The number of grafts depends upon (1) the thickness of your hair (fine, medium or coarse), (2) the donor density which tells the doctor how many hairs are present per follicular unit and (3) where the center hairline belongs (I don’t see the highest crease of the furrowed brow to measure the appropriate distances). Based upon these three factors and assuming that the center hairline is now in its final position, I would guess that the number of grafts (assuming that the grafts average 2.2 hairs/graft), that it would take 1700-2700 grafts (more if the hair is fine and less if the hair is coarse).
I also experienced shock loss behind the native grafts (even with using Fin before, during, and still on now as a preventative measure). I think this hair is growing back, but there is still significant shock loss apparent. Online I’ve seen reports that shock loss hair should come back anywhere from 3, 6, 9, to even a year after. Should I still be optimistic that this shock loss hair will grow back, if there still needs to be more regrowth at 7 months out? Thanks.
The hairs that are lost from the shock loss depend upon what type of hairs. Those hairs that were miniaturizing will usually not return even at a year. If you are on finasteride prior to the transplant, shock loss can often be prevented, but normal hairs that might be lost will come back usually in 6-8 months.
Before considering a hair transplant you might want to be evaluated by a dermatologist, possibly getting a biopsy to be sure that the cause of this loss will not also impact any eyebrow hair transplant. The loss of the lateral eyebrow is often a target for a variety of skin and autoimmune disorders. I would need to see your entire hairline looking for problems there as well, such as a loss of vellus hairs in the frontal hairline.
Taken from Reddit.com. My comments: We reported this back in 2011 (https://baldingblog.com/does-botox-prevent-or-reverse-hair-loss/). I read through this article and the three references. Thanks for sending this interesting material to me. I do not understand the mechanism here nor do I feel that any good double blind study is available. There is not enough science to make this a dependable treatment but from the 4 publications, I would expect that more information will be available in the future. I wouldn’t want someone to take on Botox instead of a more traditional treatment and then lose their hair while trying this experimental approach as time is the enemy in genetic hair loss so the longer it goes on, the more is lost. I include as much information as possible for my readership to be able to see and understand that may be coming in the future, even if it is more hope than reality.
https://sci-hub.se/10.1016/j.jaad.2020.04.082
Dihydrotestosterone (DHT) induces transforming growth factor-?1 (TGF-?1) in dermal papilla cells (DPC) to suppress follicular epithelial cell growth. Thus, TGF-?1 is one of the key players in androgenetic alopecia (AGA) and its antagonist may prevent AGA Botulinum toxin type A (BTX) may inhibit TGF-?1 secretion from DPCs as it does with scar tissue fibroblasts, which shares the mesenchymal origin. Recently, BTX has been effective for the treatment of AGA.
Herein, we evaluated the efficacy and safety of intradermal injection of BTX (Nabota®, Daewoong Pharmaceutical, Seoul, Korea) in AGA and its relationship with TGF-?1.
AGA patients were enrolled according to the basic and specific classification. Patients undergoing treatment with finasteride, minoxidil or supplements that affect hair growth were excluded. This study was approved by the institutional review board. The participants received intradermal BTX injections every four weeks for 24 weeks. A total of 30 units of BTX were injected at 20 different sites on the balding scalp in each treatment session.
The expression of TGF-?1 from cultured DPCs under 100 nM DHT was evaluated by RT-PCR analysis. Suppression of DHT-induced TGF-?1 secretion from DPCs by BTX (2.5U/106 46 cell) was assessed by immunofluorescence staining. The doses of BTX in the in vitro study were selected on the basis of a previous report investigating the effect of BTX (2.5U/106 cells) on TGF-?1 secretion from the fibroblasts.
This study comprised 18 male patients with mean age 49.00 ± 6.50. In an unblinded phototrichogram image analysis (Lead M Corp, Seoul, Korea), the number of hairs per cm2 at weeks 0, 12, and 24 were 129.61 ± 28.05, 129.11 ± 28.80, and 136.22 ± 33.05, respectively. The number of hairs significantly increased at week 24 (P = 0.012) but not at week 12 (P = 0.803). Comparison of the pre- and posttreatment photographs showed significant improvement at week 24 (P = 0.031) (Fig. 1). DHT upregulated the TGF-?1 expression of DPCs in 96 hours, whereas BTX downregulated the TGF-?1 expression in 96 hours (Fig. 2). No serious adverse events or changes in laboratory parameters were reported.
DHT-induced synthesis of paracrine mediators (Dkk-1, IL-6, TGF-?1) in balding DPCs may play a role in AGA and represent alternative treatment targets. However, clinical studies targeting these paracrine mediators have not been reported. In our in vitro study, BTX successfully abrogated DHT-induced secretion of TGF-?1 from DPC.
Intradermal injection of BTX was effective against AGA by inhibiting TGF61 ?1 secretion in the hair bulb, which is thought to suppress follicular keratinocyte growth and changes in the hair cycle. Previous studies reported the use of intramuscular BTX injections to treat AGA without elucidating the exact underlying mechanism. Considering the diffusion of the injected liquid BTX and scalp anatomy, even the intramuscular injection may indirectly inhibit the secretion of TGF-?1 from DPCs in the hair bulb. Advanced AGA or elderly age may have adversely influenced our treatment outcome.
In conclusion, we suggest that intradermal injection of botulinum toxin could be a possible treatment option for AGA by inhibiting TGF-?1 secretion from the hair follicles. However, further research and long-term follow-up are required.
