New Dermaroller Study; Thoughts, comments?

[RisingFist]

Actually, the diffuse thinners have the most aggressive hair loss. The lucky ones who recede can almost wait 10 years before they arrive at their last stage, sometimes more. It took 5 for me who is a pure diffuse thinner to reach NW5.

I'm not convinced by replies like PrincessRambo's, maybe had he chosen another name, and maybe had he not had a weird obsession with Game of Thrones, I would have taken it seriously, but I'm sorry. This is my last post in those dermaroller threads for the moment, I will come back in 3 months when there will still be no convincing results at all.

I would take this post more seriously if maybe you weren't obsessed with polar bears and maybe if you weren't The Belgian lol jk...I think with diffuse thinners the immune system plays a bigger rolse and with classic male pattern baldness, it has more to do with the genes. Either way, a solution for one is usually a solution for the other.

 

[princessRambo]

Now, next questions going further up stream:
1. What can lead to follicles producing too much DHT locally? (resulting in high PGD2)
2. What can lead to not enough aromatase around follicles? (resulting in low PGE2)

To question 2. I have no idea , but I think the answer directly lies within answering question 1, as the two prostaglandins e2 and d2 have almost opposite effects in a lot of biological processes. You answered 1 in one of your earlier post, notably immune response, overexpression of mast cells leading to degranulation and releasing PGD2 binding to PD2/CRTH2/GPR44 and totally borking the follicles.

PGD2's primary role seems to be in immune responses: "

Prostaglandin D[SUB]2[/SUB] (or PGD[SUB]2[/SUB]) is a prostaglandin that binds to the receptor PTGDR, as well as CRTH2.[SUP][1][/SUP][SUP][2][/SUP] It is a major prostaglandin produced by mast cells – recruits Th2 cells, eosinophils, and basophils." Th2 is a immune cell activator, and eosinophils are immune system "combatants" that attack cells deemed harmful.

http://www.ncbi.nlm.nih.gov/pubmed/18286292

Dermal fibrosis in male pattern hair loss: a suggestive implication of mast cells.

t was found that collagen bundles were significantly increased in balding vertexes than in non-balding occiput scalp skin. A near 4-fold increase in elastic fibers was observed in both vertex and occiput scalp skins with MPHL versus controls. Total numbers of MCs (tryptase-positive) in site-matched scalp samples were about 2-fold higher in MPHL subjects than in normal controls. Percentage elastic fiber (%) was found to be relatively well-correlated with tryptase and chymase-positive MCs. These findings suggest that accumulated MCs might be responsible for increased elastic fiber synthesis in MPHL, and indicate that future investigations are warranted.

and below from the cotsarelis study:

We also noted a unique peak of PGD2 production within hours of depilation, which was not seen in the spontaneous hair cycle in Fig. 3B. This coincides with degranulation of mast cells observed previously after depilation

I am not implying mast cell degranulation is the sole cause of PGD2 overexpression, in fact Cotsarelis has shown that lipocain type PGD2 is also overexpressed in male pattern baldness, if mast cells were the sole cause, topicals like cetirizine would be the one stop cure, but MCs are a definite major contributor downtream of fibrosis.

@FredTheBelgian: Game of Thrones is awesome, what is wrong with you . There are always people tip toeing about everything in life though, never being for or against anything, they will doubt everything, then try something, then be pessimistic about it and come back full circle about other stuff, I have quoted you perfectly in my other post

"I know what you have done, that you are neither cold nor hot. I wish you were cold or hot. But since you are lukewarm and not hot or cold, I'm going to spit you out of my mouth." - Revelation 3:15-16

 

[karankaran]

I was so convinced to start my derma roller 2.5 mm wounding treatment but a few critical voices here have dented my resolve! :-( I am worried that if my follicles get extracted by aggressive derma roller and never grew back!

 

[squeegee]

People on the ImmortalHair forum have been "proactive" for about 5 years now, coming up with all those crazy theories on how to stop hair loss "naturally". What advances have they made possible in the hair loss field? None. In a year this thread will be buried with its 200 pages.

LOL IH..

