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When is the best time of the day to take halotestin?
- Thread starter Shinobi
- Start date
bro unless your a seasoned powerlifter or top level lifter 40mg;s is a bit much..u can get great results with 20-30 a day..split the dosages up one in the morning and one in the evening.Make sure you drink lots of fluid.Also you can take them with meals because the chem structure of the halo ( 1 7-alpha alky-lated) allows no interference with absorbtion in the presence of food in the stomach...are you going to use any other aas in addition with it?
6 weeks is way too long to be on halo. esp @ 40 mg a day. 20 - 30 mg for 3 to 4 weeks tops. shits hard on your guts bro
dosage....
Devastation is right..4 weeks and no more bro especially when stacking with another toxic like fina..just alltogether hard on your system..as far as looking denser you should notice a change in a few days to a week..your strength and appearance will change more over the coming few weeks...
Shinobi said:
Devastation is right..4 weeks and no more bro especially when stacking with another toxic like fina..just alltogether hard on your system..as far as looking denser you should notice a change in a few days to a week..your strength and appearance will change more over the coming few weeks...
Fukkenshredded
New member
Halo at 40mg on top of winny/fina, which you have already been on for eight weeks. So just to understand things here, weeks 9-14 you will be taking all three, and you will go up to 40mg of halo.
You will be strong, ripped, and angry. And don't worry about the jaundice--it will clear up about three weeks after your cycle ends.
You will be strong, ripped, and angry. And don't worry about the jaundice--it will clear up about three weeks after your cycle ends.
D
DaddyX
Guest
winny/halo......not a good idea bro. why the halo anyways ?
Little Rage
New member
Corleone -
Came across some older posts yesterday but can't find them now where it actually had test results and what not about anavar being the most toxic to the liver mg to mg out of all the 17aa.
Came across some older posts yesterday but can't find them now where it actually had test results and what not about anavar being the most toxic to the liver mg to mg out of all the 17aa.
40-45 days max is all i could take. combined with winny, prop, and fina two weeks out 1/2 a bombs. this is my cutting cycle last 45 days as i remove eq, deca, and test cyp and change over to prop though I take the winny and fina for 8 weeks. my liver enzymes where very very high.
pitbullstl
New member
pittbull7 said:
Great name Pitbull....and advice.......20 mgs is more than enough for even a seasoned vet.....the longest I went was 6 weeks, but 4 is advisable......halo, and fina......look out brother....don't go out drinking in a rough part of town.....
Fukkenshredded
New member
As far as ox toxicity goes:
The dosing in some studies was as high as 20mg 4 times a day. Today the legal prescribeable limit is 20mg/day.
Am J Gastroenterol 1991 Sep;86(9):1200-8 Related Articles, Links
A randomized, controlled trial of treatment of alcoholic hepatitis with parenteral nutrition and oxandrolone. I. Short-term effects on liver function.
Bonkovsky HL, Fiellin DA, Smith GS, Slaker DP, Simon D, Galambos JT.
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
The present studies were designed to provide careful measures of effects of oxandrolone, an anabolic steroid, intravenous nutritional supplementation, and the combination of these two treatments on liver functions, metabolic balances, nitrogen metabolism, and nutritional status in patients with moderate to severe alcoholic hepatitis. Of 43 patients originally recruited, 39 (19 men, 20 women) with typical clinical and laboratory features of alcoholic hepatitis (11 Child's-Pugh class B; 28 class C) were admitted to a metabolic unit and completed a 35-day three-phase protocol. Phase I was a 10-day baseline period of observation, during which routine and special quantitative tests of liver function (galactose and antipyrine metabolism), a 7-day elemental balance study, and a 15N, 13C-leucine metabolism study were done. Phase II was a 21-day treatment period during which patients were randomly assigned to receive one of four regimens: 1) standard therapy, consisting of abstinence, a balanced, nutritionally adequate diet, and multivitamins; 2) oxandrolone (20 mg orally four times a day) plus standard therapy; 3) nutritional supplementation, consisting of 2 L daily of 3.5% crystalline amino acids (in 5% dextrose), given by peripheral vein; or 4) a combination of oxandrolone and nutritional supplementation, along with standard therapy. Metabolic balances were repeated during phase II. Phase III was 2 or 3 days posttreatment, during which special studies of liver functions and volumes and leucine metabolism were repeated. All patients who completed phase I of study and were randomly allocated to one of the four treatment groups completed the subsequent two phases. Overall, with time, patients showed highly significant improvements in most clinical and laboratory features. For most standard laboratory tests (e.g., serum albumin, transferrin, prothrombin time) improvements were more marked in patients treated with nutritional supplementation and/or oxandrolone than in those given standard therapy alone. Liver volumes fell in all treatment groups, with greater improvement in those treated with nutritional supplementation. Improvements in galactose and antipyrine metabolism rates were significant only in those treated with nutritional supplementation or oxandrolone. Effects of treatments on metabolic balances, nitrogen metabolism, and measures of nutrition are described in this issue in a companion paper. We conclude that the addition of nutritional supplementation and oxandrolone to standard therapy of moderately severe or severe alcoholic hepatitis is well tolerated, and leads to more rapid improvement in the laboratory parameters measured.
