Nolva Hairloss


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aromitase inhibitors can increase hairloss if predisposed,as they free up more receptor space to bind with 5-ar(due to aromitase being deactivated).Less binding of one enzyme free's up the possiblity of greater binding of another.If you run anti-A's in the future,concurrently run finasteride,or topical DHT blockers.

So I can lose my hair using Nolvadex with my deca???

Nolvadex is not an aromatase inhibitor & will not increase hairloss.

It's a SERM (selective estrogen receptor modulator) - selective agonist or antagonist of estrogen receptor.
That doesnt sound right, hairloss is caused by androgens (primarily DHT) binding to androgen receptors, so having less estrogen doesnt "free up" more receptors for DHT since estrogen wouldnt be attaching to the androgen receptors anyway.

However, by preventing the aromatization of test to estrogen an anti aromatase like arimidex could increase test levels and therefore indirectly increase DHT levels, so it is best to take finasteride with it to protect the hair.
I think this is a specious argument. It's not an aromatase inhibitor, as has been said, and even if it were, I think the purported increase in test and DHT is not going to be an individually major factor in hair loss. And enzymes are not generic in nature; they have VERY specific binding sites.
I suppose if you sufficiently block conversion of testosterone to estradiol then more would be shunted to the DHT pathway. In fact, in clinical trials, such was the case. However, at physiologic doses, the resultant increased androgens would inhibit at the HP, LH production reduced, and so T and DHT would return to baseline (or thereabouts). However, at Anabolic Androgenic Steroids (AAS) doses, perhaps this WOULD make a difference in serum DHT levels, since there is no longer interplay within a completely suppressed system.

I just don't like adding medications willy-nilly, though. Unless you are having difficulties with DHT, then I wouldn't use finasteride. Granted, elevated DHT can have some nasty side effects.

I also caution against dropping estrogens too low.
Increasing aromatase activity in hair follicles can decrease the conversion of test into DHT, since more test would be converted into estradiol...

Inhibiting aromatase would cause the opposite... so a combination of aromatase inhibitors + test may increase hair loss compared to test alone...

17alpha-estradiol induces aromatase activity in intact human anagen hair follicles ex vivo.

Hoffmann R, Niiyama S, Huth A, Kissling S, Happle R.

Department of Dermatology, Philipp University, Deutschhausstrasse 9, D-35033 Marburg, Germany.

For topical treatment of androgenetic alopecia (AGA) in women, solutions containing either estradiol benzoate, estradiol valerate, 17beta- or 17alpha-estradiol are commercially available in Europe and some studies show an increased anagen and decreased telogen rate after treatment as compared with placebo. At present it is not precisely known how estrogens mediate their beneficial effect on AGA-affected hair follicles. We have shown recently that 17alpha-estradiol is able to diminish the amount of dihydrotestosterone (DHT) formed by human hair follicles after incubation with testosterone, while increasing the concentration of weaker steroids such as estrogens. Because aromatase is involved in the conversion of testosterone to estrogens and because there is some clinical evidence that aromatase activity may be involved in the pathogenesis of AGA, we addressed the question whether aromatase is expressed in human hair follicles and whether 17alpha-estradiol is able to modify the aromatase activity. Herewith we were able to demonstrate that intact, microdissected hair follicles from female donors express considerably more aromatase activity than hair follicles from male donors. Using immunohistochemistry, we detected the aromatase mainly in the epithelial parts of the hair follicle and not in the dermal papilla. Furthermore, we show that in comparison to the controls, we noticed in 17alpha-estradiol-incubated (1 nM) female hair follicles a concentration- and time-dependent increase of aromatase activity (at 24 h: 1 nM = +18%, 100 nM = +25%, 1 micro M = +57%; 24 h: 1 nM = +18%, 48 h: 1 nM = +25%). In conclusion, our ex vivo experiments suggest that under the influence of 17alpha-estradiol an increased conversion of testosterone to 17beta-estradiol and androstendione to estrone takes place, which might explain the beneficial effects of estrogen treatment of AGA.

17alpha-Estradiol Induces Aromatase Activity in Isolated Human Hair Follicles.

S. Niiyama, R. Hoffmann. Dept. of Dermatology, Philipp University, Marburg, Germany.

Women tend to develop AGA later and milder than men, but with the decline of serum estrogens during the menopause many women show an accelerated progression of AGA. Estrogens may play a protective role against the development of AGA, because pregnant women are in some way protected form androgenetic hair loss, but lose their hairs again postpartum. In Europe, topically applied estrogens such as 17ß-estadiole are used to treat androgenetic alopecia, both in women and men. The femal hormone 17ß- Estradiol can be used only in women, whereas the hormonally almost inactive isomer 17a-estradiol can be used in men as well. Although some clinical studies show considerable success of such an approach, the underlying pathways of 17a-estradiol-induced hair regrowth are unknown. It is likely not a receptor mediated hormon effect, since 17ß-Estradiol is an hormon and 17a-estradiol not. Recently it has been shown that hair follicles from women with AGA express more aromatase activity compared to male hair follices, and interestingly those women taking aromatase inhibitors tend to develop rapidly progressive AGA. These circumstantial lines of evidence indicate a role of aromatase during the pathogenesis of AGA. In order to unravel the pathways of 17a-estradiol-mediated effcets on the hair follicles, we measured aromatase activity in isolated intact human occipital hair follicles by incubating hair follicles with H3-1ßandrostenedione with or without 17a-estradiol (1nM, 100nM, 1µM) for 24 or 48 hours. In comparison to the controls (female, 444fmol/mm3 = 100%), we noticed a concentration- and time-dependent increase of aromatase activity in 17a-estradiol-incubated female hair follicles (e.g. 24h: 1nM = + 18%, 100nM = + 25%, 1µM =+ 57%; 24h: 1nM = +18%, 48h: 1nM = +25%). Our ex vivo results suggest that under the influence of 17a-estradiol an increased conversion of testosterone to 17ß-estradiol and androstendione to estrone takes place. In theory this pathway may diminish the amount of intrafollicular testosterone available for conversion to DHT, and because DHT is the major mediator of AGA, this pathway may explain the beneficial effect of 17a-estradiol on the development and progression of AGA.esults suggest that SRY is a male-specific transcriptional stimulator for 5aRII in hDPCs.
hhajdo said: a combination of aromatase inhibitors + test may increase hair loss compared to test alone...

Nolvadex is not an aromatase inhibitor & will not increase hairloss.

A couple of thoughts/questions about these two studies:

1. They are saying that adding an estrogen INCREASES aromatase activity? A problem for me is that I have nothing in my library here explaining 17A- and 17B-estradiol.
2. I'm not sure a study conducted on women is really applicable to men. Although "hair follicles from female donors express considerably more aromatase activity than hair follicles from male donors", it is also true that males present DHT concentrations many times that of females.
3. I'm still trying to remember what an anogen/telogen is.
4. I want to be careful we don't leave the impression that elevated estrogen levels are beneficial, systemically.

Any questions/comments/smart-remarks?