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

Leptin resistance and insulin resistance increases mast cells--which increase hardened collagen in the scalp, ala fibrosis.

Arch Dermatol Res. 2008 Mar;300(3):147-52.

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

Department of Dermatology, Seoul National University College of Medicine, Chongno-Gu, Seoul, Republic of Korea.

A relationship has been suggested between mast cells (MCs) and male pattern hair loss (MPHL), because of histological evidence of perifollicular fibrosis and increased mast cell numbers. Two paired punch biopsies were taken from balding vertexes and non-balding occipital promontory areas of ten patients with MPHL (Ludwig-Hamilton IIIv to IV) and from five normal subjects aged from 20 to 35 years. Masson trichrome and Victoria blue staining were performed to observe collagen frameworks and elastic fiber structures. Numbers of immunoreactive MCs stained with anti-tryptase or anti-chymase antibody were counted. It 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.

Also related:

Prog Brain Res. 2004;146:279-89.
Neurotrophin presence in human coronary atherosclerosis and metabolic syndrome: a role for NGF and BDNF in cardiovascular disease?

Division of Cell Biology, Department of Forensic Medicine, Medical University, Varna, Bulgaria.

The development of atherosclerotic cardiovascular disease is a common comorbidity in patients with the metabolic syndrome, a concurrence of cardiovascular risk factors in one individual. While multiple growth factors and adipokines are identified in atherosclerotic lesions, as well as neurotrophins implicated in both cardiac ischemia and lipid and glucose metabolism, the potential role of neurotrophins in human coronary atherosclerosis and in the metabolic syndrome still remains to be elucidated. Here we describe and discuss our results that represent a novel attempt to study the cardiovascular and metabolic biology of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and mast cells (MC). The local amount of NGF, the immunolocalization of p75 neurotrophin receptor (p75NTR) and the number of MC were correlatively examined in coronary vascular wall and in the surrounding subepicardial adipose tissue, obtained from autopsy cases in humans with advanced coronary atherosclerosis. We also analyzed the plasma levels of NGF, BDNF and leptin and the number of MC in biopsies from abdominal subcutaneous adipose tissue in patients with a severe form of the metabolic syndrome. The results demonstrate that NGF levels are decreased in atherosclerotic coronary vascular tissue but increased in the subepicardial adipose tissue, whereas both tissues express a greater number of MC and a stronger p75NTR immunoreactivity, compared to controls. Metabolic syndrome patients display a significant hyponeurotrophinemia and an increased number of adipose MC; the later correlates with elevated plasma leptin levels. In effect, we provide the first evidence for (i) an altered presence of NGF, p75NTR and MC in both coronary vascular and subepicardial adipose tissue in human coronary atherosclerosis, and (ii) a significant decrease in plasma NGF and BDNF levels and an elevated amount of plasma leptin and adipose MC in metabolic syndrome patients. Together our findings suggest that neuroimmune mediators such as NGF, BDNF, leptin and MC may be involved in the development of cardiovascular disease and related disorders.

Also related:

Arch Physiol Biochem. 2001 Oct;109(4):357-60.
NGF, BDNF, leptin, and mast cells in human coronary atherosclerosis and metabolic syndrome.

Medical University, Varna, Bulgaria.

While multiple growth factor, cytokines, and immune cells are identified in atherosclerotic lesions, as well as an essential nonneuronal function of neurotrophins implicated in cardiovascular tissue development and in lipid and glucose metabolism, the role of the neurotrophins NGF and BDNF and also the adipokine leptin in human coronary atherosclerosis and related disorders, such as metabolic syndrome, remains unclear. Here we report that (i) both the amount and the immunoreactivity of NGF was reduced and the expression of p75NGF receptor and the number of mast cell increased in human atherosclerotic coronary arteries (n = 12) compared with control specimens (n = 9) obtained from autopsy cases, and (ii) NGF and BDNF plasma levels were reduced in patients with metabolic syndrome (n = 23) compared with control subjects (n = 10). Also, in metabolic syndrome patients, a positive correlation between the plasma leptin levels and the number of adipose tissue mast cells was found, suggesting that leptin may be a novel adipoimmune mediator. Altogether, the results provide the first correlative evidence for the potential involvement of NGF, BDNF, leptin, and mast cells in human coronary atherosclerosis and metabolic syndrome, implying neuroimmune and adipoimmune pathways in the pathobiology of these cardiovascular disorders.

I really think this is right on and explains a lot of what I've gone through in the past 2 years. My triglycerides were high, my HDL was low. My total cholesterol was normal though but you've told us that's not the important number. Even my blood pressure was on the high side of normal. The doctor mentioned metabolic syndrome to me once since I'm a big guy (I put on muscle easily but I also hold fat around my belly), but my tests for diabetes were all good and he said we'd track it.

I think my hair loss and the reason I was told I could have a scarring alopecia in addition to MPB by one doctor was because there was fibrosis going on in parts of my scalp that was visible by scalp biopsy. I have small patches with no visible scarring on top of my head in addition to diffuse loss. Those patches are most likely where the fibrosis occured. I've seen no regrowth in them at all.

