Vewi's picture
Vewi
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+ 7 Liver protection: Reminder If taking Orals in a Cycle (and general health)

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I see a lot of Orals being taken but I never see anything about how people are protecting their Liver.

Milk Thistle--protect the liver from toxins--you should always be using Milk Thistle when you are taking orals. However, once your done with your orals stop taking Milk Thistle 2 weeks after.

LIV52--Supports a Healthy liver, and protects it from toxins, this is something you should be taking year round for a healthy liver.

Alpha Lipoic Acid-- is a powerful antioxidant that supports healthy liver function.(spinach, broccoli, and potatoes are good sources of alpha-lipoic acid.) helps prevent certain kinds of cell damage in the body, and also restores vitamin levels such as vitamin E and vitamin C. Another thing is Alpha-lipoic acid is used in the body to break down carbohydrates and to make energy for the other organs in the body.

Vitamin C--- in particular plays a big role in liver health. Vitamin C can repair the liver following disease, or toxin Vitamin C is also proven to flush fat from the liver.

Foods--Spinach, Kiwi and asparagus are great sources for Liver aid and function.

thekaz's picture

not mine, taken from jake over @ ironmagz. great writeup none the less.

A few words on the hepatotoxicity of 17a-methylated androgens/anabolics

  1. 17a-methylated androgens/anabolics are hepatotoxic.
    The liver toxicity of steroids is an under-researched field, but there seems to be a strong correlation between how easily the body can metabolize a steroid & its toxicity. Metribolone -- a truly excessively toxic compound -- is often referred to in the literature as a 'non-metabolizable androgen'. (1, 2, 3, etc.) Mibolerone, another deadly-toxic anabolic steroid, is also effectively 'non-metabolizable': The main metabolite of mibolerone in humans is... unchanged mibolerone. And by a very wide margin.

Methylstenbolone, which is resistant to 17b-HSD and 3b-HSD, is obviously difficult for the body to clear. It should therefore be no safer, no less toxic, than Superdrol or M1T -- compounds which share very similar traits.

  1. 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.

  1. There are three fundamental ways of preventing/treating cholestasis:

Metabolic induction of hydrophobic bile acid detoxification
Stimulation of impaired bile secretion
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.

  1. Recommendations
    I strongly recommend TUDCA or UDCA to anybody considering a cycle containing oral androgens, for what should by now be obvious reasons. They are extremely potent at preventing or reversing 17aa-androgen-mediated liver damage. There's really no excuse not to take them, in my opinion, and I would advise you not to run a cycle if you can't afford them. Oral androgens can send you straight to the ER if the right precautions are not taken, & your health is much more important than a few more pounds of here-today-gone-tomorrow muscle.

Silymarin and silybin, the milk thistle extracts, are very strong antioxidants and free-radical scavengers in hepatic tissue. They impede hepatic lipid peroxidation, increase glutathione concentrations, and even have anti-inflammatory and tissue-regenerative properties... Other plant-extracted compounds, such as celastrol, have similar effects... But while these extracts are excellent to take for general liver health, they are weak protection and not an appropriate treatment for cholestasis, as they do not appear to impact bile acid secretion/metabolism at pharmacologically-relevant doses. Silymarin did increase bile secretion and improve bile acid metabolism in rats -- but that effect was primarily noticed at a dose of 100mg/kg, administered via i.p. injection (100% bioavailability), and therefore doesn't have much bearing on humans who take much smaller amounts orally (~10% bioavailability).

...But Primordial Performance's "Liver Juice" is silymarin/silybin attached to an excellent delivery complex, and should be quite effective if taken 3x/day. It is the best milk thistle supplement out there, in my opinion.

NAC is also a fine antioxidant and glutathione-booster, but it suffers from poor bioavailability & is usually very underdosed in commercially-available supplements... So I wouldn't bother with it.

Sanofi-Aventi (or is it just 'Sanofi' these days?) manufactures the popular phospholipid-complex product "Essentiale" and "Essentiale Forte". The phosphatidylcholine therein has been shown to help protect hepatic cell membranes against the damaging effects of chenodeoxycholic acid, can inhibit lipid peroxidation, and can induce cytochrome P450, which stimulates the metabolic clearance of bile acids... So there's a reason that it's the most popular OTC liver support in Europe and Asia... But "Essentiale" can be hard to find in the USA -- and, on its own, I don't believe that it is totally adequate protection for users of oral androgens.

