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Ok, now I understand why Finasteride can cause depression, it down-regulates dopamine (the feel good neurostimulator). It was determined at 4 months of Finasteride 5mg per day treatment.
________________________________
Finasteride treatment and neuroactive steroid formation.
Abstract
Finasteride is the 5alpha-reductase inhibitor that received clinical approval for the treatment of human benign prostate hyperplasia and androgenetic alopecia. The 5alpha-reductase is enzyme responsible for the reduction of testosterone to dihydrostestosterone, progesterone to dihydroprogesterone and deoxycorticosterone to dihydrodeoxycorticosterone, steroids modulating the action of gamma-aminobutyric acid on GABA receptors. These neuroactive steroids possess anticonvulsant, antidepressant and anxiolytic effects. The objective of the study was to determine the effect of finasteride therapy on a broad steroid spectrum in men with benign prostate hyperplasia. A group of 20 men with benign prostate hyperplasia was involved in the present study. Finasteride in the daily dose of 5 mg/day was administrated for 4 months. In all individuals, their hormonal profile of steroid hormones was determined before and after 4 months lasting finasteride treatment. Finasteride treatment resulted in a significant decrease all alpha-reduced and increase of most 5beta-reduced metabolites of testosterone and progesterone as well as in an increase of 7alpha-hydoxyderivatives, which are known as neuroactive steroids acting by modulation of GABAA and NMAD receptors in the brain. In the course of finasteride treatment the decrease of the concentration of circulating steroids with known inhibitory activity on GABA-ergic excitation in the brain is very probably an important factors contributing to the development of the symptoms of depression seen in some isolated cases of finasteride administration.
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(07-09-2015, 03:52 AM)Lotus Wrote: Ok, now I understand why Finasteride can cause depression, it down-regulates dopamine (the feel good neurostimulator). It was determined at 4 months of Finasteride 5mg per day treatment.
________________________________
Finasteride treatment and neuroactive steroid formation.
Abstract
Finasteride is the 5alpha-reductase inhibitor that received clinical approval for the treatment of human benign prostate hyperplasia and androgenetic alopecia. The 5alpha-reductase is enzyme responsible for the reduction of testosterone to dihydrostestosterone, progesterone to dihydroprogesterone and deoxycorticosterone to dihydrodeoxycorticosterone, steroids modulating the action of gamma-aminobutyric acid on GABA receptors. These neuroactive steroids possess anticonvulsant, antidepressant and anxiolytic effects. The objective of the study was to determine the effect of finasteride therapy on a broad steroid spectrum in men with benign prostate hyperplasia. A group of 20 men with benign prostate hyperplasia was involved in the present study. Finasteride in the daily dose of 5 mg/day was administrated for 4 months. In all individuals, their hormonal profile of steroid hormones was determined before and after 4 months lasting finasteride treatment. Finasteride treatment resulted in a significant decrease all alpha-reduced and increase of most 5beta-reduced metabolites of testosterone and progesterone as well as in an increase of 7alpha-hydoxyderivatives, which are known as neuroactive steroids acting by modulation of GABAA and NMAD receptors in the brain. In the course of finasteride treatment the decrease of the concentration of circulating steroids with known inhibitory activity on GABA-ergic excitation in the brain is very probably an important factors contributing to the development of the symptoms of depression seen in some isolated cases of finasteride administration.
And here's why (cause I know everybody is on the seat of their pants)
not!
Because of quote: Finasteride's ability to inhibit the Type II isoform of the 5alpha-reductase enzyme, which is the predominant form in human prostate and hair follicles, and the
concomitant reduction of testosterone to dihydrotestosterone (DHT). In addition to catalyzing the rate-limiting step in the reduction of testosterone, both isoforms of the 5alpha-reductase enzyme are
responsible for the reduction of progesterone and deoxycorticosterone to dihydroprogesterone (DHP) and dihydrodeoxycorticosterone (DHDOC), respectively. (Of course)
See, no biggie.
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I wonder........ Since Vitex takes an hypothalamus pituitary-adrenocortical (HPA) axis (pathway) if this would explain a down regulation of GABA A too?.
As the interprid muppet news-reporter asks, your thoughts?
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I gotta tell yah, I had real reservations about the claims of BO making you sterile in 6 months, and here's why:
inhibitor finasteride on serum levels of gonadal, adrenal, and hypophyseal hormones and its clinical significance: a prospective clinical study.
