Baldness and the Immune System?

[wookster]

Some theories propose that hair follicles are attacked by the immune system, in association with DHT miniaturization. The immune suppressant - cyclosporine, causes hair regrowth on some bald heads.

http://www.health-marketplace.com/artic ... growth.htm

Thus, a side effect of the immunosuppressive drug cyclosporine (which is used to prevent the rejection of transplanted organs) is scalp hair regrowth. It may be that cyclosporine is the most potent single hair regrowth agent known. But the drug causes potentially severe toxic side effects when used systemically, including kidney damage, hypertension (high blood pressure)-and even death-which precludes its use as a hair growth stimulant.

Another immune system suppressant - tacrolimus, causes baldness on some hairy heads.

http://www.medicinenet.com/tacrolimus/article.htm

DRUG CLASS AND MECHANISM: Tacrolimus is a drug that suppresses the immune system and is used to prevent rejection of transplanted organs. Tacrolimus accomplishes its immune-suppressing effecting by inhibiting an enzyme (calcineurin) crucial for the multiplication of T-cells, cells that are vital to the immune process.

[...]

SIDE EFFECTS: Tacrolimus is associated with many and various side effects. These include baldness (which can occur in 1 in 5 patients who take it)

Immune suppression by itself is probably not the hair growth mechanism of cyclosporine? Is it possible to discover the exact mechanism of cyclosporine hair growth and exclude the immune suppression aspect?

 

[michael barry]

I think this is interesting. Any posters want to venture guesses why one immunosuppressant helps hair growth and another inhibits it?


This is a good find.

 

[docj077]

They don’t understand how it happens, but cyclosporin increases the pigmentation density of hair and vellus and terminal hair growth. The mechanism is thought to be the same as that of minoxidil. Also, notice that this drug causes angioedema, which means angioedema does not inhibit hair growth.



CLINICAL PHARMACOLOGY:
Cyclosporine is a potent immunosuppressive agent that in animals prolongs survival of allogeneic transplants involving skin, kidney, liver, heart, pancreas, bone marrow, small intestine, and lung. Cyclosporine has been demonstrated to suppress some humoral immunity and to a greater extent, cell-mediated immune reactions such as allograft rejection, delayed hypersensitivity, experimental allergic encephalomyelitis, Freund's adjuvant arthritis, and graft versus host disease in many animal species for a variety of organs.

The effectiveness of cyclosporine results from specific and reversible inhibition of immunocompetent lymphocytes in the G0- and G1-phase of the cell cycle. T-lymphocytes are preferentially inhibited. The T-helper cell is the main target, although the T-suppressor cell may also be suppressed. Cyclosporine also inhibits lymphokine production and release including interleukin-2.

No effects on phagocytic function (changes in enzyme secretions, chemotactic migration of granulocytes, macrophage migration, carbon clearance in vivo) have been detected in animals. Cyclosporine does not cause bone marrow suppression in animal models or man.
Skin and Appendages: Abnormal pigmentation, angioedema, dermatitis, dry skin, eczema, nail disorder, pruritus, skin disorder, urticaria.
Psoriasis

The principal adverse reactions associated with the use of cyclosporine in patients with psoriasis are renal dysfunction, headache, hypertension, hypertriglyceridemia, hirsutism/hypertrichosis, paresthesia or hyperesthesia, influenza-like symptoms, nausea/vomiting, diarrhea, abdominal discomfort, lethargy, and musculoskeletal or joint pain.

CLINICAL PHARMACOLOGY:
Mechanism of Action
Tacrolimus prolongs the survival of the host and transplanted graft in animal transplant models of liver, kidney, heart, bone marrow, small bowel and pancreas, lung and trachea, skin, cornea, and limb.
In animals, tacrolimus has been demonstrated to suppress some humoral immunity and, to a greater extent, cell-mediated reactions such as allograft rejection, delayed type hypersensitivity, collagen- induced arthritis, experimental allergic encephalomyelitis, and graft versus host disease.