 

[bushbush]

People on the ImmortalHair forum have been "proactive" for about 5 years now, coming up with all those crazy theories on how to stop hair loss "naturally". What advances have they made possible in the hair loss field? None. In a year this thread will be buried with its 200 pages.

I have not frequented ImmortalHair before, but from a quick inspection it seems to be some sort of new-age, hippie, quack, pseudo-science advice site. At least this stuff has some scientific basis.

 

[benjt]

Well, Fred wants to be miserable, so let him. The problem is that this is probably a life attitude - guess his life sucks.

Anyway, back to topic.

@princessRambo:

ALL IMAGES BELOW ARE are between august and september, I started treating my hair exactly feb15, never used finasteride, started minoxidil the first week of august after the dermaroller thing started, so my regrowth can't be due to minoxidil either (though the compounding effect with dermarolling is showing good things so far).

So if you only started rolling after it started here, which was in July, what kind of treatment did you use from Feb 15 till then, as it wasn't Minxo or finasteride? Your results are pretty impressive, and it's too early to be only due to rolling and/or minoxidil.

 

[RisingFist]

I have not frequented ImmortalHair before, but from a quick inspection it seems to be some sort of new-age, hippie, quack, pseudo-science advice site. At least this stuff has some scientific basis.

almost all arguments in that forum have some scientific basis with published studies exactly as it is in this thread, dumbass.

 

[benjt]

GUYS, FFS, BACK ON TOPIC. DONT RUIN THS THREAD AGAIN BECAUSE OF PERSONAL PREFERENCES OR PROBLEMS.

 

[ganonford]

Princess,
Before anything, thanks for your valuable posts.



...then, there is something that is not very clear for me... if you started rolling last August, and you do it every three weeks, you have rolled not more than 4 times, right?

Thanks in advance...

I don't think he started on three weeks cycles

 

[bushbush]

almost all arguments in that forum have some scientific basis with published studies exactly as it is in this thread, dumbass.

Drop the poisons without losing your hair!


Natural remedy for hair loss, reversing hair loss without drugs, totally free, hair loss formula.


Each and every one of us has been inundated with spurious, fraudulent information about health. I have proof it can be short-sighted to believe FDA-approved drugs are the only reliable way to save your hair.


Information provided to the public through government institutions, media sources and politically correct dietary guidelines have corrupted objectivity surrounding health.

Right. Tinfoil hat territory.

 

[princessRambo]

Princess,
Before anything, thanks for your valuable posts.



...then, there is something that is not very clear for me... if you started rolling last August, and you do it every three weeks, you have rolled not more than 4 times, right?

Thanks in advance...

No I have, the first first 3 rolls were like 5-7 days apart, (I have also noted in this thread when it started, that I would go with the weekly roll) then I did a little more research, and started spacing them out as I was going aggresive, my last 2 rolls were the longer ones and I will keep it that way (10 days, and then held to almost 3 weeks the last one).

 

[RisingFist]

Right.

I don't even know who posted that. The amount of bull**** and snake oil that have been posted in this forum in comparison is probably 10-1. You're contradicting yourself by even using a dermaroller cause many would say it's a home made hippie solution...Sqeegee, you shouldn't laugh cause 80% of your posts about immunity gut, vitamin D, etc. I have seen the same thing on that forum with the corresponding studies so laughing at them would be the same as laughing at yourself. I personally keep an open mind and look for intelligent arguements with some supportive evidence and anecdotal on top of it. Whoever contributes to that cause at whatever forum, I don't care, but I don't jump to ignorant conclusions and join the hate bandwagon. I'll leave you guys be, it's not worth my time arguing common sense.

 

[benjt]

@princessRambo:

ALL IMAGES BELOW ARE are between august and september, I started treating my hair exactly feb15, never used finasteride, started minoxidil the first week of august after the dermaroller thing started, so my regrowth can't be due to minoxidil either (though the compounding effect with dermarolling is showing good things so far).

So if you only started rolling after it started here, which was in July, what kind of treatment did you use from Feb 15 till then, as it wasn't Minxo or finasteride? Your results are pretty impressive, and it's too early to be only due to rolling and/or minoxidil.