Uygur MC1, Arik AI, Altuğ U, Erol D.
Author information
Abstract
In the present study, we investigated the effects of a steroid 5 alpha-reductase inhibitor, finasteride, when given orally (5 mg/day), on the serum levels of gonadal, hypophyseal, and adrenal hormones and the clinical significance of these effects. Forty-eight patients with a mean age of 63 (range 49-81) were included in the study. All patients had symptoms of benign prostatic hyperplasia. Serum levels of testosterone, dihydrotestosterone, follicle-stimulating hormone (FSH) luteinizing hormone (LH), prolactin, aldosterone, cortisol, and dehydroepiandrosterone were determined before the study. The degree of symptoms in each patient and serum prostate specific antigen levels were determined together with uroflowmetric studies. Sexual status of the patients was also assessed with a self-administered questionnaire. All patients received finasteride, 5 mg/day, for 6 weeks. All of the above mentioned studies were repeated at month 3 and month 6. All of the patients had baseline hormonal values within the normal range. At month 3, the dihydrotestosterone level decreased by 60%, while the testosterone level increased by 15%. FSH and LH levels decreased by 24% and 16%, respectively. The changes in the serum levels of these hormones were further evident at month 6. No significant changes were noted in the serum levels of prolactin, aldosterone, cortisol, and dehydroepiandrosterone. Thirty-six patients (75%) were judged to be potent before the treatment. Finasteride caused erectile dysfunction in 8 patients (22%) by month 3 and in 12 (33%) by month 6. A substantial improvement was noted in symptoms of benign prostatic hyperplasia in all patients. The serum prostate specific antigen level decreased by 42% and 50% at month 3 and at month 6, respectively. Continued administration of finasteride, 5 mg/day alters the serum levels of testosterone, dihydrotestosterone, FSH, and LH significantly. Finasteride also causes sexual dysfunction in a substantial number of patients and should be offered with caution to patients who have an active sexual life.
No way BO has this kind of potential like Finasteride, (decreased by 42% and 50% at month 3 and at month 6).
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So, let me try to translate. Even though T went up, there was also a decrease in DHT. So, even though T went up, more was turned into E and tends to upset the hormonal balance in favor of feminization specifically the breast since they are presumably the easiest section of the body to attract fat deposits.
How am I doing so far.
As far as moods, it kicks dopamine to the curb.. So while you are pleased about getting breasts or growing bigger ones, it makes you feel like everything else is dumping on you.
How's that Professor Lotus?
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(07-09-2015, 05:05 AM)iaboy Wrote: So, let me try to translate. Even though T went up, there was also a decrease in DHT. So, even though T went up, more was turned into E and tends to upset the hormonal balance in favor of feminization specifically the breast since they are presumably the easiest section of the body to attract fat deposits.
How am I doing so far.
As far as moods, it kicks dopamine to the curb.. So while you are pleased about getting breasts or growing bigger ones, it makes you feel like everything else is dumping on you.
How's that Professor Lotus?
I think it explains why some who feel an initial increase in the libido department, which could be up to a month or longer until DHT levels go down. The increase comes from free T, which is the active part of testosterone, total T which isn't bio-active doesn't play a large role is this process (well, maybe slightly).
I think this could explain other anti-androgens to a certain degree, and quite possibly herbs, but BO makes this analogy quite possible too.
Iaboy, very impressive.
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(07-09-2015, 05:41 AM)Lotus Wrote: I think this could explain other anti-androgens to a certain degree, and quite possibly herbs, but BO makes this analogy quite possible too.
How so?? How do you mean?
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(07-09-2015, 06:34 AM)iaboy Wrote: (07-09-2015, 05:41 AM)Lotus Wrote: I think this could explain other anti-androgens to a certain degree, and quite possibly herbs, but BO makes this analogy quite possible too.
How so?? How do you mean?
By the same process, meaning when DHT is reduced free T surges. This by most definitions explains anti-androgens in general, and what happens when DHT is lowered.
And as we know AA's differ in strength (effectiveness), we also know everybody reacts quite differently. I think what's unique is someone who's in essence like a perfect storm, (rapid response), but, imo they'll eventually plateau (level off). That's when our body is telling us it's time to cycle.
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Lotus do you think that finasteride can raise prolactin by the effect finasteride has on dopamine?
