I am not even laughing hard in that pic, just slightly. I will not upload a full face shot, though. I have my own photos for comparison of myself from one year ago, and even when bursting out in laughter, none of those lines were to be seen.
You can also check the last two posts before mine here: http://www.hairlosstalk.com/interac...gen-synthesis-reduction?p=1131796#post1131796
I am certainly not the only guy to witness those side effects. I'll do a compilation of reports on that later.
And the next update. I did some more research throughout the whole weekend, and finally got a complete understanding of how Minoxidil works. Furthermore, I might have found out what causes the follicle miniaturization. What makes it highly likely to be true, though, is that both theories support each other. It furthermore even explains why blood flow in balded areas is significantly decreased.
How Androgenetic Alopecia/male pattern baldness is caused
Androgenetic Alopecia/male pattern baldness seems to be 100% an immune reaction. As everybody knows, follicle miniaturization is preceded by inflammation signs in the same area. Now here comes the interesting part: Permanent inflammation in dermal cells leads to fibrosis. In fact, it has been shown that the skin in bald areas of men with Androgenetic Alopecia/male pattern baldness is thicker than in the not yet bald areas (source: http://www.omicsonline.org/215.../2155-9554-3-138.pdf). Do the math: fibrosis occurs in the dermis due to inflammation, bald areas have thicker dermis. Obviously, it is fibrosis occuring there. How does fibrosis work? By accumulation of massive amounts of collagen. The collagen tissue all around the follicles becomes so thick that it basically squeezes the follicles until they are so small they can no longer work. There is even some speculation that, following fibrosis around the follicle, the lowest part of the follicle is basically completely clogged: The follicle still produces hair, but because of the fibrotic tissue around it, it cannot break through and is stuck in the follicle. Finally, the hair that is stuck in the follicle (but is still growing) and the fibrotic collagen tissue around the follicle squeeze the follicle to a degree where it can no longer fullfill its purpose. Additionally, even if it could, the hair would no longer be able to break through the fibrotic tissue composed of collagen anyway.
Source: "Minoxidil exerts different inhibitory effects on gene expression of lysyl hydroxylase 1, 2, and 3: implications for collagen cross-linking and treatment of fibrosis."
The whole theory of fibrosis causing baldness has, by the way, been backed by studies that showed the same happening to women WHO HAD FIBROSIS IN THEIR SCALP. These women, though, did not have any DHT susceptibility. Their fibrosis was a result of chemotherapy.
Source: CICATRICIAL ALOPECIA AFTER CHEMOTHERAPY/RADIOTHERAPY, by Misciali C, Tosti A, Vincenzi C, Iorizzo M, Fanti PA Department of Dermatology, University of Bologna, Italy.
As you can see, fibrosis is a known cause of baldness. With people suffering from Androgenetic Alopecia/male pattern baldness, inflammation reactions occur and later on, the scalp skin is much thicker. This hints at fibrosis taking place as a result of inflammation, as is the usual case with inflammatory reactions in the dermis.
I don't know if this has been a well established fact around here or if anybody's surprised by that, but at least to me it's new and it does make sense. Also, given that Minoxidil is known to inhibit synthesis of healthy collagen, as collagen is the material fibriotic tissue is made of.
Further reading on this theory: http://www.hairloss-reversible...html?1173668946
How Minoxidil works
Collagen depletion is not a side effect, but actually the effect of Minoxidil (or rather, of adenosine upregulation caused by Minoxidil). Minoxidil (or rather, adenosine) keeps the inflammated areas from generating collagen. As a consequence, no new thickened tissue is formed that can press and miniaturize the follicles.
My theory why adenosine does that: It dilates cells, thus prevents them from accumulating any hard substances (such as collagen parts).
