Testosterone Side Effects
In the realm of side effects, testosterone measures up as the unconditionally safest anabolic steroid to use, given the fact that it is the number one anabolic hormone produced and secreted naturally and endogenously by the human body.
It is logical then that the human body is already well aware of the effects and side effects of testosterone on its subsystems, tissues, and cells.
In addition to this, enough research has been conducted on the effects of testosterone and its side effects on the human body that almost all knowledge of testosterone side effects is well known and well documented in the medical and scientific fields.
Compared to other modified derivatives of testosterone, the risk of experiencing side effects from these other analogs is much greater, as they may exhibit unusual side effects and strange behaviors that are unfamiliar to science. This is mainly due to the fact that these analogs and derivatives are modified to essentially create completely new anabolic steroid analogs.
Since testosterone is the most natural anabolic steroid for the human body, most individuals using testosterone should not exhibit any hidden or strange side effects.
Once again, it is very important to understand that every individual reacts differently to any compound, drug, or food.
However, when compared to very mysterious compounds like anadrol or trenbolone for example, the effects of testosterone on most individuals should be more or less the same across the board.
That said, testosterone is not without side effects.
However, it is through science and medicine's almost complete understanding of this anabolic steroid that allows for a good understanding of testosterone side effects and the possibility of dealing with them.
Estrogenic Side Effects
Testosterone itself exhibits a small amount of estrogenic activity through its ability to express moderate binding affinity for the aromatase enzyme (the enzyme that converts testosterone to estrogen, also known as aromatization).
You can then expect to see a moderate amount of aromatization with testosterone use.
The conversion (aromatization) of testosterone to estrogen can result in a significant increase in plasma estrogen concentrations, especially when testosterone is used at physiological "bodybuilding doses" and doses required to enhance athletic performance and physique in general.
This is why estrogenic testosterone side effects are so dose dependent, and generally speaking, the higher the dose taken, the greater the amount of aromatization induced, which increases the likelihood and incidence of estrogenic side effects.
For this reason, estrogenic testosterone side effects should not be ignored, and as mentioned earlier, the rate of aromatization is generally always correlated to the dose used.
All potential testosterone users should understand that bodybuilding doses of testosterone often produce moderate to significant amounts of aromatization that must be dealt with in some way.
Side effect prevention and safety: There are two main ways to mitigate and deal with these potential estrogenic testosterone side effects.
One way is to use an aromatase inhibitor, which acts to deactivate (by inhibiting) the aromatase enzyme.
This effectively removes the pathway for testosterone to aromatize into estrogen, effectively preventing and blocking the increase in total circulating estrogen at the root cause (aromatization of testosterone by the aromatase enzyme).
Another slightly similar but very different approach is to use a SERM (selective estrogen receptor modulator) such as Nolvadex (tamoxifen), which works by blocking estrogen from binding to receptor sites in breast tissue.
SERMs like Nolvadex only act to reduce estrogen-induced gynecomastia in the targeted tissues, and do not actually reduce serum estrogen levels in the body, as is often misunderstood or misinformed.
Only by using an aromatase inhibitor can you achieve the effect of reducing total circulating plasma estrogen levels.
Potential estrogenic side effects include water retention and bloating, increased blood pressure (due to water retention), increased likelihood of fat retention/gain in certain body areas, and gynecomastia.
Androgenic Side Effects
Testosterone acts as the primary androgen in men, so it's no surprise that testosterone side effects actually include androgenic side effects.
In addition to its action on androgen receptors in certain tissues, testosterone's much more potent androgenic effects are actually a byproduct of its conversion (or more accurately, "reduction") to its more potent androgenic metabolite, dihydrotestosterone (DHT).
Testosterone itself has an androgenic strength rating of 100, which means that it has a moderate amount of androgenic activity and strength to bind to androgen receptors in the body.
However, as mentioned earlier, testosterone side effects are more due to the fact that testosterone is converted into the stronger and more potent androgens mentioned earlier.
This androgen is once again known as dihydrotestosterone (DHT), and the reduction (conversion) process occurs via the 5-alpha reductase (5AR) enzyme.
The 5AR enzyme is present in large amounts in a variety of specific tissues in the body, such as the scalp, prostate, and skin.