Alcohol Clin Exp Res 1995 Jun;19(3):635-41 Related Articles, Links
Relationship of protein calorie malnutrition to alcoholic liver disease: a reexamination of data from two Veterans Administration Cooperative Studies.
Mendenhall C, Roselle GA, Gartside P, Moritz T.
Department of Veterans Affairs, Medical Center, Cincinnati, OH 45220, USA.
The relationship of protein calorie malnutrition (PCM) to alcoholic liver disease was studied in 666 patients enrolled in two Veterans Administration Cooperative Studies. Some findings of malnutrition could be detected early in 62% of the comparison patients (43 subjects who were alcoholic, but had not yet developed clinical or laboratory evidence of liver injury). In those who had progressed to the stage of liver injury sufficient to manifest clinical jaundice (536 patients), some findings of malnutrition were present in every patient (100%). The degree of malnutrition correlated closely with the development of all the serious complications of the liver disease (ascites, encephalopathy, and hepatorenal syndrome), as well as the overall mortality. The degree of malnutrition was also important in predicting response to some forms of treatment. When prednisolone, a catabolic adrenal steroid, was used, efficacy was independent of the level of malnutrition. However, a relationship was observed with the severity of the liver injury [quantified by the level of jaundice and coagulopathy, i.e., Maddrey's discriminant function (DF(Maddrey)]. For prednisolone, the response was seen only when the DF was 81-100 reducing mortality 45% When oxandrolone, an androgenic anabolic steroid treatment was given, efficacy was observed only in those with moderate malnutrition (PCM score 60-79% of normal) and maximized with adequate caloric intake reducing mortality 86%. To simplify the method of calculating the PCM score for predicting response to anabolic therapy, a multiple logistic regression model was developed from the parameters used to assess nutritional status: DF(PCM) = 0.098 (peripheral blood lymphocytes) + 0.078 (creatinine height index).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Gastroenterol 1991 Sep;86(9):1209-18 Related Articles, Links
A randomized, controlled trial of treatment of alcoholic hepatitis with parenteral nutrition and oxandrolone. II. Short-term effects on nitrogen metabolism, metabolic balance, and nutrition.
Bonkovsky HL, Singh RH, Jafri IH, Fiellin DA, Smith GS, Simon D, Cotsonis GA, Slaker DP.
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
Patients with moderately severe or severe alcoholic hepatitis, described in a companion paper in this issue, had serial studies of energy and protein metabolism and elemental balances before and during treatment for 21 days with one of four randomly assigned regimens: 1) standard therapy, consisting of abstinence, a balanced, nutritionally adequate diet, and multivitamins; 2) oxandrolone (20 mg orally four times a day) plus standard therapy; 3) nutritional supplementation, consisting of 2 liters of 3.5% crystalline amino acids in 5% dextrose given by peripheral vein (PPN) plus standard therapy; and 4) a combination of the other three treatments. Dietary and intravenous intakes and weights were recorded daily, and weekly averages were calculated. Anthropometric measurements and blood studies were done weekly; blood studies included white blood cell counts and differentials, serum prealbumin, transferrin, and total protein and plasma aminograms. Four-days complete balance studies and measures of 15N,1-13C-leucine metabolism also were performed at baseline and after the treatment period. Major findings were as follows: a) Intakes of total calories and protein were significantly higher in PPN-treated than in other groups. b) All patients had positive elemental balances, both at baseline and at the end of the treatment period. However, those treated with PPN (with or without oxandrolone) had higher positive balances of nitrogen, potassium, phosphorus, and magnesium, indicating improvement in lean body mass. c) Anthropometric measurements showed no significant changes, but measures of the visceral protein compartment (serum prealbumin, transferrin, total protein, total lymphocyte count) improved significantly with time. For most of these variables, increases were significantly greater in those treated with PPN with or without oxandrolone than in the other groups. However, for prealbumin, the increase was greatest in the oxandrolone-treated group d) PPN treatment produced dramatic increases in levels of branched-chain amino acids and improvement in the ratio of plasma branched chain to aromatic amino acids. Other treatments had no effect on plasma aminograms. e) Metabolism of 15N,1-13C-leucine was normal and was not affected significantly by treatment. Therapy with PPN and/or oxandrolone was tolerated well. We conclude that PPN has favorable effects on energy and protein metabolism in florid alcoholic hepatitis; oxandrolone has lesser effects, although it may exert some additional action and particularly increases serum prealbumin levels. The results support the use of nutritional supplementation in therapy of moderately severe or severe alcoholic hepatitis.
