New Dermaroller Study; Thoughts, comments?

[princessRambo]

I don't believe PGE2 is a hair growth stimulant

From the gods of hair loss research, Garza and Cotsarelis:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/

To determine the prostaglandin content in the alopecic skin of the K14-Ptgs2 mice, we measured prostaglandin levels by HPLC-MS during the anagen phase of the hair follicle cycle. PGE2 was elevated in the K14-Ptgs2 mice compared to age-matched wild-type controls, as was previously shown using immunoassays measuring PGE2 and PGF2α content in biopsied mouse skin (14, 24). PGD2 was also elevated and was more abundant than PGE2 in both wild-type and K14-Ptgs2 mice. 15-dPGJ2 was elevated in K14-Ptgs2 mice compared to controls and demonstrated the largest fold increase (~14-fold), although baseline values were low (5.7 ng/g tissue) (Fig. 5E). We found low levels (18.4 ng/g tissue) of PGF2α, and an absence of prostacyclin (6k-PGF1α) and thromboxane (TxB2) (Fig. 5E), which are not known to be present in normal skin. Together, the balding phenotype in these mice is likely a result of the overwhelming PGD2 and 15-dPGJ2 inhibitory effects on the hair follicle, despite the presence of PGE2, a known promoter of hair growth (20).

Can someone provide links to studies that show the following?

minoxidil promotes PGE2

http://bit.ly/17lMKa9

We demonstrate here that minoxidil is a potent activator of purified PGHS-1 (AC50 = 80 microM), as assayed by oxygen consumption and PGE2 production. This activation was also evidenced by increased PGE2 production by BALB/c 3T3 fibroblasts and by human dermal papilla fibroblasts in culture. Our findings suggest that minoxidil and its derivatives may have a cytoprotective activity in vivo and that more potent second-generation hair growth-promoting drugs might be designed, based on this mechanism.

Can someone provide links to studies that show the following?

PGE2 promotes FGF9

http://bit.ly/17lNfkC

Collectively, we demonstrate, for the first time, that PGE2 can directly induce FGF-9 expression via a novel signaling pathway involving EP3, PKCδ, and a member of the ETS domain-containing transcription factor superfamily in primary human endometriotic stromal cells. Our findings may also provide a molecular framework for considering roles for PGE2 in FGF-9-related embryonic development and/or human diseases.

Also, it would be good to list everything that promotes FGF9 (directly or indirectly) and with references

Can someone please come and do me some cleaning in my house, I have a wife gone on business trip and a pile of dishes, dirty clothes and $hit all over from a baby that will not stop pooping every two hours, thanks in advance

 

[pinotq]

Jaded, Are you using a 540 pin dermaroller. If you have a fair amount of hair, this will cut and pull it and you will lose a noticeable amount of hair. I switched to a 192 pin roller and experienced no noticable hair loss after rolling.

 

[albert]

Jaded, Are you using a 540 pin dermaroller. If you have a fair amount of hair, this will cut and pull it and you will lose a noticeable amount of hair. I switched to a 192 pin roller and experienced no noticable hair loss after rolling.

Jaded, I wasn't aware you were using a 540 pin roller (if you actually have it). Of course that would be the main problem. I'm using a ~200 pin one and I've not long but either short hair and have no problems - eventually the hair tangles but it's not a big issue.

 

[closetmetrosexual]

i just went crazy with a 0.5mm roller fully pressed in. Results: I freaking loved it, almost 0 pain, except around the temples, it wasn't bad at all. Then when I was done, I closely examined everywhere, zero blood, but my scalp was as red as when I used the 1.5mm. Intersting:wow:

As I wrote in an earlier post:
Until I came across this thread, I had been rolling for a year or so, with a 1.0mm 192 needle roller - every Friday.
I never pressed hard. In fact, I followed the general instructions for dermarolling that say only to apply light pressure. It still hurt like a b**ch, though.
I did get red every time. The redness lasted for 2-3 days. About 75% of the times I rolled, I applied Tretinoin aka Retin-A (all-trans retinoic acid) immediately after rolling.

During this year, I also used minoxidil for about five months [but only on temples + hairline].

I never saw any results whatsoever. Not even shedding.
Only thing that happened was that my left temple continued to thin - and is now virtually bald. [I do not attribute the thinning of the temple to the rolling. It would've happened anyway]

So, my own personal conclusion is that if you want to roll, roll hard. Go to town, and use a 1.50-1.75mm needle length. Get bloody.
Redness alone did nothing for me.

I made my avatar for a good reason.

 

[mj9]

From the gods of hair loss research, Garza and Cotsarelis:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/





http://bit.ly/17lMKa9





http://bit.ly/17lNfkC





Can someone please come and do me some cleaning in my house, I have a wife gone on business trip and a pile of dishes, dirty clothes and $hit all over from a baby that will not stop pooping every two hours, thanks in advance

Haha thanks! I'll come by and give you a hand once we manage to get tonnes of hair growth on our heads!

