I agree. The worst cycle I ever ran was one with a designer oral that I got for free. Had me puking my guts up.
MESO-Rx
Anabolic Steroids
Anabolic Steroids & Liver [GI]
- Thread starter Michael Scally MD
- Start date
Jimmyinkedup
New Member
Thanks for sharing your experience man. I am a firm believer in UDCA as well although I do not think enough can be said for eating like you are and h2o intake as well. I think that those 2 things can prob and do prob have a profound effect on liver health.
UDCA literally has worked for me on 2 occasions where my normal protocol failed in keeping my liver enzymes within a range where I was comfortable with the #'s. Both times with no changes other than the addition of UDCA within 2 weeks my numbers were back where i felt comfortable with them.
Again thanks for sharing your real world experience.
thehogsters
Member
IMO tudca works. I ran msten a few years back at 32MG per day for 32 days. I ran it with lgi damage control. It has tudca in it but not enough to work. My liver was shot. Dark urine, light poop, and lethargy like none other. One year latter I ran dmz at 50mg for 42 days. I used Aegis (twice the amount of tudca) for my support. Not one problem during the cycle. I did not drink on either cycle. I would think 50mg of dmz would be of equal toxicity as 32MG of msten?
bigpoppachump
New Member
Dark urine and light poop is not really a good indicator of liver issues lol. I pissed fine and had some brown ass shit when my enzymes were 1000+ lmao
thehogsters
Member
How about the lethargy? It was so bad I felt like I was hung over tired, all the time. Of course my point is not very valid since I did run two different compounds. I think that msten over 20mg is like rat poison.
bigpoppachump
New Member
Orals without test in general give most folks lethargy. A fucked up liver is more like the flue with nausea,diarrhea, aches pains, brain fog, irritable to no end, the list goes on and on. Lethargy can be caused by a bunch of different shit, no testosterone, estrogen to low to high and on and on
Tahernejad Z, Baghshani H, Rashidlamir A. Blood biochemical and oxidant/antioxidant alterations following stanozolol treatment along with resistance training in rats. Andrologia. Blood biochemical and oxidant/antioxidant alterations following stanozolol treatment along with resistance training in rats - Tahernejad - 2016 - Andrologia - Wiley Online Library
This study was designed to determine the effects of anabolic steroid stanozolol (ST) in conjunction with 8 weeks of resistance training on some blood biochemical and oxidant/antioxidant profile in rats.
Twenty-four male rats were divided into four groups of six each:
group 1: sedentary + placebo (physiological saline),
group 2: training + placebo,
group 3: training + ST (2 mg kg−1 b.w.) and
group 4: training + ST (5 mg kg−1 b.w.).
Erythrocytic activity of glutathione peroxidase was increased significantly in group 4 as compared to control group.
Plasma activities of alanine aminotransferase in groups 3 and 4 and also aspartate aminotransferase in group 4 showed significant increase relative to groups 1 and 2.
Moreover, alkaline phosphatase and creatine kinase activities increased significantly in groups 3 and 4 in comparison with control group.
Elevated values of uric acid were significant in group 4, but not in groups 2 and 3, as compared to control group.
Values of other measured parameters did not have significant alterations among experimental groups.
Present findings indicate that stanozolol treatment in combination with resistance training induces some side effects especially on liver and muscle as evidenced by alterations in plasma markers of tissue damage.
This study was designed to determine the effects of anabolic steroid stanozolol (ST) in conjunction with 8 weeks of resistance training on some blood biochemical and oxidant/antioxidant profile in rats.
Twenty-four male rats were divided into four groups of six each:
group 1: sedentary + placebo (physiological saline),
group 2: training + placebo,
group 3: training + ST (2 mg kg−1 b.w.) and
group 4: training + ST (5 mg kg−1 b.w.).
Erythrocytic activity of glutathione peroxidase was increased significantly in group 4 as compared to control group.
Plasma activities of alanine aminotransferase in groups 3 and 4 and also aspartate aminotransferase in group 4 showed significant increase relative to groups 1 and 2.
