Then your on the wrong forum fella bc if you use AAS long enough COMPLICATIONS WILL OCCUR!
MESO-Rx
Anabolic Steroids
Anabolic Steroids & Liver [GI]
- Thread starter Michael Scally MD
- Start date
Then your on the wrong forum fella bc if you use AAS long enough COMPLICATIONS WILL OCCUR!
Hoping with the 2 on 4 off cycle I can avoid that... am I fooling myself?
BigNick002
New Member
Which PEDs are you referring to here? and why are they the safest? thanks
Well all oral agents are hepatotoxic, however the sixth line should read: …… unless you have some unknown predisposition to hepatic injury even oral agents do NOT cause much more than a doubling or tripling of Liver Function Tests. (unless you are a chronic, high end user)
(The point being, IF marked changes in LFT's occur while using UGL products the chances are what your using is in fact a "designer AAS" rather than LEGIT Var or A-drol)
(The point being, IF marked changes in LFT's occur while using UGL products the chances are what your using is in fact a "designer AAS" rather than LEGIT Var or A-drol)
BigNick002
New Member
What I meant was when you said, "FINALLY NOOBS should always err on the side of caution and use those PEDs which are the safest and most reliable based on existing evidence, IMO" Which are safest and most reliable based on existing evidence??
And doubling or tripling liver function isnt harmful for a few weeks at a time?
berniec
New Member
orals are bad as we all know but in moderation and with an otherwise healthy lifestyle using gear isnt anything that should be an issue. I'm on TRT and get bloods done a few times a year by my doc that include liver tests and they always are well within range, even just after i've come off a blast cycle
Bill Roberts wrote the following:
all liver values were normal (although CPK was not checked this time). That is despite the use of oral 17-alkylated anabolics: 20 mg/day each of Dianabol and oxandrolone. This I think is attributable to the dosing pattern of use only in the morning, a protocol I learned from a certain Greek physician.
https://thinksteroids.com/articles/two-week-steroid-cycle-case-study-update/
So this raises some questions for me as I've always heard it's best to split your dbol doses morning and night so as to keep blood levels constant. Is this not the best practice afterall? Is it worth the flucuating blood levels to spare the liver? I'd like to understand this more.
all liver values were normal (although CPK was not checked this time). That is despite the use of oral 17-alkylated anabolics: 20 mg/day each of Dianabol and oxandrolone. This I think is attributable to the dosing pattern of use only in the morning, a protocol I learned from a certain Greek physician.
https://thinksteroids.com/articles/two-week-steroid-cycle-case-study-update/
So this raises some questions for me as I've always heard it's best to split your dbol doses morning and night so as to keep blood levels constant. Is this not the best practice afterall? Is it worth the flucuating blood levels to spare the liver? I'd like to understand this more.
atxwarpig
New Member
I got pretty damn jacked off them oral ph's. I know most people don't see good results from them, but I lift everyday, and I've exercised my whole life, besides periods of extreme injuries.
High school and college age kids are popping them like candy. It's making steroids have a farther reach in society. It's legal, easy to get, and people you would never think take steroids probably have tried them.
Shits really dangerous too.
High school and college age kids are popping them like candy. It's making steroids have a farther reach in society. It's legal, easy to get, and people you would never think take steroids probably have tried them.
Shits really dangerous too.
Robles-Diaz M, Gonzalez-Jimenez A, Medina-Caliz I, et al. Distinct phenotype of hepatotoxicity associated with illicit use of anabolic androgenic steroids. Aliment Pharmacol Ther. http://onlinelibrary.wiley.com/doi/10.1111/apt.13023/full
BACKGROUND: We have observed an increase in hepatotoxicity (DILI) reporting related to the use of anabolic androgenic steroids (AAS) for bodybuilding.
AIM: To characterise phenotype presentation, outcome and severity of AAS DILI.
METHODS: Data on 25 cases of AAS DILI reported to the Spanish (20) and Latin-American (5) DILI Registries were collated and compared with previously published cases.
