We employed three types of estrogen control drugs with Frank

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1. ANTAGONISTS: These are drugs that act as competitive inhibitors by simply competing with the estrogen molecule for its receptor-site.

The antagonist is like a little brother that beats you to the bathroom. If he gets in first, he only sits there doing nothing but keep you out so you can't do your thing. If estrogen can't get in, nothing happens.

Contrary to what is often claimed, antagonists are not "great" at controlling water retention, in my opinion. Since they simply block receptor-sites they do not decrease the levels of circulatory estrogen. This means potential increased levels of aldosterone. They do have "some" positive effects upon water retention, but they were best utilized as a drug for prevention of gynecomastia (Gyno/ bitch tits) and female pattern fat deposits. Nolvadex and Cyclofenil are examples of antagonist.

An advantage of utilizing the properties of specific estrogen antagonist (Faslodex, Clomid or Cyclofenil) for Frank was IGF-1 production. When estrogen is deactivated by the liver, IGF-1 secretion results. It is also interesting that under the right conditions, estrogen can increase GH levels by positively influencing the pituitary gland.

So in short, antagonists inhibit estrogen at receptor-sites and some aid in GH/IGF-1 secretion.

2. AROMATASE INHIBITORS: Aromatase inhibitors are sometimes called antagonist also (which is a pretty loose term). Aromatase inhibitors control estrogen by limiting or preventing the activity of the aromatase enzyme.

Normally, the aromatase enzyme induces the conversion of some types of androgens into estrogens. By utilizing an aromatase inhibitor this conversion is either limited or prevented. In most cases the difference between limiting and preventing conversion is dose dependant. Pretty simple, huh?

By inhibiting the aromatization of androgens to estrogen there is not a build-up of estrogen in the system. This was a plus during contest prep for Frank since elevated estrogen levels inhibited fat loss and increased water retention. It also meant less of an estrogen induced negative feed-back loop inhibiting HPTA function for Frank.

Post cycle lean mass tissue loss was a significant concern.

Most AAS suppress HPTA function and therefore inhibit endogenous androgen production. Elevated estrogen levels further inhibit HPTA regeneration post-cycle. By utilizing estrogen inhibitors that decrease aromatase enzyme activity during AAS phases, there was a much lower build-up of estrogens post cycle to inhibit HPTA regeneration.

So the lesson here was that "inhibition" was finally a good thing. Arimidex, Teslac, 4-OH Testosterone, Formastane, Aromasin and Proviron are examples of aromatase inhibitors. In short, aromatase inhibitors prevent the introduction (or limit) of more estrogen into the system than is normally produced by biosynthesis. Some also possess low antagonist qualities as well.

3. BIOSYNTHESIS INHIBITORS: These inhibitors control estrogen at its very base, by preventing its endogenous biosynthesis. Normally the body begins the synthesis of most hormones with the conversion of cholesterol into pregnenolone. As usual, this is due to the activity of an enzyme. In this case it is the P-450 enzyme complex.

The hormone estrogen is several biochemical steps away from cholesterol...as you know already. If the P-450 enzyme complex is inhibited then the chain or sequence of biochemical steps are inhibited. Therefore so is the formation of estrogen and every other endogenous P-450 enzyme dependant hormone.

Cytadren is a 2-step estrogen inhibitor. First Cytadren inhibits the P-450 enzyme complex, and second it inhibits the aromatase enzyme. There are other biosynthesis inhibitors such as Trilostane and Metyrapone. Normally all 3 drugs are utilized in medicine as cortisol biosynthesis inhibitors.

That is entirely another issue. Since biosynthesis inhibitors control estrogen beginning at the very base of hormone biosynthesis, obviously they are effective at controlling water retention. Unfortunately, some negatively effect endogenous androgen production as well.


Changes in liver enzyme values can occur during AAS use. This is especially true when oral c17-alkylated steroids or high dosage Tylenol are utilized. When a c17-alkylated steroid is introduced into the system, the liver must work harder to deactivate its molecule before excretion. Levels of Bilirubin, LDH (lactate dehydrogenase), and alkaline phosphatase are all good indicators of liver health and stress. I wrote a great deal more about this in "Chemical Muscle Enhancement". The upper normal level for LDH is about 250 U/L.