Moreover, alkaline phosphatase and creatine kinase activities increased significantly in groups 3 and 4 in comparison with control group.
Elevated values of uric acid were significant in group 4, but not in groups 2 and 3, as compared to control group.
Values of other measured parameters did not have significant alterations among experimental groups.
Present findings indicate that stanozolol treatment in combination with resistance training induces some side effects especially on liver and muscle as evidenced by alterations in plasma markers of tissue damage.
BCmonster
New Member
Why does everyone have such a boner for orals. Stick to the long ester injectables and build some real muscle. Everyone using gear should be supplementing with organ products. I was experiencing dark urine after I used Anadrol a year or so ago and I ran two full months of Rich Pianos organ product and it was actually really good stuff, I felt alot better and my piss was looking really healthy in no time.
Im with you on the orals man... i dont get why soomany "need" to have a damn oral in their cycle. i run most of my cycles without orals now and avoid them.
long term health and gains = injectables IMO.
ill use a little var or dbol in future possibly, but thats because i have some to use up, i dont even look at buying orals anymore.
plus it kills my appetite so...
I can vouch for TUDCA also, took it towards the end and during pct from a pretty harsh PH cycle and it worked wonders. Although, I got bad heartburn while taking it, not sure if that was from some sort of enzymes or the PH still in my system or what but it was pretty gnarly. Also, plain cold clean water is king and IMO the most satisfying beverage in existence.
Bond P, Llewellyn W, Van Mol P. Anabolic androgenic steroid-induced hepatotoxicity. Med Hypotheses 2016;93:150-3. http://www.medical-hypotheses.com/article/S0306-9877(16)30215-8/abstract
Anabolic androgenic steroids (AAS) have been abused for decades by both professional and amateur athletes in order to improve physical performance or muscle mass. AAS abuse can cause adverse effects, among which are hepatotoxic effects. These effects include cholestatic icterus and possibly peliosis hepatis and hepatocellular carcinoma or adenoma. In particular, 17alpha-alkylated AAS appear to be hepatotoxic, whereas nonalkylated AAS appear not to be. The 17alpha-alkyl substitution retards hepatic metabolism of the AAS rendering it orally bioavailable. The mechanism responsible for the hepatotoxicity induced by 17alpha-alkylated AAS remains poorly understood. However, oxidative stress has been repeatedly shown to be associated with it. In this manuscript we present a hypothesis which describes a potential mechanism responsible for AAS-induced hepatotoxicity, based on several observations from the literature which suggest oxidative stress being a causal factor.
Anabolic androgenic steroids (AAS) have been abused for decades by both professional and amateur athletes in order to improve physical performance or muscle mass. AAS abuse can cause adverse effects, among which are hepatotoxic effects. These effects include cholestatic icterus and possibly peliosis hepatis and hepatocellular carcinoma or adenoma. In particular, 17alpha-alkylated AAS appear to be hepatotoxic, whereas nonalkylated AAS appear not to be. The 17alpha-alkyl substitution retards hepatic metabolism of the AAS rendering it orally bioavailable. The mechanism responsible for the hepatotoxicity induced by 17alpha-alkylated AAS remains poorly understood. However, oxidative stress has been repeatedly shown to be associated with it. In this manuscript we present a hypothesis which describes a potential mechanism responsible for AAS-induced hepatotoxicity, based on several observations from the literature which suggest oxidative stress being a causal factor.
For Jim and Scally:
Theoretically speaking, if LFT values remain within normal levels or are only slightly elevated by the AAS can one determine the use as practically safe?
Some people dose orals for beyond the golden rule of 4 to 6 weeks, but at lighter doses.
Theoretically speaking, if LFT values remain within normal levels or are only slightly elevated by the AAS can one determine the use as practically safe?
Some people dose orals for beyond the golden rule of 4 to 6 weeks, but at lighter doses.