Some more botox related info
A Pilot Study to Evaluate Effectiveness of Botulinum Toxin in Treatment of Androgenetic Alopecia in Maleshttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5782443/
A small dose of botulinum toxin A is effective for treating androgenetic alopecia in Chinese patientshttps://sci-hub.se/10.1111/dth.12785
Treatment of Male Pattern Baldness with Botulinum Toxin: A Pilot Studyhttps://journals.lww.com/plasreconsurg/fulltext/2010/11000/Treatment_of_Male_Pattern_Baldness_with_Botulinum.79.aspx
This 10 year study of finasteride in Japanese men is very significant. (1) it revealed improvement and prevention of disease progression in 99.1% of the 532 Japanese men with AGA treated with 1 mg/day finasteride for 10 years, (2) younger patients show more improvement than that of older patients with AGA treatment [24,25]. In this study, AGA patients at the early stage of N-H classification showed more improvement than patients at the later stage did.
https://www.oatext.com/Long-term-(10-year)-efficacy-of-finasteride-in-523-Japanese-men-with-androgenetic-alopecia.php
We evaluated the long-term (10-year) efficacy and safety of AGA treatment with 1 mg/day finasteride in a large study population (532 patients), as the first study of this kind in Japan, to our knowledge. A high objective efficacy was demonstrated by the MGPA, which revealed improvement and prevention of disease progression in 99.1% of the 532 Japanese men with AGA treated with 1 mg/day finasteride for 10 years. Furthermore, the outcome was similar to or better than that reported by other studies in Japan [8-10,13,17]. Differences have been known to occur in the progression of AGA symptoms between Japanese and Caucasian men [8,18]. This efficacy of the investigated treatment in Japanese men exceeded that reported in other studies in Caucasians. The superior response of Japanese men with AGA was reported to likely be attributable to their hair characteristics (greater diameter, black color, and lower density), which facilitated the detection of slight changes [10,19-23]. A novel finding observed in this study was the significant difference in the improvement of AGA following finasteride treatment between the N-H: I/II/III and N-H: IV/V/VI/VII groups at the first visit. The ROC analysis revealed a similar difference, that was performed to classify patients with improvement (MGPA?5) and deteriorating (MGPA<5) condition at year 10 of treatment; the cut-off point was N-H: III (AUC: 0.746). Furthermore, the MGPA of the total study population and the N-H: I/II/III group at the first visit significantly improved from treatment year 5 to 10 (P<0.001). This efficacy was different from that of a 5-year study in Japanese men, which reported that the efficacy began to plateau after 4 years of treatment [10]. Several studies have reported that AGA progresses in N-H classification with age, [7,11,12,18] and that younger patients show more improvement than that of older patients with AGA treatment [24,25]. In this study, AGA patients at the early stage of N-H classification showed more improvement than patients at the later stage did.
The swelling will go away, just give it time. I always use an elastic tape to prevent forehead swelling.
I was wanting to know if you have any information/clinical observations concerning worsening of side effects for patients who continue to take finasteride? I ask this as I am experiencing watery semen. In addition to this, I have an extremely high libido that’s way too high for my own good. In regards to such, I have a very minimal, almost non-existent refractory period after ejaculation. After having sex the first few times around, my erection quality isn’t quite what was pre-finasteride. But this is a side effect that I can very much live with. In your clinic, what observations have you made concerning patients who have manageable side effects? Do they worsen or get better with time? Or is there a general consensus that they stay the same?
Good questions. When the water semen occurs it seems to stay until you sop the finasteride. Some people report it takes 3 months before the water semen goes away. I have seen an increased sex drive from some of my patients, even my own son experienced it. He loved that side ffect.
Most people find either (1) they get accustomed to the finasteride and the side effects eventually reverse, or (2) the side effects continue or even get worse. For those who have a reduced sexual drive or ED, some doctors, including me, feel that the longer the ED on the drug, the more likely that the irreversible PFS becomes a problem (although still a very small number of people fall into this category). For doctors like me who tell the patients with significant ED that can’t mange it on the drug, I tell my patient to stop taking finasteride. As a result, of the thousands of finasteride men I have given the drug to, I have never seen a case of PFS in my practice as many of my colleagues who have similar approaches to such problems.
Im a 17y/o M and I’ve been taking fin and minoxidil from March with great results but I’m going on holiday with friends and my fin isn’t coming on time and all I have is minoxidil will it be enough to maintain my results for 2 weeks, also I expect my minoxidil usage to be inconsistent due to the nature of parties and hangovers do u guys think I’ll be ok.
Finasteride holds its value, even after you stop it for up to 10 days. Never a good idea to stop it. It is small enough to take it with you on vacation, don’t mess with it.
Ive been sitting with my prescription to fin all week and not taken it because Im terrified of the side effects. Ive been doing a ton of reading on it and it seems any side effect is rare. Im also legitimately seeing regrowth in my buddy who told me to go for it. How often have you seen side effects with this over the years? What are some things I should look for should I give in and start?
Im not sure why I am so worried.
If you talk yourself into side effect, the side effects will be 100% nocebo type effect. But if you did as my son did (he just took it and never gave it a thought), he did notice in a week that his sex drive increased significantly and he then called me about it. Normally, negative side effects, when you subtract the placebo group, is under 2% of men taking the drug.
Generally, the dermaroller (the microneedling device) induces Anagen, a single hair cycle and it should be sustained for the duration of the growth cycle. After the hair goes into telogen (about 2-3 years for men and 3-5 years for women), the pre-treatment state should return so you would have to go through the entire dermroller treatment all over again. Microneedling induces wound healing and the release of inflammatory molecules that can stimulate hair growth bringing hairs that have stem cell present back to functioning and into the anagen growth cycle.
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