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#Post#: 913--------------------------------------------------
Anabolic Steroid Side Effects- Part 2
By: guest5 Date: June 5, 2019, 12:52 pm
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By Mauro DiPasquale, M.D.
Dealing With Side Effects
While there are many possible short term and long term
consequences of anabolic steroid use, most of these side effects
can be minimized by the judicious use of, or if necessary the
discontinuation of the compound(s). As well other measures can
be taken to mitigate or eliminate potential side effects and
their consequences. The overall risks associated with the use of
anabolic steroids are not as great as the sporting federations
and the media would lead us to believe.
In men, most of the studies done so far show a reversal of any
side effects and the return of normal testicular function and
sperm count within three to six months (depending on the
duration, type and dosages used - see above) of discontinuing
the steroids.
Many of the athletes who use higher doses of two or more
anabolic steroids, for prolonged periods of time recognize the
risks involved with the use of anabolic steroids. These
athletes, whether under medical supervision or not, often use
methods and drugs to counteract or nullify these side effects9•
Unfortunately, few athletes have the benefit of proper medical
care and follow-up.
Avoiding Side Effects
Athletes in general are aware of many of the side effects
associated with the use of anabolic steroids and often use other
drugs or supplements to counteract or lessen their severity. For
example tamoxifen (Nolvadex) is used by male athletes to reduce
the estrogenic effects of testosterone and some of the anabolic
steroids that aromatize. Tetracycline and other antibiotics (as
well as acne creams etc.) are used to counteract the acne. Women
try to counteract the masculanizing effects by using the less
androgenic compounds and by using birth control pills with high
estrogenic and lower progestational effect (using oral
contraceptives in which the progestational component has minimal
androgenic properties). Evening Primrose, glutathione and
hepatoprotectants from plants and herbs are used to decrease the
hepatotoxic effects of the oral 17a-alkylated anabolic steroids.
Hypothalamic-Pituitary-Testicular Dysfunction and Anabolic
Steroids
While we may be able to discount many of the adverse effects of
anabolic steroids, such as isolated cases of liver and kidney
tumours, and are unsure of the actual long term liver and
cardiovascular consequences of anabolic steroid use, dysfunction
of the hypothalamic-pituitary-testicular axis (HPTA), resulting
in low serum levels of endogenous testosterone, may be the one
tangible serious side effect that can't be ignored or explained
away.
Although several studies have documented the hormonal
consequences of moderate to high doses of anabolic steroids in
both men and women few have reported the long term effects of
their use on the HPTA (10•11•12.) I have found that the
prolonged use of anabolic steroids can result in the long term
suppression of serum testosterone secondary to testicular and
hypothalamic-pituitary dysfunction. My data shows that there is
an
increased prevalence of both pituitary gonadotropic and
testicular dysfunction in men who have used anabolic steroids.
As well, anabolic steroids can impair reproductive function at
the gonad and/or the hypothalamo-pituitary level.
While some of the anabolic steroids (especially
dihydrotestosterone and dihydrotestosterone derivatives) do not
suppress the HPTA as much as others13, in sufficient dosages,
all anabolic steroids will suppress this axis. Perhaps this
suppression of the HPTA is the one adverse effect of anabolic
steroids that should be uppermost in the minds of those athletes
who use them.
The use of exogenous anabolic-androgenic steroids causes a
disturbance in the body's normal hormonal profile, with
decreased concentrations of serum hormone binding globulin
(SHBG), low concentrations ofluteinizing hormone (LH), follicle
stimulating hormone (FSH), testosterone precursors, and
testosterone itself, if anabolic steroids and no exogenous
testosterone are used. In athletes who use exogenous
testosterone, there is also a high ratio of testosterone to its
precursor steroids 14.
The formation, secretion, and metabolism of testosterone is a
complex process, which occurs through various sensing, feedback,
and control mechanisms. The control of the sex hormones involves
the hypothalamus, the pituitary, and the gonads. In men
regulation of testosterone secretion involves the HPTA, with
extrahypothalamic events having some influence at all three
levels15. The interaction between the various hormones and
releasing factors such as GnRH, LH, FSH, inhibin, and the
endogenous opioids, results in variations in the serum levels of
testosterone. For example, the hypothalamic decapeptide GnRH is
known to regulate the synthesis and secretion of LH and FSH by
pituitary gonadotrope cells.
The frequency of pulsatile GnRH secretion changes and LH and FSH
are differentially secreted in various physiological situations
16. As well, testosterone seems to affect the pituitary
secretion of LH and FSH directly (17•18), the response of LH and
FSH to GnRH, and the frequency of pulsatile GnRH release. It is
also thought that estrogens, produced from the aromatization of
testosterone and other anabolic steroids in parts of the brain
and hypothalamus, inhibit LH secretion, and thus decrease
testosterone production.
