For Stephen Foote, from a Doctor

[michael barry]

Dr. James Harris, through his assistant Thomas Ortiz, answered a hair transplant question of mine about donutting times on another site (HS). His reply took a few days, and must have been up for a while, as Ive just seen it.
I found this to be particularily instructive:

"In my previous life when both jugular veins had to be sacrificed
for some reason the head would swell to enormous proportions and none of my
patients ever experienced hair loss."











Here is the whole reply in context-----------------



"Sorry this is late benji from Dr. Harris. He just answered it.

"Tom,

Sorry, my filter has been sending your e-mails to the junk file.

Donutting typically becomes evident during the regrowth (6-12 months) period
after transplanting. The most logical explanation based on this observation
is that something occurs after transplantation that affects growth of
follicles in a certain position in these larger grafts. The most logical
explanation is the lack oxygen diffusion during the grafts early
revascularization process.

The scar maturation during subsequent years may have some impact but it is
probably a secondary consideration. I doubt that after the first year
changes in lymphatic flow have any role. If they did all the grafts would
start puffing up. High lymphatic pressures have never been shown to cause
hair loss. In my previous life when both jugular veins had to be sacrificed
for some reason the head would swell to enormous proportions and none of my
patients ever experienced hair loss.

Dr. H"

 

[Bryan]

A couple of shiny new nails for Stephen Foote's theory's coffin...

 

[S Foote.]

With all due respect Michael, this kind of "importance" given to the unsubstantiated comments of a "Doctor", is one of the reasons i don't post anymore.

There is just no point when these unscientific double standards are always used in these debates.

Yet again Bryan jumps in claiming a Doctors comments carry some weight when these suit Bryan, but everyone knows Bryans put downs of Doctors when their comments go against him!

Pathetic really.

Lets just look at the actual science instead of the off the cuff remarks of a "transplant Doctor".

Does this Doctor have any properly documented close up photo's, showing the development of graft doughnutting and the time period involved?

Because what studies we do have prove that the doughnutting pattern of loss does not happen within at least two years. Yet this Doctor claims it happens within months!

Is this Doctor aware of the "hard" studies involving lipedemous scalp/alopecia?


http://alopecia.researchtoday.net/archive/1/2/66.htm

Quote:

" The presence of ectatic lymphatic vessels in the two cases with hair loss was particularly emphasized. CONCLUSIONS: Our findings suggest a lessened role of racial factors, but confirms the sex implications in these related conditions, and stress the potential significance of lymphangiectatic vessels in the development of alopecia in these patients."

This is hard scientific evidence Michael, not just the opinion of some quack!


There should be some developments involving my theory within the next year. When i have any news i will post about it.

But until then i am avoiding getting involved in the ego battles on these forums.

S Foote.

 

[michael barry]

Harris used to practice medicine in another way (not hairtransplant surgery). I thought I'd make mention because he at least ventured an opinion on it.


He is a good transplant Doctor that does all the latest things (FUE, can move body hair if someone wants, small .75 instruments for little/no donor area scarring, etc.)

I did notice that he said he's never seen any hairloss associated with edema and I know that lymphedema can cause hairloss on the arms or legs of a woman who has it, but to be fair to him, thats probably a fairly obscure happenstance. He did note that he's seen mens heads swell greately when jugular veins had to be worked on and noted no hairloss. That is relevant and we all know it. I figured you would say the swelling would have to last for a year or more for the enough hairs to go into telogen or catagen for them to be "minuturized" by outside pressures , and according to the tenets of your theory, it would be a legitamate reply.


However, this is the third Doctor we know of that has commented on your idea. Sawaya, McElwee, and Harris. Fair is fair. I cannot call this a coffin nail for the hydraulic theory, but definitely something to consider. Bryan Im afraid, is much more enthusiastic about its death. :2gunsfiring_v1:

 

[wookster]

http://www.hairlosstalk.com/discussions ... c&start=30

The problem with all that theory is that an old study by Strauss, Kligman, and Pochi in the Journal of Investigative Dermatology ("The Effect of Androgens and Estrogens on Human Sebaceous Glands") clearly showed that at least in the specific experimental setup they used, topical estrogen worked EXCLUSIVELY through systemic absorption!

