06-28-2012, 04:43 PM #1
The ultimate LIVER thread and info on orals and ORAL TOXICITY!!
This post might deserve a sticky, seeing as though there is no definitive post around here concerning liver health and oral C17 alpha alkylated anabolics. No post stating what specifically happens inside the liver when C7AA steroids are consumed, what they do inside, what happens over prolonged periods, and what is the best thing to do and take in order to solve the problem. The answers to all of these questions have recently piqued my interest because in one of my biochemistry courses, we just so happen to be covering certain aspects of liver function and the biochemical processes that occur inside it. We specifically touched upon the use of ursodeoxycholic acid (UDCA) for regulating proper liver function (specifically, BILE FLOW) in the midst of liver damage from things like alcohol, hepatitis C, etc. I also ran into a small issue post-cycle that I thought may have been a liver issue (lucky it doesn't seem like it was), and that caused me to look further into this. Some or much of this information may already be known, but I feel the need to spread word about it and post this here to educate people who might be asking the same questions.
I'm a really busy guy, and I don't have very much time to take everything I have read and conjure it up into my own words here. So, to save time, I am simply going to copy and paste my findings from other sources into this post, and provide references to them.
I am, for the most part, going to just copy and paste a whole post I already made in a previous thread I posted in where a forum member was asking about liver protection, oral anabolics, etc. where I explained everything to him. Here it is, folks:
I want to start off by saying this: milk thistle is garbage. TUDCA (Tauroursodeoxycholic acid) is quite literally the primary and ONLY liver protectant people should be using if they are taking C17 Alpha Alkylated oral anabolic steroids. I think that Liv 52 is okay to use as well. But, if you could only pick ONE product and throw the rest away, I would say TAKE THE TUDCA!!!! Research has shown that it is the ONLY thing that is effective at treating anabolic steroid SPECIFIC induced cholestasis of the liver. Off the top of my head, one company that makes a product with TUDCA in it is Thermolife in their Liver Longer supplement, but they have seemed to be out of stock for a long while now. I know it is possible to pick up generic TUDCA if you look hard enough online. Just google it!
If you can find TUDCA elsewhere, get it as soon as you can.
As a matter of fact, using a liver support supplement such as TUDCA may even INCREASE the oral absorption and bioavailability of the steroid because it prevents cholestasis of the liver. You have to understand what happens in the liver when you use C17 alkylated orals. Cholestasis is defined as an impairment of bile flow in the liver. I don't know if you remember your highschool biology class, but bile is an extremely important component of the liver and of our body, because bile serves dual purposes:
1. In a way, it acts as a waste removal sewage fluid for the liver. All of the byproducts (not all necessarily bad, but stuff that your liver needs to remove on a regular basis or else it will harm the liver from an unhealthy buildup) that your liver creates from all the work it does in metabolizing a bazillion billion different things every day, gets collected as bile. In turn, bile salts really 'clean' the liver out.
2. Bile and the bile salts within it are very important to our digestion, especially of fats. It's stored in the gall bladder and then pumped into your duodenum (upper section of your small intestine) when you eat food to aid in digestion, as it assists in the breakdown of fats and such.
Now, in a nutshell, what happens when your liver gets 'damaged' from oral steroids is: (and i'm not going to get into the specific chemistry of it for ease of explanation to the layman) the liver is overloaded from processing the C17 alkylation on the anabolic steroid you are ingesting. What happens as a result is that it causes a slow down of bile flow in the liver, because the liver is getting so overloaded with the processes it is trying to undergo. The impairment of bile flow in the liver is known as cholestasis, and is a direct result of C17 alkylated steroid use . When bile flow is slowed down too much (or has outright STOPPED), the bile salts, which are very toxic to the liver cells, will start to damage those liver cells. The key idea here is BILE FLOW, and you'll see this repeated a lot in this post! The liver needs to keep churning bile through itself in all of its cells in order to clean out the metabolites resulting from all of the biochemical processes it's doing every second!
