Its actually quite logic that if we use means that are bad for our organs, it makes a difference how long wedo that and at which dose. A long heavy dosed cycle should do more harm than some short light cycles.We also know that injectable roids are safer than orals. And some orals, like Oxymetholone, are morehepatotoxic than others. The same is true for injectables, most of us know that the trenbolones do moreharm than the testosterones. But how much harm will they do? I made a comparison for you with twocase studies. One from a young bodybuilder on a low cycle and one from a professional bodybuilder witha long and heavy cycle.
Case presentationSearch... This case study presents a 23 year old male bodybuilder who, with a healthy history, incorporated the useof anabolic steroids into his training program for an upcomingcompetition. The subject administered both oral and parenteralforms of steroid over a 6 week period. Serum and urinalysiswere conducted before, during and after a six week interval ofsteroid administration. In addition, the subject recorded hissubjective side effects during this period.At 7 weeks pre*competition, the athlete initiated an anabolicsteroid program for a 6 week period. He discontinued his druguse 1 week prior to competition.During the initial 3 week period, the subject administeredparenteral agents, Nandrolone Deconoate 300 mg/wk,Bolasterone 30 mg/wk, and Mesterolone, which is an oralcompound but is altered at the 17*beta position so that itpossesses pharmacological characteristics similar to aninjectable steroid (25 mg/day).During the next 3 weeks of therapy, the steroid types used were ones which were associated with lesswater retention and therefore, minimized the "bloated" appearance which is an undesirable state forcompetition. These included most of the oral preparations which have short side chains at the 17 alphaposition of the steroid molecule. The drugs in this phase included Mesterolone 50 mg/day, Oxandrolone35 mg/day, Boldenolone Undecylenate 150 mg/wk, and Methenolone Actate 60 mg/wk.Serological assessments werecompleted prior to initiation of anabolictherapy, twice during the 6 week drugsession and at five and 13 weeksfollowing discontinuance of drug use.The results of these tests are recordedin the table below. Also recorded wereany subjective side effects noted by theathlete.DiscussionUrea values were elevated throughoutthe entire study period. This was likelydue to the high protein intake of the athlete and not necessarily attributed to any degree of renaldysfunction.34 Creatinine, also a kidney function test, was elevated throughout most of the study with theexception of 13 weeks post drug use.Creatinine excretion was consistent in a given time period and was proportional to the increased amountof muscle mass acquired by the subject. Table 2 reveals a steady increase in creatinine excretion fromthe non*drug use state to the high point of drug consumption and then steadily diminished thereafter. Thisseemed logical since the athlete acquired muscle mass in proportion to the creatinine increase. Thesubject trained little from the day of competition to the 13 week post period and hence lost approximately10 pounds of muscle mass which was reflected by diminishing creatinine levels.Bilirubin remained normal throughout the study suggesting undisturbed liver bilirubin metabolism. Totalprotein and albumin changes, in this study, were also unremarkable.
