brushing for receding hairline?
- Thread starter thomas040
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BodyDysmorphic
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total BS IMO
Brains Expel Hair
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Many different baldness treatments have an effect of increasing blood flow to the scalp. It shouldn't be all that surprising that brushing (which does increase blood flow to the scalp) would have an effect on hair health.
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Brains Expel Hair said:
Some baldness treatments have an effect of actually DECREASING blood flow to the scalp. A good example would be that doctor who tied-off the arteries going to the scalp, causing less blood to go there. He claims to have had success with that treatment.
somone uk
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just another one
there is no evidence that blood flow to the scalp is impeded in people with male pattern baldness
it's a myth
if there is no blood then you have a case but it's not like your hair needs a lot of blood
though i have never seen a treatment that talks about less bloodflow
there is no evidence that blood flow to the scalp is impeded in people with male pattern baldness
it's a myth
if there is no blood then you have a case but it's not like your hair needs a lot of blood
though i have never seen a treatment that talks about less bloodflow
S Foote.
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armandein said:
Thanks for that Armando, i think this is an important study that everyone interested in hairloss should read.
The author suggests that the significant improvement in hair follicles, is due to the induced hypoxia of the procedure, and the effect of this on local androgens.
The problem with this is that it is now known that in male pattern baldness there is already a significant hypoxia in the effected tissue, compared to hairy scalp.
http://cat.inist.fr/?aModele=afficheN&cpsidt=3068488
Titre du document / Document title
Transcutaneous P02, of the scalp in male pattern baldness : A new piece to the puzzle. Discussion
Auteur(s) / Author(s)
GOLDMAN B. E. (1) ; FISHER D. M. (1) ; RINGLER S. L. (1) ; JACKSON I. T. (Commentateur) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Plastic Surgery at Butterworth Hospital, Grand Rapids, Mich., ETATS-UNIS
Résumé / Abstract
Our study was designed to measure the transcutaneous Po2 of the scalp to determine if there was a relative microvascular insufficiency and associated tissue hypoxia in areas of hair loss in male pattern baldness. A controlled prospective study was performed at Butterworth Hospital, Grand Rapids, Michigan. Eighteen nonsmoking male volunteers aged 18 years and older were studied. Nine men had male pattern baldness (Juri degree II or III), and nine were controls (no male pattern baldness). Scalp temperature and transcutaneous Po2 were obtained at frontal and temporal sites in each subject. Peripheral circulation was assessed from postocclusive transcutaneous Po2 recovery time by means of maximum initial slope measurements. Statistical significance was assessed at p < 0.05. There was no significant difference in scalp temperature between male pattern baldness subjects and controls. Temporal scalp blood flow was significantly higher than frontal scalp blood flow in male pattern baldness subjects ; however, there was no significant difference in controls. Transcutaneous Po2 was significantly lower in bald frontal scalp (32.2 ± 2.0 mmHg) than in hair-bearing temporal scalp (51.8 ± 4.4 mmHg) in men with male pattern baldness. In controls, there was no significant difference in transcutaneous Po2 of frontal scalp (53.9 ± 3.5 mmHg) and temporal scalp (61.4 ± 2.7 mmHg). Transcutaneous Po2 also was significantly lower in the frontal scalp of male pattern baldness subjects (32.2 ± 2.0 mmHg) than in either frontal or temporal scalp of controls (53.9 ± 3.5 mmHg and 61.4 ± 2.7 mmHg, respectively). There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. We have identified a previously unreported tissue hypoxia in bald scalp compared with hair-bearing scalp.
_________________________________________
There is a history of assumptions made with circulation and male pattern baldness, as in this thread. People jump to the conclusion that we need "more blood" in the scalp to "feed" the follicles. This is clearly refuted by transplantation and this particular study.
The circulation involves a "fluid feed and return" balance". I suggest that all the things people claim help the circulation to help hair growth, are in fact helping the scalp drainage side of the equation, in particular the drainage of excess scalp tissue fluid.
The high blood feed to the scalp increases the local tissue fluid pressures, reducing this as in the ligiture study reduces the tissue fluid.
Anything that reduces tissue fluid pressure in the scalp will increase follicle size, as i have argued many times. The confirmed existence of hypoxia in the male pattern baldness scalp, also supports the low turnover of tissue fluid and drainage. Why? because we know there is more than enough blood "feed" to avoid hypoxia on the feed side of the equation.
