hello dr scally
what is the best form to protect my liver with a steroid cycle....as anadrol,dianabol,winsstrol oral...
thanks
what is the best form to protect my liver with a steroid cycle....as anadrol,dianabol,winsstrol oral...
thanks
MESO-Rx
Anabolic Steroids
Michael scally liver suggestion
- Thread starter gilmarpersonal
- Start date
Monitoring. There are NO supplements to decrease, prevent, eliminate, etc. liver changes.
cvictorg
New Member
Don't use them!!
Pericles
New Member
Liver protectors are a scam. The only way to do so, is to limit intake of things that can harm the liver, like alcohol.
Of course, oral steroids can also cause liver damage, if you take too much too long. That is why the base of any good cycle is inject-able, preferably testosterone. I personally never run orals for more than 4-5 weeks.
I entered into an agreement w/ LE, I stopped drinking, and they stopped arresting me, and it has worked for more than 23 years.
Of course, oral steroids can also cause liver damage, if you take too much too long. That is why the base of any good cycle is inject-able, preferably testosterone. I personally never run orals for more than 4-5 weeks.
I entered into an agreement w/ LE, I stopped drinking, and they stopped arresting me, and it has worked for more than 23 years.
Sounds better than the deal I got with my future ex wife. I stopped listening, but she didn't stop nagging.
Back to the topic.
Does this mean it's not worth the effort to take UDCA / NAC / SAM-e etc.? I take NAC year round for about a quarter a day.
For liver protection, WORTHLESS. If it makes you "feel" better, it's your money.
Jimmyinkedup
New Member
So Dr Scally you do not see the proven increase in bile flow and expedited removal of toxic bile salts that both UDCA and NAC induce beneficial given the primary issue that oral aas (and other hepa toxic oral substances as well) is cholestasis?
Candyskull
New Member
Proven by who?
Code:
http://www.mdpi.com/1422-0067/13/7/8882/pdfYou mean like this study here that had to be halted due to UDCA causing and accelerating hepatitis?
UDCA failed in controlling liver histology, or symptoms, in a dose of 13–15 mg/kg/day [191,192]. In a higher dose of 28–30 mg/kg/day, UDCA resulted in more than double fold increase in patient deaths, and need for liver transplantation. There is an exceptionally narrow difference between recommended dose and detrimental dose of UDCA in primary sclerosing cholangitis [13,26]
Meta-analyses of four randomized clinical trials randomizing 279 patients could not find significant differences regarding mortality or improvement in liver function tests observed after treatment with UDCA. Data on the radiological and histological responses were too scant to draw any definite conclusions [208]. High dose UDCA failed to improve the overall histology in 185 patients with NASH in comparison with placebo [209].
UDCA, is of unproven effectiveness in cholestasis, acute or chronic liver disease, colorectal carcinoma, and has specific molecular toxicity. It freezes regeneration and induces cellular hibernation. No case control double blind trial has demonstrated its true curative effects in any liver disease.
Despite high hopes and tremendous expenditure, space and chance for UDCA to effect, it does not go beyond “cellular freezing”, and arrest of cellular regeneration.
Edit- formatting.
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Jimmyinkedup
New Member
UDCA:
Ursodeoxycholic acid in cholestasis: linking... [Clin Sci (Lond). 2011] - PubMed - NCBI
Drug insight: Mechanism... [Nat Clin Pract Gastroenterol Hepatol. 2006] - PubMed - NCBI
[Long-term ursodeoxycholic acid treatme... [Klin Padiatr. 1996 May-Jun] - PubMed - NCBI
NAC:
Antifibrotic and antioxidant eff... [Eur J Gastroenterol Hepatol. 2012] - PubMed - NCBI
Acute cholestasis-induced renal failure: effects ... [Kidney Int. 1999] - PubMed - NCBI
Both;
New therapeutic option with N-acetylcysteine for p... [Am J Ther. 2011] - PubMed - NCBI
Im not claiming to know all or even any of the answers here but it is in black and white several credible places. I want Dr Scallys input and opinion on this. I have long looked to him for insight when it comes to such matters and honestly was a bit surprised at his response here but as always respect his opinion.
Ursodeoxycholic acid in cholestasis: linking... [Clin Sci (Lond). 2011] - PubMed - NCBI
Drug insight: Mechanism... [Nat Clin Pract Gastroenterol Hepatol. 2006] - PubMed - NCBI
[Long-term ursodeoxycholic acid treatme... [Klin Padiatr. 1996 May-Jun] - PubMed - NCBI
NAC:
Antifibrotic and antioxidant eff... [Eur J Gastroenterol Hepatol. 2012] - PubMed - NCBI
Acute cholestasis-induced renal failure: effects ... [Kidney Int. 1999] - PubMed - NCBI
Both;
New therapeutic option with N-acetylcysteine for p... [Am J Ther. 2011] - PubMed - NCBI
Im not claiming to know all or even any of the answers here but it is in black and white several credible places. I want Dr Scallys input and opinion on this. I have long looked to him for insight when it comes to such matters and honestly was a bit surprised at his response here but as always respect his opinion.
