My research on low-dose finasteride...

[xRedStaRx]

I think the assumption that is being made is that 5-AR has more of an affinity for Testosterone than anything else in the body. If this assumption is true, then = good proxy. If it is not, then not such a good proxy, and taking more finasteride than is necessary is causing interruptions in other reactions within the body that could be prevented by taking a lower dose. My phd is not in biochemistry so eh I dunno.

As for the cost, I get 140 mg of finasteride for 39 dollars, an 8-10 month supply. I'm not trying to be rude, but if a person can't afford 39 dollars for almost a year of finasteride, they probably should be spending their money on other things like food? I was under the impression it was super expensive.

I don't understand that line of thinking. DHT is a byproduct of 5-AR activity, the percentage drop in DHT should approximate well the percentage of inhibited 5-AR II and III enzymes. The relative affinity for testosterone is get reduced should not be relevant, as you're comparing baseline vs post dose administration.

If 100 5-AR II enzymes produce 50ng/dl of DHT, then getting a serum level of 10ng/dl should give me around ~20 5-AR II enzymes, or a 80% inhibition, all else constant.

 

[californiaoceans911]

I don't understand that line of thinking. DHT is a byproduct of 5-AR activity, the percentage drop in DHT should approximate well the percentage of inhibited 5-AR II and III enzymes. The relative affinity for testosterone is get reduced should not be relevant, as you're comparing baseline vs post dose administration.

If 100 5-AR II enzymes produce 50ng/dl of DHT, then getting a serum level of 10ng/dl should give me around ~20 5-AR II enzymes, or a 80% inhibition, all else constant.

Chemistry doesn't always work like that. You're drawing a correlation between amount of byproduct you see vs original reactants. However, Testosterone and 5-AR are not the only chemicals in this closed environment. Progesterone is also 5-AR dependent, as are others. And the affinity profile for these reactions could be complex, and dynamic. Suppressing X amount of 5-AR could redistribute the affinity profile and the body may change its priorities. I just don't know if it's that simple, and I would put my money on it NOT being that simple. I just don't know.

 

[xRedStaRx]

Chemistry doesn't always work like that. You're drawing a correlation between amount of byproduct you see vs original reactants. However, Testosterone and 5-AR are not the only chemicals in this closed environment. Progesterone is also 5-AR dependent, as are others. And the affinity profile for these reactions could be complex, and dynamic. Suppressing X amount of 5-AR could redistribute the affinity profile and the body may change its priorities. I just don't know if it's that simple, and I would put my money on it NOT being that simple. I just don't know.

Well, considering 70% of the body's serum DHT is produced from 5-AR II enzymes, it's easy to tell how much you inhibit based on that.

1 mg of finasteride maximally inhibits around 65-75% DHT.

 

[Ventures]

XredStarX and californiaoceans911,

Does 5-ard-II have other roles except converting T to DHT ? We know 5-ard-I type is found in brain but what about 5-ard-II and 5-ard-III ?
Where are those enzymes most present, in what parts of human body ?

 

[californiaoceans911]

I think this thread is dead, it's just you and me redstar lol. I do think you are missing my point. Let me try one last analogy. Suppose you have a friend, suppose he is very needy, lets call him Testosterone. Suppose he also has a girlfriend (5AR) that just moved to Europe for college at Finasteride University and he is the US working at his job at the Testes Factory.

Before she moved away your friend and his gf spent a lot of time together, they were in love. Let's call the time they spend together DHT. Now she's gone and only visits periodically because she lives in Europe at Finasteride University. When she DOES visit, she tries to spend a lot of time with him, but now also spends a lot more time with family in comparison, since her time is limited.

Here's where it gets tricky. Suppose her schoolwork at FinU starts to get easier, and she can visit more often. Does she:


a. spend all of her new extra time with her bf?
b. spend all of her new extra time with her family?
c. spend all of her new extra time split equally between her bf and her family in accordance with the ratio of time she spent with each of them on her prior visits?
d. spend all of her new extra time in a new distribution with is gauged by how she feels as her relationships progress?

The way you describe things, and many others have as well, the answer is strictly "c." However, I think "d." is a likely answer too.

Either way I'm going to try the finasteride at 0.125 mg every other day to start and probably work up to 0.125 mg ED for a few months and judge from there. I'll start a new thread with "my story" with pics and stuff. Thanks for all your comments redstar.

