New Dermaroller Study; Thoughts, comments?

[selfaware]

There is no evidence that mercury causes male pattern baldness.

sigh...

For virtually ALL systemic poisons, one of the primary symptoms is??....yeah, that's right..."hair loss".

The pituitary controls hormones....hormones control bodily processes including hair-growth....poisoning, including especially mercury, f*cks up the pituitary. These are known facts. It was long thought that Hg ends up in the kidneys, but recent research shows that mercury accumulates more in the pituitary than any other gland in the body. Pituitary is the 'master' gland of the entire body in all mammals.

Lots of guys in a "silver bullet" mindset....but this hair-restoration thing has absolutely no appearance of being solved by a single magic bullet. It's a multi-variable problem, and so every 5% improvement matters. Perhaps the healing of a long term low-level heavy metal toxicity will only help...say...5%. OK, that's 5%. Now add a PGE2 enhancer at the right time. Another 5%. Now add...
EVERY 5% matters for us.

 

[DesperateOne]

This thread is an absolute goldmine. Many MANY thanks to PrincessRambo and Squeegee for bringing forth so much information. These guys deserve a huge round of applause.

+1
I said it before and will say it again, nothing significant is coming out for the next three years, this is the only thing we have worth our time now, nothing else. The thread is getting insanely long, maybe split it into part two?

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I will add something that I goin interesting. I was watching taboo on TV and they were using bee sting therapy to improve the immune system and obviously once the bee stings, it gets inflammated. So I know it's really more like bro science, maybe at some point I will give it a try, sting my head a few times a week. The science doesn't back the procedure but the results from patients do.

 

[odalbak]

To what extend does digging small holes with the dermaroller break the fibrotic tissues of our scalps? I'm asking this because after seeing the biopsies that Squeegee posted it looks there's a huge job to be done. Fibrosis seems to be everywhere. I'm considering giving a try to that hypothetic solution to hair loss that i mentioned earlier in the thread. That friend who scratched his scalp with his nails and claimed that his hairloss had stopped as a result. At the time I was incredulous but I've since begun to give a bit of credit to it. I won't use my nails as they're short and supple, but the small tip of a pen instead, as if I wanted to cover my entire scalp with ink. Having super short hair (5mm) like I have will make it easy. And I can do that everyday, as long as I want.

 

[selfaware]

Earlier in this thread, someone posted a link to this study...

[h=1]Wound healing process may increase risk of skin cancer[/h]
For anyone doing DR who hasn't gotten to it, you might find it worth the reading. Here are a few quick excerpts. How they relate to what we're experimenting with (dermarolling) is pretty obvious...

...wound healing can promote the development of tumours due to the recruitment of tumor-initiating cells in neighboring hair follicles.


...the wound environment can enhance development of BCC via two mechanisms - promotion of tumour growth, and enhancement of tumor initiation frequency.


'We believe that exposure to UV radiation from the sun together with an active tissue regeneration process is a dangerous combination increasing the risk of developing BCC,'


Moreover, the study demonstrated that damage to the deeper parts of the skin (full-thickness wounding) is required to elicit the tumour-enhancing effect.



- I noted the ref to "enhancement of tumor initiating frequency". I think DR would certainly qualify as a very high 'frequency' of potential initiating events. I mean....ten thousand new holes a week...lol

- These results would mitigate against very deep wounding. Conversely, it suggests that non-deep wounding, not down to the base layer, may be relatively much safer.

- And, sadly for me, since I love the sun...it sounds like we might want to avoid sun for the entire many months that we do DR regularly. I also saw a paper on one of the topical agents we're discussing, which strongly urged avoiding UV while it was applied. A lot of chemicals (which includes so-called 'natural' substances; st. john's wort being a case in point) react very differently, and energetically, when UV is applied. Something to be careful of...

Also, I came across the following paper tonight...and since I haven't seen melatonin mentioned in this thread as a topical for use with DR, I thought I'd post this...

