GeorgeWBush
New Member
Well, question isn't exactly correct as it is questions plural, however I have been curious about a few things and haven't been able to find answers.
1. Use of anti-androgens concurrent with use of AAS
I know that many steroid compounds, orals mainly, exhibit their effects on cells through pathways other than the androgen receptor due to their characteristic of having a poor binding affinity. Specifically though, I am wondering why then if this is true, that many oral compounds (and some injectables, ie 'deca') aren't employed with the concurrent usage of anti-androgens alongside as the user would reap a large portion of the steroids anabolic properties while avoiding a large portion of a steroids androgenic side effects? I could see this being particularly advantageous for women who would like to use higher dosages of anabolics, like anavar, without increasing the risk of virilization.
1a. In the same vein, I further wonder why 5-alpha reductase drugs aren't employed in women who use various esters of testosterone? The only risks I am aware of, with women using such drugs as finasteride or dutasteride, is if they are pregnant with a male fetus, and the lack of 5-ar enzymes will interfere with the fetus's development of male characteristics.
2. Oral steroids in injectable solution
I have mainly 2 questions in regard to this: firstly, I am wondering if the solution used to suspend/dissolve the steroid effects the absorption time of the steroid to a significant degree. I've read that the body can absorb the BA/BB faster than carrier oils and that occurrence can cause post injection "crashing" as a result in highly concentrated steroid solutions. So, I wonder even if a carrier oil such as EO is used and the absorption of the oil is very slow, will that effect the time for the hormone to be absorbed, at least to a significant degree? I've read many anecdotal reports that orals suspended in oils take longer to "feel" similarly with test-suspension versus test in oil.
2a. Second question, is there any evidence to suggest that injecting a steroid rather than ingesting it will cause the hormone (assuming equal amounts absorbed in both cases) to be less hepatotoxic? It seems logical that if the hormone can circulate through the body, through muscles and through the various other regions where the hormone can attach, before it reaches the liver, that it would have a higher ratio of anabolism to hepatotoxicity compared to oral ingestion. However, I am basing this merely on conjecture so I defer the question to people with bigger brains than I.
3. Bill, I've read your finaplix conversion recipe and it was indeed very interesting and unique in that it suggests the use of no solvents, merely carrier oil to dissolve the tren. With the standard method, using BA/BB, I find there is a lot of half dissolved pellets and/or residue floating within the pre-filtered solution and it makes me anxious that there is loss of TA as a result. I assume most of it is bi-product and filler that shouldn't be in the final product however, it still feels as though there might be a level of TA loss. What would you say the conversation rate of finaplix - > TA is with respect to loss of TA? Merely wondering for sake of curiosity and more accurate dosing.
3a. I'd just recently brewed some TA, though due to hastiness on my part, I believe some ethanol alcohol (190 proof) managed to get into the solution. I don't believe it could be more than 0.5% of the total solution but I am getting a very irritating sting post injection that lingers for a day plus. I had used a fairly high concentration of BA/BB (2/20) though, which may also be the culprit. I am wondering what's your opinion with regard to this? For now I will cut it with a sterile oil, which I assume will alleviate the issue though I am curious what could be causing the pain - the type of pain could be described as similar to the burning sensation of alcohol poured into an open wound though in my case it is less severe and merely an irritant rather than crippling pain.
1. Use of anti-androgens concurrent with use of AAS
I know that many steroid compounds, orals mainly, exhibit their effects on cells through pathways other than the androgen receptor due to their characteristic of having a poor binding affinity. Specifically though, I am wondering why then if this is true, that many oral compounds (and some injectables, ie 'deca') aren't employed with the concurrent usage of anti-androgens alongside as the user would reap a large portion of the steroids anabolic properties while avoiding a large portion of a steroids androgenic side effects? I could see this being particularly advantageous for women who would like to use higher dosages of anabolics, like anavar, without increasing the risk of virilization.
1a. In the same vein, I further wonder why 5-alpha reductase drugs aren't employed in women who use various esters of testosterone? The only risks I am aware of, with women using such drugs as finasteride or dutasteride, is if they are pregnant with a male fetus, and the lack of 5-ar enzymes will interfere with the fetus's development of male characteristics.
2. Oral steroids in injectable solution
I have mainly 2 questions in regard to this: firstly, I am wondering if the solution used to suspend/dissolve the steroid effects the absorption time of the steroid to a significant degree. I've read that the body can absorb the BA/BB faster than carrier oils and that occurrence can cause post injection "crashing" as a result in highly concentrated steroid solutions. So, I wonder even if a carrier oil such as EO is used and the absorption of the oil is very slow, will that effect the time for the hormone to be absorbed, at least to a significant degree? I've read many anecdotal reports that orals suspended in oils take longer to "feel" similarly with test-suspension versus test in oil.
2a. Second question, is there any evidence to suggest that injecting a steroid rather than ingesting it will cause the hormone (assuming equal amounts absorbed in both cases) to be less hepatotoxic? It seems logical that if the hormone can circulate through the body, through muscles and through the various other regions where the hormone can attach, before it reaches the liver, that it would have a higher ratio of anabolism to hepatotoxicity compared to oral ingestion. However, I am basing this merely on conjecture so I defer the question to people with bigger brains than I.
3. Bill, I've read your finaplix conversion recipe and it was indeed very interesting and unique in that it suggests the use of no solvents, merely carrier oil to dissolve the tren. With the standard method, using BA/BB, I find there is a lot of half dissolved pellets and/or residue floating within the pre-filtered solution and it makes me anxious that there is loss of TA as a result. I assume most of it is bi-product and filler that shouldn't be in the final product however, it still feels as though there might be a level of TA loss. What would you say the conversation rate of finaplix - > TA is with respect to loss of TA? Merely wondering for sake of curiosity and more accurate dosing.
3a. I'd just recently brewed some TA, though due to hastiness on my part, I believe some ethanol alcohol (190 proof) managed to get into the solution. I don't believe it could be more than 0.5% of the total solution but I am getting a very irritating sting post injection that lingers for a day plus. I had used a fairly high concentration of BA/BB (2/20) though, which may also be the culprit. I am wondering what's your opinion with regard to this? For now I will cut it with a sterile oil, which I assume will alleviate the issue though I am curious what could be causing the pain - the type of pain could be described as similar to the burning sensation of alcohol poured into an open wound though in my case it is less severe and merely an irritant rather than crippling pain.