-Cal

 

[xRedStaRx]

XredStarX and californiaoceans911,

Does 5-ard-II have other roles except converting T to DHT ? We know 5-ard-I type is found in brain but what about 5-ard-II and 5-ard-III ?
Where are those enzymes most present, in what parts of human body ?

When examined in lysates of transfected cells, 5α-R1 exhibits a broad pH optimum, which ranges between 6.0 and 8.5, while 5α-R2 shows a narrow acidic pH optimum (pH 5–5.5). However, there is evidence to suggest that inside intact human cells, 5α-R2 isozyme functions optimally at a more neutral pH range (6.0–7.0). 5α-R1 has a larger turnover number, as indicated by its value and a lower substrate affinity for T, = 1–5 μM. 5α-R2 has a lower turnover number () and a higher substrate affinity, as indicated by = 0.004–1 μM for T. Under optimal conditions, 5α-R2 has a higher 5α-reducing activity than 5α-R1, as indicated by its high ratio. Both isozymes contain an NH[SUB]2[/SUB]-terminal steroid (ligand) binding domain and a COOH-terminal NADPH binding domain. The apparent dissociation constant for NADPH cofactor is similar for both isozymes (3–10 μM). No such comparisons exist for 5α-R3 except that it appears to be efficient at pH 6.5–6.9 (unpublished work from our group).

Tissue distribution of 5α-reductase 1–3 according to different authors.

