http://www.ncbi.nlm.nih.gov/pubmed/21981434

Doesn't hold for fin or dut:

http://www.ncbi.nlm.nih.gov/pubmed/12234510

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5 mg fin/day
1 application 5% minox/day
Ginger PO shampoo every day

just go to these wiki pages click edit upper right and add what you have.. pick page you want

Antiandrogen
Inhibition of androgen production occurs through a unique ..
http://en.wikipedia.org/wiki/Antiandrogen


http://en.wikipedia.org/wiki/D...-Therapeutic_target-2
this above page on advances is even far more detailed, however to bad it has the wrong title so it isn't found on google searches easily...better to edit Antiandrogen above this one.

Selective androgen receptor ...
A SARM for women would ideally stimulate bone retention, or ...

Androgen deprivation therapy
Androgen deprivation therapy (ADT), also called androgen ...

Androgen insensitivity syndrome
Androgen insensitivity syndrome (AIS) is a condition that results ...

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

Edited: 01/02/2013 at 11:02 AM by Science

this Original post study indicates why some, not all, but some reported heart conditions on RU. anti androgen medications orally, and topically if they get to the heart have this risk!


I wonder if ASC-J9 does to or perhaps it just degrades and doesn't act as an anti androgen, I just haven't seen all the literature on it yet.

However it could feasibly degrade the androgen receptors in the heart as well over time, making that heart muscle weaker, perhaps??


RU is alleged to have a 1 hour half life in the blood, so this is supposedly what makes it safe, however the binding to the androgen receptor wouldn't it happen with in that or the second hour etc..?

El Dut assumed in a post that the BINDING happened right away, not over the 24 hour period there after?

Also I did see a thread that RU may be broken down into another metabolite or a group of them, I need to find this out,.....does it enter the blood as an anti androgen or other metabolites,, do these

other metabolites and/or whatever RU is left attach to other receptors through out

the body, such as the heart?

Parsh, you may want to add RU & Spiro in the title of this thread to attract users,

ince that is the main anti androgen, as it stands now many would skip over this valuable info.

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

"however, this increased risk of HF was only found in patients taking bicalutamide 50?mg/day in combination with luteinizing hormone-releasing hormone (LHRH) receptor agonists."

"There were no cases of hospitalized HF in patients taking bicalutamide 50?mg/day as monotherapy and there was no significant association between current use of bicalutamide 150?mg/day and the risk of hospitalized HF."

To sum it up when used by itself bicalutamide showed no increased risk. When paired up with LHRH agonists, it did.

Drug Saf. 2011 Nov 1;34(11):1061-77. doi: 10.2165/11594540-000000000-00000.
Androgen deprivation therapy and the risk of coronary heart disease and heart failure in patients with prostate cancer: a nested case-control study in UK primary care.
Martín-Merino E, Johansson S, Morris T, García Rodríguez LA.
Source
Spanish Centre for Pharmacoepidemiological Research (CEIFE), Madrid, Spain.
Abstract
BACKGROUND:
Androgen deprivation therapy (ADT) is used to delay tumour development and improve survival in patients with prostate cancer. However, several randomized controlled trials and observational studies have suggested that ADT may increase the risk of cardiovascular events.
OBJECTIVE:
The aim of the study was to evaluate the risk of coronary heart disease (CHD) and heart failure (HF) in patients with prostate cancer receiving ADT in UK primary care, and to evaluate the risks associated with individual ADT and combination ADT.
METHODS:
The UK General Practice Research Database was used to identify a cohort of patients with a first prostate cancer diagnosis during 1999-2005. These patients were followed up to assess the occurrence of acute myocardial infarction (AMI), death from CHD, incident HF and hospitalization due to acute decompensated HF. Nested case-control analyses were performed to assess the risk of these outcomes associated with anti-androgen therapy, as well as different types of ADT and combinations of ADT.
RESULTS:
Current anti-androgen use was associated with a significant increase in the risk of hospitalization due to HF (odds ratio [OR] 2.15; 95% CI 1.08, 4.29), but not of incident HF, CHD or AMI. When assessed individually, there was no significant association of bicalutamide or cyproterone use with the risk of AMI or CHD. Current use of bicalutamide 50?mg/day was associated with a significant increase in the risk of HF (OR 3.28; 95% CI 1.31, 8.18); however, this increased risk of HF was only found in patients taking bicalutamide 50?mg/day in combination with luteinizing hormone-releasing hormone (LHRH) receptor agonists. There were no cases of hospitalized HF in patients taking bicalutamide 50?mg/day as monotherapy and there was no significant association between current use of bicalutamide 150?mg/day and the risk of hospitalized HF. Combination therapy with LHRH agonists and anti-androgens was associated with a significant increase in the risk of CHD (OR 4.35; 95% CI 1.94, 9.75), AMI (OR 3.57; 95% CI 1.44, 8.86), incident HF (OR 3.19; 95% CI 1.10, 9.27) and hospitalized HF (OR 3.39; 95% CI 1.07, 10.70) compared with non-use of these drugs.
CONCLUSIONS:
In men with prostate cancer, combination therapy with LHRH agonists and anti-androgens is associated with significant increases in the risk of CHD, AMI, incident HF and hospitalized HF. Individual therapies do not appear to increase the risk of these outcomes.