I don't have much time on me, so for further explanation I am going to quote a couple articles I found that explain in more detail what TUDCA does and how it literally is the ONLY liver support compound that is useful, to a much larger degree than anything else, at combating cholestasis:
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.
2. 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.
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.
How do 17-aa oral steroids cause liver damage?
Despite a lot of discussion on the forums about the "toxicity" of different oral steroids, most users are unaware of the mechanism or implications around these "toxic effects" (which is probably the reason why most users have yet to find an effective cure for the toxic effects).
Let me shed some light on this ambiguous topic.
17-aa steroids are toxic to the liver because they inhibit the excretory functions of the liver. (1-7)
More specifically, the more "liver toxic" a 17-aa steroid is, the more it inhibits the production and flow of bile from the liver.
Bile salts are known as the liver's "cleansing agents" because they act as "soaps" that carry away the toxins and flush them into the intestines for excretion. If the bile flow is restricted in the liver, then the liver cannot rid itself of toxins. When the liver loses its ability to excrete toxins, it creates a buildup of toxins throughout the entire body. (1-13)
This condition is known as cholestasis [Kola-sta-sis]. By definition, cholestasis is a condition where the flow of bile cannot flow from the liver. (1) This is the most common liver condition developed from 17-aa steroids. (1-7)
If a liver becomes cholestatic for too long, the condition can begin damaging liver cells by causing necrosis (premature death of liver cells) from excessive toxin build up in the liver. This can eventually lead to cirrhosis of the liver (development of fibrous scar tissue) when the liver attempts to regenerate the damaged liver cells. This leads to loss of liver function from the replacement of healthy liver cells with fibrous connective tissue. (2)
Although cholestasis is reversible and generally not a lethal condition, it can lead to the more serious problems mentioned above if left untreated -- not to mention costly medical bills.
To avoid serious health complications it's important to protect the liver before it becomes cholestatic or seriously damaged from prolonged cholestasis (which I will explain later).
What are signs that my liver is damaged?
When the liver has been damaged by oral steroids there are certain signs that may become obvious to the user.
Here are some of the most common signs indicating you may have a serious liver issue. Warning signs usually appear in the following order, with the later signs being the most serious -
• Reduced appetite
• Nausea and fever
• Excessive Itchiness
• Yellow eyes or skin (jaundice)
• Very dark urine (dark amber colored)
• Bloody stools
Waiting for all these signs to appear means you have waited too long. You want to take action BEFORE these signs appear. This is why I advise getting full lab values on liver function before, during and after any 17-aa oral steroid cycle. If performing lab tests for liver function, the following values are considered normal.
Normal Values -
Total bilirubin range: 0.3-1.7 mg/dl
Alanine aminotransferase (ALT) range: 10-40 IU/L
Aspartate aminotransferase (AST) range: 10-40 IU/L
Alkaline phosphatase (ALP) range: 34-125 IU/L
Gamma-glutamyl-transpeptidase (GGT) range: 7-32 IU/L
Levels above these normal values doesn't necessarily mean you have liver damage. It is common for healthy weight training athletes or bodybuilders to be slightly outside of the "normal" ALT, AST and ALP values. Therefore these "Danger Values" have been established as more appropriate levels to indicate a serious liver toxicity issue. (1-7)
Danger Values -
Total bilirubin: 10 mg/dl or higher
Alanine aminotransferase (ALT): 50 IU/L or higher
Aspartate aminotransferase (AST): 50 IU/L or higher
Alkaline phosphatase (ALP): 150 IU/L or higher
Gamma-glutamyl-transpeptidase (GGT) range: 50 IU/L or higher
NOTE: Historical research from 17-aa oral steroid induced liver toxicity suggests that lab values higher than the "Danger Values" indicate that you may be suffering from cholestasis (1-7) If your lab values are higher than the "Danger Values" listed above you should discontinue any current oral steroid use and seek medical treatment.
If the above lab tests are not an option, it is possible to get an affordable at home test for bilirubin levels, which can help diagnose a liver damage from a 17-aa oral steroid. There are tests available, such as the TestMedica Liver Home Scan, which can be purchased online for less than $5 per test. Although these home based tests lack accuracy or true diagnosis ability, it can offer a valuable insight about the condition of the liver and is recommended for any steroid user not able to get lab tests done in a clinical setting.