Author isozymes studied Tissue type Materials and methods 5α-R1 5α-R2 Notes Eicheler et al. [10] 5α-R1-2 Epidermis: genital (scrotum) nongenital (Axilla, breast, lip, eyelid) using a semiquantitative visual scale Protein expression (IHC) using rabbit polyclonal antibodies against synthetic peptides from C-terminus parts of 5α-R1-2 proteins. Antibody sensitivity and specificity confirmed by ELISA and WB on FFPE biopsy or autopsy tissues Nuclear, in epidermis from all sites: (scrotal> axilla> breast> lip> eye lid): stratum basale (++), stratum spinosum (++), absent in stratum granulosum and stratum corneum, dermal papillae, fibrous and outer epithelial RS (++), inner epithelial RS (+), matrix cells of hair bulb (++), scrotal fibroblast (++), basal and secretory cells of sebaceous glands (++), secretory and myoepithelial cells of sweat glands (++), arrector pili muscles (+), dermal adipocytes (+). No qualitative differences in males and females Cytoplasmic, in epidermis from all sites: stratum spinosum (++), stratum basale (+), absent in stratum granulosum and stratum corneum, inner epithelial RS (++), matrix cells of hair bulb (+), absent in dermal papillae, fibrous and outer epithelial RS, basal (+) and glandular (−) cells of sebaceous glands, myoepithelial (+) and secretory cells (−) of sweat glands, dermal adipocytes (+) No qualitative differences in males and females 5α-R1 more uniformly spread in skin versus 5α-R2 that is mainly found in inner epith RS Aumüller et al. [11] 5α-R1-2 Many tissue types, using a semiquantitative visual scale Protein expression (IHC) using rabbit polyclonal antibodies against synthetic peptides from C-terminus parts of 5α-R1-2 proteins. Antibody sensitivity and specificity confirmed by ELISA and WB. Tissues from surgical pts and autopsies, fixed in Bouin's or formaldehyde Mainly nuclear: Prostate: stroma (+), epithelium (+) Seminal vesicle: stroma (+), epithelium (+) Epididymis: stroma (+), epithelium (+) Testis: Leydig cells (+), Sertoli cells (+) Ovary: stroma (++), theca and granulosa cells (−) Uterus: endometrium (+), myometrium (+) Liver: hepatocytes (+/−), bile duct c (+), kupffer cells (++) Pancreas: exocrine (+), islets of Langerhans (−) Kidney: glomerulus (+), PT (−), DT (++), CD (+) Adrenal: cortex (−), medulla (−) Thyroid: thyrocytes (−), C cells (−) Cerebral cortex: pyramidal c (+), glial cells (+/−) Pituitary: prolactin cells (+), others (−) Mainly cytoplasmic: Prostate: stroma (+), epithelium (++), specially basal cells Seminal vesicle.: stroma (+), epithelium (++) Epididymis: stroma (+), epithelium (+) Testis: spermatogonia (+), Leydig and Sertoli cell (−) Ovary: stroma (+), theca and granulosa cells (+/−) Uterus: endometrium (+), myometrium (+) Liver: hepatocytes (++), bile duct c (+), kupffer cells (−) Pancreas: exocrine (+), islets of Langerhans (−) Kidney: glomerulus (−), PT (++), DT (+/−), CD (+) Adrenal: ZG (+), ZF (+/−), ZR (+/−), med (−) Thyroid: thyrocytes (−), C cells (−) Cerebral cortex: pyramidal c (++), glial c (−) Pituitary: prolactin cells (+), others (−) 5α1-2 is ubiquitous Bayne et al. [12] 5α-R1-2 Scalp biopsies from bald and non-bald men Protein expression (IHC) using validated mouse monoclonal antibodies against peptides from N-terminus parts of 5α-R1-2 and enzyme activity using [SUP]3[/SUP]H-T In balding and non-balding scalp: 5α-R1 is expressed only in sebaceous glands No expression was detected in hair follicles or in epidermis In balding and nonbalding scalp: 5α-R2 is expressed in infundibula, outer (mainly) and inner epithelial RS of hair follicles. No expression was detected in dermal papillae or in sebaceous glands Thigpen et al. [13] 5α-R1-2 Autopsy and surgical tissue samples Messenger RNA (NB) and protein expression (IHC and WB) using rabbit polyclonal antibodies against peptides from C-terminus parts of 5α-R1-2 5α-R1 protein is expressed in liver and chest skin and 5α-R1 mRNA was detected in cerebellum, hypothalamus, pons, medulla oblongata, skin, and liver 5α-R1 was not detected by WB in any fetal tissue. 