Again, who said I didnt weigh the risks? Not me, and no where in my post did I say that. I did my research at the time I ran it. I know that there are risks associated with taking any sort of compound, some of which are unknown....but my point is now that based on feedback of what others have experienced it makes me think twice, I don't understand why that is seen as so unlogical or so wrong....I didnt experince any of it, so it just makes me think more if I will thats all
so if you say that I made a huge mistake jumping into a compound without weighing the risk (which i didnt't), I would agree thats foolish if someone does......on the flip side I will say its a big mistake for one to assume that all the risks & side effects of a compound are "on the table" within a few months of a brand new compound being rolled out.
I dont miss your point bro I get it, ....however my point contradicts your point, so we will not see eye to eye on this and thats ok..
MY son took superdrol for a month, and he is now in the hospital very sick, with liver damage, we did not really know why he was so sick, he is very yellow with Jandice and serious issues, just like CW Anderson had. I found a website, and low and behold the Superdrol is the cause, here is the article PLEASE IF YOU ARE TAKING THIS STOP NOW>>>>>>>>>>> A 23-yr-old Hispanic male bodybuilder without any known past medical history presented at the Maricopa Medical Center (MMC) with a 2-wk complaint of nausea, vomiting, decreased appetite, jaundice, RUQ a**ominal pain, pale stools, dark urine, and itching. Two months before the onset of his clinical symptoms, he had started using an OTC nutritional supplement for bodybuilders named anabolic extreme (superdrol) having methasteron as its active ingredient. He consumed 72 10-mg pills of superdrol, starting at one tablet daily for 2 wk followed by two tablets daily. He did not exceed the maximal suggested dose of 126 pills (10 mg each) that was recommended over a 6-wk period. He stopped using superdrol with the onset of diffuse skin itching. He did not report any history of alcohol, recreational drugs, or tobacco use. There was no family history of liver disease. He did not have any drug allergies.
On physical examination, his vital signs were stable. He was deeply icteric with several scratch marks noted throughout the trunk and lower extremities. He was overweight with a BMI of 28. The a**omen was slightly tender in the right upper quadrant with no evidence of ascites, hepatosplen*****ly, or a Murphy's sign.
At presentation, labs revealed a total bilirubin of 36.2 g/dL, an AST of 57 U/L, ALT of 93 U/L, alkaline phosphatase of 224 U/L, total protein of 9.1 g/dL (6.3–8.2), and IgG of 669 mg/dL (751—1,560). The hepatitis viral antibodies including HAV-IgM, HB core-IgM, HBS-AG, HBV core-AB IgG, HIV-1 AB, HDV-AG as well as HCV-RNA, and HBV-DNA by polymerase chain reaction were negative. The ceruloplasmin was 76 mg/dL. Smooth muscle, antinuclear, myeloperoxidase, and LKM antibodies were negative. Alpha-fetoprotein was normal. A hepatitis A IgG-AB was positive. A 24-h urinary copper was 166 μg/dL. A urinalysis did not reveal proteinuria or hematuria. The rest of his lab reports are summarized in Table.
The patient was hospitalized for one day and discharged on oral ursodeoxycholic acid at 600 mg twice daily and hydroxyzine at 25 mg three times daily to be used as needed for pruritus. Two weeks later, he presented to the hospital because of vomiting and unrelenting skin itching. He was hypertensive with a blood pressure of 189/86 mmHg, and the use of metoprolol at a dose of 50 mg twice daily normalized his blood pressure.
A liver biopsy showed features of marked intrahepatic cholestasis, mild portal inflammation consisting predominantly of lymphocytes, foci of lobular inflammation with balloon degeneration, mild Kupffer cell iron deposition and pericellular fibrosis. There was no evidence of granulomas, peliosis, hepatic rosettes, portal fibrosis, or bile duct injury (Fig. 1). The hepatic iron index was 1.19. An a**ominal ultrasound showed mild liver enlargement at 18 cm. The gallbladder and bile duct were normal. The kidneys were slightly echogenic. The CT scan of the a**omen with IV and oral contrast did not show any liver lesion, ascites, or biliary obstruction. A kidney biopsy showed interstitial edema containing a mild lymphohistiocytic infiltrate with numerous esoinophils. An immunofluoresecence stain showed diffuse granular mesangial staining for IgA (2+) (Fig. 2). After 1 wk of hospitalization, the patient was discharged and readmitted 4 days later because of rectal bleeding and a hemoglobin level of 7.9 gm/dL with an MCV of 89 fL. The upper and lower gastrointestinal endoscopies did not reveal any varices. After receiving 2 units of packed red blood cells, his hemoglobin increased to 9.4 g/dL and he was discharged home. Two wk later, he followed up in the outpatient clinic, feeling better without any itching and near-normalization of his lab reports including both kidney and liver function.