Testosterone Side Effects


Within the arena of side effects, Testosterone is measured as the unconditionally safest anabolic steroid for use, considering the fact that it is the primary and number one anabolic hormone that the human body naturally endogenously manufactures and secretes. It makes logical sense then, that the human body is already well familiarized with the effects and side effects of Testosterone on its subsystems, tissues, and cells. In addition to this, there has been enough research performed on Testosterone’s effects and Testosterone’s side effects effects on the body that nearly all of the knowledge of Testosterone side effects is well known and well documented within medicine and science. In comparison with other modified derivatives of Testosterone, the risks of experiencing side effects from these other analogues that may exhibit abnormal side effects and strange behavior unfamiliar to science is of a far greater probability. This is primarily due to the modifications on these analogues and derivatives that serve to essentially create an entirely new anabolic steroid analogue. With Testosterone being the most natural anabolic steroid to the human body, the majority of individuals using Testosterone should never exhibit any hidden or odd side effects. Once again, it is very important to understand that all individuals will react differently to any compounds, drugs, or foods. However, compared to a very mysterious compound, such as Anadrol for example, or Trenbolone, Testosterone’s effects on most individuals should be more or less identical across the board.

With this having been said, Testosterone is not lacking its share of possible side effects. However, it is through science and medicine’s almost complete comprehension of this anabolic steroid that permits the possibility that Testosterone side effects can be well understood and dealt with.

Estrogenic Side Effects

Testosterone itself exhibits a modest amount of Estrogenic activity through its ability to express moderate binding affinity to the aromatase enzyme (the enzyme responsible for the conversion of Testosterone into Estrogen, also known as aromatization). A moderate amount of aromatization can then be expected from the use of Testosterone. Substantial rises in blood plasma levels of Estrogen as a result of the conversion (aromatization) of Testosterone into Estrogen can result, particularly when Testosterone is employed at supraphysiological ‘bodybuilding doses’ and doses generally required for performance and physique enhancement. This is why Estrogenic Testosterone side effects are also very much dose-dependent, with higher doses normally eliciting higher amounts of aromatization, and therefore higher chances and incidences of Estrogenic side effects. Estrogenic Testosterone side effects should not be disregarded for this reason, and the rate of aromatization is normally always correlated with the dose used, as previously mentioned. All potential Testosterone users should be under the understanding that bodybuilding doses of Testosterone will often produce moderate to significant amounts of aromatization that must be dealt with in some way.

SIDE EFFECT PREVENTION AND SAFETY: There exist two different primary methods of mitigating and dealing with these potential Estrogenic Testosterone side effects. One such method is through the use of an aromatase inhibitor, which serves to disable (through inhibition) the aromatase enzyme. This will effectively eliminate the pathway through which Testosterone is aromatized into Estrogen, which effectively prevents and blocks total circulating Estrogen increases at the root cause (aromatization of Testosterone by the aromatase enzyme). The other slightly similar yet very different option is through the use of a SERM (Selective Estrogen Receptor Modulator) such as Nolvadex (Tamoxifen), which alternatively acts to block Estrogen from binding to receptor sites in breast tissue. SERMs such as Nolvadex will only serve to mitigate the problem of gynecomastia caused by Estrogen at its target tissues, and will not actually reduce serum Estrogen levels in the body as commonly mistaken/misconceived. Only the use of an aromatase inhibitor is what is required for such an effect in the reduction of total circulating blood plasma levels of Estrogen.

Potential 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 in select areas of the body, and gynecomastia.

Androgenic Side Effects

Testosterone acts as the primary male androgen, and it therefore stands to reason that Testosterone side effects would indeed include that of androgenic side effects. Aside from its action on the androgen receptor in specific tissues, Testosterone’s much stronger androgenic effects are actually the byproduct of its conversion (properly termed as ‘reduction’) into an even stronger androgenic metabolite, Dihydrotestosterone (DHT).  Testosterone itself exhibits an androgenic strength rating of 100, which serves to exhibit a modest amount of androgenic activity and strength binding to androgen receptors in the body. However, androgenic Testosterone side effects, as previously mentioned are attributed more towards the fact that Testosterone is converted into the previously mentioned androgen that is stronger and more potent. This androgen is once again, known as Dihydrotestosterone (DHT) and the process of reduction (conversion) occurs via the 5-alpha reductase (5AR) enzyme.