However, during Frank's AAS phases employing oral c17-alkylated drugs, this number may have risen to 400 U/L and above. "Usually" most doctors do not note this as a major concern unless other indicators suggest excessive liver stress. If alkaline phosphatase was above its upper limit of 1 50 IU/L as well, liver stress became a factor. Often levels were reported to elevate for the first 2-3 weeks of a cycle only to return to acceptable ranges a week later. For the most part brief variations in liver enzymes were not harmful as this was potentially an adaptive reaction. Another consideration was excessive alcohol use during AAS phases.

*You should see most people's blood work after a hard night of drinking and partying. You would think Anadrol-50 was mild in comparison. This is not to say that the abuse of any drug is a good idea.


I often find myself amazed at the great lengths some athletes will go to build the ultimate living physical edifice with little regard for actual health. When reviewing blood work-ups, it often becomes necessary to explain the most fundamental reality; Destroy the inside and the outside will follow quickly. Sounds kind of silly to say, but some individuals have invested as much as $50,000.00 a year into various polypharmacological chemistries but not even $10.00 into health.

The body is an adaptive organism with Action/Reaction Factors both good and bad. In the case of building the perfect beasts each factor had to be considered and responded "to" or "with" the appropriate response for long term ultimate progress to be achieved. In most cases, the beast's bodies reacted positively to chemical muscle enhancement protocols of a brief intense nature. "Get in, grow harder, get out" was the ideal intent. However, if any phase or protocol ran too long the body would have begun counter measures that could have eventually resulted in failure and the destruction of the organism.

AAS and The Heart

Studies based upon valid research show prolonged high dose AAS use can have negative effects upon the heart. Eventually non-stop high dosage AAS cycles will lead to a decrease in high-density lipoprotein cholesterol (HDL). HDL protects against cardio vascular disease by shuttling cholesterol out of the blood and back to the liver. The liver degrades cholesterol into bile and only then can it be excreted from the body. This is the only method the body has to get rid of excess cholesterol. It is not like fat which can be burned or oxidized. A possible explanation for the significant increases in low-density lip-protein (LDL) cholesterol during long AAS protocols is simply a matter of biosynthesis.

Normally the body utilizes cholesterol to synthesize sex hormones endogenously (produced inside the body). Testosterone, estrogen and others all begin as cholesterol. When AAS are introduced exogenously, this process is inhibited. This in turn allows cholesterol to build-up to dangerous levels until discontinuance of the AAS. An interesting fact is that anything that stimulates HPTA (hypothalamus-pituitary-testes-axis) function/activity also decreases bad cholesterol levels. It does so by increasing hormone (like testosterone) production endogenously. Oral AAS have the greatest negative effects upon HDL. Nandrolones have little or no negative effect. In fact there are some studies that support the belief that nandrolones have a positive effect upon HDL levels, though I have found this not to be true in all athletes.

AAS and Red Blood Cells

Another concern realized from AAS use is due to AAS induced increases in production of red blood cells. AAS stimulate the kidneys synthesis of erythropoietin (EPO) which in turn stimulates red blood cell production. Anadrol-50 was actually medically prescribed for this purpose. An increase in red blood cell counts increases oxygen transport, vascularity, muscle fullness/hardness and to a lesser extent body weight. From Frank's point of view this was cool, to a point! Having too many red blood cells for prolonged periods increases blood volume to a point of slowing circulation. This increases the chances of blood clots and therefore also increases the chance for strokes and heart attacks.

AAS and Aldosterone

AAS induce activation of the renin-angiotension system in the kidneys. This in turn promotes the release of aldosterone from the adrenals which has a connection to some types of high blood pressure or hypertension. Aldosterone is a hormone that helps preserve blood volume via increased sodium retention and therefore water retention. High water retention increases blood pressure and heart health risk if the condition is over prolonged.

So obviously AAS abuse is a bad idea. However, brief AAS protocols were seldom reported to cause these negative effects simply due to their brief nature. Like most things in life, it is not so much a matter of what we did, as how we did it. ACTION/REACTION.

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