Here are the links for anyone wanting to see the originals

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1636777/
http://www.ncbi.nlm.nih.gov/pubmed/9008235

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Also, it would be good to list everything that promotes FGF9 (directly or indirectly) and with references

I'l get the ball rolling:

Retinoic acid
http://ac.els-cdn.com/0014579395008...t=1381594795_6a37889a7ef2fc555ab7b525fbb7c7e0
PGE2
http://www.fasebj.org/cgi/content/meeting_abstract/20/4/A71-d



We should keep in mind that these might not work on our heads as the studies were done on specific types of tissue (and animals).

 

[cthulhu2.0]

From the gods of hair loss research, Garza and Cotsarelis:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/





http://bit.ly/17lMKa9





http://bit.ly/17lNfkC





Can someone please come and do me some cleaning in my house, I have a wife gone on business trip and a pile of dishes, dirty clothes and $hit all over from a baby that will not stop pooping every two hours, thanks in advance

So I'm guessing I should lay off the fish oil??????? Maybe it's the reason I haven't been getting the gains I hoped for. btw i take a mixture of PS/omega 3 every day

 

[princessRambo]

I remember a guy Kofi that talks very well about equol daizein
http://www.disease-treatment.com/showthread.php?t=60621
http://alt.baldspot.narkive.com/52KS...d-soy-hey-kofi

Thanks Armando, this post fell through the cracks and I have missed it, . I love browsing through alt.balspot, such a wealth of information I have learned from that site when I first started looking into hair loss. So many smart and dedicated helpers with links to many good studies in there, unless you run into posts from a guy by the name of Ernie Primeau...

@closet: Thanks for the tip, are you noticing any improvement with deep rolling?

On a unrelated note, here are my daily internal drugs, I might be missing a few because of space constraint

 

[cthulhu2.0]

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



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:

I believe you are spot on with this explanation. It's like the use of ethanol for fuel vs straight up gasoline.

 

[princessRambo]

I don't understand.. where in my post did I imply that fish oil was bad? :s

 

[closetmetrosexual]

@closet: Thanks for the tip, are you noticing any improvement with deep rolling?

Nothing yet.

So far, I've only rolled twice for 'real' (bloody).
I'm doing it at two-week intervals.

I do not expect any results until we hit x-mas.
I have taken photos. Will post if I see results.


Still debating if I should keep on using Retin-A or not. (to combat fibrosis)
But a full year of Retina-A has not done anything to fight hairloss for me. Perhaps it was detrimental to use it.

 

[Kirby]

Jaded, Are you using a 540 pin dermaroller. If you have a fair amount of hair, this will cut and pull it and you will lose a noticeable amount of hair. I switched to a 192 pin roller and experienced no noticable hair loss after rolling.

I use a 192 pin roller, and lost no hair on my first rolling session - roll slowly and carefully, surgically even, and hair pulling won't be an issue from my experience.

 

[Jorged]

During this year, I also used minoxidil for about five months [but only on temples + hairline].

I never saw any results whatsoever. Not even shedding.
Only thing that happened was that my left temple continued to thin - and is now virtually bald. [I do not attribute the thinning of the temple to the rolling. It would've happened anyway]

If you were using minoxidil and then you stopped using it, a lot of the thinning in your temple may actually be because of this. minoxidil is a "funny treatment" by itself, once you start you must stick to it for life. I was stupid enough to stop using minoxidil while trying another PLOF approach (AQ Advanced Hair fraud anyone?), and my hairline and temples went to oblivion. Even after restarting using minoxidil and using it consistently for years now I could not get back all I had before.

I must say with the deep rolling approach may be wiser to give more time between sessions, and not just a week. As I said in my previous post I am only using 1.0mm needle dermaroller and, at least for me, that's enough to make my scalp bleed quite seriously. I had in fact my last session on wednesday (4th) and even today, 4 days later, the skin still looks noticeably red in some areas and painfull to touch with my hands.

I see small black dots along the hairline, and some vellus hairs are becoming thicker (blond tip, darker in the base). Also my skin is quite dry, feel a bit tight and like it's going to start peeling. Princessrambo freak the hell out of me mentioning the scarring alopecia.

 

[squeegee]

Minoxidil-induced hair growth is mediated by adenosine in cultured dermal papilla cells: possible involvement of sulfonylurea receptor 2B as a target of minoxidil.

Li M, Marubayashi A, Nakaya Y, Fukui K, Arase S.
Source

Department of Dermatology, School of Medicine, The University of Tokushima, Tokushima, Japan.

