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
Posts : 287
Join date : 2009-06-03
Re: Detumesance Therapy And Scalp Ridge
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]
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
Posts : 287
Join date : 2009-06-03
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]