As a side note, in some of these explanations, the chemical and medical literature will not be the same as you will find in genuine text books on the dry topics. We are using these terms with strict purpose of understanding the physiology and biochemistry of anabolic steroids for our purposes. Please keep this in mind.
Anti-estrogens work in a few basic ways. The first is to block the estrogen receptor itself. This is known as a second line inhibitor because estrogen is allowed to be produced, it is just blocked at the receptor. This occurs by the anti-estrogenic drug fitting into the estrogen receptor, and “taking its parking space”. When the original estrogen comes along, it can no longer fit into the receptor. Examples of second line inhibitor drugs would be Clomid or Nolvadex. Both of these drugs are actually estrogens, they are just so weak that they do not elicit any of the negative effects of the true estrogen, and thereby, block the negative estrogenic effects. These are also two of the most known drugs since the athletic usage of anabolic steroids began.
First line inhibitors are drugs such as Arimidex and Proviron. Although these two drugs are from different chemical classes, they are both first line inhibitors. Proviron is actually a steroid with zero direct anabolic activity. As we will soon describe, Proviron has other benefits aside from it's anti-estrogenic activity. It is used clinically to replace androgens in the male for the purpose of sex drive and virility. Arimidex is a drug which is a chemical antagonist. For the purpose of estrogen talk, we can consider first line inhibitors and chemical antagonists to be the same. What is meant by this, is, the estrogen is inhibited at site of production, not at the receptor. Both Arimidex and Proviron will bind to the aromatase enzyme and render it inactive. Without the aromatase enzyme the body cannot convert various anabolics into estrogen. Estrogen is essentially blocked at its root, where it is originally produced. Nolvadex is one of the most well known anti-estrogens. It is also one of the oldest and most popular medications for breast cancer victims, which is the text book clinical use for this drug. Nolvadex is actually a weak estrogen and will bind to the estrogen receptor. The receptor is then occupied and when the normal and stronger estrogen floats by the receptor, it has no where to “park”. This is what we have defined as the classic second line inhibitor. Second line, because we are allowing estrogen to be produced, we are just blocking it at the receptor. For male usage, Nolvadex is a good drug of choice to use for ant-bloating and to control gyno if you are not particularly susceptible to these estrogenic side effects. If you are not and just need minor control, 20mg per day is probably enough to keep the majority of water off and your nips from being sensitive. If you are susceptible, you may need a stronger ant-estrogen, or may need to combine Nolvadex with another anti-estrogenic drug, or may need a much higher dosage of Nolvadex (probably closer to 40mg/day). Arimidex is called a chemical inhibitor of estrogen. Actually, it is a chemical inhibitor of the enzyme aromatase. Arimidex has a high affinity (liking for) for the aromatase enzyme. As we’ve said before, it is aromatase that converts various drugs into their estrogenic metabolite that can bind to the estrogen receptor and bring about side effects. Arimidex is an effective anti-estrogen and had a great deal of popularity when physique athletes began to get a hold of it. The only problem was the cost. To top it off, not many underground companies were making legitimate arimidex so you didn’t have much choice as a buyer. Now the price has dropped considerably with the availability of other anti-estrogens such as Femara (a much stronger and often unnecessary anti-estrogen).