New Dermaroller Study; Thoughts, comments?

[Armando Jose]

Im Also at week 8 of Rolling! I allready used minoxidil mixed with ascj9 for the last 3,5 years an put mn2% on the hairline 2 times a week. I had good regrowed with this regime, only THE hairs on my temples stayed weak, but i could always Style my hair good and recession wasnt noticable!

i wanted to fill in my temples a bit more and let THE small hairs grow longer, so thats why i started Rolling like a boss till THE temples bleed like a pro! Then 24 hours later i resume my regime!

It looks like im losing ground fast now! Longer hairs on THE temples falling like THE leaves of the tree's in my backyard!

But...... Im Also noticing a ****load of very small vellus hairs among THE hairline, so im hoping this dermarolling is onlycausing a massive shed on my pumpkin and that i get THE full regrowed in a few weeks!

I cant believe that Rolling Will cause permanent loss!!!

so i'll keep Rolling like a pro!

cheers

small vellus hairs growing, .... good signal

please, if you can take some photos

 

[Bombarie]

small vellus hairs growing, .... good signal

please, if you can take some photos

I tried, but when i select a Photo From my phone it wont upload

 

[albert]

It's good to see that everyone starts shedding more or less at the same time (after 7th-9th week), including myself.

Of course if that means that those are hairs that were going to fall and the process is being accelerated to make place for the "new" hairs. But somehow seeing all of you experimenting the same stuff makes me feel a bit more OK about shedding.

I tried, but when i select a Photo From my phone it wont upload

Upload them to imgur.com (for example) and then link it here, it works like a charm.

 

[Kirby]

Are any of the week 7 to 9 shedders on finasteride or dutasteride?

 

[albert]

Are any of the week 7 to 9 shedders on finasteride or dutasteride?

I'm on finasteride.

 

[cursor]

@Princessrambo

Hey, would you advise to use cyanocobalamin or methylcobalamin, as methylcobalamin is the biologically more active form of vitamin B12. But the Study used cyanocobalamin, so I´m unsure which one to use.

Thanks!

 

[ganonford]

Thanks, my few initial sessions resulted in almost no blood, but the last few sessions more and more blood dots are showing up. And yes, I believe I did get a shed around week 7, especially in the front where my hairloss is most pronounced. I'm not on finasteride or dutasteride. I only use minoxidil(0.3ml x 2 to avoid side effects)/Regenepure/Prox-n/Azleaic acid/semen(recent addition) and sometimes my laser helmet.

I was doubtful about your results man, but without finasteride or dutasteride, and with such a small dose of minoxidil, this has to be the work of the dermaroller.

 

[DesperateOne]

Wut!?
Did I really miss that?
Did we really discuss not using Nizoral the first few days after rolling? (I've been using it daily for weeks now :thumbsdown

Why are you using it daily, isn't that thing too strong to use daily? We didn't really agreed, but we mentioned that adding only minoxidil after three days of wounding would be best.

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If any of you guys were truly bald, you would realize the futility of all this "experimentation".

That's true, but if have been paying attention, you would of understood by now that this procedure is meant for those who have hair left, preferably diffuse thinners.

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Hi squeegee. Is the Ketokonazole lotion spoken about in this article Miconazole Nitrate? I'd maybe switch to the lotion rather than the shampoo but when I search Miconazole Nitrate, all i get is vaginal cream! lol

That's because it is pus$y cream, it can be used for other things. Just that 99% if the time it is used as vaginal cream and it smells.

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It's good to see that everyone starts shedding more or less at the same time (after 7th-9th week), including myself.

Of course if that means that those are hairs that were going to fall and the process is being accelerated to make place for the "new" hairs. But somehow seeing all of you experimenting the same stuff makes me feel a bit more OK about shedding.



Upload them to imgur.com (for example) and then link it here, it works like a charm.

Haha yeah, it's a good sign that at least all of us got that shed on month two or so. Remember that the hair that sheds was destined to jump ship roughly about two months prior, that's what Kobren says anyways.

