Cardiovascular System
The use of anabolic/androgenic steroids in supratherapeutic (and often therapeutic) doses can have a number of adverse effects on the cardiovascular system. This may be noticed in several areas including unfavorable
alterations in serum cholesterol, a thickening of ventricular walls, increased blood pressure, and changes in vascular reactivity. In an acute sense these drugs are admittedly very safe. The risk of an otherwise healthy
person suffering a heart attack from an isolated steroid cycle is extremely remote. The risk of stroke is also extremely low. When these drugs are abused for long periods, however, their adverse effects on the
cardiovascular system are given time to accumulate. An increased chance of early death due to heart attack or stroke is, likewise, a valid risk with long-term steroid abuse. In order to better understand this risk, we must look specifically at how anabolic/androgenic steroids affect the cardiovascular system in several key ways.
Cholesterol/Lipids
Anabolic/androgenic steroids use can adversely affect both HDL (good) and LDL (bad) cholesterol values. The ratio of HDL to LDL cholesterol fractions provides a rough snapshot of the ongoing disposition of plaque in the arteries, either favoring atherogenic or anti-atherogenic actions. The general pattern seen during steroid use is a lowering of HDL concentrations, which is often combined with stable or increased LDL levels.Triglyceride levels may also increase.The shift can be unfavorable in all directions. Note that in some cases, the total cholesterol count will not change significantly. The total cholesterol level can, therefore, give a false representation of uncompromised
lipid health. Almost invariably the underlying HDL/LDL ratio will decrease.While this ratio should return to normal following the cessation of steroid intake, plaque deposits in the arteries are more permanent. If unfavorable shifts in
lipids are exacerbated by the long-term use of steroidal compounds, significant damage to the cardiovascular
system can result. Over time, plaque deposits may begin to narrow and
clog arteries. Anabolic/androgenic steroids are most consistent in their lowering of HDL levels. This adverse effect is mediated through the androgenic stimulation of hepatic lipase, a liver enzyme responsible for the breakdown of HDL
(good) cholesterol. With more hepatic lipase activity in the body, the favorable (anti-atherogenic) HDL cholesterol particles are cleared from circulation more quickly, and their levels drop. This is an effect that seems to be very pronounced at even modest supratherapeutic dosage levels. For example, studies with testosterone cypionate
noted a 21 % drop in HDL cholesterol with a dosage of 300 mg per week. Increasing this dosage to 600 mg did not
have any significant additional effect, suggesting that the dosage threshold for strong HDL suppression is fairly low.
Oral steroids, especially c-17 alpha alkylated compounds, are particularly potent at stimulating hepatic lipase and
suppressing HDL levels. This is due to first pass concentration and metabolism in the liver. A drug like stanozolol may, therefore, be milder than testosterone with regard to androgenic side effects, but not when it comes to cardiovascular strain. A study comparing the effects of a weekly injection of 200 mg testosterone enanthate to only a 6mg daily oral dose of stanozolol demonstrates the strong difference between these two types of drugs very wel1. After only six weeks, 6mg of stanozolol was shown to reduce HDL and HDL-2 cholesterol levels by an average of 33 and 71 %
respectively. HDL levels (mainly the HDL-3 subfraction) were reduced by only 9% in the testosterone group. LDL
cholesterol levels also rose 29% with stanozolol, while they dropped 16% with testosterone. Esterified injectable
steroids are generally less stressful to the cardiovascular system than oral agents. * It is also important to note that estrogens can have a favorable impact on cholesterol profiles. The aromatization of testosterone to estradiol may, therefore, prevent a more dramatic change in serum cholesterol. A study examined this effect by comparing the lipid
changes caused by 280 mg of testosterone enanthate per week, with and without the aromatase inhibitor testolactone. Methyltestosterone was also tested in a third group, at a dose of 20 mg daily, to judge the comparative effect of an oral alkylated steroid. The group using only testosterone enanthate in this study showed a small but not significant decrease in HDL cholesterol values over the course of the 12-week investigation. After only four weeks, however, the group using testosterone plus the aromatase inhibitor displayed an HDL reduction of an average of 25%. The group taking methyltestosterone experienced the strongest HDL reduction in the study, which dropped 35% after four weeks. This group also noticed an unfavorable rise in LDL cholesterol levels.
The potential positive effect of estrogen on cholesterol values also makes the issue of estrogen maintenance something to consider when it comes to health risks. To begin with, one may want to consider whether or not estrogen maintenance drugs are actually necessary in any given circumstance. Are side effects apparent, or is their
use a preventative step and perhaps unnecessary? The maintenance drug of choice can also have a measurable
impact on cholesterol outcomes. For example, the estrogen receptor antagonist tamoxifen citrate does not
seem to exhibit anti-estrogenic effects on cholesterol values, and in fact tends to increase HDL levels in some
patients. Many individuals decide to use tamoxifen to combat estrogenic side effects instead of an aromatase inhibitor for this reason, particularly when they are using steroids for longer periods of time, and are concerned
about their cumulative cardiovascular side effects.
