Exploring The Hormonal Route. Hair=life.

[bridgeburn]

What's its half life? I have read from 38days to 70days to 2 days - it's so confusing.

about 38 hours

Hey. So what would your recommendations be? Taking the whole 50 mg? With 4 mg estradiol daily?

that's what i did. I would recommend combining an E pill with estrogel though

but don't take cypro forever. bica is safer in the long run

 

[Yar]

Prostate cancer? You dumb f***, it is actually proven scientifically that it does nothing to prostate cancer and it actually increases the risk in developing a more stronger and more aggressive prostate cancer you uneducated analphabetic ape, that's why the FDA didn't even approve it as a prostate cancer treatment, even if Merck tried to stick it as a treatment for it, like he tried to get approved finasteride to treat and be prescribed to under 18 year olds also, but he was denied of that also, you dumb f*** that known nothing.

Do your research you dumb f*** before talking, you think your so intelligent for mimicking transgender regimes and for reading a couple of studies online that you actually don't understand sh*t from them... It's really unbelievable how dumb you are, besides the fact that in all the times spent on the internet your not even capable of writing 2 correct sentences in English, dumb f***! Prostate cancer lmao, what a retard damn. And even if it's raises the free TEST it does not mean that you get more DHT you retard because inhibiting the enzyme that actually converts it does not permit it, it just converts the free TEST to Estrogen you dumb f***, that's where the Gyno and some of the sexual sides come from, uneducated sh*t expert that you are.. So much time spent here and on the internet and you don't know the basics on how this drugs act and work, daaaaaaaamn what a retarded f*** you are!

The Dark Side of 5α-Reductase Inhibitors' Therapy: Sexual Dysfunction, High Gleason Grade Prostate Cancer and Depression

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064044/

5α-RIs therapy contributes to high Gleason grade PCa

The premise put forth by Huggins (1941) suggested that PCa is androgen-dependent and androgen deprivation results in tumor shrinkage [56]. Androgen-dependency of PCa is predictable because tumor cells are derived from normal prostate cells, which retain expression of the androgen receptor (AR). Androgen deprivation therapy (ADT) of PCa initially results in tumor regression, but the cancer often relapses into androgen-independent cancer within 18-24 months and tumors no longer require androgens for growth [5,6].

Because conversion of T to 5α-DHT is a critical pathway in normal prostate growth and function, inhibition of 5α-R activity in the prostate results in a reduction of intraprostatic 5α-DHT levels and a decrease in prostate growth and size [57]. There is no evidence that T or 5α-DHT causes initiation, promotion or development of PCa [5,6,58,59]. This hypothesis was further supported by the recent study of Muller et al. [59] in which patients enrolled in the Placebo arm of the REDUCE trial [13] showed no association between baseline total T nor 5α-DHT and PCa. The authors concluded that "baseline serum T and 5α-DHT levels were unrelated to prostate cancer detection or grade" [13,59]. This raises the question-how could 5α-RIs be useful as chemo-preventative agents if PCa development is unrelated to T or 5α-DHT? As stated by Walsh (2010) in the FDA panel discussion in 2010, "No clinical benefit has been demonstrated in patients with prostate cancer treated with PROSCAR" [16]. In addition, the potential reduction in the incidence of PCa in the general population with the use of these agents may not exceed 10%, which is not statistically significant [16]. Furthermore, the documented increase in Gleason high-grade PCa tumors in response to treatment with these agents proves that these drugs do not prevent development and growth of PCa; they merely prevent biopsies due to reduction in prostate volume. Most importantly, if 5α-RIs indeed prevent PCa development, then how come they are not approved for treatment of PCa?