There are also several other hormones and compounds, such as
inhibin and the endogenous opioids, involved in the regulation
of testosterone secretion. For example inhibin, a hormone
produced by certain testicular cells (Sertoli cells) in response
to FSH, regulates androgen production by other testicular cells
(Leydig cells); and beta-endorphin, synthesized by Leydig cells
under LH control is known to regulate Sertoli function, and thus
to affect inhibin production (19.) One recent study showed
evidence for a direct effect of naloxone on testicular
steroidogenesis in the male rats. Thus the endogenous opioids
may have an effect on not only the release of GnRHJLH, but may
also have a direct testicular effect on steroidogenesis.
The use of exogenous hormones disrupts the HPTA, with the degree
of disruption dependant on several factors including the type of
anabolic steroid used, the dosage used, the duration of
treatment, and the presence of any underlying pathology. All
male athletes using anabolic steroids experience some testicular
dysfunction, resulting in decreased serum testosterone levels,
testicular atrophy, azoospermia and sometimes the development of
a female habitus including gynecomastia. On discontinuation of
the anabolic steroids there is normally a variable time period
over which the HPTA remains depressed. In most cases the serum
hormones soon return to normal.
However, with high doses of anabolic steroids used for extended
periods oftime, there is often a prolonged impairment of
testicular endocrine function, secondary to
hypothalamic-pituitary dysfunction, and in many cases primary
testicular dysfunction. It appears from the athletes I have
followed, that the long term suppression of testicular
steroidogenesis results in not only hypothalamic-pituitary
dysfunction but also gonadal impairment that may not be as
reversible as is generally thought. Thus testosterone and the
anabolic steroids seem to have direct effects on all components
of the HPTA, and possibly even on suprahypothalamic mechanisms.
In many cases of chronic suppression of the HPTA there appears
to be a resetting of the serum testosterone - with LH and FSH
levels returning to normal values after the anabolic steroids
are discontinued, but with a markedly decreased serum
testosterone. Ordinarily one would expect elevated LH and FSH
values in light of the low serum testosterone. Such is not
usually the case. I've found a low serum testosterone associated
with elevated gonadotrophin levels in only a minority of HPTA
suppressed patients. In these patients the
hypothalamic/pituitary function was intact; the primary problem
was one of testicular dysfunction. In a few of these patients,
testicular dysfunction was irreversible.
References:
9 Bill JA; Sulter JR; Sachs K; Brigham C. Athletic polydrug
abuse phenomenon: a case report .American journal of sports
medi.ci.ne 11(4), Jul/Aug 1983, 269-271.
10 Alan M, Rahltila P, Reilti.la M, Vihlto R. Androgenicanabolic
steroid effects on serum thyroid, pituitary and steroid hormones
in athletes . Am J Sports Med 1987; 15(4):357-361.
11 Alen M, Reilti.la M, Vihlto R . Response of serum hormones to
androgen admilti.stration in power athletes Med. Sci. Sports
Bxerc 1985; 17(3) :354-359.
12 Alen M, Hakkinen K. Physical health and fitness of an elite
bodybuilder during 1 year of self* administering testosterone
and anabolic steroids a case study. Int J Sports Med 1985;
6(1):24-29.
13 Balestreri R, Bertolini s, Chiodini G, Ronzitti M. Pituitary
inhibitory and non-inhibitory effects of various anabolic
17-alkylating steroids. Arch Maragllano Pato1 Cl.in 1971; 27 (3)
:123-135.
14 Ruokonen A, A1en M, Bolton N, Vihko R. Response of serum
testosterone and its precursor steroids, SHBG and CBG to
anabolic steroid and testosterone self-administration in man. J
Steroid Biochem, 1985; 23(1) :33-38.
15 Ryzhenkov VE, Bekhtereva BP, Sapronov NS. Role of the limbic
structures in the mechanism of production of glucocorticoids and
estrogens on hypothalamic control of pituitary
adrenocorticotropic and gonadotropic functions. Bu11 Bxp Bio1
Med 1974; 77(4):362-265.
16 Dalkin AC, Haisenlecler DJ, Ortolano GA, Ellis TR, Marshall
JC. The frequency of gonadotropin releasing-hormone stimulation
differentially regulates gonadotropin subunit messenger
ribonucleic acid expression. Endocrinology 1989; 125(2):917-924.
17 Sheckter CB, Matsumoto AM, Bremner WJ. Testosterone
administration inhibits gonadotropin secretion by an effect
directly on the human pituitary. J Cl.in Endocrino1 Metab 1989;
68(2) :397-401.
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