 

[Cody1212]

For what it's worth, I initially wasn't seeing the greatest results with rolling and felt it really crushed all the hair I still had and turned them into weak beaten down hairs and it took a really long time to recover and in the meantime my hair looked like **** and hurts your daily confidence. Well what I have switched to is stamping instead of rolling and this preserves all of the existing hair that I have. I have longer straight hair and maybe it's because of the hair type that this is my case, I just think it might be worth a shot for those not seeing results from rolling to try stamping.

 

[buddyebsen1]

Im Also at week 8 of Rolling! I allready used minoxidil mixed with ascj9 for the last 3,5 years an put mn2% on the hairline 2 times a week. I had good regrowed with this regime, only THE hairs on my temples stayed weak, but i could always Style my hair good and recession wasnt noticable!

That's good news that you had regrowth with your regimen. Can you tell me more about the ascj9? How much did you add to your minoxidil? Also, where did you purchase it?

Thanks!

 

[squeegee]

Squeegee, stop being such a pus$y, you get so mad when someone talks about your **** but you are somehow free to criticize anything you please?
Everyone knows that **** is mainly used as vaginal cream, so why are you getting mad for me saying that? Look man, you're applying pus$y cream in your head, it may work for you, that's not up for discussion, the guy just wanted affirmation that it was indeed pus$y juice, that's all.

Pussy juice? WTf are you talking about? Miconazole Nitrate is a "synthetic" medical ointment that threat infections by inhibiting steroidogenesis. hahahaahahahahahhaah you such a dumb friggin ***.. a real idiot. It is no made of pussy juice. once again you just proved how a ****ing idiot your are on this forum. A pure example of an idiot.. Desperate and pathetic idiot one!


Miconazole is an imidazole antifungal agent, developed by Janssen Pharmaceutica, commonly applied topically to the skin or to mucous membranes to cure fungal infections. It works by inhibiting the synthesis of ergosterol, a critical component of fungal cell membranes. It can also be used against certain species of Leishmania protozoa which are a type of unicellular parasite that also contain ergosterol in their cell membranes. In addition to its antifungal and antiparasitic actions, it also has some limited antibacterial properties. It is marketed in various formulations under various brand names.

Miconazole is also used in Ektachrome film developing in the final rinse of the Kodak E-6 process and similar Fuji CR-56 process, replacing formaldehyde. Fuji Hunt also includes miconazole as a final rinse additive in their formulation of the C-41RA rapid access color negative developing process.

Miconazole is mainly used externally for the treatment of athlete's foot, ringworm and jock itch. Internal application is used for oral or vaginal thrush (yeast infection). The oral gel may also be used for the lip disorder angular cheilitis.

http://en.wikipedia.org/wiki/Miconazole
http://en.wikipedia.org/wiki/Imidazole
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Miconazole Nitrate blocks adrenal steroidogenesis by inhibiting cytochrome P450-dependent enzymes. Just like Keto.




Steroidogenesis:
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/basics/steroidogenesis.html


Econazole and miconazole inhibit steroidogenesis and disrupt steroidogenic acute regulatory (StAR) protein expression post-transcriptionally.

Walsh LP, Kuratko CN, Stocco DM.
Source

Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.

Abstract

The imidazole antifungal drugs econazole and miconazole have previously been shown to disrupt steroidogenesis in Leydig and adrenal cells by inhibiting 17alpha-hydroxylase/17,20-lyase (P450c17) enzyme activity, thus reducing the conversion of progesterone to androstenedione. However, a recent study in Y-1 adrenal cells indicated that these compounds may also reduce the availability of cholesterol to the cytochrome P450 side chain cleavage (P450(scc)) enzyme, the first enzyme in the steroidogenic pathway. Since the steroidogenic acute regulatory protein (StAR) mediates the transfer of cholesterol from the outer to the inner mitochondrial membrane where the P450(scc) enzyme resides, an action which constitutes the rate-limiting and acutely-regulated step in steroidogenesis, we hypothesized that these drugs may also reduce StAR expression and/or activity. Our studies demonstrate that these drugs reversibly inhibited (Bu)(2)cAMP-stimulated progesterone production in a dose- and time-dependent manner in MA-10 cells without affecting total protein synthesis or P450(scc) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) enzyme expression or activity. In contrast, they dramatically decreased (Bu)(2)cAMP-stimulated StAR protein expression post-transcriptionally. This study indicates that StAR protein is susceptible to inhibition by at least some imidazole compounds that inhibit steroidogenesis.
http://www.ncbi.nlm.nih.gov/pubmed/11282276






Steroidogenic isoenzymes in human hair and their potential role in androgenetic alopecia.