RESULTS: AAS DILI increased from representing less than 1% of the total cases in the Spanish DILI Registry in the period 2001-2009 to 8% in 2010-2013. Young men (mean age 32 years), requiring hospitalisation, hepatocellular injury and jaundice were predominating features among the AAS cases. AAS DILI caused significantly higher bilirubin values independent of type of damage when compared to other drug classes (P = 0.001).
Furthermore, the cholestatic AAS cases presented significantly higher mean peak bilirubin (P = 0.029) and serum creatinine values (P = 0.0002), compared to the hepatocellular cases. In a logistic regression model, the interaction between peak bilirubin values and cholestatic damage was associated with the development of AAS-induced acute kidney impairment (AKI) [OR 1.26 (95% CI: 1.035-1.526); P = 0.021], with 21.5 xULN being the best bilirubin cut-off point for predicting AKI risk (AUCROC 0.92). No fatalities occurred.
CONCLUSIONS: Illicit recreational AAS use is a growing cause of reported DILI that can lead to severe hepatic and renal injury. AAS DILI is associated with a distinct phenotype, characterised by considerable bilirubin elevations independent of type of damage. Although hepatocellular injury predominates, acute kidney injury develops in cholestatic cases with pronounced jaundice.
BACKGROUND: We have observed an increase in hepatotoxicity (DILI) reporting related to the use of anabolic androgenic steroids (AAS) for bodybuilding.
AIM: To characterise phenotype presentation, outcome and severity of AAS DILI.
METHODS: Data on 25 cases of AAS DILI reported to the Spanish (20) and Latin-American (5) DILI Registries were collated and compared with previously published cases.
RESULTS: AAS DILI increased from representing less than 1% of the total cases in the Spanish DILI Registry in the period 2001-2009 to 8% in 2010-2013. Young men (mean age 32 years), requiring hospitalisation, hepatocellular injury and jaundice were predominating features among the AAS cases. AAS DILI caused significantly higher bilirubin values independent of type of damage when compared to other drug classes (P = 0.001).
Furthermore, the cholestatic AAS cases presented significantly higher mean peak bilirubin (P = 0.029) and serum creatinine values (P = 0.0002), compared to the hepatocellular cases. In a logistic regression model, the interaction between peak bilirubin values and cholestatic damage was associated with the development of AAS-induced acute kidney impairment (AKI) [OR 1.26 (95% CI: 1.035-1.526); P = 0.021], with 21.5 xULN being the best bilirubin cut-off point for predicting AKI risk (AUCROC 0.92). No fatalities occurred.
CONCLUSIONS: Illicit recreational AAS use is a growing cause of reported DILI that can lead to severe hepatic and renal injury. AAS DILI is associated with a distinct phenotype, characterised by considerable bilirubin elevations independent of type of damage. Although hepatocellular injury predominates, acute kidney injury develops in cholestatic cases with pronounced jaundice.
Anabolicbrah
New Member
What sort of complications are we talking here say we cycle for about 3 years with sane dosages. There isn't really any information on the long term effects of AAS. I believe orals should be avoided but what about test only cycles. Tren seems to be unsafe.
I got 50 pills of 20mg of t bol, i got 50 pills of 20mg winny, i got 50 pills of 50.mg anadrol what do i do? Do i stack ? How many mgs per day? Im new to it allnim over weight and havent worked out in a year and im trying to get back on it
reishi mushroom and the liver:
http://www.worldscientific.com/doi/abs/10.1142/S0192415X01000526
http://www.worldscientific.com/doi/abs/10.1142/S0192415X01000526
Intercept Pharmaceuticals Inc (NASDAQ:ICPT)
http://www.interceptpharma.com/
Accelerated Path in NASH Appears Alive — A recently accepted manuscript coauthored by the FDA points to an accelerated pathway in NASH on endpoints OCA
has already shown benefit and could lessen the Street’s regulatory concerns for this
program. We view the acknowledgment of review by high level FDA officials
important in weighing the interpretation of messages in the document. We expect
an update on OCA’s Ph3 NASH trial design in the next 1-2 months that will confirm
the path for the drug and potentially transform the company’s value proposition.
Clinical Need Appears Recognized — The manuscript highlights the need to
develop therapeutics for NASH patients, and contribution of NASH to the burden of
chronic liver disease. We include a table of comments from the report we believe
are important and relevant to OCA, covering approval pathways, potential surrogate
endpoints, and views on safety and risk mitigation.