How can I protect my liver?
To prevent cholestasis, the primary condition caused by oral steroid use, it is important to ensure there is ample hydrophilic bile acid available in the liver for the proper clearance of toxins. There are two reliable options for this.
1. The first option is the drug known as Ursodiol - a.k.a. ursodeoxycholic acid. This naturally occurring bile acid is used for its ability to detoxify the liver by clearing out less hydrophilic bile acids and other toxins that cause a toxic build up, such as 17-aa oral steroids. (4,5)
Ursodiol is typically prescribed to patients admitted to the hospital for steroid induced liver toxicity, but unfortunately, it is an expensive prescription drug, and not easily obtainable.
Typical dose - 1000-1200mg/day before, during and after cycle
Everytime now that I take an oral AAS, I get massive heartburn within 3 days. I even tried an injectable oral and still got acid reflux within a week. So, I did some research and found some interesting information. This is just a random post I found on Google.
Everyone seems to miss what is happening here. If an oral kills your appetite, it is because it is too toxic for the liver. I forget exactly what happens, but to summarize, when the liver is overloaded it causes a slowing of digestion, and a backflow of bile, which is why you also see people complaining of acid reflux on harsh 17aa's. The only way to really cure your appetite is to drop the anadrol . Perhaps next time around run with liv. 52 and alpha lipoic acid?
From what I read, bile helps with digestion. Now, when I take an oral AAS, the pain I get is similar to acid reflu/heartburn, but not exactly. It feels more like the food I eat just sits in my stomach and rots, never digesting. Lets say I eat some tacos on Tuesday, by Thursday morning I am still burping that taste up.That always made me wonder if orals cause heartburn or something similar.
Now read this
In primary biliary cirrhosis, inflammation destroys the bile ducts and prevents bile from escaping the liver. The accumulated bile damages healthy liver tissue, eventually leading to cirrhosis (scarring). As scar tissue replaces healthy liver tissue, the liver loses its ability to function. All this happens very slowly. People with PBC can lead healthy, symptom-free lives for 10 years or more after diagnosis.
Though primary biliary cirrhosis is often asymptomatic, especially early on, the most common symptom is extreme itching, especially in the arms, legs and back. Other symptoms include fluid buildup in the abdomen or legs, jaundice (yellowing of the eyes and skin), or fatty deposits and darkening of the skin under the eyes.
The standard treatment for PBC is a daily dose of a medication called ursodiol. Ursodiol improves liver function and increases life expectancy in people with PBC. Other medications may be indicated for controlling symptoms
DOSING GUIDELINES FOR TUDCA/UDCA
500mg PER DAY for liver maintenance while on a cycle containing the use of oral AAS.
1,000mg or more per day for liver repair if you have done lots of damage from heavy oral use and/or you have high liver enzyme readings as shown from bloodwork, etc. The medical studies done on UDCA/TUDCA on people with liver disorders were using 1,500 - 2,000mg per day for repair purposes.
Last edited by Atomini; 11-14-2012 at 04:24 PM.
06-28-2012, 06:10 PM #2
06-28-2012, 09:45 PM #3
It seems to already have been placed into the educational threads section also.
06-28-2012, 11:08 PM #5
06-28-2012, 11:19 PM #6
Thanks for that Atomini
06-29-2012, 12:13 AM #7
Very interesting Antomini.
Was a very interesting read because I was born with Gilbert Syndrome and all of the the things in the post make everything more clear in the context of what everything in the liver does.
I go every few months to see how my liver function is doing and everythings in a good range; so its very interesting to see in more detail what an oral compound like these and others does to the liver.
Very informative post!!!! Thanks man!
06-29-2012, 12:50 AM #8
06-29-2012, 12:53 AM #9
06-29-2012, 06:58 AM #10
Yes, I am well aware that TUDCA was originally extracted from bear bile (coming from the bear's gallbladder and liver).