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Pericles
New Member
Sorry for the hijack, but I have been meaning to ask Doc about the women in Italy.
Raider72
New Member
Correct me if I am wrong (very possible) but don't a lot of the touted "liver protector" supps actually cause potential harm to the liver?? Also, from what I have read water is that one of the best liver helps, a lot of water? I personally like to mix cranberry/water (about 30/70 ratio) to help. I Eliminate alcohol, soda & lower sugar/salt intake. Maybe all worthless too but a lot cheaper then all the supps touted to help liver detox. I have milk thistle but not sold on how well it works if at all. My doc said one of the worst things for the liver is Niacin supps.
Unless the studies are done in well conducted trails in humans, the results for the most part are moot. This is by far the error (purposefully mostly) for 'bro "science." And, that is being kind.
Tackling a long-standing disconnect between animal and human studies, some charge that animal researchers need stricter safeguards and better statistics to ensure their science is solid.
For years, researchers, pharmaceutical companies, drug regulators, and even the general public have lamented how rarely therapies that cure animals do much of anything for humans. Much attention has focused on whether mice with different diseases accurately reflect what happens in sick people.
Others suggest there's another equally acute problem. Many animal studies are poorly done, they say, and if conducted with greater rigor they'd be a much more reliable predictor of human biology.
It's hard to generalize, of course: Animal studies cut across a massive swath of biology, tracking everything from the activity of single molecules in a healthy organ to side effects of a new drug poised for human testing.
And many who stake their careers on animal studies conduct them with care, judiciously weighing how to structure their experiments and chasing the science wherever their furry subjects take it.
That said, even animal research that has a big effect on human drug studies is governed by far fewer standards than clinical trials in people. There, volunteers are randomly assigned by computer to get a new drug or a placebo. Those running a trial are often blinded to who's in what category, preventing clinicians invested in a therapy's success from imagining hints of efficacy in patients they know are getting a new drug.
And look up any clinical trial seeking volunteers and you'll see a long list of "inclusion" and "exclusion" criteria governing who can participate. If you have high blood pressure or if your cancer is being treated with a certain drug, you might be out of luck.
Animal studies rarely follow these rules. For ethical and cost reasons, researchers try to use as few animals as possible, which can mean minuscule sample sizes. Unblinded, unrandomized studies are the norm. "The way we do our research with our animals is stone-age."
From various quarters, there's pressure to change that. High-profile studies showing that preclinical results often cannot be reproduced are driving funders and researchers to seek solutions—as much to mend their public image as to guarantee sound science.
Couzin-Frankel J. When Mice Mislead. Science 2013;342(6161):922-5. When Mice Mislead
Tackling a long-standing disconnect between animal and human studies, some charge that animal researchers need stricter safeguards and better statistics to ensure their science is solid.
For years, researchers, pharmaceutical companies, drug regulators, and even the general public have lamented how rarely therapies that cure animals do much of anything for humans. Much attention has focused on whether mice with different diseases accurately reflect what happens in sick people.
Others suggest there's another equally acute problem. Many animal studies are poorly done, they say, and if conducted with greater rigor they'd be a much more reliable predictor of human biology.
It's hard to generalize, of course: Animal studies cut across a massive swath of biology, tracking everything from the activity of single molecules in a healthy organ to side effects of a new drug poised for human testing.
And many who stake their careers on animal studies conduct them with care, judiciously weighing how to structure their experiments and chasing the science wherever their furry subjects take it.
That said, even animal research that has a big effect on human drug studies is governed by far fewer standards than clinical trials in people. There, volunteers are randomly assigned by computer to get a new drug or a placebo. Those running a trial are often blinded to who's in what category, preventing clinicians invested in a therapy's success from imagining hints of efficacy in patients they know are getting a new drug.
And look up any clinical trial seeking volunteers and you'll see a long list of "inclusion" and "exclusion" criteria governing who can participate. If you have high blood pressure or if your cancer is being treated with a certain drug, you might be out of luck.
Animal studies rarely follow these rules. For ethical and cost reasons, researchers try to use as few animals as possible, which can mean minuscule sample sizes. Unblinded, unrandomized studies are the norm. "The way we do our research with our animals is stone-age."
