Lxxy said:
use nizoral 2% every day and it works great <<< why to use nizoral every day when it will stay in the scalp for 3 days(HWZ)?
as for proscar 1-2 months is plenty of time for it to begin to work << no its not men read the studies plz!
and all you did was reiterate my recommendation of spiro, that i apply once nightly before bed <<< hehe no i use it in that cycle at my own
the hair re-growth from minoxidil is a joke <<< ok that right
cya
Stays in the scalp for 3 days, huh??

I assume you're refering to the 2% shampoo(20mg/g) and not the antifungal cream indicated for tinea pedis,tinea corporis and tinea cruris or for the treatment of seborrheic dermatitis or cutaneous candidiasis. Even then the recomended dose is once daily.
Ketoconazole has a short elimination half-life of 1.8 hrs after a 2.5mg/kg dose. Oral minoxidil's half-life is 4.2hrs and 5%topical is recomended 2x daily.
As for the propecia:
PRODUCT MONOGRAPH
PROPECIA®
(finasteride)
Film-coated Tablets 1 mg
THERAPEUTIC CLASSIFICATION
Type II 5 alpha-reductase inhibitor
ACTIONS AND CLINICAL PHARMACOLOGY
PROPECIA® (finasteride) is a competitive and specific inhibitor of Type II 5 alpha-reductase, an
intracellular enzyme that converts the androgen testosterone into dihydrotestosterone (DHT). Two distinct
isozymes of 5 alpha-reductase are found in mice, rats, monkeys, and humans: Type I and II. Each of
these isozymes is differentially expressed in tissues and developmental stages. In humans, Type I
5 alpha-reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and
liver. Type I 5 alpha-reductase is responsible for approximately one-third of circulating DHT. The Type II
5 alpha-reductase isozyme is primarily found in prostate, seminal vesicles, epididymides, and hair follicles
as well as liver, and is responsible for two-thirds of circulating DHT.
In humans, the mechanism of action of finasteride is based on its preferential inhibition of the Type II
isozyme. Using native tissues (scalp and prostate), in vitro binding studies examining the potential of
finasteride to inhibit either isozyme revealed a 100-fold selectivity for the human Type II 5 alpha-reductase
over Type I isozyme (IC50=500 and 4.2 nM for Type I and II, respectively). For both isozymes, the inhibition
by finasteride is accompanied by reduction of the inhibitor to dihydrofinasteride and adduct formation with
NADP+. The turnover for the enzyme complex is slow (t¹₂ approximately 30 days for the Type II enzyme
complex and 14 days for the Type I complex).
Finasteride has no affinity for the androgen receptor and has no androgenic, antiandrogenic, estrogenic,
antiestrogenic, or progestational effects. Inhibition of Type II 5 alpha-reductase blocks the peripheral
conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT
concentrations.
Finasteride produces a rapid reduction in serum DHT concentration, reaching 65%
suppression within 24 hours of oral dosing with a 1 mg tablet.
In men with male pattern hair loss (androgenetic alopecia), the balding scalp contains miniaturized hair
follicles and increased amounts of DHT compared with hairy scalp. Administration of finasteride
decreases scalp and serum DHT concentrations in these men. By this mechanism, finasteride interrupts
a key factor in the development of androgenetic alopecia in those patients genetically predisposed.
The minoxidil's efficaciousness is enhanced with the synergistic combo of propecia and nizoral @2% let alone @5%.
: J Dermatol. 2002 Aug;29(8):489-98. Related Articles, Links
Comparative efficacy of various treatment regimens for androgenetic alopecia in men.
Khandpur S, Suman M, Reddy BS.
Department of Dermatology and S.T.D., Maulana Azad Meical College and Associated Lok Nayak Hospital, New Delhi, India.
Our understanding of the aetiology of androgenetic alopecia (AGA) has substantially increased in recent years. As a result, several treatment modalities have been tried with promising results especially in early stages of AGA. However, as far as has been ascertained, there is no comprehensive study comparing the efficacy of these agents alone and in combination with each other. One hundered male patients with AGA of Hamilton grades II to IV were enrolled in an open, randomized, parallel-group study, designed to evaluate and compare the efficacy of oral finasteride (1 mg per day), topical 2% minoxidil solution and topical 2% ketoconazole shampoo alone and in combination. They were randomized into four groups. Group I (30 patients) was administered oral finasteride, Group II (36 patients) was given a combination of finasteride and topical minoxidil, Group III (24 patients) applied minoxidil alone and Group IV (10 patients) was administered finasteride with topical ketoconazole. Treatment efficacy was assessed on the basis of patient and physician assessment scores and global photographic review during the study period of one year. At the end of one year, hair growth was observed in all the groups with best results recorded with a combination of finasteride and minoxidil (Group II) followed by groups IV, I and III. Subjects receiving finasteride alone or in combination with minoxidil or ketoconazole showed statistically significant improvement (p<0.05) over minoxidil only recipients. No signifcant side-effects related to the drugs were observed. In conclusion, it is inferred that the therapeutic efficacy is enhanced by combining the two drugs acting on different aetiological aspects of AGA.