Creatinine phosphakinase (CPK) determinationswere highly elevated throughout the drug use periodbut decreased markedly in both the non*training andnon*drug use periods. The elevated titres of CPKwere attributed to muscle damage induced bysevere exercise 35'34 (4*5 hours daily) and to theintramuscular injections administered by the subject.During the pre*steroid phase, CPK titres were lowerthan both the 3 week and 5 week drug stages. Anelevation of 301 IU/L of CPK from the pre*steroid tothe 5 week steroid stage was likely the result of theintramuscular injections since the intensity oftraining did not appreciably alter during these stagesof the study.The non*specific liver function tests (LFT's), ASTand ALT, maintained higher than normal valuesthroughout the entire study. Note, these values wereelevated prior to anabolic therapy initiation. This wasnot surprising since both AST and ALT are found inskeletal muscle and are released into the serumwhen muscle damage is increased. This isexplained in a manner similar to that of CPK elevation. Strauss et al studied 32 weightlifters of which 20were using oral anabolics while the remaining 12 were not. The steroid subjects demonstrated ALT levelsgreater than normal and AST values on the high side of normal. The 12 individuals not using steroids,demonstrated ALT and AST levels virtually identical to those using the steroids.Another study conducted by Hogermant et all of 5 weightlifters, 3 of which were taking steroids and 2 whowere not, determined that all five lifters displayed elevated AST and LDH levels while ALT and ALP werenormal. The studies suggest that intense weight training alone, can elevate non*specific LFT's.At the peak of drug use, AST and ALT levels reached 98 and 137 IU/L, respectively. This could arisesecondarily to the increased drug consumption at this stage of the study and/or to the change to the oralforms of steroids, namely Oxandrolone ( see below).This specific drug, of course, has been associated with higher incidences of hepatotoxicity than theparenteral forms. Another hypothesis suggests that the elevation of LFT's is due to skeletal musclebreakdown rather than any hepatic dysfunction.There are two aspects which reinforce this conjecture. One proposes that these elevations parallel thoseof CPK which reflects muscle damage due to exercise and intramuscular injections. Secondly, the specificLFT, especially alkaline phosphatase, remained within normal parameters throughout αthe entire study,even on the lower side of normal. It appears likely that a combination of all the above exists and that thelatter factor, muscle breakdown, plays the largest role in the elevation of non*specific LFT's.Total LDH levels were monitored and since this enzyme is found in skeletal muscle as well, it is notsurprising that these changes parallel those of CPK. Haupt and Rovere suggest that measurement of thehepatic fractionation of LDH is a useful specific LFT. Biochemical analysis during this study did not includeLDH fractionation, as such LDH was considered as a non*specific liver function test.Both cholesterol and triglycerides (TG) levels were unremarkable throughout the study.Urinalysis was similarly unremarkable.
ConclusionIn view of the measured results in this isolated case study, it was considered that the only noteworthyalterations in blood chemistry were CPK, AST, ALT, and LDH. It was also felt thatno pathophysiological processes were occurring with respect to liver dysfunction and that elevated nonspecificLFT's were more a product of muscle breakdown induced by severe exercise and byintramuscular injection.Case presentation IIIn 2012 a 37*year*old male professional bodybuilder witha body height of 180 cm and a body weight of 118 kgpresented himself with increasing epigastric andabdominal pain to an outside department of hepatology.That are impressive figures other professionalbodybuilders with an height of 5′ 11″ (180 cm) and an offseason weight of 260 lb (118 kg) are Lee Haney and MilošŠarčev.For a period of at least five years he has been consumingthe following AASs in a daily medication schedule:Testosterone propionate, testosterone phenylpropionate,testosterone isocaproate, testosterone decanoate 250mg(Sustanon)Trenbolone acetate 75mg5alpha*androstanediol 100 mg (dihydrotestosterone (DHT) prohormone)Boldenone and Methandriol dipropionate 240 mg (Drive or Overdrive)Stanozolol 100 mg,Oxandrolone 4×10 mg,Letrozole 0,065 mg,Oxymetholone 3 × 50 mg or Methandienone 10 mg.Oxymetholone or Methandienone was discontinued three weeks beforecompetition. In addition, he took Spironolactone 100 mg, Mesterolone 25mg, Fluoxymesterone 10 mg four weeks, and Torasemide eighteen hoursbefore competition. Furthermore, a daily intake of amino acid, vitamins,and mineral tablets, T4 (200 μg), and growth hormones (8 I.E.) was reported.The nutritional protocol consisted of six small, protein*rich meals (chicken breast, fish, protein shakes,salad, vegetable, etc.), a high caloric and high protein*containing diet to build up muscle mass. Eightweeks before competition, the meals and consequently the caloric intake were reduced by 50% to reducesubcutaneous fat.Torasemide, a diuretic, was taken to achieve a more muscular bodily contour by reducing extracellularand subcutaneous tissue volume.The physical examination of the professional bodybuilder revealed an athletic appearance with enhancedmuscular contour. A mild tenderness in the right upper abdominal quadrant was found. Any history of alcohol consumption or smoking was denied. A hepatic lesion was discovered by abdominal ultrasound. Itappeared as a predominantly hyperechoic lesion in the right lobe of the liver. The magnetic resonanceimaging showed a hepatomegaly and confirmed the lesion which showed features of a hepatocellularadenoma[The dark patch below left.]