Abstract

The mechanism by which minoxidil, an adenosine-triphosphate-sensitive potassium channel opener, induces hypertrichosis remains to be elucidated. Minoxidil has been reported to stimulate the production of vascular endothelial growth factor, a possible promoter of hair growth, in cultured dermal papilla cells. The mechanism of production of vascular endothelial growth factor remains unclear, however. We hypothesize that adenosine serves as a mediator of vascular endothelial growth factor production. Minoxidil-induced increases in levels of intracellular Ca(2+) and vascular endothelial growth factor production in cultured dermal papilla cells were found to be inhibited by 8-sulfophenyl theophylline, a specific antagonist for adenosine receptors, suggesting that dermal papilla cells possess adenosine receptors and sulfonylurea receptors, the latter of which is a well-known target receptor for adenosine-triphosphate-sensitive potassium channel openers. The expression of sulfonylurea receptor 2B and of the adenosine A1, A2A, and A2B receptors was detected in dermal papilla cells by means of reverse transcription polymerase chain reaction analysis. In order to determine which of the adenosine receptor subtypes contribute to minoxidil-induced hair growth, the effects of subtype-specific antagonists for adenosine receptors were investigated. Significant inhibition in increase in intracellular calcium level by minoxidil or adenosine was observed as the result of pretreatment with 8-cyclopentyl-1,3-dipropylxanthine, an antagonist for adenosine A1 receptor, but not by 3,7-dimethyl-1-propargyl-xanthine, an antagonist for adenosine A2 receptor, whereas vascular endothelial growth factor production was blocked by both adenosine A1 and A2 receptor antagonists. These results indicate that the effect of minoxidil is mediated by adenosine, which triggers intracellular signal transduction via both adenosine A1 and A2 receptors, and that the expression of sulfonylurea receptor 2B in dermal papilla cells might play a role in the production of adenosine.

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.123 A RANDOMIZED TRIAL OF ADENOSINE IN ANDROGENETIC ALOPECIA

Yasushi Watanabe, Kelshi Nagashima, Noriro Hanzawa, Masashl Ogo, Akihlro Ishino, Yosuke Nakazawa, Masaaki Uemura, and Masahiro Tajima

Watanabe Dermatological clinic, Tokyo, Shinjuku Biru Clinic, Tokyo, Shiseido Science division, Tokyo and Shiseido Research Center, Yokohama, Japan

Objective: Adenosine up-regulates the expression of fibroblast growth factor 7 (FGF7) and vascular endothelial growth factor (VEGF) on cultured dermal papilla cells via adenosine receptors. We therefore speculated that adenosine stimulates growth of hair fiber due to the action of FGF7 and VEGF for epithelial cells in hair follicles. In this study,we performed a clinical trial to investigate the efficacy and safety of adenosine in hairloss associated with androgenetic alopecia (Androgenetic Alopecia).

Methods: Ahundred and four volunteers with AGAwere registered In a randomized double-blind trial that used an adenosine (0.7S%) topical lotion or niacin amide (0.1%)topical lotion twice daily for 6 months. Efficacy was evaluated by investigator assessments of change in global scalp coverage, change in the ratio of veilus-like(under 40 micrometers in diameter) and thick hairs (not less 60 micrometers or 80 micrometers in diameter), and hair density, in vertex.

Results: Fifty-one of 52 adenosine-treated subjects and 50 of 52 niacin amide-treated subjects completed the 6-month study. For global improvement, adenosine was significantly superior to niacin amide. Treatment with either lotion resulted in a significantlydecreased ratio of vellus- like hair and also significantly increased the ratio of thick hair, but did not change hair density. Regarding the Increase in the ratio of thick hair, adenosine was significantly superior to niacin amide. Adverse effects were not found.

Conclusion: In men with Androgenetic Alopecia,adenosine increased hair growth and thickened vellus-like hair without side effects. It would appear that the efficacy of hair growth results from the effects of FGF7 and VEGF which are stimulated by activation of adenosine receptors on dermal papilla cells.

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Intracellular adenosine triphosphate delivery enhanced skin wound healing in rabbits.

Ann Plast Surg. 2009 Feb;62(2):180-6. doi: 10.1097/SAP.0b013e31817fe47e.
Intracellular adenosine triphosphate delivery enhanced skin wound healing in rabbits.