Doesn't Foote's theory explain that male pattern baldness, and also body hair growth, is caused by DHT through an indirect SYSTEMIC effect via lymphatics?

If estrogen works systemically, enhancing scalp hair growth and body hair miniaturization then does DHT cause scalp hair miniaturization and increase body hair growth systemically also?

:eplus2: :jumpy: :eplus2:

 

[Bryan]

Doesn't Foote's theory explain that male pattern baldness, and also body hair growth, is caused by DHT through an indirect SYSTEMIC effect via lymphatics?

Yes, but the "systemic" part of that statement isn't particularly important. The "lymphatics" part is the key element to his theory.

If estrogen works systemically, enhancing scalp hair growth and body hair miniaturization then does DHT cause scalp hair miniaturization and increase body hair growth systemically also?

To at least some small extent. So what?

 

[wookster]

Doesn't Foote's theory explain that male pattern baldness, and also body hair growth, is caused by DHT through an indirect SYSTEMIC effect via lymphatics?

Yes, but the "systemic" part of that statement isn't particularly important. The "lymphatics" part is the key element to his theory.

If estrogen works systemically, enhancing scalp hair growth and body hair miniaturization then does DHT cause scalp hair miniaturization and increase body hair growth systemically also?

To at least some small extent. So what?

http://www.webmd.com/menopause/Estrogen ... -ERT-16198

Side effects that can occur with all forms of estrogen but are more common with oral estrogen (and less common with a patch, cream, gel, or vaginal ring) include:

[...]

Fluid retention.

Weight gain.

Breast tenderness.

[...]

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

Studies on the treatment of idiopathic gynaecomastia with percutaneous dihydrotestosterone.

[...]

Local administration of DHT was followed by the complete disappearance of gynaecomastia in 10 patients, partial regression in 19 and no change in 11 patients after 4 to 20 weeks of percutaneous DHT (125 mg twice daily).

[...]

DHT appears to have an opposite effect to estrogen in that it is beneficial for flat hairy chests, beard growth, and baldness while estrogen is benificial for voluptuous bald chests, scalp hair growth, and bald chins with no beard growth :hairy:

DHT is deactivated in skeletal muscle by a chemical with a very complex name :wink: so I don't quite understand how it can facilitate lymphatic pumping.

More research is required

 

[michael barry]

Wook,



I think the onus is on Stephen Foote to prove there is any increased pressue present in Androgenetic Alopecia scalp over occipital and donor area scalp before any of us should really even delve into his theory.


This was Stephen's great mistake. He should have established that first by getting with a doctor (a lymphedema doctor) and measuring it on some folks. Modern medical instruments can account for even small phenomena-------------it should be measurable. I personally have never felt any "tight scalp". The puffy scalp in Androgenetic Alopecia is commony accepted to be from excessive collagenous depostion around the hair follicle. We know that because we have seen it with microscopes. Its been clinically noted by tons of researchers. This is FACT. It is not speculation. If Stephen wants to prove there is mild edema, the instrumentation to measure such is surely available by now.



Ask Doctor, Im sure he'd agree with me. Stephen is asking us to believe there is higher fluid pressure from backed up lymph nodes, and it causes miniaturization and eventual immuno events, but he has never proved there is higher pressure in the first place...................or lymph nodes that are slammed shut. Its his speculation that this is taking place.



