New Dermaroller Study; Thoughts, comments?

[benjt]

http://www.hairloss-research.org/UpdateMassageStimulateHairGrowth9-13.html

Turns out there are other studies reporting a positive effect of physical stimulation for hair growth. And here comes the interesting part:

The upregulated genes included hair growth genes such as VEGF, WNT, BMP, and PDGF, and the downregulated genes included hair-removing genes such as IL-6 and TNF.

WNT is exactly what we need. If I recall correctly, WNT is upstream of FGF-9, right?

 

[odalbak]

Turns out there are other studies reporting a positive effect of physical stimulation for hair growth.

Thanks benjt. Dermarolling in itself is probably an effective enough method, but I understand that not only for the sake of sheer understanding, but also in your situation regarding minoxidil, the idea that mechanical action as such when applied to the scalp could be effective for the bio chemical reasons you're referring to, is exciting.

 

[princessRambo]

@benjt: great post about the dermis/epidermis size in balding vs non balding scalp, I was trying to find a study like this for a while now

Now I want to give my input about the role of subcutanous fat in male pattern baldness and what the Yale study really found. It seems there is confusion around this topic a bit.

In the Yale study, what they found was that adipocytes lineage cells contribute to activating the dormant stem cells and tell them to start growing hair again. In other words, it is concerned with the main signaling behind reviving dormant follicles. Furthermore I want to stress a point that was reported in the study and is somewhat being missed here. What they also found was that it was the hair follicle entering anagen that triggers adipogenesis and not the other way around.

we analyzed individual adipocytes during the hair follicle cycle by immunostaining skin sections with antibodies against caveolin 1A, which is enriched on the cell surface of mature adipocytes (Le Lay et al., 2010) and a fluorescent neutral lipid dye, Lipidtox. Morphometric analyses of individual caveolin+, Lipidtox+ cells quantified the cross-sectional area (XSA) of intradermal adipocytes. Adipocytes progressively increased in size following morphogenesis of the hair follicle (P4–P15) (Figures 1Aand S1C). Following catagen, intradermal adipocyte XSA decreased to the area of adipocytes during morphogenesis.

To analyze if de novo formation of intradermal adipocytes occurs through a proliferative precursor cell during the hair cycle, we determined if proliferative cells expressing perilipin, which is specifically expressed on mature adipocytes (Greenberg et al., 1991), exist in the skin during the hair cycle by pulsing mice for 3 days with BrdU during different stages of the hair cycle (Figure 1C).

Taken together, these data demonstrate that intradermal adipocytes regenerate through a proliferative precursor during anagen induction.

In other word when hair dies, the layer of fat in the scalp that comprises most of the skin's thickness shrinks. When hair growth begins, the fat layer expands through adipogenesis. What I am getting at is that the thinning of the subcutanous layer in Androgenetic Alopecia scalp is a direct effect of having the majority of affect follicles becoming dormant, and not the other way around. In other words, once you get follicles growing again, adipogenesis will occur automatically and thickness will resume. Also it is being suggested that one can increase adipogenesis through wounding. I do not agree. I have not seen one scientific study that supports this, on the contrary, the presence of wnt (through wounding) directly inhibit adipoginesis

http://www.jbc.org/content/280/25/24004

Wnt Signaling Inhibits Adipogenesis through β-Catenin-dependent and -independent Mechanisms

These data supported a model in which Wnt signaling inhibits adipogenesis through both β-catenin-dependent and β-catenin-independent mechanisms.

Does that mean wounding will not ultimately restore the subcutaneous fat layer? Of course not, but not directly, meaning, by wounding and potentially releasing growth factors and inducing follicular neogenesis, you will get more and more follicles, new and existing, to enter anagen, this in turn inducing adipogenesis, and at the end of the hair cycle, the expanding adypocytes in turn trigger hair stem cells to regenerate new follicles, provided you keep the effects of DHT in check to prevent major catagen induction and scalp thinning as a result, otherwise it's back to square 1.