A Silent Liver Disease Epidemic
http://cen.acs.org/articles/94/i39/silent-liver-disease-epidemic.html
For most people, the acronym NASH won’t ring any bells. But NASH, or nonalcoholic steatohepatitis, is stealthily showing up in the livers of millions of Americans. Marked by the accumulation of an unhealthy amount of fat and scar tissue in the liver, NASH is quietly reaching epidemic proportions across the globe.
By 2020, NASH is projected to overtake hepatitis C as the leading cause of liver transplants in the U.S. The disease is poised to win that dubious honor because an alarming rise in obesity and type-2 diabetes—key risk factors for NASH—is coinciding with far better treatments for hepatitis C.
Despite NASH’s prevalence, its obscurity isn’t surprising: It doesn’t cause obvious symptoms in most people, there’s no simple test to detect it, and no drugs have been approved to treat it.
Within the next five years, that could change.
…
http://cen.acs.org/articles/94/i39/silent-liver-disease-epidemic.html
For most people, the acronym NASH won’t ring any bells. But NASH, or nonalcoholic steatohepatitis, is stealthily showing up in the livers of millions of Americans. Marked by the accumulation of an unhealthy amount of fat and scar tissue in the liver, NASH is quietly reaching epidemic proportions across the globe.
By 2020, NASH is projected to overtake hepatitis C as the leading cause of liver transplants in the U.S. The disease is poised to win that dubious honor because an alarming rise in obesity and type-2 diabetes—key risk factors for NASH—is coinciding with far better treatments for hepatitis C.
Despite NASH’s prevalence, its obscurity isn’t surprising: It doesn’t cause obvious symptoms in most people, there’s no simple test to detect it, and no drugs have been approved to treat it.
Within the next five years, that could change.
…
LMAO
[OA] The Diagnosis and Manifestations of Liver Injury Secondary to Off-Label Androgenic Anabolic Steroid Use
Drug-induced liver injury (DILI) presents as a broad spectrum of adverse drug reactions which can range from a mild elevation in liver enzymes to fulminant liver failure. The primary goal is to identify DILI early when the patient's liver enzymes are elevated and to discontinue the offending agent as soon as possible to prevent further injury.
Herbal, dietary supplements and anabolic steroids represent a significant component of the drugs thought to cause DILI in the United States. Unlike all other drugs known to cause DILI, these drugs fall into a category of injury that is neither intrinsic nor idiosyncratic due to overlapping characteristics between the two.
Here, we present a case of the off-label use of androgenic anabolic steroids inducing liver injury. A combination of clinical, laboratory, and histologic workup eventually led to the diagnosis of DILI. This can be a diagnostic challenge for practitioners.
The American College of Gastroenterology (ACG) published guidelines to aid the clinician in diagnosing DILI. Proving that an episode of liver injury is caused by a drug is difficult in many cases as it requires the exclusion of alternative etiologies.
Some of the variables include temporal association, clinical-biochemical features, type of injury (hepatocellular and/or cholestatic), extrahepatic features, and the likelihood that a given agent is the culprit based on its known manifestations with prior cases.
This case illustrates the utility of the diagnostic tools used for DILI as recommended by the ACG, along with a supplemental histopathologic diagnosis.
Cabb E, Baltar S, Powers DW, Mohan K, Martinez A, Pitts E. The Diagnosis and Manifestations of Liver Injury Secondary to Off-Label Androgenic Anabolic Steroid Use. Case Rep Gastroenterol 2016;10(2):499-505. http://www.karger.com/Article/FullText/448883
An Algorithm To Evaluate Suspected Idiosyncratic DILI.
The R value cutoff numbers of 2 and 5 only serve as a guideline. Tests ordered must be based on the overall clinical picture, including risk factors for competing diagnosis [e.g., recent travel to hepatitis E virus (HEV) endemic area], associated symptoms (e.g., abdominal pain, fever), and timing of laboratory tests (i.e., the R value may change as the DILI evolves) [1].
ALT = Alanine aminotransferase;
Alk P = alkaline phosphatase;
CMV = cytomegalovirus;
EBV = Epstein-Barr virus;
HCV = hepatitis C virus;
HSV = herpes simplex virus;
MR = magnetic resonance;
ULN = upper limit of normal.
