Hi, I’m taking avodart and getting early gyne symptoms. I was wondering if anyone else here takes tamoxifen concurrently with the avodart?
I ordered some generic tamoxifen off the web, it’s called Genox. I have been taking it sporadically. I can never be sure with these online sites if the drug is real, but I think it might be helping. I’m also trying to decrease my avodart dosage to every third day. But I don’t know if that is high enough to prevent hairloss. It’s all so frustrating, a guessing game. Any advice appreciated.
» I’m taking propecia and generic tamoxifen. It has stopped the painful lump under my nip from getting worse. It is still there though. I had better results with Arimadex but it made my good cholesterol disappear. The best advice on gynoand tamoxifen can be found on the steroid websites. Good luck.
I am pretty sure tamoxifen is an estrogen blocker, it prevents estrogen from binding to tissues, it does not reduce the amount of estrogen in your body.
» I am pretty sure tamoxifen is an estrogen blocker, it prevents estrogen
» from binding to tissues, it does not reduce the amount of estrogen in your
» body.
You are right. If you want to reduce the absolute level of estrogen in your body, I think you need Arimidex. Arimidex is an aromatse (sp?) inhibitor, it can reduce the amount of estrogen produced in your body.
» Hi, I’m taking avodart and getting early gyne symptoms. I was wondering if
» anyone else here takes tamoxifen concurrently with the avodart?
» I ordered some generic tamoxifen off the web, it’s called Genox. I have
» been taking it sporadically. I can never be sure with these online sites
» if the drug is real, but I think it might be helping. I’m also trying to
» decrease my avodart dosage to every third day. But I don’t know if that
» is high enough to prevent hairloss. It’s all so frustrating, a guessing
» game. Any advice appreciated.
I think 2 to 3 times a week is probably going to give you pretty good blood levels; it all depends on how your physiology responds to the drug and to lower DHT levels.
SERM’s (selective estrogen receptor modulators) are used a lot by anabolic steroid users to avoid the side effects of high estrogen levels (eg, “gyno”).
Since DHT acts as a estrogen receptor blocker of sorts, it makes sense that a SERM would be useful for treating your gyno. However, some people are very “gyno-prone” and just a little estrogenic stimulation is enough. Good luck.
The worst case scenario is surgical intervention to remove the hypertrophied glandular tissue from the breast.
Here is the skinny on Estrogen.
- Blocking DHT does increase Estrogen (and the bad Estrogens at that)
- Blocking Testosterone production using Spiro/Flut has a similar effect on Estrogen.
- You can tackle E via diet and vitamins (aspirin, zinc, etc)
- Powerful natural (test tube) products often don’t work in the human body due to poor bioavailability or systemic interference, e.g. chrysin
- Anastrozole is very powerful and completely blocks the Aromatization of androgens; 1/4 tab every other day will work well.
- Buy generic Anastrozole; it is cheaper and less likely to be counterfeit than the Astra Zeneca branded product.
- Anastrozole is much safer (and more effective) than Tamoxifen
- As noted Tamoxifen is an early SERM; SERMs are an area of intense research as system-wide blockade of Estrogen is likely to be VERY unhealthy over a long period of time. In the short-term Anastrozole appears far less toxic than Tamoxifen.
Now a few notes on E in general.
- Estrogen plays a critical role in Prostate cancer and male pattern baldness
- It is now generally accepted that it is the T/E ratio that is critical in cancer (breast & prostate) and MPB, i.e. too much E. It is also this ratio that leads to Gyno.
- Estrogen is a complex and mis-understood subject with many recent advances, e.g. the identification of 2 Estrogen Receptors in hair; one acts like the Androgen Receptor and one acts in an opposite manner.
- Aromatase is identified late in the Anagen phase. The most likely primary impact of E in the hair cycle is the inhibition of transition to the Anagen phase.
My experience.
I took Arimidex with Proscar in Jan 2003 and shocked some regrowth of long sleeping follicles. I stopped Arimidex after 4 months and have retained my hair regrowth to this day.
Oh, I used to post here as BingBang and many will remember me and my pictures.
gc1961,
Thanks for sharing that. What prompted you to try Arimidex in the first place? Was it because of gyno or because you felt that Arimidex together with Proscar would be more effective in regrowing hair?
