Need a big favor. S Foote's theory in a nutshell?

[wookster]

Nitric oxide and prostaglandins modulate lymphatic vasomotion, and, compounds like minoxidil and latanoprost[a prostaglandin analog] stimulate hair growth. Obviously for Mr. Foote's contact inhibition and consequent follicular miniaturization to occur, a constant minimal pressure must be maintained in the scalp hypodermal tissues. I suppose that random fluctuations in hydrostatic pressure above that minimal ceiling pressure could occur though... ensativo:

 

[Bryan]

There are many theory thieves out here on the wild west of cyberspace. Why cough up everything?

I seriously doubt that there's much danger of anybody stealing Stephen's theory, for obvious reasons.

 

[The Gardener]

It has always been my understanding that the scalp has some of the most dense vascular structures on the entire surface of the skin... primarily so to protect the sensory organs. Note how a shaving knick bleeds forever, yet a similiar knick on the leg clots up within minutes.

With the head being as awash in blood as it is, I can't imagine that circulation could be much of an issue here.

 

[docj077]

Wookster,

You can post all the pictures and studies that you want. Especially, since nothing that you've posted has really helped you out.

The vessels are obliterated and sclerosed. Angiogenesis is impossible in the presence of a follice surrounded by a collagen shell with even more collagen surrounding it. You have to remove the pro-fibrotic stimulus, but unfortunately, the normally pro-angiogenesis factors like TGF-beta end up laying down more collagen than new vasculature. The body is trying to increase blood flow to the follicle, but the very molecules that are designed to do so are responsible for the increase in inflammation and fibrosis.

 

[michael barry]

WOOKIE and Doctor and BRYAN, Let me place one more burden on Stephen's assertions.


From transplantaion we know docs (mostly) nowadays move entire follicular groupings or follicular units which average between 2-3 hairs, but often have 4 or 5, and once in a blue moon 6 hairs in them.

Many times docs will move these units while one or even two of the hairs in the unit may be in catagen or telogen phases, i.e.----its not in anagen, its dermal papilla bulb is very shrunken and at the top of the dermis around the sebaceous glands. Doctor Cole has pictures of grafts culled in telogen and catagen and has posted them on his website, forhair.com. These still grow.

IF a tissue scaffold is formed around them, its all the way up near the top of the dermis. How then do they expand and grow down outside the scar formation around them into large hairs? They should be "boxed in" by edema.


Stephen has claimed that the reason that FUE hairs culled purposely from the back of the neck to fade the hairline with naturally in FUE transplantation (instead of the circumferentially large middle-of the- wreath donor hairs) dont get as large as the other hairs post-transplantaion because the tissue scaffold is created around the follicle papilla itself in healing, and it has nothing to do with how large an extraction tool was made to make the recipient site (which these days are slits most of the time made by razor-tipped instruments instead of big holes literally cut out of the dermis to jam new tissue into----now hardly any tissue is removed at all in the recipient area). So a the same sized instruments used to make recip sites should not, according to Stephen, mean small nape-o-the-neck hairs can enlarge to be as big as the better donor hairs, but the healing around those individual hairs should be the scaffold scar.


But what about hairs in rest stages, shrunken dermal papillas very small near the top of the dermis? If Stephen is right, these should never dive down outside of their scaffolds, re-enlarge, and get big. But they do. Docs will all tell you this (and Ive talked to alot of docs over the past few years and some of the best----Cole, Cooley, Umar, Woods, etc.)



I dont think we are ever going to find a magic bullet that disproves Foote's theory in a way all parties will agree with though. I think what will happen is that when ICX, Aderans, ACELL, or FOllica solves baldness in a practical way.......................all other theories will be more or less forgotten. Men just want their hair back, and dont really care about the particulars too much.

 

[bubka]

michael barry, i have read and seen you post this multiple times, and it totally understand and agree with you, my question is, what does Stephen say to this then, because it seems to put his "theory" to rest?