As suggested by Crawford et al. [60], Justman [61], and Walsh [62,63] four important points need to be considered before the decision is made to use 5α-RIs for chemo-prevention of PCa. These are: (1) 5α-RIs do not prevent PCa development and therefore, these drugs have no significant effect on reducing the real risk of metastatic PCa in men; (2) 5α-RIs reduce the risk of detecting low-grade tumors, but do not increase survival or reduced mortality [17]; (3) if these drugs indeed chemo-prevent PCa, then why aren't they used in the treatment of PCa?; and (4) to reduce the overall risk of PCa in the population, 5α-RIs as chemo-preventative agents must be entirely free of any side effects [60,61,62,63]. Theoret et al. [15] reported that even after re-evaluation of the data from the PCPT [14] and the REDUCE trial [13] with the revised Gleason scoring system, these drugs were shown to increase the incidence of Gleason high-grade PCa tumors. The authors concluded that "the trade-off inherent in using a 5αRI for prostate cancer prevention is the acceptance of one additional high-grade cancer in order to avert three to four potentially clinically relevant low-grade cancers" [15]. Put more simply, when using 5α-RIs as chemo-preventive agents - the risks outweigh the benefits.

This is not surprising since the recent follow-up data on the PCPT have clearly shown that there are no significant benefits in terms of reducing mortality and increasing survival [17]. As Ehdaie and Touijer [64] pointed out, while the medical community is eager to provide early intervention for patients with high prostate specific antigen levels after therapy, it remains critical to weigh the harm of treatments against the uncertain benefits to the patients. It is incumbent that physicians critically evaluate the current evidence and weigh the risks and benefits of such interventions [64]. Since the PCPT [14] and REDUCE trials [13], used PCa incidence as an end point instead of mortality, there is little that one can conclude about the chemo-preventive nature of these agents and their ability to prolong survival and improve quality of life [65].

Data from a large, long-term Randomized Control Trial (RCT ARI40005) raised a serious concern regarding the safety of 5α-RIs, dutasteride, because of significant increase in the risk of "cardiac failure" [13,66,67]. As pointed out by Justman [61] some of the unidentified risks of 5α-RIs may be attributed to the limitations of the clinical trials. For example, these trials had no primary or secondary endpoints to detect cardiovascular events; therefore, some of the events may have been overlooked or underestimated. Moreover, since cardiovascular events were not investigated as part of the primary or secondary endpoint, clinical trial investigators may have had different interpretations and may have not given them serious consideration [16,61,67].

Several studies have attempted to evaluate the efficacy of 5α-RIs in reducing tumor growth in the animal models. Interestingly, the study by Umekita et al. [68] showed that various PCa tumor cell lines respond differently to androgen treatment. For instance, the tumor cell line, LNCaP 104-R2, when implanted in castrated, nude, male mice continued to grow. However, treatment with TP resulted in tumor regression not tumor growth. Remarkably, treatment with TP together with finasteride resulted in increased tumor growth. These findings suggest that ADT may not necessarily be beneficial for treatment of all forms of PCa and that androgen replacement therapy may be a potential treatment for some forms but not all forms of PCa [68]. Recently, several small clinical trials have reported using testosterone therapy in patients with localized PCa, after radical prostatectomy or brachytherapy. These studies found positive results based on lack of biochemical recurrence in the treatment arms [69].

Since PCa is a heterogeneous disease, different tumors possess different metabolic properties. In a study using androgen-insensitive PCa cell lines in an animal model, it was reported that the 5α-RIs, finasteride and dutasteride, did not inhibit tumor incidence or tumor growth suggesting the limited potential benefits of 5α-RIs as chemo-preventive agents in all forms of PCa.

It should be noted that 5α-RIs alter cellular biology with uncertain outcomes. For example, treatment of animals with 5α-RIs resulted in marked increase in the expression of the AR [70]. The implication of such dysfunctional metabolism may contribute to loss of androgen dependence and to acquisition of high-grade tumors. In addition, Yun et al. [71] postulated that finasteride increases expression of hemoxygenase-1 and other related factors in PCa cell lines (PC-3). The authors suggested that finasteride-induced alteration in gene expression may be in part responsible for finasteride-induced high grade prostate tumors [71]. It is not surprising that Theoret et al. [15] reported a significantly number of high grade tumors (Fig. 4), with finasteride and dutasteride in the data from the PCPT [14] and REDUCE trials [13] respectively, even after using the revised Gleason scoring system [15].

