New Dermaroller Study; Thoughts, comments?
- Thread starter Jlyncher
- Start date
- Status
resu
Senior Member
- Reaction score
- 1,339
Watch this video:
https://www.youtube.com/watch?v=9WQaw80NyfU
And this:
[video=youtube;VuXJbqDlNug]https://www.youtube.com/watch?v=VuXJbqDlNug[/video]
https://www.youtube.com/watch?v=9WQaw80NyfU
And this:
[video=youtube;VuXJbqDlNug]https://www.youtube.com/watch?v=VuXJbqDlNug[/video]
squeegee
Banned
- Reaction score
- 132
[video=youtube;9WQaw80NyfU]https://www.youtube.com/watch?v=9WQaw80NyfU[/video]
guy here is using the same technique.. https://www.youtube.com/watch?v=VuXJbqDlNug
- - - Updated - - -
Been 4 days since I stabbed my head with a 1.5mm derma roller. I am shedding dead skin like a mofo. not even funny. It looks like the derma roller accelerates skin turn over which cause hair growth.
http://www.mtsroller.com/faqs/
- - - Updated - - -
Topical EGF: http://www.dr-roller-shop.com/100-egf-serum
Pretreatment of epidermal growth factor promotes primary hair recovery via the dystrophic anagen pathway after chemotherapy-induced alopecia.
Paik SH, Yoon JS, Ryu HH, Lee JY, Shin CY, Min KH, Jo SJ, Kim KH, Kwon O.
Abstract
Epidermal growth factor (EGF) is not only a cell growth stimulant but also has a catagen-inducing effect. Because chemotherapeutic agents primarily damage anagen hair follicles, it would be important to investigate whether catagen inducers have beneficial effects in chemotherapy-induced alopecia (CIA). We pretreated hair follicles with topical EGF-liposomal solution in the C57BL/6 mouse model of cyclophosphamide-induced alopecia and observed the catagen-inducing property and damage response pathway after CIA. We confirmed that topical EGF application induced a catagen-like stage and found that these catagen-like hairs were protected from chemotherapy-mediated damage. Moreover, our results showed that EGF treatment favoured primary hair recovery via the dystrophic anagen pathway after CIA. Given that hair follicles subjected to less severe chemotherapeutic insult enter the dystrophic anagen pathway followed by primary recovery, the results of this study suggest that catagen inducers could be useful as a new alopecia-protection strategy, especially in the context of CIA.
[h=1]Epidermal Growth Factor as a Biologic Switch in Hair Growth Cycle[SUP]*[/SUP][/h] http://www.jbc.org/content/278/28/26120.long
@Bombarie: Minoxidil will still be helpful, as it resolves fibrotic collagen tissue which is a crucial part in restoring balding (and maybe even bald) areas to prior health. Just make sure that you do not apply any minoxidil within the first 24 to 48 hours after treatment (depending on roller needle size), to make sure that no minoxidil enters your blood stream.
@Chelaxing: I myself am not applying anything right now due to a pertaining lack of a derma roller, but a mild anti inflammatory can be used. Just make sure it's nothing that's known to cause harm to liver or kidneys (some anti inflammatories actually do), as it can enter your blood stream through those tiny wounds.
@everyone: I am pretty sure after having a good look at crossections of scalp skin that there are two pathways of action with dermarolling:
1) everything below 1.5mm will only help delivery of topicals. Those wounds are simply not deep enough. They only go as far as the dermis. And as everybody knows, we have a regular permanent dermis renewal protocol anyway. As the dermis is constantly dying off and renewing anyway, wounds at this level will certainly not lead to regrowth of DP. There is nothing to be gained by increasing cell turnover and tissue regeneration in an area that is constantly renewed anyway.
2) 1.5mm and more: Only when damaging the layer below the dermis regrowth of DP can be triggered at all. This was also demonstrated by one study by Cotsarelis, where they made sure to remove tissue below the dermis as well. It goes in accordance with 1), as dermis and epidermis are renewed all the time anyway. In many places of the male body, dermis and epidermis are even 2mm (3mm on the back and some parts of the chest, and sometimes even 4mm, but only on palms and feet AFAIK), so we would need 1.5mm with high pressure, or bigger needles to hit anything below dermis, if we want to replicate what Cotsarelis did. We need to trigger regrowth in the subcutis to form new DP or to trigger their repair.
@Chelaxing: I myself am not applying anything right now due to a pertaining lack of a derma roller, but a mild anti inflammatory can be used. Just make sure it's nothing that's known to cause harm to liver or kidneys (some anti inflammatories actually do), as it can enter your blood stream through those tiny wounds.