 

[princessRambo]

@benjt, when I started I wanted to replaced minoxidil with something else, and topical capsaicin was ideal, this burns like a mofo, but I attributed most of the initial growth spurt to that plus use of topical calcipotriol (VDR is critical for hair cycling and calcitriol strongly increases wnt/b catenin in the hair follicle for up to 48 hours), I noted way back in the beginning of my treatment (in my calcipotriol thread) that I was going to try dermarolling everytime before applying calcipotriol, for absorption as I had ordered many batches of the cream instead of the scalp ointment (dummy me) this I did up to starting the aggressive dermarolling in august, this wasn't wounding theory based, it was very light rolling 3-4 times a week with a 0.5mm roller and apply calcipotriol.

I have used other topical including topical EGCG, resveratrol, and something else that I will no longer mention here . I think my internals were the most aggressive one, I basically wanted to blunt dht and fibrosis without using finasteride. There are a lot of things that will work but absorption is necessary and critical. I will have an unrelated post about those internals backed by publications. The reason I don't like mentioning stuff is some people will show up, and say x y z doesn't work for $hit because they have done it 2000 bc.

There are some french publications that show that even saw palmetto, when absorbed properly can inhibit 5AR 3 times more than 5mg finasteride. Again this is something I don't like mentioning but since you asked..., but soon, some random dude will start yelling at me... *waiting for random dude to mingle*.

Now let's go back to the wounding and PGD2 talk

 

[squeegee]

I don't even know who posted that. The amount of bull**** and snake oil that have been posted in this forum in comparison is probably 10-1. You're contradicting yourself by even using a dermaroller cause many would say it's a home made hippie solution...Sqeegee, you shouldn't laugh cause 80% of your posts about immunity gut, vitamin D, etc. I have seen the same thing on that forum with the corresponding studies so laughing at them would be the same as laughing at yourself. I personally keep an open mind and look for intelligent arguements with some supportive evidence and anecdotal on top of it. Whoever contributes to that cause at whatever forum, I don't care, but I don't jump to ignorant conclusions and join the hate bandwagon. I'll leave you guys be, it's not worth my time arguing common sense.

This is called learning process.. But I never said that Amalgam filings causes hairloss and laser helmets are the cure hahaha

- - - Updated - - -

@benjt, when I started I wanted to replaced minoxidil with something else, and topical capsaicin was ideal, this burns like a mofo, but I attributed most of the initial growth spurt to that plus use of topical calcipotriol (VDR is critical for hair cycling and calcitriol strongly increases wnt/b catenin in the hair follicle for up to 48 hours), I noted way back in the beginning of my treatment (in my calcipotriol thread) that I was going to try dermarolling everytime before applying calcipotriol, for absorption as I had ordered many batches of the cream instead of the scalp ointment (dummy me) this I did up to starting the aggressive dermarolling in august, this wasn't wounding theory based, it was very light rolling 3-4 times a week with a 0.5mm roller and apply calcipotriol.

I have used other topical including topical EGCG, resveratrol, and something else that I will no longer mention here . I think my internals were the most aggressive one, I basically wanted to blunt dht and fibrosis without using finasteride. There are a lot of things that will work but absorption is necessary and critical. I will have an unrelated post about those internals backed by publications. The reason I don't like mentioning stuff is some people will show up, and say x y z doesn't work for $hit because they have done it 2000 bc.

There are some french publications that show that even saw palmetto, when absorbed properly can inhibit 5AR 3 times more than 5mg finasteride. Again this is something I don't like mentioning but since you asked..., but soon, some random dude will start yelling at me... *waiting for random dude to mingle*.