You have to consider Wook, that he could be every bit as wrong as Armando is and there might not be any fluid back up at all. We know there is less blood flow in balding scalp (capillary damage, miniaturized follicles) and less oxygen (same thing---------and less hemoglobin because there is less blood). No other researcher has noted this. Bryan has pointed out a couple of his "favorite" researchers, Hoffman and Harper (or whatever their names are). These people have been looking at hair for years at the University of British Columbia microscopially. They have never noticed evidence of higher tissue fluid pressure or backed up lymphatic pumps. Stephen could be right and all the worlds hair researchers, cloning researchers, dermatolgists, and surgeons wrong..............................................but isn't that a very long shot? Even for a man who trusts no doctors like yourself?



Personal bias admittance--------------my mom was a nurse.




By the way.......................here are Dr. James Harris' credidentials (a man Stephen so easily dismisses):

"Dr. Harris is also at the forefront of biotechnology in the investigation of cell multiplication for the treatment of hair loss.

James Harris, MD, FACS, received his medical degree with honors from the University of Colorado School of Medicine in 1989. He is a Diplomate of the American Board of Otolaryngology, Fellow of the American College of Surgeons, and a member of the American Academy of Otolaryngology and the International Society of Hair Restoration Surgery. A facial plastic surgeon by training, Dr. Harris' practice is now limited exclusively to follicular unit hair transplantation and follicular unit extraction. He is a Clinical Instructor of Hair Transplantation at the University of Colorado Health Sciences Center in Denver, Colorado. Additional credentials, publications, lectures, and research activities may be seen in the Curriculum Vitae."




Dr. Harris, along with Dr. Emmanuel Marrit, wrote "The Hair Replacement Revolution: A Consumers Guide to Effective Hair Replacement Techniques". His terrific book offers solid advice on all legitamate hair loss treatments, including hair transplants. It can be purchased online at Amazon.



NOTE: Otolaryngology is the branch of medicine that specializes in the diagnosis and treatment of ear, nose, throat, and head & neck disorders






I imagine Stephen thinks Im a cruel man (and possibly you yourself Wook), actually I believe in the rigorous application of the scientific method to arrive at conclusions apart from any personal bias as a wedge against human frailty. I think the scientific method and a culture influenced by Judeo-Christian ethics and values is what has made the West the most advanced and influential culture the world has ever known and has lifted us into the modern age. Any inquiry into a dermatological occurence like baldness should proceed the same way. With cold, unflinching trial and error, tests and test results, hypothesises formed by reason and tested by science and either discarded, reformulated, or further tested. Thats it. Thats how we solve problems. Bryan and Doctor probably feel about the same way.

 

[wookster]

Wook,



The puffy scalp in Androgenetic Alopecia is commony accepted to be from excessive collagenous depostion around the hair follicle.

I notice morning puffiness in my shaved scalp which diminishes after doing a few sets of the scalp exercise. Unless someone is already very bald or has a shaved head it would be difficult to observe. I can take pics and send them to you via e-mail or post them here if you are determined to see "proof" of the water retention[edema] or "fluid shifting" as docj077 put it. Fluid shifting is just another term for edema...

The puffiness must be water retention of some kind because collagen deposition would not disappear after doing exercises.

Shelton says that the effect of baldness is mainly one of androgen sensitivity where cell receptors play only a small role in baldness, if my interpretation is correct. Foote says that baldness is caused by androgens via a more systemic indirect effect and DHT is produced by conversion of T to DHT via 5AR in the peripheral tissues for a reason. Since DHT has the opposite effect of estrogen it must inhibit the estrogenic effect to a certain degree.

Beard growth shifts the sweating efficiency from chin to scalp...

 

[wookster]

James Harris, MD, FACS, received his medical degree with honors from the University of Colorado School of Medicine in 1989. He is a Diplomate of the American Board of Otolaryngology, Fellow of the American College of Surgeons, and a member of the American Academy of Otolaryngology and the International Society of Hair Restoration Surgery. A facial plastic surgeon by training, Dr. Harris' practice is now limited exclusively to follicular unit hair transplantation and follicular unit extraction. He is a Clinical Instructor of Hair Transplantation at the University of Colorado Health Sciences Center in Denver, Colorado. Additional credentials, publications, lectures, and research activities may be seen in the Curriculum Vitae."

