New Dermaroller Study; Thoughts, comments?

[selfaware]

PGE2 is supposed to raise FGF-9 levels which Follica states induces new hair growth. Thus:

Wound -> minoxidil -> PGE2 -> FGF-9 -> New Hair Follicle -> Look Good -> Get Laid

ROFL...

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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

tee hee...

hey, this bit just caught my eye....not sure I've seen discussion of it...

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.


'derivatives' ??....WHAT derivatives? Did this tenderfoot with the very green horns miss something??

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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).

...and 95% of all such work is done in CULTURE DISHES...NOT in living bodies. Still, it's better than no research at all!

 

[squeegee]

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.

Are we talking about the same stuff Benjit? ATP or adenosine Trisphophate is what makes your heart beat, it is the fuel for cellular activity. No ATP, no life.

http://faculty.clintoncc.suny.edu/f...01 lectures/cellular respiration/cellular.htm

 

[princessRambo]

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 enzymatic activity. There are guys out there lifting with 800x the DHT level in their blood with a full head of hair.

+1 trillion to that. I always thought completely inhibiting 5AR, which is used everyone in the body, including the brain, is borderline insanity, I am all for compromise, slightly reducing it might be okay, like lowering bad cholesterol vs almost complete inhibition with a synthetic drug. It's all about balance imo.

 

[DesperateOne]

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.

I did the same ****ingmistake, switching from finasteride to dutasteride because I was greedy thinking I could gain more. I would be pretty good right now if I had not done that, even worse I ordered from an Indian online site which is not even online anymore because they sold sugar pills instead. When is this madness going to end...

 

[mj9]

I wonder if Follica havent released anything yet because they still trying to figure out how to stop people from replicating the technique at home with a demaroller and this other "compound"

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This other compound is probably something really stupid like semen or something...

 

[Jorged]

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

I do actually believe is a combination of both. As we all know already in male pattern baldness alopecia you don't go bald from one day to the next like in other types of alopecias. It is an overall thinning process that in some people goes faster than in others. minoxidil not only works awakening hairs that are already miniaturized, it also starts "feeding" hairs that have just started the process, so when you stop minoxidil you will not only lose those awakened hairs, but also other thinning hairs that have become "addicted" to it.

I don't want to be on minoxidil for life either, not on finas. For being in 2013 both "officially approved" products by the FDA sucks big time. Now, that been said, I already learned my lesson by quitting minoxidil (and finas) once. I am NW2 and 31yo now, started fighting this sickness when I was 24, without them I would most probably be totally bald by now.

Our only hope is in neogenesis, as totally brand new hairs (pure and innocent baby hairs) would theoretically take quite a lot of time to be affected again by DHT, thinning and whatever other things that are happening down there in our scalp. I just would like Follica to stop being so shady, show once for all a proof of concept (from this infamous trials they have "supposedly" already done in humans) and work faster, way faster. It's been like 6 years already waiting for them...

 

[princessRambo]

I wonder if Follica havent released anything yet because they still trying to figure out how to stop people from replicating the technique at home with a demaroller and this other "compound"

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This other compound is probably something really stupid like semen or something...

Follica is the shadiest company known to man, these doctors are more worried about money than anything else. Look at the filing date for the fgf9 patent:

http://www.google.com/patents/EP2361119A1?cl=en

Filing date	Nov 11, 2009
Priority date	Nov 12, 2008

Now look at when the study was published and it took over the news like wildfire.

http://www.ncbi.nlm.nih.gov/pubmed/23727932

Nat Med. 2013 Jul;19(7):916-23. doi: 10.1038/nm.3181. Epub 2013 Jun 2.

They knew about fgf9 and wound healing for 5 f*king years and immediately applied for a patent in 2008, it wasn't until summer 2013 that they released the study. What else do you think they have up their sleeves? :censored:

 

[cthulhu2.0]

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

I was referring to the part where you state that minoxidil is unlikely to significantly effect fgf9 production. I remember reading that high levels of pge2 correlate with higher fgf9 to an extent but that it levels off at higher amounts.