OCA Shown Benefit in Main Reference Surrogate Endpoint — The manuscript
suggests the strongest support for an approvable surrogate endpoint of prevention
of progression to cirrhosis. In the Ph 2 FLINT trial, OCA showed convincing
evidence of benefit here and broader reversal of fibrosis in patients. Additionally, the authors highlight the importance of addressing the metabolic drivers of NASH and not solely hitting fibrosis.
CV Risk Highlighted, but Detailed Lipids Considered — Commentary about CV
risk balanced. While the manuscript did note importance of not raising CV risk, an
included table indicated this assessment will be based on detailed lipid profiles and
not LDL-C alone. Based on our analysis of OCA mechanism on atherogenic lipid in
NASH, we expect OCA could ultimately provide a net benefit in CV risk. Also the
manuscript points to the utility of Data monitoring Committees in monitoring safety,
while there were no comments around CV outcomes trials.
Next NASH Update for ICPT — We continue to expect ICPT to announce the
outcome of meeting with the FDA regarding the Ph 3 NASH trial design in the next
month. The company continues to appear confident in starting the Ph 3 trial during
the 1H:15.
Sanyal AJ, Friedman SL, McCullough AJ, Dimick L. Challenges and opportunities in drug and biomarker development for nonalcoholic steatohepatitis: Findings and recommendations from an American Association For The Study Of Liver Diseases (AASLD) - Food and Drug Administration (FDA) Joint Workshop. Hepatology. http://onlinelibrary.wiley.com/doi/10.1002/hep.27678/abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in North America. It is a growing contributor to the burden of chronic liver disease requiring liver transplantation. Cirrhosis is also associated with an increased risk of hepatocellular cancer which may occur even in the absence of cirrhosis in subjects with nonalcoholic steatohepatitis (NASH) the histological form of NAFLD associated with increased liver-related mortality. The diagnosis of NASH currently requires a liver biopsy. There are also no FDA-approved therapies for NASH. There is therefore a need to develop better diagnostic and therapeutic strategies for patients with NASH targeting both those with early stage disease as well as those with advanced liver fibrosis. There are unique challenges in the design of studies for these target populations. The long relatively asymptomatic time interval in the progression of NAFLD and NASH to cirrhosis and ultimately liver failure, along with gaps in knowledge regarding disease modifiers combine to present significant challenges in trial design. There is therefore an urgent need to develop methods to identify the populations at particular risk of disease progression and to validate endpoints that reflect meaningful changes in health status in this population.
This manuscript summarizes the discussion at a joint workshop held September 5th and 6th, 2013, in Silver Spring, Maryland, sponsored by the FDA and the AASLD to develop guidance on diagnostic and therapeutic modalities for NASH.
http://www.interceptpharma.com/
Accelerated Path in NASH Appears Alive — A recently accepted manuscript coauthored by the FDA points to an accelerated pathway in NASH on endpoints OCA
has already shown benefit and could lessen the Street’s regulatory concerns for this
program. We view the acknowledgment of review by high level FDA officials
important in weighing the interpretation of messages in the document. We expect
an update on OCA’s Ph3 NASH trial design in the next 1-2 months that will confirm
the path for the drug and potentially transform the company’s value proposition.
Clinical Need Appears Recognized — The manuscript highlights the need to
develop therapeutics for NASH patients, and contribution of NASH to the burden of
chronic liver disease. We include a table of comments from the report we believe
are important and relevant to OCA, covering approval pathways, potential surrogate
endpoints, and views on safety and risk mitigation.
OCA Shown Benefit in Main Reference Surrogate Endpoint — The manuscript
suggests the strongest support for an approvable surrogate endpoint of prevention
of progression to cirrhosis. In the Ph 2 FLINT trial, OCA showed convincing
evidence of benefit here and broader reversal of fibrosis in patients. Additionally, the authors highlight the importance of addressing the metabolic drivers of NASH and not solely hitting fibrosis.