Massage, lasers, scalp exercises, reducing the fluid "feed" as in this study, all have the effect of reducing tissue fluid pressure. This is the only common factor in the circulation debates.
S Foote.
Hi Stephen;
Nice to see you again.
This a important study, mainly because is real in persons that the doctor lligate the arteries of scalp. No trick....
But Dr. Marcchal also said:
"These histologic images show that the circulatory slowing obtained by the arterial ligatures at the level of the scalp is a treatment of primary value in reducing the sebum production which improves the cellular life of the dermis, epidermis, and hair follicle."
I think that your theory can be strenghted if you take in account the sebaceous gland and the sebum as part of the "fluids" in scalp tissue.
have a nice day
Armando
Nice to see you again.
This a important study, mainly because is real in persons that the doctor lligate the arteries of scalp. No trick....
But Dr. Marcchal also said:
"These histologic images show that the circulatory slowing obtained by the arterial ligatures at the level of the scalp is a treatment of primary value in reducing the sebum production which improves the cellular life of the dermis, epidermis, and hair follicle."
I think that your theory can be strenghted if you take in account the sebaceous gland and the sebum as part of the "fluids" in scalp tissue.
have a nice day
Armando
S Foote.
Experienced Member
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armandein said:
Hi Armando.
If you think cause and effect, all we can be sure of from this study is that reducing blood feed to the scalp, "causes" the reported effects.
You cannot claim for example that the reduced blood feed causes an effect on sebum which "then" causes an effect on hair follicles, based on this study.
I think the Doctor was wrong to give that impression in his wording.
As in most studies you have to seperate the facts, like reducing blood flow reduces sebum and increases follicle size, from the speculation. I could just as easily argue that the expanding follicles squeeze the sebaceous glands, reducing sebum.
I quote this study in support of my theory of hair growth, because other reported fluid reducing methods as i quoted above, also help hair growth. But do these factors "also" reduce sebum Armando?
Regards
S Foote.
S Foote.
Experienced Member
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- 66
Armando.
Since i last posted i have been thinking about what could explain the stated effects in that study, and any one mechanism that would explain both the effect on follicles and sebum production.
It turns out after some basic searching, that there are studies that support my theory "directly" increasing sebum production alongside reducing hair growth.
I think this is important as the known increased sebum production in male pattern baldness has not been adequately explained yet.
A brief recap:
My theory says that hair follicles evolved to adjust their size according to the pressure in the surrounding tissue. As a hollow structure, follicle growth has to move surrounding tissue away, and normal cellular contact inhibition of follicle cell growth will happen sooner if there is increased resistence from the surrounding tissue. The higher the local tissue fluid pressure, the greater the force pushing dermal tissue into the hollow space being formed by the enlarging follicle. This greater resistence creates smaller follicles, by earlier onset of normal contact inhibition of cell growth.
I have argued that male pattern baldness is caused by a DHT induced reduction in lymphatic function in the male pattern baldness area (lymphedema), creating increased tissue fluid pressure and the effect described above.
The quoted study here reduces scalp blood feed, so reducing tissue fluid pressure and the effect of lymphedema, therefore allowing follicles to enlarge more.
So how could lymphedema "ALSO" increase sebum production in the same local tissue?
The Studies author makes these claims, quote:
"The adult's alopecia bound
to lipid or hormonal troubles is a
secondary indication. The contraindication
is constituted by the union of
the following factors: (1) a hyperbetalipoproteinemia
level exceeding 80
percent;"
"These patients always show a distinct
increase in blood lipids, an elevation of
beta-lipoproteins, and a high Burnstein
test."
"Sebum is borne by blood lipids and
recaptured by the sebaceous glands.
Lipemia in patients who have developed
seborrheic alopecia is extremely
important."
So the amount of lipids reaching the sebaceous glands is important in increasing sebum production.
There are many studies that prove that in tissues subject to Lymphedema, there is a significant increase the deposition of lipids in the effected tissue.
This local increase in the raw material for sebum increases sebum production, simple.
After the procedure in this study, Quote:
"The sebaceous glands, functioning
abundantly before the operation, become
reduced, less dense, and show
spaces empty of all cellular elements.
This signifies a necrobiosis devoid of
lipid inclusions."
So the lipid levels are reduced.
