yanez
Member
- Reaction score
- 0
I have a theory
I was wondering what is the mechanism that triggers the gynecomastia
Then I found this text
Other drugs may produce gynecomastia by interfering with androgen production or action ,thus increasing the estrogen/androgen ratio effect at the breast. The antifungal agent ketoconazole is a potent inhibitor of testosterone biosynthesis and can cause gynecomastia.However ,because of its pharmacokinetics,the incidence of gynecomastia is low when the drug is given in a once-a-dy dosage this regimen allows the serum testosterone levels to normalize before each succeding dose.Traditional antiandrogens (cyproterone,flutamide).as well as the H2-blocker cimetidine,appear to cause gynecomastia by blocking androgen receptor at the breast rather than by decresing androgen production; they cause an increased effective estrogen/androgen ratio in the breast tissue.This side effect of cimetidine is most common when high doses are used to treat Zollinger_ellison syndrome and is seen much less frequently with other antiulceral drugs,such as rantidine or omeprazole.The blockade of androgen action at the breast by a commercial insecticide has been implicated in an epidemic of gynecomastia in Haitian immigrants.The aldosterone antagonist spironolactone ,frequetly used as a diuretic ,may block androgen receptor as well as interfere with androgen production,thereby leading to an increased effective estrogen/adnrogen ratio at the breast.here ,too,the breast enlargement is seen most commonly at high dosages,as in the treatment of primary hyperaldosteronism.Finasteride ,wich is used in the treatment of prostate disorders and which inhibits 5-a- reductase and reduces intracellular levels of active androgen (dihydrosterone) in targets issues,has also been associated with gynecomastia.
A wide variety of neurotransmitter agonists,antagonists,or modulators that are used to treat hypertension or pshychiatric disorders have been associated with gynecomastia,but the nature and mechanism of this connection are largely unexplored.Also ,such agents commonly are associated with hyperprolactinemia,which may cause secondary hypogonadism.
An increasingly frequent cause of drug-related gynecomastia is cancer chemotherapeutic agents.Gynecomastia associated with such medications may be increasing in prevalence as their spectrum of use is extended to nonmaligant conditions (e.g.,gynecomastia following methrotrexate treatment of rheumatoid arthirtis.
It has been known for many years that such drugs ,particularly alkylating agents ,are highly toxic to spermatogenic epithelium ,causing primary testicular failure with azzospermia,small testicles ,and high serum LH and FSH levels.Serum testosterone levels ,however,usually are normal or low normal,but in some cases of chemotherapy-related gynecomastia,serum estrogen levels have been elevated.A reasonable,but unproven ,theory is that chemotherapy agents produce compensated Leydig cell failure,with normal or low-normal serum testosterone levels maintained only with the stimulus of high serum LH.This incresed serum LH then causes a relative increase in testicular estrogen output,leading to an increase in the circulating estrogen/adnrogen ratio and then gynecomastia.
http://books.google.com/books?id=FVfzRv ... #v=onepage
but then if the gynecomastia is due to a relationship (ratio) in the breast of unbalanced estrogen / androgen (with an excess of the first then)
.. And inhibit aromatase in the long run creates hypogonadism
here explains why antiaromatase have a negative effect leading to hypogonadism
see
Aromatase inhibitors Have Also Been shown to reverse age-related declines in testosterone, as well as primary hypogonadism.
http://www.ncbi.nlm.nih.gov/pubmed/15001605
.. So why not try to apply any creams for topical use in the breast just there blocking the estrogen receptors ER?
melatonin is a well tolerated substance that blocks the estrogen receptors, .. you could maybe use a cream of melatonin topically
I need
a confirmation by some competent person
http://www.fasebj.org/cgi/content/abstract/13/8/857
http://www.ncbi.nlm.nih.gov/pubmed/10224229
http://www.ncbi.nlm.nih.gov/pubmed/15229223
if this would give protection to the mammary glands with regard to the estrogenic activity and hypertrophy of these .... it would be useful, for example, you could continue to use all antiandrogens you would like the sides having gynecomastia precluded
anyway I heard that melatonin block even AR receptor a bit..mmmm...
only if the gynecomastia is given by an excess of estrogen in the ratio estrogen / androgen in the breast and melatonin receptors inhibits both estrogen and androgen those that happen ..? Well I think that is sufficient to block estrogen to inhibit hypertrophy
could this be useful ?