 

[Armando Jose]

Does it have something to do that subcutaneous fat layer with the product delivered by the sebaceous gland?
seems that when the hair is in the anagen phase, the sebaceous gland works harder. I personally think that fat is not only directed towards the outside, but has a path to inside

 

[ganonford]

Sorry for the little off topic-guys, I know most of you don't like this topic, but as the original thread disapeared, I have no other way...

princessRambo, I know we should not depend that much on you, and that we should take our own decisions and make our own mistakes. Having said that, I would like to know your opinion.

You said before that you think it would be best to avoid topicals during the first days (except for minoxidil). But would you said the same thing about semen?...

 

[squeegee]

@benjt: great post about the dermis/epidermis size in balding vs non balding scalp, I was trying to find a study like this for a while now

Now I want to give my input about the role of subcutanous fat in male pattern baldness and what the Yale study really found. It seems there is confusion around this topic a bit.

In the Yale study, what they found was that adipocytes lineage cells contribute to activating the dormant stem cells and tell them to start growing hair again. In other words, it is concerned with the main signaling behind reviving dormant follicles. Furthermore I want to stress a point that was reported in the study and is somewhat being missed here. What they also found was that it was the hair follicle entering anagen that triggers adipogenesis and not the other way around.

In other word when hair dies, the layer of fat in the scalp that comprises most of the skin's thickness shrinks. When hair growth begins, the fat layer expands through adipogenesis. What I am getting at is that the thinning of the subcutanous layer in Androgenetic Alopecia scalp is a direct effect of having the majority of affect follicles becoming dormant, and not the other way around. In other words, once you get follicles growing again, adipogenesis will occur automatically and thickness will resume. Also it is being suggested that one can increase adipogenesis through wounding. I do not agree. I have not seen one scientific study that supports this, on the contrary, the presence of wnt (through wounding) directly inhibit adipoginesis

http://www.jbc.org/content/280/25/24004

Wnt Signaling Inhibits Adipogenesis through β-Catenin-dependent and -independent Mechanisms



Does that mean wounding will not ultimately restore the subcutaneous fat layer? Of course not, but not directly, meaning, by wounding and potentially releasing growth factors and inducing follicular neogenesis, you will get more and more follicles, new and existing, to enter anagen, this in turn inducing adipogenesis, and at the end of the hair cycle, the expanding adypocytes in turn trigger hair stem cells to regenerate new follicles, provided you keep the effects of DHT in check to prevent major catagen induction and scalp thinning as a result, otherwise it's back to square 1.

This is good stuff Princess!!:salut:

 

[opti]

how about injecting subcutanous fat in the temples or bald areas?

 

[DesperateOne]

I guess that clears up things about the fat being the their of hairs, it's simply the after math of baldness. Thanks Rambo, please keep up the good work.

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Sorry for the little off topic-guys, I know most of you don't like this topic, but as the original thread disapeared, I have no other way...

princessRambo, I know we should not depend that much on you, and that we should take our own decisions and make our own mistakes. Having said that, I would like to know your opinion.

You said before that you think it would be best to avoid topicals during the first days (except for minoxidil). But would you said the same thing about semen?...

I also would like this answered.

 

[benjt]

Sorry for the little off topic-guys, I know most of you don't like this topic, but as the original thread disapeared, I have no other way...

princessRambo, I know we should not depend that much on you, and that we should take our own decisions and make our own mistakes. Having said that, I would like to know your opinion.

You said before that you think it would be best to avoid topicals during the first days (except for minoxidil). But would you said the same thing about semen?...

It shouldn't be a problem as long as you give the wounds a couple of hours (3 should be enough) to close.

Does it have something to do that subcutaneous fat layer with the product delivered by the sebaceous gland?
seems that when the hair is in the anagen phase, the sebaceous gland works harder. I personally think that fat is not only directed towards the outside, but has a path to inside

The authors of the study on Detumescence Therapy argued exactly the same, but came to the conclusion that due to fibrosis, "grease" (whatever that may be; might include the fat you#re speaking of) cannot be transported away and accumulates.