To be more precise: When minoxidil, and throug it adenosine, is present, collagen is still produced, but it is much weaker. (Source: "Minoxidil exerts different inhibitory effects on gene expression of lysyl hydroxylase 1, 2, and 3: implications for collagen cross-linking and treatment of fibrosis.", Zuurmond AM; van der Slot-Verhoeven AJ; van Dura EA; De Groot J; Bank RA; Matrix Biol. 2005; 24(4):261-70 (ISSN: 0945-053X))).
The side effects many people experience are actually how Minoxidil protects our follicles from miniaturizing. The only problem with people experiencing side effects is that the minoxidil does not only work locally.
If you want to continue using minoxidil, find out what makes it spread from your scalp to your face, or potentially even system wide.
The thing about these two findings I made is: They are sound. The theory on how Androgenetic Alopecia causes baldness by thickening fibriotic collagen tissue makes sense. It also explains why Minoxidil, upregulating adenosine, which is known to inhibit collagen and thus fibrosis works. The theory of follicles being squeezed and miniaturized by sourrounding fibriotic tissue (made of collagen) is also backed by the fact that skin in bald areas is thicker than in not yet bald areas.
To me, all of this makes perfectly sense.
Furthermore, all of this also explains why zinc works (and actually has to work!) for treating Androgenetic Alopecia/male pattern baldness: It is anti-inflammatory. I hope all of you can see the soundness in those theories.
The next questions that need to be answered are:
a) What causes the auto-immune reactions in the scalp?
b) How can they be treated?
c) How can they be stopped?
d) How can we counteract fibrosis?
My own theories on these matters:
a) No idea. It might actually be that it is not the DHT causing the immune reaction, as many studies have shown that DHT values of people with Androgenetic Alopecia/MBP and of people without Androgenetic Alopecia/MBP do not differ very much. What has been shown, however, with 100% certainty is that SHBG is much lower in men with Androgenetic Alopecia/MBP. Lowered SHBG just causes DHT to be higher - which is why often DHT is higher with Androgenetic Alopecia affected men. This does not mean, however, that DHT is the cuplrit causing the local inflammation in the scalp that leads to fibrosis that leads to collagen tissue being generated that squeezes follicles which in turn are miniaturized by all the fibrotic tissue around them.
What has to be found out, through, is
a.1) What potential causes there are for SHBG to be very low. This might lead us to the root of the problem of Androgenetic Alopecia/male pattern baldness.
a.2) What other effects low SHBG has. This might lead us to the substance which causes the inflammation of the scalp. It might be DHT, but it might also be something completely different.
Expanding on why DHT might wrongfully be thought to be the culprit: finasteride/dutasteride work by inhibiting 5a reductase. Its primary function is metabolising T to DHT. However, lower DHT has a number of side effects, including higher SHBG (as less SHBG is bound by DHT). So, ultimately, one of the side effects of lower DHT (such as higher SHBG) might actually be what makes Androgenetic Alopecia/MBP stop, not the lower DHT itself. This hints at some other hormone that can bind to SHBG being the culprit (but does not deny the possibility that it can in fact be DHT - this is supported by the fact that Androgenetic Alopecia is much less frequent in women). Anybody care to compile a list of hormones that can bind to SHBG?
b) Any local treatment that reduces immune reactions and/or inflammation. Any strong wound healing creme with high zinc concentration will help fight Androgenetic Alopecia/MBP, completely side effect free. Anything else that fights inflammatory reactions will also help. Anybody got some ideas what else could help? Furthermore, local immune suppressiva will also help reduce the speed of Androgenetic Alopecia/MBP progress. Any hints on local immune suppressiva?
I will start using zinc shampoo (Head & Shoulders has some) and also using highly concentrated zinc wound healing creme and report back.
c) The trickiest question and the holy grail. Finding this out means finding the cure for Androgenetic Alopecia/male pattern baldness. Essentially, we are dealing with some immune reaction that should not occur. Typically, this is known as allergies. Funnily enough, all friends of mine who suffer from Androgenetic Alopecia/MBP also suffer from pollen and/or fruit and/or nut allergies. People with a lot of allergies are often also more allergies they do not know of. Furthermore, allergies are a sign of an overreactive immune system. This is basically exactly what we are facing here.
