New Dermaroller Study; Thoughts, comments?

[Sparky4444]

Well said. I think that's exactly right. The skin is becoming unhealthy, and so the follicles die off. ...

That just doesn't wash...Why do I have a few perfectly good, thick hairs on my temples, surrounded by slick bald skin??? One follicle perfectly good, the next door neighbor crap...????

 

[hellouser]

Alright, I am going to document with different pictures my hair loss journey.

First, my genetic makeup, I am bi-racial african-american/white, so my hair phenotype is the crazy afro a la beyonce or lenny kravitz, kind of like that when it used to grow crazy:

As far as hairline goes, it is very similar to Kobe Bryant's, in fact, it is almost identical, very high, never receded, just thinned out of nowhere (like kobe did as well):

Brothers, dad and my son all have the same high hairline. So that gives you a little picture of how my hair and hairline looked pre-balding.

Here is my hairline in my high teens:

https://www.dropbox.com/s/smhlvh3k3hns8oa/beforeBalding2.jpg



Here is my crazy afro all growned out (note, these photos are very old, so quality may not be the best, and some of them are actually scans of printouts as fancy digital cams weren't a commodity back in the days .



https://www.dropbox.com/s/70xg5skn3pnyli3/afroBeforeBalding.jpg


The above is the last afro I could successfully pull, with every subsequent hair cycle, the top kept getting thinner and thinner. You can clearly see in the picture below that the top is noticeably thinner, and it kept going.

https://www.dropbox.com/s/lzic6e56p6juikk/BaldingGettingObvious2.jpg

Below, I cut my hair because the afro wasn't fooling anyone anymore ;(. You can see the sides already thicker and growing way faster than the top.

https://www.dropbox.com/s/fqbie9ghsoz78j5/BaldingMoreShowingSidesLongerThanTop2.jpg

Below, as a kept shaving my head, bald patches can be seen getting obvious, the top is growing as a snails pace. Look at dat shiny reflection on top :woot:

https://www.dropbox.com/s/emu2uox5ong6kxj/baldingShowingMore.jpg

In the picture below, I am totally fcked!! the top will simply not grow past half an inch, even waiting a whole year, most hair are thin an vellus like with no dark pigment at all, the hair on top will simply not grow, period.



ALL IMAGES BELOW ARE are between august and september, I started treating my hair exactly feb15, never used finasteride, started minoxidil the first week of august after the dermaroller thing started, so my regrowth can't be due to minoxidil either (though the compounding effect with dermarolling is showing good things so far).

Before I started treatment, I only had to trim the sides every week or so to get rid of the annoying horseshoe pattern, the top not growing no matter what, I didn't need to shave it.

Around the end of June the top kept growing darker, terminal looking hair slowly, so I had to start trimming both sides and top to have something cosmetically decent.


This is after I started dermarolling, minoxidil can clearly be seen dried around the hairline, it also makes my scalp and hair look whitish.

https://www.dropbox.com/s/15olt9ga542apyb/another.jpg

Below is grown slightly, you see the top is still composed of non-fully pigmented terminal hair, but it is definitely semi-terminal and grows at a little faster rate, nowhere near how fast the sides grow though

https://www.dropbox.com/s/jl61we456eh0sro/last.jpg

Below is a clearer view of the top directly under light, close up look with hair cut very short, you can see the sides still way thicker than the top, semi terminal and few patches of terminal hair can be seen all over, what you can't see is the thousands of thin/vellus looking peach fuzz all over. What is also happening is that the scalp is getting thicker and tiny black hair follicles ready to sprout are all over seems to be spreading all over the top and that is changing the texture of the scalp


Below is the longest I have grown it so far, lighting isn't the best though, top still look thin compared to the sides, but I came from literally nothing, so I can't be complaining, darn it, the forum only allows attaching 8 picture per post, so I am attaching this a different way:

https://www.dropbox.com/s/28smibu8rx3eqvc/grownedSlightly.jpg

Scalp can still be seen through the top because of not having fully terminal hair all over. I wasn't going to post anything till around the january timeframe because I wanted to assess how effective the derma rolling works (started early august). Time will tell but I am happy so far. I came from nearly a norwood 7, I say nearly because random peach fuzz would still grow half an inch but the growth was stunted. Am I happy? heck yes, but I think I can improve to the point of full recovery with time. What I noticed so far is that my balding is going away exactly in reverse order. What I attribute most my success also is consistency.