Tacrolimus inhibits T-lymphocyte activation, although the exact mechanism of action is not known. Experimental evidence suggests that tacrolimus binds to an intracellular protein, FKBP-12. A complex of tacrolimus-FKBP-12, calcium, calmodulin, and calcineurin is then formed and the phosphatase activity of calcineurin inhibited. This effect may prevent the dephosphorylation and translocation of nuclear factor of activated T-cells (NF-AT), a nuclear component thought to initiate gene transcription for the formation of lymphokines (such as interleukin-2, gamma interferon). The net result is the inhibition of T-lymphocyte activation (i.e., immunosuppression).

Skin: Acne, alopecia, exfoliative dermatitis, fungal dermatitis, herpes simplex, herpes zoster, hirsutism, neoplasm skin benign, skin discoloration, skin disorder, skin ulcer, sweating.

 

[docj077]

Basically, cyclosporin decreases apoptosis in hair follicle keratinocytes.

Cyclosporin A-induced hair growth in mice is associated with inhibition of calcineurin-dependent activation of NFAT in follicular keratinocytes
Anat Gafter-Gvili1, Benjamin Sredni2, Rivka Gal1, Uzi Gafter1, and Yona Kalechman2

One of the most common side effects of treatment with cyclosporin A (CsA) is hypertrichosis. This study shows that calcineurin activity is associated with hair keratinocyte differentiation in vivo, affecting nuclear factor of activated T cells (NFAT1) activity in these cells. Treatment of nude or C57BL/6 depilated normal mice with CsA inhibited the expression of keratinocyte terminal differentiation markers associated with catagen, along with the inhibition of calcineurin and NFAT1 nuclear translocation. This was associated with induction of hair growth in nude mice and retardation of spontaneous catagen induction in depilated normal mice. Furthermore, calcineurin inhibition blocked the expression of p21waf/cip1 and p27kip1, which are usually induced with differentiation. This was also associated with an increase in interleukin-1 expression (nude mice), a decrease in transforming growth factor- (nude and normal mice), and no change in keratinocyte growth factor expression in the skin. Retardation of catagen in CsA-treated mice was accompanied by significant alterations in apoptosis-related gene product expression in hair follicle keratinocytes. The ratio of the anti-apoptotic Bcl-2 to proapoptotic Bax expression increased, and expression of p53 and interleukin-1 converting enzyme activity decreased. These data provide the first evidence that calcineurin is functionally active in follicular keratinocytes and that inhibition of the calcineurin-NFAT1 pathway in these cells in vivo by CsA enhances hair growth.
catagen; epithelial cells; terminal differentiation; apoptosis; hypertrichosis; nuclear factor of activated T cells

 

[docj077]

Also, just to throw this out there.

Tacrolimus can be used as a topical in alopecia areata as an immunomodulator.

It induces anagen during the telogen phase and causes hair regrowth. It's very effective in the absence of T-lymphocytes, which it eventually causes.

However, in some patients it also causes hair loss. It can help or hurt.

 

[CCS]

OK, so tacrolimus may be a safe alternative to cyclosporine as a topical, but might cause hair loss in some people? Just did a quick skim. I'm using boswellia seratta, or something like that, as a topical. I wonder if it suppresses immune recruiting signals locally or if that is just hype.

 

[michael barry]

Doctor,
Cyclosporine causes edema in other parts of the bod like the legs and feet, not the head. Where it causes edema, there is hairloss. Im just bein' fair man.

Thats some fabulous info youve posted. Stephen is at work on getting his theory tested in finality by the way. I imagine in a year he will be able to say with clarity it holds promise or is wrong.


I noticed you got off finasteride (Im lucky I guess, and tolerate it well). Your basically taking 333% of vitamin E, tumeric, and green tea extract correct?