» gc1961,
»
» Thanks for sharing that. What prompted you to try Arimidex in the first
» place? Was it because of gyno or because you felt that Arimidex together
» with Proscar would be more effective in regrowing hair?
I read an article by a weight-trainer that claimed Tamoxifen had help him grow his hair back. Then I did a pile of research on Endocrinology and Intracrinology; If I had started sooner I would have had even better results based on my current understanding.
Tamoxifen also inhibits (IGF-1) and stimulates sulfur-transferase; this enzyme is responsible for Minoxidil conversion to Minox Sulphate - the active metabolite.
IMO IGF-1 is both bad and good; it unregulates Androgen and Estrogen Receptors (bad), but is critical for growth cycle (good).
I attach my images for reference…
hey looking good ! Where did you get generic Anastrozole from? I looked up Arimidex and that stuff is soooooooooo expensive. :surprised:
gc1961,
I took arimidex myself two years ago along with proscar (1/2). My experience doesn’t concur. I don’t believe arimidex made me grow a single strand (dosage was 1pill1/2 over a week time for two months). Arimidex does not work wonders as well on E serum levels. I tested mine prior to taking arimidex and at the very end of the treatment as well: unchanged. Arimidex did not clear either my minor gyno case. As to your own case, I understand you’re still on proscar and this is the very reason why you retained your extra hair. Arimidex has probably nothing to do with that. What’s more, whether you like it or not, T prevented from conversion into E because of arimidex becomes new candidate to conversion into DHT which can only induce extra hairloss. Unless the said T remains free or gets bound by SHBG, which is a rare consequence of AI use if I remember correctly. What I am very curious about is whether you happen(ed) to change your proscar dosage and what kind of sexual sides you notice(d). Please tell us. Thank you.
» gc1961,
» I took arimidex myself two years ago along with proscar (1/2). My
» experience doesn’t concur. I don’t believe arimidex made me grow a single
» strand (dosage was 1pill1/2 over a week time for two months). Arimidex
» does not work wonders as well on E serum levels. I tested mine prior to
» taking arimidex and at the very end of the treatment as well: unchanged.
» Arimidex did not clear either my minor gyno case. As to your own case, I
» understand you’re still on proscar and this is the very reason why you
» retained your extra hair. Arimidex has probably nothing to do with that.
» What’s more, whether you like it or not, T prevented from conversion into
» E because of arimidex becomes new candidate to conversion into DHT which
» can only induce extra hairloss. Unless the said T remains free or gets
» bound by SHBG, which is a rare consequence of AI use if I remember
» correctly. What I am very curious about is whether you happen(ed) to
» change your proscar dosage and what kind of sexual sides you notice(d).
» Please tell us. Thank you.
Maybe you had counterfeit Arimidex; there is a ton of research on its effectiveness on inhibiting E. I doubt you could take it and not see a result unless you were taking fake meds; I work in the industry and outside the US >20% of meds are fake - especially branded, high-priced meds like Arimidex.
As for more DHT as a result of taking Arimidex, I have not seen research that suggests this. Have you? Without such research I can just as easily speculate that HPTA feedback would maintain the T level; BTW the amount of E relative to T is 1/100th, so you would only be increasing T by 1% by completely blockading E production. Further, it is very clear that a complete blockade on T-to-DHT does not prevent hairloss in the majority of people. There are many more factors to hairloss (or prostate cancer) than DHT; much of the new research points to E.
Regarding SHBG, there are many question marks around your point. Firstly >50% of T at the hair folicle is generated at the follicle; either from cholesterol or from Adrenal DHEA. This is not transported via SHBG or Albumin binding. Secondly, hormones that are bound by SHBG can and do dissociate and there are suggestions that SHBG-bound-DHT might be active in binding to the follicle (the SHBG aligns the DHT in one theory); so the classical view of bioactive T is very questionable for sites that express the 450 class enymes as hair does).
No one knows the answers.
gc1961 can you recommend a place online for generic Anastrozole?
