Calcification Theory Suggest It Inhibits Vellus Hair Turning Terminal

proscar2

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May help explain the difficulty of chems getting the desired effects EVEN with chems

an old post on people using manual pressure to reduce calcification and fibrosis and how it links to lympth- Argues the reason why vellus hair doesn't easily turn terminal

There is no doubt that increased fenestrations (increasing leakiness of capillaries) reduces blood pressure. This is precisely the way that Minoxidil lowers blood pressure: http://www.ncbi.nlm.nih.gov/pubmed/10233226

Apart from genetics and nutrition - the biggest thing that affects hair thickness is the size of the sheath of the papilla. In other words, the number of cells on the end.This is DIRECTLY determined by the presence of a capiliary loop feeding the Papilla. Without a loop - the hair is vellus. The more blood delivered to the area, the stronger the loop and the thicker the papilla = thicker hair.

All the above are verifiable facts - I've posted numerous papers backing up each assertion in the past. We have strong anecdotal evidence that manual methods can cause at least some hair growth - and good evidence that they can cause substantial regrowth.Let's assume though - that only the odd random hair will occur from manual methods.

What causes the random hair to grow? I don't think it's a leap to suggest that it was due to capillary loop developing for that hair. The only real way to explain that is to say that it was due to increased blood flow - even if you don't accept that as a sound method to regrow hair en mass.

Which strongly suggests that increasing blood flow will cause the capillary loop to develop regardless of if the hair 'demands' the resources as is normal for hair growth. In other words the mechanism goes both ways - hair growth demands blood flow to generate the cells for the papilla. Also, increased bloodflow will cause the same mechanism to activate.

At this point - I find it hard to believe that this isn't the primary method of action of minoxidil. Take away the increased blood diffused in the tissue and the capiliary loops collapse - causing a massive shed - precisely because fenestration not capillary growth was the cause of the increased blood flow.

The lymphodema angle is still more theoretical - but if as I'm observing the ridge can be reduced through deep massage, then this is identical to the treatment used for lymphodema massage treatment. Again this is proven and can be referenced.

A lack of capillaries might also create a low oxygen environment - encouraging DHT to be increased to compensate for the hypoxia. DHT is known to drive lymphatic drainage harder than in normal tissue.

So why the lymph fluid clogged tissue if DHT accelerates the flow of lymph fluid? I'm wondering if it pushes too hard and causes a backlog of fluid that can't escape the top of the scalp fast enough and pools. This is pure speculation right now.

I'll keep on massaging.


gbp2000
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Re: Detumesance Therapy And Scalp Ridge

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despacio on Sat Apr 05, 2014 7:01 am

Fibrosis is a key inhibitor of lymphatic regeneration.

Avraham T1, Clavin Norwood, Daluvoy SV, Fernandez J, Soares MA, Cordeiro AP, Mehrara BJ.



Author information



Abstract

BACKGROUND:

Lymphedema is a common debilitating sequela of lymph node dissection. Although numerous clinical studies suggest that factors that lead to fibrosis are associated with the development of lymphedema, this relationship has not been proven. The purpose of these experiments was therefore to evaluate lymphatic regeneration in the setting of variable soft-tissue fibrosis.

METHODS:

A section of mouse tail skin including the capillary and collecting lymphatics was excised. Experimental animals (n = 20) were treated with topical collagen type I gel and a moist dressing, whereas control animals (n = 20) underwent excision followed by moist dressing alone. Fibrosis, acute lymphedema, lymphatic function, gene expression, lymphatic endothelial cell proliferation, and lymphatic fibrosis were evaluated at various time points.

RESULTS:

Collagen gel treatment significantly decreased fibrosis, with an attendant decrease in acute lymphedema and improved lymphatic function. Tails treated with collagen gel demonstrated greater numbers of lymphatic vessels, more normal lymphatic architecture, and more proliferating lymphatic endothelial cells. These findings appeared to be independent of vascular endothelial growth factor C expression. Decreased fibrosis was associated with a significant decrease in the expression of extracellular matrix components. Finally, decreased soft-tissue fibrosis was associated with a significant decrease in lymphatic fibrosis as evidenced by the number of lymphatic endothelial cells that coexpressed lymphatic and fibroblast markers.

CONCLUSIONS:

Soft-tissue fibrosis is associated with impairment in lymphatic regeneration and lymphatic function. These defects occur as a consequence of impaired lymphatic endothelial cell proliferation, abnormal lymphatic microarchitecture, and lymphatic fibrosis. Inhibition of fibrosis using a simple topical dressing can markedly accelerate lymphatic repair and promote regeneration of normal capillary lymphatics.