5α-R1 was detected by WB in newborn liver, skin, and scalp.5α-R1 was detected by WB in all scalp samples from balding and nonbalding men (except one). It was not detected in any normal prostate, BPH, or PC sample 5α-R2 protein is expressed in prostate, seminal vesicles, epididymis, and liver. 5α-R2 mRNA was detected in prostate, SV, epididymis. and liver. 5α-R2 was detected by WB only in fetal genital skin (not detected in fetal liver, adrenal, testis, ovary, scalp, and brain). 5α-R2 was detected by WB in newborn prostate, SV, epididymis, liver, skin. and scalp. 5α-R2 was not detected by WB in any sample of balding and nonbalding scalp from one man. It was detected in all normal prostate, BPH, and PC samples 5α-R1 protein was not detected in any prostate sample Thomas et al. [14] 5α-R1-2 Prostate: BPH (TURP), ASCaP (RP), CaP metastasis in androgen deprivation-treated men (autopsy) Protein expression (IHC) using rabbit polyclonal antibodies against peptides from N-terminus of 5α-R1-2 proteins. Antibody specificity confirmed with WB on naïve, 5α-R1- and 5α-R2- transfected COS-1 cells and IHC on transfected COS-1 cells-Evaluated by measuring percentage of moderate- and high-intensity immunostaining areas in relation to total epithelial, PIN, or tumor area in PE tissues Nuclear in BPH, shifts to cytoplasm in HGPIN and CaP Immunostaining intensity: Metastasis> CR-CaP> AS-CaP = HGPIN> BPH Mainly cytoplasmic in all specimens Immunostaining intensity: BPH = Metastasis = CR-CaP> AS-CaP = HGPIN All differences are statistically significant Thomas et al. [14] 5α-R1-2 Prostate: AS-CaP (RP) with Gleason score <7, 7, >7 Protein expression (IHC) using validated rabbit polyclonal antibodies, evaluated by visually estimating percent of total tumor area showing low-, moderate, and high-intensity in relation to Gleason score Mainly nuclear in BPH, nuclear and cytoplasmic in CaP (all grades), and in adjacent benign epithelial tissue Immunostaining intensity: High grade > moderate grade = low grade > PC-adjacent benign tissue > BPH Mainly cytoplasmic in all samples (benign and malignant) Immunostaining intensity: BPH> high grade> moderate grade = low grade = adjacent benign tissue Staining in CaP-adjacent benign tissue is not significanty different from low- and high-grade CaP for either isozyme Söderstöm et al. [15] 5α-R1-2 Prostate: BPH (TURP) and AS-CaP via RP or RC Messenger RNA expression (sqRT-PCR) and measurement of 5α-R enzyme activity at pH 5.5 and 7 using [SUP]14[/SUP]C-T at 37°C in homogenized frozen pulverized prostate tissue 5α-R1 mRNA expression is similar in BPH and AS-CaP. There was no correlation between enzyme activity at pH (5.5 and 7) and 5α-R1 mRNA expression as expressed on the basis of β-actin 5α-R2 mRNA and enzyme activity were higher in BPH than in AS-CaP. There was a positive correlation between enzyme activity at pH 5.5 and expression of 5α-R2 mRNA as expressed on the basis of β-actin Lehle et al. [61] 5α-R 1-2 BPH and CaP tissue post prostate biopsy or RP frozen in liquid nitrogen, one human liver sample Messenger RNA expression (ISH, sqRT-PCR) ISH showed that 5α-R1 mRNA is expressed in epithelium > stroma mRNA expression levels by sqRT-PCR: liver> CaP > BPH> Normal prostate ISH showed that 5α-R2 mRNA is expressed in epithelium > stroma mRNA expression levels by sqRT-PCR: liver = BPH > Normal prostate > CaP Habib et al. [16] 5α-R1-2 BPH tissue (TURP) frozen in liquid nitrogen or in ice-cold RPMI with FBS and archival PE-BPH tissue Messenger RNA expression (ISH, RT-PCR) and measurement of enzyme activity at pH 5 and 7.5 using [SUP]3[/SUP]H-T at 37°C in homogenized pulverized frozen prostate tissue 5α-R1 mRNA expressed in epithelium > stroma 5α-R1 mRNA expressed in epithelium > stroma 5α-R2 mRNA > 5α-R1 mRNA in BPH 5α-R2 enzyme activity ≫ 5α-R1 enzyme activity in homogenized BPH tissue Bonkhoff et al. [17] 5α-R1-2 BPH (TURP), AS-CaP (RP), CR-CaP (channeling TUR) Protein expression (IHC) using polyclonal rabbit antibodies against peptides from C-terminus parts of 