Sorry if brought up before but: Best topical to help aid in breaking up fibrosis?

Anything viable out there with studies backing it up?


Thanks in advance!

Mag oil

Oh yeah I forgot apple cider vineger too.

what is fibrosis ?? Collagen cross linking ?? or is that something else ?


I thought carnosine was scientifically the best thing for this , even better than MSM or magnesium oil.

http://www.hairloss-research.org says that taurine breaks up fibrosis in the scalp and is the best thing. But that website has been the same for literally the past 5 years.

Try them all

carnosine
magnesium oil
apple cider vinegar
taurine
MSM
ginger/cinnamon

I don't think a topical carnosine exists though

Maybe caustic symmetry knows something

As someone who tried MSM for years with no results, I am now going with carnosine to see what results I get

MSM only works for resolving scar tissue (fibrosis) when a pure, unadulterated form is used without any excipients (even the capsule of gelatin or other wise can reduce its efficacy). So it's best to take it 30 minutes away from other elements.

Vitamin K2 is helpful for preventing and/or reducing crosslinking.

Nutr Rev. 2011 Mar;69(3):162-7. doi: 10.1111/j.1753-4887.2011.00380.x. Epub 2011 Feb 14.
Bone quality and vitamin K2 in type 2 diabetes: review of preclinical and clinical studies.
Iwamoto J1, Sato Y, Takeda T, Matsumoto H.

Type 2 diabetic patients are at high risk of bone fractures even if their bone mineral density is normal or high. This is likely explained by poor bone quality and extraskeletal factors. The present review was conducted to provide an overview of the currently available preclinical and clinical evidence on the effect of vitamin K(2) on bone quality in persons with type 2 diabetes. Vitamin K(2) stimulates γ-carboxylation of osteocalcin and can increase bone formation through steroid and xenobiotic receptors. Clinical studies of type 2 diabetic patients have shown detrimental collagen cross-links in bone; low serum insulin-like growth factor-I and osteocalcin concentration are associated with an increased risk of fractures. A therapeutic strategy for preventing fractures in type 2 diabetic patients remains to be established. One recent preclinical study showed that vitamin K(2) administration in a type 2 diabetic rat model had the following skeletal benefits: increased serum osteocalcin, improved collagen cross-link profiles, and increased bone strength. These new findings suggesting a possible beneficial effect of vitamin K(2) supplementation on bone quality in type 2 diabetes warrant further investigation.

Following calcium and phosphorus, sulfur is the third most abundant mineral in the body. A grown man of average height and weight has approximately 140 grams of sulfur distributed through their system. Nearly half of all sulfur is contained in muscular tissue, skin, and bones.

Sulfur-based amino acids such as Taurine and Cysteine are synthesized from MSM. Therefore it isn't necessary to take these other substances.

When plants absorb MSM from rainwater, they convert it into sulfur containing the amino acids methionine and cysteine. Taurine and cysteine, the other two known sulfur amino acids, are synthesized from cysteine. The body manufactures about 80% of the amino acids it needs, and these are classified as nonessential. The remaining 20%, called essential amino acids, must be obtained from food. Methionine and cysteine are considered two of them. There are approximately 28 known amino acids. Each type of protein is made up of a unique collection of amino acids in a specific combination. Two molecules of cysteine can oxidize and bond together through sulfur (-S-S-) bonds. These sulfur bonds are the key factors that hold proteins in shape, and determine the form, properties, and biological activities of proteins.

Mindell, E.L.: The MSM Miracle. Enhance Your Health with Organic Sulfur. Good Health Guides, Keats Publishing, Inc, Connecticut, USA: 1997.

Ley, B.M.: The Forgotten Nutrient MSM: on Our Way Back to Health with Sulfur. Health Learning Handbooks, BL Publications, California: 1998.

Maybe taurine as a topical also ?

iuyyighghghgkh wrote:Maybe taurine as a topical also ?