PMID: 19644258 [PubMed - indexed for MEDLINE]
 

Iah11

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Fair play i appreciate that youre passionate about all this and you seem to read up a lot but this post is just incorrect in so many assertions.

First, when you state minoxidil works by increasing blood flow to the scalp, thats just false. Just think about it. Do users of caffeine, or people who exercise more suffer from lower rates of Androgenetic Alopecia? Minoxidil is a wonder drug for hair loss because it directly changes up/down regulates genes related to hair loss and increases keratin production. Just google minoxidil gene analysis.

Secondly, theres a study with over a 1000 patients who suffered from seborrhoic alopecia and hair loss slowing was observed in the vast majority of patients.

I dont even know what the link to lymphodema is here.

Sigh
 

Iah11

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Secondly, theres a study with over a 1000 patients who suffered from seborrhoic alopecia and hair loss slowing was observed in the vast majority of patients.

Sigh

Supposed to read that the patients had ligation of superficial scalp arteries performed
 

Georgie

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On find that my hair shedding is actually a little worse after exercise. :(
Increased blood flow never did much for me.
 

alebaba

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I've done Detumesance Therapy And Scalp Ridge before for about 2 years, got some vellus hairs and thats pretty much it. I was on nothing else tho, maybe I should give it another go along with seti. That sh*t also f*** up my wrist pretty good too, gave me carpal tunnel. I did it for 30 mins to an hr, twice a day.
 

arnoldd

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I had an allergic reaction to dutasteride, a general swelling of the face , salivary glands and swelling nodes. It last 6 months because the long half life of dutas.
Now i have a lot of scar tissue in the beard, especially where the lymph nodes were swelling.
So its true, chronic activation of lymph nodes lead to fibrosis.
But i cant see why a healthy person need to worry about that. Just stay away from inflammation
 

Georgie

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I had an allergic reaction to dutasteride, a general swelling of the face , salivary glands and swelling nodes. It last 6 months because the long half life of dutas.
Now i have a lot of scar tissue in the beard, especially where the lymph nodes were swelling.
So its true, chronic activation of lymph nodes lead to fibrosis.
But i cant see why a healthy person need to worry about that. Just stay away from inflammation
Oh dude that is rough. I’m sorry that happened. For whatever reason after starting duta I got localised bilateral
rashes on my shoulders. Lasted almost a month and a half, went away, now seem to be returned. Didn’t change anything else so it had to be duta.
Honestly wtf is with this drug.
 

arnoldd

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Oh dude that is rough. I’m sorry that happened. For whatever reason after starting duta I got localised bilateral
rashes on my shoulders. Lasted almost a month and a half, went away, now seem to be returned. Didn’t change anything else so it had to be duta.
Honestly wtf is with this drug.

Pay attention to that. Allergic reaction is inflammation and you know its nothing good for hairs
 

Georgie

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Pay attention to that. Allergic reaction is inflammation and you know its nothing good for hairs
A really good point!
I actually have 0% eosinophils shown on the same blood test that I got after I started avodart. That means an inflammatory response to something. Hmmm.

On another note, I’m really interested
I’m trying Sulfasalazine
 

arnoldd

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A really good point!
I actually have 0% eosinophils shown on the same blood test that I got after I started avodart. That means an inflammatory response to something. Hmmm.

On another note, I’m really interested
I’m trying Sulfasalazine

No no. Normal range of eosinophils is 1-3%. You are fine. When you have an illness or allergy reaction they go high.
 
Last edited:

Georgie

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No no. Normal range of eosinophils is 0-3%. You are fine. When you have an illness or allergy reaction they go high.
So do you think if I take sulfa even with low eos I won’t like.. leave myself totally open to infection?
 

ALightInTheDark

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I've made a hair fibrosis protocol
- Epsom Salt mask
- 30% Glycolic Acid Scalp Peel 1x/month (Enzyme Peel Papain Bromelain Serrapeptase/ MyChelle Dermaceuticals Incredible Pumpkin Peel 1.2 Fluid Ounce)
- Topical Iodine / Lugol 2% + DMSO (80/20)
- Topical Taurine
- Topical NAC
- SOD (Copper Peptides,Tricomin,Folligen)
- Green Tea Extract,Pomegranate Extract,Resveratrol,Grape Seed Extract
- Magnesium Orotate + Magnesium Oil
- Derminaneedling once every 3 weeks (1.5mm with erythema)
- Decorin

Tell me yall what u think
 

proscar2

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sorry in case people misunderstand
Fair play i appreciate that youre passionate about all this and you seem to read up a lot but this post is just incorrect in so many assertions.