This is the major problem with most people in my opinion. They will try every single treatment in the world as soon as they hear something good about it. They jump from topical to topical every month or so and never consistent with anything. They will quickly abandon an existing treatment that maybe doing incredible things (not yet noticeable) as soon as they read a post from some random dude on the internet claiming they have been on the same treatment since they were in their mother's womb and it didn't do $hit for them.

I think a lot of things work given adequate consistency, heck, I think even vigorously scratching your head with your nail might give you some results if you are consistent enough (I think odabalk or someone else mentioned that is what a friend of theirs does, this was months back early in this thread). My point is, treat your hair or do nothing, don't be wishy washy in what you are doing, pick something smart and be consistent:

Revelation 3:15-16

Holy macro. That is some serious regrowth without the use of fvcking finasteride! NICE!!!!!!!!!!!!

 

[LayZ]

PrinRam,

I see you're on an EQUOL diet. I'm gonna try that very soon. Supposedly does a number on free dht.

Don't know how you intend to apply the IBU, just keep in mind that it can keep wound channels open for a much longer time. Dunno if that's good or bad for what peeps are doing here.

 

[squeegee]

Hi squeegee,

Years ago, I used dermaroller to remove some scars from my face (forehead) and used to apply emu oil almost immediately after the bleeding stopped. This gave me pretty good results and my scars were removed almost completely (it took time, though: a couple of years or more). I used emu oil because of its regenerative properties but ALSO because of its anti-inflammatory properties.... (and I think it is very similar to the castor oil many people use here.



Do you think that, in this case, the regenerative properties of the emu oil are less beneficial than the anti-inflammatory ones?
In other words, would you recommend not to use it at the inflammatory stage of the healing process?

...many thanks

Acute inflammation triggers regeneration, you should not using emu oil for at least the first 3 days. It has anti-inflammatory properties..

 

[princessRambo]

PrinRam,

I see you're on an EQUOL diet. I'm gonna try that very soon. Supposedly does a number on free dht.

Don't know how you intend to apply the IBU, just keep in mind that it can keep wound channels open for a much longer time. Dunno if that's good or bad for what peeps are doing here.

Yes when I first started my journey one of the goals I wanted to achieve was to become a natural equol producer, thus the high amount of daidzein and miso paste. Thanks for the tip on IBU, If I ever use it, I would only do it after wound closure.

 

[squeegee]

in theory, if bald areas have low (or lower) blood flow, which prevents hair to "live" on that area, how come transpanted hair on such areas survives?

My theory is that perifollicular fibrosis is really the bad boy of hairloss..

Look at my growing pictures from bald temples, the newborn hairs are coming out of the punctured holes from the derma roller. You see where I am going with this! What his the first step in hair transplantation?



Perifollicular fibrosis: pathogenetic role in androgenetic alopecia.

Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH.
Source

Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University, Seoul, Korea.

Abstract

Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 microg/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia.

Article: Perifollicular fibrosis: pathogenetic role in androgenetic alopecia. Source: Biol Pharm Bull. 2006 Jun;29(6):1246-50. Author(s): Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University.

Summary:
Fibrosis is a scarring process in the skin that can damage the hair follicle (hair loss). This study shows that increased Testosterone speeds up fibrosis while treatment with Finasteride helps slow fibrosis. Stopping or slowing fibrosis may be another method by which Finasteride may help prevent hair loss.​

Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 mug/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia. http://www.derma-haarcenter.ch/files/Directory/News/06_07_2012/EHRS+2012+Barcelona.pdf

Cosmet Dermatol. 2009 Jun;8(2):83-91
Androgenetic alopecia in males: a histopathological and ultrastructural study.
El-Domyati M, Attia S, Saleh F, Abdel-Wahab H.