I'm not sure if I've seen anything yet on anyone trying it topically. Wouldn't be surprised if it worked, because it is a sulfur-based amino acid. There's definitely some efficacy internally to some extent.

http://www.nature.com/nrrheum/journal/v10/n7/full/nrrheum.2014.53.html

One figure from this study.

http://www.nature.com/nrrheum/journal/v10/n7/fig_tab/nrrheum.2014.53_F1.html

"The activation of fibroblasts and the differentiation of myofibroblasts are hallmarks of fibrosis. Activated myofibroblasts synthesize and deposit ECM components, leading to ECM accumulation, increased collagen crosslinking, contraction and fibrosis. Fibrotic tissues exhibit increased tissue pressure and hypoxia, which further activate resident fibroblasts and escalate fibrotic mechanisms."

It's how they achieve their immortality there if not treated. Perpetuum mobile with inflammation.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725728/


" Using a transgenic model of overexpression of a constitutively active form of HIF1α, we determined that HIF1α fails to induce the expected proangiogenic response. In contrast, we observed that HIF1α initiates adipose tissue fibrosis, with an associated increase in local inflammation. “Trichrome- and picrosirius red-positive streaks,” enriched in fibrillar collagens, are a hallmark of adipose tissue suffering from the early stages of hypoxia-induced fibrosis. Lysyl oxidase (LOX) is a transcriptional target of HIF1α and acts by cross-linking collagen I and III to form the fibrillar collagen fibers. Inhibition of LOX activity by β-aminoproprionitrile treatment results in a significant improvement in several metabolic parameters and further reduces local adipose tissue inflammation. Collectively, our observations are consistent with a model in which adipose tissue hypoxia serves as an early upstream initiator for adipose tissue dysfunction by inducing a local state of fibrosis."

On a side note, http://www.nature.com/mt/journal/v17/n10/images/mt2009136f7.gif  -  interesting Stem cell VEGF model.

Also, depending on your level of recession, you might not have developed fibrosis YET. But there is inflammation for sure.

http://www.ncbi.nlm.nih.gov/pubmed/19527330

RESULTS:

"The frontal bald area of patients showed highly significant increase in telogen hairs and decrease in anagen/telogen ratio and terminal/vellus hair ratio (P < 0.001). Perifollicular inflammation was almost a constant feature in early cases and showed a significant inverse correlation with perifollicular fibrosis (P = 0.048), which was more marked with thickening of the follicular sheath in advanced cases.

CONCLUSION:

Follicular microinflammation plays an integral role in the pathogenesis of AGA in early cases. Over time, thickening of perifollicular sheath takes place due to increased deposition of collagen, resulting in marked perifollicular fibrosis, and sometimes ends by complete destruction of the affected follicles in advanced cases."

Billa asked in another thread about calcification too.

http://www.ncbi.nlm.nih.gov/pubmed/21597007

"OPN exerts stage-specific roles in arteriosclerosis in LDLR-/- mice. Actions phenocopied by the OPN metabolite SVVYGLR promote osteogenic calcification processes with disease initiation. OPN limits vascular chondroid metaplasia, endochondral mineralization, and collagen accumulation with progression. Complete deficiency yields a net increase in arteriosclerotic disease, reducing aortic compliance and conduit vessel function in LDLR-/- mice."


http://en.wikipedia.org/wiki/Atherosclerosis

http://upload.wikimedia.org/wikipedia/commons/9/9a/Endo_dysfunction_Athero.PNG

Look at Fibroatheroma stage from the picture maybe.

-Single or multiple lipid cores.
-Fibrotic/calcific layers

is calcification

collagen cross linking

fibrosis

the same ?

also, does k2 decalcify the skin ?

iuyyighghghgkh wrote:is calcification

collagen cross linking

fibrosis

the same ?

also, does k2 decalcify the skin ?

Yes, K2 decalcifies the skin, arteries and vascular system. It's also beneficial for the liver and hormone regulation.

