Anabolic steroids (AS) are effective in enhancing athletic performance. The
trade off, however, is the occurrence of adverse side effects which can
jeopardize health. Since AS have effects on several organ systems, a myriad of
side effects can be found. In general, the orally administered AS have more
adverse effects than parenterally administered AS. In addition, the type of AS
is not only important for the advantageous effects, but also for the adverse
effects. Especially the AS containing a 17-alkyl group have potentially more
adverse affects, in particular to the liver. One of the problems with athletes,
in particular strength athletes and bodybuilders, is the use of oral and
parenteral AS at the same time ("stacking"), and in dosages which may be several
(up to 40 times) the recommended therapeutical dosage. The frequency and
severity of side effects is quite variable. It depends on several factors such
as type of drug, dosage, duration of use and the individual sensitivity and
response.
Liver Function
AS may exert a profound adverse effect on the liver. This is particularly
true for orally administered AS. The parenterally administered AS seem to have
less serious effects on the liver. Testosterone cypionate, testosterone
enanthate and other injectable anabolic steroids seem to have little adverse
effects on the liver. However, lesions of the liver have been reported after
parenteral nortestosterone administration, and also occasionally after injection
of testosterone esters. The influence of AS on liver function has been studied
extensively. The majority of the studies involve hospitalized patients who are
treated for prolonged periods for various diseases, such as anemia, renal
insufficiency, impotence, and dysfunction of the pituitary gland. In clinical
trials, treatment with anabolic steroids resulted in a decreased hepatic
excretory function. In addition, intra hepatic cholestasis, reflected by itch
and jaundice, and hepatic peliosis were observed. Hepatic peliosis is a
hemorrhagic cystic degeneration of the liver, which may lead to fibrosis and
portal hypertension. Rupture of a cyst may lead to fatal bleeding.
Benign (adenoma's) and malign tumors (hepatocellular carcinoma) have been
reported. There are rather strong indications that tumors of the liver are
caused when the anabolic steroids contain a 17-alpha-alkyl group. Usually, the
tumors are benign adenoma's, that reverse after stopping with steroid
administration. However, there are some indications that administration of
anabolic steroids in athletes may lead to hepatic carcinoma. Often these
abnormalities remain asymptomatic, since peliosis hepatis and liver tumors do
not always result in abnormalities in the blood variables that are generally
used to measure liver function.
AS use is often associated with an increase in plasma activity of liver
enzymes such as aspartate aminotransferase (AST), alanine aminotransferase
(ALT), alkaline phosphatase (AP), lactate dehydrogenase (LDH), and gamma
glutamyl transpeptidase (GGT). These enzymes are present in hepatocytes in
relatively high concentrations, and an increase in plasma levels of these
enzymes reflect hepatocellular damage or at least increased permeability of the
hepatocellular membrane.
In longitudinal studies of athletes treated with anabolic steroids,
contradictory results were obtained on the plasma activity of liver enzymes
(AST, AST, LDH, GGT, AP). In some studies, enzymes were increased, whereas in
others no changes were found. When increases were found, the values were
moderately increased and normalized within weeks after abstinence. There are
some suggestions that the occurrence of hepatic enzyme leakage, is partly
determined by the pre-treatment condition of the liver. Therefore, individuals
with abnormal liver function appear to be at risk.
Anabolic Steroids and the
Male Reproductive System
AS are derivatives of testosterone, which has strong genitotropic effects.
For this reason, it will not be surprising that side effects include the
reproductive system. Application of anabolic steroids leads to
supra-physiological concentrations of testosterone or testosterone derivatives.
Via the feed back loop, the production and release of luteinizing hormone (LH)
and follicle stimulation hormone (FSH) is decreased.
Prolonged use of anabolic steroids in relatively high doses will lead to
hypogonadotrophic hypogonadism, with decreased serum concentrations of LH, FSH,
and testosterone.
There are strong indications that the duration, dosage, and chemical
structure of the anabolic steroids are important for the serum concentrations of
gonadotropins. A moderate decrease of gonadotropin secretion causes atrophy of
the testes, as well as a decrease of sperm cell production. Oligo, azoospermia
and an increased number of abnormal sperm cells have been reported in athletes
using AS, resulting in a decreased fertility. After stopping AS use, the gonadal
functions will restore within some months. There are indications, however, that
it may take several months.
In bodybuilding, where usually high dosages are uses, after stopping steroid
use, often choriogonadotropins are administered to stimulate testicular
function. The effectiveness of this therapy is unknown.
The various studies suggest that using more than one type of anabolic steroid
at the same time ("stacking") causes a stronger inhibition of the gonadal
functions than using one single anabolic steroid. After abstention from anabolic
steroids these changes in fertility usually reverse within some months. However,
several cases of have been reported in which the situation of hypogonadism
lasted for more than 12 weeks.