Department of Dermatology, Faculty of Medicine, Al-Minya University, Al-Minya, Egypt.

Background Androgenetic alopecia is a common cosmetic hair disorder, resulting from interplay of genetic, endocrine, and aging factors leading to a patterned follicular miniaturization. Microinflammation seems to be a potential active player in this process. Aims To study the histopathological and ultrastructural changes occurring in male androgenetic alopecia (Androgenetic Alopecia). Patients/methods Fifty-five subjects were included in this study (40 with Androgenetic Alopecia and 15 as normal age-matched controls). Skin biopsies from frontal bald area and occipital hairy area were subjected to histopathological examination, immunohistochemical staining for collagen I and ultrastructural study. Results The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases. Conclusion Follicular microinflammation plays an integral role in the pathogenesis of Androgenetic Alopecia in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases.

http://www.biomediclaser.com/pdf/Inflammation-in-Androgenetic-Alopecia.pdf

Formation of fibrous tissue or fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the
miniaturization. Involution of the pilosebaceous unit in this form of baldness and sustained microscopic
follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is
considered a possible cofactor in the complex etiology of androgenetic alopecia. However, till date, the
inflammatory component has not been explored in developing treatment protocols for androgenetic
alopecia.


Fibrosing Alopecia in a Pattern DistributionPatterned Lichen Planopilaris or Androgenetic Alopecia With a Lichenoid Tissue Reaction Pattern?


Patients developed progressive fibrosing alopecia of the central scalp, without the multifocal areas of involvement typical of lichen planopilaris and pseudopelade. Perifollicular erythema, follicular keratosis, and loss of follicular orifices were limited to a patterned area of involvement. Biopsy specimens of early lesions demonstrated hair follicle miniaturization and a lichenoid inflammatory infiltrate targeting the upper follicle region. Advanced lesions showed perifollicular lamellar fibrosis and completely fibrosed follicular tracts indistinguishable from end-stage lichen planopilaris, pseudopelade, or follicular degeneration syndrome.