FIG. 4
Relative and absolute risk of prostate cancer according to modified Gleason score (mGS), PCPT and REDUCE trial. 5α-RI, 5α-reductase inhibitors. I bars indicate 95% confidence intervals. Adapted from Theoret MR, et al. N Engl J Med 2011;365:97-9, with permission of Massachusetts Medical Society [15].

The overwhelmingly negative decision by the FDA panel of scientists and medical experts [16] speaks volumes and raises a significant concern about the safety and the efficacy of these drugs as chemo-preventive agents for PCa, given that they elicit many serious adverse side effects [16]. With the postmarketing increase in reported adverse events, the FDA has mandated a revision to the labeling for all 5α-RIs [16]. The labeling changes included a warning of increased sexual dysfunction, depression, and increased risk of high-grade PCa.

I don’t need to tell me for finasteride, I took the drug on this other than the hair problems I didn’t get from him anymore. Only increased oily hair! It doesn’t make any estrogen, it increases testosterone, bodybuilders take it to increase strength! This is not an antiandrogen pure androgen!

 

[Yar]

Prostate cancer? You dumb f***, it is actually proven scientifically that it does nothing to prostate cancer and it actually increases the risk in developing a more stronger and more aggressive prostate cancer you uneducated analphabetic ape, that's why the FDA didn't even approve it as a prostate cancer treatment, even if Merck tried to stick it as a treatment for it, like he tried to get approved finasteride to treat and be prescribed to under 18 year olds also, but he was denied of that also, you dumb f*** that known nothing.

Do your research you dumb f*** before talking, you think your so intelligent for mimicking transgender regimes and for reading a couple of studies online that you actually don't understand sh*t from them... It's really unbelievable how dumb you are, besides the fact that in all the times spent on the internet your not even capable of writing 2 correct sentences in English, dumb f***! Prostate cancer lmao, what a retard damn. And even if it's raises the free TEST it does not mean that you get more DHT you retard because inhibiting the enzyme that actually converts it does not permit it, it just converts the free TEST to Estrogen you dumb f***, that's where the Gyno and some of the sexual sides come from, uneducated sh*t expert that you are.. So much time spent here and on the internet and you don't know the basics on how this drugs act and work, daaaaaaaamn what a retarded f*** you are!

The Dark Side of 5α-Reductase Inhibitors' Therapy: Sexual Dysfunction, High Gleason Grade Prostate Cancer and Depression

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064044/

5α-RIs therapy contributes to high Gleason grade PCa

The premise put forth by Huggins (1941) suggested that PCa is androgen-dependent and androgen deprivation results in tumor shrinkage [56]. Androgen-dependency of PCa is predictable because tumor cells are derived from normal prostate cells, which retain expression of the androgen receptor (AR). Androgen deprivation therapy (ADT) of PCa initially results in tumor regression, but the cancer often relapses into androgen-independent cancer within 18-24 months and tumors no longer require androgens for growth [5,6].

Because conversion of T to 5α-DHT is a critical pathway in normal prostate growth and function, inhibition of 5α-R activity in the prostate results in a reduction of intraprostatic 5α-DHT levels and a decrease in prostate growth and size [57]. There is no evidence that T or 5α-DHT causes initiation, promotion or development of PCa [5,6,58,59]. This hypothesis was further supported by the recent study of Muller et al. [59] in which patients enrolled in the Placebo arm of the REDUCE trial [13] showed no association between baseline total T nor 5α-DHT and PCa. The authors concluded that "baseline serum T and 5α-DHT levels were unrelated to prostate cancer detection or grade" [13,59]. This raises the question-how could 5α-RIs be useful as chemo-preventative agents if PCa development is unrelated to T or 5α-DHT? As stated by Walsh (2010) in the FDA panel discussion in 2010, "No clinical benefit has been demonstrated in patients with prostate cancer treated with PROSCAR" [16]. In addition, the potential reduction in the incidence of PCa in the general population with the use of these agents may not exceed 10%, which is not statistically significant [16]. Furthermore, the documented increase in Gleason high-grade PCa tumors in response to treatment with these agents proves that these drugs do not prevent development and growth of PCa; they merely prevent biopsies due to reduction in prostate volume. Most importantly, if 5α-RIs indeed prevent PCa development, then how come they are not approved for treatment of PCa?