Fibrosis and be caused by crosslinking, but it is not always the same. For example as we age there is less plasmin and greater levels of antiplasmin, so the level of fibrinogen levels can build up (pre-collagen strands), which can thicken the blood or create coagulation defects.

Oman Med J. 2014 May;29(3):172-7. doi: 10.5001/omj.2014.44.
Vitamin k dependent proteins and the role of vitamin k2 in the modulation of vascular calcification: a review.
El Asmar MS1, Naoum JJ2, Arbid EJ2.

Vascular calcification, a cause of cardiovascular morbidity and mortality, is an actively regulated process involving vitamin K dependent proteins (VKDPs) among others. Vitamin K is an essential micronutrient, present in plants and animal fermented products that plays an important role as a cofactor for the post-translational γ-carboxylation of glutamic acid residues in a number of proteins. These VKDPs require carboxylation to become biologically active, and they have been identified as having an active role in vascular cell migration, angiogenesis and vascular calcification. This paper will review the process of vascular calcification and delineate the role that vitamin K2 plays in the modulation of that process, through the activation of VKDPs. One such VKDP is Matrix Gla Protein (MGP), which when activated inhibits osteogenic factors, thereby inhibiting vascular and soft tissue calcification.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4052396/

CS - this is a bit off topic, but I want to ask since it's your expertise. I have an opportunity to do a full orthomolecular diagnostics as I have gotten a significant discount through some coupons my family participates in for some time. The test is blood and urine and they test out all organic acids and nutrients, intolerancies/allergies for about 100 different foods, and more, I don't know the exact details but I'm sure you are familiar with the test. They said it's a wide picture of metabolism and functions and also after the testing they study it and give suggestions with foods and supplements to optimize the metabolism. I shouldn't skip this opportunity right?

What about emu oil ,which contains Vitamin K and an oily capsule of Vitamin D? Would that do something for the hair if applied topically? You could add Magnesium oil too.

What are people's opinions on this?

Is fibrosis really a factor here? Think about this for a moment; alopecia areata sufferers' follicles are subjected to continuous auto-immune attack, yet their hair often times regenerates after months, years or decades. So, if this theory had any merit, then these people would also have scalps which are laced with internal scar tissue, yet their follicles regenerate and regrow hair. Secondly, the papilla continues to produce micro-vellus hairs; the sweat and sebaceous glands continue to function normally. Given their close proximity to the papilla, then wouldn't fibrotic scar tissue also impede their functioning also? 

There seems to be only one area of the follicle which inflames and that is the extra-cellular matrix surrounding the papilla, but this area is constantly renewed by the hair bulge during growth cycles unless it enters into the telogen phase and remains there. When the matrix (in the case of alopecia areata) stops inflaming, it regenerates and the follicle starts to produce terminal hairs. So, I'm failing to see how fibrosis is a factor here.

Christos wrote:What about emu oil ,which contains Vitamin K and an oily capsule of Vitamin D? Would that do something for the hair if applied topically? You could add Magnesium oil too.

What are people's opinions on this?

May not work topically. internally is good.

see the list of things I mentioned to see what breaks up fibrosis.

Xenon wrote:Is fibrosis really a factor here? Think about this for a moment; alopecia areata sufferers' follicles are subjected to continuous auto-immune attack, yet their hair often times regenerates after months, years or decades. So, if this theory had any merit, then these people would also have scalps which are laced with internal scar tissue, yet their follicles regenerate and regrow hair. Secondly, the papilla continues to produce micro-vellus hairs; the sweat and sebaceous glands continue to function normally. Given their close proximity to the papilla, then wouldn't fibrotic scar tissue also impede their functioning also? 