» Maybe you had counterfeit Arimidex; there is a ton of research on its
» effectiveness on inhibiting E. I doubt you could take it and not see a
» result unless you were taking fake meds; I work in the industry and
» outside the US >20% of meds are fake - especially branded, high-priced
» meds like Arimidex.
»
» As for more DHT as a result of taking Arimidex, I have not seen research
» that suggests this. Have you? Without such research I can just as easily
» speculate that HPTA feedback would maintain the T level; BTW the amount of
» E relative to T is 1/100th, so you would only be increasing T by 1% by
» completely blockading E production. Further, it is very clear that a
» complete blockade on T-to-DHT does not prevent hairloss in the majority of
» people. There are many more factors to hairloss (or prostate cancer) than
» DHT; much of the new research points to E.
»
» Regarding SHBG, there are many question marks around your point. Firstly
» >50% of T at the hair folicle is generated at the follicle; either from
» cholesterol or from Adrenal DHEA. This is not transported via SHBG or
» Albumin binding. Secondly, hormones that are bound by SHBG can and do
» dissociate and there are suggestions that SHBG-bound-DHT might be active
» in binding to the follicle (the SHBG aligns the DHT in one theory); so the
» classical view of bioactive T is very questionable for sites that express
» the 450 class enymes as hair does).
»
» No one knows the answers.
I had the astra zeneca thing… Tested my E2 before taking it:17pg/ml if I remember, and two months later: 17pg/ml (same lab)…
I’m on 2.5mg finasteride daily and know that the ideal dosage would be 4mg (I tested it) to retain my hair. Problem is: libido is weak at 2.5, so what would it be at 4, long term? What’s your own dosage of finasteride currently? What would you advise me? You seem to be very knowledgeable.
gc, what about estradiol? How come some guys use topical that has estradiol in it? What is the reason for that?
» » Maybe you had counterfeit Arimidex; there is a ton of research on its
» » effectiveness on inhibiting E. I doubt you could take it and not see a
» » result unless you were taking fake meds; I work in the industry and
» » outside the US >20% of meds are fake - especially branded, high-priced
» » meds like Arimidex.
» »
» » As for more DHT as a result of taking Arimidex, I have not seen
» research
» » that suggests this. Have you? Without such research I can just as
» easily
» » speculate that HPTA feedback would maintain the T level; BTW the amount
» of
» » E relative to T is 1/100th, so you would only be increasing T by 1% by
» » completely blockading E production. Further, it is very clear that a
» » complete blockade on T-to-DHT does not prevent hairloss in the majority
» of
» » people. There are many more factors to hairloss (or prostate cancer)
» than
» » DHT; much of the new research points to E.
» »
» » Regarding SHBG, there are many question marks around your point.
» Firstly
» » >50% of T at the hair folicle is generated at the follicle; either from
» » cholesterol or from Adrenal DHEA. This is not transported via SHBG or
» » Albumin binding. Secondly, hormones that are bound by SHBG can and do
» » dissociate and there are suggestions that SHBG-bound-DHT might be
» active
» » in binding to the follicle (the SHBG aligns the DHT in one theory); so
» the
» » classical view of bioactive T is very questionable for sites that
» express
» » the 450 class enymes as hair does).
» »
» » No one knows the answers.
»
» I had the astra zeneca thing… Tested my E2 before taking it:17pg/ml if
» I remember, and two months later: 17pg/ml (same lab)…
» I’m on 2.5mg finasteride daily and know that the ideal dosage would be 4mg
» (I tested it) to retain my hair. Problem is: libido is weak at 2.5, so
» what would it be at 4, long term? What’s your own dosage of finasteride
» currently? What would you advise me? You seem to be very knowledgeable.
Like you, I take 2.5mg; 1/4 generic proscar in the morning 1/4 in the evening. I think Bryan could and would point to research showing little serum DHT reduction from 1.25mg to 2.5mg.
I am not sure going to 4mg will make a difference.
Re the libido thing, I never had a problem with it; while I suspect this is just a difference in the hormone balance in certain individuals, I have also been continuously supplementing with NO2 (Nitric Oxide) from GNC. NO is a vasodilator and may help with the libido. I also believe that NO2 (or other Arginine supplements) is very supportive in fighting hair-loss.
