- Blood Pressure
- Cholesterol & Lipids
- Hair Loss
- Kidney stress
- Liver stress
- Stunned Growth
- Testicular Atrophy
- Water & Salt retention
High levels of androgens will stimulate the sebaceous glands in the skin to secrete an oily substance called sebum. When the secretion of sebum becomes too much the hair follicles may clot, resulting in acne. For mild cases of acne there are a number of over the counter topical medications to help clean the skin from excess oil. For more severe acne breakouts require stronger medications like isotretinoin (Accutane). Acne is typically resolved with the cessation of steroids.
While on a steroid cycle a common side effect that users experience is increased aggression resulting in mood swings, irritability and a short temper, some users have even reported rare cases of verbal and physical violence. I’m guessing these extremely rare cases are more so due to their general behaviour of the individual and less so to the drug itself.
We cannot dispute that aggression exist among steroid users or names like ‘roid rage’ or a metaphor used when you hit a long golf shot for example ‘he must be on steroids’ would exist. The other side of this could also be the psychological outlook and belief system that taking steroids you will actually cause aggression and so this behavior is created rather by a thought than the actual drug. It is documented in animals however the link between natural testosterone and aggression however these tests have not been conclusive in humans.
One must also take into account that increased aggression is largely dependent upon dose and stacking different highly androgenic compounds. Many athletes in explosive strength sports like cage fighting, bodybuilding, power lifters, sprinters and so forth specifically favour highly androgenic steroids due to their alleged abilities to support aggression and the mental and physical drive they offer. However the only way to achieve factual evidence that steroids increase aggression would be to conduct a clinical trial with two groups of patience’s, one group being administered a high doses of anabolic steroids and the other a placebo drug. I do not see this happening any time soon.
Anabolic Steroids may increase blood pressure when used in dosages above therapeutic levels. In most cases elevations in blood pressure are relatively modest, but it’s advisable to keep a close eye on levels and action should be taken if blood pressure exceeds 140/90. There are a number of factors responsible in elevating blood pressure, but the most common causes are increased water retention, increased vascular stiffness and increases in the proportion of blood volume that is occupied by red blood cells. Aromatizing or highly estrogenic steroids tend to cause the greatest influences over blood pressure, although any steroid may cause elevated blood pressure. Blood pressure tends to normalize with the cessation of steroids.
Cholesterol & Lipids:
Some steroids may cause a harmful increase in LDL (Bad) cholesterol and a decrease in HDL (Good) cholesterol. 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. The drug tamoxifen citrate (Nolvadex) has shown to exhibit positive effects on HDL values whereas other anti-estrogens like aromatase inhibitors show the opposite.
During the time that steroids are being administered, natural hormone production is diminished because the body recognizes the excess hormone levels. When the steroid drugs are abruptly discontinued, however, the body can enter a state of temporary hypogonadism (low androgen levels). This may be associated with a number of psychological symptoms including depression, insomnia, and loss of interest. This condition is usually referred to as anabolic steroid withdrawal depression, and can persist for weeks or even months as the body slowly resumes normal hormone production. The best way to combat this is by following a proper PCT cycle. The other reason could very well be due to the toxins that have built up in your body following a steroid cycle, so it is best advised to detoxify your body after each and every cycle.
Anabolic steroids with significant estrogenic or progestational activity may cause gynecomastia (female breast development in males). This disorder is specifically characterized by the growth of excess glandular tissue in men, due to an imbalance of male and female sex hormones in the breast. The first sign is typically pain in the nipple area. This may quickly coincide with minor swelling. This is sometimes referred to as pseudo-gynecomastia, as it primarily involves fat and not glandular tissue. At this stage, it may be possible to address mild nipple swelling by reducing or eliminating the offending steroidal compounds, and administering an appropriate anti-estrogenic medication for several weeks. If left untreated, however, this may quickly progress to clear gynecomastia, which involves significant fat, fibrous, and glandular tissue growth. The hard tissue growth may be easily felt in the early stages when pinching deeply around the nipple. Noticeable gynecomastia is likely to require corrective cosmetic.
Careful steroid selection and reasonable dosing are usually regarded as the most basic and reliable methods for preventing its onset. Many steroid users also frequently take some form of estrogen maintenance medication, which may effectively counter the effects of elevated estrogenicity. Common options include aromatase inhibitors such as anastrozole. The use of a PCT program at the conclusion of steroid administration (which usually includes several weeks of anti-estrogen use) is also commonly advised, as gynecomastia is sometimes reported in the post-cycle hormone imbalance phase when steroids are not actually being taken.