From various quarters, there's pressure to change that. High-profile studies showing that preclinical results often cannot be reproduced are driving funders and researchers to seek solutions—as much to mend their public image as to guarantee sound science.
Couzin-Frankel J. When Mice Mislead. Science 2013;342(6161):922-5. When Mice Mislead
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Jimmyinkedup
New Member
BMC Surgery | Full text | The effect of ursodeoxycholic acid in liver functional restoration of patients with obstructive jaundice after endoscopic treatment: a prospective, randomized, and controlled study
In many studies, it was shown the positive effect of UDCA administration in patient with cholestatic liver desease.
The hypothesis of this trial is that patients with obstructive jaundice, in which will be administered UDCA, in the early phase after endoscopic intervention will have better and faster functional restoration of the liver than patients in the control group.
Dr Scally Im confused because then there is a bunch of info like the above available. IS it too soon to say you think or u really believe despite studies like this supps like UDCA are useless for the liver?
In many studies, it was shown the positive effect of UDCA administration in patient with cholestatic liver desease.
The hypothesis of this trial is that patients with obstructive jaundice, in which will be administered UDCA, in the early phase after endoscopic intervention will have better and faster functional restoration of the liver than patients in the control group.
Dr Scally Im confused because then there is a bunch of info like the above available. IS it too soon to say you think or u really believe despite studies like this supps like UDCA are useless for the liver?
There is no need for confusion. Apparently, the clinical trial you reference is also at odds on the benefit. In these cases, there is some evidence for benefit.
In aggregate, the data suggest that ursodeoxycholic acid (UDCA) for the treatment of primary biliary cirrhosis (PBC) is associated with improvement in liver biochemical tests, a reduction in disease progression, and possibly transplant-free survival.
Several additional conclusions can be made from these data:
•UDCA appears to be more effective in patients with early disease.
•Patients with advanced PBC and complications of portal hypertension (eg, ascites or variceal bleeding) do not benefit from UDCA. Such patients should be considered for liver transplantation.
The thread is aimed at AAS induced liver changes, NOT obstructive jaundice or PBC. For AAS induced changes, I am unable to find any benefit as well as direct clinical experience showing none.
Again, I caution is translating study findings to those for AAS. This is by far the most common error in AAS forums.
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Jimmyinkedup
New Member
Gotcha. Am I incorrect in my line of thinking that cholestasis is one the primary downfalls and contributing factors towards aas incuded liver damage? Or even that improving it may improve liver health and function? Thats a large portion my general belief I hang my contentions on when it comes to these 2 particular supps --so that would make a big diff in how i potentially view them. I know we cant always get studies done with patients on aas with the particular issue or taking the particular compound we want info on. I however dont think its imprudent not to 100% dismiss like symptomology and outcome post administration said compound when its effects appear to lower one of the primary contributing factors in liver damage period .
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Pericles
New Member
Bla Bla Bla UDCA, Bla Bla Milk Thistle, Blah: Lets try and get back to the important question I posed: Are Italian chicks hotter than American?
Come on Doc, get your priorities straight!
Nice concise summary of the studies however. So many researchers use 300 words to say what could be said in 50:
"The thread is aimed at AAS induced liver changes, NOT obstructive jaundice or PBC. For AAS induced changes, I am unable to find any benefit as well as direct clinical experience showing none".
Again, I caution is translating study findings to those for AAS. This is by far the most common error in AAS forums.
Come on Doc, get your priorities straight!
Nice concise summary of the studies however. So many researchers use 300 words to say what could be said in 50:
"The thread is aimed at AAS induced liver changes, NOT obstructive jaundice or PBC. For AAS induced changes, I am unable to find any benefit as well as direct clinical experience showing none".
Again, I caution is translating study findings to those for AAS. This is by far the most common error in AAS forums.
It seems you are talking prophylactic or preventative treatment. I know of no studies for such a use. From numerous posts, this is a common reason for use. [Along this line, DeTox is no more than a scam.]
In very rare cases and I mean very very rare, there have been reports of AAS induced cholestasis. In fact, I posted on a case recently. Might this be effective? In that case, the treatment was discontinuation.
conquistador
New Member
Anabolic-androgenic steroids and liver injury. [Liver Int. 2008] - PubMed - NCBI
for a breakdown of the study: Ursodeoxycholic acid restores anabolic liver
Liver injury due to oral anabolic use typically manifests itself as cholestasis.
Hepatotoxicity induced by oral anabolic compounds tends to be characterized by enlargement of periportal hepatocytes, impairment of bile flow & dramatically increased serum levels of AST, ALT and GGT. In other words, cholestasis... but let's examine this a little bit further.