Wang J, Zhang Q, Wan R, Mo Y, Li M, Tseng MT, Chien S.
Source

Department of Surgery, University of Louisville School of Medicine, KY, USA. j0wang19@louisville.edu

Abstract

Small unilamellar lipid vesicles were used to encapsulate adenosine triphosphate (ATP-vesicles) for intracellular energy delivery. This technique was tested in full-thickness skin wounds in 16 adult rabbits. One ear was rendered ischemic by using a minimally invasive surgery. The other ear served as a normal control. Four circular full-thickness wounds were created on the ventral side of each ear. ATP-vesicles or saline was used and the wounds were covered with Tegaderm (3M, St. Paul, MN). Dressing was changed and digital photos were taken daily until all the wounds were healed. The mean healing times of ATP-vesicles-treated wounds were significantly shorter than that of saline-treated wounds on ischemic and nonischemic ears. Histologic study indicated better-developed granular tissue and reepithelialization in the ATP-vesicles-treated wounds. The wounds treated by ATP-vesicles exhibited extremely fast granular tissue growth. More CD31 positive cells were seen in the ATP-vesicles-treated wounds. This preliminary study shows that direct intracellular delivery of ATP can accelerate the healing process of skin wounds on ischemic and nonischemic rabbit ears. The extremely fast granular tissue growth was something never seen or reported in the past.​

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Use of minoxidil for wound healing
Abstract
A method for the promotion or acceleration of wound healing by a treatment with minoxidil is disclosed. The minoxidial can be administered by topical application, oral administration, injection or any combination thereof. Treatment with minoxidil is effective for promoting the migration of epithelial cells in a wound or in tissues such as cornea and the like. Methods for identifying binding sites for minoxidil in cells based on their affinity for the compound in attachment or chemotactic assays are described.

http://www.google.ca/patents/US4912111

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J Dermatol. 2008 Dec;35(12):763-7. doi: 10.1111/j.1346-8138.2008.00564.x.
Adenosine increases anagen hair growth and thick hairs in Japanese women with female pattern hair loss: a pilot, double-blind, randomized, placebo-controlled trial.

Oura H, Iino M, Nakazawa Y, Tajima M, Ideta R, Nakaya Y, Arase S, Kishimoto J.
Source

Department of Dermatology, School of Medicine, University of Tokushima, Tokushima, Japan.

Abstract

Adenosine upregulates the expression of vascular endothelial growth factor and fibroblast growth factor-7 in cultured dermal papilla cells. It has been shown that, in Japanese men, adenosine improves androgenetic alopecia due to the thickening of thin hair due to hair follicle miniaturization. To investigate the efficacy and safety of adenosine treatment to improve hair loss in women, 30 Japanese women with female pattern hair loss were recruited for this double-blind, randomized, placebo-controlled study. Volunteers used either 0.75% adenosine lotion or a placebo lotion topically twice daily for 12 months. Efficacy was evaluated by dermatologists and by investigators and in phototrichograms. As a result, adenosine was significantly superior to the placebo according to assessments by dermatologists and investigators and by self-assessments. Adenosine significantly increased the anagen hair growth rate and the thick hair rate. No side-effects were encountered during the trial. Adenosine improved hair loss in Japanese women by stimulating hair growth and by thickening hair shafts. Adenosine is useful for treating female pattern hair loss in women as well as androgenetic alopecia in men.

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Dermal benefits of topical D-ribose

Abstract

Our aging skin undergoes changes with reductions in collagenous and elastic fibers, fibroblasts, mast cells, and macrophages with free radical production, which can result in reduced skin tone and wrinkle formation. Fibroblasts are important for dermal integrity and function with a decrease in function producing less skin tone, thinning, and wrinkle formation. Dermal levels of adenosine triphosphate (ATP) decline with aging, potentially altering dermal function. Supplemental D-ribose, a natural occurring carbohydrate, enhances ATP regeneration. D-ribose-based studies demonstrated benefits in both cell culture fibroblastic activities and a subsequent clinical study in women with decreased skin tone with wrinkles. Supplemental D-ribose may offer this needed cellular benefit.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047922/

Dermal penetration of creatine from a face-care formulation containing creatine

J Cosmet Dermatol. 2011 Dec;10(4):273-81. doi: 10.1111/j.1473-2165.2011.00579.x.
Dermal penetration of creatine from a face-care formulation containing creatine, guarana and glycerol is linked to effective antiwrinkle and antisagging efficacy in male subjects.

Peirano RI, Achterberg V, Düsing HJ, Akhiani M, Koop U, Jaspers S, Krüger A, Schwengler H, Hamann T, Wenck H, Stäb F, Gallinat S, Blatt T.
Source

Department of Skin Biology and Skin Structure, Beiersdorf AG Research and Development, Unnastrasse 48, Hamburg, Germany.