. The patient was transferred to the Department of Visceral Surgery,University of Cologne for a laparoscopic resection of the suspected HCA.If steroids users develop liver tumours thenthey usually have hepatocellular adenoma:benign swellings that do not spread throughthe rest of the body. Nevertheless manydoctors think it's a good idea to remove theswellings because they may start to bleed orcould change into a more malignant form oftumour: hepatocellular carcinoma.Hepatocellular carcinoma is liver cancer.This form of cancer is most common amongalcoholics, but very rare among steroidsusers. That's why doctors at UniversityHospital of Cologne were surprised whenthey found hepatocellular carcinoma in thisbodybuilder.The doctors in Cologne decided to operate on the man. They removed the part of the liver where thetumour was located; the tumour itself measured 6 x 5 x 5 cm. In the lab they discovered that it washepatocellular carcinoma that the man had developed.In the literature the doctors only found 7 cases of bodybuilders who had developed hepatocellularcarcinoma as a result of steroids use. The chance of steroids users developing this form of cancer istherefore small, but not zero."Bodybuilders who abuse anabolic androgen steroids over a long period of time have a risk of developingan hepatocellular adenoma or hepatocellular carcinoma and should therefore be well monitored", thedoctors write. "Periodic hepatic ultrasound seems to be an adequate screening procedure to detect thedevelopment of hepatic lesions.""Although most of the tumors developing by anabolic androgenic steroids misuse or intake are benign,early detection is important in order to avoid the associated risk of malignant transformation and lifethreateninghemorrhages", they continue. "In these cases a surgical excision is recommended."Fortunately the bodybuilder in the study recovered. Just seven days after his operation the doctors senthim home and when they examined him 27 months later he was completely healthy.OxandroloneA growing number of reports about abuse of anabolic androgen steroids in Western Europe and the USAby competitive and noncompetitive bodybuilders is reported in the literature. A correlation between AASuse and hepatocellular adenoma has been increasingly recognized in athletes taking AAS. While danazolis associated with hepatocellular adenoma formation, other preparations like oxymetholone, respectively,methyltestosterone can lead to hepatocellular carcinoma. In addition to other synthetical androgenicsteroids, the 37 year old bodybuilder in the case study above consumed the prospective carcinogenicoxymetholone (50mg) three times a day.There is one reported case of a steroid induced hepatic tumor in an athlete resulted in his death. Thiswas a male bodybuilder who succumbed to hepatocellular carcinoma and hepatic cholangiocarcinoma. The athlete employed both oral and parenteralcompounds for four years preceding his deathincluding; Methandrostenolone (oral), Oxandrolone(oral), Stanozol (oral), Methenolone andNandrolone Decanoate (administeredintramuscularly).This individual utilized the 17*alpha alkyl derivativesof testosterone for a protracted period of time, aswas the case with almost all of the other reportedinstances of hepatic tumors attributed to the use of anabolic steroids. It is significant to note thatOxymetholone (Anadrol) was the preparation most frequently associated with the incidences ofboth peliosis hepatis and hepatic carcinoma.It will be clear by now but, … extended use of high doses of oral anabolic steroids can cause liver tumorsor hepatocellular adenoma. We might call this 'liver cancer', but doctors would not use this term here.Real liver cancer, in which liver cells mutate into cancer cells, is even more rare among steroids usersthan hepatocellular adenoma. But it does happen, report doctors at the University Hospital of Cologne.Cholestasis, peliosis hepatis and liver tumours, are the possible consequences of steroid use for the liver.Cholestasis is a condition whereby the liver can no longer remove waste products via the bile to theintestines. Faeces become grey, skin colour yellow, you start to itch and if you don't receive treatmentquickly your liver tissue starts to die off.Peliosis hepatis is a condition in which blood filled cavities form in the liver. It was probably the cause ofdeath of Andreas Muenzer. Doctors don't yet know how peliosis hepatis arises, but they do know how totreat the problem: you just need to remove the cause. If Andreas Muenzer had stopped taking steroids intime he could very well still be alive today – and his liver would have recovered.What we can do is ..if you want to use oral steroids as a kickstarter for your cycle or in the cut, don’tcombine it with recreational drugs, oral medication, alcohol.