@princessRambo: That raises - at least for me - two questions:
1. Does that mean there is a circular dependence? Hair needs BAT, but hair only creates BAT during anagen. BAT dies, hair no longer receives nutrients, hair dies, hair can no longer create new BAT. That's what it looks lie to me right now.
2. Wnt inhibits BAT growth, but helps follicle neogenesis, which kicks off BAT production? Doesn't make much sense to me.

 

[princessRambo]

It shouldn't be a problem as long as you give the wounds a couple of hours (3 should be enough) to close.

This would be my answer as well.

@princessRambo: That raises - at least for me - two questions:
1. Does that mean there is a circular dependence? Hair needs BAT, but hair only creates BAT during anagen. BAT dies, hair no longer receives nutrients, hair dies, hair can no longer create new BAT. That's what it looks lie to me right now.
2. Wnt inhibits BAT growth, but helps follicle neogenesis, which kicks off BAT production? Doesn't make much sense to me.

This is a good point, but we have to ask ourselves where exactly is wnt expressed when hair enters into anagen. Is the expression within the hair follicle, or is it expressed within the BAT which lies much lower in the dermis, or both? My answer will be within the follicle itself only.

 

[squeegee]

I finally did some in-depth research as to scalp skin thickness. The source is the well cited paper THE THICKNESS OF HUMAN SCALP: NORMAL AND BALD.

They offer value ranges which I wrote down for males:
Epidermis - min: 0.035 mm, max: 0.07 mm
Dermis - min: 0.6 mm, max: 1.6 mm
Subcutis/Hypodermis - min: 1.15 mm, max: 1.9 mm

So, let's make the assumption that we want to hit at least the lowest layer of the dermis - where the follicles are - to damage the perifollicular fibrosis (and maybe even the follicle?) and have new tissue formed there. Then, if we add up the minimum values which probably describe completely bald areas, we get 0.635 mm. As I said, this is the absolute minimum and probably only applies if the areas is 100% bald.
If we make the assumption that we want to trigger regrowth of BAT in the subcutis (let's say, we want to penetrate the subcutis till the middle), then we need needles of at least 1.21 mm absolute minimum.

For those that want to be on the safe side and by no means go any further than the subcutis (which makes sense, cause we don't want to damage the galea), then we should not get needles above 1.785 mm (this is the depth where the subcutis ends and the galea begins, in completely bald areas).

So, effectively, even if your scalp is the thinnest possible, you will not penetrate deep enough to hit the galea unless your needles are longer than 1.785 mm. Thus, a 1.5 mm roller should be 100% safe to use. If we want to hit the lowest levels of the dermis, we need at least 0.6 mm in completely bald areas, and if we want to trigger BAT regrowth, we need at least 1.21 mm.
These values will of course differ for everyone and depend on your age and the progress of your Androgenetic Alopecia/male pattern baldness. In any case, acc. to the study linked above, you will not damage anything by using a 1.5 mm roller. And most likely, you will not have significantly deep needles if you use anything shorter than 0.7 mm.

My advice would be to use 1.5 mm. It's still completely safe no matter how thin your skin (I repeat: the absolut minimum thickness measured by the authors of above paper in 100% bald areas is 1.785 mm), and you make sure that you hit deep enough to kill both perifollicular fibrosis, and also hit the subcutis for BAT regeneration.
By the way: These values also mean that you can actually damage your galea if you go for 2.0 mm or longer if you roll in areas that are 100% bald. Does not mean that you necessarily will, cause even with baldness skin thickness will differ from individual to individual. Nonetheless, with 2.0 mm or longer, there's at least a chance you inflict deep damage. Go for 1.5 mm. Safe to use in any case, and definitely long enough to go subcutis deep.


I also advice everybody interested in the science to take a look at the values for the subcutis (hypodermis) in the paper from above. The values for males vs. females differ the most for the subcutis. This hints at the subcutis (and thus BAT) playing a huge role here, in my opinion.

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There is only an indirect correlation between fibrosis and blood here. 100% of blood comes from the subcutis/hypodermis (or deeper, if you do damage below that which I'd not advise). The balder you are, the more fibrosis, and the thinner your upper skin layers, so you will more easily hit the subcutis where the blood vessels are.