Abstract

BACKGROUND:

  The dermal extracellular matrix provides stability and structure to the skin. With increasing age, however, its major component collagen is subject to degeneration, resulting in a gradual decline in skin elasticity and progression of wrinkle formation. Previous studies suggest that the reduction in cellular energy contributes to the diminished synthesis of cutaneous collagen during aging.
AIMS:

  To investigate the potential of topically applied creatine to improve the clinical signs of skin aging by stimulating dermal collagen synthesis in vitro and in vivo.
PATIENTS/METHODS:

  Penetration experiments were performed with a pig skin ex vivo model. Effects of creatine on dermal collagen gene expression and procollagen synthesis were studied in vitro using cultured fibroblast-populated collagen gels. In a single-center, controlled study, 43 male Caucasians applied a face-care formulation containing creatine, guarana extract, and glycerol to determine its influence on facial topometric features.
RESULTS:

  Cultured human dermal fibroblasts supplemented with creatine displayed a stimulation of collagen synthesis relative to untreated control cells both on the gene expression and at the protein level. In skin penetration experiments, topically applied creatine rapidly reached the dermis. In addition, topical in vivo application of a creatine-containing formulation for 6 weeks significantly reduced the sagging cheek intensity in the jowl area as compared to baseline. This result was confirmed by clinical live scoring, which also demonstrated a significant reduction in crow's feet wrinkles and wrinkles under the eyes.
CONCLUSIONS:

  In summary, creatine represents a beneficial active ingredient for topical use in the prevention and treatment of human skin aging.
© 2011 Wiley Periodicals, Inc.


Adenosine promotes wound healing and mediates angiogenesis in response to tissue injury via occupancy of A(2A) receptors.

Montesinos MC, Desai A, Chen JF, Yee H, Schwarzschild MA, Fink JS, Cronstein BN.
Source

Department of Medicine, New York University School of Medicine, New York, New York, USA.

Abstract

Recent evidence indicates that topical application of adenosine A(2A) receptor agonists, unlike growth factors, increases the rate at which wounds close in normal animals and promotes wound healing in diabetic animals as well as growth factors, yet neither the specific adenosine receptor involved nor the mechanism(s) by which adenosine receptor occupancy promotes wound healing have been fully established. To determine which adenosine receptor is involved and whether adenosine receptor-mediated stimulation of angiogenesis plays a role in promotion of wound closure we compared the effect of topical application of the adenosine receptor agonist CGS-21680 (2-p-[2-carboxyethyl]phenethyl-amino-5'-N-ethylcarboxamido-adenosine) on wound closure and angiogenesis in adenosine A(2A) receptor knockout mice and their wild-type littermates. There was no change in the rate of wound closure in the A(2A) receptor knockout mice compared to their wild-type littermates although granulation tissue formation was nonhomogeneous and there seemed to be greater inflammation at the base of the wound. Topical application of CGS-21680 increased the rate of wound closure and increased the number of microvessels in the wounds of wild-type mice but did not affect the rate of wound closure in A(2A) receptor knockout mice. Similarly, in a model of internal trauma and repair (murine air pouch model), endogenously produced adenosine released into areas of internal tissue injury stimulates angiogenesis because there was a marked reduction in blood vessels in the walls of healing air pouches of A(2A) receptor knockout mice compared to their wild-type controls. Inflammatory vascular leakage and leukocyte accumulation in the inflamed air pouch were similarly reduced in the A(2A) receptor knockout mice reflecting the reduced vascularity. Thus, targeting the adenosine A(2A) receptor is a novel approach to promoting wound healing and angiogenesis in normal individuals and those suffering from chronic wound

http://www.ncbi.nlm.nih.gov/pubmed/12057906

Adenosine receptors in wound healing, fibrosis and angiogenesis.

Feoktistov I, Biaggioni I, Cronstein BN.
Source

Division of Cardiovascular Medicine, Vanderbilt University, Nashville, TN 37232-6300, USA. igor.feoktistov@vanderbilt.edu

Abstract

Wound healing and tissue repair are critical processes, and adenosine, released from injured or ischemic tissues, plays an important role in promoting wound healing and tissue repair. Recent studies in genetically manipulated mice demonstrate that adenosine receptors are required for appropriate granulation tissue formation and in adequate wound healing. A(2A) and A(2B) adenosine receptors stimulate both of the critical functions in granulation tissue formation (i.e., new matrix production and angiogenesis), and the A(1) adenosine receptor (AR) may also contribute to new vessel formation. The effects of adenosine acting on these receptors is both direct and indirect, as AR activation suppresses antiangiogenic factor production by endothelial cells, promotes endothelial cell proliferation, and stimulates angiogenic factor production by endothelial cells and other cells present in the wound. Similarly, adenosine, acting at its receptors, stimulates collagen matrix formation directly. Like many other biological processes, AR-mediated promotion of tissue repair is critical for appropriate wound healing but may also contribute to pathogenic processes. Excessive tissue repair can lead to problems such as scarring and organ fibrosis and adenosine, and its receptors play a role in pathologic fibrosis as well. Here we review the evidence for the involvement of adenosine and its receptors in wound healing, tissue repair and fibrosis.

