Hair loss

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Kasper
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Hair loss

Post by Kasper »

I've studied hair loss quite for a well now (with some other guys on hair loss fora).
Vitamin E (from red palm oil) seems to be the most hopefull thing out there at the moment.
Here is an study:
http://www.tocotrienol.org/images/stori ... beyond.pdf

Or you should go for DHT blockers, but that has much side effects, and is absolutely not the way to go.
It sort of creates a female scalp, but the rest of your body becomes more female as well...

Do you have inflammation/itching/redness going on in your scalp ?
dime
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Re: Hair loss

Post by dime »

No I would never take something like DHT blockers even if it means going bald :)

There is tiny bit of itching sometimes yes, but I can't notice redness.
What is worrying me lately is that hair comes out with hardened sebum (white bulb at the end), since I started putting a drop of peppermint oil in my shampoo. The shampoo is just two eggs that I blend, sometimes with a bit of coconut oil.

It would be better to figure out how does vitamin E actually affect hair, I wouldn't trust that study much.
It's quite hard to get the RDA of E from food, so it's possible that defficiency may affect hair loss for example.

Ray Peat also recommends getting a lot of vit. E btw, like at least 100mg from supplements daily: http://raypeat.com/articles/articles/vitamin-e.shtml
dime
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Re: Hair loss

Post by dime »

I ordered from here, much cheaper than amazon http://www.vitacost.com/jarrow-formulas-toco-sorb
dime
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Re: Hair loss

Post by dime »

Quite interesting:
"Sebaceous glands as transporters of vitamin E"
http://www.ncbi.nlm.nih.gov/pubmed/16477469

Another good read: www.ysonut.es/pdf/Ysodoc/D030202.pdf from where I learned that UVA/UVB exposure rapidly depletes vitamin E in the skin.
dime
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Sebum and acne

Post by dime »

A couple of things related to sebum in people with acne (may be relevant for hair loss too)

Lower vitamin E

http://www.hindawi.com/journals/mi/2010/858176/
In vitro experiments have shown that squalene peroxides, beyond induction of keratinocytes proliferation, led also to the upregulation and release of inflammatory mediators, such as interleukine-6. Overall, these effects clearly suggest a proinflammatory activity of squalene oxidation products [34]. The onset of inflammatory reactions appears to be an early event in the development of acne lesions [35, 36]. The oxidative challenge supplied with peroxidated squalene can be aggravated by its potential glutathione-depleting activity which results in an increased cytotoxicity and comedogenicity [37].
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835893/
The strategy that skin adopts to limit the potentially harmful effects of peroxidated squalene relies on the vitamin E supply to the skin surface. Vitamin E is found in the skin surface lipids as a significant constituent of human sebum. In sites with elevated sebaceous glands density continuous secretion of vitamin E is detected, which is in tight correlation with the levels of cosecreted squalene.20 The role played by squalene peroxidation in acne development is strengthened by the observation that skin surface and comedones lipids collected from acne patients are enriched in polar lipids mainly derived from squalene oxidation.21,22

More recent data collected in vivo have confirmed these findings and indicated significant differences in sebum composition of acne patients in comparison with healthy subjects with regard to squalene and vitamin E amount. In particular, higher amounts of squalene peroxide and consequently decreased levels of vitamin E level have been detected in acne subjects23 further supporting the role of squalene peroxidation,24 and, in general, of lipid peroxidation in acne development (Figure 1).25 A lower 16:0/16:1 ratio in triglycerides and wax esters has been also found, underlying another kind of alteration characteristic of sebum from acne patients.23
Lower linoleic acid