Hoffmann R.
Source

Department of Dermatology, Philipp University, Marburg, Germany. rolf.hoffmann@mailer.uni-marburg.de

Abstract

Androgenetic alopecia (Androgenetic Alopecia) is the most common type of hair loss. The relatively strong concordance of the degree of baldness in fathers and sons is not consistent with a simple Mendelian trait, and a polygenic basis is considered to be most likely. So far, the predisposing genes for Androgenetic Alopecia are unknown and we do not understand the molecular steps involved in androgen-dependent beard growth versus androgen-dependent hair loss, but Androgenetic Alopecia can be defined as a dihydrotestosterone (DHT)-dependent process with continuous miniaturization of sensitive hair follicles. The type 2 5alpha-reductase plays a central role by the intrafollicular conversion of testosterone to DHT. However, due to the increasing knowledge in this field, we now know that there are many more steroidogenic enzymes involved in the onset and development of Androgenetic Alopecia, and this article shall provide a critical overview of recent discoveries.
http://www.cunliffe-awards.de/pdfs/publikation_hofmann.pdf
http://www.ncbi.nlm.nih.gov/pubmed/12592073


Steroidogenic enzymes in skin.

Andersson S.
Source

Department of Obstetrics-Gynecology and Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9032, USA. stefan.andersson@UTSouthwestern.edu

Abstract

The gonadal synthesis of testosterone from cholesterol involves four enzymes, namely, cytochrome P-450 side-chain cleavage enzyme, cytochrome P-450 17a-hydroxylase/lyase, 3b-hydroxysteroid dehydrogenase, and 17b-hydroxysteroid dehydrogenase. A significant part of the plasma-borne testosterone is converted in androgen target tissues, such as the skin, to the more potent androgen dihydrotestosterone by the steroid 5a-reductase type 1 and type 2 isoenzymes. Dihydrotestosterone, which binds to the nuclear androgen receptor with much greater affinity than testosterone, is the androgen responsible for a process leading to androgenetic alopecia. Consequently, the 5a-reductase inhibitor finasteride was developed and has proven efficacious in promoting hair growth as a consequence of lowering scalp and plasma dihydrotestosterone levels. In contrast to the direct synthesis of dihydrotestosterone from testosterone, biologically inactive C19-steroids produced by glandular and peripheral tissues may also feed into the scalp skin production of dihydrotestosterone by the local expression of reductive 17b-hydroxysteroid dehydrogenase, oxidative 3a-hydroxysteroid dehydrogenase, and 3b-hydroxysteroid dehydrogenase enzymes. Aberrant expression of one or more of these enzymes, could conceivably result in increased scalp dihydrotestosterone levels, and possibly, acceleration of the balding process in genetically predisposed men and women.




http://www.ncbi.nlm.nih.gov/pubmed/11399532

Human skin is a steroidogenic tissue: steroidogenic enzymes and cofactors are expressed in epidermis, normal sebocytes, and an immortalized sebocyte cell line (SEB-1).

Thiboutot D, Jabara S, McAllister JM, Sivarajah A, Gilliland K, Cong Z, Clawson G.
Source

Department of Dermatology, The Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA. dthiboutot@psu.edu