And with regards to halotestin:
The reason that halotestin is the harshest on the liver is because halo incorporates a combination of features including a 17-a methyl group, a 9-a fluorine, and a 11-OH group. (Andronergic activity is increased 10 times and anabolic activity increased 20 times over that of 17-a methyl testosterone.)
The chemical name for fluoxymesterone is androst-4-en-3-one, 9-fluoro11,17-dihydroxy-1,7-methyl-,(11b,7b)-.
So let's look...we find that it has 17A methyl(17alpha alkylated) which is absolutely toxic--this is the 17aa that is always referred to in most orals, but in addition to this halo also has two more bonds that must be broken down--a 9alpha fluorine (flluorine is used to protect substances from breaking down as in sodium fluoride) wich is an additional toxicity, and an 11-hydroxyl group which is must be enzymatically reduced to the corresponding 11-hydroxy derivative before the steroid can become biologically active. This reaction is carried out by a distinct 11-hydroxysteroid dehydrogenase isozyme in the liver that operates in a reductive mode, a process that in and of itself is very toxic, not only to the liver but to the kidneys.
These three bonds are the reason that halotestin exceeds other steroids in relative toxicity, despite what most bodybuilders say.
So, halo is more toxic than anadrol, and anadrol is more toxic than, say, D-bol or winstrol, but not because of the number of bonds only but also the fact that anadrol decreases glutathione production in hepatocytes in a way that stanozolol does not cause (Welder AA, et al., J Pharmacol Toxicol Methods 33(4)187-95 1995 Aug)
Winstrol would be about as hepatotoxic as oxandrolone except for the additional hygroscopic impact and the pyrogenic aspect, both of which combine to enhance the relative stress put on the internal organs in general, so the net effect is that it is more harsh than oxandrolone.
The term 'halotestin' is derived from the halogen of flourine combined with the term 'testin' which is a shortened version of 'testosterone'.
So there ya go, folks. This information has been posted here before, by me and several others, but since ol' Georgie decided to truncate the search results I am glad to post it as often as necessary to get this point across:
HALOTESTIN IS TOXIC. BE CAREFUL WITH IT.
FS
--------------------------------------------------------------------------------
The dosing in some studies was as high as 20mg 4 times a day. Today the legal prescribeable limit is 20mg/day.
Am J Gastroenterol 1991 Sep;86(9):1200-8 Related Articles, Links
A randomized, controlled trial of treatment of alcoholic hepatitis with parenteral nutrition and oxandrolone. I. Short-term effects on liver function.
Bonkovsky HL, Fiellin DA, Smith GS, Slaker DP, Simon D, Galambos JT.