Have you heard about Roxythromicyn? Its a immunosuppressant thats in clinical trials right now for alopecia. You can read about it at clinicaltrials.gov I think. Just out of curiousity, have you ever considered trying a copper peptide or a prostaglandin analogued? Any hypertrichotic up there or skin remodeller like emu oil? Would be interested to hear your thoughts on these when you find the time.........................

 

[CCS]

emu oil is a skin remodeler? Like copper peptides? Where did you read this?

 

[docj077]

OK, so tacrolimus may be a safe alternative to cyclosporine as a topical, but might cause hair loss in some people? Just did a quick skim. I'm using boswellia seratta, or something like that, as a topical. I wonder if it suppresses immune recruiting signals locally or if that is just hype.

Apparently, B. seratta inhibits p-selectin mediated recruitment of inflammatory cells. It also enhances apoptosis induced by cytokines and chemotherapeutic agents and inhibits osteoclastogenesis through inhibition of NF-kappaB regulated gene expression.

It basically does the same thing curcumin does in as far as the NF-kappa B gene system. That's why they are both very potent anti-cancer agents.

However, curcumin does not induce this pathway in healthy cells. I can not speak for B. seratta however.

 

[docj077]

Doctor,
Cyclosporine causes edema in other parts of the bod like the legs and feet, not the head. Where it causes edema, there is hairloss. Im just bein' fair man.

Thats some fabulous info youve posted. Stephen is at work on getting his theory tested in finality by the way. I imagine in a year he will be able to say with clarity it holds promise or is wrong.


I noticed you got off finasteride (Im lucky I guess, and tolerate it well). Your basically taking 333% of vitamin E, tumeric, and green tea extract correct?


Have you heard about Roxythromicyn? Its a immunosuppressant thats in clinical trials right now for alopecia. You can read about it at clinicaltrials.gov I think. Just out of curiousity, have you ever considered trying a copper peptide or a prostaglandin analogued? Any hypertrichotic up there or skin remodeller like emu oil? Would be interested to hear your thoughts on these when you find the time.........................

Yes, that's all I'm taking right now.

Curcumin for it's TGF-beta and TNF-alpha inhibitory effects, Green Tea for its TNF-alpha inhibitory effects, and Vitamin E, which pretty much negates any undesirable effect Curcumin has on DNA.

Also, I did quit propecia. In my opinion, it's just way too harmful to my brain. Since I've stopped propecia and began my new plan, my hair has become thicker, my scalp is far less oily, I have vellus growth, and I'm no longer losing any hair. I guess I'll have to see if it lasts. My plan is the only way that I can see of for me to modulate my immune system without actually destroying it.

You're right about the cyclosporin, but it must just be that the cyclosporin causes gravity induced edema secondary to the angioedema (however, I have seen is cause facial and scalp edema, but those patients were bedridden and supine). Hirsutism is very common actually with the use of this drug and it seems like it's very common with pretty much any given immunosuppressant.

Who knows? Perhaps, the answer could one day be eating a lot of curry and the use of an anti-inflammatory topical for the rest of your life to fight male pattern baldness. That would actually be funny, in my opinion, but it's starting to seem like the reality of this disease.

As for the other meds you mentioned, no, I have not considered using them. I may have to do some research, however.

I just don't want to use topicals...at all.

 

[wookster]

:freaked: :freaked:

http://en.wikipedia.org/wiki/Curcumin

Curcumin

[...]

A 2004 UCLA-Veterans Affairs study involving genetically altered mice suggests that curcumin might inhibit the accumulation of destructive beta-amyloid in the brains of Alzheimer's disease patients and also break up existing plaques associated with the disease. It was published that curcumin inhibits cyclooxygenase-2 (COX-2) as well as lipoxygenase (LOX), two enzymes involved in inflammation.

[...]


However, as pointed out by Kawanishi et al. (2005) curcumin is a "double-edged sword" having both anti-cancer and carcinogenic effects.