A well known side effect of AS in males is breast formation (gynecomastia).
Gynecomastia is caused by increased levels of circulating estrogens, which are
typical female sex hormones. The estrogens estradiol and estrone are formed in
males by peripheral aromatization and conversion of AS. The increased levels of
circulation estrogens in males stimulate breast growth. In general, gynecomastia
is irreversible.
AS may affect sexual desire. Although few investigations on this issue have
been published, it appears that during AS use sexual desire is increased,
although the frequency of erectile dysfunction is increased. This may seem
contradictory, but sexual appetite is androgen dependent, while erectile
function is not. Since sexual desire and aggressiveness are increased during AS
use, the risk of getting involved in sexual assault may be increased.
Anabolic Steroids and the
Female Reproductive System
In the normal female body small amounts of testosterone are produced, and as
in males, artificially increasing levels by administration of AS will affect the
hypothalamic-pituitary-gonadal axis. An increase in circulating androgens will
inhibit the production and release of LH and FSH, resulting in a decline in
serum levels of LH, FSH, estrogens and progesterone. This may result in
inhibition of follicle formation, ovulation, and irregularities of the menstrual
cycle. The irregularities of the menstrual cycle are characterized by a
prolongation of the follicular phase, shortening of the luteal phase or
amenorrhea. Although these changes are generally more pronounced in younger
women, large inter-individual responsiveness to anabolic steroids exists. The
effects of AS dosages as generally used in sport, on the
hypothalamic-pituitary-gonadal axis in females are hardly studied.
Other side effects of anabolic steroid use in females are increased sexual
desire and hypertrophy of the clitoris. The few systematic studies that have
been conducted suggest that the effects are similar to the effects in patients,
treated with anabolic steroids.
Anabolic steroid use by pregnant women may lead to pseudohermaphroditism or
to growth retardation of the female fetus. Anabolic steroid use may even lead to
fetal death. However, these side effects have not been studied systematically.
It is likely that the severity of the side effects is related to the dosage,
duration of use and the type of the drug.
Additional side effects of anabolic steroids specifically in women are acne,
hair loss, withdrawal of the frontal hair line, male pattern boldness, lowering
of the voice, increased facial hair growth, and breast atrophy. The lowering of
the voice, decreased breast size, clitoris hypertrophy and hair loss are
generally irreversible. Females using AS may develop masculine facial traits,
male muscularity, and coarsening of the skin.
When anabolic steroids are administered in growing children side effects
include virilization, gynecomastia, and premature closure of the epiphysis,
resulting in cessation of longitudinal growth.
Serum Lipoproteins and the
Cardiovascular System
AS also affect the cardiovascular system and the serum lipid profile.
Relatively few studies have been done to investigate the effect of anabolic
steroids on the cardiovascular system. No longitudinal studies have been
conducted on the effect of anabolic steroids on cardiovascular morbidity and
mortality.
Most of the investigations have been focused on risk factors for
cardiovascular diseases, and in particular the effect of anabolic steroids on
blood pressure and on plasma lipoproteins. In most cross-sectional studies serum
cholesterol and triglycerides between drug-free users and non-users is not
different. However, during anabolic steroid use total cholesterol tends to
increase, while HDL-cholesterol demonstrates a marked decline, well below the
normal range. Serum LDL-cholesterol shows a variable response: a slight increase
or no change. The response of total cholesterol seems to be influenced by the
type of training that is done by the athlete. When a great deal of the exercise
consists of aerobic exercise, the increasing effect of AS is counterbalanced by
an exercise-induced increasing effect, which may result in a net decline in
total cholesterol. Aerobic training does not seem to be able to offset the
steroid-induced decline in HDL-cholesterol and its subfractions HDL-2, and
HDL-3.
The precise effect of anabolic steroids on LDL-cholesterol is unknown yet. It
appears that anabolic steroids influence hepatic triglyceride lipase (HTL) and
lipoprotein lipase (LPL). Males usually have higher levels of HTL, while females
have higher LPL activity. HTL is primarily responsible for the clearance of
HDL-cholesterol, while LPL takes care of cellular uptake of free fatty acids and
glycerol. Androgens and anabolic steroids stimulate HTL, presumably resulting in
decreased serum levels of HDL-cholesterol.
The effect of anabolic steroids on triglycerides is not well known. It is
suggested that relatively low doses do not affect the serum triglyceride levels,
while it cannot be excluded that higher doses elicit an increase.
No unanimity exists about the influence of anabolic steroids on arterial
blood pressure. The response is most probably dose dependent. There is some data
suggesting that high doses increase diastolic blood pressure, whereas low doses
fail to have a significant effect on diastolic blood pressure. Increases in
diastolic blood pressure normalize within 6-8 weeks after abstinence from
anabolic steroids. It appears that repeated intermittent use of anabolic
steroids does not affect diastolic blood pressure during drug free periods.
