In the area of side effects, Testosterone is considered the absolute safest anabolic steroid considering it is the anabolic hormone that the human body endogenously produces naturally. Following this logic, the human body is well accustomed to the effects of Testosterone on its systems, and enough research has been conducted on Testosterone and its effects on the body that nearly all of the knowledge of Testosterone Enanthate side effects is known to man. This is in contrast with other modified analogues of Testosterone that may exhibit odd side effects and odd behavior unknown to science due to its modifications that essentially create an entirely new anabolic steroid. Testosterone being the most natural anabolic steroid to the human body should never exhibit any hidden or odd side effects (compared to a very mysterious compound, such as Anadrol for example, or Trenbolone).
With this having been established, Testosterone is not without its share of potential side effects. But it is our almost complete understanding of this compound that allows Testosterone Enanthate side effects to be efficiently understood and dealt with.
Estrogenic Side Effects of Testoseterone Enanthate
Testosterone is easily aromatized by the aromatase enzyme, and Testosterone is known to possess moderate interaction with the aromatase enzyme. This results in significant rises in Estrogen levels resulting from the conversion of Testosterone into Estrogen. Estrogenic Testosterone Enanthate side effects should not be ignored, and the rate of aromatization is correlated directly with the dose of Testosterone used, with increasingly higher doses corresponding with an increase in aromatization of Testosterone into Estrogen. Without a doubt, bodybuilding doses of Testosterone will generate significant amounts of aromatization that must be dealt with in some way. Individuals can elect to use an aromatase inhibitor, which serves to disable the aromatase enzyme so that Testosterone cannot be converted into Estrogen, effectively controlling Estrogen increases as the root cause. The other possible option is the use of a SERM (Selective Estrogen Receptor Modulator) such as Nolvadex, which serves to block Estrogen from attaching to receptor sites in breast tissue. SERMs such as Nolvadex will only serve to remedy the issue of gynecomastia caused by Estrogen, and will not actually reduce serum Estrogen levels in the body – an aromatase inhibitor is what is required for this. Estrogenic side effects include the following: water retention and bloating, blood pressure elevations (as a result of the water retention), increased possible fat retention/gain, and gynecomastia.
Androgenic Side Effects of Testosterone Enanthate
Testosterone Enanthate side effects do include androgenic side effects as well, considering Testosterone is the human body’s primary androgenic hormone next to Dihydrotestosterone (DHT). Testosterone possesses an androgenic strength rating of 100, which serves to exhibit a considerable amount of androgenic activity in the body. However, Testosterone Enanthate side effects in the arena of androgenic strength has more to do with the fact that Testosterone is converted into the far stronger and more potent androgen Dihydrotestosterone (DHT) by way of the 5-alpha reductase enzyme. The 5-alpha reductase enzyme is present in large amounts in certain tissues, such as the scalp, prostate, and the skin. When Testosterone reaches these tissues, it undergoes a high rate of reduction into its more potent androgenic metabolite DHT. It is DHT that is responsible for the greater severity of androgenic side effects. Ancillary drugs such as Proscar or Dutasteride can be utilized to effectively inhibit the 5-alpha reductase enzyme and thereby eliminate DHT at the root of its cause. This will not, however, eliminate androgenic side effects due to the fact that Testosterone itself possesses an androgenic strength rating of 100 and will still act as an androgen in various tissues throughout the body. An alternative (or an adjunct) to 5-alpha reductase inhibitors such as Proscar is the topical use of Nizoral 2% shampoo, where its active ingredient Ketoconazole acts as a topical DHT blocker in skin and scalp, effectively reducing the probability of androgens triggering male pattern baldness as well as acne breakouts caused by increased oily skin. Androgenic side effects include: increased sebum secretion (oily skin), increased bouts of acne (linked to increased sebum secretion), bodily and facial hair growth, and the increased risk of triggering Male Pattern Baldness (MPB) in individuals that possess the genetic trait required for the condition to manifest itself.
