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- 967
What minoxidil are you using @Somebody? watched your video where you put Foligain foam into the bottle with a pin, still doing that?
Somebody's Story | 25 Finasteride Results | 7 Mo Treatment (pics)
- Thread starter Somebody
- Start date
What minoxidil are you using @Somebody? watched your video where you put Foligain foam into the bottle with a pin, still doing that?
- Reaction score
- 967
Yeah again, but Somebody is doing it everyday, so you can't deny that everyday works.
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Where do you guys buy perilla?
Also what other anti inflammation stuff has somebody used? Hesistent to use salicylic acid shampoo as wouldn’t it limit pge?
Also what other anti inflammation stuff has somebody used? Hesistent to use salicylic acid shampoo as wouldn’t it limit pge?
- Reaction score
- 967
Google ‘Perilla Allermin’, you should get some results from a couple of stores who are selling perilla leaves in capsules.
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- 133
My perilla is coming in the mail, in the mean time using Claritin... also shampooing with tea tree/peppermint oil shampoo followed by a mix of Argan oil shampoo with Alpecin.
My inflammation is ALMOST gone. I get a light bit of irritation a few time an hour. Hopefully as my hormones keep coming into balance I’ll keep improving... anything I can add? I feel like if I can completely kill the inflammation I’ll get great regrowth from dermarolling+rogaine
My inflammation is ALMOST gone. I get a light bit of irritation a few time an hour. Hopefully as my hormones keep coming into balance I’ll keep improving... anything I can add? I feel like if I can completely kill the inflammation I’ll get great regrowth from dermarolling+rogaine
- Reaction score
- 133
I feel like my only goal in life currently is to have the thickness to pull off somebody’s slicked back look lol. Don’t think I’ll ever regrow my nw2 temples but I would really like to have the thickness...
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- 133
Hey dude just curious how your hair is doing... I remember you had some really nasty inflammation on avodart, since you’ve dealt with that are you getting regrowth?
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My itch is pretty much gone. I guess duta started working or/and combo of perilla/taurine/omega3. No regrowth, but a least I have a feeling that it’s not becoming worse.
Nice. Are you on minoxidil? Strongly recommended if you are dermarolling.
What needle size are you using?
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Just dermarolling. I’m gonna start with minoxidil in november just to see what dutasteride did after a year. If some miracle happens ( which is highly unlikely) and I got some regrowth, I will stay away from minoxidil. If not, I’m gonna use minoxidil and pray for a good response.
I’m using 1.5mm just to get used to it.
Light pressure till some drops of blood appears. Apply minoxidil right after
Thats good but minoxidil its key for regrowth.
Used minoxidil in the past (without wounding of course) and it didnt do jack sh*t on its own.
Its the synergy with skin disruption doing the trick for me.
BTW, 1.5mm its what im using too. Its the ideal depth for light wounding.
Never had any problem.
- Reaction score
- 967
How many times/week are you dermarolling? Are you doing the same way somebody does (=everyday)?
Once per week. Sometimes twice not more.
My approach is light to moderate dermarolling sessions, and stop right after little drops of blood appears.
Im really convinced its not necessary to wound hard. I mean there are obviously cases of success when people butcher their head but i learned antiandrogens combined with minoxidil can boost results to the same degree.
Dry hair in my case.
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5α-Reductase inhibitors like finasteride and dutasteride inhibit 5α-reductase type II and/or other isoforms and are able to decrease circulating DHT levels by 65 to 98% depending on the 5α-reductase inhibitor in question.[26][27][28][20] As such, similarly to the case of 5α-reductase type II deficiency, they provide useful insights in the elucidation of the biological functions of DHT.[29] 5α-Reductase inhibitors were developed and are used primarily for the treatment of BPH. The drugs are able to significantly reduce the size of the prostate gland and to alleviate symptoms of the condition.[14][30] Long-term treatment with 5α-reductase inhibitors is also able to significantly reduce the overall risk of prostate cancer, although a simultaneous small increase in the risk of certain high-grade tumors has been observed.[15] In addition to prostate diseases, 5α-reductase inhibitors have subsequently been developed and introduced for the treatment of pattern hair loss in men.[31] They are able to prevent further progression of hair loss in most men with the condition and to produce some recovery of hair in about two-thirds of men.[13] 5α-Reductase inhibitors seem to be less effective for pattern hair loss in women on the other hand, although they do still show some effectiveness.[32] Aside from pattern hair loss, the drugs are also useful in the treatment of hirsutism and can greatly reduce facial and body hair growth in women with the condition.[33][16]
5α-Reductase inhibitors are overall well-tolerated and show a low incidence of adverse effects.[34] Sexual dysfunction, including erectile dysfunction, loss of libido, and reduced ejaculate volume, may occur in 3.4 to 15.8% of men treated with finasteride or dutasteride.[34][35] A small increase in the risk of affective symptoms including depression, anxiety, and self-harm may be seen.[36][37][38] Both the sexual dysfunction and affective symptoms may be due partially or fully to prevention of the synthesis of neurosteroids like allopregnanolone rather necessarily than due to inhibition of DHT production.[36] A very small risk of gynecomastia has been associated with 5α-reductase inhibitors (1.2 to 3.5%).[34][39] Based on reports of 5α-reductase type II deficiency in males and the effectiveness of 5α-reductase inhibitors for hirsutism in women, reduced body and/or facial hair growth is a likely potential side effect of these drugs in men.[13][16] There are very few studies evaluating the side effects of 5α-reductase inhibitors in women. However, due to the known role of DHT in male sexual differentiation, 5α-reductase inhibitors may cause birth defects such as ambiguous genitalia in the male fetuses of pregnant women. As such, they are not used in women during pregnancy.[34]