Case presentationSearch... This case study presents a 23 year old male bodybuilder who, with a healthy history, incorporated the useof anabolic steroids into his training program for an upcomingcompetition. The subject administered both oral and parenteralforms of steroid over a 6 week period. Serum and urinalysiswere conducted before, during and after a six week interval ofsteroid administration. In addition, the subject recorded hissubjective side effects during this period.At 7 weeks pre*competition, the athlete initiated an anabolicsteroid program for a 6 week period. He discontinued his druguse 1 week prior to competition.During the initial 3 week period, the subject administeredparenteral agents, Nandrolone Deconoate 300 mg/wk,Bolasterone 30 mg/wk, and Mesterolone, which is an oralcompound but is altered at the 17*beta position so that itpossesses pharmacological characteristics similar to aninjectable steroid (25 mg/day).During the next 3 weeks of therapy, the steroid types used were ones which were associated with lesswater retention and therefore, minimized the "bloated" appearance which is an undesirable state forcompetition. These included most of the oral preparations which have short side chains at the 17 alphaposition of the steroid molecule. The drugs in this phase included Mesterolone 50 mg/day, Oxandrolone35 mg/day, Boldenolone Undecylenate 150 mg/wk, and Methenolone Actate 60 mg/wk.Serological assessments werecompleted prior to initiation of anabolictherapy, twice during the 6 week drugsession and at five and 13 weeksfollowing discontinuance of drug use.The results of these tests are recordedin the table below. Also recorded wereany subjective side effects noted by theathlete.DiscussionUrea values were elevated throughoutthe entire study period. This was likelydue to the high protein intake of the athlete and not necessarily attributed to any degree of renaldysfunction.34 Creatinine, also a kidney function test, was elevated throughout most of the study with theexception of 13 weeks post drug use.Creatinine excretion was consistent in a given time period and was proportional to the increased amountof muscle mass acquired by the subject. Table 2 reveals a steady increase in creatinine excretion fromthe non*drug use state to the high point of drug consumption and then steadily diminished thereafter. Thisseemed logical since the athlete acquired muscle mass in proportion to the creatinine increase. Thesubject trained little from the day of competition to the 13 week post period and hence lost approximately10 pounds of muscle mass which was reflected by diminishing creatinine levels.Bilirubin remained normal throughout the study suggesting undisturbed liver bilirubin metabolism. Totalprotein and albumin changes, in this study, were also unremarkable.
Creatinine phosphakinase (CPK) determinationswere highly elevated throughout the drug use periodbut decreased markedly in both the non*training andnon*drug use periods. The elevated titres of CPKwere attributed to muscle damage induced bysevere exercise 35'34 (4*5 hours daily) and to theintramuscular injections administered by the subject.During the pre*steroid phase, CPK titres were lowerthan both the 3 week and 5 week drug stages. Anelevation of 301 IU/L of CPK from the pre*steroid tothe 5 week steroid stage was likely the result of theintramuscular injections since the intensity oftraining did not appreciably alter during these stagesof the study.The non*specific liver function tests (LFT's), ASTand ALT, maintained higher than normal valuesthroughout the entire study. Note, these values wereelevated prior to anabolic therapy initiation. This wasnot surprising since both AST and ALT are found inskeletal muscle and are released into the serumwhen muscle damage is increased. This isexplained in a manner similar to that of CPK elevation. Strauss et al studied 32 weightlifters of which 20were using oral anabolics while the remaining 12 were not. The steroid subjects demonstrated ALT levelsgreater than normal and AST values on the high side of normal. The 12 individuals not using steroids,demonstrated ALT and AST levels virtually identical to those using the steroids.Another study conducted by Hogermant et all of 5 weightlifters, 3 of which were taking steroids and 2 whowere not, determined that all five lifters displayed elevated AST and LDH levels while ALT and ALP werenormal. The studies suggest that intense weight training alone, can elevate non*specific