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
The present studies were designed to provide careful measures of effects of oxandrolone, an anabolic steroid, intravenous nutritional supplementation, and the combination of these two treatments on liver functions, metabolic balances, nitrogen metabolism, and nutritional status in patients with moderate to severe alcoholic hepatitis. Of 43 patients originally recruited, 39 (19 men, 20 women) with typical clinical and laboratory features of alcoholic hepatitis (11 Child's-Pugh class B; 28 class C) were admitted to a metabolic unit and completed a 35-day three-phase protocol. Phase I was a 10-day baseline period of observation, during which routine and special quantitative tests of liver function (galactose and antipyrine metabolism), a 7-day elemental balance study, and a 15N, 13C-leucine metabolism study were done. Phase II was a 21-day treatment period during which patients were randomly assigned to receive one of four regimens: 1) standard therapy, consisting of abstinence, a balanced, nutritionally adequate diet, and multivitamins; 2) oxandrolone (20 mg orally four times a day) plus standard therapy; 3) nutritional supplementation, consisting of 2 L daily of 3.5% crystalline amino acids (in 5% dextrose), given by peripheral vein; or 4) a combination of oxandrolone and nutritional supplementation, along with standard therapy. Metabolic balances were repeated during phase II. Phase III was 2 or 3 days posttreatment, during which special studies of liver functions and volumes and leucine metabolism were repeated. All patients who completed phase I of study and were randomly allocated to one of the four treatment groups completed the subsequent two phases. Overall, with time, patients showed highly significant improvements in most clinical and laboratory features. For most standard laboratory tests (e.g., serum albumin, transferrin, prothrombin time) improvements were more marked in patients treated with nutritional supplementation and/or oxandrolone than in those given standard therapy alone. Liver volumes fell in all treatment groups, with greater improvement in those treated with nutritional supplementation. Improvements in galactose and antipyrine metabolism rates were significant only in those treated with nutritional supplementation or oxandrolone. Effects of treatments on metabolic balances, nitrogen metabolism, and measures of nutrition are described in this issue in a companion paper. We conclude that the addition of nutritional supplementation and oxandrolone to standard therapy of moderately severe or severe alcoholic hepatitis is well tolerated, and leads to more rapid improvement in the laboratory parameters measured.
Alcohol Clin Exp Res 1995 Jun;19(3):635-41 Related Articles, Links
Relationship of protein calorie malnutrition to alcoholic liver disease: a reexamination of data from two Veterans Administration Cooperative Studies.
Mendenhall C, Roselle GA, Gartside P, Moritz T.
Department of Veterans Affairs, Medical Center, Cincinnati, OH 45220, USA.
The relationship of protein calorie malnutrition (PCM) to alcoholic liver disease was studied in 666 patients enrolled in two Veterans Administration Cooperative Studies. Some findings of malnutrition could be detected early in 62% of the comparison patients (43 subjects who were alcoholic, but had not yet developed clinical or laboratory evidence of liver injury). In those who had progressed to the stage of liver injury sufficient to manifest clinical jaundice (536 patients), some findings of malnutrition were present in every patient (100%). The degree of malnutrition correlated closely with the development of all the serious complications of the liver disease (ascites, encephalopathy, and hepatorenal syndrome), as well as the overall mortality. The degree of malnutrition was also important in predicting response to some forms of treatment. When prednisolone, a catabolic adrenal steroid, was used, efficacy was independent of the level of malnutrition. However, a relationship was observed with the severity of the liver injury [quantified by the level of jaundice and coagulopathy, i.e., Maddrey's discriminant function (DF(Maddrey)]. For prednisolone, the response was seen only when the DF was 81-100 reducing mortality 45% When oxandrolone, an androgenic anabolic steroid treatment was given, efficacy was observed only in those with moderate malnutrition (PCM score 60-79% of normal) and maximized with adequate caloric intake reducing mortality 86%. To simplify the method of calculating the PCM score for predicting response to anabolic therapy, a multiple logistic regression model was developed from the parameters used to assess nutritional status: DF(PCM) = 0.098 (peripheral blood lymphocytes) + 0.078 (creatinine height index).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Gastroenterol 1991 Sep;86(9):1209-18 Related Articles, Links
A randomized, controlled trial of treatment of alcoholic hepatitis with parenteral nutrition and oxandrolone. II. Short-term effects on nitrogen metabolism, metabolic balance, and nutrition.
Bonkovsky HL, Singh RH, Jafri IH, Fiellin DA, Smith GS, Simon D, Cotsonis GA, Slaker DP.