Abstract

Although the human sebaceous gland can synthesize cholesterol from acetate and can further metabolize steroids such as dehydroepiandrosterone into potent androgens, the de novo production of steroids from cholesterol has not been demonstrated in human skin. The goal of this study was to delineate the steroidogenic pathway upstream from dehydroepiandrosterone by documenting the presence of members of the P450 side chain cleavage system (P450scc). This system catalyzes the initial step in steroid hormone synthesis following translocation of cholesterol to the inner mitochondrial membrane. In concert with its cofactors, adrenodoxin and adrenodoxin reductase, and the transcription factor steroidogenic factor 1, P450scc converts cholesterol to pregnenolone. An SV40 immortalized human sebaceous gland cell line (SEB-1) was established in order to facilitate investigation of the P450scc system. The sebaceous phenotype of SEB-1 sebocytes was confirmed using immunohistochemistry, Oil Red O staining, and gene array expression analysis. Presence of P450scc, adrenodoxin reductase, cytochrome P450 17-hydroxylase (P450c17), and steroidogenic factor 1 was documented in human facial skin, human sebocytes, and SEB-1 sebocytes. Using immunohistochemistry, antibodies to the above proteins localized to epidermis, hair follicles, sebaceous ducts, and sebaceous glands in sections of facial skin. Results of immunohistochemistry were confirmed with Western blotting. Biochemical activity of cytochrome P450scc and P450c17 was demonstrated in SEB-1 sebocytes using radioimmunoassay. The relative abundance of mRNA for P450scc, P450c17, and steroidogenic factor 1 in SEB-1 sebocytes and sebaceous glands was compared to mRNA levels in ovarian theca and granulosa cells using real-time quantitative polymerase chain reaction. Gene array expression analysis and quantitative polymerase chain reaction indicated that mRNA for P450scc is more abundant than mRNA for both P450c17 and steroidogenic factor 1 in sebaceous glands and SEB-1 cells. These data demonstrate that the skin is in fact a steroidogenic tissue. The clinical significance of this finding in mediating androgenic skin disorders such as acne, hirsutism, or androgenetic alopecia remains to be established.

http://www.ncbi.nlm.nih.gov/pubmed/12787114


Molecular mechanisms of androgenetic alopecia
http://www.derma-haarcenter.ch/files/Directory/Publikationen/Androgenetic+alopecia.pdf



Higher Levels of Steroidogenic Acute Regulatory Protein and Type I 3

-Hydroxysteroid Dehydrogenase in the Scalp of Men with Androgenetic Alopecia

http://www.nature.com/jid/journal/v126/n10/full/5700442a.html


Cutaneous Androgen Metabolism: Basic Research
and Clinical Perspectives

http://www.klinikum-dessau.de/fileadmin/user_upload/Hautklinik/PDF-Files/157_androgens.pdf



The human skin as a hormone target and an endocrine gland

Christos C. Zouboulis
Department of Dermatology, Charité University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany
Abstract
Hormones influence the development and function of human skin which also produces and releases hormones. Recently attention has been focused on identifying and understanding the complex endocrine properties of human skin, such as expression and function of specific hormone receptors, synthesis of hormones from major classes of compounds used by the body for general purposes, organized metabolism, activation, inactivation and elimination of the hormones in specialized cells of the tissue, exertion of biological activity and release of tissue hormones in the circulation. Specifically, hormones exert their biological effects on the skin through interaction with high-affinity receptors, such as several receptors for peptide hormones and neurotransmitters, steroid and thyroid hormones. Hormones exhibit a wide range of biological activities on the skin with distinct effects caused by growth hormone/insulin-like growth factor-I, neuropeptides, sex steroids, glucocorticoids, retinoids, vitamin D, peroxisome proliferator-activated receptor ligands, eicosanoids, melatonin and serotonin. Human skin produces, activates or inactivates metabolically numerous hormones which are probably important for skin functions but also for functions of the entire human organism, such as sex hormones, especially in aged individuals, insulin-like growth factor and -binding proteins, neuropeptides, prolactin, catecholamines, retinoids, steroids, vitamin D and eicosanoids. These functions are undertaken in most cases by different skin cell populations in a coordinated way, indicating the endocrine autonomy of the skin. Characteristic examples are the metabolic pathways of the corticotropin-releasing hormone/propiomelanocortin axis, steroidogenesis, vitamin D and retinoids. The human skin is, thus, the largest, peripheral endocrine organ.

http://www.hormones.gr/49/article/article.html



Ketoconazole blocks adrenal steroidogenesis by inhibiting cytochrome P450-dependent enzymes.