A couple of related studies:
http://www.jlr.org/cgi/content/full/41/8/1317
Quote:
" Reichl et al. (53) showed that HDLs in human lymphedema fluid were enriched in polar lipids compared with plasma HDLs."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2676671/
Quote:
"Here, we provide a detailed characterization of secondary lymphedema in the mouse tail and correlate the evolution of tissue swelling to changes in tissue architecture, infiltration of immune cells, deposition of lipids, and proliferation and morphology of the lymphatic vessels. We show that sustained swelling leads to lymphatic hyperplasia and upregulation of vascular endothelial growth factor (VEGF)-C, which may exacerbate the edema because the hyperplastic vessels are poorly functional. The onset of lymphatic hyperplasia occurred prior to the onset of lipid accumulation and peak VEGF-C expression. Langerhans dendritic cells were seen in the dermis migrating from the epidermis to the lymphatic capillaries in edematous tissue "
So here is one mechanism (lymphedema), that explains all the observations in the quoted study, and people should note from the abstact above, the immunology in male pattern baldness also.
S Foote.
Since i last posted i have been thinking about what could explain the stated effects in that study, and any one mechanism that would explain both the effect on follicles and sebum production.
It turns out after some basic searching, that there are studies that support my theory "directly" increasing sebum production alongside reducing hair growth.
I think this is important as the known increased sebum production in male pattern baldness has not been adequately explained yet.
A brief recap:
My theory says that hair follicles evolved to adjust their size according to the pressure in the surrounding tissue. As a hollow structure, follicle growth has to move surrounding tissue away, and normal cellular contact inhibition of follicle cell growth will happen sooner if there is increased resistence from the surrounding tissue. The higher the local tissue fluid pressure, the greater the force pushing dermal tissue into the hollow space being formed by the enlarging follicle. This greater resistence creates smaller follicles, by earlier onset of normal contact inhibition of cell growth.
I have argued that male pattern baldness is caused by a DHT induced reduction in lymphatic function in the male pattern baldness area (lymphedema), creating increased tissue fluid pressure and the effect described above.
The quoted study here reduces scalp blood feed, so reducing tissue fluid pressure and the effect of lymphedema, therefore allowing follicles to enlarge more.
So how could lymphedema "ALSO" increase sebum production in the same local tissue?
The Studies author makes these claims, quote:
"The adult's alopecia bound
to lipid or hormonal troubles is a
secondary indication. The contraindication
is constituted by the union of
the following factors: (1) a hyperbetalipoproteinemia
level exceeding 80
percent;"
"These patients always show a distinct
increase in blood lipids, an elevation of
beta-lipoproteins, and a high Burnstein
test."
"Sebum is borne by blood lipids and
recaptured by the sebaceous glands.
Lipemia in patients who have developed
seborrheic alopecia is extremely
important."
So the amount of lipids reaching the sebaceous glands is important in increasing sebum production.
There are many studies that prove that in tissues subject to Lymphedema, there is a significant increase the deposition of lipids in the effected tissue.
This local increase in the raw material for sebum increases sebum production, simple.
After the procedure in this study, Quote:
"The sebaceous glands, functioning
abundantly before the operation, become
reduced, less dense, and show
spaces empty of all cellular elements.
This signifies a necrobiosis devoid of
lipid inclusions."
So the lipid levels are reduced.
A couple of related studies:
http://www.jlr.org/cgi/content/full/41/8/1317
Quote:
" Reichl et al. (53) showed that HDLs in human lymphedema fluid were enriched in polar lipids compared with plasma HDLs."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2676671/
Quote:
"Here, we provide a detailed characterization of secondary lymphedema in the mouse tail and correlate the evolution of tissue swelling to changes in tissue architecture, infiltration of immune cells, deposition of lipids, and proliferation and morphology of the lymphatic vessels. We show that sustained swelling leads to lymphatic hyperplasia and upregulation of vascular endothelial growth factor (VEGF)-C, which may exacerbate the edema because the hyperplastic vessels are poorly functional. The onset of lymphatic hyperplasia occurred prior to the onset of lipid accumulation and peak VEGF-C expression. Langerhans dendritic cells were seen in the dermis migrating from the epidermis to the lymphatic capillaries in edematous tissue "
So here is one mechanism (lymphedema), that explains all the observations in the quoted study, and people should note from the abstact above, the immunology in male pattern baldness also.
