Endocrine Effects of Anabolic Steroids

Misuse of steroids can interfere with the regular synthesis of hormones within the body, resulting in alterations that can be either reversible or permanent. It is worth noting that the adverse effects of anabolic-androgenic steroids (AAS) predominantly manifest with prolonged usage [1]. The primary side effects commonly observed are primarily related to appearance and are reversible once the use of steroids is discontinued. AAS classified as Class B can induce liver toxicity [2], resulting in jaundice that typically emerges within a timeframe of 2 to 5 months. Hepatotoxicity has not been associated with the intramuscular administration of testosterone esters. Significant liver and lipoprotein-related adverse effects are primarily observed with high doses of alkylated AAS [3], whereas parenteral AAS use appears to impact heart muscles, which may become clinically evident after a number of years. Fortunately, the occurrence of severe, life-threatening effects appears to be relatively rare.

Acute adverse effects

Some of the minor and temporary side effects commonly associated with steroid use include headaches, fluid retention (particularly in the extremities), gastrointestinal discomfort, diarrhea, stomach pains, and increased oiliness of the skin. Jaundice, menstrual irregularities, and hypertension are among the acute effects that can have more noticeable clinical implications. In the case of injection use, infections can occur at the injection site, leading to pain and the formation of abscesses. Both males and females may experience acne during puberty while undergoing androgen treatment, which is attributed to the increased activity of sebaceous glands and the secretion of sebum, a natural oil [4].

Aromatization refers to the conversion of steroid hormones into different forms. Testosterone and other anabolic steroids that can be aromatized are partially metabolized into estradiol and other estrogen agonists. Consequently, males who use high doses of AAS may experience elevated estrogen levels comparable to those observed in women during a regular menstrual cycle [5]. Elevated estrogen levels in men due to the aromatization of anabolic steroids can result in breast pain and the development of gynecomastia, a condition characterized by the enlargement of breast tissue. Observational studies indicate that a significant majority of anabolic steroid users (88-96%) encounter at least one observable side effect. These side effects include acne (40-54%), testicular atrophy (40-51%), gynecomastia (10-34%), cutaneous striae (34%), and injection-site pain (36%). It’s worth noting that these percentages represent the reported occurrence rates among steroid users in these studies [6].

Chronic adverse effects

• Somatic effects

Anabolic steroid abuse can lead to various health consequences, including urogenital issues, acne, and cardiovascular and hepatic diseases. Studies conducted by Melchert and Welder [7], Rogol and Yesalis [8], and Sullivan et al. [9] have highlighted the association between anabolic steroid abuse and these conditions.

In males, certain changes caused by anabolic steroid use can be reversible. These changes include decreased sperm production, impotence, difficulties or pain during urination, and testicular atrophy (shrinkage of the testicles). According to a study conducted on male bodybuilders, more than half of the participants experienced testicular atrophy and/or reversible or irreversible breast development (gynecomastia) [10]. Females who have elevated levels of anabolic androgenic steroids (AAS) may experience menstrual irregularities and the development of masculinizing characteristics. These include decreased body fat and breast size, deepening of the voice, excessive growth of body hair, irreversible scalp hair loss (baldness), and enlargement of the clitoris. It is important to note that with prolonged use of steroids, some of these effects can become irreversible [10, 11]. Steroid use has been linked to prostate cancer, as indicated in a study by Creagh et al. [12]. One significant concern associated with steroid use in children and adolescents is premature closure of the growth plates, which can lead to a reduction in adult height. However, in certain cases, AAS may be clinically employed to manage abnormal body length. It is important to note that the use of AAS carries an elevated risk of developing fatal liver cysts, other liver alterations, and liver cancer, as suggested by studies conducted by Soe et al. [13] and Stimac et al. [14]. Class B and C AAS (anabolic-androgenic steroids) are known to possess significant hepatotoxicity. Alkylated AAS, in particular, have been demonstrated to elevate hepatic triglyceride lipase activity by 21% to 123% and increase low-density lipoprotein levels by as much as 29%. These findings were reported in studies conducted by Bagatell and Bremner [15] and Thompson et al. [16]. It is worth noting that the hepatic pathology induced by AAS use can often be reversed when AAS administration is discontinued, as indicated by Modlinski and Fields [17]. Furthermore, the overall occurrence of adverse hepatic effects among long-term AAS users is likely low, according to a study by Pope and Katz [18].