Blood drawing depends 100% on whether you reach the subcutis when rolling, as there is simply no blood in dermis and epidermis. Fibrosis doesnt really matter directly here.

My scalp also looked like that of hellouser's the first three times that I rolled, but by now it's completely impossible for me to draw that much blood no matter how much pressure I apply. I hope the reason for that is tissue regeneration, thus adding thickness to my scalp skin where I rolled.

Benjit! I love you man!:love: great post!

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Look at the older baldies.. with the norwood male pattern baldness pattern.. Their scalps on top are thin, lifeless with no sebum at all. Where the fat Subcutaneous fat remains on the sides of the pumpkin.. hair are still alive and growing. Brown adipose tissue serves a supportive role for hair follicles and hair growth for sure and share same functions as the bone marrow. Androgen have big influence on adipose tissue functions.

 

[cthulhu2.0]

I finally did some in-depth research as to scalp skin thickness. The source is the well cited paper THE THICKNESS OF HUMAN SCALP: NORMAL AND BALD.

They offer value ranges which I wrote down for males:
Epidermis - min: 0.035 mm, max: 0.07 mm
Dermis - min: 0.6 mm, max: 1.6 mm
Subcutis/Hypodermis - min: 1.15 mm, max: 1.9 mm

So, let's make the assumption that we want to hit at least the lowest layer of the dermis - where the follicles are - to damage the perifollicular fibrosis (and maybe even the follicle?) and have new tissue formed there. Then, if we add up the minimum values which probably describe completely bald areas, we get 0.635 mm. As I said, this is the absolute minimum and probably only applies if the areas is 100% bald.
If we make the assumption that we want to trigger regrowth of BAT in the subcutis (let's say, we want to penetrate the subcutis till the middle), then we need needles of at least 1.21 mm absolute minimum.

For those that want to be on the safe side and by no means go any further than the subcutis (which makes sense, cause we don't want to damage the galea), then we should not get needles above 1.785 mm (this is the depth where the subcutis ends and the galea begins, in completely bald areas).

So, effectively, even if your scalp is the thinnest possible, you will not penetrate deep enough to hit the galea unless your needles are longer than 1.785 mm. Thus, a 1.5 mm roller should be 100% safe to use. If we want to hit the lowest levels of the dermis, we need at least 0.6 mm in completely bald areas, and if we want to trigger BAT regrowth, we need at least 1.21 mm.
These values will of course differ for everyone and depend on your age and the progress of your Androgenetic Alopecia/male pattern baldness. In any case, acc. to the study linked above, you will not damage anything by using a 1.5 mm roller. And most likely, you will not have significantly deep needles if you use anything shorter than 0.7 mm.

My advice would be to use 1.5 mm. It's still completely safe no matter how thin your skin (I repeat: the absolut minimum thickness measured by the authors of above paper in 100% bald areas is 1.785 mm), and you make sure that you hit deep enough to kill both perifollicular fibrosis, and also hit the subcutis for BAT regeneration.
By the way: These values also mean that you can actually damage your galea if you go for 2.0 mm or longer if you roll in areas that are 100% bald. Does not mean that you necessarily will, cause even with baldness skin thickness will differ from individual to individual. Nonetheless, with 2.0 mm or longer, there's at least a chance you inflict deep damage. Go for 1.5 mm. Safe to use in any case, and definitely long enough to go subcutis deep.


I also advice everybody interested in the science to take a look at the values for the subcutis (hypodermis) in the paper from above. The values for males vs. females differ the most for the subcutis. This hints at the subcutis (and thus BAT) playing a huge role here, in my opinion.

- - - Updated - - -


There is only an indirect correlation between fibrosis and blood here. 100% of blood comes from the subcutis/hypodermis (or deeper, if you do damage below that which I'd not advise). The balder you are, the more fibrosis, and the thinner your upper skin layers, so you will more easily hit the subcutis where the blood vessels are.

Blood drawing depends 100% on whether you reach the subcutis when rolling, as there is simply no blood in dermis and epidermis. Fibrosis doesnt really matter directly here.

