In 1981, in an experiment by Pierre Gagné, 48 males with long-standing histories of sexually deviant behaviour were given medroxyprogesterone acetate for as long as 12 months. Forty of those subjects were recorded as having diminished desires for deviant sexual behaviour, as well as less frequent sexual fantasies and greater control over sexual urges. The research recorded a continuation of this improved behaviour after the administration of the drug had ended, with no evidence of adverse side effects, and so recommended medroxyprogesterone acetate along with counselling as a successful method of treatment for serial sex offenders.
Chemical castration
Chemical castration is castration via anaphrodisiac drugs, whether to reduce libido and sexual activity, to treat cancer, or otherwise. Unlike surgical castration, where the gonads are removed through an incision in the body, chemical castration does not remove organs and is not a form of sterilization.
Chemical castration is generally reversible when treatment is discontinued, although permanent effects in body chemistry can sometimes be seen, as in the case of bone density loss increasing with length of use of depot medroxyprogesterone acetate (DMPA). In men, chemical castration reduces sex drive and the capacity for sexual arousal, side effects of some drugs may include depression, suicidal ideation, hot flashes, anemia, infertility, increase in body fat and higher risks of cardiovascular diseases and osteoporosis. In women, chemical castration acts by decreasing testosterone levels in order to lower their sex drive, side effects include the deflation of breast glands, expansion of the size of the nipple and shrinking of bone mass.
In some jurisdictions, chemical castration has been used to reduce the libido of sexual offenders. The effectiveness of chemical castration in decreasing recidivism among sex offenders is controversial.
When used on males, these drugs can reduce sex drive, sexual fantasies, and capacity for sexual arousal. Life-threatening side effects are rare, but some users show increases in body fat and reduced bone density, which increase long-term risk of cardiovascular disease and osteoporosis, respectively. Males may also experience gynecomastia (development of larger-than-normal mammary glands in males); full development is less common unless chemical castration is combined with feminizing oestrogen therapy.
Some drugs, such as medroxyprogesterone acetate, cyproterone acetate, and LHRH agonists can decrease serum testosterone and estradiol in the body, thus impairing the metabolism of glucose and lipid. These drugs can also cause depression, hot flashes, infertility, and anemia, aside from cardiovascular diseases and osteoporosis. The risk of side effects caused by chemical castration drugs can increase depending on the length of time under which they are administered. A 2004 study in which eleven men were chemically castrated ended with one committing suicide after one year of treatment; in another 2020 study, increases in suicidal ideations was reported by 8% of its treatment group, which led to the hospitalization of two of the 25 subjects who had been administered degarelix.
When used on females, the effects are similar, though there is little research about chemically lowering female's sex drive or female-specific anaphrodisiacs, since most research focuses on the opposite, but anti-androgenic hormone regimens would lower testosterone in females which can impact sex drive or sexual response. These drugs also deflate the breast glands and expand the size of the nipple. Also seen is a sudden shrinking in bone mass and discoloration of the lips, reduced body hair, and muscle mass.
The first use of chemical castration occurred in 1944, when diethylstilbestrol was used with the purpose of lowering men's testosterone. The antipsychotic agent benperidol was sometimes used to decrease sexual urges in people who displayed what was thought of as inappropriate sexual behavior, and as likewise given by depot injection, though benperidol does not affect testosterone and is therefore not a castration agent. Chemical castration was often seen as an easier alternative to life imprisonment or the death penalty because it allowed the release of the convicted.
In 1981, in an experiment by Pierre Gagné, 48 males with long-standing histories of sexually deviant behaviour were given medroxyprogesterone acetate for as long as 12 months. Forty of those subjects were recorded as having diminished desires for deviant sexual behaviour, as well as less frequent sexual fantasies and greater control over sexual urges. The research recorded a continuation of this improved behaviour after the administration of the drug had ended, with no evidence of adverse side effects, and so recommended medroxyprogesterone acetate along with counselling as a successful method of treatment for serial sex offenders.