Drug-induced liver injury (DILI) presents as a broad spectrum of adverse drug reactions which can range from a mild elevation in liver enzymes to fulminant liver failure. The primary goal is to identify DILI early when the patient's liver enzymes are elevated and to discontinue the offending agent as soon as possible to prevent further injury.
Herbal, dietary supplements and anabolic steroids represent a significant component of the drugs thought to cause DILI in the United States. Unlike all other drugs known to cause DILI, these drugs fall into a category of injury that is neither intrinsic nor idiosyncratic due to overlapping characteristics between the two.
Here, we present a case of the off-label use of androgenic anabolic steroids inducing liver injury. A combination of clinical, laboratory, and histologic workup eventually led to the diagnosis of DILI. This can be a diagnostic challenge for practitioners.
The American College of Gastroenterology (ACG) published guidelines to aid the clinician in diagnosing DILI. Proving that an episode of liver injury is caused by a drug is difficult in many cases as it requires the exclusion of alternative etiologies.
Some of the variables include temporal association, clinical-biochemical features, type of injury (hepatocellular and/or cholestatic), extrahepatic features, and the likelihood that a given agent is the culprit based on its known manifestations with prior cases.
This case illustrates the utility of the diagnostic tools used for DILI as recommended by the ACG, along with a supplemental histopathologic diagnosis.
Cabb E, Baltar S, Powers DW, Mohan K, Martinez A, Pitts E. The Diagnosis and Manifestations of Liver Injury Secondary to Off-Label Androgenic Anabolic Steroid Use. Case Rep Gastroenterol 2016;10(2):499-505. http://www.karger.com/Article/FullText/448883
An Algorithm To Evaluate Suspected Idiosyncratic DILI.
The R value cutoff numbers of 2 and 5 only serve as a guideline. Tests ordered must be based on the overall clinical picture, including risk factors for competing diagnosis [e.g., recent travel to hepatitis E virus (HEV) endemic area], associated symptoms (e.g., abdominal pain, fever), and timing of laboratory tests (i.e., the R value may change as the DILI evolves) [1].
ALT = Alanine aminotransferase;
Alk P = alkaline phosphatase;
CMV = cytomegalovirus;
EBV = Epstein-Barr virus;
HCV = hepatitis C virus;
HSV = herpes simplex virus;
MR = magnetic resonance;
ULN = upper limit of normal.
Diaz FC, Saez-Gonzalez E, Benlloch S, et al. Albumin dialysis with MARS for the treatment of anabolic steroid-induced cholestasis. Ann Hepatol 2016;15(6):939-43. Albumin dialysis with MARS for the treatment of anabolic steroid-induced cholestasis. - PubMed - NCBI
BACKGROUND AND AIMS. Steroid-related hepatotoxicity has become one of the most relevant causes of drug induced liver cholestasis. Some patients do not improve after standard medical treatment (SMT) and may therefore require other approaches, like extracorporeal liver support.
MATERIAL AND METHODS: We report four cases of patients with pruritus, abnormal liver function tests and biopsy-proven anabolic steroid-induced cholestasis who were unresponsive to SMT. They underwent treatment with albumin dialysis (Molecular Adsorbent Recirculating System -MARS(R)-). A minimum of two MARS sessions were performed.
RESULTS: After MARS(R) procedure, patients' symptoms improved, as well as liver function tests, thus avoiding liver transplantation.
CONCLUSION: Albumin dialysis appears as a valuable therapeutic option for the management of anabolic steroid-induced cholestasis in patients that are unresponsive to SMT.
BACKGROUND AND AIMS. Steroid-related hepatotoxicity has become one of the most relevant causes of drug induced liver cholestasis. Some patients do not improve after standard medical treatment (SMT) and may therefore require other approaches, like extracorporeal liver support.