My scalp also looked like that of hellouser's the first three times that I rolled, but by now it's completely impossible for me to draw that much blood no matter how much pressure I apply. I hope the reason for that is tissue regeneration, thus adding thickness to my scalp skin where I rolled.

Good stuff benjt, you rock!

 

[benjt]

squeegee, my post also means that you run the risk of damaging your galea with your 3 mm roller. I don't know how advanced your male pattern baldness is, but if you roll in completely bald areas, you might really hit your galea.

@princessRambo: Remains question 1 I just think that a circular dependence is very unlikely, processes in the body usually dont work that way. I think we're missing something here.

An idea of mine for explanation: Estrogen is related to fat tissue generation, this includes BAT. It has been shown that in Androgenetic Alopecia/male pattern baldness patients, the hair follicles themselves produce huge amounts of DHT. Is it possible that Androgenetic Alopecia/male pattern baldness patients' follicles commit suicide by not creating theright environment for creating their own BAT during anagen phase? Usually, you'd have estrogen around when creating adipose tissue; instead, you have DHT.
Spinning that theory even further: Is that maybe the reason why the immune system starts attacking locally and thus triggering fibrosis? DHT might be harmful to BAT in the making.

 

[squeegee]

Benjit..the roller don't cause any adverse conditions. Dermal roller is not big enough to induce damage to anything. At the very worst, it will reinforces the galea LOL. It is not a meat tenderizer!, it is a micro-roller. Deeper is better because you have more chances to recruit blood from bigger capillaries. Blood is the keyword. This is why the derma roller works at 1.5mm and not that much at .25mm. Older practitioner uses the 3.0mm in the face for a reason for worst skin conditions, burn, scars,deeper wrinkles..or older patients. Even with the 3mm, I rinse my hair after couple hours and I can apply minoxidil if I want with no sides whatsoever. The problem is deeper in the tissue. The BBQ guy was successful for a reason. A lot of you over thinking everything. Roll deep, get bloody messy. Wait then repeat. Stay consistent. Get hair on your pumpkin.

The advantage of dermarolling compared to those other methods is that it doesn’t remove the outermost layer of skin and there is no danger of burns and other thermal damage.Wound healing has 3 stages - Inflammation, proliferation and remodeling.Inflammation is a reaction of our body to heal the injury.During the inflammation stage, the blood vessels dilate, resulting in an increased blood flow to the area. The area becomes red and warm. Plasma fluids will flood the area and cause swelling. When the immune system cleans the area of damaged cells, the damaged cells will be replaced by new ones.The skin consists of 3 layers. The epidermis, the dermis and subdermis.The epidermis has no blood supply. The dermis has irregular blood vessels and the deeper the dermis the more blood vessels. If you puncture a blood vessel you end up with pinpoint bleeding or even bruises.The more damage in the dermis you cause, the more remodeling you will get.


http://files.kotisivukone.com/karl-ludwig.kotisivukone.com/tiedostot/clinicsdermatology2008_pci.pdf

 

[karankaran]

I feel that the key here is going deep enough! I will not be happy if I do not see a bloody mess on my head when I do it! I also think that the key is to derma roll vertically, horizontally and diagonally (left and right). From Nov 1, I will start this! I would like to just press the entire 2.5 mm inside my head and roll, I am ordering a numbing cream, just in case!

 

[Sparky4444]

4th stabbing session with the 1.5mm Friday nite...Japanese Mint Oil did help quite a bit, again...Drew pretty good blood, but the real slick area of my temple needed some good stabbing to get blood...

...Next morning it was a little bit red, but nothing dramatic...

...so far, at 4th week, nothing to report....I doubt I will see anything at 5 weeks..this is being stubborn...

 

[DesperateOne]

4th stabbing session with the 1.5mm Friday nite...Japanese Mint Oil did help quite a bit, again...Drew pretty good blood, but the real slick area of my temple needed some good stabbing to get blood...

...Next morning it was a little bit red, but nothing dramatic...