Curcumin has devastating effects on healthy human cells. A study done by Kelly et al. (2001) in the journal of Mutation Research, proves that curcumin has prooxidant activity based on its effects on the DNA pattern achieved by alkaline gel electrophoresis. However, the undesired effects of curcumin can be suppressed by the lipophilic antioxidant, α-tocopherol.

 

[michael barry]

Wook,

α-tocopherol , is that the normal version of vitamin E?

Its in Alpecin...............maybe thats why they put that in there?


It would seem that taking alot of vitamin E along with curcumin might be necessary. I still have hope for the barley extract's effect on TGF-beta one and the apple B-2's effect on PKC. Nobody would have to nudge me too awfully hard to have a couple of beers a day.

 

[Felk]

Wook,

α-tocopherol , is that the normal version of vitamin E?

Its in Alpecin...............maybe thats why they put that in there?


It would seem that taking alot of vitamin E along with curcumin might be necessary. I still have hope for the barley extract's effect on TGF-beta one and the apple B-2's effect on PKC. Nobody would have to nudge me too awfully hard to have a couple of beers a day.

Docj077 takes 3 times the RDI of Vit. E for this reason i believe. He said it's there to stop any damage to your DNA from curcumin.

God damn though, you always hear the "other side" of supposedly beneficial supplements, and then grudge a nod to the wise people who say nothing we take into our bodies is harm free, natural or not. I think i'll just stick with my finasteride at .5mg a day, at least that's meant for hair loss and it's effects well studied.

 

[docj077]

I'll put it this way. There are people in India that put turmeric spice in their curry everyday of their lives. They don't suffer from curcumin's carcinogenic effects. You have to take multiple grams of the stuff before their is even a cancerous effect. I'm only taking 600mg.

 

[michael barry]

Guys,

for some reason I got on male pattern baldness-research mailing list (by mistake, I didnt sign up for it). But I got this great info in a newsletter. Enjoy:

Herbal Aromatase Inhibition




There is evidence indicating men with androgenetic hair loss in fact have *lower* testosterone levels than men who are not balding, (as if losing hair weren't bad enough).

It seems counterintuitive being that hair loss is actually androgen mediated. That being the case, the expected corollary would be that one would anticipate finging higher estrogen in those with hair loss. It was not at all surprising when we found a study showing that men with acne, (another classic"androgen mediated" disorder) indeed do have higher estrogen levels than men with no acne. The hormonal pathogenesis of acne is almost identical to that of male pattern baldness, i.e. elevated 5AR activity, increased sebum emission, inflammation, bacterial infiltrates etc .The available evidence indicates that male pattern baldness, like acne, involves higher levels of DHT and estrogen, and lower testosterone. Of additional interest is that it has been established that men with prostate disorders typically have higher estrogen as well.


Chin Med J (Engl). 1989 Mar;102(3):236-8.

Testosterone and estradiol serum levels in acne
45 acne patients and 38 healthy subjects were assayed for serum testosterone and estradiol levels by RIA. The results showed that serum testosterone levels of male patients were normal, but serum estradiol levels were significantly higher (40%) than in healthy males. In female patients, estradiol levels were normal, but testosterone levels were significantly higher (47%) than in healthy females. Of the 18 female patients, 16 had various degrees of menstrual dysfunction, and some even had slight hirsutism. Therefore, male acne patients should not be treated with estrogen and in female acne patients with ovarian dysfunction, artificial menstrual cycle therapy is recommended.


Further evidence indicates that lowering DHT alone, as with Propecia and Avodart, is only partially effective at best for stopping the progression of male pattern baldness, and even then for a limited amount of time. Both Propecia and Avodart are known for raising estrogen as well as reducing serum DHT levels, thus compromising the full potential benefit of lowering DHT for scalp hair growth and prostate disorders.

It's a classic case of 2 steps forward and one and a half steps back for hair growth.

This isn't even taking into account the well established side effects of increased estrogen in men, i.e., increase in belly fat, decrease in libido, increased disposition to inflammation, decreased immunity, etc..