MK-386 is a selective 5α-reductase type I inhibitor which was never marketed.[40] Whereas 5α-reductase type II inhibitors achieve much higher reductions in circulating DHT production, MK-386 decreases circulating DHT levels by 20 to 30%.[41] Conversely, it was found to decrease sebum DHT levels by 55% in men versus a modest reduction of only 15% for finasteride.[42][43] However, MK-386 failed to show significant effectiveness in a subsequent clinical study for the treatment of acne.[44]
Biological activity[edit]
DHT is a potent agonist of the AR, and is in fact the most potent known endogenous ligand of the receptor. It has an affinity (Kd) of 0.25 to 0.5 nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0 nM)[45] and 15–30 times higher than that of adrenal androgens.[46] In addition, the dissociation rate of DHT from the AR is 5-fold slower than that of testosterone.[47] The EC50 of DHT for activation of the AR is 0.13 nM, which is about 5-fold stronger than that of testosterone (EC50 = 0.66 nM).[48] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[45]
The elimination half-life of DHT in the body (53 minutes) is longer than that of testosterone (34 minutes), and this may account for some of the difference in their potency.[49] A study of transdermal DHT and testosterone treatment reported terminal half-lives of 2.83 hours and 1.29 hours, respectively.[50]
Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase into an estrogen like estradiol. Therefore, it is frequently used in research settings to distinguish between the effects of testosterone caused by binding to the AR and those caused by testosterone's conversion to estradiol and subsequent binding to and activation of ERs.[51] Although DHT cannot be aromatized, it is still transformed into metabolites with significant ER affinity and activity. These are 3α-androstanediol and 3β-androstanediol, which are predominant agonists of the ERβ.[17]
Biochemistry
5α-Reductase inhibitors are overall well-tolerated and show a low incidence of adverse effects.[34] Sexual dysfunction, including erectile dysfunction, loss of libido, and reduced ejaculate volume, may occur in 3.4 to 15.8% of men treated with finasteride or dutasteride.[34][35] A small increase in the risk of affective symptoms including depression, anxiety, and self-harm may be seen.[36][37][38] Both the sexual dysfunction and affective symptoms may be due partially or fully to prevention of the synthesis of neurosteroids like allopregnanolone rather necessarily than due to inhibition of DHT production.[36] A very small risk of gynecomastia has been associated with 5α-reductase inhibitors (1.2 to 3.5%).[34][39] Based on reports of 5α-reductase type II deficiency in males and the effectiveness of 5α-reductase inhibitors for hirsutism in women, reduced body and/or facial hair growth is a likely potential side effect of these drugs in men.[13][16] There are very few studies evaluating the side effects of 5α-reductase inhibitors in women. However, due to the known role of DHT in male sexual differentiation, 5α-reductase inhibitors may cause birth defects such as ambiguous genitalia in the male fetuses of pregnant women. As such, they are not used in women during pregnancy.[34]
MK-386 is a selective 5α-reductase type I inhibitor which was never marketed.[40] Whereas 5α-reductase type II inhibitors achieve much higher reductions in circulating DHT production, MK-386 decreases circulating DHT levels by 20 to 30%.[41] Conversely, it was found to decrease sebum DHT levels by 55% in men versus a modest reduction of only 15% for finasteride.[42][43] However, MK-386 failed to show significant effectiveness in a subsequent clinical study for the treatment of acne.[44]
Biological activity[edit]
DHT is a potent agonist of the AR, and is in fact the most potent known endogenous ligand of the receptor. It has an affinity (Kd) of 0.25 to 0.5 nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0 nM)[45] and 15–30 times higher than that of adrenal androgens.[46] In addition, the dissociation rate of DHT from the AR is 5-fold slower than that of testosterone.[47] The EC50 of DHT for activation of the AR is 0.13 nM, which is about 5-fold stronger than that of testosterone (EC50 = 0.66 nM).[48] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[45]
The elimination half-life of DHT in the body (53 minutes) is longer than that of testosterone (34 minutes), and this may account for some of the difference in their potency.[49] A study of transdermal DHT and testosterone treatment reported terminal half-lives of 2.83 hours and 1.29 hours, respectively.[50]
Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase into an estrogen like estradiol. Therefore, it is frequently used in research settings to distinguish between the effects of testosterone caused by binding to the AR and those caused by testosterone's conversion to estradiol and subsequent binding to and activation of ERs.[51] Although DHT cannot be aromatized, it is still transformed into metabolites with significant ER affinity and activity. These are 3α-androstanediol and 3β-androstanediol, which are predominant agonists of the ERβ.[17]
Biochemistry
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Little update,
I was derma rolling for about a month and a half, two months now. minoxidil for about 4. Not sure if its derma rolling or just the consistent minoxidil use, but my shedding has practically halted, regrowth is hard to tell but I've been using 1.5 consistently every night and followed with minoxidil right after.
recently haven't been rolling as hard, still hurts like crazy for me. Anyone think it'd be bad to use some numbing gel? any tips for the pain? thanks
I was derma rolling for about a month and a half, two months now. minoxidil for about 4. Not sure if its derma rolling or just the consistent minoxidil use, but my shedding has practically halted, regrowth is hard to tell but I've been using 1.5 consistently every night and followed with minoxidil right after.
recently haven't been rolling as hard, still hurts like crazy for me. Anyone think it'd be bad to use some numbing gel? any tips for the pain? thanks