Now let's go back to the wounding and PGD2 talk

PGd2 is induced by inflammation.
PGD[SUB]2[/SUB] and Inflammation

PGD[SUB]2[/SUB] is a major eicosanoid that is synthesized in both the central nervous system and peripheral tissues and appears to function in both an inflammatory and homeostatic capacity.[SUP]101[/SUP] In the brain, PGD[SUB]2[/SUB] is involved in the regulation of sleep and other central nervous system activities, including pain perception.[SUP]102,103[/SUP] In peripheral tissues, PGD[SUB]2[/SUB] is produced mainly by mast cells but also by other leukocytes, such as DCs and Th[SUB]2[/SUB] cells.[SUP]104–106[/SUP] Two genetically distinct PGD[SUB]2[/SUB]-synthesizing enzymes have been identified, including hematopoietic- and lipocalin-type PGD synthases (H-PGDS and L-PGDS, respectively). H-PGDS is generally localized to the cytosol of immune and inflammatory cells, whereas L-PGDS is more restrained to tissue-based expression.[SUP]107[/SUP]
PGD[SUB]2[/SUB] can be further metabolized to PGF[SUB]2α[/SUB], 9α,11β-PGF[SUB]2[/SUB] (the stereoisomer of PGF[SUB]2α[/SUB]) and the J series of cyclopentanone PGs, including PGJ[SUB]2[/SUB], Δ[SUP]12[/SUP]-PGJ[SUB]2[/SUB], and 15d-PGJ[SUB]2[/SUB].[SUP]108[/SUP] Synthesis of J series PGs involves PGD[SUB]2[/SUB] undergoing an initial dehydration reaction to produce PGJ[SUB]2[/SUB] and 15d-PGJ[SUB]2[/SUB], after which PGJ[SUB]2[/SUB] is converted to 15d-PGJ[SUB]2[/SUB] and Δ[SUP]12[/SUP]-PGJ[SUB]2[/SUB] via albumin-dependent and albumin-independent reactions, respectively.[SUP]109[/SUP]
PGD[SUB]2[/SUB] activity is principally mediated through DP or DP1 and CRTH2 or DP2, as described previously (Table). Also, 15d-PGJ[SUB]2[/SUB] binds with low affinity the nuclear PPARγ.[SUP]110[/SUP]
PGD[SUB]2[/SUB] has long been associated with inflammatory and atopic conditions, although it might exert an array of immunologically relevant antiinflammatory functions as well.
PGD[SUB]2[/SUB] is the predominant prostanoid produced by activated mast cells, which initiate IgE-mediated type I acute allergic responses.[SUP]104,111[/SUP] It is well established that the presence of an allergen triggers the production of PGD[SUB]2[/SUB] in sensitized individuals. In asthmatics, PGD[SUB]2[/SUB], which can be detected in the bronchoalveolar lavage fluid within minutes, reaches biologically active levels at least 150-fold higher than preallergen levels.[SUP]112[/SUP] PGD[SUB]2[/SUB] is produced also by other immune cells, such as antigen-presenting DCs and Th[SUB]2[/SUB] cells, suggesting a modulatory role for PGD[SUB]2[/SUB] in the development of antigen-specific immune system responses.[SUP]104,105[/SUP] PGD[SUB]2[/SUB] challenge elicits several hallmarks of allergic asthma, such as bronchoconstriction and airway eosinophil infiltration,[SUP]113,114[/SUP] and mice that overexpress L-PGDS have elevated PGD[SUB]2[/SUB] levels and an increased allergic response in the OVA-induced model of airway hyperreactivity.[SUP]115[/SUP]
The proinflammatory effects of PGD[SUB]2[/SUB] appear to be mediated by both DP1 and DP2/CRTH2 receptors. Because both receptors bind PGD[SUB]2[/SUB] with similar high affinity, PGD[SUB]2[/SUB] produced by activated mast cells or T cells would be capable of activating multiple signaling pathways leading to different effects, depending on whether the DP1 or DP2/CRTH2 receptors or both are locally expressed.
The DP1 receptor is expressed on bronchial epithelium and has been proposed to mediate production of chemokines and cytokines that recruit inflammatory lymphocytes and eosinophils, leading to airway inflammation and hyperreactivity seen in asthma.[SUP]116[/SUP] Mice deficient in DP1 exhibit reduced airway hypersensitivity and Th2-mediated lung inflammation in the OVA-induced asthma model, suggesting that the DP1 plays a key role in mediating the effects of PGD[SUB]2[/SUB] released by mast cells during an asthmatic response.[SUP]62[/SUP] Furthermore, PGD[SUB]2[/SUB] may inhibit eosinophil apoptosis via the DP1 receptor.[SUP]117[/SUP]