Long-term use of AAS has been linked to an increased risk of cardiovascular disease (CVD), including hypertension, heart attacks, and strokes. Steroids contribute to the development of CVD by altering the levels of lipoproteins responsible for transporting cholesterol in the bloodstream. Specifically, steroids, especially oral steroids, elevate low-density lipoprotein cholesterol (LDL-cholesterol) levels and decrease high-density lipoprotein cholesterol (HDL-cholesterol) levels. These changes in lipoprotein profiles can contribute to the development of cardiovascular complications associated with AAS use. Indeed, alkylated AAS, including orally administered ones like stanozolol (at a dosage of 6 mg/day orally for 6 weeks), have been observed to significantly decrease HDL-cholesterol levels. Specifically, HDL2-cholesterol can be reduced by 23% to 80%, while overall HDL-cholesterol levels can be lowered by approximately 33%. These findings have been reported in studies conducted by Bagatell and Bremner [15] and Thompson et al. [16]. In contrast to orally administered AAS, the impact of parenteral testosterone enanthate (at a dosage of 200 mg/week for 6 weeks) on HDL-cholesterol levels is less pronounced. Studies suggest that parenteral testosterone enanthate use is associated with a modest reduction of approximately 9% in HDL-cholesterol levels [16]. Generally, after discontinuation of AAS use, serum levels tend to return to their baseline levels within a few weeks to months, as reported by Hartgens et al. [19]. Additionally, even when high doses of testosterone enanthate (600 mg/week, administered parenterally for 20 weeks) are used, the impact on HDL-cholesterol levels appears to be minimal, as indicated by Singh et al. [20].

Elevated levels of LDL-cholesterol and reduced levels of HDL-cholesterol are associated with an increased risk of atherosclerosis. Power lifters, for instance, are reported to have a higher risk of atherosclerosis due to higher concentrations of LDL-cholesterol and lower concentrations of HDL-cholesterol, as noted in a study by Hurley et al. [21]. Furthermore, the use of steroids can induce blood clotting as a result of increased platelet count and aggregation, as indicated by studies conducted by Ferenchick et al. [22] and Togna et al. [23]. Steroid use can contribute to myocardial hypertrophy, which increases the risk of arrhythmias, sudden death, systolic and diastolic hypertension, and myocardial infarction. Studies by Frankle et al. [24] and Karila et al. [25] have highlighted these cardiovascular effects of AAS. Certain cardiovascular effects, such as hypertension, dyslipidemia, and coagulation abnormalities, may improve after discontinuation of AAS use. However, effects like atherosclerosis and cardiomyopathy appear to be irreversible, as noted by Hartgens and Kuipers [26] and Sullivan et al. [9].

• Effects on the neuropsychiatric system

The misuse of AAS is linked to various behavioral and psychiatric effects, which range from mild irritability and an increased drive for body training (which may still be socially acceptable) to uncontrolled aggression, hostility, and even symptoms of depression and mania. The occurrence of these effects is generally low and heavily dependent on the dosage of AAS used. Additionally, it can be challenging to determine whether the behavioral and psychiatric effects are directly caused by AAS use itself or if they are influenced by underlying personality traits of the individual or psychosocial factors related to AAS misuse. It is important to note that chronic AAS users often exhibit traits associated with antisocial behavior, narcissism, and histrionic personality. However, studies have suggested that supraphysiological doses of AAS can directly induce hypomanic or manic symptoms, which may be accompanied by aggression and violence. It is worth mentioning that not all studies have consistently reported mood changes, indicating significant variability in symptom presentation. This variability can be attributed to factors such as the dosage, specific compound used, duration of AAS use, individual personality traits, and concurrent or past use of other recreational drugs. Some individuals may exhibit prominent symptoms, while others may not display any noticeable mood changes [27, 28].

