Almost perfect? Why did you start with propecia then?
Somebody's Story | 25 Finasteride Results | 7 Mo Treatment (pics)
- Thread starter Somebody
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Almost perfect? Why did you start with propecia then?
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Man @Somebody I have been doing your daily rolling for absorption method for about 3 months now and my hair basically looks no different than before I started. Maybe a few extra wispy looking hairs but nothing that seems to be cosmetically relevant. Results with this method are supposed to happen pretty quickly, no?
I may have just already maxed out my regrowth potential on the big 3 prior to starting. I'm trying to decide if it's worth me continuing on with this for another few months and see if anything worthwhile comes of it. I don't really want to continue exposing my scalp to needles every day if I'm getting no benefit from it
I may have just already maxed out my regrowth potential on the big 3 prior to starting. I'm trying to decide if it's worth me continuing on with this for another few months and see if anything worthwhile comes of it. I don't really want to continue exposing my scalp to needles every day if I'm getting no benefit from it
What about vitaminis?
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hey somebody! nice thread and progress your hair is perfect congrats
couple of questions.
How long do you wait before applying minoxidil after you dermaroll everynight?
this might be strange but do you have any tips for finding Perilla leaves in Australia? lol. I can only find Perilla oil supps online.
thanks man, keep up the fight. You're an inspiration
couple of questions.
How long do you wait before applying minoxidil after you dermaroll everynight?
this might be strange but do you have any tips for finding Perilla leaves in Australia? lol. I can only find Perilla oil supps online.
thanks man, keep up the fight. You're an inspiration
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I think I'm just going to cut back on the rolling some as I do think it has made some new hairs appear (albeit not cosmetically helping hairs at this point)
I think I'll take 2-3 days off from rolling to let my scalp kind of "reset", then go to doing it somewhere between 3-5 days a week
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Just found two pictures in old usb drive. Both are from 2004. I was 19 half at that time. As I look back to hair loss timeline, I think I had really agresseive hair loss between 2003-2005 and that it stabilazed between 2006-2007 and afterwords it accelated again, to finaly I did take action in end of 2008 and got propecia.
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If you can respond to your opinion I would be very happy
https://www.hairlosstalk.com/intera...estion-about-side-effects-of-propecia.111422/
https://www.hairlosstalk.com/intera...estion-about-side-effects-of-propecia.111422/
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Hey somebody thanks for answering my minoxidil question, I have 2 more questions do you drink perilla leaf tea as well? and does the egg mask really reduce oily scalp? thanks again brother.
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Yes, from time to time I do drink perilla as tea. But I prefer coffee. The way I take perilla powder is as folllowing: in morning on empty stomach and I drink it down with water. About egg white mask, yes it should work. I have got postive feedback from others who have tried it. From my experice it's good for reducing light inflammation. Also you can google up benifits of applying egg white mask.
Ok, so it's a year and a half now since the first post, how many people have a new head of hair? Anyone had great results at all besides Somebody using this method? Anybody? I'm 14 months in with zero new hair, and I'm a fanatic, never missed a single day. I would love it if maybe a few more guys had some great results, but I see the same questions being answered today as they were a year ago. Maybe the guys who grew hair left when they got results??? Or it just doesn't work. Fire away
What defines Somebody's method? Only thing I've added since I started to follow this thread (unregistered hehe) is perilla which may or may not help out. derma + minoxidil I did before.
I am getting zero gains since I started the hair treatment journey in July last year so there isn't really any bulletproof method.
Granted, Somebody's story is phenomenal and a great follow.
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I'm going away from the every day plan back to the once or twice a week plan of doing it less but harder. Also I'm not going to apply it straight after, going to wait half a day at least. Heard that applying directly afterwards actually cancels out all the effects of dermarolling, but again it's a theory. Like you say, there's no bulletproof method. I just know that my hair is terrible, it's actually worse now than when I started, so I have to try something different. I wish it worked like Somebody, but he just got lucky I suppose. Will keep you updated on the new programme, this is week 2 now
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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]
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]
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Damn your hairline is gorgeous dude. No homo. I'm super jelly
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To be far, the lighting is a little different in the pictures. Hair still looks great though.