Abstract

Ketoconazole has recently been shown to interfere with steroidogenesis in patients and rat in vitro systems. In this study we attempted to elucidate the site of inhibition in the adrenal gland. Although ketoconazole impaired adrenocorticotropic hormone stimulated cyclic (c)AMP production, dibutyrl cAMP addition did not bypass the steroidogenic blockade indicating that the critical ketoconazole-inhibited step was distal to cAMP. Addition of radiolabeled substrates to isolated adrenal cells and analysis of products by high performance liquid chromatography demonstrated a ketoconazole block between deoxycorticosterone (Doctor) and corticosterone. This 11-hydroxylase step is carried out by a P450-dependent mitochondrial enzyme. No restriction of progesterone or pregnenolone conversion to Doctor was detected, steps carried out by non-P450-dependent microsomal enzymes. Inhibition of cholesterol conversion to pregnenolone by mitochondrial fractions indicated a second block at the side chain cleavage step, another mitochondrial P450-dependent enzyme. Adrenal malate dehydrogenase, a non-P450-dependent mitochondrial enzyme was not inhibited while renal 24-hydroxylase, a P450-dependent mitochondrial enzyme in another organ, was blocked by ketoconazole. We conclude that ketoconazole may be a general inhibitor of mitochondrial P450 enzymes. This finding suggests that patients receiving ketoconazole be monitored for side effects relevant to P450 enzyme inhibition. Further, we raise the possibility that this drug action may be beneficially exploited in situations where inhibition of steroidogenesis is a therapeutic goal.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC437014/


The effect of ketoconazole on steroidogenesis: I. Leydig cell enzyme activity in vitro.

Albertson BD, Frederick KL, Maronian NC, Feuillan P, Schorer S, Dunn JF, Loriaux DL.
Source

Developmental Endocrinology Branch, NICHD, NIH, Bethesda, Maryland 20892.

Abstract

The in vitro inhibition of Leydig cell microsomal steroidogenesis by ketoconazole, a potent P-450 dependent enzyme blocker, was evaluated in the human, stallion and pig. Purified Leydig cells were isolated by mechanical dispersion of teased, decapsulated whole testes and sieving through a 0.25 mm stainless steel mesh. The activity of 3 beta-hydroxysteroid dehydrogenase/isomerase (3 beta-HSD), 17-hydroxylase (17-OHase), 17,20-desmolase (17,20D), 17-ketosteroid reductase (17-KSR) and aromatase were measured using a constant amount (50 microM) of 14C-labelled substrates in the presence of varying concentrations of pure ketoconazole. Products were isolated by thin layer chromatography and verified by derivative formation. 17-OHase and 17,20D activities were significantly inhibited (p less than .001) by ketoconazole at concentrations as low as 5 microM. 3 beta-HSD, 17-KSR and aromatase activities were only significantly inhibited by ketoconazole at concentrations of 500 and 5000 microM. These data describe the specific loci of inhibition of ketoconazole on testicular steroidogenesis and confirm the observations that ketoconazole is an effective inhibitor of androgen biosynthesis in several species.

http://www.ncbi.nlm.nih.gov/pubmed/3262906


The influence of ketoconazole on human adrenal steroidogenesis: incubation studies with tissue slices


Summary. objective The influence of ketoconazole on the various enzymes of human adrenal steroid biosynthesis was examined in vitro.

measurements After Incubation of human adrenal tissue slices with labelled precursors and ketoconazole (0–2000 μM), radioactive metabolites were separated by thin-layer chromatography and quantified by liquid scintillation counting. Enzyme activity was assessed by measuring conversion of tritium-labelled precursors to products.

resultsIn vitro, ketoconazole showed a significant Inhibition on the following adrenal enzyme systems (with decreasing activity): C17,20-desmolase (IC[SUB]50[/SUB] 2 μM), 16α-hydroxylase (IC[SUB]50[/SUB] 9 μM), 17α-hydroxylase (IC[SUB]50[/SUB] 18 μM), 18-hydroxylase (IC[SUB]50[/SUB] 28 μM), and 11 β-hydroxylase (IC[SUB]50[/SUB] 35 μM). In the tested concentrations ketoconazole had no Inhibitory effect on the 21-hydroxylase, the 3β-hydroxysteroid dehydrogenase and the 20-hydroxysteroid dehydrogenase component of the C17,20-desmolase enzyme system.


conclusions

The data are in accordance with clinical findings where a strong suppression of serum androgen levels by relatively selective inhibition of C17,20-desmolase has been assumed. The predominant blocking effect of ketoconazole on adrenal as well as on gonadal androgen biosynthesis might be of clinical benefit in the management of hyperandrogenic states.