These Doctors are highly intelligent individuals and dedicated PROFESSIONALS -- determined to maintain their standards of living... Why should they take any unecessary risks by bucking the system? They probably have families to support along with two or three ex wives.

It is hard to break free from the beurocratic inertia and super magnetic stability of the status quo. It takes a lifetime to build a name for oneself but that can all be totally destroyed by one risky venture into the world of alternative ideas.

How does hair become sensitive to androgens?

The hippocratic wreath thins with age? Does the beard thin also? If so, then both types of end stage hair thinning must be unrelated to DHT...?

 

[michael barry]

I can take pics and send them to you via e-mail or post them here if you are determined to see "proof" of the water retention[edema] or "fluid shifting" as docj077 put it. Fluid shifting is just another term for edema...

Hey, post em', I'd like to see this and see Bryans rationlalization of it.

Shelton says that the effect of baldness is mainly one of androgen sensitivity where cell receptors play only a small role in baldness, if my interpretation is correct

Actually, people with non-working androgen receptors never go bald and never grow beard hair to amount to much of anything. I'd say thats more than a small role, but the whole shebang wouldn't you? I mean you can have all the DHT on earth, but if your androgen receptors dont work, you dont go bald, and you dont get chest and arm and neck hair, etc.

Beard growth shifts the sweating efficiency from chin to scalp...

.................This is something under contention. Hairs look like a forrest of follicles if youve ever seen a strip scar transplant where the strip of hair-bearing flesh is removed. The big anagen follicles, the large dermal papillas. Look at your beard Wookie, pluck a whisker. See how large that is? Compare it to a vellus hair on your shoulder. Look close, you will see the tiny white vellus hair covering your entire body. That great big whisker dermal papilla have alot of androgen receptors on the dermal papilla which uptake the DHT and other androgens and grows large in response. In an area with only vellus hairs, the androgens bind with other androgen receptors. Which receptors? The onese in your sebaceous glands and your sweat glands. Sweat glands have androgen receptors. Men sweat more efficiently than women.

The hippocratic wreath thins with age? Does the beard thin also? If so, then both types of end stage hair thinning must be unrelated to DHT...?

This is a good question. Everyone notices it. Men with good heads of hair on "Just For Men" commercials coloring their beard hair because their beard hair is grey and ageing, and not as thick as it probably was in their 20's-30's. Perhaps testosterone elicits an oxide response over time that ages all dermal tissues to an extent. I keep going back to the pictures of the female to male transexuals and how much their faces age. Remember the Buck Angel pictures I posted? The other one's of the Ophrah Twins? How much older the faces looked. The greying goatee on the one girl along with all the facial wrinkles. Hair, to quote Tom Hagerty, is just a specialized skin cell. The alpecin researchers noted that testosterone erodes a protective layer of the dermis and subjects it to oxidant damage.




[/quote]How does hair become sensitive to androgens?

Dunno, perhaps they can handle them up to a point, and then they "flip" their response because too much is too much, and the mitochondrial DNA starts sending out bad signals in response to uptake in the papilla. Perhaps there really is a "genetic clock" inside the follicles or the stem cells located in the arrector pilli muscle or a part of the follicle that remains during all three growth phases where stem cell materials are present. Its the $64 question isn't it? We know follicles dont need male hormone at all though dont we? People with androgen sensitivity grow hair just fine, but no body/beard hair right? We know that if you put spironolactone on a woman's moustache, it will lessen. Ive posted pictures of fluridil making a woman's moustache lessen a good deal. So body hair needs it, and needs it directly to grow. Ex vivo experiments with healthy beard follicles prove beard hair grows weaker if no androgens are around.

 

[michael barry]

Picture of Larry Craig, who is bald.


Does that really look like edema to you? Anyone?
Does his face, beard hair obviously not going to be as thick as it once was, look like its suffering any kind of edema either?