5α-R1 and 2, validated by ELISA and WB Mainly nuclear, in normal prostate and BPH tissue (luminal epithelial > basal) and in stroma 5α-R1 immunostaining > 5α-R2 in BPH (in both epithelium and stroma). In CaP, 5α-R1 immunostaining became nuclear and cytoplasmic and more intense in HGPIN and CaP versus adjacent benign tissue (specially CR-CaP) Mainly cytoplasmic (weak), in normal prostate and BPH tissue (basal > luminal epithelial) and stroma. In CaP, 5α-R2 immunostaining became nuclear and cytoplasmic and more intense in HGPIN and CaP versus adjacent benign tissue (specially CR-CaP) Shirakawa et al. [18] 5α-R1-2 BPH (RC) fixed in formaldehyde and paraffin-embedded Messenger RNA (qRT-PCR), protein (IHC) expression using polyclonal rabbit antibodies against peptides from C-terminus parts of 5α-R1 and 2, validated by ELISA and enzyme activities at pH 5 and 7.5 using [SUP]3[/SUP]H-T at 37°C 5α-R1 mRNA copy numbers> 5α-R2 mRNA in BPH 5α-R1 protein expression is intense in epithelium of BPH (higher than 5α-R2 protein) 5α-R1 enzyme activity at pH 7.5 is similar to 5α-R2 enzyme activity at pH 5.0 5α-R2 mRNA < 5α-R1 mRNA in BPH 5α-R2 protein expression is detected in epithelium and stroma of BPH (less intense than 5α-R1) Titus et al. [19] 5α-R1-2 ASBP, AS-CaP and CR-CaP (RP or channeling TURP) tissue that was FFPE or snap frozen in liquid nitrogen Protein expression (by IHC in TMAs that are quantified by visual scoring and digital image analysis and by WB) and enzyme activity in homogenized pulverized prostate tissue using [SUP]3[/SUP]H-ASD at 37°C 5α-R1 is nuclear and cytoplasmic in all 3 tissues Nuclear 5α-R1 staining intensity: ASBP = AS-CaP = CR-CaP Cytoplasmic 5α-R1 staining intensity: ASBP = AS-CaP> CR-CaP Not detected in stroma in any of the 3 tissues In WB, 5α-R1 > 5α-R2 in all 3 tissues 5α-R1 enzyme activity > 5α-R2 in CR-CaP (3 folds) 5α-R2 is mainly cytoplasmic in all 3 tissues Nuclear 5α-R2 staining intensity: ASBP = AS-CaP> CR-CaP Cytoplasmic 5α-R2 staining intensity: ASBP = AS-CaP> CR-CaP Not detected in stroma in any of the 3 tissues In WB, 5α-R2 was undetectable in CR-CaP 5α-R2 activity > 5α-R1 in ASBP and AS-CaP In all 3 tissues, expression of 5α-R1 is consistenty more than 5α-R2 (in nucleus) but similar in cytoplasm Godoy et al. [20] 5α-R3 Benign and malignant human tissue TMAs Protein expression (IHC) using validated monoclonal mouse antibody against peptide from N-terminus of 5α-R3 protein and quantified by visual scoring and digital image analysis 5α-R3 was mainly cytoplasmic Benign tissue immunostaining: Kidney (PT,DT ++), liver (++), exocrine pancreas (++), skeletal muscle (+), skin (strata basale and spinosum ++), gastric epithelial cells (+), myometrium (++) Malignant tissue: colon adenoCA (++), esophageal adenoCA (++), RCC (++), HCC (++), ovarian mucinous CA (++), stomach adenoCA (++), testis seminoma and YS tumor (++), thyroid papillary CA (++), endometrioid CA (++), breast CA (+) ASBP: basal epithelial cells, HGPIN: benign basal and neoplastic epithelial cells, AS-CaP and CR-CaP: in neoplastic cells (5α-R3 immunostaining intensity: AS-CaP = CR-CaP > ASBP) 5α-R3 protein expression ↑ in the cytoplasm of malignant cells versus benign cells in prostate, testis, thyroid, lung and breast CA Yamana et al. [21] 5α-R3 20 benign human tissues, CaP, and breast cancer cell lines 5α-R1-3 mRNA expression (RT-PCR) and measurement of 5α-R 1–3 enzyme activity using [SUP]14[/SUP]C-labelled ASD and T in intact cells in culture 5α-R3 expression at the mRNA level is higher than 5α-R1 and 2 in frontal cortex, heart, colon, stomach, liver, pancreas, lung, BPH, prostate, testis, mammary gland, brain, cervix, ovary, dermis, epidermis, total skin, small intestine, spleen, and kidney 5α-R2 mRNA was the most abundant in BPH and muscle Finasteride inhibits 5α-R2 and 5α-R3 with similar potency (IC[SUB]50[/SUB] = 14.3 nM, 17.4 nM, resp.). Dutasteride is a more potent inhibitor of 5α-R3 than finasteride (IC[SUB]50[/SUB] = 0.33 nM) 5α-R3 is ubiquitous Dutasteride is a triple 5α-RI in vitro