CV Risk Highlighted, but Detailed Lipids Considered — Commentary about CV
risk balanced. While the manuscript did note importance of not raising CV risk, an
included table indicated this assessment will be based on detailed lipid profiles and
not LDL-C alone. Based on our analysis of OCA mechanism on atherogenic lipid in
NASH, we expect OCA could ultimately provide a net benefit in CV risk. Also the
manuscript points to the utility of Data monitoring Committees in monitoring safety,
while there were no comments around CV outcomes trials.
Next NASH Update for ICPT — We continue to expect ICPT to announce the
outcome of meeting with the FDA regarding the Ph 3 NASH trial design in the next
month. The company continues to appear confident in starting the Ph 3 trial during
the 1H:15.
Sanyal AJ, Friedman SL, McCullough AJ, Dimick L. Challenges and opportunities in drug and biomarker development for nonalcoholic steatohepatitis: Findings and recommendations from an American Association For The Study Of Liver Diseases (AASLD) - Food and Drug Administration (FDA) Joint Workshop. Hepatology. http://onlinelibrary.wiley.com/doi/10.1002/hep.27678/abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in North America. It is a growing contributor to the burden of chronic liver disease requiring liver transplantation. Cirrhosis is also associated with an increased risk of hepatocellular cancer which may occur even in the absence of cirrhosis in subjects with nonalcoholic steatohepatitis (NASH) the histological form of NAFLD associated with increased liver-related mortality. The diagnosis of NASH currently requires a liver biopsy. There are also no FDA-approved therapies for NASH. There is therefore a need to develop better diagnostic and therapeutic strategies for patients with NASH targeting both those with early stage disease as well as those with advanced liver fibrosis. There are unique challenges in the design of studies for these target populations. The long relatively asymptomatic time interval in the progression of NAFLD and NASH to cirrhosis and ultimately liver failure, along with gaps in knowledge regarding disease modifiers combine to present significant challenges in trial design. There is therefore an urgent need to develop methods to identify the populations at particular risk of disease progression and to validate endpoints that reflect meaningful changes in health status in this population.
This manuscript summarizes the discussion at a joint workshop held September 5th and 6th, 2013, in Silver Spring, Maryland, sponsored by the FDA and the AASLD to develop guidance on diagnostic and therapeutic modalities for NASH.
An ayurvedic herbal combination has been studied for the treatment of cirrhosis, but current evidence supporting its use remains incomplete and contradictory. http://www.med.nyu.edu/content?ChunkIID=21393
Mendal JN, Roy BK. Studies with Liv.52 in the treatment of infective hepatitis, chronic active hepatitis and cirrhosis of the liver. Probe . 1983;22:217.
Huseini HF, Alavian SM, Heshmat R, et al. The efficacy of Liv-52 on liver cirrhotic patients: a randomized, double-blind, placebo-controlled first approach. Phytomedicine. 2005;12:619-624. http://himalayawellness.com/pdf_files/liv260.pdf
de Silva HA, Saparamadu PA, Thabrew MI, Pathmeswaran A, Fonseka MM, de Silva HJ. Liv.52 in alcoholic liver disease: a prospective, controlled trial. J Ethnopharmacol 2003;84(1):47-50. https://www.sciencedirect.com/science/article/pii/S0378874102002635
Liv.52, a hepatoprotective agent of herbal origin, is used empirically for the treatment of alcoholic liver disease in Sri Lanka. We conducted a controlled trial to assess the efficacy of Liv.52 in patients with alcoholic liver disease. Patients with evidence of alcoholic liver disease attending outpatient clinics were included in a prospective, double blind, randomized, placebo controlled trial. During the trial period, 80 patients who fulfilled inclusion criteria were randomly assigned Liv.52 (cases; n = 40) or placebo (controls) the recommended dose of three capsules twice daily for 6 months. All patients underwent clinical examination (for which a clinical score was computed), and laboratory investigations for routine blood chemistry and liver function before commencement of therapy (baseline). Thereafter, clinical assessments were done monthly for 6 months, while laboratory investigations were done after 1 and 6 months of therapy. There was no significant difference in the age composition, alcohol intake and baseline liver function between the two groups. The two-sample t-test was used to analyze data obtained after 1 and 6 months of therapy against baseline values. There was no significant difference in clinical outcome and liver chemistry between the two groups at any time point. There were no reports of adverse effects attributable to the drug. Our results suggest that Liv.52 may not be useful in the management of patients with alcohol induced liver disease.
