Oral Hormones and Liver Health

Oral hormones are frequently used to kick start cycles. For years rumor and "broscience" has held that they are extremely toxic to the liver and can cause a host of serious medical issues. I was interested in researching this topic as a user, because I like to know what I'm getting myself into, and because pharmocology is a passion of mine. (In other words I like doing research, because I'm weird.)

Here is a summary of the research I have done regarding oral hormones (and specifically 17aa oral hormones) and the potential complications of their use.

Orals versus Injectable Hormones

First off, it's important to understand how oral hormones are different than hormones we use via injection.

When a steroid is injected directly into muscle it enters the blood stream and is able to act on androgen receptors in muscle cells and other bodily tissues before it encounters the liver, which is responsible for breaking down a large percentage of the wastes in our bodies (the kidneys also work on ridding the body of toxins.) By interacting with these androgen receptors the hormone directly increases protein synthesis, leading to faster muscle repair and muscle growth. (1) Basically they make us bigger and stronger faster than our bodies can on their own. Obviously this is a much simplified explanation of how hormones work, but it gives you the basic idea.

Unlike injectable hormones oral steroids must travel through the gastric system (our stomachs and intestines) prior to being released into the blood stream. A step of this process (which is called "first pass metabolism" essentially the first path anything takes in being processed by the body) is travel through the liver which works as a filter and waste remover. The majority of steroids used via injection are broken down almost completely by the liver which is why they are ineffective orally. (2)

So, since these hormones are so effectively metabolized by the liver researchers looked to develop a method of making them orally active while studying the effects of increased testosterone on males. The researchers found that by alkylating the basic hormone molecule at the alpha position of the 17th carbon (by adding either a methyl or ethyl group at that location) the hormone was able to pass through the liver relatively unchanged and into the blood stream. It was then able to act on muscle and other bodily tissue just like an injected steroid. (3) These hormones became known as the 17aa steroids (17-alpha alkylated.) Almost (if not all) orally active steroids belong to the 17aa group including Dianabol, Var, Anadrol, Halo and Winny being the most well known.

A Little History...

Dianabol (methandrostenolone or metandienon) was actually developed back in 1955 by a team of researchers including Albert Wettstein, Alfred Hunger, Charles Meystre, Ludwig Ehmann, Ernst Vischer, Hans Peter Frey and Walter Voser. It was the first orally active hormone. (3) It was popularized in the U.S. by Dr. John Ziegler in 1959 who prescribed it to the U.S. Olypmic lifters, in an attempt to combat the Russians use of testosterone on their lifters. This was at the height of the cold war, remember, and the U.S. needed all the good press they could get. (4)

Since Dianabol has been around the longest it has, arguably, the largest volume of research of any of the oral steroids, however many of the other orals have been studied at length regarding their effects on the liver.

Enough history about their development and how they get into our systems and work. We know they work, ample clinical evidence has demonstrated their ability to cause significant strength and muscle gains in users.

The Real Deal on Oral Steroids and the Liver

I approach everything with a harm reduction view. People are going to use hormones, how can they do so in the most safe way possible? How bad are orals for us really?

Well, the biggest issue with orals is that we're overworking the liver by putting a chemical through it that it is unable to break down easily. This leads the liver to produce additional enzymes to aid in breaking down the substance (AST and ALT, which are often elevated in labs of those using oral hormones.) Because the liver is working so hard to try to break these compounds down it can lead to inhibition in its ability to break down not only the hormone but everything else it is trying to deal with. Another complicating factor is that the breakdown of 17aa hormones leads to the creation of 17-glucuronides which are toxic metabolites and which also (arguably) can lead to the majority of the negative liver effects seen with 17aas. (10) This also causes the liver to produce additional biles (called bile salts) which work to clear toxins out of the liver and into the excretory system. When these bile sites become saturated they can stop working as effectively as they normal do and decrease or stop the production and elimination of bile from the liver. (5) Current research is inconclusive as to the mechanism of action that 17aa hormones exhibit which specifically causes this decrease in bile production and excretion. (7) (Obviously this is an oversimplified description of the process, but it works for this explanation.)