However, I doubt very much that it is still today harvested from bears. Bears are usually used as the supply for bear bile found in eastern Chinese medicine, and not western pharmaceutical medicine. I believe that most western pharmaceuticals use bile extracted from animals which had been killed for their meat in modern slaughterhouses. You can then extract the bile and purify it in a lab to make UDCA and TUDCA.
06-29-2012, 02:22 PM #11
06-29-2012, 02:51 PM #12
lol, now you won't feel so guilty when you swallow down a capsule or 2 of TUDCA knowing that no bears died to keep your liver healthy from a cycle of orals.
Over here in North America and western medicine in general, would likely never allow the extraction of TUDCA from bears because of the moral issue. They found a way around that. Just like how HGH was originally extracted from the hypothalamus of dead bodies. They haven't done that in over 25 years.
06-29-2012, 03:00 PM #13
06-29-2012, 03:22 PM #14
Make no mistake, the issue of extracting bile from bear livers and gall bladders (sometimes while they're still alive might I add!!!!) is still a common practice in China and such. There are still major outcries concerning it.
Either way, no worries with TUDCA. And if you're ever unsure, you can always email or somehow contact the company that makes whatever TUDCA you buy and ask them as to how they obtain their ingredient. Thermolife, for example, clearly stated that they didn't obtain TUDA for their Liver Longer supplement from sources that extract it from bears.
06-29-2012, 10:04 PM #15
06-30-2012, 12:49 AM #16
Wow - amazing - thanks. ANd to back up what you say about Milk Thistle --Im an idiot. My actual DR told me 3 years ago that Milk Thistle was bogus....and I didn't listen. He told me you would literally need 20 pills a day to even stir up what it is supposed to do. I will chuckin my bottle tonight....
07-01-2012, 06:49 AM #17
07-01-2012, 07:21 AM #18
Good post. Can I be one of the typical 19 yr old who say I'm different, it wont happen to me, I am the exception to the rule. lol
I have a friend who had liver failure due to toxidity. Went from looking formal to looking 8 months pregnant in less than a week and took over a year to get back close to normal and now had to be EXTREMELY careful.
07-01-2012, 08:54 AM #19
Great post Atomini. It seems milk thistle (silymarin and silybin) is a very good antioxidant it just needs a greater dose to be effective and better bioavailability such as in Primordial Liver Juice correct? Also it looks like Thermolife Liver Longer is no longer available. It's still listed on a bunch of sites just out of stock and some boards are saying it was discontinued. I know my last 5 week dbol jumpstart through my liver bw all out of range. Lots of water is also key to liver function.
07-01-2012, 12:45 PM #20
07-02-2012, 09:34 AM #21
07-02-2012, 09:38 AM #22
I still maintain it's a much better idea to buy straight TUDCA and use that instead of a milk thistle supplement.
07-02-2012, 10:51 AM #23
Just ordered some STuff is not cheap but then again,...Im sure liver failure is costly. lol
07-02-2012, 10:52 AM #24New Member
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- Jun 2012
I'm concerned about not wanting to mess up my liver and get all my gains during my cycle of test 600 and winn. I have been on this cycle for two weeks and I'm not gaining any weight but to early to tell if I'm builing muscle. My diet which is my protein and carbs calories are all in tune. My concern is previous I used animal stak and then cycled off for two weeks. I did not do a pxt after that and just jumped into my cycle of test and Winn. Does anyone have any ideas whether I should jeep going or pct?
07-02-2012, 11:32 AM #25
We need more details as to how long your cycle will be, what you have used before and how long ago, etc.
07-02-2012, 02:02 PM #26
07-02-2012, 07:22 PM #27Banned
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I have a question for you knowledgeable members. I plan on doing my first cycle around twenty three or twenty four. I am not so sure I want to be injecting myself cause there seems to be so many things that could go wrong from injecting. Most of you say that test is a perfect place to start for a first cycle. But I just dunno if I would ever get my head around the idea of injecting. So basically, you guys strongly advise test as a first cycle over an oral steroid ? I'm not looking to cycle now just asking a general question so I know for the future.
