ifyouwannabemylover
Chasing Vanity
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In this thread we appreciate finasteride to counteract the overly negative reputation it has.
Finasteride has likely saved dozens of lives and even if you factor in suicides that, allegedly, resulted from finasteride use (which is questionable to say the least), it has probably saved more lives than it's (allegedly) taken.
Finasteride long-term (10 years) safety profile according to a Japanese study (not related to Merck):
www.oatext.com
More information:
The effect of androgens on the physiology of the penis has been a topic of discussion for many years. In 1974, Imperato‐McGinley and colleagues (1974) discovered an autosomal recessive form of incomplete male pseudohermaphroditism, which was shown to result from 5 α‐reductase deficiency. This disorder, also known as pseudovaginal perineoscrotal hypospadias, or type 2 familial male pseudohermaphroditism, is characterized by a 46,XY karyotype, ambiguity of the external genitalia (female phenotype at birth), and virilization at puberty. During fetal development, the decrease in DHT results in incomplete masculinization of the external genitalia. Later in puberty, affected individuals develop a muscular male habitus with growth of the phallus and scrotum, and their voices change into adulthood. In adulthood, they have decreased body hair, a scant to absent beard, no temporal hair line recession, and a small prostate. However, subjects have normal erections and ejaculations and a libido directed towards females (Imperato‐McGinley et al, 1974).
All ferrets were gonadectomized when they were 11 weeks of age and were subsequently tested for masculine sexual behavior after a latin‐square sequence of treatments with subcutaneous silastic capsules containing T, estradiol, or DHT. After T administration, control males displayed significantly more neck gripping, mounting, and pelvic thrusting than males treated neonatally with ATD. After DHT administration, little masculine sexual behavior was shown by any group. These consequences suggest that behavioral masculinization in the male ferret results primarily from the neonatal action of T itself in the brain, and not from its estrogenic or 5 α‐reduced androgenic metabolites (Baum et al, 1983).
Clinicians counsel more or less on a drug's sexual side effects. Could this counseling trigger ED as a placebo effect? Mondaini et al (2007) investigated whether a discrepancy exists in finasteride‐related sexual adverse effects between double‐blind trials and clinical practice, and if the difference might be partially related to a placebo effect. The patients were asked to complete the International Index of Erectile Function (IIEF) and the Male Sexual Function‐4 (MSF‐4; contains questions about interest in sex, quality of erection, achievement of orgasm, and achievement of ejaculation) questionnaires (Mondaini et al, 2007). Finasteride was prescribed to 120 patients with or without counseling on the drug's sexual side effects. The estimation of side effects was conducted at 6 and 12 months using the MSF‐4 questionnaire and a self‐administered questionnaire. In this study, finasteride was associated with a significantly higher proportion of ED in patients informed of possible erectile side effects as compared with that in patients for whom the same information was withheld. The incidence of ED was 9.6% for the group without counseling and 30.9% for the group with counseling (Mondaini et al, 2007). The placebo effect demonstrated here has to be taken into account when managing finasteride‐related EDs.
In this review, we summarized the effect of 5ARIs with respect to erectile function. It is likely that androgens are vital for the development, maintenance and function of penile tissue and regulation of erectile physiology. However, the critical androgenic substance for these effects is most likely T rather than DHT.
onlinelibrary.wiley.com
*Let me end this by saying that finasteride is anything but an ideal solution, but it's pretty much the best option there is and even if you dislike the idea, it could be of use until better options are available.
Finasteride has likely saved dozens of lives and even if you factor in suicides that, allegedly, resulted from finasteride use (which is questionable to say the least), it has probably saved more lives than it's (allegedly) taken.