MATERIAL AND METHODS: We report four cases of patients with pruritus, abnormal liver function tests and biopsy-proven anabolic steroid-induced cholestasis who were unresponsive to SMT. They underwent treatment with albumin dialysis (Molecular Adsorbent Recirculating System -MARS(R)-). A minimum of two MARS sessions were performed.
RESULTS: After MARS(R) procedure, patients' symptoms improved, as well as liver function tests, thus avoiding liver transplantation.
CONCLUSION: Albumin dialysis appears as a valuable therapeutic option for the management of anabolic steroid-induced cholestasis in patients that are unresponsive to SMT.
Liane BJ, Magee C. Guerilla Warfare on the Pancreas? A Case of Acute Pancreatitis From a Supplement Known to Contain Anabolic-Androgenic Steroids. Mil Med 2016;181(10):e1395-e7. Military Medicine - International Journal of AMSUS
INTRODUCTION: Performance-enhancing drugs (PEDs) are commonly consumed in the United States with high prevalence of use in athlete populations and increased use by deployed service members. Many PEDs may contain anabolic-androgenic steroids (AAS), which are legally restricted and prohibited by many agencies due to their health risk.
CASE DESCRIPTION: A unique case of acute pancreatitis associated with the use of the PED "Guerilla Warfare," a labeled AAS-containing supplement, is presented. The patient is a healthy 20-year-old male Marine who presented with multiple episodes of abdominal cramps each day for a month with decreased appetite and nonbilious vomiting. He reported a 6-week history of "Guerilla Warfare" PED use and review of systems identified fatigue and 12 lb reported weight loss. He presented with normal vital signs, tenderness in upper abdominal quadrants, elevated lipase (909 units/L), lactate dehydrogenase (193 units/L), and an enlarged pancreas with surrounding inflammation on computed tomography.
SUMMARY: This constitutes the first report of acute pancreatitis with the use of "Guerilla Warfare," and the second reported case with the use of any AAS-containing PED. Increased awareness of significant PED-associated adverse effects by both the civilian and military communities is needed to better characterize these risks moving forward.
INTRODUCTION: Performance-enhancing drugs (PEDs) are commonly consumed in the United States with high prevalence of use in athlete populations and increased use by deployed service members. Many PEDs may contain anabolic-androgenic steroids (AAS), which are legally restricted and prohibited by many agencies due to their health risk.
CASE DESCRIPTION: A unique case of acute pancreatitis associated with the use of the PED "Guerilla Warfare," a labeled AAS-containing supplement, is presented. The patient is a healthy 20-year-old male Marine who presented with multiple episodes of abdominal cramps each day for a month with decreased appetite and nonbilious vomiting. He reported a 6-week history of "Guerilla Warfare" PED use and review of systems identified fatigue and 12 lb reported weight loss. He presented with normal vital signs, tenderness in upper abdominal quadrants, elevated lipase (909 units/L), lactate dehydrogenase (193 units/L), and an enlarged pancreas with surrounding inflammation on computed tomography.
SUMMARY: This constitutes the first report of acute pancreatitis with the use of "Guerilla Warfare," and the second reported case with the use of any AAS-containing PED. Increased awareness of significant PED-associated adverse effects by both the civilian and military communities is needed to better characterize these risks moving forward.
Ed Plucker
New Member
Why anyone would use prohormones is beyond me. If you want to use performance enhancement drugs, use injectable anabolic steroids. They work so much better than orals and have no virtually liver toxicity. I know a lot of bros are afraid of needles but if you want to juice you had better suck it up and learn how to inject. Your liver and kidneys are pretty irreplaceable.
I know I'm a lightweight compared to most here, but I run a 12 wk orals-only cycle (which includes a 4 wk NO ORALS, mini-PCT break in the middle) with 50mg Var and 30-40 mg Winny. I use an assload of milk thistle stand. extract coupled with my Liv-52 (a must), before, during and after....but I try to take my liver protectants at least 4 hours before OR after my orals, bcuz I've heard a couple bros at my gym say it might limit my gains. But I never personally experienced that before, so who knows. But better safe then sorry.
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