The ideal solution to this dilemma is to simultaneously inhibit aromatase AND 5 alpha reductase, not just 5-alpha reductase alone. Aromatase, as many already know, is the enzyme that converts estrogens from androgens. Aromatase and consequently estrogen, increase as men age and is largely implicated in abdominal mass increase, prostate enlargement, hirsutism (body hair growth, particularly on back), and depression. This combination of medical problems, seen in the majority of American middle aged men has been termede the "Estrogen Syndrome" among endocrinologists.

By inhibiting both 5 alpha reductase and aromatase, one increases testosterone and decreases both DHT and estrogen, optimizing the hormone profile for muscle mass maintenance, libido, bodyfat, and for our purposes, hair growth.

How to inhibit aromatase???
There are several compounds, both herbal, and pharmaceutical, that are useful.

Arimidex is an aromatase inhibiting drug that is used in the treatment of breast cancer. It has been in vogue for years in the bodybuilding community who found that it generally prevents breast enlargement among anabolic steroid users. It has interestingly also been used to increase final adult height in children, (for those sports parents). Its drawback is its cost- typically $280.00 or more a month. Insurance will only cover in certain cases of diagnosed breast cancer.

Alternatives do exist.
Several compounds, some of which are already recommended in our treatment protocol, have been shown to inhibit aromatase and have additional benefits for health, anti-aging, and hair growth. Most notable among these compounds are Green Tea Extract, Grape Seed/Resveratrol Extract, Pomegranate Extract, Melatonin, and Chrysin/piperine (Chrysin without piperine is useless , as it is not absorbed).


Cancer Res. 2006 Jun 1;66(11):5960-7.

Grape seed extract is an aromatase inhibitor and a suppressor of aromatase expression.

Department of Surgical Research, Beckman Research Institute of the City of Hope, Duarte, California, USA.
Aromatase is the enzyme that converts androgen to estrogen. It is expressed at higher levels in breast cancer tissues than normal breast tissues. Grape seed extract (GSE) contains high levels of procyanidin dimers that have been shown in our laboratory to be potent inhibitors of aromatase. In this study, GSE was found to inhibit aromatase activity in a dose-dependent manner and reduce androgen-dependent tumor growth in an aromatase-transfected MCF-7 (MCF-7aro) breast cancer xenograft model, agreeing with our previous findings. We have also examined the effect of GSE on aromatase expression. Reverse transcription-PCR experiments showed that treatment with 60 mug/mL of GSE suppressed the levels of exon I.3-, exon PII-, and exon I.6-containing aromatase mRNAs in MCF-7 and SK-BR-3 cells. The levels of exon I.1-containing mRNA, however, did not change with GSE treatment. Transient transfection experiments with luciferase-aromatase promoter I.3/II or I.4 reporter vectors showed th!
e suppression of the promoter activity in a dose-dependent manner. The GSE treatment also led to the down-regulation of two transcription factors, cyclic AMP-responsive element binding protein-1 (CREB-1) and glucocorticoid receptor (GR). CREB-1 and GR are known to up-regulate aromatase gene expression through promoters I.3/II and I.4, respectively. We believe that these results are exciting in that they show GSE to be potentially useful in the prevention/treatment of hormone-dependent breast cancer through the inhibition of aromatase activity as well as its expression.

Breast Cancer Res Treat. 2002 Feb;71(3):203-17
Chemopreventive and adjuvant therapeutic potential of pomegranate (Punica granatum) for human breast cancer.