This decrease in the liver's ability to process and expel bile results in a condition known as choleostasis. When a liver becomes choleostatic it greatly reduces or loses it's ability to process toxins out of itself. This can lead to liver damage as toxins remain in the liver, causing continued damage to hepatic (liver cells) tissues. This buildup can lead to lesions within the liver. (6) The liver responds by increasing enzymatic activity (leading to higher AST/ALT levels) and the circle repeats unless treated, which I'll go into later.

Multiple studies indicate that after an extended period of oral steroid use clinical liver damage will occur, including the aforementioned lesions, drug induced hepatitis and jaundice*. However studies indicate that the extent of this damage is time and dose mediated, that is, if one is taking reasonable dosages for a period no greater than 2 months (although periods of up to 6 months have been observed with similar results) lasting damage should be non-existent. (7) ( 8 )

*As a side note, just because I thought it was an interesting fact) Jaundice is an interesting symptom of liver dysfunction. Jaundice is caused by a buildup of bilirubin. Bilirubin is a waste product of the breakdown of red blood cells, which is normally processed through the liver and excreted in bile. (Fun fact, bilirubin is what causes the yellow color of bruises.) When the liver is unable to process bile bilirubin builds up leading to a yellow tone to the skin and eyes of the patient. This is jaundice. If you turn yellow do not pass go, do not collect 200 fucking dollars, go to the hospital.

Current research indicates that if 17aa oral hormones are not used for extended periods and at sane dosages any changes in liver functioning (i.e. increased AST/ALT/Bilirubin values in labwork) should self correct with time. (6)

Conclusions

So, the conclusion we can draw from current peer reviewed research is that common "bro-science" of the severity of liver damage associated with oral hormone use has been, if not completely over-estimated than blatantly blown out of proportion.

Now, I'm not saying go out and gobble down Dbol by the dozens. As noted dosage and length of use are the two highest indicators of adverse liver issues with oral 17aa hormone use. However I feel that following this review I would not place too much concern on responsible oral hormone use and long term liver complications provided orals are maintained to short dosing periods and run at sane doses.

Safer Oral Hormone Use

That being said, there are some very simple methods for providing support to the liver while running oral cycles.
The first method is stupid easy. If you cannot do it you should 100%, absolutely, no fucking way, I'm not even kidding, not use hormones at all. DON'T DRINK ALCOHOL WHILE USING ORAL HORMONES. NOT ANY. Not a beer. Not a shot. Just don't do it. Your liver is already being taxed eliminating the orals from your body. Alcohol causes inflammation* of liver cells, hardening of liver cells and is generally just shitty to your liver. DON'T DRINK!

The second method takes a little bit of work. Get some TUDCA. Then you have to take it orally. TUDCA is effective at decreasing liver damage because when you take it it causes your body to more effectively create and clear bile in liver tissue, which moves toxins out of the liver. TUDCA also increases the expression (creation) of certain proteins in the liver which are associated with pumping bile out of the liver, so it also helps in clearing other biles from the liver, allowing it to more effectively process all toxins coming through it. (6) (9) Dosing protocol is 250mg-500mg per day for maintenance with doses for up to 1000mg per day if lab works indicates significantly elevated liver values.

TUDCA has also been shown to increase insulin sensitivity which is something we all want. For more information on this see my post here.

Milk Thistle (or, more accurately Silymarin, the active component in Milk Thistle) has shown good evidence of liver protection. If you want to be extra safe consider taking a supplement containing Milk Thistle. Make sure to look for one with at least 150mg of Silymarin standardized, as this will be the most effective. Dose like it says on the bottle. If you have to choose between Milk Thistle and TUDCA go with TUDCA, it has much more evidence backing it's efficacy.