Topical Melatonin for Treatment of Androgenetic Alopecia
Int J Trichology. 2012 Oct-Dec
Tobias W Fischer, Ralph M Trüeb,1 Gabriella Hänggi,2 Marcello Innocenti,3 and Peter Elsner
Five clinical studies showed positive effects of a topical melatonin solution in the treatment of Androgenetic Alopecia in men and women while showing good tolerability:

 

[princessRambo]

Right now there are 3 approaches:

1. Follow the original derma roller study, this is the simplest. One thing we should ask is, did they induce follicular neogenesis in that trial, or did they somehow revive dormant existing follicle through the 1.5mm rolling + minoxidil when they stated that new hair growth was noticed at 6 weeks. I highly suspect it was existing miniaturized comatosed follicle that sprung back to life. In any case, this is by far the easiest approach to follow

2. Follow the gory wounding approach, the perfect example for this is the BBQ old man. This is also stated in the 2012 follica patent, notably, removing portions of the scalp at 5-7mm depth, by completing scraping off the epidermis, dermis and sub-dermis. A dermaroller cannot achieve this, period. Only a scalpel or worse, falling asleep head first into a hot george foreman grill

3. This is what some of the crazy mad scientist wanna be like myself are trying to achieve. This is based on the latest follica discovery of the fgf9 link. For this to occur, you need to somehow induce fgf9 at a given stage of wound healing, and bam, new hair. Since there is a complexity and somewhat bio-hazard uncertainty about buying fgf9 from some random guy in china, we think it is possible to induce fgf9 through PGE2, because PGE2 induces FGF9. Minoxidil also induces PGE2. That said, from my personal research, this is a quite difficult to achieve, the reason is because it is dose dependent and time dependent. For one, I will go ahead and say that this cannot be achieved by minoxidil, the concentration of PGE2 necessary for this is just too high.

http://mcb.asm.org/content/26/22/8281.full.pdf

To investigate the effects of PGE2 on FGF-9 expression, primary culture human endometriotic stromal cells weretreated with various doses of PGE2 (0.01 to 100 uM) and concentrations of mRNA were quantified using quantitativeRT-PCR (see Fig. S1A and B in the supplemental material).The result demonstrated that PGE2 induced FGF-9 mRNAexpression in dose- and time-dependent manners (Fig. 1A andB). The expression of FGF-9 mRNA was induced by 0.1, 1, and10 uM PGE2, whereas higher concentrations of PGE2 failed toexert such effect. Administration of cells with 1 uM PGE2 enhanced FGF-9 mRNA expression at 8 h; expression reached a maximum at 12 h and then declined toward the basal level at24 h after PGE2 treatment. The induction of FGF-9 mRNA byPGE2 was mirrored by the increase in FGF-9 protein (Fig. 1C).

So basically they treated with different dosages between 0.01uM and 100uM and found that it is dose dependent and the lowest concentration to be 0.1uM and highest concentration 10uM. Therefore if you need to induce fgf9 through the PGE2 pathway you need a source of PGE2 that falls right in between those two number.

incidentally, PGE2 having a molecular weight of 352g/M, the dosage 23uM/ml of PGE2 in semen falls within the FGF9 inducing margin.... just saying :whistle:

 

[Armando Jose]

http://www.bmj.com/highwire/filestream/339492/field_highwire_article_pdf/0/1645.2

BBQ OLD MAN FTW! no minoxidil, fast recovery of hair. Deep wound.

Thank you squeegee for the link

 

[selfaware]

Maybe it's not the chemicals involved in the product but the fact that since it's peeling the skin it causes some sort of repeated little inflammation. Adding dermaroller wounding to it would make it worse.

That might be the case odal, although I think they did quite a bit of in-vitro testing also. In other words, in a culture dish...nothing to do with peeling...at least a few of the Retin family of compounds initiated tumors. I think for peels, it's not such an issue because it's done so seldom. But for DR'ing...where it might be applied daily, for a long time, perhaps it's something to be cautious with the dosing...especially considering how deeply DR'ing helps topicals be absorbed. I do plan on including it in my regime, but very selectively. As PR has always maintained....timing is everything. And I think my senior wife has mentioned that too...