There seems to be only one area of the follicle which inflames and that is the extra-cellular matrix surrounding the papilla, but this area is constantly renewed by the hair bulge during growth cycles unless it enters into the telogen phase and remains there. When the matrix (in the case of alopecia areata) stops inflaming, it regenerates and the follicle starts to produce terminal hairs. So, I'm failing to see how fibrosis is a factor here.

www.hairloss-research.org has a lot of articles about taurine and fibrosis

read and see what you think

There are already plenty of studies showing perifollicular fibrosis (scarring) in "androgenetic alopecia". Like the one I posted page back.


EDIT: If you don't believe me, check this entire page out.

http://www.hairlosstalk.com/interact/showthread.php/76578-Fibrosis-Inflammation-amp-Androgen-Alopecia?s=855040f597a7079e76502eb11fb18ec7

OK, I will repeat myself once more; if fibrosis was such an issue, then why do alopecia areata sufferers regrow their hair in many cases after months, years or decades? What part of that is difficult to understand? I could care less about studies on fibrotic scar tissue allegedly affecting hair growth; I have presented evidence that a) alopecia areata sufferer's follicles come under auto-immune attack b) suffer inflammation c) experience hair regrowth in many cases. 

Again, if inflammation is causing scar tissue, and scar tissue is affecting hair growth, then why do alopecia areata sufferers experience regrowth?

Xenon I don't understand what are we discussing here. We also can't really discuss this unless we do some studies ourselves. Alopecia areata and typical "mpb" is different in the signalling pathway scene regulated by everything AND androgens. Are you suggesting and rejecting that there is no fibrosis generated by inflammation in mpb? If you ask WHY alopecia areata reverses itself I do not know. You also say this in a fashion, like it's impossible to regrow hair in androgenetic alopecia. Also, fibrosis isn't the only problem. I posted obvious pictures of regrowth with a MANUAL during androgenetic alopecia and so have others.


"I have presented evidence that a) alopecia areata sufferer's follicles come under auto-immune attack b) suffer inflammation c) experience hair regrowth in many cases. "

Here's the problem mate. You can't go from a) to b) to c) because there is a LOT happening in between and NOBODY studied this. You do understand that right? What do you expect me to say, if you don't know the answer, and nobody else does? Maybe there was some psycho-nutritional-lifestyle-heavy metal- etc. until endless strawmans - stressor that when it got removed, the regrowth was initiated because the hard set androgen transcription enviroment wasn't set up, aka it was a situational specific auto-immune impairment and not the typical mpb signalling cascade that ends up in forever-apoptosis-mode.

Anegdotally, my follicles were also under inflammation and everything was the same and I experienced regrowth. Why didn't it come by itself but I had to do some work I really do not know. Also why did it even initiate I do not know. Was it because of low SHBG? Lol. Shear fact that this STOPPED all further hair loss and started regrowing and thickening hair for me really puts a high end perspective on the theories that explain it in a pattern-fashion. And by that simple logic, which we can overwhelmingly complicate through various scientific fields until endless strawmans, it provided the regrowth in the same vice-versa pattern that it miniaturized at the beginning. So I can't answer your question about alopecia areata but I don't see how that means that we aren't tackling fibrosis in mpb? What if inflammation in mpb directs different signalling pathways in which cytokines and collagen formation play a different role in apoptosis signalling along with androgens, and in alopecia areata it doesn't? We can speculate, but hard evidence about fibrosis in mpb is just that, and there is no reason that we shouldn't be trying to reverse it. For all we may know, fibrosis may directly somehow prevent spontaneous regrowth in "mpb" and it plays a whole different role in alopecia areata coming from different multiple signal initiators.

Bottomlime, this thread mainly refers to how to tackle fibrosis in androgenetic alopecia, since 95% of us are suffering from it. If you want to question the importance of fibrosis in the process, this isn't the place to do so. Fibrosis and androgens in the role of male pattern baldness are in a direct relationship or very close to it.