@everyone: I am pretty sure after having a good look at crossections of scalp skin that there are two pathways of action with dermarolling:
1) everything below 1.5mm will only help delivery of topicals. Those wounds are simply not deep enough. They only go as far as the dermis. And as everybody knows, we have a regular permanent dermis renewal protocol anyway. As the dermis is constantly dying off and renewing anyway, wounds at this level will certainly not lead to regrowth of DP. There is nothing to be gained by increasing cell turnover and tissue regeneration in an area that is constantly renewed anyway.
2) 1.5mm and more: Only when damaging the layer below the dermis regrowth of DP can be triggered at all. This was also demonstrated by one study by Cotsarelis, where they made sure to remove tissue below the dermis as well. It goes in accordance with 1), as dermis and epidermis are renewed all the time anyway. In many places of the male body, dermis and epidermis are even 2mm (3mm on the back and some parts of the chest, and sometimes even 4mm, but only on palms and feet AFAIK), so we would need 1.5mm with high pressure, or bigger needles to hit anything below dermis, if we want to replicate what Cotsarelis did. We need to trigger regrowth in the subcutis to form new DP or to trigger their repair.
Guys, I have just a couple of questions/considerations:
1) in case of deep bloody 1,5 mm microneedling, how long to wait until the next application to allow the complete scalp recovery? I guess one week should not be enough!!
2) I thinK that the idea of not applying minoxidil after the procedure is not only linked to the risk of excessive absorption but also because it is desirable promote the inflammatory process as long as possible, and avoid application of antinflammatory products as emu oil, estrogens, pgd2 blockers, minoxidil, ecc.
Thank you and sorry form my english
1) in case of deep bloody 1,5 mm microneedling, how long to wait until the next application to allow the complete scalp recovery? I guess one week should not be enough!!
2) I thinK that the idea of not applying minoxidil after the procedure is not only linked to the risk of excessive absorption but also because it is desirable promote the inflammatory process as long as possible, and avoid application of antinflammatory products as emu oil, estrogens, pgd2 blockers, minoxidil, ecc.
Thank you and sorry form my english
squeegee
Banned
- Reaction score
- 132
nope, let your body do his job. Go to bed inflamed lol
- - - Updated - - -
well said Benjt!:salut:
- - - Updated - - -
From my own perspective it looks like 2 weeks would be the best for recovery time with 1.50mm or+.
odalbak
Established Member
- Reaction score
- 11
Aren't you just speculating here? That guy PrettyFly83 on BTT is having great success with only 0.5mm. He looked pretty much bald all over. I know minoxidil can help but in his case things seem to be going far beyond regular minoxidil possibillities.
http://www.*********talk.com/showthread.php?t=13420&page=5
Yes odalbak, that indeed is speculation, though based on the paper of Cotsarelis where he and his team removed tissue to induce regrowth. I assume they went that deep for the same reason.
In my layman's understanding, it just does not make sense to damage something that is constantly thrown out anyway and on top of that does not have anything to do with hair follicles. I think that just inducing FGF-9 is not enough; if it was, there would already be a treatment composed of just this. I think the key here is to force the body into creating scalp tissue from scratch, namely in the layer that hosts the DPs. Growth factors are not enough on their own, I am pretty sure of that. Otherwise the solution to all our problems would've already been found.
@princessRambo: Valid points under the assumption that minoxidil indeed is the only way to increase PGE2 and thus FGF9. After having read more than a dozen studies about minoxidil, I am pretty sure that minoxidil per se does not even increase PGE2 levels. That is only a side effect of its vasodilatory function. PGE2 is a product and signaler down the inflammation cascade, which is, by the way, comprised of many, many different substances. I think the diagrams showing which readings are elevated when after wounding were also posted earlier in this thread.
Anyway: The only confirmed primary function of minoxidil is vasodilation. This is not a surprise given that it is an NO compound similar to adenosine (there also exists a paper that for this reason tries to establish that minoxidil only works THROUGH adenosine, while I speculate it is either metabolised into adenosine or an agonist). As such, it will just flush everything where it does its workings. This can include pro-inflammatory substances such as PGD2, thus triggering the inflamed area to enter the next stage, where the body will upregulate PGE2 by itself. Additionally, minoxidil and adenosine in their role as neurotransmitter blockers just put all body processes to a halt where applied, including new collagen formation but also inflammationary processes in general.
FGF-9 however will also be expressed just by itself, when deep scalp tissue renews. FGF-9 will only be elevated by the body where it "makes sense", i.e., you will not find elevated levels of FGF-9 in inflamed kidneys or tonsils. So while minoxidil may be beneficial, it is not crucial, and PGE2 will also be expressed by itself after wounding. I think that FGF-9 will be elevated by the body anyway as a response to deep wounding in that area.
Edit:
Just to make my point clear: We have two papers here.
1) The indian one, which did not induce deep wounds, but used minoxidil. Worked.