 

[wookster]

Wookster,

The vessels are obliterated and sclerosed. Angiogenesis is impossible in the presence of a follice surrounded by a collagen shell with even more collagen surrounding it. You have to remove the pro-fibrotic stimulus, but unfortunately, the normally pro-angiogenesis factors like TGF-beta end up laying down more collagen than new vasculature. The body is trying to increase blood flow to the follicle, but the very molecules that are designed to do so are responsible for the increase in inflammation and fibrosis.

:boid: :boid: :boid:

People from countries that consume ample amounts of curcuminiods still suffer from male pattern baldness.

That simple observation seems to expose a flaw in your theoretical infrastructure also.

Fibrosis, sclerosed tissue, inflammation, are also consequences of sustained lymph stagnation.

http://www.pubmedcentral.nih.gov/articl ... id=1502157

Sustained lymph stagnation engenders a pathological response that is complex and not well characterized. Tissue inflammation in lymphedema may reflect either an active or passive consequence of impaired immune traffic.

[...]

The molecular pattern in the RNA extracted from the whole tissue was dominated by the upregulation of genes related to acute inflammation, immune response, complement activation, wound healing, fibrosis, and oxidative stress response.

 

[wookster]

It has always been my understanding that the scalp has some of the most dense vascular structures on the entire surface of the skin... primarily so to protect the sensory organs. Note how a shaving knick bleeds forever, yet a similiar knick on the leg clots up within minutes.

With the head being as awash in blood as it is, I can't imagine that circulation could be much of an issue here.

http://findarticles.com/p/articles/mi_m ... ody_middle

A link exists between the lack of oxygen in the cells of the scalp and male pattern baldness, according to a study by plastic surgeon Steven L. Ringler, Butterworth Hospital, Grand Rapids, Mich. "Hair requires oxygen to grow. When circulation is inadequate, the cells will have insufficient oxygen, which may prevent the hair from growing. The apparent hereditary nature of baldness may actually be a genetic predisposition to insufficient circulation."

Approximately two-thirds of the male Caucasian population is affected by male pattern baldness as they get older. Numerous causes have been proposed, from scalp tension to age, genetic predisposition, the presence of androgens, a steroid hormone that increases male characteristics.

During the test, scalp temperatures and transcutaneous [PO.sub.2] (availability of oxygen in the cells) of all subjects were measured over the temples above the ears and on the frontal scalp at the top of the forehead. While scalp temperatures varied slightly, the difference in transcutaneous [PO.sub.2] between bald and control subjects was significant. The oxygen level in the bald scalps was almost 38% less that of the control group. Additionally, in those with male pattern baldness, the [PO.sub.2] was less in the frontal scalp than over the temples. In the control group, there was no significant difference between the frontal scalp and the temporal areas.

The area around the temples is not likely to be bald because the circulation to the temples and back of the head is fed by the external carotid artery, which provides a sufficient flow of blood. The frontal scalp receives circulation from the internal carotid artery, which supplies the brain, and small branches pass through the eye sockets to the scalp. Hair transplants may be able to grow in what previously was bald scalp because they are inserted at a level deeper than the normal hair follicle, where there is greater circulation.

In recent years, the reduction of baldness has been noted as a side effect in male patients receiving minoxidil for hypertension. While this phenomena has not been explained fully, the increased circulation that results from the treatment may change the availability of oxygen in the frontal scalp.

"This study is just part of ongoing research to identify specific treatments and possible prevention of male pattern baldness," Ringler explains. "Current studies show very promising results." In the meantime, he suggests that people with male pattern baldness consider hair transplants, which increasingly are successful.

 

[wookster]

There are many theory thieves out here on the wild west of cyberspace. Why cough up everything?

I seriously doubt that there's much danger of anybody stealing Stephen's theory, for obvious reasons.