http://www.hindawi.com/journals/mi/2010/858176/
A diminished amount of linoleic acid in the sebum has been suggested to affect the composition of sphingolipids in the follicle. Acne patients show a lower percentage of acyl-ceramides containing linoleic acid. Depletion of linoleic acid in sphingolipids has been hypothesized to be involved in the follicular hyperkeratosis, which is a crucial event involved in the comedones formation [20]. Moreover, low levels of linoleic acid also lead to impairment of the epidermal barrier function and predispose to the increased permeability of comedonal wall to inflammatory substances [21].
Oxidative stress, inflammation
Prostaglandins are other pro-inflammatory mediators thought to be involved in acne lesion development [52]. Mouse with increased cyclooxygenase-2 (COX-2) expression and prostaglandins E2 (PGE2) levels showed sebaceous gland hyperplasia and enhanced sebum production [53] suggesting an important role for COX-2 signaling pathway in sebocytes biology. In in vitro models, it has been demonstrated that expression and activation of COX-2 is PPARtive stressors, including lipid oxidizing agents, have been shown to activate PPAR and to induce lipogenesis in sebocytes [52–55]. All these findings allow to hypothesize that sebocytes proliferation and/or lipogenesis as well as inflammatory reactions may be regulated by PPAR-mediated pathways. Clinical data, demonstrating upregulated expression of both COX-2 and PPAR in acne involved skin, support this hypothesis [47] and add new insights on acne pathogenesis. Taken together, all these findings suggest a comprehensive link between inflammation and sebogenesis supporting the definition of acne as an inflammatory disease in which lipid mediators play a central role.
Kasper
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Re: Hair loss

Post by Kasper »

Vitamin E helps preventing dergranulation of mast cells.
How vitamin E does this I'm not sure of.
I think it's or by inhibting chymase, or by limiting lipid perodixation.
But either way, mast cell degranulation is something you definitely not want in your scalp.
This will raise your PGD2 level, and PGD2 seems to be the major factor in male hair loss.

Can you read dutch dime (I don't know which country you're from .. ? ).
I've written a lot of long post with scientific reference about hair loss/mast cell degranulation/vitamine E/chimase/omega 3/lipid perodixation etc. etc. in dutch.
If you can read dutch I can give you the links, if you want..
dime
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Re: Hair loss

Post by dime »

I can try with google translate, let me know about the links.

I find Dutch very amazing, with all the double (probably there are even triple) letters, like 'kk' for example, I have no idea how do you pronounce them?! :D
Kasper
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Re: Hair loss

Post by Kasper »

from hair loss forum:

I've been to me a while to study mast cells.
Mast cells are the cells that produce PGD 2.
And most people will now know that PGD2 deadly for your hair turns out to be.
It is now mainly suggested to PGD 2 blocks to go, or go to the PGD 2 receptor blocks.
And I think this stand is an effective way, but somehow it is also intresant the cause of these high levels of PGD2 in the scalp further.
And I think that causes activation of mast cells in the scalp. If that mast cells are activated, PGD2 produced.
Without activation of mast cells, may be I do not think (or barely) produced PGD2 in the scalp.
Now it appears to be that only PGD 2 (of these mast cells) for AGA sure, but I think only by PGD 2 to blocks, you might solve the AGA, but still active on mast cells in your scalp have.
What this means, I do not know.
But I think your best / healthiest / natural situation creates, the real source address (overactive mast cells), instead of only 1 product of these mast cells to block.

It is known that there are three types of mast cells. MCT, MCTC, MCC mast cells.
MCT cells were the predominant type seen in the alveoli of the lung (93%) and in the small intestinal mucosa (81%). MCTC cells predominanted in the skin (99%) and in the small intestinal submucosa (77%) and, to a lesser degree, in the tonsils (60%).
Mast cell subsets expressing tryptase and chymase (MCTC) tend to be abundant in the dermis, while mast cells expressing tryptase, but little or no
chymase (MCT), tend to be located in the mucosa or organ systems. A third and minor population expresses or mast cell chymase and cathepsin G (MCC).