07-02-2012, 08:02 PM #28
testosterone in some form as a base. There are very few steroids that can be run on their own without the need to use testosterone with it. This is because when you use any anabolic , you are shutting down your body's natural testosterone production (or at the very least, severely lowering it). This will result in normal bodily functions that require testosterone to function to go defunct without the presence of testosterone. You MUST at least run testosterone at a normal physiological dose. It is also ideal to run testosterone only for your first cycle, as testosterone is the basis by which all other anabolic steroids come from. It only makes sense considering that your body ALREADY produces testosterone, and that you are merely putting more of something your body already produces inside you. If you react adversely to testosterone, then chances are you will react worse to other anabolics. We use testosterone as a baseline by which all other anabolic steroids are measured off of, and we use it to gauge our body's natural reactions to it seeing as though it is the #1 anabolic steroid our bodies are already used to.
Furthermore, oral anabolics, if they ARE going to be used should strictly be used as a jumpstart or as some sort of a complimentary supplemental component of a cycle. As you continue to do your research, you will quickly realize the inflexibility of oral anabolic steroids and how little their capabilities are. I only ever used injectables, as they offer far more flexibility, options, and ease of use over oral tablets any day. I've only ever used 2 orals in all of my 5 years of AAS use: turinabol and anadrol . And I can definitely say after all is said and done, that I would have much rather put my money elsewhere. What a waste. The capabilities of oral AAS are so minimal in terms of how you can use them that it's really a waste of money. Thinking of using dbol ? Just use trenbolone at a lower dosage. Thinking of using anavar or oral primo? Try masteron instead. Winny? I wouldn't even use the injectable.
Lastly, there is the issue of liver damage. I don't even need to start opening up the book on that, considering I have a full writeup just above. After all, that's what this giant thread is about. Because of the liver issues, oral anabolics are not advised to be run for long periods of time (3-6 weeks maximum). Does this mean you can't run them without risking damage? No... you can do whatever you want, but the risks increase greatly. I have personally run Anadrol (touted as the MOST liver toxic oral) for 10 weeks along with test prop. At the end of the cycle my liver enzymes were slightly elevated, and the anadrol left me with a stomach ulcer (though that was probably an issue of the tablets themselves and me taking them on an empty stomach over the 10 weeks).
Bottom line: at first glance, orals might SEEM like they're so much more convenient to use than injectables. But when you look deeper into it, they're actually far less convenient. Give me a syringe over a tablet any day! Easier on my dosing schedule, fits into my life schedule better, don't have to carry pills around with me, and I have a healthier liver AND cholesterol values.
07-02-2012, 08:46 PM #29Banned
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07-02-2012, 09:12 PM #30
And there's no way to know until you go. This is why we reccomend testosterone to start with. And a relatively lightly dosed cycle to boot. 300mg per week of testosterone should be more than enough for a beginner to test the waters. And this is where you'll know if you are sensitive to estrogen buildup, or acne, or testicular shrinkage, or hard shutdown, or any other side effects. Some are very lucky like me, who experience absolutely nothing. Others find they are very sensitive to one particular side effect, lets say acne, and see nothing else. Others get a whole plethora of side effects just from a small dose. Your first cycle or 2 are all about testing the waters and seeing how you respond and react. And only after you have explored every nook and cranny of it will you be ready to move on to other compounds and explore those to find what works better for you, etc.
What determines how you react to anything is first and foremost: genetics. The next thing is dose and duration. Then age is a factor as well, because as we age, our bodies change and react differently to things than we did at a previous age. After that comes what compound(s) you use.
For example, I know a guy who recently did his first cycle and finished it about 3 weeks ago. Not only was he not ready for it at all (hadn't built up a proper base of muscle beforehand, etc.), he was a moron and used test E at 750mg per week! First off, I think 500mg per week is too much, let alone seven fifty! But that's not the end of it. He originally planned his cycle to be 10 weeks long. For whatever reason, he decided to extend it to 14 weeks, and for the last 3 weeks or something he upped his dose to 1,000mg per week. A whole gram per week of test... on a BEGINNER 1st TIME CYCLE.