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What Cots is basically saying here is even after you chop off the ballz, completely annihilating further DHT synthesis, hair won't grow back unless you factor in other stuff, he still noted tremendous amount of growth, but not complete regrowth, there might still large amount of fibrosis and inflammation even after turning into a women by high estrogen therapy.

makes one wonder about applying readily available Estrogen (estradiol) cream topically with the shallower DR sessions....

 

[squeegee]

To what extend does digging small holes with the dermaroller break the fibrotic tissues of our scalps? I'm asking this because after seeing the biopsies that Squeegee posted it looks there's a huge job to be done. Fibrosis seems to be everywhere. I'm considering giving a try to that hypothetic solution to hair loss that i mentioned earlier in the thread. That friend who scratched his scalp with his nails and claimed that his hairloss had stopped as a result. At the time I was incredulous but I've since begun to give a bit of credit to it. I won't use my nails as they're short and supple, but the small tip of a pen instead, as if I wanted to cover my entire scalp with ink. Having super short hair (5mm) like I have will make it easy. And I can do that everyday, as long as I want.

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

 

[shivers20]

You guys are spot in with fibrosis/collagen accumulation stopping hair from growing. Bimatoprost causes eyelid sucus which is a result of collagen being degraded. A good example showing
why it has an effect on hair growth.

 

[odalbak]

I wonder how Benjt is doing without minoxidil. Any minimal change like vellus hairs benjt?

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

Ink is full of growth factors, E prostaglandins, glutathione…

 

[squeegee]

I made fibrosis my #1 enemy. It is the villain of male pattern baldness. Period. The Biopsies proved it. I will physically attack it with 3mm derma roller and Retin-a to soften the scalp prior to rolling, every 2 weeks. I want to regenerate the fibrotic environment of my scalp. I read somewhere that people were using that technique to soften their scars before using the derma roller. After reading this..This is what Derma roller initiates.. Simultaneously, the cells that line the inner aspect of blood vessels called endothelial cells, proliferate creating new blood vessels. New tiny blood vessels (capillaries) migrate into the (old) perforated scar tissue and provide the newly formed tissue with nutrition, oxygen and blood pigments (haemoglobin). . I have a lot of hope that the derma roller can reverse baldness. Also, I will attack fibrosis from the inside by overloading my blood of proteolityc enzymes. Serrapeptase and nattokinase which is now cheaper than before. These enzymes digest dead matters in your blood, fibrin, plaque.. I also think that us early balders have less enzymatic activities in the first place which support DTH negative sides. This is maybe why us balders have many connections with cardiovascular diseases and prostate cancer.



http://dermaroller.com/all-about-scars

Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells
http://www.jci.org/articles/view/44478

[video=youtube;rYEDA3JcQqw]http://www.youtube.com/watch?v=rYEDA3JcQqw[/video]

 

[jason5]

Right now there are 3 approaches:

So basically they treated with different dosages between 0.01uM and 100uM and found that it is dose dependent and the lowest concentration to be 0.1uM and highest concentration 10uM. Therefore if you need to induce fgf9 through the PGE2 pathway you need a source of PGE2 that falls right in between those two number.

incidentally, PGE2 having a molecular weight of 352g/M, the dosage 23uM/ml of PGE2 in semen falls within the FGF9 inducing margin.... just saying :whistle:

Don't want to start another troll fest regarding semen, but assuming sperm is just a set of chemicals, can anyone argue against the actual chemistry of sperm and why it would or would not help in hair-loss after wounding. I'm strongly considering using this at least 3 times per week due to the high PGE2 content. Our bodies are the most advanced chemical factories in the universe, to discredit this particular substance without proper investigation would be a shame. Imagine how much money and research would be required to produce something as complex as semen.