...so far, at 4th week, nothing to report....I doubt I will see anything at 5 weeks..this is being stubborn...

lol funny how sometimes that Japanese oil seems to work and others it doesn't. Are you applying it with a dry scalp? I noticed that if I applied it with a kinda wet head, it actually hurt less, I guess because it distributed across better.

 

[karankaran]

Here is what I found out today - epidermis (outermost layer) thickness ranges from 0.05mm to 1.5mm. And dermis thickness ranges from 0.6 mm to 3.00 mm. The skin is thickest at palm, soles of feet and back. Considering it is different for scalp (which it is), you can definitely assume =1.5mm for wounding and >=2.5mm for deep wounding. And I mean complete insertion of needles in the scalp and rolling while the needles are inserted. Btw, hair follicles are rooted a bit far inside the dermis.

 

[princessRambo]

1. Does that mean there is a circular dependence? Hair needs BAT, but hair only creates BAT during anagen. BAT dies, hair no longer receives nutrients, hair dies, hair can no longer create new BAT. That's what it looks lie to me right now.

1. Does that mean there is a circular dependence? Hair needs BAT, but hair only creates BAT during anagen. BAT dies, hair no longer receives nutrients, hair dies, hair can no longer create new BAT. @princessRambo: Remains question 1 I just think that a circular dependence is very unlikely, processes in the body usually dont work that way. I think we're missing something here.

benjt, There is an inherent assumption in 1 that I have bolded above which makes it a slippery slope , let me elaborate.

Hair does not die because it doesn't receive nutrient from BAT, hair enters into premature catagen in Androgenetic Alopecia because of overexpression of PGD2 signaling from hematopoietic prostaglandin D synthase (histamine release from mast cell degranulation) and lipocalin type prostaglandin D synthase: this is the level that one of Cotsarelis' studies measured and found to be 11 fold increased or some scary number like that in Androgenetic Alopecia, and is probably why topicals like cetirizine don't always have great results with some people as it only inhibits HPGDS induced PGD2 (now i am getting off topic ).

The bottom line is that PGD2 is what tells hair to go to sleep. This isn't necessarily a bad thing, as even with normal people without Androgenetic Alopecia, it is the same signaling that regulates the normal hair cycle, in Androgenetic Alopecia there is just too much of the "go to sleep" signal, the compounding effect of dht also inhibit wnt through dkk1, thus the hair follicle receive less and less of the "keep growing" (wnt) signal and it shrivels up, gets thinner and thinner, sleeps longer and longer and eventually goes to permanent sleep. This increased in catagen all over parallels with reduced adipogenesis and as a result, dormant stem cells at the base of hair follicles don't receive any more signal to wake up.

Now the role of adipocytes as far as I can tell from the Yale study is the "Wake up" signal. They also showed that platelet derived growth factor from adipocytes precursor cells contribute to the promoting of hair growth, but keep in mind they are not the only type of cells that induce PDGF, but they help in growth, but are not the chief actor for growth, so to speaks.

we propose that adipocyte precursor cells secrete PDGF to promote hair growth. Mice lacking PDGF-A display similar hair follicle defects as Ebf1 null mice, namely a lack of anagen entry (Karlsson et al., 1999). In addition, PDGF ligands have been implicated in hair growth induction based on experiments analyzing conditioned media from SVF derived adipocytes (Park et al., 2010). Adipocyte lineage cells are not the only cell type in the skin that expresses PDGF ligands, multiple cells in the follicular epithelium, the matrix and the hair germ, have been shown to express PDGF (Karlsson et al., 1999). Additional signals expressed by intradermal adipocytes may also be involved in signaling to the DP or epithelium (Park et al., 2010). Future experiments will clarify the cellular target of adipocyte signals in the skin and further define how PDGF signaling promotes bulge cell activation.

 

[Sparky4444]

lol funny how sometimes that Japanese oil seems to work and others it doesn't. Are you applying it with a dry scalp? I noticed that if I applied it with a kinda wet head, it actually hurt less, I guess because it distributed across better.

I'm using Hagina Japanese Mint Oil...it is very strong and it acts like an anesthetic...I'm also rolling very aggressively and quickly..it's the "scrunching" sound that actually makes my stomach turn more than the pain...