Excessive doses of AAS (more than 1000 mg/week) can indeed produce distinct psychiatric effects in individuals. The most notable psychiatric features observed in such cases are manic-like presentations characterized by irritability, aggression, euphoria, grandiose beliefs, hyperactivity, and engaging in reckless or dangerous behavior. A study by Clark and Henderson [29] has reported these prominent psychiatric symptoms. It is important to note that while some users may experience a positive self-perception while using anabolic steroids, extreme mood swings, including manic-like symptoms, can occur, potentially leading to violent behavior [30]. AAS users can experience various psychological symptoms, including paranoid jealousy, extreme irritability, delusions, and impaired judgment, which may arise from a sense of invincibility. Additionally, individuals may exhibit acute psychosis, exacerbation of tics, or the development of acute confusional states as a result of AAS use. These presentations have been reported in studies conducted by Hartgens and Kuipers [26] and Perry et al. [31]. Case reports and studies involving individuals and groups using AAS, such as bodybuilders, have documented various psychiatric episodes. These include hypomania or manic episodes, as reported by Freinhar and Alvarez [32] and Pope and Katz [18], episodes of depression or suicide, as noted by Parssinen et al. [33], Pope and Katz [18], and Thiblin et al. [34], and psychotic episodes reported by Freinhar and Alvarez [32]. These findings highlight the potential psychiatric risks associated with AAS use.

The prevalence of psychiatric symptoms among AAS abusers is indeed significant. It is noteworthy that 23% of individuals using high doses of AAS (>1000 mg/week) met the DSM-III-R criteria for major mood syndrome, including mania, hypomania, and major depression. Additionally, a percentage ranging from 3% to 12% developed psychotic symptoms. These findings, as reported by Pope and Katz [18], emphasize the importance of recognizing and addressing the potential psychiatric effects associated with AAS abuse.

Muscle dysmorphia, characterized by an excessive and pathological preoccupation with muscularity, is prevalent among AAS users. It has been reported that muscle dysmorphia affects approximately 1.5% to 6% of Swedish gym visitors, as indicated by a student thesis [35]. AAS users may develop this condition due to an obsession with the belief that their muscularity is not sufficient. Pope et al. [36] suggested that the significant gap between men’s actual muscularity and their body ideals could contribute to the rise in disorders like muscle dysmorphia and anabolic steroid abuse. This suggests that societal pressures and unrealistic body standards may play a role in the development of such conditions.

In summary, high doses of AAS have the potential to induce neuropsychiatric symptoms, although the overall prevalence of such symptoms is relatively low. It is important to note that a subset of AAS abusers may already have pre-existing psychiatric conditions, which can complicate the causal relationship between AAS abuse and neuropsychiatric effects. Therefore, while neuropsychiatric symptoms can occur with AAS use, it is crucial to consider individual factors and pre-existing psychiatric morbidity when evaluating the relationship between AAS abuse and these effects.

Endocrine consequences

Indeed, while anabolic effects refer to the promotion of muscle growth, tissue repair, and increased protein synthesis, androgenic effects are related to the development of male secondary sexual characteristics. These effects are mediated through the binding of AAS to androgen receptors in various tissues. While efforts are made to develop AAS with more selective anabolic effects and reduced androgenic effects, it is challenging to completely dissociate the two. Consequently, AAS use carries the risk of both desired anabolic effects and unwanted androgenic effects, which can vary among individuals [37]. Indeed, the adverse effects of AAS abuse can be influenced by several factors, including the age and sex of the individual, the duration and total dose of AAS exposure, and the specific type of steroid used. These factors can contribute to variations in the manifestation and severity of side effects. For example, certain side effects may be more pronounced in younger individuals whose bodies are still developing, while others may be more common in specific genders. Additionally, the type of AAS used, such as oral or injectable steroids, can also impact the nature and extent of adverse effects. It is crucial to consider these factors when assessing the potential risks associated with AAS abuse [8]. Indeed, the effects of AAS abuse can be categorized into two main types: androgenic effects and toxic effects. Androgenic effects refer to the exaggeration of normal physiological effects of androgens in the body. These can include increased muscle mass, facial hair growth, deepening of the voice, and other masculinizing effects.