In other words, for AGA involve only the mast cells in the dermis (dermis), the MCTC type.
AGA makes no sense to PGD 2 produced by the MCT type mast cells to block, since in the lungs, mucous membrane occur, not in the skin.
This MCTC type cells are distinguished because they produce chymase.
Intresant whole to the fabric chymase is, that it is not only produced by MCTC mast cells, but also a very important role to play in the activation of these cells.

http://www.ncbi.nlm.nih.gov/pubmed/10525066
This study shows that chymase-specific activation of the MCTC type of mast cells causes. This blocking you so that the PGD 2 is produced by mast cells.

Vitamin E seems to play an important role in reducing chymase production.
The activity of chymase tended to Decrease, but the tryptase activity of C2 cells was not Influenced by vitamin E.
http://www.ncbi.nlm.nih.gov/pubmed/10525066
Vitamin E, which focuses on the important mast cells for AGA.

To the best study that I took today to close. Check out this chymase occurs in the hair of mice:
http://www.cps.org.tw/docs/Vol54% 20N ... rticle% 204.pdf

The cause of alopecia in Tg mice is Unclear. Clinical studies have Shown That mast cells are Involved in the Pathogenesis of Various types of hair loss and alopecia. In scarring alopecias (19, 20) and androgenetic alopecia (9), the number of skin mast cells is remarkably Increased. However, determination of the infiltration of mast cells in the skin of human chymase-Tg mice was beyond the scope of this study and was not Carried Out.

Unfortunately, this study is really out of AGA, but on diabetes. They found by chance that chymase also played a role in AGA. But the results speak for themselves.
Also, this study shows that AGA indeed more mast cells occur in the scalp.
Besides that vitamin E seems a good option, I think it's also a good option is to look into the possibility to use specific chymase inhibitors.
This was used in the study I quoted:
Z-Ile-Glu-Pro-Phe-CO (2) Me
http://www.ncbi.nlm.nih.gov/pubmed/10525066

Ohter post :

I've just read on whether we can really exclude that other cells (besides mast cells) for significant increase in PGD 2 can provide, and I found this:

In humans, mast cells are an almost exclusive cellular source of PGD 2. Although there is some evidence or PGD 2 formation by platelets, macrophages and T lymphocytes' certain, the reported amounts are 100-1000 times lowerthan Those consistently produced IgE dependent activation of mast cells. More importantly, Whereas the basophil and the mast cell release Both histamine and leukotriene (LT) C4, it is only the mast cell That Produces significantly Quantities or PGD2.
http://thorax.bmj.com/content/59/6/453.1.full

So I think we can safely say that activation of mast cells are the cause of the increase in PGD 2 seen in aga.
dime
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Re: Hair loss

Post by dime »

Thanks for copying it here!
And especially thanks for mentioning vitamin E in the other thread!

I see a lot less hairs falling since I got the wheat germ oil 2-3 days ago and no hard sebum anymore, whereas hair fall was consistently bad for months before.
I added a teaspoon to the shampoo then and I'm eating one teaspoon per day.
I got red palm oil (so expensive, 10eur for 325ml..), so I will switch to that and see how it goes.
The red palm oil really seems like the best deal (aside from the money), high in vitamin E and low in PUFA. Usually only foods/oils that are high in PUFA are also high in vit. E, which protect the fats from going rancid.
Kasper
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Re: Hair loss

Post by Kasper »

I'm still flabbergasted that I never heard of red palm oil...
But I also have really good results since I introduced vitamin E (red palm oil) in my diet.

My hair just look completely stable if you know what I mean, no dead looking hairs.
My skin is much more colorful/shiny/healthy.