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Follica is the shadiest company known to man, these doctors are more worried about money than anything else. Look at the filing date for the fgf9 patent:

http://www.google.com/patents/EP2361119A1?cl=en

Filing date	Nov 11, 2009
Priority date	Nov 12, 2008

Now look at when the study was published and it took over the news like wildfire.

http://www.ncbi.nlm.nih.gov/pubmed/23727932

Nat Med. 2013 Jul;19(7):916-23. doi: 10.1038/nm.3181. Epub 2013 Jun 2.

They knew about fgf9 and wound healing for 5 f*king years and immediately applied for a patent in 2008, it wasn't until summer 2013 that they released the study. What else do you think they have up their sleeves? :censored:

This is rather suspicious, but why would they wait so long if they could profit from this discovery if it is as simple as injecting fgf9 after inducing wounds

 

[squeegee]

Personal observation: my hair looks thicker during the first 3 days after derma roller. Why? releases of ATP during acute inflammation? Bringing extracellular ATP to an Hypoxic environment is a winning situation.


[h=1]Increased release of ATP from endothelial cells during acute inflammation.[/h]Bodin P, Burnstock G.
[h=3]Source[/h]Autonomic Neuroscience Institute, Royal Free Hospital School of Medicine, London, UK.

[h=3]Abstract[/h][h=4]OBJECTIVE AND DESIGN:[/h]The effects of lipopolysaccharide (LPS), a potent inflammatory mediator, on the shear stress stimulated release of adenosine triphosphate (ATP) were investigated on endothelial cells from human umbilical vein in primary culture.
[h=4]METHODS:[/h]Human umbilical vein endothelial cells (HUVEC) in primary cultures were subjected to shear stress using a cone and plate apparatus. ATP released by the cells was measured by luminometry, using a luciferin-luciferase assay.
[h=4]RESULTS:[/h]Under conditions of shear stress alone (25dyn/cm2), ATP accumulates into the culture medium and reaches a maximum after 3 to 5 min of stimulation (121.7+/-13.2 pmol/ml). The shear stress-stimulated release of ATP was significantly increased after a 4 h pre-incubation of endothelial cells with 50 microg/ml (314.4+/-26.7 pmol/ml) and 10microg/ml lipopolysaccharide (207.7+/-22.2 pmol/ml). Dexamethasone, an anti-inflammatory glucocorticoid, inhibited the effects of lipopolysaccharide.
[h=4]CONCLUSIONS:[/h]These results show that non-damaged endothelial cells release ATP under experimental inflammatory conditions and support an early role of extracellular ATP in the inflammatory process.




Microvascular insufficiency and local tissue hypoxia (male pattern baldness)

1: Med Hypotheses 2002 Apr;58(4):261-3

Hormone-induced aberrations in electromagnetic adhesion signaling as a developmental factor of androgenetic alopecia.

Matilainen VA, Keinanen-Kiukaanniemi SM.

Department of Public Health Science and General Practice, University of Oulu, Finland.

In androgenetic alopecia, overactivation of the androgen hormone cascade in genetically predisposed persons leads to miniaturization of the dermal papilla of the hair follicle and to reduction in the number of papilla cells in the scalp, but the mechanisms explaining this miniaturization have remained unclear. According to our hypothesis, the increase of dihydrotestosterone (DHT) production in the overactive androgen state inhibits cell mitosis in the dermal papilla and contributes to the induction of programmed cell death (apoptosis). Normally, DNA molecules have a negative charge, which doubles in every cell mitosis. In the catagen and telogen phases, the sulphur-rich hair moves upwards, dehydrates and develops an increasing positive charge. In a normal hair-growth cycle, the epithelial column shortens and the secondary germ is formed and it invaginates the dermal papilla by electromagnetic attraction. In the mitotic inhibition state induced by DHT, the negative charge decreases, leading to a weakening of the electromagnetic adhesion forces and weaker electrical attraction between the undifferentiated germ cells and the dermal papilla. Insulin resistance has an additional pathogenic role in the excessive miniaturization of the hair follicle. The vasoactive substances associated with endothelial dysfunction in insulin resistance induce microcirculatory disturbance, perifollicular vasoconstriction and stimulation of smooth muscle cell proliferation in the vascular wall. This leads to microvascular insufficiency and local tissue hypoxia and progressive miniaturization of hair follicles.


1: Plast Reconstr Surg 1996 May;97(6)1109-16; discussion 1117

Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.