 

[IBM]

michael barry: what would happen to a 30's men if they estrogen raise the double and testosterone lower to half?

 

[michael barry]

michael barry: what would happen to a 30's men if they estrogen raise the double and testosterone lower to half?

They'd be very unhappy men if they were heterosexuals. Would it not be better to use spironolactone or perhaps fluridil topically along with internal finasteride if you wanted to safely use anti-androgens with minimal/no side effects?



Doubling your estrogen and halving your testosterone is aksing for gyno, erectile problems (you'd be cutting DHT in half in all probability because you'd only have half the testosterone-------------and a bunch of estrogen in your androgen receptors). Your skin might get nice and soft though, which would help you if you were a Larry Craig type-of guy :lol:

 

[IBM]

michael barry: what would happen to a 30's men if they estrogen raise the double and testosterone lower to half?

They'd be very unhappy men if they were heterosexuals. Would it not be better to use spironolactone or perhaps fluridil topically along with internal finasteride if you wanted to safely use anti-androgens with minimal/no side effects?

But it would be better for our scalp? In physical terms a men would be feminine? Or he would be unchangeable?

 

[michael barry]

I think just plain finasteride would be much more effective than what you propose.

DHT is the primary culprit in baldness. Cutting T in half gets you about a fifty percent reduction in DHT hypothetically, and doubling your estrogen would probably block a few androgen receptors----maybe 10 more percent of them (you dont have much estrogen----so that may be optomistic), while taking finasteride should lower DHT 65-70% in the aggregate, and 85% or so of the type 2 DHT that primarily miniaturizes your hair.

Remember, the type two alpha five reductase enzyme that makes the DHT that fukkcs up your hair is located in the prostate tisues and the root sheath's of each and every hair follicle on your body. Since globulin binds all but about one percent of DHT in the bloodstream, the conclusion is unmistakable.......................almost all the DHT that is the problem with your hair is made right there at the hair follicle, and binds with the androgen receptors on the cytoplasm of the cellular walls of the dermal papilla cells.

Have you ever seen the RU58841 (topical androgen receptor blocker) pictures with the stumptailed macaques? Pretty impressive regrowth..........................just by blocking androgen receptors topically. Topicals will be the future in resisting alopecia. A finasteride with a longer half life would be an improvement, but dutasteride is going to be about as effective an anti-androgen with acceptably small side effects as can be synthesized. I guess you could take internal spironolactone with it or flutamide, but you'd better be wanting to be a transexual, because you will not be getting hard ons if you take therapuetic levels of these indications as a male.

 

[wookster]

Picture of Larry Craig, who is bald.


Does that really look like edema to you? Anyone?
Does his face, beard hair obviously not going to be as thick as it once was, look like its suffering any kind of edema either?

His top scalp looks like it has the reflective shine associated with male pattern baldness and Foote's description of the male pattern baldness edema.


http://www.hairlosstalk.com/discussions ... ell#223191

Music, if minoxidil made your face swell, it was no doubt because it SHIFTED fluid pressure from your scalp to your face. Minoxidil sulfate, as well as the alchohol carrier vehicle (and probably propylene glycol in it too) are diurectics. Diruetics shift fluid volume away from themselves. They "push" water away.

The after-sex headache is something all men face after orgasm for a few seconds/minutes. A chemical releases in your head for that "druggy" feeling.................it takes a bit for you to recover. Actually that chemical that releases can help you go to sleep if you just roll over and shut your eyes. Its kind of a "springboard" sleeping pill if you use it. If you, however, get up and go make a sandwich and watch the late show.......its effects wear off. We dont think about this, but sex can be a bit dehydrating as an activity anyway. Wake up with a headache? Lack of water in your brain perhaps. Vodka is a great deyhyrator, and thus vodka hangovers are really painful.