When testosterone enters these tissues, it is rapidly reduced to the more potent androgenic metabolite DHT due to the high concentration of 5ARs in the area.
It is DHT that is responsible for most of the serious androgenic side effects associated with testosterone (or anabolic steroids in general that are reduced to a more potent metabolite via the 5AR enzyme).
Side effect prevention and safety: Supplements exist that work to inhibit the 5-alpha reductase enzyme, essentially eliminating DHT.
These compounds are known as 5-alpha reductase inhibitors (or 5-alpha blockers) and include Proscar (aka finasteride and Propecia) and Dutasteride (aka Avodart).
It is important to note that the use of these ancillary compounds does not completely eradicate androgenic side effects, and testosterone itself has an androgenic strength rating of 100, so even if the potential for conversion/reduction to DHT is eliminated or reduced, it can still act as an androgen in various tissues throughout the body.
As an alternative (or in addition) to 5AR inhibitors, topical androgen blockers can be used.
These products are applied topically to areas of concern (e.g., common acne prone areas or the scalp to prevent androgen-induced male pattern baldness).
By far the most popular and most effective topical androgen blocker is Nizoral shampoo (in two forms, 1% and the more potent 2%), whose active ingredient, ketoconazole, acts as a topical DHT blocker that is applied to the skin and scalp.
Applying it at least twice a week, usually in the shower, is enough to mitigate androgenic effects such as oily skin and acne over time.
Androgenic side effects include increased sebum secretion (oily skin), increased acne breakouts (associated with increased sebum secretion), body and facial hair growth, and an increased risk of developing benign prostatic hyperplasia (BPH) and male pattern baldness (MPB) (if you have the genetic traits necessary to develop these conditions).
HPTA and Endogenous Testosterone Production Side Effects
All anabolic steroids suppress or shut down endogenous testosterone production.
Testosterone side effects, like all anabolic steroids in existence, actually exhibit these specific side effects (albeit to varying degrees).
The possibility of total and long-term suppression and disruption of this endocrine system can also occur, especially with excessive abuse of testosterone or anabolic steroids in the form of excessive cycle lengths as well as excessive dosing plans.
The specific axis of the endocrine system that governs the endogenous production of testosterone is called the hypothalamic-pituitary-testicular axis (HPTA), and with the use of exogenous androgens, this entire axis is suppressed and worsens as a result of Leydig cell desensitization the longer the duration of use continues.
Side effect prevention and safety
A comprehensive and appropriate post cycle therapy (PCT) program protocol is always essential after the end of a testosterone administration cycle, which should include the co-use of testosterone stimulating ancillary compounds such as SERMS (e.g. Nolvadex), aromatase inhibitors (e.g. Aromasin) and/or HCG to promote the recovery of HPTA and subsequent endogenous testosterone production as quickly as possible.
The duration of a PCT program typically begins in the 4-6 week range after the end of the cycle, after all anabolic steroids have been eliminated from the body.
Failure to engage in a proper PCT program can permanently damage HPTA, resulting in low or deficient testosterone levels (a medical condition known as hypogonadism), and may require treatment in the form of testosterone replacement therapy (TRT) for the rest of your life.
Hepatotoxic Side Effects
All types of testosterone, including the oral variant known as Andriol (testosterone undecanoate), are not C17-alpha alkylated anabolic steroids and therefore do not exhibit liver toxicity.
Confirmation of this fact comes from a study that examined the potential for liver toxicity when testosterone was used at high doses (400 mg daily, equivalent to 2,800 mg weekly) for 20 days in several male subjects, administered orally rather than by intramuscular injection.
The idea of oral administration, as opposed to traditional intramuscular injection, is to saturate the liver with large amounts of testosterone (all substances taken orally make a 'first pass' through the liver, interacting with it at a much faster rate than the injection route of administration).
In studies, no changes were observed [1].
It is also important to note that even if liver toxicity of testosterone propionate has been measured, its route of administration is by injection, which avoids the aforementioned first pass through the liver (a phenomenon that only occurs with oral ingestion).
Therefore, liver toxicity is not a concern when it comes to testosterone side effects.
Cardiovascular side effects
Increased cardiovascular tension and negative changes in cholesterol levels are both normal effects that fall under the category of testosterone side effects.