LFT's.At the peak of drug use, AST and ALT levels reached 98 and 137 IU/L, respectively. This could arisesecondarily to the increased drug consumption at this stage of the study and/or to the change to the oralforms of steroids, namely Oxandrolone ( see below).This specific drug, of course, has been associated with higher incidences of hepatotoxicity than theparenteral forms. Another hypothesis suggests that the elevation of LFT's is due to skeletal musclebreakdown rather than any hepatic dysfunction.There are two aspects which reinforce this conjecture. One proposes that these elevations parallel thoseof CPK which reflects muscle damage due to exercise and intramuscular injections. Secondly, the specificLFT, especially alkaline phosphatase, remained within normal parameters throughout αthe entire study,even on the lower side of normal. It appears likely that a combination of all the above exists and that thelatter factor, muscle breakdown, plays the largest role in the elevation of non*specific LFT's.Total LDH levels were monitored and since this enzyme is found in skeletal muscle as well, it is notsurprising that these changes parallel those of CPK. Haupt and Rovere suggest that measurement of thehepatic fractionation of LDH is a useful specific LFT. Biochemical analysis during this study did not includeLDH fractionation, as such LDH was considered as a non*specific liver function test.Both cholesterol and triglycerides (TG) levels were unremarkable throughout the study.Urinalysis was similarly unremarkable.
ConclusionIn view of the measured results in this isolated case study, it was considered that the only noteworthyalterations in blood chemistry were CPK, AST, ALT, and LDH. It was also felt thatno pathophysiological processes were occurring with respect to liver dysfunction and that elevated nonspecificLFT's were more a product of muscle breakdown induced by severe exercise and byintramuscular injection.Case presentation IIIn 2012 a 37*year*old male professional bodybuilder witha body height of 180 cm and a body weight of 118 kgpresented himself with increasing epigastric andabdominal pain to an outside department of hepatology.That are impressive figures other professionalbodybuilders with an height of 5′ 11″ (180 cm) and an offseason weight of 260 lb (118 kg) are Lee Haney and MilošŠarčev.For a period of at least five years he has been consumingthe following AASs in a daily medication schedule:Testosterone propionate, testosterone phenylpropionate,testosterone isocaproate, testosterone decanoate 250mg(Sustanon)Trenbolone acetate 75mg5alpha*androstanediol 100 mg (dihydrotestosterone (DHT) prohormone)Boldenone and Methandriol dipropionate 240 mg (Drive or Overdrive)Stanozolol 100 mg,Oxandrolone 4×10 mg,Letrozole 0,065 mg,Oxymetholone 3 × 50 mg or Methandienone 10 mg.Oxymetholone or Methandienone was discontinued three weeks beforecompetition. In addition, he took Spironolactone 100 mg, Mesterolone 25mg, Fluoxymesterone 10 mg four weeks, and Torasemide eighteen hoursbefore competition. Furthermore, a daily intake of amino acid, vitamins,and mineral tablets, T4 (200 μg), and growth hormones (8 I.E.) was reported.The nutritional protocol consisted of six small, protein*rich meals (chicken breast, fish, protein shakes,salad, vegetable, etc.), a high caloric and high protein*containing diet to build up muscle mass. Eightweeks before competition, the meals and consequently the caloric intake were reduced by 50% to reducesubcutaneous fat.Torasemide, a diuretic, was taken to achieve a more muscular bodily contour by reducing extracellularand subcutaneous tissue volume.The physical examination of the professional bodybuilder revealed an athletic appearance with enhancedmuscular contour. A mild tenderness in the right upper abdominal quadrant was found. Any history of alcohol consumption or smoking was denied. A hepatic lesion was discovered by abdominal ultrasound. Itappeared as a predominantly hyperechoic lesion in the right lobe of the liver. The magnetic resonanceimaging showed a hepatomegaly and confirmed the lesion which showed features of a hepatocellularadenoma[The dark patch below left.]