Mendal JN, Roy BK. Studies with Liv.52 in the treatment of infective hepatitis, chronic active hepatitis and cirrhosis of the liver. Probe . 1983;22:217.
Huseini HF, Alavian SM, Heshmat R, et al. The efficacy of Liv-52 on liver cirrhotic patients: a randomized, double-blind, placebo-controlled first approach. Phytomedicine. 2005;12:619-624. http://himalayawellness.com/pdf_files/liv260.pdf
de Silva HA, Saparamadu PA, Thabrew MI, Pathmeswaran A, Fonseka MM, de Silva HJ. Liv.52 in alcoholic liver disease: a prospective, controlled trial. J Ethnopharmacol 2003;84(1):47-50. https://www.sciencedirect.com/science/article/pii/S0378874102002635
Liv.52, a hepatoprotective agent of herbal origin, is used empirically for the treatment of alcoholic liver disease in Sri Lanka. We conducted a controlled trial to assess the efficacy of Liv.52 in patients with alcoholic liver disease. Patients with evidence of alcoholic liver disease attending outpatient clinics were included in a prospective, double blind, randomized, placebo controlled trial. During the trial period, 80 patients who fulfilled inclusion criteria were randomly assigned Liv.52 (cases; n = 40) or placebo (controls) the recommended dose of three capsules twice daily for 6 months. All patients underwent clinical examination (for which a clinical score was computed), and laboratory investigations for routine blood chemistry and liver function before commencement of therapy (baseline). Thereafter, clinical assessments were done monthly for 6 months, while laboratory investigations were done after 1 and 6 months of therapy. There was no significant difference in the age composition, alcohol intake and baseline liver function between the two groups. The two-sample t-test was used to analyze data obtained after 1 and 6 months of therapy against baseline values. There was no significant difference in clinical outcome and liver chemistry between the two groups at any time point. There were no reports of adverse effects attributable to the drug. Our results suggest that Liv.52 may not be useful in the management of patients with alcohol induced liver disease.
Qureshi K, Sarwar U, Khallafi H. Severe Aplastic Anemia following Acute Hepatitis from Toxic Liver Injury: Literature Review and Case Report of a Successful Outcome. Case Reports Hepatol. 2014:216570. http://www.hindawi.com/journals/crihep/2014/216570/
Hepatitis associated aplastic anemia (HAAA) is a rare syndrome in which severe aplastic anemia (SAA) complicates the recovery of acute hepatitis (AH). HAAA is described to occur with AH caused by viral infections and also with idiopathic cases of AH and no clear etiology of liver injury.
Clinically, AH can be mild to fulminant and transient to persistent and precedes the onset SAA. It is assumed that immunologic dysregulation following AH leads to the development of SAA.
Several observations have been made to elucidate the immune mediated injury mechanisms, ensuing from liver injury and progressing to trigger bone marrow failure with the involvement of activated lymphocytes and severe T-cell imbalance.
HAAA has a very poor outcome and often requires bone marrow transplant (BMT). The findings of immune related myeloid injury implied the use of immunosuppressive therapy (IST) and led to improved survival from HAAA.
We report a case of young male who presented with AH resulting from the intake of muscle building protein supplements and anabolic steroids. The liver injury slowly resolved with supportive care and after 4 months of attack of AH, he developed SAA. He was treated with IST with successful outcome without the need for a BMT.
Hepatitis associated aplastic anemia (HAAA) is a rare syndrome in which severe aplastic anemia (SAA) complicates the recovery of acute hepatitis (AH). HAAA is described to occur with AH caused by viral infections and also with idiopathic cases of AH and no clear etiology of liver injury.
Clinically, AH can be mild to fulminant and transient to persistent and precedes the onset SAA. It is assumed that immunologic dysregulation following AH leads to the development of SAA.
Several observations have been made to elucidate the immune mediated injury mechanisms, ensuing from liver injury and progressing to trigger bone marrow failure with the involvement of activated lymphocytes and severe T-cell imbalance.