Goldman BE, Fisher DM, Ringler SL.

Department of Plastic Surgery, Butterworth Hospital, Grand Rapids, Mich., USA.

Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
​

 

[hellouser]

I was referring to the part where you state that minoxidil is unlikely to significantly effect fgf9 production. I remember reading that high levels of pge2 correlate with higher fgf9 to an extent but that it levels off at higher amounts.

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This is rather suspicious, but why would they wait so long if they could profit from this discovery if it is as simple as injecting fgf9 after inducing wounds

One of my theories is that they'll first release a weaker version of their product, something that grows hair but now as much. They'll charge a ridiculous amount of money and people WILL pay for it as anything health related doesnt have a monetary value. Then, after they've milked the public for long enough, release an improved method of hair restoration.

Wanna know a company thats model is very much the same?

APPLE.

Steve Jobs and the rest of the marketing scum at Apple are the worlds *best* at making small incremental improvements and making ridiculous profit.

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+1 trillion to that. I always thought completely inhibiting 5AR, which is used everyone in the body, including the brain, is borderline insanity, I am all for compromise, slightly reducing it might be okay, like lowering bad cholesterol vs almost complete inhibition with a synthetic drug. It's all about balance imo.

So, would you say combining RU or CB-03-01 with dermarolling and minoxidil would be beneficial?

 

[Jlyncher]

Personal observation: my hair looks thicker during the first 3 days after derma roller. Why? releases of ATP during acute inflammation? Bringing extracellular ATP to an Hypoxic environment is a winning situation.


Increased release of ATP from endothelial cells during acute inflammation.

Bodin P, Burnstock G.
Source

Autonomic Neuroscience Institute, Royal Free Hospital School of Medicine, London, UK.

Abstract

OBJECTIVE AND DESIGN:

The effects of lipopolysaccharide (LPS), a potent inflammatory mediator, on the shear stress stimulated release of adenosine triphosphate (ATP) were investigated on endothelial cells from human umbilical vein in primary culture.
METHODS:

Human umbilical vein endothelial cells (HUVEC) in primary cultures were subjected to shear stress using a cone and plate apparatus. ATP released by the cells was measured by luminometry, using a luciferin-luciferase assay.
RESULTS:

Under conditions of shear stress alone (25dyn/cm2), ATP accumulates into the culture medium and reaches a maximum after 3 to 5 min of stimulation (121.7+/-13.2 pmol/ml). The shear stress-stimulated release of ATP was significantly increased after a 4 h pre-incubation of endothelial cells with 50 microg/ml (314.4+/-26.7 pmol/ml) and 10microg/ml lipopolysaccharide (207.7+/-22.2 pmol/ml). Dexamethasone, an anti-inflammatory glucocorticoid, inhibited the effects of lipopolysaccharide.
CONCLUSIONS:

These results show that non-damaged endothelial cells release ATP under experimental inflammatory conditions and support an early role of extracellular ATP in the inflammatory process.




Microvascular insufficiency and local tissue hypoxia (male pattern baldness)

1: Med Hypotheses 2002 Apr;58(4):261-3

Hormone-induced aberrations in electromagnetic adhesion signaling as a developmental factor of androgenetic alopecia.

Matilainen VA, Keinanen-Kiukaanniemi SM.

Department of Public Health Science and General Practice, University of Oulu, Finland.

In androgenetic alopecia, overactivation of the androgen hormone cascade in genetically predisposed persons leads to miniaturization of the dermal papilla of the hair follicle and to reduction in the number of papilla cells in the scalp, but the mechanisms explaining this miniaturization have remained unclear. According to our hypothesis, the increase of dihydrotestosterone (DHT) production in the overactive androgen state inhibits cell mitosis in the dermal papilla and contributes to the induction of programmed cell death (apoptosis). Normally, DNA molecules have a negative charge, which doubles in every cell mitosis. In the catagen and telogen phases, the sulphur-rich hair moves upwards, dehydrates and develops an increasing positive charge. In a normal hair-growth cycle, the epithelial column shortens and the secondary germ is formed and it invaginates the dermal papilla by electromagnetic attraction. In the mitotic inhibition state induced by DHT, the negative charge decreases, leading to a weakening of the electromagnetic adhesion forces and weaker electrical attraction between the undifferentiated germ cells and the dermal papilla. Insulin resistance has an additional pathogenic role in the excessive miniaturization of the hair follicle. The vasoactive substances associated with endothelial dysfunction in insulin resistance induce microcirculatory disturbance, perifollicular vasoconstriction and stimulation of smooth muscle cell proliferation in the vascular wall. This leads to microvascular insufficiency and local tissue hypoxia and progressive miniaturization of hair follicles.