It is important to note that progesterone can also augment the stimulatory effect of estrogen on mammary tissue growth. As such, progestational drugs may be able to trigger the onset of gynecomastia in sensitive individuals, even without elevating levels of estrogen. Many anabolic steroids, particularly those derived from nandrolone, are known to exhibit strong progestational activity. While gynecomastia is not a common compliant with these drugs, they are occasionally linked to this side effect in anecdotal reports. The anti-prolactin cabergoline (Cabaser) is usually taken in such instances.
Although dihydrotestosterone is identified as the primary hormone involved in the progress of androgenetic alopecia, it does not possess a unique ability to influence this condition. All anabolic/androgenic steroids stimulate the same cellular receptor, and as a result are capable of providing the necessary androgenic stimulation. Baldness can result from steroid use, even in the absence of steroids that convert to, or are derived from, dihydrotestosterone. Treatment for androgenetic alopecia in men usually involves topical minoxidil and oral finasteride, as-alpha reductase enzyme inhibitor.
Anabolic steroid use may be associated with insomnia. This adverse reaction appears to be related to an imbalance of hormone levels, and has been noticed during both excess and insufficient hormonal states. While insomnia may be frequently reported among steroid users, this side effect rarely reaches a clinically significant level.
Direct damage to the kidneys from anabolic steroids usage are very rare and usually even the opposite might be the case. However high blood pressure as a result from steroid usage is usually to blame here. In healthy individuals, clinical renal toxicity caused by the short-term administration of anabolic steroids is unlikely. Cranberry extract is sometimes used in an attempt to prevent kidney damage.
Many steroids are toxic to the liver (hepatotoxic). These compounds can cause serious and sometimes life-threatening damage when abused, and occasionally even under therapeutic conditions. Those agents commonly associated with clinical hepatotoxicity include (but are not limited to) fluoxymesterone, methandrostenolone, methylandrostenediol, methyltestosterone, norethandrolone, oxymetholone, and stanozolol. Liver strain, as assessed by elevated liver enzymes, has also been reported with non-alkylated esterified injectable steroids including nandrolone decanoate and testosterone enanthate in extremely rare instances. These steroids have never been associated with serious hepatic damage, however, and are not regarded as liver toxic.
Early liver toxicity is usually visible in blood test results for hepatic function before physical symptoms or dysfunction develop. Screening for abnormalities in hepatic markers is regarded as the most effective way of preventing liver damage from steroid administration. Should asymptomatic toxicity go unnoticed and without a change in drug intake, it is likely to progress to more severe hepatic strain, injury, or hepatic dysfunction. Immediate cessation of anabolic steroid use and a full assessment of liver and full-body health are advised should any signs of unacceptable liver toxicity become apparent.
Symptoms may include anorexia, malaise, nausea, vomiting, upper abdominal pain, or pruritus (itching). The stool may also change to a clay color (alcholic stool) due to the reduced excretion of bile, and the urine may become amber. Cholestatic jaundice may develop, which is characterized by a yellowing of the skin, eyes, and mucous membranes due to high levels of bilirubin in the blood.
Supplements containing Milk Thistle are often used in an attempt to limit hepatotoxicity but effectiveness is fairly limited. More recent findings show that using the liver detoxifier "SAMe" can actually be very effective positive influence on our liver while on a anabolic steroid cycle, the other way to do this is with TMG which actually converts to SAMe.
Anabolic steroids may inhibit linear growth when administered before physical maturity. These hormones actually can have a dichotomous influence on linear height. Steroid use may cause premature closure of the growth plates, which inhibits further linear growth. There have been a number of cases of noticeably stunted growth (short stature) in juvenile athletes that have taken these drugs.
While androgens, estrogens, and glucocorticoids all inherently participate in bone maturity, estrogen is regarded as the primary inhibitor of linear growth in both men and women. Women are shorter on average than men, and also tend to stop growing at a slightly earlier age, due to the effects of this hormone. Anabolic steroids that either convert to estrogen or are inherently estrogenic are, likewise, more likely to inhibit linear growth than other agents. Individuals are warned of the potential for growth interruption when anabolic steroids are used before physical maturity.
Anabolic steroids may produce atrophy (shrinkage) of the testicles. Although testicular atrophy is very common in frequency, it is also regarded as a temporary reversible side effect. Atrophy should not produce permanent damage and reversal is likely to happen during a properly constructed PCT cycle.
Water & Salt retention:
Anabolic steroids may increase the amount of water and sodium stored in the body. Estrogen is a regulator of fluid retention in both men and women. Increased levels of estrogen tend to increase hypothalamic arginine vasopressin levels, which can promote the increased storage of water. Anabolic steroids that convert to estrogen, or possess inherent estrogenic activity are associated with increased extracellular water retention.