 

[squeegee]

Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process. This can be a reactive, benign, or pathological state. In response to injury this is called scarring and if fibrosis arises from a single cell line this is called a fibroma. Physiologically this acts to deposit connective tissue, which can obliterate the architecture and function of the underlying organ or tissue. Fibrosis can be used to describe the pathological state of excess deposition of fibrous tissue, as well as the process of connective tissue deposition in healing.[SUP][1][/SUP]

Fibrosis is similar to the process of scarring, in that both involve stimulated cells laying down connective tissue, including collagen and glycosaminoglycans. Immune cells called Macrophages, and damaged tissue between surfaces called interstitium release TGFbeta. This can be because of numerous reasons, including inflammation of the nearby tissue, or a generalised inflammatory state, with increased circulating mediators. TGFbeta stimulates the proliferation and activation of fibroblasts, which deposit connective tissue.[SUP][2]

[/SUP]
http://en.wikipedia.org/wiki/Fibrosis

 

[Donc83]

I know my hair does not itch nearly as much since rolling. I guess this is a good thing.

 

[squeegee]

Cellular and molecular mechanisms of chronic inflammation-associated organ fibrosis

Satoshi Ueha[SUP]1,2[/SUP], Francis H. W. Shand[SUP]1,3[/SUP] and Kouji Matsushima[SUP]1,2[/SUP]*

• [SUP]1[/SUP] Department of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan
• [SUP]2[/SUP] Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Tokyo, Japan
• [SUP]3[/SUP] Department of Pharmacology, University of Melbourne, Melbourne, VIC, Australia

Organ fibrosis is a pathological condition associated with chronic inflammatory diseases. In fibrosis, excessive deposition of extracellular matrix (ECM) severely impairs tissue architecture and function, eventually resulting in organ failure. This process is mediated primarily by the induction of myofibroblasts, which produce large amounts of collagen I, the main component of the ECM. Accordingly, the origin, developmental pathways, and mechanisms of myofibroblast regulation are attracting increasing attention as potential therapeutic targets. The fibrotic cascade, from initial epithelial damage to eventual myofibroblast induction, is mediated by complex biological processes such as macrophage infiltration, a shift from Th1 to Th2 phenotype, and by inflammatory mediators such as transforming growth factor-β. Here, we review the current understanding of the cellular and molecular mechanisms underlying organ fibrosis.

http://www.frontiersin.org/Journal/10.3389/fimmu.2012.00071/abstract

 

[DesperateOne]

male pattern baldness is a complex beast and has lots of reasons why it affects hair follicles. From fibrosis to increased pgd2, it is just that some have a effect on some people because we are all different.

By the way since on the subject. There really shouldn't be any reason we can't use say bull semen right? As long as it falls in the range of it inducing fgf9, we should be good. After all, isn't injected testosterone extracted from bulls. Iron dragon and Kane store are both selling pge2, need to check if it falls within the range of inducing fgf9.

Fibrosis is defensively a primary enemy and should not be expected to be eliminated in days, unless you throw on a very intense peeler. Maybe that's why the peeler worked on a few people who knows.

 

[odalbak]

There really shouldn't be any reason we can't use say bull semen right?

Bull**** !

No, seriously. Why not using your own semen? It's free and easily available.

 

[DesperateOne]

Bull**** !

No, seriously. Why not using your own semen? It's free and easily available.

Good question, well since my hair loss affects my entire scalp including my sides, I particularly need full coverage. Applying twice a day will only give me so much to put on, I guess if I buzz my hair I would be able to leverage more of it, was just curious.

 

[theRA]

seriously, bull semen?.... as if your own wouldn't be disgusting enough , not judging but....... seriously? Think where it "came" from

 

[zombiehair]

roll call 6 for me.

It has been 10 days since my last roll.


I started off my session with a 1.5mm 540 needle roller.
I rolled quite aggressively applying a decent amount of pressure.
I then swapped to a 2 mm 192 needle.

Observations

rolling with 1.5mm I experienced none of the crunching needle popping the scalp sensation I had experienced previously.
rolling with the 2.mm I did experience a little popping but still nothing like the first 3 or 4 weeks of rolling.

To me this appears to suggest I have continued to break down to some extent a hardened stretched layer of my scalp .

Again after rolling my scalp was peppered with a few red blood spots .This time I was out for blood but still no signs of much bleeding no more or less than previous rolls.

Think Ill wait a full 2 weeks till my next session.
Still to early to say for sure of any results but still very positive.