The word "cholestasis" gets thrown around a lot, but it can mean two very different things: The physical obstruction of hepatic bile flow -or- the impairment of bile secretion. In the former case, there is a mechanical block in the bile duct system; in the latter, bile is held in hepatocytes or cholangiocytes as it cannot be secreted. In both cases, what happens thereafter is that the retained hydrophobic bile salts -- which are strongly cytotoxic -- lead to cellular injury, then apoptosis, then necrosis, often followed by an inflammatory reaction and tissue fibrosis. This tissue damage, if advanced enough, can physically destroy bile ducts, worsening the condition.
The obstruction of bile flow is typically not something you'd experience after exposure to any toxin; it is the almost exclusive domain of inherited or autoimmune diseases which leave fibrotic lesions or scar-tissue in the liver, such as cystic fibrosis, primary biliary cirrhosis, and so on. Exposure to oral anabolic compounds can, however, result in the second form of cholestasis -- bile retention in hepatocytes -- thus the enlarged hepatocytes observed after their use.
3. There are three fundamental ways of preventing/treating cholestasis:
1. Metabolic induction of hydrophobic bile acid detoxification
2. Stimulation of impaired bile secretion
3. Protection of hepatocytes from the toxic effects of hydrophobic bile acids and/or inhibition of hepatocyte apoptosis.
Cholestatic liver damage is caused by bile acid accumulation... But not all bile acids are toxic. Generally speaking, the fewer hydroxyl groups they bear, the more hydrophobic and cytotoxic they are. Hence lithocholic acid is markedly cytotoxic, deoxycholic acid is very slightly cytotoxic, and cholic acid is essentially non-cytotoxic. Treatment #1 would involve hastening the metabolic conversion of the more toxic bile acids to hydrophilic, less toxic compounds --- or increasing the synthesis of hydrophilic bile acids from cholesterol, which would decrease the cytotoxicity of the entire bile pool as a whole. This can seemingly be achieved with the oral administration of ursodeoxycholic acid (UDCA), which has been reported to activate the PXR/SXR nuclear receptor in hepatocytes, which then activates bile acid–metabolizing enzymes. It is reasonable to assume that Tauroursodeoxycholic acid (TUDCA), the taurine conjugate of UDCA, should have the same effect.
As for #2... Bile secretion at the level of the hepatocyte is carried out by a group of transporter proteins: The bile salt export pump (BSEP), the phospholipid export pump (MDR3), the canalicular bilirubin conjugate export pump (MRP2), and a chloride-bicarbonate anion exchanger (AE2) for bicarbonate excretion. BSEP is the driving factor behind bile-acid dependent secretion, and MRP2/AE2 are the major forces behind bile-acid-independent bile secretion. Hydrophilic bile acids such as UDCA & TUDCA (and even, partially, cholic acid) have been shown to increase expression of BSEP mRNA; they activate BSEP coactivators by binding to the Farnesoid X Receptor (the "bile acid receptor"); they phosphorylate the BSEP protein via a Ca+/PKCa-mediated mechanism; lastly, they stimulate Cl -/HCO3 - exchange via this same PKCa induction, thus increasing AE2 levels.
Taken together, the above effects drastically enhance secretion of potentially toxic bile acids.
#3 can be complicated, but I will explain briefly: Certain toxic bile salts activate the Fas Death Receptor on hepatocytes. This leads to a cascade of dozens of protein interactions & ultimately to cell death. TUDCA, UDCA, and certain other compounds can diminish Fas–induced apoptosis, but, as far as I am aware, the exact mechanism is not known at this time. Fas activation here is not ligand-dependent, so the 'obvious' mechanism is out the window. The mechanism could, however, involve activation of the EGFR, which activates MAPK & the MAPK-mediated 'survival pathway' in hepatocytes; it might also involve inhibition, somewhere along the line, of the proapoptotic proteins Bax and Bid.
taken from: http://antaeuslabs.blogspot.com/2011/07/few-words-on-hepatotoxicity-of-17a.html
conquistador
New Member
Take the dang UDCA/TUDCA. That's what I would do. At the end of the day, you're still gonna take the steroids, right? Right. So be proactive about minimizing liver damage. I don't see what's the problem. Unless you're shitting your money on herbal supplements with no bioavailability. Liv-52, Milk thistle...what a fucking joke.
Candyskull
New Member
And the studies that show UDCA just masking liver damage without actually preventing/reversing it, and in some cases accelerating it? Honestly the stuff kind of scares me.
My liver is a champ so I don't sweat it that much, but I really feel like the best coarse of action is just minimizing intake, and if you're the type of person who's liver enzymes hit the roof with orals; you should probably just jab all your juice. There's always TNE.