I was wondering what is the mechanism that triggers the gynecomastia
Then I found this text
Other drugs may produce gynecomastia by interfering with androgen production or action ,thus increasing the estrogen/androgen ratio effect at the breast. The antifungal agent ketoconazole is a potent inhibitor of testosterone biosynthesis and can cause gynecomastia.However ,because of its pharmacokinetics,the incidence of gynecomastia is low when the drug is given in a once-a-dy dosage this regimen allows the serum testosterone levels to normalize before each succeding dose.Traditional antiandrogens (cyproterone,flutamide).as well as the H2-blocker cimetidine,appear to cause gynecomastia by blocking androgen receptor at the breast rather than by decresing androgen production; they cause an increased effective estrogen/androgen ratio in the breast tissue.This side effect of cimetidine is most common when high doses are used to treat Zollinger_ellison syndrome and is seen much less frequently with other antiulceral drugs,such as rantidine or omeprazole.The blockade of androgen action at the breast by a commercial insecticide has been implicated in an epidemic of gynecomastia in Haitian immigrants.The aldosterone antagonist spironolactone ,frequetly used as a diuretic ,may block androgen receptor as well as interfere with androgen production,thereby leading to an increased effective estrogen/adnrogen ratio at the breast.here ,too,the breast enlargement is seen most commonly at high dosages,as in the treatment of primary hyperaldosteronism.Finasteride ,wich is used in the treatment of prostate disorders and which inhibits 5-a- reductase and reduces intracellular levels of active androgen (dihydrosterone) in targets issues,has also been associated with gynecomastia.
A wide variety of neurotransmitter agonists,antagonists,or modulators that are used to treat hypertension or pshychiatric disorders have been associated with gynecomastia,but the nature and mechanism of this connection are largely unexplored.Also ,such agents commonly are associated with hyperprolactinemia,which may cause secondary hypogonadism.
An increasingly frequent cause of drug-related gynecomastia is cancer chemotherapeutic agents.Gynecomastia associated with such medications may be increasing in prevalence as their spectrum of use is extended to nonmaligant conditions (e.g.,gynecomastia following methrotrexate treatment of rheumatoid arthirtis.
It has been known for many years that such drugs ,particularly alkylating agents ,are highly toxic to spermatogenic epithelium ,causing primary testicular failure with azzospermia,small testicles ,and high serum LH and FSH levels.Serum testosterone levels ,however,usually are normal or low normal,but in some cases of chemotherapy-related gynecomastia,serum estrogen levels have been elevated.A reasonable,but unproven ,theory is that chemotherapy agents produce compensated Leydig cell failure,with normal or low-normal serum testosterone levels maintained only with the stimulus of high serum LH.This incresed serum LH then causes a relative increase in testicular estrogen output,leading to an increase in the circulating estrogen/adnrogen ratio and then gynecomastia.
http://books.google.com/books?id=FVfzRv ... #v=onepage
but then if the gynecomastia is due to a relationship (ratio) in the breast of unbalanced estrogen / androgen (with an excess of the first then)
.. And inhibit aromatase in the long run creates hypogonadism
here explains why antiaromatase have a negative effect leading to hypogonadism
see
Aromatase inhibitors Have Also Been shown to reverse age-related declines in testosterone, as well as primary hypogonadism.
http://www.ncbi.nlm.nih.gov/pubmed/15001605
.. So why not try to apply any creams for topical use in the breast just there blocking the estrogen receptors ER?
melatonin is a well tolerated substance that blocks the estrogen receptors, .. you could maybe use a cream of melatonin topically
I need
a confirmation by some competent person
http://www.fasebj.org/cgi/content/abstract/13/8/857
http://www.ncbi.nlm.nih.gov/pubmed/10224229
http://www.ncbi.nlm.nih.gov/pubmed/15229223
if this would give protection to the mammary glands with regard to the estrogenic activity and hypertrophy of these .... it would be useful, for example, you could continue to use all antiandrogens you would like the sides having gynecomastia precluded
anyway I heard that melatonin block even AR receptor a bit..mmmm...
only if the gynecomastia is given by an excess of estrogen in the ratio estrogen / androgen in the breast and melatonin receptors inhibits both estrogen and androgen those that happen ..? Well I think that is sufficient to block estrogen to inhibit hypertrophy
could this be useful ?