Alternatively, instead of trying to control the immune system, we can also try to find out what exact substance/hormone/condition causes the immune reaction and try to reduce/elliminate that. This is not trivial, obviously.
Substances whose blood concentration is linked to Androgenetic Alopecia/MBP:
- T3
T4
TSH
Cortisol
Progesterone
Prostaglandin D2
SHBG
Insuline
Insuline-like growth factors
Ethanol and methanol (!! - the theory is that ethanol and methanol have a negative effect on a) the liver where many of the above mentioned substances are produced, and b) on the immune system - in fact, it has been shown that very frequent consumption of high amounts of alcohol slows down MBP/Androgenetic Alopecia)
The problem with those substances is that they are linked. T3, T4 and TSH regulate SHBG. Insuline also regulates SHBG. The next problem is, that the chain of actions is not always clear (at least not to me). E.g., it could be that T3/T4/TSH regulate insuline and insuline-like growth factors which in turn regulates SBHG. Then we would need to find out how to correct T3/T4/TSH.
It could also be the other way around, with Insuline -> T3/T4/TSH -> SBHG.
d) Kerastase might be helpful here, as it was developed to untighten collagen sheaths. Product names are Aminexil, Capiplus and Densitive. All of them should help in one form or the other; Capiplus contains saw palmetto, densitive helps break up fibriotic collagen. Anybody knows something about these products?
As you can see, the whole matter is very complex. However, by understanding how Androgenetic Alopecia/male pattern baldness works, I think we got a whole step further.
Again, any input would be much appreciated. Also, any anti inflammatory and anti fibrosis products you know of, please list them here.
Edit: All of this of course also means that Androgenetic Alopecia/MBP is pretty much irreversible. You can plant new follicles into your scalp all you want - if the scalp skin is too thick for new hair to penetrate, you will not profit from newly grown follicles at all. Unless somebody knows a way to remove fibriotic tissue and replace it with new, soft tissue, newly grown follicles will not help at all.
Also, it would completely suffice then to "unclog" the old follicles and transform the fibriotic scalp skin to "new skin" - if that was so easy... but actually, this also means that the "scarring" approach that destroys old tissue might be promising, or triggers growth of completely new, unfibriotic tissue from the lower dermal layers. I have no idea if this is possible, though.
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Update: The scalp fibrosis might be reversed using a hormone called relaxin. A biotech company has also found a different approach, where they take fibroblasts (the collagen producing cells) from non-bald areas and insert them multiplied into bald areas, so they can produce new non-fibriotic tissue. Source: http://www.news-medical.net/news/2005/05/03/9736.aspx A funny side effect: These areas also started producing hair again!
Might as well be that Androgenetic Alopecia/MBP is reversible after all.
Furthermore, Androgenetic Alopecia/MBP might be caused by a lack of relaxin in the scalp in the first place. An idea worth looking into. Funnily, relaxin is reduced by ejaculation.
Edit: In case anybody can use that info, TGF-b is the hormone triggering the fibrosis of the tissue around the follicles. Anyone know how to inhibit that? But please not systemwide, as it is needed for wound healing.
Edit2: For the record, T3 and T4 up-regulate SHBG. (Source: http://jme.endocrinology-journ...g/content/43/1/19.full ). Now, the question is: How do we get T3/T4 to increase? One way seems to be intense work-out (source: http://www.nel.edu/26-2005_6_pdf/NEL260605A14_Ciloglu.pdf ).
Edit3: Bad news: T3, and as a consequence SHBG, decrease as a consequence of inflammation, not the other way around (source: http://chriskresser.com/inflammation-strikes-again ). In case there is no circular dependency here, this means that increasing T3 or SHBG will not help stop or slow down Androgenetic Alopecia/MBP, as they are only low as a consequence of the inflammation causing Androgenetic Alopecia/MBP. They are not the reason for or a contributor to Androgenetic Alopecia/MBP (unless there is circular dependency, which I have no knowledge about as of now.)