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.1991.tb03516.x/abstract

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Reversal of androgenetic alopecia by

topical ketoconzole: Relevance of anti-
androgenic activity

http://www.netwidesales.com/pdf/hairloss/nizoral_shampoo_ketoconazole.pdf



Effect of antifungal drugs on cytochrome P450 (CYP) 2C9, CYP2C19, and CYP3A4 activities in human liver microsomes.

Niwa T, Shiraga T, Takagi A.
Source

Post-marketing Development Research Center, Fujisawa Pharmaceutical Co., Ltd., Osaka, Japan. toshiro.niwa@jp.astellas.com

Abstract

The effects of five antifungal drugs, fluconazole, itraconazole, micafungin, miconazole, and voriconazole, on cytochrome P450 (CYP) 2C9-mediated tolbutamide hydroxylation, CYP2C19-mediated S-mephenytoin 4'-hydroxylation, and CYP3A4-mediated nifedipine oxidation activities in human liver microsomes were compared. In addition, the effects of preincubation were estimated to investigate the mechanism-based inhibition. The IC50 value against tolbutamide hydroxylation was the lowest for miconazole (2.0 microM), followed by voriconazole (8.4 microM) and fluconazole (30.3 microM). Similarly, the IC50 value against S-mephenytoin 4'-hydroxylation was the lowest for miconazole (0.33 microM), followed by voriconazole (8.7 microM) and fluconazole (12.3 microM). On the other hand, micafungin at a concentration of 10 or 25 microM neither inhibited nor stimulated tolbutamide hydroxylation and S-mephenytoin 4'-hydroxylation, and the IC50 values for itraconazole against these were greater than 10 microM. These results suggest that miconazole is the strongest inhibitor of CYP2C9 and CYP2C19, followed by voriconazole and fluconazole, whereas micafungin would not cause clinically significant interactions with other drugs that are metabolized by CYP2C9 or CYP2C19 via the inhibition of metabolism. The IC50 value of voriconazole against nifedipine oxidation was comparable with that of fluconazole and micafungin and higher than that of itraconazole and miconazole. The stimulation of the inhibition of CYP2C9-, CYP2C19-, or CYP3A4-mediated reactions by 15-min preincubation was not observed for any of the antifungal drugs, suggesting that these drugs are not mechanism-based inhibitors.

http://www.ncbi.nlm.nih.gov/pubmed/16141567

 

[DesperateOne]

Pus$y juice as Mico being that, not that it literally contained that, sigh. Ask anyone you know and 99% of people will tell you it is used as a vaginal cream, hence you enjoy applying vaginal cream. I stated that it may work, but you seem to only comprehend things you like. My point is, its primary is as a pus$y cream, no abstract medical journals are going to change that. So stop trying to defend your pus$y juice already.

 

[Agahi]

im loling here you guys are too much.

 

[karankaran]

Guys, please do not kill pus$y for me lol...

 

[DesperateOne]

I wish I can slap your little **** face until your passed out crying. yeah bitchslap. The drug is used to threat infections , yeast infections included. What is the big deal about it? Grow up little maggot.

There is no big deal, you made it a big deal, as you always do when someone metions your snatch lube.

Read first, I answered that guys question, I never mentioned you or anything, he was the first to mention vaginal cream. Then you come in barking and acting all tough like you always do, stupid little French man.
I am not against anyone using it, you just go beserk when someone mentions its primary use.

So far we can conclude one thing, it may not thicken up your hair or it might, but it defenetively thickens up your skull.

 

[Sparky4444]

...I saw this at the drug store...so you can buy it off the shelf and just apply it once per day???

 

[badgenetics1]

Can we please not let this thread devolve into a shouting match again? This thread almost got closed once, and I'm pretty sure none of us want that given what a great resource it has been for all of us. Can the insults/fights be done over PMs and not this thread?

 

[closetmetrosexual]

Why are you using it daily, isn't that thing too strong to use daily? We didn't really agreed, but we mentioned that adding only minoxidil after three days of wounding would be best.

I don't know if its too strong.
Daily use has not given me irritation or anything that I've noticed.

 

[Jlyncher]

Sparta!!!!!

God, I love rolling day!

 

[karankaran]

guys, i am worried if all the hair that is falling out coz of rolling , what if it does not grow back :-(