Proof is in the pudding buddy

 

[wookster]

WOOKIE and Doctor and BRYAN, Let me place one more burden on Stephen's assertions.


From transplantaion we know docs (mostly) nowadays move entire follicular groupings or follicular units which average between 2-3 hairs, but often have 4 or 5, and once in a blue moon 6 hairs in them.

Many times docs will move these units while one or even two of the hairs in the unit may be in catagen or telogen phases, i.e.----its not in anagen, its dermal papilla bulb is very shrunken and at the top of the dermis around the sebaceous glands. Doctor Cole has pictures of grafts culled in telogen and catagen and has posted them on his website, forhair.com. These still grow.

IF a tissue scaffold is formed around them, its all the way up near the top of the dermis. How then do they expand and grow down outside the scar formation around them into large hairs? They should be "boxed in" by edema.


Stephen has claimed that the reason that FUE hairs culled purposely from the back of the neck to fade the hairline with naturally in FUE transplantation (instead of the circumferentially large middle-of the- wreath donor hairs) dont get as large as the other hairs post-transplantaion because the tissue scaffold is created around the follicle papilla itself in healing, and it has nothing to do with how large an extraction tool was made to make the recipient site (which these days are slits most of the time made by razor-tipped instruments instead of big holes literally cut out of the dermis to jam new tissue into----now hardly any tissue is removed at all in the recipient area). So a the same sized instruments used to make recip sites should not, according to Stephen, mean small nape-o-the-neck hairs can enlarge to be as big as the better donor hairs, but the healing around those individual hairs should be the scaffold scar.


But what about hairs in rest stages, shrunken dermal papillas very small near the top of the dermis? If Stephen is right, these should never dive down outside of their scaffolds, re-enlarge, and get big. But they do. Docs will all tell you this (and Ive talked to alot of docs over the past few years and some of the best----Cole, Cooley, Umar, Woods, etc.)

ensativo: ensativo: ensativo:


Good question.

 

[docj077]

Wookster,

The vessels are obliterated and sclerosed. Angiogenesis is impossible in the presence of a follice surrounded by a collagen shell with even more collagen surrounding it. You have to remove the pro-fibrotic stimulus, but unfortunately, the normally pro-angiogenesis factors like TGF-beta end up laying down more collagen than new vasculature. The body is trying to increase blood flow to the follicle, but the very molecules that are designed to do so are responsible for the increase in inflammation and fibrosis.

:boid: :boid: :boid:

People from countries that consume ample amounts of curcuminiods still suffer from male pattern baldness.

That simple observation seems to expose a flaw in your theoretical infrastructure also.

Fibrosis, sclerosed tissue, inflammation, are also consequences of sustained lymph stagnation.

http://www.pubmedcentral.nih.gov/articl ... id=1502157

Sustained lymph stagnation engenders a pathological response that is complex and not well characterized. Tissue inflammation in lymphedema may reflect either an active or passive consequence of impaired immune traffic.

[...]

The molecular pattern in the RNA extracted from the whole tissue was dominated by the upregulation of genes related to acute inflammation, immune response, complement activation, wound healing, fibrosis, and oxidative stress response.

The amount of curcuminoids needed to reverse fibrosis is impossible to ingest. Especially, since those compounds are not easily absorbed and many studies demonstrate that oral intake does not equal a high concentration in the blood.

Also, remind me again why you think the lymphatics are damaged in male pattern baldness? There is no evidence for such a process to my knowledge. I would argue that androgens cause the inflammation and fibrosis first with any damage to the lymphatics simply being a result of the initial process. That process would continue with further lymphatic destruction.

As for the oxygen levels in the scalp that you gave another poster, that is easily explained by the hyperkeratinization of the epidermal layer preventing oxygen diffusion and vessel obliteration preventing nutrient diffusion across capillaries.

opsblush: opsblush: opsblush:

 

[michael barry]

Wookie,

http://youtube.com/watch?v=L5GlPTom3U0

Watch that speech by Karl Rove. He moves his head alot and you get to see him sideways as well as frontally. He is going tremendously bald. He hardly has eyebrows. His side recession is almost back to his ears, and his hippocratic wreath has receeded downwards.