ELISA: enzyme-linked immunosorbant assay; IHC: immunohistochemistry; WB: western blot; NB: northern blot; FFPE: formalin fixed paraffin embedded; RS: root sheath; RP: radical prostatectomy; sqRT-PCR: semiquantitative reverse transcriptase-polymerase chain reaction; PE: paraffin-embedded; RPMI: Roswell Park Memorial Institute; FBS: fetal bovine serum; PT: proximal tubules; DT: distal tubules; CD: collecting ducts; TURP: transurethral resection of prostate; RC: radical cystectomy; HGPIN: high-grade prostate intraepithelial neoplasia; ISH: in situhybridization; RCC: renal cell carcinoma; HCC: hepatocellular carcinoma; adenoCA: adenocarcinoma; CA: carcinoma; YS: yolk sac; TMA: tissue microarray.

 

[xRedStaRx]

I think this thread is dead, it's just you and me redstar lol. I do think you are missing my point. Let me try one last analogy. Suppose you have a friend, suppose he is very needy, lets call him Testosterone. Suppose he also has a girlfriend (5AR) that just moved to Europe for college at Finasteride University and he is the US working at his job at the Testes Factory.

Before she moved away your friend and his gf spent a lot of time together, they were in love. Let's call the time they spend together DHT. Now she's gone and only visits periodically because she lives in Europe at Finasteride University. When she DOES visit, she tries to spend a lot of time with him, but now also spends a lot more time with family in comparison, since her time is limited.

Here's where it gets tricky. Suppose her schoolwork at FinU starts to get easier, and she can visit more often. Does she:


a. spend all of her new extra time with her bf?
b. spend all of her new extra time with her family?
c. spend all of her new extra time split equally between her bf and her family in accordance with the ratio of time she spent with each of them on her prior visits?
d. spend all of her new extra time in a new distribution with is gauged by how she feels as her relationships progress?

The way you describe things, and many others have as well, the answer is strictly "c." However, I think "d." is a likely answer too.

Either way I'm going to try the finasteride at 0.125 mg every other day to start and probably work up to 0.125 mg ED for a few months and judge from there. I'll start a new thread with "my story" with pics and stuff. Thanks for all your comments redstar.

-Cal

You aren't completely wrong, nor right.

You're trying to say that free T molecules affinity for 5-AR II increases when it is inhibited to compensate for the less quantities of metabolites produced. However, their affinity is strictly biochemical and constant for the most part. What you can change is the turnover activity of 5-AR enzymes, making your body produce more of them, and not make them stronger.

The same could be said about androgen receptors. However, their number and sensitivities are mostly controlled by endocrine hormones, and paracrine signaling for the underlying tissue, as far as I'm aware.

 

[baldchewbacca]

Hey californiaoceans,

How have you found the minoxidil foam? U mentioned it's re grown a bit. How long have u been using it? Any sides?

Im already on finasteride but only thinning at hairline so considering going on it. Maybe even test patching one temple first to see how it goes. Any advice?

 

[californiaoceans911]

Thanks for all that info redstar! Chewbac I have had a few hairs sprout up in the corner of my temples but they are small and I'm not sure 100% that it's the minoxidil working that fast. Also had a lot of shedding in the front line from it, it has become really diffuse. For example, when it's a windy day, the whole frontal hairline tickles because wind is passing through my hair. That's how I first noticed my balding was progressing too. I tolerate minoxidil very well. With the keto shampoo added I get very little itching.

 

[baldchewbacca]

Thanks for all that info redstar! Chewbac I have had a few hairs sprout up in the corner of my temples but they are small and I'm not sure 100% that it's the minoxidil working that fast. Also had a lot of shedding in the front line from it, it has become really diffuse. For example, when it's a windy day, the whole frontal hairline tickles because wind is passing through my hair. That's how I first noticed my balding was progressing too. I tolerate minoxidil very well. With the keto shampoo added I get very little itching.

That's great it's working even if slowly though.

Has the hairline recovered? If you she's I've read its a good sign. That's what I'm a bit worried about. I'm only thinning front cm to temples and if that was to shed my hairline would jump up noticeably. That's my one hesitation.

Really unsure. I want to thicken it up and minoxidil seems like only option after finasteride.

 

[californiaoceans911]

University finally found the Gormley et al. paper I requested, if anyone wants a copy I can scan with my smartphone and email it. First author is a Merck scientist. Conclusion is that even a dose of 0.1 is likely to reach the same DHT inhibition as 1mg, but it would take longer to reach the level of suppression whereas 1mg reaches it after 1 dose. 0.2 mg reaches the same level as 1mg after two doses.

That being said, I think the reason Merck doesn't change the dose again is because of the first court battle they had with Actavis. Too much of a headache for them legally. They probably figure people will cut the pills anyway. If I were them I would want more money.....

 

[xRedStaRx]

University finally found the Gormley et al. paper I requested, if anyone wants a copy I can scan with my smartphone and email it. First author is a Merck scientist. Conclusion is that even a dose of 0.1 is likely to reach the same DHT inhibition as 1mg, but it would take longer to reach the level of suppression whereas 1mg reaches it after 1 dose. 0.2 mg reaches the same level as 1mg after two doses.

That being said, I think the reason Merck doesn't change the dose again is because of the first court battle they had with Actavis. Too much of a headache for them legally. They probably figure people will cut the pills anyway. If I were them I would want more money.....