Xenon wrote:OK, I will repeat myself once more; if fibrosis was such an issue, then why do alopecia areata sufferers regrow their hair in many cases after months, years or decades? What part of that is difficult to understand? I could care less about studies on fibrotic scar tissue allegedly affecting hair growth; I have presented evidence that a) alopecia areata sufferer's follicles come under auto-immune attack b) suffer inflammation c) experience hair regrowth in many cases. 

Again, if inflammation is causing scar tissue, and scar tissue is affecting hair growth, then why do alopecia areata sufferers experience regrowth?

You're implying the same mechanism for alopecia areata is the same as MPB. They are completely different. Dht + fibrosis is what mpb is. maybe alopecia is fibrosis + something else. Whatever it is, they're completely different.

Keanoseg wrote:Xenon I don't understand what are we discussing here. We also can't really discuss this unless we do some studies ourselves. Alopecia areata and typical "mpb" is different in the signalling pathway scene regulated by everything AND androgens. Are you suggesting and rejecting that there is no fibrosis generated by inflammation in mpb? If you ask WHY alopecia areata reverses itself I do not know. You also say this in a fashion, like it's impossible to regrow hair in androgenetic alopecia. Also, fibrosis isn't the only problem. I posted obvious pictures of regrowth with a MANUAL during androgenetic alopecia and so have others.


"I have presented evidence that a) alopecia areata sufferer's follicles come under auto-immune attack b) suffer inflammation c) experience hair regrowth in many cases. "

Here's the problem mate. You can't go from a) to b) to c) because there is a LOT happening in between and NOBODY studied this. You do understand that right? What do you expect me to say, if you don't know the answer, and nobody else does? Maybe there was some psycho-nutritional-lifestyle-heavy metal- etc. until endless strawmans - stressor that when it got removed, the regrowth was initiated because the hard set androgen transcription enviroment wasn't set up, aka it was a situational specific auto-immune impairment and not the typical mpb signalling cascade that ends up in forever-apoptosis-mode.

Anegdotally, my follicles were also under inflammation and everything was the same and I experienced regrowth. Why didn't it come by itself but I had to do some work I really do not know. Also why did it even initiate I do not know. Was it because of low SHBG? Lol. Shear fact that this STOPPED all further hair loss and started regrowing and thickening hair for me really puts a high end perspective on the theories that explain it in a pattern-fashion. And by that simple logic, which we can overwhelmingly complicate through various scientific fields until endless strawmans, it provided the regrowth in the same vice-versa pattern that it miniaturized at the beginning.  So I can't answer your question about alopecia areata but I don't see how that means that we aren't tackling fibrosis in mpb? What if inflammation in mpb directs different signalling pathways in which cytokines and collagen formation play a different role in apoptosis signalling along with androgens, and in alopecia areata it doesn't? We can speculate, but hard evidence about fibrosis in mpb is just that, and there is no reason that we shouldn't be trying to reverse it. For all we may know, fibrosis may directly somehow prevent spontaneous regrowth in "mpb" and it plays a whole different role in alopecia areata coming from different multiple signal initiators.

Bottomlime, this thread mainly refers to how to tackle fibrosis in androgenetic alopecia, since 95% of us are suffering from it. If you want to question the importance of fibrosis in the process, this isn't the place to do so. Fibrosis and androgens in the role of male pattern baldness are in a direct relationship or very close to it.

Yes, signalling pathways may be different, but, according to the conventional knowledge, both ultimately result in inflammation of the follicle and hairloss. According to what you and the studies are stating, inflammation leads to scarring (yes, I get that), but, as I pointed out, it is only the extra-cellular matrix which suffers inflammation. This portion of the follicle is continually renewed via signaling from the hair bulge anyway, so even if the matrix is destroyed by inflammation, it will redevelop, so long as the environment is healthy. This is why alopecia areata sufferers are able to regrow hair in many cases, simply based upon the fact that the matrix is able to redevelop and reproduce terminal hairs. Now, also take into account the fact that many MPB sufferers report regrowth when taking fin or minox. Did they have to undergo manuals in order to get rid of scar tissue in order for their hair to regrow? No, the lowering of DHT assisted in helping the hair regrow, not the manual removal of internal scar tissue. Of course there are other factors impeding hairgrowth where MPB is concerned, but my point being, fin / dut helps to regrow hair without the requirement of scar tissue removal. 