http://www.ncbi.nlm.nih.gov/pubmed/19639289



​

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Abstract

Adenosine—a purine nucleoside generated extracellularly from adenine nucleotides released by cells as a result of direct stimulation, hypoxia, trauma, or metabolic stress—is a well-known physiologic and pharmacologic agent. Recent studies demonstrate that adenosine, acting at its receptors, promotes wound healing by stimulating both angiogenesis and matrix production. Subsequently, adenosine and its receptors have also been found to promote fibrosis (excess matrix production) in the skin, lungs, and liver, but to diminish cardiac fibrosis. A commonly ingested adenosine receptor antagonist, caffeine, blocks the development of hepatic fibrosis, an effect that likely explains the epidemiologic finding that coffee drinking, in a dose-dependent fashion, reduces the likelihood of death from liver disease. Accordingly, adenosine may be a good target for therapies that prevent fibrosis of the lungs, liver, and skin.



http://f1000.com/prime/reports/b/3/21/

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Use of D-ribose, including as a topical vehicle, to promote faster healing, including from surgical procedures

http://www.google.com/patents/US20040127428

 

[princessRambo]

Should we be limiting our intake of Omega-3 fats during days 1-3 during the inflammation/increased pge2 stage,

Dietary Fish Oil Reduces Basal and Ultraviolet B-Generated PGE2 Levels in Skin and Increases the Threshold to Provocation of Polymorphic Light Eruption

The sunburn response is markedly reduced by dietary fish oil rich in -3 polyunsaturated fatty acids. Because prostaglandins mediate the vasodilatation, we examined the effect of fish oil on ultraviolet (UV) B-induced prostaglandin metabolism. In addition we assessed the potential photoprotective effect of fish oil in light-sensitive patients. Thirteen patients with polymorphic light eruption received dietary supplements of fish oil rich in -3 polyunsaturated fatty acids for 3 months. At baseline and 3 months, the minimal erythema dose of UVB irradiation was determined, and a graded UVA challenge given to a forearm to assess the threshold dose for papule provocation. Suction blisters were raised on the other forearm, on control skin, and on skin irradiated with four times the minimal erythema dose of UVB 24 h previously, and blister fluid prostaglandin E2 was measured by radioimmunoassay. Following 3 months of fish oil, the mean minimal erythema dose of UVB irradiation increased from 19.8 2.6 to 33.8 3.7 mJ/cm2 (mean SEM), p < 0.01. The UVA provocation test was positive in 10 patients at baseline, and after 3 months nine of these showed reduced sensitivity to papule provocation, p < 0.001. Before fish oil, PGE2 increased from 8.6 (SEM 2.1) ng/ml in control skin to 27.2 (11) ng/ml after UVB, p < 0.01. Following 3 months of fish oil, PGE2 decreased to 4.1 (1) and 9.6 (2.4) ng/ml in control and irradiated skin, respectively, p < 0.05. Reduction of UV-induced inflammation by fish oil may be due, at least partially, to lowered prostaglandin E2 levels. The photoprotection against UVA-provocation of a papular response suggests a clinical application for fish oil in polymorphic light eruption.

This is the kind of study I mentioned before where you have to be really careful to interpret what the study means, or it could be very very misleading. I have said earlier that both Cox1 and Cox 2 produce both PGE2 and PGD2, the difference is it depends on context. Usually (not always), prostaglandins resulting from Cox 1 are used for carrying out the body's regular functions, while the PGs from Cox 2 are usually the result of an inflammatory response. Below is a neat site describing the differences, you can even download a pdb file and play with the molecules in 3D if you want to experience some pure nerdgasm:

http://cti.itc.virginia.edu/~cmg/Demo/pdb/cycox/cycox.html

There are two isoforms of COX in animals: COX-1, which carries out normal, physiological production of prostaglandins, and COX-2, which is induced by cytokines, mitogens and endotoxins in inflammatory cells, and which is responsible for the production of prostaglandins in inflammation.

This is not an absolute truth as they are cases where the major inflammatory response is induced by COX 1, in short, the body is a complex.

http://www.ncbi.nlm.nih.gov/pubmed/20880055

Now in your study above, does it mean that omega 3 suppressing PGE2 is evil? Of course not, it is the wrong kind of PGE2 as result of inflammation. The PGE2 in the male pattern baldness context is in fact lowered because of inflammation, PGD2 is the resulting inflammatory prostaglandin. Fish oil being highly anti-inflammatory, what do you think it does in this context? Your deduction from looking at this fish oil study reminds me of a recent fish oil study where the idiots concluded that fish oils increases prostate cancer in a correlative manner, and it polluted the media for a few weeks. Looking at that same study, you can look at the same data-set they used and correlate that people driving a Cadillac have an increased risk of prostate cancer.