Androgenic side effects from testosterone

The 5AR enzyme is present in great quantities in various particular tissues in the body such as the scalp, prostate, and the skin. Upon entering these tissues, Testosterone will undergo a high rate of reduction into its more potent androgenic metabolite DHT due to the high concentrations of 5AR in these areas. It is DHT that is then responsible for the majority of the greater severity of androgenic side effects associated with Testosterone (or any anabolic steroid that commonly reduces into a stronger metabolite via the 5AR enzyme).

SIDE EFFECT PREVENTION AND SAFETY:  Ancillary drugs exist that act to inhibit the 5-alpha reductase enzyme and as a result, eliminate DHT at the root of its cause. These compounds are, as such, known as 5AR inhibitors (or 5AR blockers), such as Proscar (AKA Finasteride and Propecia), and Dutasteride (AKA Avodart). It is important to note that the use of these ancillary compounds will not entirely eradicate androgenic side effects due to the fact that Testosterone itself expresses an androgenic strength rating of 100 and will therefore still serve to function as an androgen in various tissues throughout the body, even if the possibility for conversion/reduction into DHT is eliminated or reduced.

An alternative (or an addition) to 5AR inhibitors is through the use of topical androgen blockers. These items are applied topically to any area of concern (for example, areas of common acne breakouts or on the scalp for the avoidance of androgen triggered male pattern baldness). The most popular and most effective topical androgen blocker to date is Nizoral shampoo (both in 1% and the stronger 2% formats), where its active ingredient Ketoconazole acts as a topical DHT blocker where it is applied on the skin and scalp. Application at least two times weekly, normally during showers, is normally enough to mitigate androgenic effects such as oily skin and acne over time.

Androgenic side effects include: increased sebum secretion (oily skin), increased bouts of acne (linked to increased sebum secretion), bodily and facial hair growth, benign prostatic hypertrophy (BPH), and the increased risk of triggering Male Pattern Baldness (MPB) in individuals that possess the genetic trait required for the condition to manifest itself.

Acne from anabolic steroid abuse

HPTA and Endogenous Testosterone Production Side Effects

All anabolic steroids exhibit endogenous Testosterone production subdual and/or shutdown. Testosterone side effects indeed exhibit this particular side effect as well, as does each and every anabolic steroid in existence (to varying degrees). The possibility of total and long term suppression and shutdown of these endocrine systems can result as well, and can develop in particular from the excessive abuse of Testosterone or any anabolic steroids both in the form of excessive cycle lengths as well as excessive dosing schemes. The specific axis of the endocrine system that governs the endogenous production of Testosterone is known as the Hypothalamic Pituitary Testicular Axis (HPTA), and this whole axis will become inhibited when the use of exogenous androgens are used, and becomes worse as the duration of use continues as a result of Leydig cell desensitization.

SIDE EFFECT PREVENTION AND SAFETY: After the conclusion of any cycle of Testosterone, a comprehensive and suitable Post Cycle Therapy (PCT) program protocol is always essential, which involves the collective use of Testosterone-stimulating ancillary compounds such as SERMS (Nolvadex, for example), the possible use of an aromatase inhibitor (such as Aromasin) and/or HCG should be utilized in order to facilitate the recovery of the HPTA and subsequent endogenous Testosterone production as quickly as possible. The duration of PCT programs normally land in the 4 – 6 week range after all anabolic steroids have cleared from the body after the end of a cycle. Failure to engage in a proper PCT program can result in permanent damage to the HPTA, whereby the individual produces insufficient/deficient levels of Testosterone (a medical condition known as hypogonadism), and medical treatment in the form of TRT (Testosterone Replacement Therapy) for life will be required.

Hepatotoxic Side Effects

Testosterone of all types, including the oral variant known as Andriol (Testosterone Undecanoate) are not C17-alpha alkylated anabolic steroids, and therefore do not exhibit any measure of toxicity on the liver. The assurance of this fact rests in the studies that 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 in administering it orally rather than the traditional intramuscular injection is 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]. It is also important to note that even if there were any measure of hepatotoxicity with Testosterone Propionate, its route of administration lies in injection, which avoids the aforementioned first pass through the liver (something that only occurs with oral ingestion of a substance). Therefore, hepatotoxicity is not of any concern where Testosterone side effects are concerned.