HAAA has a very poor outcome and often requires bone marrow transplant (BMT). The findings of immune related myeloid injury implied the use of immunosuppressive therapy (IST) and led to improved survival from HAAA.
We report a case of young male who presented with AH resulting from the intake of muscle building protein supplements and anabolic steroids. The liver injury slowly resolved with supportive care and after 4 months of attack of AH, he developed SAA. He was treated with IST with successful outcome without the need for a BMT.
Volley_Fire
New Member
Cristina RT, Hanganu F, Brezovan D, et al. Cytoarchitecture of steroid dependent target tissues after testosterone administration compared to nandrolone decanoate in castrated rats in the aim of Hershberger bio test. Rom J Morphol Embryol 2014;55(3 Suppl):1143-8. http://www.rjme.ro/RJME/resources/files/55131411431148.pdf
The objective was the cytoarchitecture evaluation of known steroid dependent target tissues after administering of testosterone, compared to action of its more active ester, nortestosterone (nandrolone decanoate) in castrated rat males in the aim of Hershberger bio test.
Study was performed on 30 castrated male Wistar rats, aged between 35 and 39 days, in peripubertal period, divided into five groups. Androgen doses administration begun at the rats' age of 49 days. Animals were injected i.m., daily, for 10 consecutive days as follows: Aquatest (Balkan Pharmaceuticals Ltd., Moldova) testosterone aqueous solution: Testosterone I group (0.4 mg/animal); Testosterone II (0.8 mg/animal); (Deca-Durabolin, Balkan Pharmaceuticals); nandrolone decanoate oily solution: Nortestosterone I (1.5 mg/kg body weight); Nortestosterone II (7.5 mg/kg body weight) and Control (White sesame oil, Manicos, Romania, 0.1 mL/animal).
Gonadectomy (GDX) induced modifications of target tissues wet weight accompanied by important modifications in cytoarchitecture. Changes following exogenous administration of testosterone and nortestosterone decanoate were found in: liver (granular dystrophy, mega-mitochondria, tubular intumescences), prostate (increasing of the structural elements), seminal vesicles (hyalinosis, thickening of cell walls and the hyaline presence), levator ani-bulbo-cavernosus muscle (muscle fibbers dilacerations), bulbourethral glands (muscular fibbers rarefaction by fluid accumulation) demonstrating the disruptor activity especially for overdosed nandrolone decanoate.
The objective was the cytoarchitecture evaluation of known steroid dependent target tissues after administering of testosterone, compared to action of its more active ester, nortestosterone (nandrolone decanoate) in castrated rat males in the aim of Hershberger bio test.
Study was performed on 30 castrated male Wistar rats, aged between 35 and 39 days, in peripubertal period, divided into five groups. Androgen doses administration begun at the rats' age of 49 days. Animals were injected i.m., daily, for 10 consecutive days as follows: Aquatest (Balkan Pharmaceuticals Ltd., Moldova) testosterone aqueous solution: Testosterone I group (0.4 mg/animal); Testosterone II (0.8 mg/animal); (Deca-Durabolin, Balkan Pharmaceuticals); nandrolone decanoate oily solution: Nortestosterone I (1.5 mg/kg body weight); Nortestosterone II (7.5 mg/kg body weight) and Control (White sesame oil, Manicos, Romania, 0.1 mL/animal).
Gonadectomy (GDX) induced modifications of target tissues wet weight accompanied by important modifications in cytoarchitecture. Changes following exogenous administration of testosterone and nortestosterone decanoate were found in: liver (granular dystrophy, mega-mitochondria, tubular intumescences), prostate (increasing of the structural elements), seminal vesicles (hyalinosis, thickening of cell walls and the hyaline presence), levator ani-bulbo-cavernosus muscle (muscle fibbers dilacerations), bulbourethral glands (muscular fibbers rarefaction by fluid accumulation) demonstrating the disruptor activity especially for overdosed nandrolone decanoate.
Waste of money.
Volley_Fire
New Member
So do any hepatoprotective agents exist that may reduce or prevent liver damage from AAS? My perspective is: an ounce of prevention is worth a pound of cure....
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