I would recommend everyone to try out virgin red palm oil in their diet.
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Oscar
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Re: Hair loss

Post by Oscar »

dime wrote:I find Dutch very amazing, with all the double (probably there are even triple) letters, like 'kk' for example, I have no idea how do you pronounce them?! :D
Just like a single one ;) The difference is that the vowel before the double consonant will be pronounced as the short version. For example: stoken ~ stoke-n vs. stokken ~ stock-n.
dime
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Re: Hair loss

Post by dime »

Ok that sounds easy, I was trying to litterally pronounce as it's written :D

About my comment on the wheat germ oil.. now I'm again seing a lot of hair loss, so nothing has changed :(
Perhaps it was some temporary condition.
Will make me a red palm oil mayonaisse and see how that goes.
dime
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Re: Hair loss

Post by dime »

Still fighting with this issue. Latest research points to PGD2, from wikipedia:
In August 2012, Scientists at the University of Pennsylvania announced that they had discovered an enzyme which caused baldness. They found that the enzyme Prostaglandin D2 (PGD2) was found to be present on the scalp of balding men at far higher levels than normal, preventing hair follicles from maturing and therefore stopping them from working and growing hair. Dr George Cotsarelis and his dermatological team at the University say that they are in talks with several pharmaceutical companies about developing treatments which could be available in two years.[25][26][27]
Although I rather think PGD2 comes up as a result, not as a cause.. there's probably something else which causes inflammation.
Kasper
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Re: Hair loss

Post by Kasper »

Some time ago I had a real PGD2 obsession, this what I found intresting:

In humans, mast cells are an almost exclusive cellular source of PGD2. Although there is evidence of some PGD2 formation by platelets, macrophages and certain T lymphocytes, the reported amounts are 100–1000 times lower than those produced during IgE dependent activation of mast cells. More importantly, whereas the basophil and the mast cell both release histamine and leukotriene (LT) C4, it is only the mast cell that produces significant quantities of PGD2.
http://thorax.bmj.com/content/59/6/453.1.full

Assuming that those studies are correct, in other words:
1. PGD2 is a usefull in vivo marker of mast cell degranulation.
2. PGD2 is present in higher levels of the scalp of balding man than normal.

We can conclude that in the balding scalp mast cell degranulation is far higher than normal.
About mast cell degranulation is done much more research than about PGD2, so if you want to search for more insight, search on mast cell degranulation (especially the MCTC subclass)


Buteyko connection

Allergy(European Journal of Allergy and Clinical Immunology) 2010 JW Strider, CG Masterson, PL Durham
Treatment of mast cells with carbon dioxide suppresses degranulation via a novel mechanism involving repression of increased calcium levels
Background: Intranasal noninhaled delivery of carbon dioxide (CO2) is efficacious in the symptomatic treatment of seasonal allergic rhinitis. The goal of this study was to determine whether and how 100% CO2 inhibits mast cell degranulation, thereby possibly contributing to the reduction of symptoms in seasonal allergic rhinitis.
Conclusions: Results from this study provide the first evidence of a unique regulatory mechanism by which CO2 inhibits mast cell degranulation and histamine release by repressing stimulated increases in intracellular calcium. Thus, our data provide a plausible explanation for the reported therapeutic benefit of noninhaled intranasal delivery of 100% CO2 to treat allergic rhinitis.


Truth is, buteyko was quite balding...
It could be that he would have been balder and balder earlier in his life, if he wouldn't have mastered his breathing.

I don't know where I read this study, but I'm quite sure this was the conclussion:
Testosteron is shown to be inflammatory in hypoxic conditions. And to be anti-inflammatory in normoxic conditions.
Also interesting regarding acne.

More about mast cell degranulation:
http://www.ncbi.nlm.nih.gov/pubmed/19700409
Lipid peroxidation seems to activate mast cells as well.
Fat soluble anti-oxidants therefore seem to be important.
I think my hair improved since using astaxanthin and red palm oil.
dime
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Re: Hair loss

Post by dime »

So it's possible that the cause is not enough oxygen (blood) reaching the top of the head where I see most hair fall creating a hypoxic condition there, which makes testosteron/DHT inflammatory? And then PGD2 is released in response to this inflammation? This makes a lot of sense to me.
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