Needless to say, he recently contacted me freaking out that he is having problems over his PCT with being able to get erections and whatnot. Now, he may have messed himself up by going extreme on his first cycle. OR he may just be sensitive to HPTA shutdown and he is one of those types that requires longer to recover (it's only been 3 weeks PCT so far for him). I told him to keep up his nolva and an aromatase inhibitor (aromasin ), and wait it out another week or 2 before taking further steps. Never know, he may fully recover by then.
But this is an example of why we use a basic compound such as testosterone only for a first cycle, and use a sensible dose and duration to gauge how we respond. I have never been an advocate of cycles longer than 8 weeks. Maximum I advise people is 10 weeks.
07-02-2012, 09:24 PM #31Banned
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07-02-2012, 09:48 PM #32
You know what I always say? For the superficial side effects like acne, etc. I tell people to look back at puberty. If you had a bad pizza face when you were going through puberty, chances are you are probably going to return to that if you go on a cycle.
I wouldn't try to figure out your genetics by looking at yourself the way you are. You can't know if you're gyno prone or not by looking at where fat deposits are on your pec area... it tells you nothing. The only way you know if you're gyno prone is to do a cycle and see for yourself (or get genetic testing done). But we all know nobody is going to perform the latter. Some may start to get gyno at 500mg per week, and others won't see gyno unless they go up to 2,000mg per week. My point here is that the answer to all your questions are: you never know until you go.
I can't tell you if you wait until 25 that you aren't going to mess yourself up permanently. There are no guarantees in life except death and taxes. I can definitely say that you have a better chance of not developing contraindications if you wait until 25 years of age and take the proper precautions when you cycle, doing proper PCT, etc. Any way you slice it, you are taking a gamble when you decide to start doing cycles of AAS. The idea here is that when you gamble, it's a game of odds. When you spin the roulette wheel of anabolic steroids , you can tip the odds in your favor by taking all of the proper safety precautions and following all healthy stipulations and guidelines for anabolic steroid use . This way, you can guarantee yourself that you will have the lowest possible chance of anything permanently damaging happening. But you cannot GUARANTEE that you are 100% safe.
Some people may do everything properly to the T and mess themselves up for good, because they just had the unfortunate genetics to respond badly. Other people may do a cycle of extreme doses, have no side effects, and furthermore stay on for a year, and come off with no PCT and never have problems for the rest of their lives. Some people are allergic to peanuts and will die from anaphylactic shock just by smelling the scent, and some won't. Such is life.
Last edited by Atomini; 07-02-2012 at 09:50 PM.
07-02-2012, 10:43 PM #33Banned
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- Jun 2012
07-02-2012, 11:50 PM #34
07-03-2012, 12:34 AM #35
Where can you even order TUDCA (Tauroursodeoxycholic Acid) by Nutra planet? Its sold out everywhere I look.
07-03-2012, 05:05 PM #36
My PREDICTION with the knowledge I have would be that it would likely have no change. The liver itself produces bile, and the bile flushes through the liver as it is produced. The gallbladder acts as a reservoir for the bile for the purpose of secreting it into the duodenum for digestion of fats and food.
I know TUDCA is difficult to find, but you can with enough searching. I havent had a need to look recently because I still have a box left over of Liver Longer that I bought a while ago. I will try searching for some more shortly.
One of the reasons it has become so hard to get is because mainstream medicine has jumped all over TUDCA because they've realized the immense benefits it has for people with all types of liver disorders. Countless studies have been done, and the results speak for themselves. So, the popularity of TUDCA has shot up into the stratosphere. Now it is in very short supply because manufacturers are overloaded with requests. This is one of the reasons Thermolife's Liver Longer has been out of stock for so long.
In time, i'm sure the supply issue will improve.
07-03-2012, 08:01 PM #37
What is the best thing to take for slightly elevated liver enzymes?
07-03-2012, 09:29 PM #38
07-03-2012, 11:34 PM #39
07-04-2012, 07:32 PM #40
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