Hopefully, the supplementing I'm doing with the Krill and Lecithin in addition to the other supps will help me change my blood profiles for the rest of my life. My diet is clean with little to no saturated fats in it. I exercise regularly. I just think I'm genetically pre-disposed to this kind of condition. My Dad had it. His Dad had it. His brother had it.

I'm hoping the knowledge I've gained here will give me an edge that they never had.

If you have any other advice on what to add to a regimen please let me know, IH. I'm hopeful that I'm taking steps to not let history repeat itself in my family.

I do know since I've gone high dose Krill oil and Lecithin, something is happening with my hair. Like I said in the other forum, it's thicker and fuller than it's been in 2 years. Something is kicking in.

Hadrion--

You're doing the right thing. Attack the root of the problem so you can stop it from occurring again. To reverse the damage, wounding is your best friend, seconded by laser therapy at some point down the road to restructure collagen. They go hand-in-hand, but you can definitely bust up that Fibrosis.

I second Nidhogge, your best hope to over come any fibrosis is to do the wounding.

In addition, Magnesium Oil could help too, as it can diffuse calcium deposits which contribute to fibrosis.

Don't worry about Saturated fat, it gets a bad rap just about everywhere, but really saturated fat is not bad. It's reputation
had been maligned due to epidemiological studies lumping it in with the highly negative trans-fats. Since no distinction was made,
many biased researchers continue to assume that saturated fat is bad.

Studies have vindicated it, so no worries there.

One thing to add is that Niacinamide is great (very cheap) and effective for dealing with mast cells. Niacinamide inhibits mast cell degranulation.

Good. I'm already on the Niacinamide from the Candida suggestion so I've got a lot of things covered.

I definitely feel that I, too, have fibrosis issues. Actually, this was a subjective impression that I got long before I started reading about such things on these sites. When you guys say "wounding" I assume you include chemical peels in that as well? If so, that is something I want to do on a regular basis, say once a month. Speaking of which, Did you get my reply e-mail on the peels, Nidhogge?

-EIC/Benisrosi

Beni--

Refresh my memory on the peels? I may have read the e-mail with the intention to reply, and then forgot.

I will say that I formulated four ounces of 30% Salicylic Acid/70% PEG yesterday. Once I test this on myself to determine the efficacy, I'll start selling to people. Unfortunately, I'll have to order a lot more PEG and Salicylic Acid if the demand is more than just a few people, lol...I have a feeling it will be.

nidhogge wrote:Beni--

Refresh my memory on the peels? I may have read the e-mail with the intention to reply, and then forgot.

I will say that I formulated four ounces of 30% Salicylic Acid/70% PEG yesterday. Once I test this on myself to determine the efficacy, I'll start selling to people. Unfortunately, I'll have to order a lot more PEG and Salicylic Acid if the demand is more than just a few people, lol...I have a feeling it will be.

It was nothing big. I just asked if the peels were something you can do yourself or if you had to go to the salon. For example, I saw a salon here wanted to charge $50 for a Nioxin Scalp Renew treatment, but I can by the NSR for $15 myself. I was just wondering if you have to have any know-how to do it.

Also, is this something you plan on doing, say, every month or less often? Nioxin said to do the NRS 3 times with 4-6 between treatments. Didn't seem to indicate what to do afterwards, though! Maybe once every three months?

This acid peel can be done every 10 days. I'm going to gauge this on my own though...some trial-and-error. 2 weeks might be better given the need to provide enough WNT-signalling and EGFR-inhibition. Nioxin Scalp Renew--I'd stick with the directions. Once a month. Got a 3-pack off Ebay for (including S&H), 47 bucks.

Should arrive today or tomorrow.

You definitely don't need to pay someone $50 to do the Nioxin Scalp Renew. My wife did it for me one month at home. You just have to make sure you make the grid with the concoction all over your scalp and then really rub it in. It's better if you have someone with strong hands, but not essential. You can do it yourself.

Sorry for this stupid question but, what are you guys talking about?

nidhogge said "bust up that Fibrosis" and Caustic Summetry said "do the wounding yourself".

Are you guys talking about this new trendy hurt-your-scalp routine?

Thanks, guys. I'll be ordering the Nioxin Scalp Renew and doing it myself then. (BTW, nice find on eBay, Nidhogge.)

Misirlou - You asked a good question, since this subject deserves its own thread.

We were talking about different ways to intentionally wound your scalp. Here's what I mean--when you either sandpaper an area of your scalp that has no hair (just skin) using 400 grade sandpaper or using a scalp peel that "eats" away at the superficial layers of skin, it is a form of "gentle" wounding.

You're probably wondering why gentle wounding is a good thing. First of all we have plenty of stem cells in the skin. Without wounding they will not doing anything remarkable other than just be there for future need if the skin has to repair itself.

Something special happens when you wound the skin and research has found that wounding the skin brings back the "embryonic stage," where skin cells can differentiate into other tissue. When we add either powdered lithium orotate or Lithium chloride along with some DMSO to the wounded area, they increase Wnt signaling .