As suggested by Crawford et al. [60], Justman [61], and Walsh [62,63] four important points need to be considered before the decision is made to use 5α-RIs for chemo-prevention of PCa. These are: (1) 5α-RIs do not prevent PCa development and therefore, these drugs have no significant effect on reducing the real risk of metastatic PCa in men; (2) 5α-RIs reduce the risk of detecting low-grade tumors, but do not increase survival or reduced mortality [17]; (3) if these drugs indeed chemo-prevent PCa, then why aren't they used in the treatment of PCa?; and (4) to reduce the overall risk of PCa in the population, 5α-RIs as chemo-preventative agents must be entirely free of any side effects [60,61,62,63]. Theoret et al. [15] reported that even after re-evaluation of the data from the PCPT [14] and the REDUCE trial [13] with the revised Gleason scoring system, these drugs were shown to increase the incidence of Gleason high-grade PCa tumors. The authors concluded that "the trade-off inherent in using a 5αRI for prostate cancer prevention is the acceptance of one additional high-grade cancer in order to avert three to four potentially clinically relevant low-grade cancers" [15]. Put more simply, when using 5α-RIs as chemo-preventive agents - the risks outweigh the benefits.

This is not surprising since the recent follow-up data on the PCPT have clearly shown that there are no significant benefits in terms of reducing mortality and increasing survival [17]. As Ehdaie and Touijer [64] pointed out, while the medical community is eager to provide early intervention for patients with high prostate specific antigen levels after therapy, it remains critical to weigh the harm of treatments against the uncertain benefits to the patients. It is incumbent that physicians critically evaluate the current evidence and weigh the risks and benefits of such interventions [64]. Since the PCPT [14] and REDUCE trials [13], used PCa incidence as an end point instead of mortality, there is little that one can conclude about the chemo-preventive nature of these agents and their ability to prolong survival and improve quality of life [65].

Data from a large, long-term Randomized Control Trial (RCT ARI40005) raised a serious concern regarding the safety of 5α-RIs, dutasteride, because of significant increase in the risk of "cardiac failure" [13,66,67]. As pointed out by Justman [61] some of the unidentified risks of 5α-RIs may be attributed to the limitations of the clinical trials. For example, these trials had no primary or secondary endpoints to detect cardiovascular events; therefore, some of the events may have been overlooked or underestimated. Moreover, since cardiovascular events were not investigated as part of the primary or secondary endpoint, clinical trial investigators may have had different interpretations and may have not given them serious consideration [16,61,67].

Several studies have attempted to evaluate the efficacy of 5α-RIs in reducing tumor growth in the animal models. Interestingly, the study by Umekita et al. [68] showed that various PCa tumor cell lines respond differently to androgen treatment. For instance, the tumor cell line, LNCaP 104-R2, when implanted in castrated, nude, male mice continued to grow. However, treatment with TP resulted in tumor regression not tumor growth. Remarkably, treatment with TP together with finasteride resulted in increased tumor growth. These findings suggest that ADT may not necessarily be beneficial for treatment of all forms of PCa and that androgen replacement therapy may be a potential treatment for some forms but not all forms of PCa [68]. Recently, several small clinical trials have reported using testosterone therapy in patients with localized PCa, after radical prostatectomy or brachytherapy. These studies found positive results based on lack of biochemical recurrence in the treatment arms [69].

Since PCa is a heterogeneous disease, different tumors possess different metabolic properties. In a study using androgen-insensitive PCa cell lines in an animal model, it was reported that the 5α-RIs, finasteride and dutasteride, did not inhibit tumor incidence or tumor growth suggesting the limited potential benefits of 5α-RIs as chemo-preventive agents in all forms of PCa.

