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Posted this in response to another current thread. Just something I found laying around.
On The Issue Of Tren Toxicity
I wanted to share this with everyone on Elite because this is a question I see commonly asked on the boards. This is Author L. Rea's commentary on trenbolone toxicity and first appeared on www.anabolicbeast.com .
Question: I've got the following problem: In many books(including CME, WAR) I can read trenbolone is quite toxic, and you should use low dosages for short periods. I now some people who used Parabolan p*issed blood. BUT I can also read that trenbolone isn't toxic (Bill Roberts: WAR revisited):
"I have found no indication in the scientific literature of particular kidney toxicity with trenbolone. I know of a number of users, at doses of typically 50 mg/day, who have experienced no problems. There are however anecdotal claims of kidney problems. It seems to me, however, that this is occurring only with athletes stacking an incredible amount of drugs, and how the blame can fairly be laid at trenbolone (actually at Parabolan, not trenbolone acetate) is not clear."
In Anabolics 2002 nor William Llewellyn mentioned anything about this toxicity.
I know people using trenbolone acetate 100mg/day for 10weeks without any problem. Just see Nevertoobig's stack: he uses 100mg trenbolone acetate ED.
As I know liver toxicity is in connection with the hexahydrobenzylcarbonate ester and it can be a problem with Parabolan but you don't have to worry if you uses other ester like acetate. So what is the truth? And if I'm right why was finajet so toxic? Just because it was for animals and the oil was not clear enough?
Answer: Trenbolone acetate preperations are toxic to both liver and kidney tissue. The extent is a matter of period of administration for the most part. The reasons are strange but true.
At one time there were the many black-market preperations of Finaplix, FinaJect and others. Most of these contained simple ground Finaplex-H implants...as most are painfully aware. With the process (if you can refer to a caveman approach as a process. The idea of "I have a rock and can make my own AAS" is not a good one) came many foreign non-kidney-friendly materials, some of which were non-soluable. The use of Fina-kits eleminated some of the material concerns due to the use of benzyl alcohol as a solvent to seperate the binders from the AAS in Finaplex-H implants. But there is another concern. The EOD or ED administration of trenbolone acetate preperations also means an accumulation of benzyl alcohol (which is quite high in these kits). Personally I felt that in itself this would not be a huge concern. Unfortunately athlete liver and kidney stress markers consistantly showed in those who utilized the drug. (A little research to discuss)
TR-343
Toxicology and Carcinogenesis Studies of Benzyl Alcohol (CAS No. 100-51-6) in F344/N Rats and B6C3F1 Mice (Gavage Studies)
Chemical Formula: C7H8O - 3D Structure*
Toxicology and carcinogenesis studies of technical-grade benzyl alcohol (99% pure), a textile dye additive, solvent, and food flavoring agent, were conducted by administering the chemical by gavage in corn oil vehicle to groups of F344/N rats and B6C3F1 mice of each sex for 16 days, 13 weeks, or 2 years.
Short-Term Studies:
In 16-day studies, all five male and five female rats and mice dosed with 2,000 mg/kg benzyl alcohol died. Two of five male and 3/5 female rats and 1/5 male and 2/5 female mice dosed with 1,000 mg/kg died. Rats and mice of each sex in the two highest dose groups were lethargic after dosing. Other toxic responses to benzyl alcohol in these dose groups included blood around the mouth and nose, subcutaneous hemorrhages, and blood in the urinary and gastrointestinal tracts of rats and blood in the urinary bladder of mice. Animals administered lower doses of benzyl alcohol (125, 250, or 500 mg/kg) had no compound-related histologic lesions.
Doses selected for the 13-week studies were 0, 50, 100, 200, 400, and 800 mg/kg for rats and mice. Eight of 10 male rats dosed with 800 mg/kg died during weeks 7 and 8; four of these deaths were described as gavage related. Rats dosed with 800 mg/kg exhibited clinical signs indicative of neurotoxicity including staggering, respiratory difficulty, and lethargy. Hemorrhages occurred around the mouth and nose, and there were histologic lesions in the brain, thymus, skeletal muscle, and kidney.
In truth I now feel that it is the accumulative benzyl alcohol that had altered the liver and kidney markers disfavorably far more so than the trenbolone itself. One must remember that the amount of benzyl alcohol in 1ml of most kit preperations is several times higher than an entire 10ml vial of testosterone enanthate.