HPTA and Endogenous Testosterone Production Side Effects
Every single anabolic steroid exhibits a suppressive effect on the endogenous production of Testosterone by way of the Hypothalamic Pituitary Testicular Axis (HPTA) negative feedback loop. Testosterone Enanthate side effects are no exception to this rule. The exogenous administration of Testosterone Enanthate will suppress and/or shut down natural endogenous Testosterone production for the duration of its use. Immediately following the end of any anabolic steroid cycle, it is highly advised that the user engage in a proper PCT (Post Cycle Therapy) protocol, which includes the use of Testosterone production stimulating ancillary compounds, such as Nolvadex and/or HCG (Human Chorionic Gonadotropin) for a typical PCT period of 4 – 6 weeks following the end of a cycle. Failure to do so can result in permanent damage to the HPTA (Hypothalamic Pituitary Testicular Axis) whereby the individual will insufficiently produce proper levels of Testosterone for life, ultimately requiring medical intervention in the form of TRT (Testosterone Replacement Therapy).
Hepatotoxic Side Effects
Testosterone Enanthate is not a C17-alpha alkylated anabolic steroid and therefore does not exhibit any measure of toxicity on the liver. In fact, studies have investigated the potential for hepatotoxicity with Testosterone used at high doses (400mg daily, which equates to 2,800mg weekly) in several male test subjects for a 20 day period where the route of administration was actually oral instead of intramuscular injections. The idea here was to saturate the liver with high amounts of Testosterone (all orally ingested substances make what is known as a ‘first pass’ through the liver and interact with the liver at a far greater rate than the injectable route of administration). The result of the study was that no changes were observed[1]. Therefore, hepatotoxicity is not of any concern where Testosterone Enanthate side effects are concerned.
Cardiovascular Side Effects of Testosterone Enanthate
Cardiovascular strain and negative cholesterol changes are all peripheral effects that fall under Testosterone Enanthate side effects. It is one side effect that is exhibited by every single anabolic steroid in existence and is inherent to the nature of anabolic steroids, especially oral anabolic steroids. This involves the reduction of HDL (the good cholesterol) and increases of LDL (the bad cholesterol). The result of such changes involves an increased risk of arteriosclerosis, and the degree to which these changes occur for the worse are usually dose-dependent (with higher doses increasing the negative changes and the risks). Other factors that affect these negative cholesterol changes are: duration of use, and route of administration. Testosterone itself actually happens to exhibit far less of an impact on cholesterol values in this case than all other anabolic steroids, as one of the contributing factors in this case is due to the liver’s ability to freely metabolize Testosterone, and the fact that Testosterone is not extremely resistant to hepatic breakdown and metabolism. The issue where hepatotoxicity is concerned mostly stems from certain anabolic steroids that possess the trait of exhibiting heavier resistance to hepatic metabolism than Testosterone is. This is one of the main reasons as to why oral anabolic steroids exhibit varying levels of hepatotoxicity – the C17-alpha alkylation causes the anabolic steroid to become further resistant to being metabolized or broken down by the liver. The concern as to whether an anabolic steroid has a high resistance to hepatic metabolism or a low resistance is a factor in how much impact a given anabolic steroid has on the liver’s management of cholesterol.
Testosterone in particular has demonstrated in one clinical study to have only a mild impact on HDL cholesterol after a 12 week period where 280mg of Testosterone Enanthate was administered weekly. The cholesterol profiles had later changed for the worse when an aromatase inhibitor was included, which resulted in a significant 25% drop in HDL cholesterol[2]. Conversely, other studies have been conducted whereby 300mg weekly of Testosterone Enanthate was administered for a 20 week period without the use of an aromatase inhibitor which resulted in a 13% reduction of HDL cholesterol, however, when Testosterone doses were raised to 600mg weekly, reduction of HDL cholesterol had dropped to 21%[3]. From the data examined, it is very evident that the increase in Estrogen via aromatization and liver metabolism actually helps to offset the negative cholesterol changes from the use of supraphysiological amounts of anabolic steroids. This makes sense, considering Estrogen itself is known to promote positive impacts on cholesterol levels. Therefore, the use of an aromatase inhibitor and its impact on cholesterol profiles should always be remembered when any user is considering the addition of an aromatase inhibitor on cycle. It is advisable to instead use minimal doses of an aromatase inhibitor while on a cycle for the purpose of Estrogen control rather than total Estrogen level elimination. The idea in such a case is to keep Estrogen levels within normal ranges and not allow them to skyrocket as a result of aromatization, but at the same time prevent them from dropping to near zero from the use of full doses of an aromatase inhibitor.
Testosterone Enanthate References:
[1] Enzyme induction by oral testosterone. Johnsen SG, Kampmann JP, Bennet EP, Jorgensen F. 1976 Clin Pharmacol Ther 20:233-237