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

I see no reason why Luteinizing Hormone would be at the root of this? In fact if it were, you'd think they'd title the study that, or include it at least. Has anyone seen full text of study, we can't rely on just an abstract, this is to important ..life or death literally here...please post full text if someone finds it.

we know that RU is closely related to MDV and nilutamide.


In fact one of the metabolities of RU is cyanolutamide ...still don't know about the other metabolites if there are any and to what extent RU is absorbed in blood unmetabolized as an anti androgen floatiing around blood stream and through heart looking for androgen receptors to attach to?



that bateman study on thread is questionable if using 300 mcg RU and some low systemics , when standard dose is 50-100 mg here.
this one on RU sides seems to give more.

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

Edited: 01/02/2013 at 07:53 PM by Science

There is a huge amount of data on both sides of the argument. My understanding is that testosterone and DHT appear to have cardioprotective (read: anti-inflammatory to blood vessel walls) effects. Some things that cause inflammation at hair follicles may prevent it in the arteries wrapped around our heart.

this. people freaking out over heart failure due to antiandrogens are going over board. Androgen deprivation they are talking about is CAB(Complete androgen blockade). Not just using fin/dut or a topical antiandrogen.

I agree that Finasteride or Dutasteride is not likely an issue since they do not attach to the androgen receptors found in the body the way an antiandrogen does.

Can you say definitively though you have not heard of one case of alleged heart failure or heart conditions on antiandrogens including but not limited to RU58841?

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

it is amazing how a subject about anti androgen get's derailed by those talking about fin and dut, which are not the foregoing. When people have alleged heart complications from a topical RU, that is of relevance to be discussed and that is what the thread is seeking answers to is the risk of all oral and topical anti androgen in heart complications, as androgen receptors alleged to be in heart muscle.

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

If androgen deprivation is so bad for your heart, why do eunuchs, on the average, live 14 years longer?

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5 mg fin/day
1 application 5% minox/day
Ginger PO shampoo every day

gumbo boy throwing a spanner into the works again. Drats, foiled again thay say!

el dut also said one of the metabolites of RU (the antiandrogenic one) has something like a 2 day half life, so it could build up in the body over time.

was he talking about Cyanolutamide?

It is alleged to be converted into 1% Cyanolutamide.
However I wonder if the heart problems experienced if related to RU are related to KB in particular as the vehicle is a occlusion dressing left on scalp for 8 hours if this info is accurate, and thus one is increasing amount of RU that goes systemic, thus increasing the amount of Cyanolutamide perhaps by significant concentration in the blood to lead to heart problems and to build up far more quickly... much of the foregoing is conjecture at this point to be investigated.

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this is for information purposes I am not a Dr. for hair loss my advice should not be considered medical/expert advice for such. The poster will not be liable for any direct, indirect, consequential, special, exemplary, or other damages arising therefrom.

El Dut was calling it "RU 56279".

Is that identical to "cyanolutamide"?

while its purely associational, a lot of the guys thought that it shouldnt be a huge issue because the prostate drug nilutamide is used in doses of 300 mg... we are using ~100 mg RU which would translate to 1 mg RU 56279 / cyanolutamide. Assuming its comparable to nilutamide that seems to be a small amount. But this could be misleading. nilutamide is given for prostate cancer, not for hair. But you'd think 1/100th of a dose (assuming they are comparable in strength) shouldnt cause a huge issue.

Get a C-reactive protein test during your next doctor visit.

Take care of your smellf

bumping an old thread

maybe someone more knowledgeable then me in this could help. I see a lot of guys on other forums are using RU58841 as a way to prevent hairloss while they are on gear. but as the abstract states above
" combination therapy with LHRH agonists and anti-androgens is associated with significant increases in the risk of CHD, AMI, incident HF and hospitalized HF"

now I don't know exactly which chemicals are LHRH agonist but I thought hcg and clomid promotes the same effect as LHRH? I do not know if nolvadex does the same. but is promoting those effects the same as taking an LHRH agonist?

but my question is are this people taking a huge gamble running RU and these serms or hcg together? could it cause them heart failure like the study suggest?

I do not take RU or those other drugs. I know a decent amount about RU from all the forums but i am not that knowledgeable on the other drugs. i just see a lot of people taking it and thought if someone answered these questions it could potential help someone.

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Finastride 1.25mg