http://archderm.jamanetwork.com/article.aspx?articleid=189906


INFLAMMATORY PHENOMENA AND FIBROSIS

The implication of microscopic follicular inflammation in the pathogenesis of Androgenetic Alopecia has emerged from several independent studies: An early study referred to an inflammatory infiltrate of activated T cells and macrophages in the upper third of the hair follicles, associated with an enlargement of the follicular dermal sheath composed of collagen bundles (perifollicular fibrosis), in regions of actively progressing alopecia.[25] Horizontal section studies of scalp biopsies indicated that the perifollicular fibrosis is generally mild, consisting of loose, concentric layers of collagen that must be distinguished from cicatricial alopecia.[26] The term 'microinflammation' has been proposed, because the process involves a slow, subtle, and indolent course, in contrast to the inflammatory and destructive process in the classical inflammatory scarring alopecias.[27] The significance of these findings has remained controversial. However, morphometric studies in patients with male pattern Androgenetic Alopecia treated with minoxidil showed that 55% of those with microinflammation had regrowth in response to treatment, in comparison to 77% in those patients without inflammation and fibrosis.[26] Moreover, some forms of primary fibrosing alopecia may represent pathological exaggeration of Androgenetic Alopecia associated with follicular inflammation and fibrosis, specifically postmenopausal frontal fibrosing alopecia,[28] and fibrosing alopecia in a pattern distribution.[29]
An important question is how the inflammatory reaction pattern is generated around the individual hair follicle. Inflammation is regarded as a multistep process which may start from a primary event. Some authors proposed that alopecia may result from cumulative physiological degeneration of selected hair follicles. They described in healthy murine skin clusters of perifollicular macrophages as perhaps indicating the existence of a physiological program of immunologically controlled hair follicle degeneration by which malfunctioning follicles are removed by programmed organ deletion, and suggested that perhaps an exaggerated form of this process might underlie some forms of primary scarring alopecia.[30] The observation of a perifollicular infiltrate in the upper follicle near the infundibulum of human hair follicles in Androgenetic Alopecia suggests that the primary causal event for the triggering of inflammation might occur near the infundibulum.[27] On the basis of this localization and the microbial colonization of the follicular infundibulum with Propionibacterium sp., Staphylococcus sp., Malassezia sp., or other members of the transient flora, one could speculate that microbial toxins or antigens could be involved in the generation of the inflammatory response. Alternatively, keratinocytes themselves may respond to oxidative stress from irritants, pollutants, and UV irradiation, by producing nitric oxide, and by releasing intracellularly stored IL-1α. This pro-inflammatory cytokine by itself has been shown to inhibit the growth of isolated hair follicles in culture. [31] Moreover, adjacent keratinocytes, which express receptors for IL-1, start to engage the transcription of IL-1 responsive genes: mRNA coding for IL-1β, TNFα, and IL-1α, and for specific chemokine genes, such as IL-8, and monocyte chemoattractant protein-1 (MCP-1) and MCP-3, themselves mediators for the recruitment of neutrophils and macrophages, have been shown to be upregulated in the epithelial compartment of the human hair follicle.[27] Besides, adjacent fibroblasts are also fully equipped to respond to such a pro-inflammatory signal. The upregulation of adhesion molecules for blood-borne cells in the capillary endothelia, together with the chemokine gradient, drives the transendothelial migration of inflammatory cells, which include neutrophils through the action of IL-8, T cells, and Langerhans cells at least in part through the action of MCP-1. After processing of localized antigen, Langerhans cells, or alternatively keratinocytes, which may also have antigen presenting capabilities, could then present antigen to newly infiltrating T lymphocytes and induce T-cell proliferation. The antigens are selectively destroyed by infiltrating macrophages, or natural killer cells. On the occasion that the causal agents persist, sustained inflammation is the result, together with connective tissue remodeling, where collagenases, such as matrix metalloproteinase (also transcriptionally driven by pro-inflammatory cytokines) play an active role.[27] Collagenases are suspected to contribute to the tissue changes in perifollicular fibrosis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929555/

 

[RisingFist]

Yes when I first started my journey one of the goals I wanted to achieve was to become a natural equol producer, thus the high amount of daidzein and miso paste. Thanks for the tip on IBU, If I ever use it, I would only do it after wound closure.

can you elaborate on this? I tried searching but couldn't find much. It might be of interest to all those people who tried that equol scam from some company. If there's a natural way to do it then I'm sure many would be interested. It almost sounds like you're balancing the body back to controlling dht naturally.

 

[princessRambo]

@squeegee: very informative post, will have to digest all this . I do believe fibrosis is key, even if we had a magical pill today that will neutralize 100% of the downstream effect of dht in the scalp. Do you think a slick norwood 7 will regrow everything just by taking that one pill? The already fuc*ked up state of the fibrotic scalp that was pounded for years will have to slowly revert completely before full recovery, this might take up to a year or more with such magical pill. I think dermarolling will definetely speed up the process

can you elaborate on this? I tried searching but couldn't find much. It might be of interest to all those people who tried that equol scam from some company. If there's a natural way to do it then I'm sure many would be interested. It almost sounds like you're balancing the body back to controlling dht naturally.