On The Issue Of Tren Toxicity
I wanted to share this with everyone on Elite because this is a question I see commonly asked on the boards. This is Author L. Rea's commentary on trenbolone toxicity and first appeared on www.anabolicbeast.com .
Question: I've got the following problem: In many books(including CME, WAR) I can read trenbolone is quite toxic, and you should use low dosages for short periods. I now some people who used Parabolan p*issed blood. BUT I can also read that trenbolone isn't toxic (Bill Roberts: WAR revisited):
"I have found no indication in the scientific literature of particular kidney toxicity with trenbolone. I know of a number of users, at doses of typically 50 mg/day, who have experienced no problems. There are however anecdotal claims of kidney problems. It seems to me, however, that this is occurring only with athletes stacking an incredible amount of drugs, and how the blame can fairly be laid at trenbolone (actually at Parabolan, not trenbolone acetate) is not clear."
In Anabolics 2002 nor William Llewellyn mentioned anything about this toxicity.
I know people using trenbolone acetate 100mg/day for 10weeks without any problem. Just see Nevertoobig's stack: he uses 100mg trenbolone acetate ED.
As I know liver toxicity is in connection with the hexahydrobenzylcarbonate ester and it can be a problem with Parabolan but you don't have to worry if you uses other ester like acetate. So what is the truth? And if I'm right why was finajet so toxic? Just because it was for animals and the oil was not clear enough?
Answer: Trenbolone acetate preperations are toxic to both liver and kidney tissue. The extent is a matter of period of administration for the most part. The reasons are strange but true.
At one time there were the many black-market preperations of Finaplix, FinaJect and others. Most of these contained simple ground Finaplex-H implants...as most are painfully aware. With the process (if you can refer to a caveman approach as a process. The idea of "I have a rock and can make my own AAS" is not a good one) came many foreign non-kidney-friendly materials, some of which were non-soluable. The use of Fina-kits eleminated some of the material concerns due to the use of benzyl alcohol as a solvent to seperate the binders from the AAS in Finaplex-H implants. But there is another concern. The EOD or ED administration of trenbolone acetate preperations also means an accumulation of benzyl alcohol (which is quite high in these kits). Personally I felt that in itself this would not be a huge concern. Unfortunately athlete liver and kidney stress markers consistantly showed in those who utilized the drug. (A little research to discuss)
TR-343
Toxicology and Carcinogenesis Studies of Benzyl Alcohol (CAS No. 100-51-6) in F344/N Rats and B6C3F1 Mice (Gavage Studies)
Chemical Formula: C7H8O - 3D Structure*
Toxicology and carcinogenesis studies of technical-grade benzyl alcohol (99% pure), a textile dye additive, solvent, and food flavoring agent, were conducted by administering the chemical by gavage in corn oil vehicle to groups of F344/N rats and B6C3F1 mice of each sex for 16 days, 13 weeks, or 2 years.
Short-Term Studies:
In 16-day studies, all five male and five female rats and mice dosed with 2,000 mg/kg benzyl alcohol died. Two of five male and 3/5 female rats and 1/5 male and 2/5 female mice dosed with 1,000 mg/kg died. Rats and mice of each sex in the two highest dose groups were lethargic after dosing. Other toxic responses to benzyl alcohol in these dose groups included blood around the mouth and nose, subcutaneous hemorrhages, and blood in the urinary and gastrointestinal tracts of rats and blood in the urinary bladder of mice. Animals administered lower doses of benzyl alcohol (125, 250, or 500 mg/kg) had no compound-related histologic lesions.
Doses selected for the 13-week studies were 0, 50, 100, 200, 400, and 800 mg/kg for rats and mice. Eight of 10 male rats dosed with 800 mg/kg died during weeks 7 and 8; four of these deaths were described as gavage related. Rats dosed with 800 mg/kg exhibited clinical signs indicative of neurotoxicity including staggering, respiratory difficulty, and lethargy. Hemorrhages occurred around the mouth and nose, and there were histologic lesions in the brain, thymus, skeletal muscle, and kidney.
In truth I now feel that it is the accumulative benzyl alcohol that had altered the liver and kidney markers disfavorably far more so than the trenbolone itself. One must remember that the amount of benzyl alcohol in 1ml of most kit preperations is several times higher than an entire 10ml vial of testosterone enanthate.
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