DP1 antagonists exert antiinflammatory properties in several experimental models, including inhibition of antigen-induced conjunctival microvascular permeability in guinea pigs and OVA-induced airway hyperreactivity in mice.[SUP]118,119[/SUP]
DP2/CRTH2 receptors contribute largely to pathogenic responses by mediating inflammatory cell trafficking and by modulating effector functions. PGD[SUB]2[/SUB] released from mast cells may mediate recruitment of Th2 lymphocytes and eosinophils directly via the DP2/CRTH2 receptor. In humans, the DP2/CRTH2 receptor is expressed on Th2 lymphocytes, eosinophils, and basophils,[SUP]8,120,121[/SUP] and an increase in DP2/CRTH2[SUP]+[/SUP] T cells has been positively associated with certain forms of atopic dermatitis.[SUP]122[/SUP] The DP2/CRTH2 receptor has been demonstrated to mediate PGD[SUB]2[/SUB]-stimulated chemotaxis of these cells in vitro and leukocyte mobilization in vivo.[SUP]123[/SUP]
In contrast to the proinflammatory role of PGD[SUB]2[/SUB] in allergic inflammation, PGD[SUB]2[/SUB] may act to inhibit inflammation in other contexts. The DP1 receptor is expressed on DCs that play a key role in initiating an adaptive immune response to foreign antigens. PGD[SUB]2[/SUB] activation of the DP1 receptor inhibits DC migration from lung to lymph nodes following OVA challenge, leading to reduced proliferation and cytokine production by antigen specific T cells.[SUP]124[/SUP] DP1 activation also reduces eosinophilia in allergic inflammation in mice and mediates inhibition of antigen-presenting Langerhans cell function by PGD[SUB]2[/SUB].[SUP]125,126[/SUP] As mentioned, PGD[SUB]2[/SUB] and its degradation product 15d-PGJ[SUB]2[/SUB] have been suggested as the COX-2 products involved in the resolution of inflammation.[SUP]28,127[/SUP] Administration of a COX-2 inhibitor during the resolution phase exacerbated inflammation in a carrageenan-induced pleurisy model [SUP]28[/SUP]. In a zymosan-induced peritonitis model, deletion of H-PGDS induced a more aggressive inflammatory response and compromised resolution, findings that were moderated by addition of a DP1 agonist or 15d-PGJ[SUB]2[/SUB].[SUP]123[/SUP] Although these data appear to implicate PGD[SUB]2[/SUB] and 15d-PGJ[SUB]2[/SUB] in resolution, there is a large disparity between the nanomolar to picomolar amounts of 15d-PGJ[SUB]2[/SUB] detected by physicochemical methodology in in vivo settings and the amount needed to have a biological effect in vitro on PPARγ or nuclear factor-κB (micromolar amounts).[SUP]32,128,129[/SUP] This discrepancy is supported by recent data reported in zymosan-induced peritonitis, where we observed evoked biosynthesis of PGD[SUB]2[/SUB] only during the proinflammatory phase and not during resolution. Consistent with this observation, DP2/CRTH2 deletion reduced the severity of acute inflammation, but neither DP1 or DP2/CRTH2 deletion affected resolution. Although 15d-PGJ[SUB]2[/SUB] is readily detected when synthetic PGD[SUB]2[/SUB] is infused into rodents,[SUP]130[/SUP] endogenous biosynthesis of 15d-PGJ[SUB]2[/SUB] was not detected during promotion or resolution of inflammation (J. Mehta et al, unpublished data, 2010).
PGD[SUB]2[/SUB] may play a role in the evolution of atherosclerosis. In the context of inflamed intima, PGD[SUB]2[/SUB] in part derives from H-PGDS-producing inflammatory cells that are chemotactically compelled to permeate the vasculature.[SUP]131,132[/SUP] Additionally, L-PGDS expression is induced by laminar sheer stress in vascular endothelial cells and is actively expressed in synthetic smooth muscle cells of atherosclerotic intima and coronary plaques of arteries with severe stenosis.[SUP]133–135[/SUP] PGD[SUB]2[/SUB] has been shown to inhibit expression of proinflammatory genes, such as inducible nitric oxide synthase and plasminogen activator inhibitor.[SUP]136,137[/SUP] Indeed, L-PGDS deficiency accelerates atherogenesis.[SUP]138[/SUP]
In summary, studies with COX-2 inhibitors suggest that products of this enzyme may play a role in resolution in several models of inflammation. However, the identity of such products, whether formed directly by COX-2 or because of substrate diversion consequent to COX-2 inhibition, remains, in many cases, to be established.