1: Plast Reconstr Surg 1996 May;97(6)1109-16; discussion 1117

Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle.

Goldman BE, Fisher DM, Ringler SL.

Department of Plastic Surgery, Butterworth Hospital, Grand Rapids, Mich., USA.

Our study was designed to measure the transcutaneous PO2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous PO2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous PO2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects; however, there was no significant difference in controls. Transcutaneous PO2 was significantly lower in bald frontal scalp (32.2 +/- 2.0 mmHg) than in hair-bearing temporal scalp (51.8 +/- 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous PO2 of frontal scalp (53.9 +/- 3.5 mmHg) and temporal scalp (61.4 +/- 2.7 mmHg). Transcutaneous PO2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 +/- 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 +/- 3.5 mmHg and 61.4 +/- 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
​

Interesting, I've noticed the same thing. Also, I can practically watch my hair grow during those first 3 days after rolling.

 

[squeegee]

Interesting, I've noticed the same thing. Also, I can practically watch my hair grow during those first 3 days after rolling.

We are not the only ones reporting the same observation. L-carnitine promotes atp synthesis.. and hair growth at the same time.. Without ATP, there is no normal cellular functions, no progenitor cell migration.

Reduced human lymphocyte blastogenesis and enhancement of adenosine triphosphate (ATP) by L-carnitine.

Conti P, Reale M, Stuard S, Spoto G, Picerno F, Ferrara T, Placido FC, Barbacane RC, Albertazzi A, Errichi BM.
Source

Immunology Division, University of Chieti Medical School, Italy.

Abstract

Carnitine is associated with lipid synthesis and its deficiency may lead to cardiomegaly with parenchymal lipid in the heart, kidney and liver. In our study we found that pretreatment of peripheral blood mononuclear cells (PBMC) with serial dilutions of L-Carnitine (100 micrograms/ml-1 pg/ml) inhibits, in a dose-dependent manner, lymphocyte DNA synthesis stimulated with PHA (20 micrograms/ml). L-Carnitine did not have any effect on resting PBMC. The maximum inhibition was found at 10 micrograms/ml of L-Carnitine. Moreover, in a time-course study and using an enzymatic analysis (ATP monitoring reagent), L-Carnitine enhanced ATP production on PBMC treated and untreated with PHA, reaching a maximum effect at 30 min incubation. In another set of experiments PBMC were treated with L-Carnitine alone and in combination with PHA, and the percent of receptors CD3, CD4, and CD8 were calculated with flow cytometry. After the cell incubation with L-Carnitine, the percent of all receptors studied did not change compared to L-Carnitine-untreated cells (controls). These data suggest that L-Carnitine inhibits, in a dose-dependent manner, lymphocyte blastogenesis induced by PHA, probably through the enhancement of ATP synthesis, which is considered an inhibitor of phospholipase C activity and a suppressor in lymphocyte cultures.




L-carnitine-L-tartrate promotes human hair growth in vitro.

Foitzik K, Hoting E, Förster T, Pertile P, Paus R.
Source

Department of Dermatology, University Hospital Hamburg-Eppendorf, University of Hamburg, Hamburg, Germany. kfoitzik@yahoo.com