Administration of Equol-Producing Bacteria Alters the Equol Production Status in the Simulator of the Gastrointestinal Microbial Ecosystem (SHIME)[SUP]1[/SUP]

http://nutrition.highwire.org/content/136/4/946.full

The bacterial strains used in this study were previously isolated from a human fecal sample at our laboratory (26). This stable mixed culture, which efficiently transforms daidzein into equol, consists of 4 dominant bacterial strains:Enterococcus faecium EPI1, Lactobacillus mucosae EPI2, Finegoldia magna EPI3, and a Veillonella sp.-related strain EP. The culture was grown anaerobically in brain heart infusion (Oxoid) supplemented with 0.5 g/L L-cystein (BHI[SUB]a[/SUB]) as described previously (26).

So basically in the above study they identified the Enterococcus faecium strain as a group of bacterium compable of converting daidzein in the gut into equol. The study below confirms Enterococcus faecium as one of the dominant strains from miso paste.

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2672.2002.01573.x/full

Method and Results: Nine Miso-pastes were sampled for isolation of bacteriocin-producers. Almost all isolated enterococcal strains produced bacteriocins but no isolated tetragenococci did so. The bacteriocin-producing isolates were divided into nine groups by phenotypic tests. As the phenotypic characters were highly diverse, these strains could not be identified to species level on the basis of their phenotypes. The nine representative strains from each group were identified by 16S rRNA analysis. These bacteriocin-producers with one exception (Lactococcus sp.) were identified as strains of the Enterococcus faecium `species group'.

Thus

1. take soy isoflavones pill containing daidzein,
2. eat miso paste frequently,
3. pray to god it works

On a serious note, there are studies implying that just having a diet rich in isoflavones can turn a non-equol producer into equol producer within months. Some people will scare you that taking high amount of phytoestrogens will give you gyno, or turn you into a woman or some other non-sense like that. Well I have been taking close to 3000mg of phytoestrogens from tea alone (probably contining close to 1000mg of pure EGCG), combining that with close to a 100 mg of phytoestrogens from soy isoflavones, combining with 1280mg of phytoestrogens from curcumin, further I use piperine to increase bioavailability, for almost 8 months now. According to those guys on the internet, I should have a 36 DD by now and breastfeeding my son instead of my wife...

 

[odalbak]

I do believe fibrosis is key, even if we had a magical pill today that will neutralize 100% of the downstream effect of dht in the scalp.

Not surprising balding guys don't get their hair back after losing their balls.

 

[squeegee]

Not surprising balding guys don't get their hair back after losing their balls.

unk::agree: Odal always comes up with the most random funny **** LOL

 

[odalbak]

unk::agree: Odal always comes up with the most random funny **** LOL

And semen topical application is no longer available unless they get into ipads… haha

 

[squeegee]

In 2006, Dr. Laaff, a dermato-pathologist, evaluated 20 blinded biopsies from a study performed by Dr. M. Schwarz, a plastic surgeon from Freiburg, into the effects of the Dermaroller on collagen and elastin formation. Biopsies were taken by Dr Schwarz from various parts of the body of 10 patients undergoing elective cosmetic surgery. A first 'control' biopsy was taken adjacent to the site that was needled with the Dermaroller. Six to eight weeks later, another biopsy was taken from the needled skin. New collagen and elastin fiber formation was obvious and quite dramatic. On average, an increase of new fibers of 206% was observed by the pathologist and in one case a 1,000% increase was recorded. In the absence of any signs of overt tissue damage, a new hypothesis for a possible mechanism of action of CIT is proposed.

http://www.genuinedermaroller.com.au/science/science

- - - Updated - - -

Few studies : http://www.ncbi.nlm.nih.gov/pubmed/?term=Percutaneous+Collagen+Induction+Therapy

 

[Billy_Elvis]

Hi guys,

I have been rollering with a 1.5mm 540 needle roller with minoxidil twice a day (except 24 hours post roller) for 5 weeks now and think I can see slight thickening in the places I lost hair the more recently. I am thin at the crown and am hoping in a few months to see my crown looking less thin. I have taken lots of before photos in different light with different lengths of hair so I should have a good baseline. This is my last ditch attempt to recover some hair before I start buzzing it with a 1 guard.