It should be noted that 5α-RIs alter cellular biology with uncertain outcomes. For example, treatment of animals with 5α-RIs resulted in marked increase in the expression of the AR [70]. The implication of such dysfunctional metabolism may contribute to loss of androgen dependence and to acquisition of high-grade tumors. In addition, Yun et al. [71] postulated that finasteride increases expression of hemoxygenase-1 and other related factors in PCa cell lines (PC-3). The authors suggested that finasteride-induced alteration in gene expression may be in part responsible for finasteride-induced high grade prostate tumors [71]. It is not surprising that Theoret et al. [15] reported a significantly number of high grade tumors (Fig. 4), with finasteride and dutasteride in the data from the PCPT [14] and REDUCE trials [13] respectively, even after using the revised Gleason scoring system [15].

FIG. 4
Relative and absolute risk of prostate cancer according to modified Gleason score (mGS), PCPT and REDUCE trial. 5α-RI, 5α-reductase inhibitors. I bars indicate 95% confidence intervals. Adapted from Theoret MR, et al. N Engl J Med 2011;365:97-9, with permission of Massachusetts Medical Society [15].

The overwhelmingly negative decision by the FDA panel of scientists and medical experts [16] speaks volumes and raises a significant concern about the safety and the efficacy of these drugs as chemo-preventive agents for PCa, given that they elicit many serious adverse side effects [16]. With the postmarketing increase in reported adverse events, the FDA has mandated a revision to the labeling for all 5α-RIs [16]. The labeling changes included a warning of increased sexual dysfunction, depression, and increased risk of high-grade PCa.

5a inhibition only worsens the hair situation.

 

[keepcoolmybabies]

5a inhibition only worsens the hair situation.

For the majority of people 5ari's will at least maintain the existing hair, while some will experience some regrowth. I've seen some anecdotes about 5ari's worsening hair loss, but that seems to be a small minority of cases.

There's also no guarantee HRT will bring back hair. I think it offers a powerful option for those willing to go down that route, but it's far from a sure bet that you'll regrow all your hair. For every reddit transgender hair loss success story, there several more that resort to wigs. Estrogen, AA's (depending on which one used), and 5ari's all offer different mechanisms by which they can combat hair loss and some are more or less responsive in different people.

 

[Yar]

smeared eggs and the prostate with estrogel

 

[robincurtz]

@Yar , @Ikarus ; Hey faggots, you are gonna look like this.

 

[finastride23]

Please help me
I am taking cyproteron acetate for about 2 month and I dont see any changes even my hairs get worse but 6 month ago I took cpa for about 2 month and it gave me some nice regrowth,what should I do?what will happen if I drop it?
my hair will be get worse?
my libido is so low after this two month and I have puffy nipples but I don’t see any changes in my hair

 

[Yar]

[QUOTE = "keepcoolmybabies, post: 1841299, member: 142367"] Для большинства людей 5ari's, по крайней мере, сохранит существующие волосы, в то время как некоторые испытают некоторый отрастание. Я видел несколько анекдотов об ухудшении выпадения волос 5ari, но это, кажется, небольшое меньшинство случаев.

Там также нет гарантии, что HRT вернет волосы. Я думаю, что он предлагает мощный вариант для тех, кто хочет пойти по этому пути, но это далеко не верная ставка, что вы вырастите все свои волосы. Для каждой истории успеха выпадения волос reddit есть еще несколько, которые прибегают к парикам. Эстрогены, АА (в зависимости от того, какой из них используется) и 5ari предлагают разные механизмы, с помощью которых они могут бороться с выпадением волос, а некоторые более или менее реагируют на разных людей. [/ QUOTE]

Please help me
I am taking cyproteron acetate for about 2 month and I dont see any changes even my hairs get worse but 6 month ago I took cpa for about 2 month and it gave me some nice regrowth,what should I do?what will happen if I drop it?
my hair will be get worse?
my libido is so low after this two month and I have puffy nipples but I don’t see any changes in my hair

You do not take estradiol? Without estradiol, cipro can not be taken!

