New Dermaroller Study; Thoughts, comments?

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zombiehair

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Checking in my latest rolling observations.
I now have quite the collection of rollers.
I believe this was roll call 5 for me.

I started off my session with a 1.5mm 540 needle roller.
I rolled quite aggressively applying a decent amount of pressure for 5 minutes or so.
I then swapped to a 2 mm 192 needle and continued for another 5 or so minutes.

Observations

during this sessions I didnt notice as much of the needle popping the scalp sensation I had experienced during earlier rolls.
To me this appears to suggest I have broken down to some extent a hardened stretched layer of my scalp ?
After rolling my scalp was peppered with a few red blood spots nothing like some of the post rolling images some members have kindly posted.
I don't believe the lack of blood to be caused by lack of pressure on my part.
My scalp just doesn't appear to bleed as much .

At the moment I'm In 2 minds whether to wait one or two weeks until my next session.

For anyone considering trying out the rolling Id suggest starting out by following the study initially and see how it works for them.
You can always move on to some of the variations discussed in the thread further down the road if better results are reported.

roll on roll day :)
 

squeegee

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hey squeegee, you have some photo documentation of the results? :) any new terminal hair or just velus?

Here is a pic of my bald temple slowly filing in!

I will get more pics tomorrow.. friggin 2.00 am here lol
 

zombiehair

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Looking good squeegee :)
Id read earlier in the thread a few suggestions that new hair was growing directly from needle puncture sites.
Can Anyone seeing results add anything to this ?
 

isishearmyplea

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squeegee can you post a before/after pic of your whole pumpkin :p, that d be gr8. thanks and best wishes!!
 

mas80

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Been rolling for about 8 weeks now and I think I'm seeing new hairs along the hairline, so I'm cautiously optimistic. I've noticed that I don't get that same velcro feeling anymore like I did when I rolled the first few times and blood comes much easier now. Not sure what to make of it. I'm using a 1.5 mm with 192 needles and going all the way in. Haven't jumped on the sperm wagon yet.

EDIT: I'm considering rolling every 2nd or 3rd week or maybe even just once a month instead of every week. Any thoughts?
 
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zombiehair

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I'm considering something similar myself maybe every second week.
This is based on the healing timeline posted by princessrambo in the semen thread.
still undecided here.
 

Jaded

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I just found out this thread, 119 pages less than two months, general consensus unlike any other treatment, no side effects and it could actually work, this thing looks like a winner. Just one question, for people that still have more hair than bald spots, dermarolling will cause a massive shed initially right? I just ordered a 1.5mm and i was thinking about doing it once a month.
 

DesperateOne

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I guess only you can decide, do your research, listen to your body, I personally suggest this: if you only rolled mildly with very little blood, by all means, roll weekly, you will likely be fine, but if you butcher your scalp, wait a minimum of two weeks, the magic happens in the post inflammation and re-epithelazation and later stages, not before. As for 1.5mm roller, you are right on, I don't personally feel the need to go any deeper, you will get all necessary wound healing growth factors to be released that way.

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Timing depends on the kind of damage you do, if you are unsure, you can just stick to the dermaroller study in the original post, 1.5mm wound weekly with mild erythema, they got great results ;)

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The most recent Follica patent was just released 3 days ago (thanks Kirby ;)). It is addressing the big elephant in the male pattern baldness room, the one that not only prevents follicular neogenesis, but also inhibits growth of existing hair, namely prostaglandin D2. We have failed to address how to tackle that giant elephant so far in this thread.

http://patentscope.wipo.int/search/en/WO2013142295

The patent mainly revolves around inhibition of the Prostaglandin D2 receptor, GPR44 (CRTH2). This has been debated to death before and there already exist products that selectively inhibit the PGD2 receptor, namely ramatroban. I think in terms of wound healing neo genesis, it is critical to address this as well, as studies have shown that PGD2 prevent new hair birth. In any case, I was reviewing the study to figure out what particular time point was PGD2 inhibition critical:




So in this study, it seems that 7 days after wounding till complete healing is where factors affecting neo genesis become important and where pgd2 inhibition is important (I will also note that this is a larger wound so taking this time frame literally for our dermarolling purpose might be erroneous). We also know that over the counter drugs such as aspirin and ibuprophen block both the bad PGD2 and good PGE2. So I am thinking if at the critical time we use those cheap drugs topically, but at the same time add exogenous concentrated good prostaglandins (yes semen might serve this purpose, now bite me :D), or even increasing minoxidil dosage during those critical wounding periods (as minoxidil induces PGE2), it might be beneficial. Just my an opinionated analysis though.

I was also wondering where pgd2 was fitting in the whole thing, if I remember correctly, it was Dr. cots first breakthrough and we have seem to forgotten about it. Aspirin is one of the things people have suggested in the past but I think after some research from people on forums, the and the winner turned to be zyrtec(Cetirizine). I think it was because it only blocked pgd2 and not the good pge2, but even if that is the case, we should still be able to do as you suggest. During the morning add some pge2 topically and then at night add some aspirin or Cet to block the pgd2. This would be great because I had ordered a box full of Kirkland Cet from Amazon about a month ago, which I haven't even opened. One problem is that we need to mix it with everclear, or something else if remember correctly.
 

zombiehair

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If I remember right I read a few contradicting studies on cetirizine when I was looking into it before.
Ill have to have another look.
Here is a study that implies cetirizine ups pge2 .

