Yea it's all wishful thinking only on my part... just like every other guy who has experienced depression thanks to finasteride or Avodart... or the below experiences, or that others have already researched on their own:
http://www.keratin.net/forums/viewtopic.php?t=6857
http://www.hairlosshelp.com/forums/mess ... SGDBTABLE=
http://www.hairsite7.com/m586dutas26/_d ... 000236.htm
http://www.hairsite7.com/m586dutas26/_d ... 00023c.htm
If you want to believe the below mechanisms of action thanks to finasteride may not have any impact on a person's brain or behaviour, go right ahead -- whatever makes you sleep better at night. Either way, seems more like wishful thinking on YOUR part, pal.
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http://www.pubmedcentral.nih.gov/articl ... id=1622749
Selected bits:
"
Animal studies suggested that finasteride could alter 5alpha-reductase activity in some regions of the brain, and lead to behavioral and mood changes. It has been shown that finasteride is able to inhibit 5alpha-reductase in medial basal hypothalamus in pregnant rats, and induce behavioral changes [13]. Significant inhibition of hypothalamic and pituitary 5alpha-reductase is also noticed in adult male rats [14]. In addition to animal studies, although there are some case reports suggesting finasteride induction of depressive symptoms and anxiety in humans, [15] but no prospective study has been carried out, in order to investigate finasteride behavioral effects. In the present study, we have investigated any depressive symptoms or anxiety induced by finasteride administration, in the patients with diagnosis of androgenetic alopecia."
5alpha-reductase is a critical enzyme in the conversion of several steroids such as testosterone, progesterone, aldosterone and corticosterone in the brain. This enzyme converts testosterone to the most natural potent androgen DHT, and also it acts an important role in conversion of progesterone to dihhydroprogesterone (DHP). DHP is further converted to allopregnanolone (5alpha, 3alpha-tetrahydroprogesterone) by 3alpha-HSD [9,21].
Allopregnanolone is a modulator of gamma amino butyric acid type A receptor (GABA-A), and increases chloride conductance.
This neurosteroid has been found to exert anti-convulsant, anesthetic and anxiolytic effects [22-24]. Moreover, change in the levels of allopregnanolone is found to be associated with depressive disorders. [25,26]
Our results are in agreement with the past published reports [15], and indicate that finasteride might induce depressive symptoms. The 95% confidence interval, for the difference in the means of the BDI scores, was ranging from 0.34 to 1.04. This shows that the overall change induced by finasteride is minimal, but statistically significant. Anxiety scores were also increased, but the difference was not significant.
A decline in serum DHT level occurs after finasteride administration [27]. This may contribute to finasteride induced depression.
Some studies have been shown that serum DHT level, which is in equilibrium with the brain [28], is inversely associated with depression. A study by Barrett-Connor E. et al. showed that
BDI scores were inversely associated with bioavailable testosterone and DHT level [29]. Furthermore, it was found that
DHT had anti-depressant effects on behavior of male rats and its replacement in castrated rats was able to partially decrease the immobility behavior, which is indicative of depression [30].
Finasteride induced psychiatric dysfunction can also be attributed to its inhibitory effect on androgen and steroid 5alpha-reduction in the brain. Animal studies suggest that finasteride has inhibitory effects on 5alpha-reduction of testosterone and progesterone in the brain and inhibits the formation of allopregnanolone [31,32].
Allopregnanolone has an important role in depressive disorders [26]. In 1998 Romeo E. et al, revealed that
episodes of unipolar major depressive disorder in men is associated with a decline in the plasma concentrations of allopregnanolone [25]. Furthermore, a study carried out by Uzunova V. et al. showed that
CSF levels of allopregnanolone were significantly lower in depressed patients, and there was negative correlation between allopregnanolone levels in CSF and HAM-D scores. [33].
Since finasteride is a potent 5AR type2 inhibitor and the predominant isoform of the enzyme in human brain is 5AR type1 [34,35], some points should be noted concerning finasteride inhibitory effect on brain steroid metabolism. (i) Although finasteride is a potent 5AR type2 inhibitor, but it has also some inhibitory effects on 5AR type1 [36]. (ii)
Finasteride administration in humans has been reported to be associated with some behavioral and mental disorders related to low levels of allopregnanolone in the brain [37]. This may also improve the concept of brain allopregnanolone suppression by finasteride in humans
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Depression circumstantially related to the administration of finasteride for androgenetic alopecia.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12433001
ABSTRACT:
In this paper we report
19 patients (14 males, 5 females; mean age 28.16 years +/- 7.68 SD) out of a series of 23 (17 males, 5 females)
who developed a mood disturbance (moderate to severe depression) during treatment with finasteride, 1 mg/day orally, for androgenetic alopecia (Hamilton subtypes III-V; Ludwig subtypes I-II).
Depression, which significatively impaired sociofamilial relations, sleep and eating behaviour, was associated to marked anxiety in some cases,
developed after 9-19 weeks of treatment with finasteride, and promptly resolved after suspension of the drug.
Two patients accepted reintroduction of the drug, and depression relapsed within 2 weeks.
Depression as an adverse effect of finasteride has been reported only once.
Further studies are needed to confirm our circumstantial observations, which are based on a retrospective series of patients.
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Finasteride: suspected association with depression
PAGE 3, Canadian Adverse Reaction Report:
http://dsp-psd.pwgsc.gc.ca/Collection/H42-4-1-14-1E.pdf
A white man in his mid-40s with no prior history of psychiatric problems was treated with finasteride for male-pattern hair loss. Clinical depression developed about 3 months after the onset of therapy.
The depression was described as moderately severe but was unresponsive to treatment with various antidepressants. Treatment was maintained for 4 years.
Following cessation of the finasteride therapy, the depression resolved in about 2 weeks, and the patient made a complete recovery.
A published report has described 19 cases (14 males, 5 females) in whom moderate to severe depression developed during treatment with finasteride (1 mg/d orally) for androgenetic alopecia.1