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
Patients with moderately severe or severe alcoholic hepatitis, described in a companion paper in this issue, had serial studies of energy and protein metabolism and elemental balances before and during treatment for 21 days with one of four randomly assigned regimens: 1) standard therapy, consisting of abstinence, a balanced, nutritionally adequate diet, and multivitamins; 2) oxandrolone (20 mg orally four times a day) plus standard therapy; 3) nutritional supplementation, consisting of 2 liters of 3.5% crystalline amino acids in 5% dextrose given by peripheral vein (PPN) plus standard therapy; and 4) a combination of the other three treatments. Dietary and intravenous intakes and weights were recorded daily, and weekly averages were calculated. Anthropometric measurements and blood studies were done weekly; blood studies included white blood cell counts and differentials, serum prealbumin, transferrin, and total protein and plasma aminograms. Four-days complete balance studies and measures of 15N,1-13C-leucine metabolism also were performed at baseline and after the treatment period. Major findings were as follows: a) Intakes of total calories and protein were significantly higher in PPN-treated than in other groups. b) All patients had positive elemental balances, both at baseline and at the end of the treatment period. However, those treated with PPN (with or without oxandrolone) had higher positive balances of nitrogen, potassium, phosphorus, and magnesium, indicating improvement in lean body mass. c) Anthropometric measurements showed no significant changes, but measures of the visceral protein compartment (serum prealbumin, transferrin, total protein, total lymphocyte count) improved significantly with time. For most of these variables, increases were significantly greater in those treated with PPN with or without oxandrolone than in the other groups. However, for prealbumin, the increase was greatest in the oxandrolone-treated group d) PPN treatment produced dramatic increases in levels of branched-chain amino acids and improvement in the ratio of plasma branched chain to aromatic amino acids. Other treatments had no effect on plasma aminograms. e) Metabolism of 15N,1-13C-leucine was normal and was not affected significantly by treatment. Therapy with PPN and/or oxandrolone was tolerated well. We conclude that PPN has favorable effects on energy and protein metabolism in florid alcoholic hepatitis; oxandrolone has lesser effects, although it may exert some additional action and particularly increases serum prealbumin levels. The results support the use of nutritional supplementation in therapy of moderately severe or severe alcoholic hepatitis.
And with regards to halotestin:
The reason that halotestin is the harshest on the liver is because halo incorporates a combination of features including a 17-a methyl group, a 9-a fluorine, and a 11-OH group. (Andronergic activity is increased 10 times and anabolic activity increased 20 times over that of 17-a methyl testosterone.)
The chemical name for fluoxymesterone is androst-4-en-3-one, 9-fluoro11,17-dihydroxy-1,7-methyl-,(11b,7b)-.
So let's look...we find that it has 17A methyl(17alpha alkylated) which is absolutely toxic--this is the 17aa that is always referred to in most orals, but in addition to this halo also has two more bonds that must be broken down--a 9alpha fluorine (flluorine is used to protect substances from breaking down as in sodium fluoride) wich is an additional toxicity, and an 11-hydroxyl group which is must be enzymatically reduced to the corresponding 11-hydroxy derivative before the steroid can become biologically active. This reaction is carried out by a distinct 11-hydroxysteroid dehydrogenase isozyme in the liver that operates in a reductive mode, a process that in and of itself is very toxic, not only to the liver but to the kidneys.
These three bonds are the reason that halotestin exceeds other steroids in relative toxicity, despite what most bodybuilders say.
So, halo is more toxic than anadrol, and anadrol is more toxic than, say, D-bol or winstrol, but not because of the number of bonds only but also the fact that anadrol decreases glutathione production in hepatocytes in a way that stanozolol does not cause (Welder AA, et al., J Pharmacol Toxicol Methods 33(4)187-95 1995 Aug)
Winstrol would be about as hepatotoxic as oxandrolone except for the additional hygroscopic impact and the pyrogenic aspect, both of which combine to enhance the relative stress put on the internal organs in general, so the net effect is that it is more harsh than oxandrolone.
The term 'halotestin' is derived from the halogen of flourine combined with the term 'testin' which is a shortened version of 'testosterone'.
So there ya go, folks. This information has been posted here before, by me and several others, but since ol' Georgie decided to truncate the search results I am glad to post it as often as necessary to get this point across:
HALOTESTIN IS TOXIC. BE CAREFUL WITH IT.
FS
--------------------------------------------------------------------------------
Halo is Unreal
Just ran it at the end of a two wk cutter, 25mg zambons ED for 2 wks, start of 2nd wk, halo starts at 5 mg a day, split into 2 doses of 2.5 , i felt this!!! did for 4 days and then ran 10 mg a day , two 5 mg doses and was a friggin lunatic, the pumps were ridcolous, what a structurely enhanced hormone!! like a friggin Blockbuster on the 4th of July
Just ran it at the end of a two wk cutter, 25mg zambons ED for 2 wks, start of 2nd wk, halo starts at 5 mg a day, split into 2 doses of 2.5 , i felt this!!! did for 4 days and then ran 10 mg a day , two 5 mg doses and was a friggin lunatic, the pumps were ridcolous, what a structurely enhanced hormone!! like a friggin Blockbuster on the 4th of July
Enigmaxxx7
New member
DaddyX said:
I know this is great for cutting and hardening, but both of these 17AA at once is hard on your liver. Are you taking the Winny orally or shooting it? If you are taking the Winny orally, I wouldn't cycle the Halo more than 4 weeks and 20mg ED is plenty good.
Peace and chicken grease