Finasteride long-term (10 years) safety profile according to a Japanese study (not related to Merck):
Safety evaluation
Adverse reactions were recorded in 6.8% (36/532) in the safety evaluation in this study, which was slightly higher than that observed in other studies in Japanese men [8,9,17]. This observation was thought to have been caused by the fact that the investigation period of this study was longer than that of others and, therefore, the patients had aged more. Incidences of decreased libido and erectile dysfunction have been known to increase in proportion with age. In the investigation in 40 years or older of Asians, the incidences of decreased libido and erectile dysfunction were 6.0–38.7% and 40.6–70.0%, respectively [29,23]. Overall, the adverse reactions were all mild, and the incidence was lower than the generic incidence of decreased libido and erectile dysfunction in Asians. As adverse reactions were recorded by patients in a subjective questionnaire, the result was thought to be slightly different from the correct number of adverse reactions in this study. Strict safety evaluation was not investigated in this study. Several studies on AGA treatment with finasteride have reported that there are no significant differences from the placebo in adverse reactions, [13,30,31] and that the risk of discontinuing the treatment because of adverse reaction is similar to that of the placebo [32].Long-term (10-year) efficacy of finasteride in 523 Japanese men with androgenetic alopecia
OA Text is an independent open-access scientific publisher showcases innovative research and ideas aimed at improving health by linking research and practice to the benefit of society.
More information:
The effect of androgens on the physiology of the penis has been a topic of discussion for many years. In 1974, Imperato‐McGinley and colleagues (1974) discovered an autosomal recessive form of incomplete male pseudohermaphroditism, which was shown to result from 5 α‐reductase deficiency. This disorder, also known as pseudovaginal perineoscrotal hypospadias, or type 2 familial male pseudohermaphroditism, is characterized by a 46,XY karyotype, ambiguity of the external genitalia (female phenotype at birth), and virilization at puberty. During fetal development, the decrease in DHT results in incomplete masculinization of the external genitalia. Later in puberty, affected individuals develop a muscular male habitus with growth of the phallus and scrotum, and their voices change into adulthood. In adulthood, they have decreased body hair, a scant to absent beard, no temporal hair line recession, and a small prostate. However, subjects have normal erections and ejaculations and a libido directed towards females (Imperato‐McGinley et al, 1974).
All ferrets were gonadectomized when they were 11 weeks of age and were subsequently tested for masculine sexual behavior after a latin‐square sequence of treatments with subcutaneous silastic capsules containing T, estradiol, or DHT. After T administration, control males displayed significantly more neck gripping, mounting, and pelvic thrusting than males treated neonatally with ATD. After DHT administration, little masculine sexual behavior was shown by any group. These consequences suggest that behavioral masculinization in the male ferret results primarily from the neonatal action of T itself in the brain, and not from its estrogenic or 5 α‐reduced androgenic metabolites (Baum et al, 1983).
Clinicians counsel more or less on a drug's sexual side effects. Could this counseling trigger ED as a placebo effect? Mondaini et al (2007) investigated whether a discrepancy exists in finasteride‐related sexual adverse effects between double‐blind trials and clinical practice, and if the difference might be partially related to a placebo effect. The patients were asked to complete the International Index of Erectile Function (IIEF) and the Male Sexual Function‐4 (MSF‐4; contains questions about interest in sex, quality of erection, achievement of orgasm, and achievement of ejaculation) questionnaires (Mondaini et al, 2007). Finasteride was prescribed to 120 patients with or without counseling on the drug's sexual side effects. The estimation of side effects was conducted at 6 and 12 months using the MSF‐4 questionnaire and a self‐administered questionnaire. In this study, finasteride was associated with a significantly higher proportion of ED in patients informed of possible erectile side effects as compared with that in patients for whom the same information was withheld. The incidence of ED was 9.6% for the group without counseling and 30.9% for the group with counseling (Mondaini et al, 2007). The placebo effect demonstrated here has to be taken into account when managing finasteride‐related EDs.
In this review, we summarized the effect of 5ARIs with respect to erectile function. It is likely that androgens are vital for the development, maintenance and function of penile tissue and regulation of erectile physiology. However, the critical androgenic substance for these effects is most likely T rather than DHT.
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*Let me end this by saying that finasteride is anything but an ideal solution, but it's pretty much the best option there is and even if you dislike the idea, it could be of use until better options are available.
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