2) Cotsarelis. Deep wounding, no minoxidil. Worked, as long as FGF9 expression was ensured - which is, to my knowledge at least, the case when you hit the subcutis with wounds. minoxidil by itself does not increase FGF9 anyway - as long as inflammation does not go chronic, the body is going to send PGE2 (and thus FGF9) anyway. This image also seems to imply that follicles formed in completely new tissue in this study, i.e., they went quite deep, where the DP usually sit.
And that is exactly my point: Two ways of working here.
In my layman's understanding, it just does not make sense to damage something that is constantly thrown out anyway and on top of that does not have anything to do with hair follicles. I think that just inducing FGF-9 is not enough; if it was, there would already be a treatment composed of just this. I think the key here is to force the body into creating scalp tissue from scratch, namely in the layer that hosts the DPs. Growth factors are not enough on their own, I am pretty sure of that. Otherwise the solution to all our problems would've already been found.
@princessRambo: Valid points under the assumption that minoxidil indeed is the only way to increase PGE2 and thus FGF9. After having read more than a dozen studies about minoxidil, I am pretty sure that minoxidil per se does not even increase PGE2 levels. That is only a side effect of its vasodilatory function. PGE2 is a product and signaler down the inflammation cascade, which is, by the way, comprised of many, many different substances. I think the diagrams showing which readings are elevated when after wounding were also posted earlier in this thread.
Anyway: The only confirmed primary function of minoxidil is vasodilation. This is not a surprise given that it is an NO compound similar to adenosine (there also exists a paper that for this reason tries to establish that minoxidil only works THROUGH adenosine, while I speculate it is either metabolised into adenosine or an agonist). As such, it will just flush everything where it does its workings. This can include pro-inflammatory substances such as PGD2, thus triggering the inflamed area to enter the next stage, where the body will upregulate PGE2 by itself. Additionally, minoxidil and adenosine in their role as neurotransmitter blockers just put all body processes to a halt where applied, including new collagen formation but also inflammationary processes in general.
FGF-9 however will also be expressed just by itself, when deep scalp tissue renews. FGF-9 will only be elevated by the body where it "makes sense", i.e., you will not find elevated levels of FGF-9 in inflamed kidneys or tonsils. So while minoxidil may be beneficial, it is not crucial, and PGE2 will also be expressed by itself after wounding. I think that FGF-9 will be elevated by the body anyway as a response to deep wounding in that area.
I am fully aware of that. In this case, with small needles, the minoxidil indeed is crucial. minoxidil dissolves hard fibrotic collagen tissue where it has "access", and the small wounds give minoxidil that access. Otherwise, the minoxidil is held off by the collagen it has not yet dissolved. minoxidil acts like acid on collagen - it first needs to dissolve the top layer until it can go deeper. The small wounds (that are first filled by very soft tissue) provide channels for the minoxidil to go deeper than without. That's at least my understanding.princessRambo said:
Edit:
Just to make my point clear: We have two papers here.
1) The indian one, which did not induce deep wounds, but used minoxidil. Worked.
2) Cotsarelis. Deep wounding, no minoxidil. Worked, as long as FGF9 expression was ensured - which is, to my knowledge at least, the case when you hit the subcutis with wounds. minoxidil by itself does not increase FGF9 anyway - as long as inflammation does not go chronic, the body is going to send PGE2 (and thus FGF9) anyway. This image also seems to imply that follicles formed in completely new tissue in this study, i.e., they went quite deep, where the DP usually sit.
And that is exactly my point: Two ways of working here.
That is not 100% true, as shown by other studies:
a) that one boy (age 14 I think) that started growing a lot of hair on one of his arms after injury there
b) the senior that got major burn wounds and regrew ALL of his hair
b) again hints at replacing tissue from scratch does work.
All of us are doing speculative work here. In fact, that is the only thing we can do, as we are unable to do primary research: We can only try to piece the puzzle together. Some theories make sense, some don't. To determine which of them make sense, we discuss.
That's basically what I mean: We cannot rely on minoxidil inducing PGE-2. As I said, I think all of this has to do with minoxidil being basically the same as adenosine, which boils down to two mechanisms:
a) shutting down running processes (s. wikipedia article on adenosine)
b) levelling all substances in the area where applied (s. wikipedia article on vasodilators)
As this topic was already discussed in this thread here and some seem to take it personal, I will leave it out this time. There is at least one scientific report of the same happening in vivo, and many reports of users on the net.
Cotsarelis was not the first one to try this. However, he was the first to induce deep (as in: deeper than just dermis) wounds alongside. And that's my point: Cotsarelis probably assumes that deep wounding is necessary, otherwise he wouldntve done it.
From my layman's understanding its also logical. What happens to the bald areas in the first place? Fibrosis. While fibrosis advances, the follicles shrink. Now just injecting growth factors into the bald areas leaves the newly repaired follicles in a fibrotic environment. How long will they be able to produce new hair in that same environment that killed the follicles in the first place?