Abstract

The trimethylated amino acid l-carnitine plays a key role in the intramitochondrial transport of fatty acids for beta-oxidation and thus serves important functions in energy metabolism. Here, we have tested the hypothesis that l-carnitine, a frequently employed dietary supplement, may also stimulate hair growth by increasing energy supply to the massively proliferating and energy-consuming anagen hair matrix. Hair follicles (HFs) in the anagen VI stage of the hair cycle were cultured in the presence of 0.5-50 microm of l-carnitine-l-tartrate (CT) for 9 days. At day 9, HFs treated with 5 microm or 0.5 microm of CT showed a moderate, but significant stimulation of hair shaft elongation compared with vehicle-treated controls (P < 0.05). Also, CT prolonged the duration of anagen VI, down regulated apoptosis (as measured by TUNEL assay) and up regulated proliferation (as measured by Ki67 immunohistology) of hair matrix keratinocytes (P < 0.5). By immunohistology, intrafollicular immunoreactivity for TGFbeta2, a key catagen-promoting growth factor, in the dermal papilla and TGF-beta II receptor protein in the outer root sheath and dermal papilla was down regulated. As shown by caspase activity assay, caspase 3 and 7, which are known to initiate apoptosis, are down regulated at day 2 and day 4 after treatment of HFs with CT compared with vehicle-treated control indicating that CT has an immediate protective effect on HFs to undergo programmed cell death. Our findings suggest that l-carnitine stimulates human scalp hair growth by up regulation of proliferation and down regulation of apoptosis in follicular keratinocytes in vitro. They further encourage one to explore topical and nutraceutical administration of l-carnitine as a well-tolerated, relatively safe adjuvant treatment in the management of androgenetic alopecia and other forms of hair loss.

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Extracellular ATP and adenosine as regulators of endothelial cell function ...

http://books.google.ca/books?id=UbT...EwBjgU#v=onepage&q=ATP GROWTH FACTORS&f=false

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Detection of ATP-binding to growth factors.

König S, Hasche A, Pallast S, Krieglstein J, Klumpp S.
Source

Integrated Functional Genomics, Interdisciplinary Center of Clinical Research, University of Münster, Münster, Germany. koenigs@uni-muenster.de

Abstract

It was shown in previous work that the interaction of growth factors (GFs) with adenosine triphosphate (ATP) is essential for their neuroprotective effect. Here we investigated the nature of the association of human basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and brain-derived neurotrophic factor (BDNF) with ATP. It was demonstrated that this interaction involves the formation of non-covalent ATP-GF complexes that are labile at low pH and that could be selectively purified and subjected to electrospray and MALDI-TOF mass spectrometry. The results obtained with these techniques indicated that the stability of the complexes is high. Main features of the procedure used here are: (1) reversed-phase purification of nucleotide-protein non-covalent complexes, (2) their detection with MALDI-TOF-MS using acid-free matrix, and/or (3) their measurement with ESI-MS using soft desolvation conditions. The methodology was successful in providing proof for the presence of various nucleotide-GF complexes. It was extended to other nucleotide-binding proteins (ribonuclease A) as well as proteins that do not exhibit nucleotide binding (lysozyme) as positive and negative control, respectively. Thus, the method demonstrated its general use for the investigation of a wide range of proteins interacting with nucleotides as long as their complexes are sufficiently stable to accommodate the experimental conditions.
http://www.ncbi.nlm.nih.gov/pubmed/18055212

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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.

 

[cthulhu2.0]

I read this on another forum, its too bad. He was a big contributor in the hair loss community
""Hey guys,

I don't know if you know Bryan Sheldon, sometimes known as Bryan on many Hairloss forums. He was very knowledgeable about Hairloss treatments and was one of the best posters I have ever came across. Unfortunately, I just found out he passed away 2 weeks ago. Rest in peace brother and thank you for all your contributions over the last decade.

It's a shame he never got the chance to see Hair multiplication come to fruition. He was always very enthusiastic and did a lot of research to keep everyone up to date.

Wherever you are Bryan, we wont forget you.""

 

[Donc83]

Where can I find a 192 roller for cheap. Everyone i see online is like 160 that is crazy I have a roller with 540 pins but it pulls way too much hair out. Thanks

 

[Armando Jose]

can someone besides princessRambo please post pictures. I have been doing the treatment since the beginning of August and although I am getting okay results, I am expecting more in terms of regrowth. Btw I am using a 1.5mm, switched from 1.0mm beginning of sept

have you your own photos? you achieve good results?

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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.