» gc, what about estradiol? How come some guys use topical that has estradiol
» in it? What is the reason for that?
Like male androgens, there are many hormones classsed as Estrogens; and just like T and DHT, some Estrogens are stronger than others.
Estrogen is currently a hot topic in breast and prostate cancer; in both cases it is viewed negatively. Yet in hairloss discussion the majority of people believe that Estrogen is a benefit, and hence the supplementation.
I do not share this opinion and have read many medical papers that increasingly identify Estrogen as very negative.
A thing to remember here is that a lot of our knowledge here is <10 years old, for example the fact that there are two different Estrogen Receptors (alpha and beta) expressed in human hair. These seem to be in opposition in many of their properties, so the balance of the two may be critical.
The net of the E research I have done suggests that the primary action of E in MPB is that it inhibits new hair from entering anagen (growth) phase.
BTW there are herbal supplements that modify E metabolism significantly, e.g. Indole-3-Carbinol. These promote less active forms of Estrogen and appear as an alternative to toxic cancer drugs like Tamoxifen.
This is a big subject.
Estrogen is a very confusing topic. There are a lot of conflicting studies about estrogen. This one was posted by Martinb from the old forum.
Wozel, G.; Narayanan, S.; Jäckel, A.; Lutz, G. A.
Alfatradiol (0,025 %) - Eine wirksame und sichere Therapieoption zur Behandlung der androgenetischen Alopezie bei Frauen und Männern (Alfatradiol (0.025 %) - an Effective and Safe Therapy for the Treatment of Androgenetic Alopecia in Women and Men).
Akt Dermatol 2005; 31: 553-560 DOI: 10.1055/s-2005-870188
Abstract
Androgenetic alopecia (AGA), also referred to as male pattern baldness, is the most common cause of hair loss in both sexes in adulthood. An option for topical treatment that selectively targets the metabolic pathways involved in the balding process is alfatradiol, an estrasterid without hormonal activity. In a drug monitoring study, efficacy and safety of alfatradiol (0.025 %) was assessed in 233 patients with AGA (192 women, aged 14-76 years, and 41 men, aged 17-56 years). After 7.5 months of treatment, trichograms of 112 patients (92 women, 20 men) were evaluated. Under treatment with alfatradiol the proportion of frontal anagen hair increased statistically significantly, in women from 69% to 77% (means) and in men from 56% to 65%. The proportion of telogen hair decreased accordingly. In 12% of women and 21% of men a further decline in the number of anagen hair was observed. Merely three patients (1,3 %) reported mild local adverse reactions. In conclusion, Alfatradiol appears to be effective and safe in the topical treatment of AGA in both men and women.
» Under treatment with alfatradiol the proportion of frontal anagen hair
» increased statistically significantly, in women from 69% to 77% (means)
» and in men from 56% to 65%.
Well, the improvement is really not that significant. The women grew 8% more hair, and men grew 9% more, it s not that much more.
17-Estradiol Induces Aromatase Activity in Human Hair Follicles
Dept of Derm, Philipp University, Marburg, Germany
“…Our results suggest that under the influence of 17 a-Estradiol an increased conversion of testosterone to 17 b-estradiol and androstendione to estrone takes place. In theory this pathway may diminish the amount of intrafollicular testosterone available for conversion to DHT, ane because DHT is the major mediator of AGA, this pathway may explain the beneficial effect of 17 a-estradiol on the development and progression of AGA.”
» 17-Estradiol Induces Aromatase Activity in Human Hair Follicles
» Dept of Derm, Philipp University, Marburg, Germany
»
» “…Our results suggest that under the influence of 17 a-Estradiol an
» increased conversion of testosterone to 17 b-estradiol and androstendione
» to estrone takes place. In theory this pathway may diminish the amount of
» intrafollicular testosterone available for conversion to DHT, ane because
» DHT is the major mediator of AGA, this pathway may explain the beneficial
» effect of 17 a-estradiol on the development and progression of AGA.”
I don’t really buy the last sentence. All the recent reseach shows that E is as bad for hair and prostate as DHT. I think they made too much of a jump in their conclusion. A definite case of separating the science results from a bad interpretation.