Department of Pharmacy, Pusan National University, Korea.
Fresh organically grown pomegranates (Punica granatum L.) of the Wonderful cultivar were processed into three components: fermented juice, aqueous pericarp extract and cold-pressed or supercritical CO2-extracted seed oil. Exposure to additional solvents yielded polyphenol-rich fractions ('polyphenols') from each of the three components. Their actions, and of the crude whole oil and crude fermented and unfermented juice concentrate, were assessed in vitro for possible chemopreventive or adjuvant therapeutic potential in human breast cancer. The ability to effect a blockade of endogenous active estrogen biosynthesis was shown by polyphenols from fermented juice, pericarp, and oil, which inhibited aromatase activity by 60-80%. Fermented juice and pericarp polyphenols, and whole seed oil, inhibited 17-beta-hydroxysteroid dehydrogenase Type 1 from 34 to 79%, at concentrations ranging from 100 to 1,000 microg/ml according to seed oil >> fermented juice polyphenols > pericarp poly!
phenols. In a yeast estrogen screen (YES) lyophilized fresh pomegranate juice effected a 55% inhibition of the estrogenic activity of 17-beta-estradiol; whereas the lyophilized juice by itself displayed only minimal estrogenic action. Inhibition of cell lines by fermented juice and pericarp polyphenols was according to estrogen-dependent (MCF-7) >> estrogen-independent (MB-MDA-231) > normal human breast epithelial cells (MCF-10A). In both MCF-7 and MB-MDA-231 cells, fermented pomegranate juice polyphenols consistently showed about twice the anti-proliferative effect as fresh pomegranate juice polyphenols. Pomegranate seed oil effected 90% inhibition of proliferation of MCF-7 at 100 microg/ml medium, 75% inhibition of invasion of MCF-7 across a Matrigel membrane at 10 microg/ml, and 54% apoptosis in MDA-MB-435 estrogen receptor negative metastatic human breast cancer cells at 50 microg/ml. In a murine mammary gland organ culture, fermented juice polyphenols effected 47% inhi!
bition of cancerous lesion formation induced by the carcinogen 7,12-di
methylbenz[a]anthracene (DMBA). The findings suggest that clinical trials to further assess chemopreventive and adjuvant therapeutic applications of pomegranate in human breast cancer may be warranted.

Food Chem Toxicol. 2002 Jul;40(7):925-33
Inhibition of aromatase activity by green tea extract catechins and their endocrinological effects of oral administration in rats.
Department of Toxicology, The Tokyo Metropolitan Research Laboratory of Public Health, 24-1 Hyakunincho 3 chome, Shinjuku-ku, Japan. sato@tokyo-eiken.go.jp
We orally administered polyphenone-60 (P-60), green tea extract catechins, in the diet (0, 1.25 and 5%) to male rats for 2, 4 and 8 weeks initiated at 5 weeks old. It was found that a 5% dose to male rats for 2-8 weeks induced goiters and decreased weights of the body, testis and prostate gland. Endocrinologically, elevating plasma thyroid stimulating hormone (TSH), luteinizing hormone (LH) and testosterone levels and decreasing tri-iodothyronine (T(3)) and thyroxine (T(4)) levels were induced by this treatment. We also found that P-60 as a whole and some of its constituents exhibited inhibitory effects on human placental aromatase activity by in vitro assay. The concentration of P-60 that required producing 50% inhibition of the aromatase activity (IC(50) value) was 28 microg/ml. The IC(50) values of (-)-catechin gallate (Cg), (-)-epigallocatechin (EGC), (-)-epigallocatechin gallate (EGCg) and (-)-gallocatechin gallate (GCg) were 5.5 x 10(-6), 1.0 x 10(-4), 6.0 x 10(-5) and!
1.5 x 10(-5) M, respectively. (-)- Epicatechin gallate (ECg) at 1.0 x 10(-4) M produced 20% inhibition. (-)-Epicatechin (EC) and (+)-catechin (CT) exhibited no effects on aromatase activity. The endocrinological changes observed in vivo were in conformity with antithyroid effects and aromatase inhibition effects of P-60 and its constituents.
Melatonin modulates aromatase activity in MCF-7 human breast cancer cells.
Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, Santander, Spain.
Most of the current knowledge about the mechanisms by which melatonin inhibits the growth of breast cancer cells point to an interaction of melatonin with estrogen-responsive pathways, thus behaving as an antiestrogenic hormone. However, a possible effect of melatonin on the local synthesis of estrogens had not been examined. The objective of this work was to study whether melatonin may modify the aromatase activity in MCF-7 breast cancer cells thus modulating the local estrogen biosynthesis. In MCF-7 cells cultured with testosterone in estradiol-free media, melatonin (1 nM) counteracts the testosterone-induced cell proliferation dependent on the local biosynthesis of estrogens from testosterone by the aromatase activity of the cells. We found that melatonin reduces the aromatase activity (measured by the tritiated water release assay) of MCF-7 cells both at basal conditions and when aromatase activity was stimulated by cAMP or cortisol. The greatest inhibition of the aromat!
ase activity was obtained with 1 nm melatonin, the same concentration that gives the highest antiproliferative and anti-invasive effects of MCF-7 cells. Finally, by RT-PCR, we found that melatonin downregulates aromatase expression at the transcriptional level in the MCF-7 cells. We conclude that melatonin, at physiological concentrations, decreases aromatase activity and expression in MCF-7 cells. This aromatase inhibitory effect of melatonin, together with its already known antiestrogenic properties interacting with the estrogen-receptor, makes this indoleamine an interesting tool to be considered in