On the other hand, toxic effects are considered the more serious consequences associated with prolonged and excessive use of AAS at pharmacological doses. These effects can vary and may involve multiple organs and systems in the body. Examples of toxic effects include liver damage (hepatotoxicity), cardiovascular complications, psychiatric disturbances, endocrine disruptions, and metabolic abnormalities.

It is important to note that the distinction between androgenic and toxic effects is not always clear-cut, as some effects may have overlapping characteristics. Moreover, the severity and occurrence of these effects can vary among individuals depending on factors such as dosage, duration of use, and individual susceptibility.

The adverse consequences of AAS abuse can be particularly detrimental in females and adolescents. In females, the excessive use of AAS can lead to irreversible virilization, which includes the development of masculine characteristics such as deepening of the voice, excessive body hair growth (hirsutism), and enlargement of the clitoris. These effects are difficult to reverse once they occur.

In adolescents, AAS abuse can interfere with normal growth and development, potentially resulting in stunted linear growth. This occurs because AAS can prematurely close the growth plates in the long bones, limiting the individual’s potential for reaching their full adult height.

Another reversible effect of AAS abuse is the suppression of the hypothalamic-pituitary-gonadal axis, which can lead to disruptions in menstrual function and infertility in females. Once AAS use is discontinued, normal hormonal function can typically be restored.

Additionally, AAS abuse can stimulate the sebaceous glands, leading to increased production of sebum (oily substance) in the skin. This can contribute to the development of severe acne in AAS users, especially at higher doses.

It is important to emphasize that the use of AAS should be approached with caution, and individuals should be aware of the potential risks and adverse effects, particularly in vulnerable populations such as females and adolescents.

Anabolic steroid abuse is accompanied by a significant issue involving the consistent reduction in the levels of HDL-cholesterol in the bloodstream due to the impact of androgens, which suppress the activity of hepatic endothelial lipase. This decline in HDL-cholesterol levels could potentially have long-term implications by increasing the risk of ischemic heart disease. However, it is unlikely to be linked to conditions such as cardiomyopathy, cerebral vascular accident, or pulmonary embolism, which are associated with the use of anabolic androgenic steroids (AAS). These conditions might be independent effects of androgens on the blood vessels and the process of blood clotting. The potential negative effects on the prostate gland resulting from prolonged use of anabolic steroids have not been fully understood yet, with the available data limited to occasional case reports. In clinical trials for male contraception, participants were administered a weekly dosage of 200 mg of testosterone enanthate for a duration of up to 18 months. The collected data revealed that there were no significant alterations observed in the plasma concentrations of prostate-specific antigen (PSA), a marker commonly used for prostate health assessment. Additionally, the transverse diameter of the prostate gland only increased by a modest 14% during the study period [38]. Severe liver abnormalities are predominantly linked to orally active 17a-alkylated androgens, including substances like methyltestosterone, methandrostenolone, oxandrolone, and stanozolol. Individuals using anabolic steroids have displayed a spectrum of behavioral changes, ranging from heightened aggression to the infamous “roid rage” and even psychosis [39]. The withdrawal effects experienced after discontinuing the use of exogenous testosterone are likely connected to the gradual restoration of natural testosterone production by the body.

While there are individual case reports available in the literature, the precise frequency of severe or fatal adverse effects associated with anabolic androgenic steroid (AAS) use is uncertain. Consequently, it is challenging to accurately assess the true extent of the risks associated with AAS usage. It is reasonable to assume that there is likely significant underreporting of AAS use. However, the overall occurrence of serious and fatal complications is probably low. These isolated cases of pathological conditions may be attributed to specific reactions in susceptible individuals exposed to high doses of anabolic androgenic steroids (AAS) used by abusers. It is important to note that these reported effects cannot be generalized to indicate a consistent effect of androgens, except for the 17a-alkylated compounds which are considered the most harmful among the anabolic agents. There is a claim that intermittent usage of anabolic steroids might mitigate long-term side effects and that their use may not be as detrimental to overall well-being or as addictive as other recreational drugs. However, it is essential to highlight that such assertions lack supporting data and should not be widely accepted at this time.

Contraindications

The use of testosterone cypionate is not recommended in individuals with severe renal, cardiac, and hepatic diseases. It is contraindicated in men with breast cancer or prostate cancer, as well as in cases of venous thromboembolism. Testosterone cypionate should not be used by pregnant women, women who may become pregnant, breastfeeding women, or individuals with hypersensitivity to any component of the formulation.