 

[squeegee]

Thanks Armando, this post fell through the cracks and I have missed it, . I love browsing through alt.balspot, such a wealth of information I have learned from that site when I first started looking into hair loss. So many smart and dedicated helpers with links to many good studies in there, unless you run into posts from a guy by the name of Ernie Primeau...

@closet: Thanks for the tip, are you noticing any improvement with deep rolling?

On a unrelated note, here are my daily internal drugs, I might be missing a few because of space constraint

Here is my daily intake.. I have more but I could not fit everything in the pic..

 

[benjt]

Nothing new exactly regarding adenosine, at least not for me

You can read up on adenosine in the first thread that I created here - the one where I detailed my story with minoxidil. I substituted minoxidil with adenosine temporally, which definitely had some funny results. You can basically put a human to sleep with adenosine instantly (but at the same time also make them feel nauseous).

Long story short, summarizing my findings:
- adenosine puts many processes in the body to a halt or slows them down strongly; this includes nerve and neural activity, but also dermal metabolic stuff and muscles
- The study saying that "minoxidil's effects are mediated by adenosine" is not necessarily correct as indicated by some other studies. It may just be that the metabolic outcome of minoxidil in the body (minoxidil sulf... something) is chemically close to adenosine, thus they are agonists.
- The effects of adenosine and minoxidil are very similar
- Disadvantage: Dosing of adenosine is not easy, small overdoses (example: 8 drops instead of 6) leed to nausea, dizziness, extreme sleepiness (12 to 14 drops and you'll fall asleep within 5 minutes and maybe puke on the way)
- Advantage: very much lowered half life, thus no permanent side effects like those of minoxidil; probably though also the positive effects are not as strong as minoxidil

If you want details, read about it in my minoxidil thread. I did an in-depth account of my experience with adenosine there.

 

[closetmetrosexual]

If you were using minoxidil and then you stopped using it, a lot of the thinning in your temple may actually be because of this. minoxidil is a "funny treatment" by itself, once you start you must stick to it for life. I was stupid enough to stop using minoxidil while trying another PLOF approach (AQ Advanced Hair fraud anyone?), and my hairline and temples went to oblivion. Even after restarting using minoxidil and using it consistently for years now I could not get back all I had before.

Well, my temple was already thinning at the time I began minoxidil. Its really seems to have kept the same pace of thinning ever since.
minoxidil did not seem to impact it positively or negatively. But I cannot know for sure, of course.

@ Being on mix for life... I hope this isn't true. I had heard this before.

But I have also heard that all you lose when you quit minoxidil is whatever minoxidil gave you in the time you used it.
Say you were losing 100 hairs a month (not just shedding, but 100 follicles kicking the bucket for good) without minoxidil.
Then you introduce minoxidil, and reduce the death toll of your hairs down to 20 (instead of 100). That's a 80 hair per month 'surplus'.
Now, say you were on minoxidil for 24 months. Normally, you would have lost 2400 (24 x 100) hairs in this period. But you only lost 480 (24 x 20) hairs due to using minoxidil.

Now you quit minoxidil, and you rapidly lose 1920 hairs (2400 - 480 = 1920). This will look bad because its so quick and sudden.
But in fact, you only lost the hairs that minoxidil was keeping you from losing in the time you were on minoxidil.

So, which one is true? I really don't want to be on minoxidil for life. 8O

 

[princessRambo]

@squeegee I am not seeing anything to fight DHT or a strong NF Kb inhibitor. Are you taking finasteride? Do you use each of these religiously daily?

@benjt I personally believe minoxidil's major hair growth benefit is simply upregulation of VEGF and increase of PGE2 synthesis, that's about the size of it. I never took the potassium channel opener crap seriously.

@fred: I have no idea, I buy in bulk from amazon most of the time. Also, If you live in a socialist country like Canada you can get everything for free :woot:

*bracing for onslaught from angry sausage with yellow mustard*

 

[selfaware]

i just went crazy with a 0.5mm roller fully pressed in. Results: I freaking loved it, almost 0 pain, except around the temples, it wasn't bad at all. Then when I was done, I closely examined everywhere, zero blood, but my scalp was as red as when I used the 1.5mm. Intersting:wow:

Interesting indeed. Makes one wonder....

Just what does constitute 'wounding' ?

For instance...you walk right into the corner of a table...owww!...f*ck!...and next day, you see a small but deep-red bruise on your leg. Is this a 'wound' ? Sure seems like it to me...even tho the skin was not broken.

For a while, I've been doing a 'tapping' of the two frontal bald zones, using my fingernails to focus pressure into tiny area to create highest impact force and depth. I tap hard enough so it hurts, but is endurable....move around, and also rotate hands, while doing it. Is this causing some 'micro-bruising' ? If so, is that enough of a 'wounding' to stimulate dermal remodeling/regrowth ?