And Liv-52? Mostly a waste of money. A blend of mild antioxidants is all there is to it.

The bottom line here is this: Oral anabolics/androgens are hepatotoxic. Period. If you are going to use them, I implore you to take sensible precautions. Antaeus shall release a novel and powerful liver-support product in the very near future. In the meantime, there's Thermolife's "Liver Longer" and Primordial's "Liver Juice". Both are cheap enough that there's no excuse not to take them.

thekaz's picture

any side effect issues with TUDCA/UDCA?

whats the reason to choose tudca over udca?

Optimus Prime's picture

I didn't about the Estro conversion in Milk Thistle either....thanks

Beastmode11's picture

For my upcoming cycle I will be running tbol weeks 1-4 and var 14-20.oils are prop (taper) 16-18, eq weeks 1-16, test e weeks 1-16. For liver protection I have liv 52 ds and UDCA 250mg capsules. I was informed that for UDCA to be effective I should take 500-750 mg daily?? Does anyone have any experience or knowledge on the subject?
Thanks, Beast

GRIMEY's picture

I read somewhere that 500mg/day UDCA/TUDCA was the common dose for "maintenance"and 1g/day was the common dose for "repair".

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Beastmode11's picture

Much appreciated. 500 mg seems as though it should do the job along with liv 52 ds

GRIMEY's picture

yeah it should, personally if I take more than 500mg I feel nauseous, the one time I took 1g I vomitted 10 minutes after consuming it.

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Beastmode11's picture

Well that doesn't sound fun, I'm gonna stay away from that high of a dose for sure. Also, I take liv 52 year round, but I only plan on taking UDCA while on Orals, does that work or do I need to get my body accustomed to it first and cycle it 2-4 weeks before using Orals?

Makwa's picture

Whenever I take any orals I preload my liver support 2 weeks before and continue for 2weeks after I am done with them.

GRIMEY's picture

x2

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Makwa's picture

Most of the studies I have seen on it for cirrhosis patients is in the range of 10mg/kg bodyweight. Here is an abstract from Pubmed

http://www.ncbi.nlm.nih.gov/pubmed/10524634

Beastmode11's picture

Thanks man, looks like I will need more than expected lol

Makwa's picture

All these studies are on people who already have severe liver distress. I would think that you could take less if you are just trying to protect your liver and not trying to reverse an existing condition.

Beastmode11's picture

No liver disease here that I am aware of lol, just know I am double dipping Orals next run and want to be extra protected ya know?

j223's picture

Yes I take vitamin C, milk thistle and N-acetyl Cysteine anytime I use orals for more than 2 weeks

mujeriego's picture

Very very good, I would say even better than milk thistle and liv 52

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Makwa's picture

TUDCA (Tauroursodeoxycholic acid) and UDCA (Ursodeoxycholic acid) are a couple of other important ones for liver health that I take, especially when I was taking PH's.

The TUDCA helps metabolize the fats in your liver which helps to prevent cholestasis. It also can help increase insulin sensitivity.

UDCA has actually been shown to reduce jaundice and is also used to treat cirrhosis, so it must be doing something good for the liver.

SuperMax's picture

Goodstuff, this is the info people need!!!

Big Pimp Daddy's picture

Yah tudca is king. I take that and liv 52. 1 each a day now and ill take 2 each a day when I run var here soon.

Barabbas's picture

Good post bro. You remind me of someone who helped me tremendously throughout my first cycle, but his name started with a Z. Could it be?

Barabbas's picture

FR sent.. Good to see ya again.

Barabbas's picture

FR sent.. Good to see ya again.

TheFlash85's picture

add beetroot to the list of foods, by far the best, doctors have actually recommended drinking the juice for alcoholics with chirrossis of the liver!!!

TheFlash85's picture

interesting! never knew about that one!!!

FinMan's picture

I take milk thistle year round... And pretty much that's all. Should I really be needing ALA? I take vitamin c daily as well.
I run anadrol somewhat often.

FinMan's picture

That's good to know. I have literally been taking milk thistle for years and didnt really think about the estro fact. Thanks. Very helpful as always ;-)