Sparky4444
Senior Member
- Reaction score
- 44
You guys..my question is this:" Is it worth it to go through all this for just a few hairs that won't be cosmetically noticeable"??
- Reaction score
- 2,634
If it maintains, HELL YES.
But notice the interesting part about those incidents of regrowth: Deep wounding, where deep tissue had to be replaced by the body. The body is in fact capable of generating follicles completely anew, as shown by these incidents - but only with deep wounding. If it also happened without deep wounds, (a) the solution for us would be easy, and (b) scratches would lead to undesired hair growth.
I do believe that the key lies in wounding of the subcutis.
The study shows exactly where they cut - below the DP. And where are the DP nested? At the lowest part of the dermis, right on top of the subcutis.
Furthermore, given that the 2011 Yale study showed that bald areas lack brown adipose tissue completely (!) - which is located in the subcutis - which also goes hand in hand with the effectiveness of PRP and stem cell treatment approaches (cf. recent study posted in this forum on lack of stem cell supply which is usually carried out via the brown adipose tissue-mediated angiogenesis), in my opinion at least its safe to say that it is very important to induce wounding there.
I know that those are speculations, but for all intents and purposes, they just fit too well together with other research and approaches at treatment that showed positive results, such as PRP + wounding.
@Sparx4444: Given that recently there has been going a lot of research in that area which actually showed some results - no matter if w/ minoxidil or without - it is definitely worth a shot. We have a number of people trying this out now, so in a few months we can tell more. And the more people join in for the test, the better - maybe someone finds just the right "settings" for the treatment to work (as in: needle length, regimen, frequency of application, and so on).
@the others: What do you use for disinfection of the roller and the skin?
squeegee
Banned
- Reaction score
- 132
According to the study.. they were not going crazy with the derma-roller...
Microneedling procedure
The shaven scalp was prepared with betadine and normal saline. A dermaroller of 1.5 mm sized needles was rolled over the affected areas of the scalp in a longitudinal, vertical, and diagonal directions until mild erythema was noted, which was considered as the end point of the procedure. All patients were instructed not to apply Minoxidil on the day of procedure and to resume its application only 24 h after the Microneedling procedure.
- - - Updated - - -
Erythema is redness of the skin, caused by hyperemia of the capillaries in the lower layers of the skin. It occurs with any skin injury, infection, or inflammation.
So... go mild with it every weeks or got a bit harder on it but go bi-weekly.. It is my 5th day since rolling times.. and my pumpkin is still sensitive lol... so and I want to try the 2.5mm ASAP.. argh!
Mechanisms of hair re-growth induced by Microneedling include:
Microneedling procedure
The shaven scalp was prepared with betadine and normal saline. A dermaroller of 1.5 mm sized needles was rolled over the affected areas of the scalp in a longitudinal, vertical, and diagonal directions until mild erythema was noted, which was considered as the end point of the procedure. All patients were instructed not to apply Minoxidil on the day of procedure and to resume its application only 24 h after the Microneedling procedure.
- - - Updated - - -
Erythema is redness of the skin, caused by hyperemia of the capillaries in the lower layers of the skin. It occurs with any skin injury, infection, or inflammation.
So... go mild with it every weeks or got a bit harder on it but go bi-weekly.. It is my 5th day since rolling times.. and my pumpkin is still sensitive lol... so and I want to try the 2.5mm ASAP.. argh!
Mechanisms of hair re-growth induced by Microneedling include:
- Release of platelet derived growth factor, epidermal growth factors are increased through platelet activation and skin wound regeneration mechanism
- Activation of stem cells in the hair bulge area under wound healing conditions which is caused by a dermaroller
- Overexpression of hair growth related genes vascular endothelial growth factor, B catenin, Wnt3a, and Wnt10 b.
supermusic
Established Member
- Reaction score
- 34
I wonder if this procedure could help to reverse the gray hair too..
i was just wondering the same thing. i started seeing a ton of grey hairs in the past 6 months, mostly in the areas not affected by male pattern baldness (sides and back of head). it looks really weird. I'm 28 years old so i don't know whats up with these grey hairs deciding to show up so early. if dermarolling can help with this then i will start dermarolling my whole head :woot:
odalbak
Established Member
- Reaction score
- 11
I bought betadine and normal saline like they used in the Indian study, but it's not very convenient since you need to have 10 doses of normal saline for 1 dose of betadine and I have no idea what amounts to use anyway. I haven't dermaroll yet but I think I'll use a simple disinfection spray like hexamidine on my scalp instead. It's a mix of alcohol, sodium acetate, acetic acid and purified water.
I have an old Ray violet wand that I may use to sterilize the roller. It produces ozone which is meant to be very germicidal.
- Status