Billy

 

[odalbak]

Biopsies were taken by Dr Schwarz from various parts of the body of 10 patients undergoing elective cosmetic surgery.

It's a pity no patient had surgery on his scalp. We could have found the solution to hair loss 6 years ago…

 

[opti]

so what happens if using anti inflammatory creams after dermarolling?side effect or will it result in no regeneration?

 

[bushbush]

so what happens if using anti inflammatory creams after dermarolling?side effect or will it result in no regeneration?

No one knows for sure.

 

[opti]

Wanna try to use castor oil the next time dermarolling with a 0,5mm (though its bleeding) on one temple , hope i wont get cancer or anything from that . Used minoxidil directly after rolling and im pretty sure it works a lot more systematic then :O

 

[Morinohtar]

Acute inflammation triggers regeneration, you should not using emu oil for at least the first 3 days. It has anti-inflammatory properties..

So, using Aloe Vera is out of question too, right?

 

[bryan87]

I think one full week should be enough, that's what I am going by recently.

On an unrelated noted, since some people asked what I use: here is my anti 5AR regimen:

As soon as waking up in a fasted state:

10mg piperine in the morning on empty stomach followed by 320mg saw palmetto, +5000mcg biotin + 400mg Green tea extract (containing 200mg EGCG), 650mg curcumin, 2000mg evening primrose oil, 1000mg omega 3 (exact amount of omega 3, not fish oil containing fillers). 1000 mg MSM, 1000MG sililca, 5000iu cholecalciferol, 2 cups soy milk, walnuts and almonds, generic multi vitamin.

2 hours later:

a cup of concentrated tea infusion with white and black tea with a spoon of coconut oil into the tea (lauric acid) and a tea spoon of cayenne peper in the tea

Noon
60mg of soy isoflavones pill + iodine kelp cap + 10 mg piperine followed by 500mg of resveratrol + 650 mg of curcumin, followed by the tea infusion stated above + 2000mg of evening primrose oil + 1000 mg omega 3 (exact amount of omega 3 with no fillers) + 1000mg msm+ 1000mg silica,

2 hours later:
my custom tea infusion again (as listed above),

Before bed: 2000mg evening primrose oil + 1000mg pure omega 3 + 1000mg msm +1000mg silica + 16000% daily value worth of b12 + 450 mg of magnesium + the custom tea infusion state above + 1 scoop of fermented soy (japanese miso paste).

There is too many studies backing a lot of these and many people have tried these in the past, I personally attribute my success so far to consistency (never missed a dosage, except on unsual circumstances, like when traveling internationally on a long flight when the drugs are in the checked in luggage or some weird occasion like that). Use of piperine is key in my opinion as it dramatically increases pills bio-availability, curcumin for example is very poorly absorbed but piperine can increase the absorption rate by up to 2000%. Same with ECGC, Saw palmetto etc.

Lets look the study behind saw palmetto alone compared to finasteride:

Inhibition of the activity of 'basic' 5 alpha-reductase (type 1) detected in DU 145 cells and expressed in insect cells.



A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia.



Inhibition of androgen metabolism and binding by a liposterolic extract of "Serenoa repens B" in human foreskin fibroblasts.



There is also the famous merck sponsorded research (not bothering posted that here) that completely discredited LSERs in comparison to finasteride but to me it's a matter of increased absorption and consistency, heck you will find users here who have used finasteride even dutasteride for years with nothing to show for, but nobody really knows how consistent anybody is.

The last and most important aspect of my regiment is... prayer lol. Since people asked, this is what I use, on a side note, I have zero side effects, now back on topic.

For how long have you been doing this? Have you notice an improvement?

 

[squeegee]

So, using Aloe Vera is out of question too, right?

The goal of using the derma roller is to trigger small local acute inflammation so it regenerates itself. Why, you wanna use aloe vera and slow it down? Leave your pumpkin alone for few days.. you want to maximize your results. Armando was spot on few posts ago!