Cardiovascular Side Effects

Increased incidence of cardiovascular strain and negative alterations in cholesterol profiles are all normal effects that fall under Testosterone side effects. This is a side effect expressed by all anabolic steroids, and some impact this better or worse than others. It is characteristic to the nature of anabolic steroids in general, and particularly oral anabolic steroids are the worst involving these effects. Negative cardiovascular effects primarily involve the reduction of HDL (commonly labeled as the “good” cholesterol) and increases of LDL (commonly labeled as the “bad” cholesterol). This occurs by way of the fact that Testosterone (and all androgens in general) increases the activity of the enzyme hepatic lipase in the liver. Hepatic lipase is the enzyme manufactured in the liver that is responsible for the breakdown of HDL (good) cholesterol[2]. The result of these alterations involves an augmented potential risk increase of arteriosclerosis and cardiovascular disease (CVD). However, the degree to which these changes occur for the worse are usually dose-dependent (with higher doses increasing the negative changes and the risks) as well as duration, where extended cycle lengths will present a greater increasing risk of CVD rather than short cycles. The negative alterations of cholesterol and the subsequent increased risk for CVD is why shorter cycles are advised, and it is one of the Testosterone side effects that are as temporary as the cycle length itself (negative alterations in cholesterol are normally fairly quick to return to normal following the end of a cycle).

The other major factor that will affect these cholesterol changes is the route of administration of the anabolic steroid. Testosterone itself actually happens to display far less of bearing on cholesterol values in this case than all other anabolic steroids. This is due to due to the liver’s aptitude to freely metabolize Testosterone, which is resultant of the fact that Testosterone is not tremendously resistant to hepatic breakdown and metabolism, unlike many other anabolic steroid analogues that have been altered to increase their resistance to hepatic metabolism. The increases in hepatotoxicity frequently results from various anabolic steroids which possess the aforementioned trait of exhibiting a greater degree of resistance to hepatic metabolism than Testosterone. This is one of the main reasons as to why oral anabolic steroids express greater degrees of hepatotoxicity (which also vary among the different C17-alpha alkylated orals. The C17-alpha alkylation is the origin for the anabolic steroid becoming further resistant to liver metabolism, or to undergo breakdown by the liver. The concern involving whether or not an anabolic steroid exhibits a high resistance to hepatic metabolism (or a low resistance) is an influence as to how much of a bearing a given anabolic steroid holds 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[3]. 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 dosages were raised to 600mg weekly, reduction of HDL cholesterol had dropped to 21%[4]. 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.

SIDE EFFECT PREVENTION AND SAFETY: It is therefore advised that individuals utilize minimal doses of an aromatase inhibitor during cycles for the purpose of Estrogen control rather than entire Estrogen level elimination. The concept of such a practice is to maintain Estrogen levels within normal ranges and disallow them to increase dramatically as a result of aromatization, but at the same time prevent Estrogen levels from dropping below normal physiological levels to almost undetectable levels from the use of full doses of an aromatase inhibitor. It is also extremely important that any user of anabolic steroids, no matter the type or preparation (oral or injectable), to take exquisite care in making the proper adjustments in their nutritional habits that favor positive cholesterol maintenance and changes, especially when running cycles of anabolic steroids.



Medical References:


[1] Enzyme induction by oral testosterone. Johnsen SG, Kampmann JP, Bennet EP, Jorgensen F. 1976 Clin Pharmacol Ther 20:233-237

[2] Hepatic lipase activity influences high density lipoprotein subclass distribution in normotriglyceridemic men: genetic and pharmacological evidence. Grundy S et al. J Lipid Res 1999 40:229-34.

[3] High-density lipoprotein choilesterol is not decreased if an aromatizable androgen is administered. Friedl K, Hannan C et al. Metabolism 39(1) 1990;

[4] Testosterone dose-response relationships in healthy young men. Bhasin S, Woodhouse L. et al. Am J Physiol Endocrinol Metab 281:E1172-81, 2001