Questions questions....always with the questions! (tip o' the hat to Kelly's Heroes.. )

By the way, I wanted to mention, in ref to the Emu oil study....note how it said that emu ALONE had no effect on healing. It was Emu "lotion" that gave double the healing. Which contains Vit-E and 'botanical' oil. I need to read the whole study text again, and see if they specify WHICH vitamin-E ! Since it appears that 90% of available E's are all tocopherols, not tocotrienols....and tocopherols don't do squat. Worse than that, I just found a study showing that tocopherols CANCEL the beneficial actions of tocotrienols...at least in some situations (study was on internal disease/health, not hair stuff). That would mean that even if we source straight tocotrienols, if we're eating anything with "vitamin E" in it, then we are surely getting tocopherols, and perhaps canceling out our pricey fancy tocotrienols. And every damn thing in the world is 'enriched' with vitamins these days...can't seem to get away from it. Anyway, thought I'd mention this. And back to my main point...that emu-oil study may be showing us that Emu is valuable as a -carrier- of lipid-soluble vitamins and other helpful things....but doesn't contribute on its own.

Also...this cracked me up today...

"RadiantLife HRx is a Low Level Laser Therapy (LLLT) device, designed for hair rejuvenation. The device supplies pulsed 655 nm laser light energy to the scalp. This wavelength of laser light is able to penetrate 8 - 10 mm into the scalp tissue, that is just beyond the hair bulb."

sheet!....10mm is 3/8" of an inch!...uhh...yeah...that's "beyond the hair-bulb" all right!...like, 7mm into the damn skull-bone!...lol..

Gawd...there is just SO much garbage out there......thank the gods for this thread and the members who contribute real, proven, info, I say.

 

[squeegee]

@squeegee I am not seeing anything to fight DHT or a strong NF Kb inhibitor. Are you taking finasteride? Do you use each of these religiously daily?

@benjt I personally believe minoxidil's major hair growth benefit is simply upregulation of VEGF and increase of PGE2 synthesis, that's about the size of it. I never took the potassium channel opener crap seriously.

@fred: I have no idea, I buy in bulk from amazon most of the time. Also, If you live in a socialist country like Canada you can get everything for free :woot:

*bracing for onslaught from angry sausage with yellow mustard*

Princess.. I go to the gym daily. I am a man, I embrace DHT! I took heavy doses of finasteride in the past. It worked, I had no sides whatsoever, then tried dutasteride just because and had the worst side effects ever. I was weak and that **** killed my hairline. I reconstructed my hairline with minoxidil/ Miconazole NItrate 4% while taking internal DHEA LOL.. so **** DHT inhibitor.. I learned to not ****ing around with your endocrine system. Inflammation is the b**ch. I believe us balders that the missing link is the lack of endogenous antioxidants or proteolytic enzymatic activity. There are guys out there lifting with 800x the DHT level in their blood with a full head of hair.


Decrease in glutathione may be involved in pathogenesis of acne vulgaris.

Ikeno H, Tochio T, Tanaka H, Nakata S.
Source

Ikeno Clinic of Dermatology and Dermatologic Surgery, 1-14-4 Ginza Chuo-ku, Tokyo 104-0061, Japan. cubikeno@tea.ocn.ne.jp

Abstract

BACKGROUND:

Some past studies reported that oxidative stress components such as reactive oxygen species (ROS) or lipid peroxide (LPO) are involved in the pathogenesis and progression of acne vulgaris. In this study, we hypothesized that the pathogenesis of acne vulgaris may depend on the differences in antioxidative activity among antioxidants in our body. We collected samples of stratum corneum from acne patients and healthy subjects and compared the quantity of gluthathione (GSH), one of many antioxidative components in our body, for comparison.
METHODS:

Samples of stratum corneum were collected from facial acne-involved lesion, facial uninvolved area, and the medial side of the upper arm in acne vulgaris patients. Similarly, samples were collected from a facial uninvolved area and the medial side of the upper arm in healthy subjects. The quantity of GSH was measured in each area. In vitro effects of alpha-melanocyte stimulating hormone (α-MSH) on GSH synthesis-related gene were also examined.
RESULTS:

The quantity of GSH in stratum corneum from each area was significantly lower in acne vulgaris patients than that of healthy subjects. There was no significant difference in quantity of GSH between the acne-involved lesion and uninvolved area in acne patients. In vitro studies showed that the expression level of Glutamate-cysteine ligase catalytic subunit (GCLC), one of the GSH synthesis-related genes, was significantly decreased by the additional use of α-MSH.

CONCLUSIONS:

We conclude that a decline in antioxidative activity led by a decrease in GSH quantity may play an important role in pathogenesis of acne vulgaris. The use of α-MSH may further decrease the GSH level.