THis is why its hard to believe edema is the cause of hairloss for me personally. If thats the case, his whole cranium has it because his wreath hair is greying and thinning also. It would seemingly imply that his lymph drainage sucks even close to his ears. Its kinda hard to believe that would be the case, but much easier to believe he just has a high genetic amount of androgen receptors in the skin of his cranium, and a bit more active alpha five reductase enzymes up there in the hairs that he does have. His scalp does not look inflammed to me either.




You mentioned something in one of your earlier post from Kevin McElwee's site (who disagrees with Stephen by the way, and believes healthy hairs use enzymes to eat through collagenous deposits, which is why transplants thrive when moved to shiny bald scalp, etc.). McElwee mentioned "something happens during puberty" that makes hairs male pattern baldness hairs and makes body hair terminal.


This is wrong. Ive posted pictures and links of female to male transexuals who are going male pattern bald. They went through puberty as females. There is no "change" in hairs during puberty.....................there is just an increase in male hormone----thats all. If you have bad hair genetics, this increase in male hormone is bad for the hair. Ive applied peppermint oil and green tea extract to beard hair and reduced it some. I applied revivogen to body hair and reduced it a great deal. If you blocked androgen receptors long enough on body hair, Im pretty sure it would finish its growth cycles and not re-emerge as terminal hairs. This might take a couple of years though on something like beard hairs which have long growth cycles.



That mouse experiment with RU58841, in which only 2% of non-treated male pattern baldness hairs had a second cycle on the mice vs. 28% of RU58841 treated follicles (but not treated every day as they should have been), pretty much sealed Foote's theory in my eyes. Tissue scaffolds were formed. All the damned follicles should have grown forever, treated or not....................................but hardly any did in the untreated group and less than a third did in the treated group. THESE mice DEFINITELY had a decent amount of male hormone, enough to keep the hairs miniaturized.



We have noted that balding men's hair ages and greys faster than men who keep their hair, even in wreath areas. Stephen has noted that stagnant protiens would create an environment for this to be so, but why do balding mens BEARD hairs also seem to grey quicker? If you pay attention, you'll not that balding men's CHEST hair also seems to grey quicker. I dont think Stephen is claiming they have back up in the beard and chest...............................



I seen that you noted there is more oxygen in non-balding scalp. Of course there is, it has hair and capillary networks to support that hair. It has to have more blood, and blood carries oxygen. It only makes sense that that would be the case. Perhaps this lack of oxygen as we bald is the one of the primary reasons balding scalp ages so much worse.

 

[bubka]

We have noted that balding men's hair ages and greys faster than men who keep their hair, even in wreath areas. Stephen has noted that stagnant protiens would create an environment for this to be so, but why do balding mens BEARD hairs also seem to grey quicker? If you pay attention, you'll not that balding men's CHEST hair also seems to grey quicker. I dont think Stephen is claiming they have back up in the beard and chest...............................

i may say i have observed the total opposite, i don't see a link in running out of pigment with male pattern baldness

 

[michael barry]

melanocytes, which stain the hair shaft with pigment, only comprise about one percent of the hair follicle.


oxides in particular might promote a slowing of their activity or cell death within them......................

 

[wookster]

The amount of curcuminoids needed to reverse fibrosis is impossible to ingest. Especially, since those compounds are not easily absorbed and many studies demonstrate that oral intake does not equal a high concentration in the blood.

opsblush: opsblush: opsblush:

Of course, people who consume curcuminoids their whole life still go through all the stages of male pattern baldness. Ergo, curcuminoids don't appear to be a very strong preventative against the fibrotic processes of male pattern baldness ...in the scalp tissues.