Back to minoxidil, if you use alot of it, your hands will swell and possibly your feet. These are observed side-effects of it. Its a fluid-volume shifter. Proanthocyanidins do this even more (almost painfully) if you use too much. This doesn't mean Stephen's theory is right, however. But it is an interesting coincidence........like cyclosporin shifting fluid volume in rodents.

http://www.path.sunysb.edu/coursemat/hbp310inflam.htm

There are two types of edema:


Exudate: an exudate consists of protein-rich fluid. It is the type of edema seen in inflammation, since the gaps in the endothelial lining of the blood vessels are large enough to allow the passage of proteins as well as water. If the gaps are quite big, the large plasma protein fibrinogen will pass into the tissues. Fibrinogen is the major component of blood clots. It may form clots within the tissues, leading to what is termed a fibrinous exudate. Exudates that are rich in bacteria, leukocytes, and debris are called purulent exudates (more popularly known as pus).

Transudate: Transudates are collections of fluid in the tissues that contain relatively little protein. They form when the normal hydrostatic and osmotic forces that control the balance of water between blood and tissues are out of whack, but the endothelium is normal. Since the endothelium is intact, only small molecules such as water and salts can cross the vessel wall; larger protein molecules stay within the blood plasma. A transudate is not the type of edema that forms during inflammation.

 

[wookster]

Shelton says that the effect of baldness is mainly one of androgen sensitivity where cell receptors play only a small role in baldness, if my interpretation is correct

Actually, people with non-working androgen receptors never go bald and never grow beard hair to amount to much of anything. I'd say thats more than a small role, but the whole shebang wouldn't you? I mean you can have all the DHT on earth, but if your androgen receptors dont work, you dont go bald, and you dont get chest and arm and neck hair, etc.

http://www.hairlosstalk.com/discussions ... ors#359968

It seems that the main difference between the Big 3 - proponents description of the balding process and the Stephen Foote description of male pattern baldness is that the conventional baldness science describes the problem as one of cell receptors, that is to say androgen receptors...

Oh horseshit, Wookster! It has nothing to do with androgen receptors, except very very indirectly. Can't you think of a more sophisticated way to explain it than just that??

 

[wookster]

:freaked: :freaked2: :freaked:

http://www.emedicine.com/derm/topic439.htm

Background: Tufted hair folliculitis is a rare, progressive pattern of scarring alopecia that affects the scalp. Its characteristic feature is the presence of groups of 10-15 hairs emerging from a single follicular opening. The cause of this disorder is unknown. Tufts of hair associated with scars have been described in association with several other forms of alopecia. It is probable that tufted hair folliculitis represents an advanced stage of follicular injury seen in several types of scarring alopecia.

[...]

Physical: The most prominent feature of this disorder is the presence of tufts of 8-15 hairs that appear to emerge from a single follicular orifice in a "doll's hair" pattern. Adjacent to and intermingled with the tufts are areas of scarring alopecia, with complete loss of follicles. The area of tufts and scarring is somewhat well circumscribed and may be accompanied by varying degrees of edema, erythema, and tenderness. Boggy plaques have been described. There may be crust adherent to the scalp or hair, often in a collarette around the most proximal portion of the hair. Pustules are not common, but pus may be expressed from the follicular openings. Several reports have noted that a high percentage of telogen hairs are obtained when tufts of hair are extracted forcibly.

 

[docj077]

This is such a ridiculous conversation. Some individuals with male pattern baldness have spongiosis associated with their disorder. This spongiosis is considered by Andrews' Disease of the Skin: Clinical Dermatology to be "due to seborrheic folliculitis."

If an individual develops edema in the scalp secondary to male pattern baldness, it is likely lipedematous alopecia. Unfortunately, the development of lipedematous alopecia has no real bearing on one's prognosis.