http://atvb.ahajournals.org/content/31/5/986.full


Introduction to the Eicosanoids

http://themedicalbiochemistrypage.org/eicosanoids.php



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Prostaglandin D2 inhibits wound-induced hair follicle neogenesis through the receptor, Gpr44.

Nelson AM, Loy DE, Lawson JA, Katseff AS, Fitzgerald GA, Garza LA.
Source

Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Abstract

Prostaglandins (PGs) are key inflammatory mediators involved in wound healing and regulating hair growth; however, their role in skin regeneration after injury is unknown. Using wound-induced hair follicle neogenesis (WIHN) as a marker of skin regeneration, we hypothesized that PGD2 decreases follicle neogenesis. PGE2 and PGD2 were elevated early and late, respectively, during wound healing. The levels of WIHN, lipocalin-type prostaglandin D2 synthase (Ptgds), and its product PGD2 each varied significantly among background strains of mice after wounding, and all correlated such that the highest Ptgds and PGD2 levels were associated with the lowest amount of regeneration. In addition, an alternatively spliced transcript variant of Ptgds missing exon 3 correlated with high regeneration in mice. Exogenous application of PGD2 decreased WIHN in wild-type mice, and PGD2 receptor Gpr44-null mice showed increased WIHN compared with strain-matched control mice. Furthermore, Gpr44-null mice were resistant to PGD2-induced inhibition of follicle neogenesis. In all, these findings demonstrate that PGD2 inhibits hair follicle regeneration through the Gpr44 receptor and imply that inhibition of PGD2 production or Gpr44 signaling will promote skin regeneration.

 

[benjt]

In my opinion, from squeegee's latest findings, this sentence might yield another approach:

PGD[SUB]2[/SUB] can be further metabolized to PGF[SUB]2α[/SUB]

[SUB]
Maybe we baldies are lacking the converting substances, and that's the reason why PGD2 is overexpressed? It is produced in normal amounts, but not correctly converted to PGF2a?
[/SUB]

 

[squeegee]

In my opinion, from squeegee's latest findings, this sentence might yield another approach:
[SUB]
Maybe we baldies are lacking the converting substances, and that's the reason why PGD2 is overexpressed? It is produced in normal amounts, but not correctly converted to PGF2a?
[/SUB]

I really think that Androgen Alopecia is an aftermath of a local chronic inflammation fueled by Androgen.
Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. Consequently, chronic inflammation is almost always accompanied by tissue destruction.

The activation of macrophages also resulted in the extracellular production of PGD2....

http://www.jbc.org/content/early/2002/01/10/jbc.M110314200.full.pdf



,


Androgen activity and markers of inflammation among men in NHANES III.

Schooling CM.
Source

CUNY School of Public Health at Hunter College, New York, New York.

Abstract

OBJECTIVES:

Inflammation contributes to chronic diseases. Lower serum testosterone among men is associated with less inflammation, yet immune defense is thought to trade-off against reproduction with androgens adversely affecting immune function. Anti-androgens are effective at castrate levels of serum testosterone, suggesting serum testosterone may not capture all androgen activity. The association of two androgen biomarkers with key markers of inflammation was examined.
METHODS:

The adjusted association of serum testosterone and androstanediol glucuronide with C-reactive protein, white blood cell, granulocyte and lymphocyte count, fibrinogen, and hemoglobin, as a control outcome because testosterone administration raises hemoglobin, were examined in a nationally representative sample of 1,490 US men from the National Health and Nutrition Examination Survey III phase 1 (1988-1991) using multivariable linear regression.
RESULTS:

Serum testosterone and androstanediol glucuronide were weakly correlated (0.13). Serum testosterone was associated with lower white blood cell count [-0.26 × 10(-9) per standard deviation, 95% confidence interval (CI) -0.37 to -0.14] and granulocyte count (-0.21 × 10(-9) , 95% CI -0.29 to -0.13) but not with hemoglobin (0.02 g/l, 95% CI -0.89 to 0.92), adjusted for age, education, race/ethnicity, smoking, and alcohol. Similarly adjusted, androstanediol glucuronide was not associated with white blood cell count (0.10 × 10(-9) , 95% CI -0.05 to -0.25), granulocyte count (0.12 × 10(-9) , 95% CI -0.02 to 0.25), or fibrinogen (0.05 g/l, 95% CI -0.004 to 0.11), but was with hemoglobin (0.70 g/l, 95% CI 0.07 to 1.32).
CONCLUSIONS:

Different androgen biomarkers had different associations with inflammatory markers, highlighting the need to consider several androgen biomarkers. The possibility remains that androgens may generate inflammatory processes with implications for chronic diseases. Am. J. Hum. Biol., 25:622-628, 2013. © 2013 Wiley Periodicals, Inc.

 

[baldnesssadness]

hello everyone

I have used topical ceterizine which gave me little growth on the temples. this was from september 2012- March 2013. Hair loss didn't stop and my hairline still receeded.
Then i used Voltaren(diclofenac) which gave me more vellus hairs adding minoxidil improved the results but it was far from terminal.
Now i have dermarolled for over a month and temple hairs grow stronger and i also get new vellus hair.

My question is this, should we add diclofenac to the dermaroller regime? what do you think? dermarolling+ minoxidil+ diclofenac think theoreticly it will give better results than minoxidil alone ?

im sure u seen this before but this a study of minoxidil+diclofenac+ tea tree oil which gave better results than minoxidil alone.

http://www.ncbi.nlm.nih.gov/pubmed/23807837

can someone pls answer this?

 

[squeegee]

hello everyone

I have used topical ceterizine which gave me little growth on the temples. this was from september 2012- March 2013. Hair loss didn't stop and my hairline still receeded.
Then i used Voltaren(diclofenac) which gave me more vellus hairs adding minoxidil improved the results but it was far from terminal.
Now i have dermarolled for over a month and temple hairs grow stronger and i also get new vellus hair.

My question is this, should we add diclofenac to the dermaroller regime? what do you think? dermarolling+ minoxidil+ diclofenac think theoreticly it will give better results than minoxidil alone ?

im sure u seen this before but this a study of minoxidil+diclofenac+ tea tree oil which gave better results than minoxidil alone.

http://www.ncbi.nlm.nih.gov/pubmed/23807837

can someone pls answer this?

I think that any topical anti inflammatory should be stopped with derma-rolling involved. When you are introducing the derma roller into your regimen, you want to introduces, promotes reconstruction. Inflammation (acute inflammatory), proliferation and remodeling are they keywords for results. Also, cox-2 inhibitor on a long term use is not a good idea.

 

[princessRambo]

hello everyone

I have used topical ceterizine which gave me little growth on the temples. this was from september 2012- March 2013. Hair loss didn't stop and my hairline still receeded.
Then i used Voltaren(diclofenac) which gave me more vellus hairs adding minoxidil improved the results but it was far from terminal.
Now i have dermarolled for over a month and temple hairs grow stronger and i also get new vellus hair.

My question is this, should we add diclofenac to the dermaroller regime? what do you think? dermarolling+ minoxidil+ diclofenac think theoreticly it will give better results than minoxidil alone ?

im sure u seen this before but this a study of minoxidil+diclofenac+ tea tree oil which gave better results than minoxidil alone.

http://www.ncbi.nlm.nih.gov/pubmed/23807837

can someone pls answer this?

Out of curiosity, did you mix the cetirizine with anything but water? Cet only supress PGD2 from mast cells (which is still a problem). I am seriously contemplating topical ibuprophen to non-selectively blunt both cox1 and 2 at the same time completely annihilating PGD2 regardless of where it is being produced,, and then add exogenous PGE2 at a different time, all this after making sure the initial inflammatory burst from wounding has ended.