Yhis study can be useful, from Gaza
http://www.nature.com/jid/journal/v96/n4/pdf/5612584a.pdf

[h=2]Glutathione S-Transferases in Human and Rodent Skin: Multiple Forms and Species-Specific Expression[/h]

 

[zombiehair]

Interesting post on hypoxia squeegee.
One thing I have noticed and mentioned previously is the lack of bleeding on my own scalp after aggressive rolling.
In comparison to some of the post rolling blood bath pics some users have posted.
I have been hoping to see increased blood spots after each consecutive rolling session but haven't seen this happen so far after six rolling sessions.
I have recently been leaving a longer healing time between sessions now about 10 days.
I might consider a lighter roll with a smaller needled roller every 5 days or so between the major more aggressive sessions .
Not to do so much of an injury based damage but to Increase blood flow and all the goodies it brings to the area including oxygen.
Thoughts anyone ?

 

[Jorged]

One of my theories is that they'll first release a weaker version of their product, something that grows hair but now as much. They'll charge a ridiculous amount of money and people WILL pay for it as anything health related doesnt have a monetary value. Then, after they've milked the public for long enough, release an improved method of hair restoration.

I am afraid you may be right here, but why to do this? Even if Follica procedure is able to, in the best case scenario, recuperate a 100% of the hair that has been lost by neogenesis, theoretically this brand new hair will still be "attacked" by the hairloss process, therefore multiple treatments will be needed during a liftime, let's say once every 5, 10 or 15 years depending on how agressive is the process in each individual. With new young men (and women) also joining the hairloss club every year, the amount of possible clients is virtually infinite. The first company that honestly deliver a valid procedure whithout thinking exclusively in profit will ultimately be the winner.

 

[albert]

Interesting post on hypoxia squeegee.
One thing I have noticed and mentioned previously is the lack of bleeding on my own scalp after aggressive rolling.
In comparison to some of the post rolling blood bath pics some users have posted.
I have been hoping to see increased blood spots after each consecutive rolling session but haven't seen this happen so far after six rolling sessions.
I have recently been leaving a longer healing time between sessions now about 10 days.
I might consider a lighter roll with a smaller needled roller every 5 days or so between the major more aggressive sessions .
Not to do so much of an injury based damage but to Increase blood flow and all the goodies it brings to the area including oxygen.
Thoughts anyone ?

I guess everyone is different, maybe you just have a thick scalp. In my case, I bled a good amount the very first time and it continues to be like that (and I'm not going extreme).

 

[benjt]

@squeegee: Don't confuse adenosine with ATP. I will quote wikipedia on the effects that I described:

It is also an inhibitory neurotransmitter, believed to play a role in promoting sleep and suppressing arousal. [...] In general, adenosine has an inhibitory effect in the central nervous system (CNS).

Apart from that, the wikipedia article on adenone also explains the effects on the heart some people get on minoxidil.

@zombiehair: Are you a diffuse thinner, or standard male pattern baldness pattern? Diffuse thinners will not bleed as easily.

@somebody else (sorry, don't know who it was ) : Somebody asked me for my scalp massage protocol. It's not extremely easy to describe massage movements in natural language, but I'll do my best:
I mostly use my finger tips, or rather the full area of the first and half of the second joint of the four fingers of my hands. I'm just trying to press with the inside of my fingers as much as possible.
1) Then, using this surface, I do "shifting" (imagine putting a tangent to your scalp into all directions; that's the movement direction here) into all directions. If "tangent" confuses you, think of rapid rotating and shifting movements into all "horizontal" directions of the scalp. It's as if you were trying to push the skin from it's current position onto another place of the scalp; I do this both in straight lines and in rotation of the skin patch where I currently have my fingers. I carry out this movement as rapidly and rigorously as possible.
2) I also exert full force from above, like kneading, i.e. this time the direction of force is vertical, pressing down from above. I use both my fingers' surface and my knuckles for this. The horizontal movement here is marginal and only done to make the vertical force spread to a small area (instead of just hitting a very small spot).
3) Last thing I do is squeezing skin patches together, so I have two opposing forces as if you were trying to introduce folds into your scalp skin.

I do all of these movements for all my scalp, i.e. I relocate my hands after a few seconds (20 to 30) in one spot. For ease of doing this, I first do 1) all over my scalp, then 2), and then 3).

But I think you should be fine with anything, as long as you're shifting your scalp skin into all possible directions as rigorously as possible, applying force in all horizontal directions on all patches of the scalp, and applying vertical force from above.

 

[albert]

benjt: It was me, thank you.

Also, would like to mention that I do also notice more thickness at least the day after the rolling.