Interesting find, goes in hand with the figure I put up earlier.

It would be nice if you could attach it here.

 

[californiaoceans911]

Interesting find, goes in hand with the figure I put up earlier.

It would be nice if you could attach it here.

This Gormley et al. paper is the original source of that figure. Research done by Gormley and Stoner of Merck. I'll scan it when I get to work tomorrow.

- - - Updated - - -

I am trying to upload the paper, but it only allows 19.5 kilobytes

It is 8.5 megabytes, and even when I try to reduce it I can only get it down to 2.5 megabytes. Any suggestions?

 

[superhairy]

This Gormley et al. paper is the original source of that figure. Research done by Gormley and Stoner of Merck. I'll scan it when I get to work tomorrow.

- - - Updated - - -

I am trying to upload the paper, but it only allows 19.5 kilobytes

It is 8.5 megabytes, and even when I try to reduce it I can only get it down to 2.5 megabytes. Any suggestions?

I don't think you can compress it this low.
Just upload it in dropbox or in a free hosting website?

But interesting thread. Does a 0.1mg dose bring the same results as a 1mg dose in the long term?

 

[xRedStaRx]

I don't think you can compress it this low.
Just upload it in dropbox or in a free hosting website?

But interesting thread. Does a 0.1mg dose bring the same results as a 1mg dose in the long term?

No.

~0.5mg ED was probably the closest thing to 1 mg ED with almost the same results.

There should be a threshold level of DHT where male pattern baldness is not triggered. Presumably, all effective doses of finasteride should work well in that regard. Which is above and including 0.05mg.

- - - Updated - - -

This Gormley et al. paper is the original source of that figure. Research done by Gormley and Stoner of Merck. I'll scan it when I get to work tomorrow.

- - - Updated - - -

I am trying to upload the paper, but it only allows 19.5 kilobytes

It is 8.5 megabytes, and even when I try to reduce it I can only get it down to 2.5 megabytes. Any suggestions?

Upload it here and paste the link.

http://tinyupload.com/

 

[californiaoceans911]

No.

~0.5mg ED was probably the closest thing to 1 mg ED with almost the same results.

There should be a threshold level of DHT where male pattern baldness is not triggered. Presumably, all effective doses of finasteride should work well in that regard. Which is above and including 0.05mg.

I think 0.2 mg ED was about 80% as effective in HAIR REGROWTH as 1 mg ED, but any dose over 0.04 mg is thought to reach the same level of DHT inhibition as 1mg after a couple of weeks.


Here is the Gormley paper:

http://s000.tinyupload.com/?file_id=05291166525636673775


I wonder if I can create a zip file full of finasteride and ketaconazole papers and upload it for the community.

 

[aero1976]

I think 0.2 mg ED was about 80% as effective in HAIR REGROWTH as 1 mg ED, but any dose over 0.04 mg is thought to reach the same level of DHT inhibition as 1mg after a couple of weeks.


Here is the Gormley paper:

http://s000.tinyupload.com/?file_id=05291166525636673775


I wonder if I can create a zip file full of finasteride and ketaconazole papers and upload it for the community.

You said you went to college, right? Took statistics? Then you know there is a world of difference between 80% of effectiveness and being effective, which 1mg is. The more relevant statistic is taking any will hurt your liver if in fact it will.

 

[californiaoceans911]

You said you went to college, right? Took statistics? Then you know there is a world of difference between 80% of effectiveness and being effective, which 1mg is. The more relevant statistic is taking any will hurt your liver if in fact it will.

No I didn't take statistics in college, my courses started a few notches above statistics. You're trying to use semantics to break down my argument, and it just makes you look silly. If it wasn't clear before I'll make it more clear for you. I'll put it in caps so maybe you'll read it a few times and get the point.

CLINICAL STUDIES BY ROBERTS ET AL. AND LEYDEN ET AL. HAVE SHOWN THAT DOSES BELOW 1 mg ARE EFFECTIVE AT HALTING HAIR LOSS AND REGROWTH OF HAIR IN THE VERTEX AND FRONTAL SCALP.