 

[Yar]

Please help me
I am taking cyproteron acetate for about 2 month and I dont see any changes even my hairs get worse but 6 month ago I took cpa for about 2 month and it gave me some nice regrowth,what should I do?what will happen if I drop it?
my hair will be get worse?
my libido is so low after this two month and I have puffy nipples but I don’t see any changes in my hair

urgently take 2mg of estradiol sublingually

 

[finastride23]

[QUOTE = "keepcoolmybabies, post: 1841299, member: 142367"] Для большинства людей 5ari's, по крайней мере, сохранит существующие волосы, в то время как некоторые испытают некоторый отрастание. Я видел несколько анекдотов об ухудшении выпадения волос 5ari, но это, кажется, небольшое меньшинство случаев.

Там также нет гарантии, что HRT вернет волосы. Я думаю, что он предлагает мощный вариант для тех, кто хочет пойти по этому пути, но это далеко не верная ставка, что вы вырастите все свои волосы. Для каждой истории успеха выпадения волос reddit есть еще несколько, которые прибегают к парикам. Эстрогены, АА (в зависимости от того, какой из них используется) и 5ari предлагают разные механизмы, с помощью которых они могут бороться с выпадением волос, а некоторые более или менее реагируют на разных людей. [/ QUOTE]

You do not take estradiol? Without estradiol, cipro can not be taken!

I apply elestrin on my temples and some one did this also said to me it will take three month but your shed should be stop at month two

 

[Yar]

Please help me
I am taking cyproteron acetate for about 2 month and I dont see any changes even my hairs get worse but 6 month ago I took cpa for about 2 month and it gave me some nice regrowth,what should I do?what will happen if I drop it?
my hair will be get worse?
my libido is so low after this two month and I have puffy nipples but I don’t see any changes in my hair

how much cypro do you take? urgently take estradiol !!!

 

[Yar]

I apply elestrin on my temples and some one did this also said to me it will take three month but your shed should be stop at month two

tablets with estradiol 2mg.Cipro taken only with estradiol then hair growth in temples and on the head will germinate

 

[robincurtz]

Please help me
I am taking cyproteron acetate for about 2 month and I dont see any changes even my hairs get worse but 6 month ago I took cpa for about 2 month and it gave me some nice regrowth,what should I do?what will happen if I drop it?
my hair will be get worse?
my libido is so low after this two month and I have puffy nipples but I don’t see any changes in my hair

Don't take estradiol unless you are a transgender. At most, you can try anti-androgens. Don't be delusional about that the society would start loving you once you grow tits and big butts.

 

[Yar]

Don't take estradiol unless you are a transgender. At most, you can try anti-androgens. Don't be delusional about that the society would start loving you once you grow tits and big butts.

you are a fool antiandrogen without estradiol does not work !!! estrogen gives hair growth!

 

[Yar]

I apply elestrin on my temples and some one did this also said to me it will take three month but your shed should be stop at month two

take 2mg of estradiol sublingually every day. For some time I began to apply estrogel 0.75 estrogel to the scrotum. This should give high-quality growth in the temples and give nw0

 

[Yar]

Why don't you actually cut them off or inject acid into them like that guy did, wouldn't it be more effective? Your not gonna use them ever anyways...

f*** you tell me? go to the branch of finasteride fool!

 

[Yar]

Lmao, i was asking serious you mongoloid retarded f***, why do you apply estrogel on scrotum when you can actually cut them off and achieve the desired results you are seeking? Your chemically castrated anyways with that treatment, it's not like your balls are gonna function anymore, ever in your shitty life, why are you keeping them, go full eunuch and your saved for life lmao

I'll cut it off, put it in your shitty mouth

 

[Manochoice]

take 2mg of estradiol sublingually every day. For some time I began to apply estrogel 0.75 estrogel to the scrotum. This should give high-quality growth in the temples and give nw0

Does applying A female hormone to your balls not scare you?

 

[Yar]

Does applying A female hormone to your balls not scare you?

no, it gives higher levels of estradiol for hair growth. You either do or remain bald bald and watch others get what they want!

 

[Father_of_Shiseido]

Don't take estradiol unless you are a transgender. At most, you can try anti-androgens. Don't be delusional about that the society would start loving you once you grow tits and big butts.

I took spironolactone for almost 1 year, and you know what? My face began to feminise, my jaws have shrunken. I stopped taking it all. Now I am only on dutasteride. Probably I would consider a hair transplant in future.