S Foote.
Dear friend Stephen;
It is clear that you have given the problem a lot of thought, it’s good.
Nowadays there is only a few ideas regarding sebum and hair loss despite that it is usually described in the aetiology of the problem. The hair don’t survive without sebaceous gland and even SG is more antique that hair shaft, did you read some study?
www.nature.com/jid/journal/v128/n6/full/5701200a.html
Sebogenic hypothesis of hair follicle phylogeny
Kurt S, Stenn
Aderans Reseach Institute, Philadelphia, PA, USA
Recognizing that virtually all hair follicles are associated with a sebaceous gland it is relevant when
considering the evolutionary origin of the hair follicle to ask which came first: the hair follicle, or its sebaceous gland. The cutaneous challenge for organisms adapting to land from a water environment was/is the development of a water-impermeable cover. Plant and animal forms have successfully executed this adaptation by means of an integument rich in surface waxes and lipids. We present here associated evidence supporting the sebaceous gland first hypothesis where the hair shaft precursor is viewed to have derived from a sebaceous gland lobe as a wick to efficiently draw the secretions of the deep-lying, lipid secretions to the surface. While the paleontological record is scant to silent, some support for this hypothesis is found in extant Mammalia. Moreover, cell and molecular mechanistic studies show that hair follicle inductive signals, when weak, result in a sebaceous gland, suggesting that the first, primitive, signal is for lipid gland formation. Needed studies to test, and implications of, the hypothesis will be reviewed.
OTOH, hair pilosebaceous unit are only created in the embrionary step, and the distance among hairs are genetically designed, mainly with biological signals where the pressure in the surrounding tissue is only a minor factor, the size of the skull is small. Also, I think that lipids level on blood plasma are not a important factor in common baldness, why? Because only fall the hairs from the top of the head and blood is equal on all scalp. I don’t concur with the idea that Sebaceous gland make sebum from blood lipids,….
Dermatologica. 1986 ;173 (2):61-5 3792601 [Select] [Hide]
Follicule to follicule heterogeneity of sebum excretion.
G E Piérard
We have evaluated the normal variations in the sebum excretion rate from follicle to follicle on the forehead by using the noninvasive techniques of the Lipometre and Sebutape. For a given overall amount of sebum excreted to the surface of the skin during a limited period of time, both the number of active sebaceous follicles and the amount of lipids excreted by them may vary. Significant intraindividual and interindividual differences may be found for these parameters. Such a noninvasive approach to the biology of sebaceous glands represents a new tool allowing a precise evaluation of diseases of the sebum excretion and of their treatments.
Honestly, sebum can modified its reological properties easily, and must be in the “fluid equation†of your theory.
http://www.john-libbey-eurotext.fr/en/r ... icle.phtml
There is a study regarding the possiblility of the formation of “crystals†in sebum,
Armando
It is clear that you have given the problem a lot of thought, it’s good.
Nowadays there is only a few ideas regarding sebum and hair loss despite that it is usually described in the aetiology of the problem. The hair don’t survive without sebaceous gland and even SG is more antique that hair shaft, did you read some study?
www.nature.com/jid/journal/v128/n6/full/5701200a.html
Sebogenic hypothesis of hair follicle phylogeny
Kurt S, Stenn
Aderans Reseach Institute, Philadelphia, PA, USA
Recognizing that virtually all hair follicles are associated with a sebaceous gland it is relevant when
considering the evolutionary origin of the hair follicle to ask which came first: the hair follicle, or its sebaceous gland. The cutaneous challenge for organisms adapting to land from a water environment was/is the development of a water-impermeable cover. Plant and animal forms have successfully executed this adaptation by means of an integument rich in surface waxes and lipids. We present here associated evidence supporting the sebaceous gland first hypothesis where the hair shaft precursor is viewed to have derived from a sebaceous gland lobe as a wick to efficiently draw the secretions of the deep-lying, lipid secretions to the surface. While the paleontological record is scant to silent, some support for this hypothesis is found in extant Mammalia. Moreover, cell and molecular mechanistic studies show that hair follicle inductive signals, when weak, result in a sebaceous gland, suggesting that the first, primitive, signal is for lipid gland formation. Needed studies to test, and implications of, the hypothesis will be reviewed.