Finally, do the simple stuff. Make sure you are staying extremely hydrated. Eat right. Get enough rest.

So every one knows I was the one that recommended 12 Liv 52 a day. As he was talking of doing a heavy cycle of D-bol. What he fails to mention is the recommended dosage of Liv 52 on the bottle for an adult is 2-3 pills 3 x day which is 6-9 pills. The fact that castoja weights 255lb and was going to be on D-bol I upped it 1 tab per dose. What I fine amazing is your worried about 12 herbal pill but yet not concerned about doing 100 mg of d-bol which is 10-20 tabs a day depending on size.
I don't have a gallbladder because of D-bol usage. What it does, really what most 17's do is not cause liver damage per say but cause cholestasis. Look up any new liver protection product that's being marketed for steroid users and what your being protected from is cholestasis. Liv-52 does that.
Praxis (Bern 1994). 2002 Sep 18;91(38):1561-4.
[Cholestatic jaundice and pruritus].
[Article in German]
Stocker C, Hardmeier B, Looser M, Scharf C, Greminger P.
Source
Medizinische Poliklinik, Departement für Innere Medizin, Universitätsspital Zürich.
Abstract
The 38 year old male patient was admitted to our clinic with jaundice and invalidating pruritus of unknown origin. The primary evaluation made by the practitioner of the patient and the initial examinations performed in the clinic revealed no diagnosis. In particular, an infectious liver disease could be excluded. Reevaluation of anamnestic data revealed then the in-take of Dianabol, an often used anabolic steroid as the most possible reason for the cholestatic hepatopathy.
http://www.ncbi.nlm.nih.gov/pubmed/12369223
http://www.ncbi.nlm.nih.gov/pubmed/18720005
http://www.ncbi.nlm.nih.gov/pubmed/10506840

Anabolic steroid-induced hepatotoxicity: is it overstated?

Abstract-

OBJECTIVE:

There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders.

DESIGN:

This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis.

PARTICIPANTS:

The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls.

MAIN OUTCOME MEASURES:

The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels.

RESULTS:

In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT.

CONCLUSION:

Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.

Dickerman RD, Pertusi RM, Zachariah NY, Dufour DR, McConathy WJ. Clin J Sport Med 1999;9:34-9.

Basically they're saying that people using AAS vs. just bodybuilding had no evidence of liver issues. Again, the small sample size is a bit of a concern. They also note that bodybuilders can show higher levels of liver enzyme due to muscle breakdown through lifting, the byproducts of which are processed through the liver. I.E. if someone lifted heavy than had a liver function test their levels could be elevated from that alone.

I ended up in the hospital from being jaundice don't know if it was the Dbol test or tren but something did it. I was on my 2nd cycle about 4 years ago cant remember what the dosage was on the dbol but i remember taking 1mL of test E 250 2x a week and 1ml of tren E 2 times a week

over rated probably so but better safe then sorry.

All orals are liver toxic. They have to be in order to survive the first pass. Liv 52 and regular milk thistle will do ya good. Never run an oral past 6 weeks and don't do things that add liver stress like drinking or using other meds.

Noone would waste primo with a dbol run. Thats just crazytalk! And hells yes it's toxic! You gonna die!

It is absolutely liver toxic just as any 17aa oral compound can be. Running it at 30-40mg ed in conjunction with a quality AI and a liver supp is relatively safe. It's the guys that run substantially higher doses for longer periods of time that end up having problems. That's not to say that you can't have issues at your dosage and cycle length. Nothing will hammer you with gyno quicker than dbol. Get a week to ten days in and find out your AI is bunk. That's gonna piss you off. You also have to pay close attention to your blood pressure because it can absolutely spike and get out of control from all the water retention. Anyone with BP issues should avoid running dbol. You have to be careful with it and stay on top of everything while running it. I've used it multiple times with each experience being a little different. Good luck.