According to the Endocrinology Society, it may be prudent to avoid testosterone treatment in men who have experienced a myocardial infarction or stroke within the past six months [40, 41].

Monitoring

Before starting testosterone treatment, it is necessary to confirm the diagnosis of hypogonadism by measuring early morning testosterone levels on two different days. Additionally, certain assessments should be conducted prior to initiating treatment. These include obtaining a lipid profile, conducting hepatic function tests, measuring hemoglobin and hematocrit levels, and assessing prostate-specific antigen (PSA) levels. In patients aged 40 years and older, a prostate exam is also recommended before starting testosterone treatment. These evaluations help ensure appropriate monitoring and management during testosterone therapy.

During the course of treatment with anabolic steroids, healthcare professionals should regularly obtain and monitor certain parameters. These include the patient’s lipid profile, hepatic function tests, hemoglobin, and hematocrit levels. It is recommended to assess these parameters at 3 to 6 months after initiation of therapy and then annually.

In the case of women receiving testosterone treatment for breast cancer, close monitoring is necessary to detect any signs of virilization, which refers to the development of male characteristics.

Patients undergoing testosterone therapy should be regularly monitored to evaluate their response to treatment and to identify any potential adverse effects. This monitoring should occur at 3 to 6 months after starting therapy and then annually, with particular attention given to cardiac adverse events. Regular follow-up and evaluation are crucial to ensure the safety and efficacy of testosterone treatment.

For men aged 40 years and above, specific guidelines exist regarding the monitoring of prostate-specific antigen (PSA) levels and prostate examination during testosterone treatment. These recommendations include:

1. Men with a baseline PSA level higher than 0.6 ng/mL should have their PSA levels measured and undergo a prostate examination at 3 to 6 months after initiating testosterone therapy.
2. Treatment should be withheld in men who have a palpable prostate nodule or a PSA level exceeding 4 ng/mL.
3. In patients at high risk of prostate malignancy, defined as having a PSA level higher than 3 ng/mL, treatment should also be withheld.

These guidelines aim to ensure appropriate monitoring and minimize the potential risks associated with testosterone therapy, particularly in relation to prostate health. It is important for healthcare professionals to consider these factors and individual patient characteristics when making decisions about testosterone treatment in men.

To ensure optimal testosterone levels during treatment with testosterone enanthate and testosterone cypionate, it is recommended to measure testosterone levels midway between injections. Based on the guidelines provided by the Endocrine Society in 2010, dose and frequency adjustments should be made to maintain testosterone concentrations within the range of 400 ng/dL to 700 ng/dL.

In the case of topical testosterone therapy, the serum testosterone level should be measured two to eight hours after application. This measurement is typically done after fourteen days of starting the therapy or during dose titration to assess the effectiveness of the treatment.

Regular monitoring of testosterone levels helps to ensure that patients are receiving appropriate doses and achieving target testosterone concentrations for their specific treatment goals. It allows healthcare providers to make necessary adjustments to maintain hormonal balance and optimize therapy outcomes.

Conclusions

According to this review, the misuse and abuse of anabolic androgenic steroids (AAS) can result in detrimental effects on various tissues and organs throughout the body. The mechanisms commonly involved in AAS-related damage include oxidative stress, apoptosis (programmed cell death), and alterations in protein synthesis.

The review highlights that the long-term administration of high doses of AASs can have serious consequences, including hypogonadism (diminished function of the gonads), cardiac impairment, neurodegeneration, coronary artery disease, and even sudden cardiac death. Among the long-term side effects, cardiovascular issues such as cardiomyopathy (disease of the heart muscle) and atherosclerotic disease (hardening and narrowing of arteries) are commonly reported.

Hypogonadism is frequently observed in individuals who abuse AAS and should be considered when AAS use is suspected. Prompt and aggressive treatment is necessary to address this condition.

Overall, this review underscores the significant risks and adverse effects associated with long-term, high-dose AAS use, emphasizing the importance of understanding and addressing these potential complications in individuals who engage in AAS misuse or abuse.

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