PARTICULARLY, ROBERTS ET AL. SHOWED THAT AFTER 6 MONTHS AND 12 MONTHS, PATIENTS ON 0.2 mg of FINASTERIDE REGREW ROUGHLY 80% AS MUCH HAIR ON THEIR VERTEX AS THOSE PATIENTS ON 1 mg. EVEN A DOSE OF 0.01 mg WAS STATISTICALLY EFFECTIVE AT SLOWING DOWN HAIR LOSS RELATIVE TO THE PLACEBO GROUP.

The reason 1 mg is prescribed is because the drug was believed to be very safe and well tolerated, and obvious Merck, Sharp, and Co. wanted the drug to be as powerful as possible so that it would be as effective as possible for the largest statistical group of people. NOT EVERYONE NEEDS 1 mg and NOT EVERYONE WILL SEE RESULTS ON 1 mg. Now please STFU and stop going on every thread annoying people.

I keep citing research and you keep citing "some doctor told me this". It's annoying.

 

[aero1976]

No I didn't take statistics in college, my courses started a few notches above statistics.

I was mistaken. I thought you had gone to college. Anyone who "starts a few notches" above a base course is assumed and usually tested to make sure they have the base knowledge of the base class. Next time when you make up a story for yourself learn these things first. My comment about my doctor in another thread was spot on. Short of another doctor posting, he does know more than you.

People come here to find out the basics of hair loss and learn. You pretending to be knowledgeable is irresponsible. There is no reason to risk taking a drug in a way that diminishes what the original study found should you be taking. Once you get through a Stat class you will understand 80% effectiveness is not 80% of the good of a whole. To all people who come here and read your crap, et al, caveat emptor

 

[xRedStaRx]

I think 0.2 mg ED was about 80% as effective in HAIR REGROWTH as 1 mg ED, but any dose over 0.04 mg is thought to reach the same level of DHT inhibition as 1mg after a couple of weeks.


Here is the Gormley paper:

http://s000.tinyupload.com/?file_id=05291166525636673775


I wonder if I can create a zip file full of finasteride and ketaconazole papers and upload it for the community.

Yes, 0.2 mg did 80% as good as 1 mg in positive hair counts after six months. I have reason to believe though, that 0.2 mg on the long run should close the gap even more on 1 mg, but I'm not sure if such a study exists for more than 24 weeks on 0.2 mg vs 1 mg.

Serum DHT levels are not an exact correlate to tissue DHT levels, which is what's really important. But it is a fairly good proxy nonetheless. In that sense, 0.2 mg and above are superior to lower doses for their ability to lower intra-follicular DHT levels even further, possibly breaking the critical threshold for some resistant individuals. This is why I always say that 0.5-0.625 mg EOD, or 0.2 mg ED up to 1 mg EOD or 0.5-0.625 mg ED are the optimal doses for treatment, barring in mind a margin of safety for people who do not respond as well to lower doses. I'm currently on 0.625 mg EOD myself with good results.

You said you went to college, right? Took statistics? Then you know there is a world of difference between 80% of effectiveness and being effective, which 1mg is. The more relevant statistic is taking any will hurt your liver if in fact it will.

There isn't a world of difference between 80% and 100% when you consider that hair counts measured in on themselves are maximally achieved at an increase of 60-70 hairs in an area unit with at least a 1,000 follicles for 1 mg. That would be 10 less hairs than the full dose, which is 1% less hair overall

I was mistaken. I thought you had gone to college. Anyone who "starts a few notches" above a base course is assumed and usually tested to make sure they have the base knowledge of the base class. Next time when you make up a story for yourself learn these things first. My comment about my doctor in another thread was spot on. Short of another doctor posting, he does know more than you.

People come here to find out the basics of hair loss and learn. You pretending to be knowledgeable is irresponsible. There is no reason to risk taking a drug in a way that diminishes what the original study found should you be taking. Once you get through a Stat class you will understand 80% effectiveness is not 80% of the good of a whole. To all people who come here and read your crap, et al, caveat emptor

The original study means nothing. Science is not static. New studies are constantly being conducted and updating our pool of knowledge, what a crappy argument you're making.

Doctors don't know as much as you think. I'd venture to say that some internet hair loss posters and the scientists conducting the studies on chemical hair loss treatments are more knowledgeable than your local dermatologist or cosmetic surgeon. They have much more important readings and practices to consider than studying the pharma-dynamics of a suicide enzyme inhibitor.