These are side effects seen with all anabolic steroids, some more severe or less affecting than others.
This is a characteristic of anabolic steroids in general, with oral anabolic steroids being the most severe when it comes to these side effects.
Negative cardiovascular effects primarily include a decrease in HDL (commonly categorized as "good" cholesterol) and an increase in LDL (commonly categorized as "bad" cholesterol).
This occurs because testosterone (and all androgens in general) increases the activity of the hepatic lipase enzyme in the liver.
Hepatic lipase is an enzyme produced by the liver that is responsible for the breakdown of HDL (good) cholesterol [2].
As a result of these changes, the potential risk of arteriosclerosis and cardiovascular disease (CVD) can increase.
However, the extent to which these changes are exacerbated is generally dose-dependent (higher doses result in more negative changes and increased risk), with longer duration resulting in a greater increase in CVD risk than shorter duration.
Negative changes in cholesterol and the resulting increased CVD risk is why shorter cycles are recommended, and is one of the side effects of testosterone that is as temporary as the cycle itself (negative changes in cholesterol typically return to normal fairly quickly after the cycle ends).
Another major factor affecting these cholesterol changes is the route of administration of the anabolic steroid.
Testosterone itself actually has much less of an effect on cholesterol levels than all other anabolic steroids.
This is due to the liver's ability to metabolize testosterone freely, as testosterone is not highly resistant to hepatic breakdown and metabolism, unlike many other anabolic steroid analogs that have been modified to be more resistant to hepatic metabolism.
Increased hepatotoxicity is often caused by various anabolic steroids with the aforementioned characteristics that exhibit more resistance to hepatic metabolism than testosterone.
This is one of the main reasons why oral anabolic steroids are more hepatotoxic (oral anabolic steroids have different degrees of hepatotoxicity depending on the C17-alpha alkylated steroid).
C17-alpha alkylation is the origin of anabolic steroids becoming highly resistant to hepatic metabolism or being broken down by the liver.
An issue related to whether an anabolic steroid is highly resistant (or less resistant) to hepatic metabolism is how much a particular anabolic steroid affects the liver's management of cholesterol.
Testosterone, in particular, was shown in one clinical study to have only a mild effect on HDL cholesterol when 280 mg of testosterone enanthate was administered weekly for 12 weeks.
When an aromatase inhibitor was subsequently administered, the cholesterol profile changed for the worse, with a significant 25% reduction in HDL cholesterol [3].
Conversely, another study using 300 mg of testosterone enanthate weekly for 20 weeks without the use of an aromatase inhibitor showed a 13% reduction in HDL cholesterol, but when the testosterone dose was increased to 600 mg weekly, the HDL cholesterol reduction dropped to 21% [4].
Based on the data examined, it is very clear that the increase in estrogen through aromatization and hepatic metabolism actually helps to offset the negative cholesterol changes caused by anabolic steroid use in excess of physiological amounts.
This is not surprising considering that estrogen itself is known to have a positive effect on cholesterol levels.
Therefore, the use of aromatase inhibitors and their effects on cholesterol levels should always be kept in mind when considering adding an aromatase inhibitor to your cycle.
Side effect prevention and safety
It is therefore recommended that a minimum dose of aromatase inhibitors be used during the menstrual cycle with the goal of regulating estrogen rather than eliminating total estrogen levels.
The idea behind this approach is to keep estrogen levels within the normal range and prevent aromatization from causing a sharp increase in estrogen levels, while at the same time preventing the use of full doses of aromatase inhibitors from causing estrogen levels to drop below normal physiological levels to almost undetectable levels.
It is also very important for all anabolic steroid users, regardless of the type of anabolic steroid or formulation (oral or injectable), to pay close attention to properly adjusting their nutritional habits to ensure that they are making positive choices.
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 the distribution of high-density lipoprotein subclasses in normotriglyceridemic men: Genetic and pharmacologic evidence. Grundy S et al. J Lipid Res 1999 40:229-34.
[3] High-density lipoprotein cholesterol is not reduced by administration of aromatizing androgens. Friedl K, Hannan C et al. Metabolism 39(1) 1990;
[4] Testosterone dose-response relationship in healthy young men. Bhasin S, Woodhouse L. et al. Am J Physiol Endocrinol Metab 281:E1172-81, 2001