 

[wookster]

http://www.emedicine.com/derm/topic548.htm

Baldness, thoracic hairiness, hair graying, and earlobe crease

A recent case-control study examined the association of dermatological signs, such as baldness, thoracic hairiness, hair graying, and diagonal earlobe crease, with the risk of myocardial infarction in male subjects younger than 60 years. It included 842 male subjects admitted for the first nonfatal myocardial infarction; the controls were 712 male subjects admitted with noncardiac diagnoses, without clinical signs of coronary disease.

The relative risks were estimated as odds ratios. Logistic regression was used to control for the confounding variables. Baldness, thoracic hairiness, and earlobe crease were approximately 40% more prevalent in noncontrol subjects. After allowing for age and other established coronary risk factors, the relative risk of myocardial infarction for frontoparietal baldness compared with no hair loss was 1.77 (95% confidence interval 1.27-2.45) and it was 1.83 (95% confidence interval 1.4-2.3) for men with thick, extended thoracic hairiness. The presence of a diagonal earlobe crease yielded a relative risk of 1.37 (95% confidence interval 1.25-1.5), while hair graying was associated with myocardial infarction only in male subjects younger than 50 years.

The authors concluded that baldness, thoracic hairiness, and diagonal earlobe crease indicate an additional risk of myocardial infarction in men younger than 60 years, independent of age and other established coronary risk factors. In a recent report by Matilainen et al, the presence of insulin resistance that increases coronary disease risk has been shown to be associated with an early onset of male-pattern baldness or alopecia. This may represent a common pathogenetic mechanism for baldness and coronary atherosclerosis.

 

[wookster]

You mentioned something in one of your earlier post from Kevin McElwee's site (who disagrees with Stephen by the way, and believes healthy hairs use enzymes to eat through collagenous deposits, which is why transplants thrive when moved to shiny bald scalp, etc.). McElwee mentioned "something happens during puberty" that makes hairs male pattern baldness hairs and makes body hair terminal.


This is wrong. Ive posted pictures and links of female to male transexuals who are going male pattern bald. They went through puberty as females. There is no "change" in hairs during puberty.....................there is just an increase in male hormone----thats all. If you have bad hair genetics, this increase in male hormone is bad for the hair. Ive applied peppermint oil and green tea extract to beard hair and reduced it some. I applied revivogen to body hair and reduced it a great deal. If you blocked androgen receptors long enough on body hair, Im pretty sure it would finish its growth cycles and not re-emerge as terminal hairs. This might take a couple of years though on something like beard hairs which have long growth cycles.

It seems that there are flaws in the studies that Kevin McElwee bases his conclusions on. The old donor dominance ideas are not completely true then....

Too bad you didn't take before and after pictures of your body hair reduction experiments. Without such evidence it is hard to differentiate the objective consensus reality from the lone subjective interpretation that you present.

 

[Bryan]

It seems that there are flaws in the studies that Kevin McElwee bases his conclusions on. The old donor dominance ideas are not completely true then....

What "flaws" are you referring to, and what makes you think that the old donor dominance ideas are not completely true?

 

[powersam]

In a recent report by Matilainen et al, the presence of insulin resistance that increases coronary disease risk has been shown to be associated with an early onset of male-pattern baldness or alopecia. This may represent a common pathogenetic mechanism for baldness and coronary atherosclerosis.

woot

 

[wookster]

It seems that there are flaws in the studies that Kevin McElwee bases his conclusions on. The old donor dominance ideas are not completely true then....

What "flaws" are you referring to, and what makes you think that the old donor dominance ideas are not completely true?

http://www.ncbi.nlm.nih.gov/sites/entre ... stractPlus

Does the recipient site influence the hair growth characteristics in hair transplantation?

[...]

CONCLUSION: These results strongly suggest that the recipient site affects some characteristics of transplanted hairs, such as their growth and survival rates.