When used in full or partial combination, one would obtain the benefits of aromatase inhibition without having to resort to Arimidex, and would get a plethora of health and hair growth promoting benefits in the process.
When used in conjunction with Propecia or Avodart, the side effects of these drugs would significantly diminish, and their benefit for hair growth enhanced. Feedback from the steroid using bodybuilding community, (often a source of good information) has been positive about the ability of these herbal/supplements to prevent "gyno" or breast enlargement.
To reiterate-5 AR inhibition plus aromatase inhibition equals better hair growth

 

[htownballa]

Mike,

Thanks for the good find. So: Green Tea Extract, Grape Seed/Resveratrol Extract, Pomegranate Extract, Melatonin, and Chrysin/piperine supposedly reduce estrogen levels. In what dosage/vehicle are these best taken in?

 

[CCS]

it sure is funny that some people are trying to turn testosterone into estrogen, and now this article says estrogen is the enemy. I think both hormones are bad for scalp hair. But maybe the estrogen is worse. I think women have good hair because they have 5% our testosterone levels, not because they have more estrogen.

I'm not going run out and buy estrogen inhibitors, but I think taking grapeseed extract and green tea extract with soy and meat is a good idea, along with drinking pomagranit juice. I'm already putting all those anti-oxidants on my head.

 

[htownballa]

it sure is funny that some people are trying to turn testosterone into estrogen, and now this article says estrogen is the enemy. I think both hormones are bad for scalp hair. But maybe the estrogen is worse. I think women have good hair because they have 5% our testosterone levels, not because they have more estrogen.

I'm not going run out and buy estrogen inhibitors, but I think taking grapeseed extract and green tea extract with soy and meat is a good idea, along with drinking pomagranit juice. I'm already putting all those anti-oxidants on my head.

Why are people trying to turn testosterone into estrogen?! :freaked2:

Actually you are right though, test AND estrogen are bad for hairs. There is really no safe way to reduce both of them, and if you lower one don't you increase the other?

 

[Bryan]

it sure is funny that some people are trying to turn testosterone into estrogen, and now this article says estrogen is the enemy. I think both hormones are bad for scalp hair.

{SIGH}

As I've been pointing out for years, the preponderance of the evidence suggests that estrogen is good for scalp hair. It's just those crappy Web sites like hairloss-research.org which have been trying to convince people otherwise for years. Their main goal seems to be to try to sell useless supplements like chrysin which don't even work in the first place to reduce estrogen.

Bryan

 

[CCS]

I'm just going to block the receptor and downstream effects, and make sure DHT is gone, and not worry about which of the two, test or est, is worse.