There is evidence that the use of anabolic steroids does elicit structural
changes in the heart and that the ischemic tolerance is decreased after steroid
use. Echocardiographic studies in bodybuilders, using anabolic steroids,
reported a mild hypertrophy of the left ventricle, with a decreased diastolic
relaxation, resulting in a decreased diastolic filling. Some investigators have
associated cardiomyopathy, myocardial infarction, and cerebro-vascular accidents
with abuse of anabolic steroids. However, a possible causal relationship could
not been proved, because longitudinal studies that are necessary to prove such a
relationship, have not been conducted yet. There is convincing evidence that
oral administration of anabolic steroids has stronger adverse effects on the
mentioned variables than parenteral administration.
Although the effects of anabolic steroids have an unfavorable influence on
the risk factors for cardiovascular disease, no data are available about the
long term effects. Most of the mentioned effects appear to reverse within 6-8
weeks after abstention. It is unknown, however, whether the structural changes
as reported in the heart, are reversible as well.
Psychological
Effects
Administration of AS may affect behavior. Increased testosterone levels in
the blood are associated with masculine behavior, aggressiveness and increased
sexual desire. Increased aggressiveness may be beneficial for athletic training,
but may also lead to overt violence outside the gym or the track. There are
reports of violent, criminal behavior in individuals taking AS. Other side
effects of AS are euphoria, confusion, sleeping disorders, pathological anxiety,
paranoia, and hallucinations.
Anabolic steroid users may become dependent on the drug, with symptoms of
withdrawal after cessation of drug use. The withdrawal symptoms consist of
aggressive and violent behavior, mental depression with suicidal behavior, mood
changes, and in some cases acute psychosis. At present it is unknown which
individuals are particularly at risk. It is likely that great individual
differences in responsiveness may exist. Some individuals try to minimize the
withdrawal affects by administration of human choriogonadotropins (hCG), in
order to enhance endogenous testosterone production. However, it is unknown in
how far the hCG administration is successful in ameliorating the withdrawal
effects.
Additional Side
Effects
In addition to the mentioned side effects several others have been reported.
In both males and females acne are frequently reported, as well as hypertrophy
of sebaceous glands, increased tallow excretion, hair loss, and alopecia. There
is some evidence that anabolic steroid abuse may affect the immune system,
leading to a decreased effectiveness of the defense system. Steroid use
decreases the glucose tolerance, while there is an increase in insulin
resistance. These changes mimic Type II diabetes. These changes seem to be
reversible after abstention from the drugs.
There are some case reports suggesting a causal relationship between anabolic
steroid use and the occurrence of Wilms tumor, and prostatic carcinoma. In the
literature also sleep apnea has been reported, which has been associated with
AS-induced increased in hematocrit, leading to blood stasis and thrombosis.
AS use may affect thyroid function. Administration of AS has been found to
decrease thyroid stimulation hormone (TSH), and the products of the thyroid
gland. In addition, thyroid binding globulin (TBG). These changes reversed
within weeks after discontinuation of AS use.
A serious consequence of AS use may be the multiple drug abuse. On the one
hand athletes use different kinds of drugs in an attempt to counterbalance the
side effects: hCG, thyroid hormones, anti-estrogens, anti-depressants. On the
other hand people try to support the anabolic effects of AS by using additional
anabolic hormones as for instance: different types of AS at the same time,
growth hormone, insulin, erythropoietine, and clenbuterol. Because most of this
takes place outside the official medical circuit, it is likely that these
practices may lead to serious conditions.
References
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1988
2. American College of Sports Medicine. Position
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19(5): 534-539, 1987
3. Bahrke, M.S., C.E. Yesalis, J.E. Wright.
Psychological and behavioral effects of endogenous testosterone levels and
anabolic-androgenic steroids among athletes; a review. Sports Med. 10(5):
303-337, 1990
4. Cohen, J.C., R. Hickman. Insulin resistance and
diminished glucose tolerance in power lifters ingesting anabolic steroids.
J. Clin. Endocrinol. Metab. 64: 960-963, 1987
5. De Piccoli, B., F. Giada, A. Benettin, F.
Sartori, E. Piccolo. Anabolic steroid use in body builders: an echocardiographic
study of left ventricular morphology and function. Int. J. Sports Med. 12(4): 408-412,
1991
6. Haupt, H.A. Anabolic steroids and growth hormone.
Am. J. Sports Med. 21(3): 468-474, 1993
7. Wilson, J.D. Androgen abuse in athletes.
Endocr. Rev. 9(2): 181-199, 1988
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