Edit4: There are some hints that there is a circular dependency: http://immortalhair.forumandco...and-hair-growth
Means:
- Androgenetic Alopecia/male pattern baldness triggers lower T3/T4
- Lower T3/T4 accelerates Androgenetic Alopecia/male pattern baldness
Edit5: Iodine seems to play a key role in a) T3/T4 regulation and b) body inflammation handling. In fact, it is crucial for transporting growth and healing agents to areas of inflammation. Given that huge portions of the population lack sufficient iodine supply and its role in inflammation handling, it likely play a role in Androgenetic Alopecia/male pattern baldness. In some parts of the world it has been used in traditional medicine to treat hair loss successfully.
So: Inflammation does not cause T3 and T4 to be low, but lack of iodine causes a lack of T3 and T4 and inflammation. Thus, there is a correlation, but no causality of T3/T4 and inflammation. A discussion on this matter with a lot of sources for further reading can be found here: http://immortalhair.forumandco...male-pattern-hair-loss
Edit6: Next candidate found, Prostaglandin D2. It has been shown that in Androgenetic Alopecia/male pattern baldness affected persons, Prostaglandin D2 concentration was three times higher in bald areas than in non-bald areas. And guess what?
"They are mediators and have a variety of strong physiological effects, such as regulating the contraction and relaxation of smooth muscle tissue. [...] Smooth muscle-containing tissue needs to be stretched often, so elasticity is an important attribute of smooth muscle. Smooth muscle cells may secrete a complex extracellular matrix containing collagen (predominantly types I and III), elastin, glycoproteins, and proteoglycans." Source: Wikipedia.
Question is, now: is Prostaglandin D2 increased because of inflammation, or due to another reason? Also, how can we decrease Prostaglandin D2?
I think this is pretty smart. Last year I was told I could be allergic to my own progesteron after having rashes on and off for almost a year (progesteron autoimmune dermatitis). Of course another derm laughed it of and told me I have sebhorreic dermatitis/rosacea ( although the rash was all over my face even on the back of my arms). Anyway after that my hair started to fall out, so it totally made sense to me that the allergic reaction to progesteron could be the culprit. Of course when I mentioned this to the derm, all I got was a big smurk again , so I fired him :uglylol:
Look at women who took BCP , after getting of the BCP or even during taking it their hair started falling out. Could chemical fake hormones make your body sensitive to the bodies own hormones?
About the skinthickening, could it also be because the lymphvessels and bloodvessels are inflamed, so the blood pooling into the skin can't be drained as well because of the impaired lymphvessels? Sorry if this all sounds stupid, just had to spit it outuke:
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I think this is pretty smart. Last year I was told I could be allergic to my own progesteron after having rashes on and off for almost a year (progesteron autoimmune dermatitis). Of course another derm laughed it of and told me I have sebhorreic dermatitis/rosacea ( although the rash was all over my face even on the back of my arms). Anyway after that my hair started to fall out, so it totally made sense to me that the allergic reaction to progesteron could be the culprit. Of course when I mentioned this to the derm, all I got was a big smurk again , so I fired him :uglylol:
Look at women who took BCP , after getting of the BCP or even during taking it their hair started falling out. Could chemical fake hormones make your body sensitive to the bodies own hormones?
About the skinthickening, could it also be because the lymphvessels and bloodvessels are inflamed, so the blood pooling into the skin can't be drained as well because of the impaired lymphvessels? Sorry if this all sounds stupid, just had to spit it outuke:
So would Androgenetic Alopecia be considered an autoimmune disorder, and if so would it be somewhat the same as AA and the cure for AA could be beneficial for Androgenetic Alopecia as well. Has it been tested on Androgenetic Alopecia?