The Wnt signaling allows the stem cells to morphologically transform into hair follicles. So we are talking about turning skin into hair.

This is based in part what http://www.follicabio.com/ is doing.

IH--

Great reply man, couldn't have said it better myself!

Misirlou--

I'd start off with a good chemical peel first. Sandpapering is tough to gauge because it's very easy to overdo it. You won't know until the next day that you probably sandpapered too much. Took me about 3 weeks to completely heal up the skin. Fresh skin looks great though.

Misirlou--

One more thing. You occasionally see Fibrosis thrown around with hairloss, though it is not a hairloss specific term. Fibrosis is scarring of an organ...so it can mean any organ. For example, cirrhosis of the liver (hardening of the liver) can be, I believe, considered a form of Fibrosis. Skin is an organ as well, so when your skin gets scarred, that's Fibrosis. Scar tissue is a lot tougher than regular skin, and as a result, can affect follicular development. So, by "busting up" that scar tissue and applying solutions that facilitate hair follicle growth, that is how gengle wounding works. As for HOW your skin gets scarred, it's a result of inflammation that is a reaction to any number of things...mites, DHT, etc. These are things that you keep under control with a healthy diet, IH's regime, and topicals/lasers.

Well fellas, I found a different salon that did the Nioxin Scalp Renew for $35. Since the NSR costs at least $15 on its own, I thought it was worth $20 to have a good looking young woman massage it into my scalp for awhile. I can confirm that it feels awesome. My scalp feels like a million bucks. This will definitely become a regular part of my plan.

Nid: You suppose that stripping the fibrosis and crud off the scalp will enhance the effectiveness of laser therapy? I bet it will!

EIC--

I have no doubt in my mind about it. I believe that the two are very synergistic with one another.

Thanks for the replies guys! Now I'm a bit more in the game, so to speak.

How much "time" is bought if the wounding process works? I mean, the newly created organs would still be genetically sensitive, right?

Do we have any proofs that this works?

If feels as if a stronger version of Azelaic acid could help burn off some skin too?

This method sounds to me as the one most promising ones since RU 58841 was first heard of.

Someone mentioned laser. I might be totally wrong now but, 650-655 nanometer is basically how deep down through the tissue the light will travel. Wouldn't a laser that had some kind of dynamic nanometer technology be better if we are talking about wounds? Or are all the stem cells / WNT / repairing action occurring on the same depth/level? It feels as if we would like to stimulate more then just what 650 nm can offer.

So if one does the dermabrasion via Nioxin Scalp Renew and then uses the DMSO/lithium rinse, you are effectively doing the Follica patent, right? Or does it require additional lithium/DMSO over and above the rinse?

Yes presumably EIC. However, Im convinced that enzyme peels are more economical and well known as far as effectiveness is concerned. But at this time theres no consensus on which chemical or enzyme peel is best in terms of cost and value. I hope someone with experience or knowledge points us in the right direction.

The new forum rocks by the way

Zerx--

I'm about to wash off my first treatment with my formulated 30% Salicylic Acid/70% PEG solutions. Scalp doesn't feel irritated at all, which is good.

EIC--

Sorta and not really. The Lithium/DMSO rinse lacks an EGFR-inhibitor. Also, I'd want to apply a Lithium/DMSO/DMI solution a few times a day as well, and leave it on. The shampoo will help, but shouldn't be the sole way.

Misirlou--

The lasers that I use when constructing people's helmets and that other people have been using when construction theirs are the ones that ideal for hair loss. Studies have shown this over the years.

nidhogge - I remember IH being opposed to the use of salicylic acid for some reason. I also remember someone suggesting TCA peels at one point. And Im sure you know the Scalpskin lady from regrowth.com and her enzyme peels. Im basically not sure which way to go between the TCA and the enzyme peels. Even then which percentage of the TCA to go with. There are really so many schools of thought on countering scalp fibrosis that Im just adamant to jump into any one of them without careful consideration.

As far as lithium is concerned Im honestly scared what side effects I might get from some of it getting in my bloodstream. I read somewhere that criminals have the common characteristic of having excessive lithium in their blood. That is a scary proposition for me so Im searching for something else to improve Wnt signaling.

zerx - Actually, the Lithium information you heard is the opposite.

Criminals have 400 times LESS lithium in their hair than normal people.

If I had the opportunity to change the world so to speak, I would replace fluroide, a neurotoxin with lithium instead.

What would happen is criminal behavior would drop.

Also Lithium has been found recently to completely halt ALS (Amotrophic Lateral Sclerosis) or what I like to call, "Stephen Hawking's Disease."

It's also a way to completely prevent Alzheimer's. and drastically reduce Parkinson's disease risks.

Further, Lithium as Orotate prevents your brain from shrinking with age.

This may be a totally stupid question, but when you guys talk about scalp peels and such are you just applying them to thin/bald spots with no hair or are you actually putting them over your entire scalp? If the latter, when you do the peels are you peeling off a lot of hair?

When I do the Scalp Renew, a good amount of hair comes out from the massage. That always freaks me out a bit, but I'm rolling with and seeing what 6 months on it will yield.