[h=2]Abstract[/h]Cetirizine was first described as a specific anti-H1 molecule displaying potent antiallergic activity. It was later found that its pharmacological properties extended to cellular actions as on eosinophil recruitment at inflammatory sites in allergic patients. Monocytes and macrophages participate in allergic mechanisms, particularly through high affinity H1 and H2 membrane receptors and generation of pro- and anti-inflammatory agents; among them histamine-induced factors, IL-1 and prostanoids are of importance. The aim of this work was to investigate the effect exerted by various concentrations of cetirizine (0.1–10 μg/ml) appliedin vitro to human monocytes and peritoneal rat macrophages cultured for 24 h. Peritoneal macrophages were collected either from normal or experimentally inflamed rats. Human monocytes, isolated from peripheral blood, were studied either in a resting state or after stimulation by LPS fromEscherichia coli (1 and 10 μg/ml). Cetirizine (10 μg/ml) significantly enhanced IL-1 release by human monocytes stimulated by a weak LPS concentration (1 μg/ml) but could not modify the maximal increase of IL-1 release induced by 10 μg/ml of LPS. It did not exert any effect on resting cells. Cetirizine (0.1–10 μg/ml) enhanced PGE2release by resting human monocytes. Concentrations of 1 and 10 μg/ml enhanced PGE2 release by LPS-stimulated monocytes, and by healthy and inflamed rat macrophages. This effect was concentration-dependent. Our findings point to an anti-inflammatory action of cetirizine via PGE2release and histamine H2 interactions. Cetirizine did not directly modify IL-1 generation by resting monocytes but the IL-1 production observed after LPS stimulation could promote the mechanisms by which PGE2 is released.
 

DesperateOne

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If I remember right I read a few contradicting studies on cetirizine when I was looking into it before.
Ill have to have another look.
Here is a study that implies cetirizine ups pge2 .

[h=2]Abstract[/h]Cetirizine was first described as a specific anti-H1 molecule displaying potent antiallergic activity. It was later found that its pharmacological properties extended to cellular actions as on eosinophil recruitment at inflammatory sites in allergic patients. Monocytes and macrophages participate in allergic mechanisms, particularly through high affinity H1 and H2 membrane receptors and generation of pro- and anti-inflammatory agents; among them histamine-induced factors, IL-1 and prostanoids are of importance. The aim of this work was to investigate the effect exerted by various concentrations of cetirizine (0.1–10 μg/ml) appliedin vitro to human monocytes and peritoneal rat macrophages cultured for 24 h. Peritoneal macrophages were collected either from normal or experimentally inflamed rats. Human monocytes, isolated from peripheral blood, were studied either in a resting state or after stimulation by LPS fromEscherichia coli (1 and 10 μg/ml). Cetirizine (10 μg/ml) significantly enhanced IL-1 release by human monocytes stimulated by a weak LPS concentration (1 μg/ml) but could not modify the maximal increase of IL-1 release induced by 10 μg/ml of LPS. It did not exert any effect on resting cells. Cetirizine (0.1–10 μg/ml) enhanced PGE2release by resting human monocytes. Concentrations of 1 and 10 μg/ml enhanced PGE2 release by LPS-stimulated monocytes, and by healthy and inflamed rat macrophages. This effect was concentration-dependent. Our findings point to an anti-inflammatory action of cetirizine via PGE2release and histamine H2 interactions. Cetirizine did not directly modify IL-1 generation by resting monocytes but the IL-1 production observed after LPS stimulation could promote the mechanisms by which PGE2 is released.

Well, I think one contradiction was that Cet reduces inflammation, however, we would be applying post inflamation anyways, so it will not matter much. I had also forgotten that Cet also increases pge2, and people saw vellus hair in the past, at least the pictures I saw from the a German forum. I think it had to be pointed out that there were some horror stories with Cet in the German forum and maybe a few here. ramatroban seems promising.
 

JonnyKid

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Dermaroller cant hurt....

Hello guys-I have been using a dermaroller for years. Not sure how well it works to help absorption of my minoxidil but I know it cant hurt!
 
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badgenetics1

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Hello guys-I have been using a dermaroller for years. Not sure how well it works to help absorption of my minoxidil but I know it cant hurt!

What size having you been using? Also, we aren't using the dermaroller to increase the absorption of minoxidil, rather we are using it to induce the creation of new hair follicles.
 

squeegee

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More pics :




I am recovering from a shed which is totally normal. All these hairs are growing in bald areas. Pretty impressive for 9 weeks in of rolling. I used the 2.5mm last week and still recovering from it as you can see the dead skin left on my pumpkin. Patience and consistency are the keywords!

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Hello guys-I have been using a dermaroller for years. Not sure how well it works to help absorption of my minoxidil but I know it cant hurt!

The study don't use the derma roller for better absorption of Minoxidil, they use it to induce growth factors, platelets and progenitor cell for reconstruction.
 

theRA

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I am recovering from a shed which is totally normal. All these hairs are growing in bald areas. Pretty impressive for 9 weeks in of rolling. I used the 2.5mm last week and still recovering from it as you can see the dead skin left on my pumpkin. Patience and consistency are the keywords!

damn nice, also... seems that the new hair grows from the dermarolling punctures/holes, interesting
 

DesperateOne

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We need to find out what techniques the scientist use to see what stage in the wounding cycle we're in for any individual. Most likely some of it can be visible under a different frequency Of light, but who knows. Does anyone remember the correct vehicle for Cet and the ratios?
I also think one of the final pieces of the puzzle might be that lithium to keep the wound open longer.
 
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