Let's also consider this; if fibrosis was such a huge factor, then why is the papilla not destroyed and replaced by collagen fibers? If most balding guys look at their scalps under a certain angle of light, they can see it is laced with micro-vellus hairs -- formerly terminal hairs now in the telogen phase. All that needs to be achieved here is the reduction of inflammation, which will ultimately lead to renewal of a new matrix.

That's really for another thread man. Make a thread about that, this thread is about what can be done about the fibrosis... not a debate on whether or not this is contributing to our hair loss...

carnosine
magnesium oil
apple cider vinegar
Limes/lemons
taurine
MSM / vitamin c
ginger/cinnamon
vitamin k2/d3
EDTA

anymore you can think of ?

Xenon wrote:Yes, signalling pathways may be different, but, according to the conventional knowledge, both ultimately result in inflammation of the follicle and hairloss. According to what you and the studies are stating, inflammation leads to scarring (yes, I get that), but, as I pointed out, it is only the extra-cellular matrix which suffers inflammation. This portion of the follicle is continually renewed via signaling from the hair bulge anyway, so even if the matrix is destroyed by inflammation, it will redevelop, so long as the environment is healthy. This is why alopecia areata sufferers are able to regrow hair in many cases, simply based upon the fact that the matrix is able to redevelop and reproduce terminal hairs. Now, also take into account the fact that many MPB sufferers report regrowth when taking fin or minox. Did they have to undergo manuals in order to get rid of scar tissue in order for their hair to regrow? No, the lowering of DHT assisted in helping the hair regrow, not the manual removal of internal scar tissue. Of course there are other factors impeding hairgrowth where MPB is concerned, but my point being, fin / dut helps to regrow hair without the requirement of scar tissue removal.

Let's also consider this; if fibrosis was such a huge factor, then why is the papilla not destroyed and replaced by collagen fibers? If most balding guys look at their scalps under a certain angle of light, they can see it is laced with micro-vellus hairs -- formerly terminal hairs now in the telogen phase. All that needs to be achieved here is the reduction of inflammation, which will ultimately lead to renewal of a new matrix.

Hey Xenon, this is exactly why I said that we need more research. You make very good points and this is why.

Minox is a vasolidator - period. The ion channel it opens can be opened by anything at different situations. Potassium channels are not a primary reason why it works. Minox was developed for heart conditions look it up. Minox is also less effective at areas already bald so why could this be? Only because of enviroment makes sense to me.

You could say the same thing with Botox, reliever, etc studies. Relaxed muscles, more blood flow = everything reversed, even potential (most probable) fibrosis. Now how and why is that? There is a connected mechanism between the stuff. Not only minox and fin through blood increase , DHT decrease achieved that, how would you explain the botox etc. mechanisms? There seems to be some common mechanisms which as a background, can create and reverse given enviroments and transcriptions. We can only know if we precisely research it. Just goes to show that the enviroment can be changed by multiple mechanisms.

For example, Xenon take a look at this study.

http://www.jbiomedsci.com/content/21/1/3

It's how just blood flow, lack of it, or volumetrically improper blood flow, can express and create inflammatory enviroment, reduce antioxidant activity etc... There are a bunch of studies scattered throughout the internet that no one connected, and there's also lack of research. It's definitely a complex process, but you can say that some things will always be good (like proper blood flow, no fibrosis, etc.)

Yes it can be dangerous and the side effects, even though often mentioned, are not taken seriously by most people. It's used in certain conditions, given for the heart, this is a specific situation, so I don't think it's safe for everyone to just be spilling it over the scalp. IMO taking minox for hair regrowth isn't worth it at all.

edit: disappeared message before lol