Lipedematous alopecia of the scalp
Bianca Maria Piraccini, Stylianos Voudouris, Massimiliano Pazzaglia, Giulia Rech, Colombina Vicenzi, and Antonella Tosti
Dermatology Online Journal 12 (2): 6


"Lipedematous scalp is a rare disease, mainly reported in black women, and is characterized by diffuse or circumscribed thickening of the scalp, more palpable than visible [1-12]. It can be associated with subjective symptoms, such as pain and pruritus, as well as with diffuse hair loss or inability of the hair on the thickened areas of the scalp to grow longer than a few centimeters. We describe two caucasian male patients who presented with lipedematous scalp associated with androgenetic alopecia. In one of the two patients, treatment with finasteride 1 mg produced hair regrowth.


In July 2003 a 48-year-old healthy man presented to our clinic with a 10-year history of hair loss. Physical examination revealed Hamilton-IV androgenetic alopecia and a soft, cotton-like diffuse swelling of the scalp on the vertex (Fig. 1). The skin of the thickened scalp did not have signs of inflammation, and the patient was unaware of the abnormality. On palpation the scalp was thick, boggy, and had a spongy texture without fluctuation.

In November 2003 a 53-year-old man, in good health, consulted us because of a 4-year history of diffuse hair loss associated with intermittent scalp itching. Physical examination revealed a Hamilton V vertex androgenetic alopecia and thickening of the scalp of the vertex and the occipital region. On palpation the scalp had a spongy texture without fluctuation. Videodermoscopy of the areas of scalp thickening revealed in both cases linear areas of erythema along the scalp creases. The erythematous areas showed fine arborizing telangiectasia and small coiled capillary loops (Figs. 2a, 2b). Both patients submitted to a scalp biopsy. Vertical and horizontal sections were performed.


The clinical features and the histopathologic findings of our patients led us to the diagnosis of lipedematous scalp associated with male pattern androgenetic alopecia.

***Both patients were treated with finasteride 1mg/day. The 1-year followup assessed by global photography and digital videodermoscopy of the scalp showed no changes of the lipedematous scalp in both patients and a mild improvement of androgenetic alopecia in the first patient. The androgenetic alopecia of the second patient remained stable.***


The pathogenesis of lipedematous scalp and the associated alopecia are not known. Some authors report the presence of edema of the thickened adipose tissue [6, 8, 10] and dilated lymphatic vessels [10] and suggest that lymphangiectasia may be responsible for hair loss because it is found only in those patients with lipedematous scalp and alopecia. The two cases we reported are adult caucasian males with lipedematous scalp, very uncommon for their race and sex. They both exhibited androgenetic alopecia. They are the first patients with lipedematous scalp studied by dermoscopy, which showed striking and exclusive features, consisting in vascular abnormalities restricted to the areas of scalp thickening. In fact in both patients at videodermoscopy, the lipedematous scalp areas presented linear areas of telangiectasia within the scalp creases. This was possibly caused by compression of the superficial blood capillaries by the increased volume of the subcutaneous fat layer within the thickened scalp. This finding is not related to androgenetic alopecia, because it has never been described in this disease [13]. Neither lymphatic nor blood vessel dilation was seen in the biopsies of our patients and we could not make a correlation between dermoscopic and pathological features.

The association of lipedematous scalp and androgenetic alopecia in our two patients is, in our opinion, coincidental and resulting from the high frequency of androgenetic alopecia in men. The fact that the lipedematous scalp coincided with the areas affected by androgenetic alopecia is possibly related to the fact that both conditions tend to be localized in the vertex. The casual correlation of lipedematous scalp and androgenetic alopecia in our patients is furthermore suggested by results of treatment with finasteride 1 mg. One year of finasteride treatment in fact induced improvement of androgenetic alopecia in one patient and stabilization in the other, but it did not affect the lipedematous scalp, which remained unchanged in both cases."






You'll notice that edema can be associated with male pattern baldness, but reversal and maintaince of male pattern baldness does not require reversal of edema. Instead, inhibition of androgen action is required. Thus, edema is not the underlying cause of the reason for continued deterioration.