Download 2a_ Endogenous Testosterone - St. Raymond High School for Boys

Endogenous Testosterone
Testosterone is an anabolic androgenic hormone (AAS). Although it is normally thought as a male hormone, it is naturally produced in both men and women. Its anabolic
properties include the maintenance and growth of muscle and bone tissue. Increases in muscular size appear to be due to the effect of testosterones upon protein
synthesis. Testosterone increases skeletal muscle size through hypotrophy not by hyperplasia. . Testosterone has been reported to enhance glycogen synthesis,
reabsorption of sodium in the kidneys, and secretion of sebaceous glands .Testosterone is also associated with bone growth, calcium retention, sodium reabsorption, and
increased metabolic rate. Testosterone levels have been linked to aggressive behavior in animals and humans
The negative feedback loop of the hypothalamic-pituitary-testicular axis regulates the production of endogeneous testosterone. The hypothalamus secretes gonadotropin
releasing hormone (GnRH), which stimulates luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the anterior pituitary. LH can then stimulate the
membrane receptors of the Leydig cells in the testes to stimulate the production of testosterone
Testosterone can be converted to estradiol through aromatization in adipose tissue, certain brain tissue, and other specific tissues. The production of
dyhydrotestosterone (DHT) is 1/20th of the production of testosterone. Dihydrotestosterone is related to facial hair, genetic balding, prostate growth, and the
development of male external genitalia. Testosterone decreases by approximately 1% per year after age 30.
Exogenous testosterone can have severe adverse effects on spermatogenesis by suppresses intratesticular testosterone production Therapies that protect the testis
involve Human Chorionic Gonadotropin (hCG) therapy or selective estrogen receptor modulators (SERMs) such as clomiphene citrate Most men on hormonal
contraception therapy return of normal sperm production within 1 year after discontinuation
Long Term Effects
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Long term effect of AAS in general are unknown
Specifically, as related to:
o Type of AAS
o Dose
o Frequency of use
o Age at initiation
o Concurrent drug use
Other confounds
o Varied AAS practices of individuals
 large dosages for prolonged time
 therapeutic dosages intermittently
Investigation has been proposed
o Study the long term effects of AAS
o Costing approximately $1 million
o Approved but never funded
Physical effects
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All effects fully reversible (adult males)
o Within several months after cessation
o Except postulated changes in the myocardium
 which have not been followed
Effect vary significantly
o Types of AAS
o Dosages of AAS
o Individuals
o Other situations
Best documented effects
o Liver
o Serum lipids
o Reproductive system
Other effects
o Psyche and behavior
o Glucose tolerance and hyperinsulinism
o Cerebrovascular accidents
o Prostatic Changes
o Immune function
o Altered collagen production possibly effecting tendon integrity
Cardiovascular risk factor
o Hyperinsulinism and decreased glucose tolerance
o Changes in lipoprotein fraction
o Increased triglyceride levels
o Increased concentration of several clotting factors
o Hypertension (via estrogen conversion)
o Changes in myocardium
Liver structure and function
o Cholestatic jaundice
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Peliosis hepatis
Hepatocellular hyperplasia
Hepatocellular adenomas
Associated with 17 alpha-alkylated (oral) steroids
Male reproductive system
o Decreased endogenous testosterone
o Decreased gonadotrophic hormones
o Decreased sex hormone-binding globulin (SHBG)
o Decreased testicle size
o Sperm
 decreased count
 decreased mobility
 altered morphology
o Gynecomastia
Women
o Some effects not reversible
o Menstrual abnormalities
o Deepening of the voice
o Shrinkage of the breasts
o Male pattern baldness
o Increased libido, acne, body hair, clitoris size
o Greatly increased testosterone levels
o Decreased sex hormone-binding globulin (SHBG)
o Decreased follicle-stimulating hormone
o Decreased thyroid-binding proteins
It is difficult to access the effects associated with AAS due to numerous methodological shortcomings of many investigations. They
include inappropriate sampling strategies, lack of adequate control groups, use of varying types, doses and length of administration of
AAS, and the variety of techniques employed to evaluate the psychological and behavioral outcomes
To further problems, most AAS used by athletes are obtained through the black market making its actual content uncertain. Samples of
AAS found in the black market often do not contain the ingredients declared on the label
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The effects of AAS vary significantly depending upon the type and dose of AAS as well as for different individuals and situations . It may
be a serious error to over generalize the effects and potential side effects of specific AAS to all other AAS. Likewise, it may be also
erroneous to assume the effects and potential side effects of certain steroid use in relatively large dosage and/or long duration will have
the same effects and potential side effects at a relatively lower and/or shorter duration.
Some authors attempt to dramatize the dosages of AAS used by the athletes by drawing reference to the dose usually administered for
specific diseased individuals. This is a misleading reference to judge athletic dosages, since AAS are often used in varying dosages for
different purposes. For example, Hurley, Seals, Hagberg, Goldberg, Ostrove, Holloszy, Wiest, & Goldberg (1984) explain that
Oxymetholone (Anadrol) was used by one subject in an average dosage of 87.5 mg/day. They point out that this dosage is 5.8 times
that usually administered for androgen deficiency. The subjects dosage was approximately 1 mg/kg body weight per day. The actual
recommend dosage for children and adults is 1-5 mg/kg body weight per day for a minimum of 3 to 6 months (Physicians Desk
Reference, 1993)! Conversely, it is difficult to extrapolate the potential side effects of a certain steroid therapy on medical patients, or
even a "normal" population for that matter, to a given athletic population.
Members of the sports medicine community have, with the best intentions, adapted a conservative strategy and used strong, but often unfounded,
pronouncements regarding the adverse effects of AAS. Athletes, on the other hand, have simply not witnessed long time AAS users 'dropping like
flies'. This aggressive health education strategy does not seem to have had a major impact on use of AAS and has very likely added to the lack of
credibility of the sports medicine and scientific communities in this area. For over 2 decades it was denied (and still is by some) that AAS enhance
physical capacities or performance. Athletes were told, until 1984, that any weight gained while taking AAS was merely the result of fluid retention
and that any strength gain was largely psychological (a placebo effect)."
Furthermore, Yesalis, Wright, & Bahrke, (1989) point out all of the effects of AAS have been demonstrated to be fully reversible within
several months following cessation of use; except changes in myocardium which has not been followed. Although, it has been argued
that the long term effects of chronic AAS use can not be determined with current data. A epidemiological investigation has been
proposed to study the long term effects of AAS. The study costing approximately $1 million was approved but was never funded.
Some experts believe legislation against drugs in sports will only increase an already thriving black market and organized crime (as
what has already began to occur with AAS) (Di Pasquale, 1992b). Traditional drug education has been ineffective. The use of drugs will
likely continue, especially if the incentives associated with winning remain so high (Di Pasquale, 1992b; Landry & Primos, 1990).
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