. The patient was transferred to the Department of Visceral Surgery,University of Cologne for a laparoscopic resection of the suspected HCA.If steroids users develop liver tumours thenthey usually have hepatocellular adenoma:benign swellings that do not spread throughthe rest of the body. Nevertheless manydoctors think it's a good idea to remove theswellings because they may start to bleed orcould change into a more malignant form oftumour: hepatocellular carcinoma.Hepatocellular carcinoma is liver cancer.This form of cancer is most common amongalcoholics, but very rare among steroidsusers. That's why doctors at UniversityHospital of Cologne were surprised whenthey found hepatocellular carcinoma in thisbodybuilder.The doctors in Cologne decided to operate on the man. They removed the part of the liver where thetumour was located; the tumour itself measured 6 x 5 x 5 cm. In the lab they discovered that it washepatocellular carcinoma that the man had developed.In the literature the doctors only found 7 cases of bodybuilders who had developed hepatocellularcarcinoma as a result of steroids use. The chance of steroids users developing this form of cancer istherefore small, but not zero."Bodybuilders who abuse anabolic androgen steroids over a long period of time have a risk of developingan hepatocellular adenoma or hepatocellular carcinoma and should therefore be well monitored", thedoctors write. "Periodic hepatic ultrasound seems to be an adequate screening procedure to detect thedevelopment of hepatic lesions.""Although most of the tumors developing by anabolic androgenic steroids misuse or intake are benign,early detection is important in order to avoid the associated risk of malignant transformation and lifethreateninghemorrhages", they continue. "In these cases a surgical excision is recommended."Fortunately the bodybuilder in the study recovered. Just seven days after his operation the doctors senthim home and when they examined him 27 months later he was completely healthy.OxandroloneA growing number of reports about abuse of anabolic androgen steroids in Western Europe and the USAby competitive and noncompetitive bodybuilders is reported in the literature. A correlation between AASuse and hepatocellular adenoma has been increasingly recognized in athletes taking AAS. While danazolis associated with hepatocellular adenoma formation, other preparations like oxymetholone, respectively,methyltestosterone can lead to hepatocellular carcinoma. In addition to other synthetical androgenicsteroids, the 37 year old bodybuilder in the case study above consumed the prospective carcinogenicoxymetholone (50mg) three times a day.There is one reported case of a steroid induced hepatic tumor in an athlete resulted in his death. Thiswas a male bodybuilder who succumbed to hepatocellular carcinoma and hepatic cholangiocarcinoma. The athlete employed both oral and parenteralcompounds for four years preceding his deathincluding; Methandrostenolone (oral), Oxandrolone(oral), Stanozol (oral), Methenolone andNandrolone Decanoate (administeredintramuscularly).This individual utilized the 17*alpha alkyl derivativesof testosterone for a protracted period of time, aswas the case with almost all of the other reportedinstances of hepatic tumors attributed to the use of anabolic steroids. It is significant to note thatOxymetholone (Anadrol) was the preparation most frequently associated with the incidences ofboth peliosis hepatis and hepatic carcinoma.It will be clear by now but, … extended use of high doses of oral anabolic steroids can cause liver tumorsor hepatocellular adenoma. We might call this 'liver cancer', but doctors would not use this term here.Real liver cancer, in which liver cells mutate into cancer cells, is even more rare among steroids usersthan hepatocellular adenoma. But it does happen, report doctors at the University Hospital of Cologne.Cholestasis, peliosis hepatis and liver tumours, are the possible consequences of steroid use for the liver.Cholestasis is a condition whereby the liver can no longer remove waste products via the bile to theintestines. Faeces become grey, skin colour yellow, you start to itch and if you don't receive treatmentquickly your liver tissue starts to die off.Peliosis hepatis is a condition in which blood filled cavities form in the liver. It was probably the cause ofdeath of Andreas Muenzer. Doctors don't yet know how peliosis hepatis arises, but they do know how totreat the problem: you just need to remove the cause. If Andreas Muenzer had stopped taking steroids intime he could very well still be alive today – and his liver would have recovered.What we can do is ..if you want to use oral steroids as a kickstarter for your cycle or in the cut, don’tcombine it with recreational drugs, oral medication, alcohol.
