This is a great write up I think everyone should give a read to exactly understand what’s going on in your body.
Oral Hormones and Liver Health
Oral hormones are frequently used to kick start cycles.
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, 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 enyzmatic 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 )