First, when you state minoxidil works by increasing blood flow to the scalp, thats just false. Just think about it. Do users of caffeine, or people who exercise more suffer from lower rates of Androgenetic Alopecia? Minoxidil is a wonder drug for hair loss because it directly changes up/down regulates genes related to hair loss and increases keratin production. Just google minoxidil gene analysis.

Secondly, theres a study with over a 1000 patients who suffered from seborrhoic alopecia and hair loss slowing was observed in the vast majority of patients.

Sigh

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1 @ lah11 I actually never said that regarding minoxidil? I started THE ISSUE ON CALCIFICATION BY SAYING I WANT NOT HIGHLIGHTING BLOOD FLOW SPECIFICALLY! The post was an old post by another user on another forum; maybe i wasn't clear?



2 PLEASE PEOPLE don't focus on 'blood=flow' ' as it produces 'sigh's from members that dont get what I'm trying to promote.Its more regarding calcification and the lympth.

and this is @LAH11,i'm well aware of the many theories regarding minoxidil -
here is the (possible) MAIN reasons (until very recently) why minoxidil is thought to work. from other OLD posts.

note that although they can be placed roughly under the hypotheses of 'blood-flow' this is not what I'm specifically trying to highlight; it's not simply blood-flow, remember minoxidil is a calcium channel blocker.

1 There are lots of theories about minoxidil, without even including possible effects on AR. Which one to believe? Since minoxidil is designed to reduce intracellular calcium in order to relax blood vessels, I’m guessing that’s probably what it actually does.

Mechanism of action
Minoxidil is thought to have a direct mitogenic effect on epidermal cells, as has been observed both in vitro in vivo. Though the mechanism of its action for causing cell proliferation is not very clear, minoxidil is thought to prevent intracellular calcium entry. Calcium normally enhances epidermal growth factors to inhibit hair growth, and Minoxidil by getting converted to minoxidil sulfate acts as a potassium channel agonist and enhances potassium ion permeability to prevent calcium ions from entering into cells.

Though the exact action of minoxidil preventing the formation of DHT has not been shown but the drug has been shown to have a stabilizing effect on the hair loss. The result of the drug takes about few months time to be evident since it is the time which is necessary for restoring the normal growth cycle of hair fibers.


2 And yet another study, which says minoxidil simply increases blood flow (I’m still going with decreasing intracellular calcium, just like it is supposed to work):

“Intracellular ATP (up to 5 mM) or glibenclamide (20 nM), a specific ATP-sensitive K channel blocker, did not block these channels. Minoxidil sulfate (5 micrograms/ml) or pinacidil (10 microM) did not open these two types of K channels or increase 86Rb efflux. These results suggest that minoxidil sulfate or pinacidil did not activate K channel current in hair follicles, and that the drug effect on hair growth might be mediated by other mechanisms such as increased blood flow.”


3 Minoxidil has been seen to promote growth of hair fiber though how the drug works is still not very clear. Minoxidil is supposed to be working as an agent that promotes cell division rather than having an effect as an immunosuppressant or influencing the hormones. It has been observed that Minoxidil enhances the keratinocyte process thereby helping hair growth. Even vitro keratinocytes can be kept for a longer time with minoxidil. The drug has also been found to increase the number of hairs in monkeys and humans during anagen.

Minoxidil may also enhance hair growth by reducing the calcium influx in the cells. Calcium triggers off those epidermal growth factors that inhibit the growth of hair fibers. Minoxidil sulphate being a potassium channel opener induces the potassium ions to enter the cells and blocks the influx of calcium in the cells thereby facilitating hair growth.

Minoxidil being initially a drug for hypertension, was once thought to enhance hair growth by increasing the blood flow into the follicles but it has been found that dilation of blood vessels do not play a direct role in hair growth.


I spend more time on rebuttal than all else- christ!
 

balda

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I've made a hair fibrosis protocol
- Epsom Salt mask
- 30% Glycolic Acid Scalp Peel 1x/month (Enzyme Peel Papain Bromelain Serrapeptase/ MyChelle Dermaceuticals Incredible Pumpkin Peel 1.2 Fluid Ounce)
- Topical Iodine / Lugol 2% + DMSO (80/20)
- Topical Taurine
- Topical NAC
- SOD (Copper Peptides,Tricomin,Folligen)
- Green Tea Extract,Pomegranate Extract,Resveratrol,Grape Seed Extract
- Magnesium Orotate + Magnesium Oil
- Derminaneedling once every 3 weeks (1.5mm with erythema)
- Decorin

Tell me yall what u think
@ALightInTheDark
Have you finally tried the protocol? Results? Thanks
 
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