OTOH, hair pilosebaceous unit are only created in the embrionary step, and the distance among hairs are genetically designed, mainly with biological signals where the pressure in the surrounding tissue is only a minor factor, the size of the skull is small. Also, I think that lipids level on blood plasma are not a important factor in common baldness, why? Because only fall the hairs from the top of the head and blood is equal on all scalp. I don’t concur with the idea that Sebaceous gland make sebum from blood lipids,….
Dermatologica. 1986 ;173 (2):61-5 3792601 [Select] [Hide]
Follicule to follicule heterogeneity of sebum excretion.
G E Piérard
We have evaluated the normal variations in the sebum excretion rate from follicle to follicle on the forehead by using the noninvasive techniques of the Lipometre and Sebutape. For a given overall amount of sebum excreted to the surface of the skin during a limited period of time, both the number of active sebaceous follicles and the amount of lipids excreted by them may vary. Significant intraindividual and interindividual differences may be found for these parameters. Such a noninvasive approach to the biology of sebaceous glands represents a new tool allowing a precise evaluation of diseases of the sebum excretion and of their treatments.
Honestly, sebum can modified its reological properties easily, and must be in the “fluid equation†of your theory.
http://www.john-libbey-eurotext.fr/en/r ... icle.phtml
There is a study regarding the possiblility of the formation of “crystals†in sebum,
Armando
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- 42
armandein said:
I've asked you many times over the years to provide evidence to support that claim, but you have never done that.
armandein said:
But Kligman et al have clearly demonstrated that hairs do NOT act as "wicks" to draw sebum from the sebaceous glands!
armandein said:
So how do you think they make sebum?
Dear Bryan
Its good ask for studies (*), but I know that you are a formed person that like read the current investigations
. There is a lot of them regarding the term “pilosebaceous unit†better than hair follicle in the investigation of hair biology. Do you know a single study or observation where exist hair follicle without sebaceous gland? Surely don’t.
BTW Dr. Kligman made a lot of well defined experiments, but he is human as all:
An excerpt of Journal of Investigative Dermatology (2006), Volume 126
As Albert Kligman himself put it when I asked him what he considered to be his
major contributions to research in dermatology
“[I made] a bevy of…original observations which make up my life work…, not all of which were stellar or even true!â€
armandein wrote:
I don’t concur with the idea that Sebaceous gland make sebum from blood lipids,….
So how do you think they make sebum?
Please, don’t take my words, in this case, seriously. Blood lipids are implicated, I’m sorry, I had a mistake.
Armando
(*) Examples:
Doxorubicin-Induced Alopecia Is Associated with Sebaceous Gland Degeneration
Report from the Cicatricial Alopecia Colloquium
Insights from the asebia mouse: a molecular sebaceous gland defect leading to cicatricial alopecia
Defolliculated (D¯): A Dominant Mouse Mutation Leading to Poor Sebaceous Gland Differentiation and Total Elimination of Pelage Follicles
Asebia-2J (Scd1ab2J): A New Allele and a Model for Scarring Alopecia
Its good ask for studies (*), but I know that you are a formed person that like read the current investigations
. There is a lot of them regarding the term “pilosebaceous unit†better than hair follicle in the investigation of hair biology. Do you know a single study or observation where exist hair follicle without sebaceous gland? Surely don’t.BTW Dr. Kligman made a lot of well defined experiments, but he is human as all:
An excerpt of Journal of Investigative Dermatology (2006), Volume 126
As Albert Kligman himself put it when I asked him what he considered to be his
major contributions to research in dermatology
“[I made] a bevy of…original observations which make up my life work…, not all of which were stellar or even true!â€
armandein wrote:
I don’t concur with the idea that Sebaceous gland make sebum from blood lipids,….
So how do you think they make sebum?
Please, don’t take my words, in this case, seriously. Blood lipids are implicated, I’m sorry, I had a mistake.
Armando
(*) Examples:
Doxorubicin-Induced Alopecia Is Associated with Sebaceous Gland Degeneration
Report from the Cicatricial Alopecia Colloquium
Insights from the asebia mouse: a molecular sebaceous gland defect leading to cicatricial alopecia
Defolliculated (D¯): A Dominant Mouse Mutation Leading to Poor Sebaceous Gland Differentiation and Total Elimination of Pelage Follicles
Asebia-2J (Scd1ab2J): A New Allele and a Model for Scarring Alopecia