Transcript Anabolic Steroids

Anabolic Steroids
MacGregor Brown & Bryce Inman
Psyc 472
1
History of Performance Drug
Abuse
 Greeks reported using certain mushrooms and plant seed to increase
performance.
 Romans used drugs to increase performance of horses and gladiators to increase
crowd response.
 Steroids first developed in the 1930’s
 Used by the Germans on their soldiers and animals during WW2 to make up for
a lack of nutrition.
 1950’s first used for athletic purposes in Russia and Europe.

Primarily for weightlifting.
 Mid 1950’s it was discovered that testosterone was the driving force behind
increased athletic performance.
 Used in all levels of sports, in the 1972 Olympics 68% of athletes reported using
anabolic steroids.
 1991 the Federal Anabolic Control Act classified steroids as a schedule 3 drug.
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Performance Enhancing Drug
Statistics
 3.6% of high school students abuse steroids.

Risen nearly 2% in 2002, only drug other than ecstasy to show an
increase.
 Men that abuse steroids have a high incidence of some form
of opioid abuse.
 Over 3,000,000 people in the USA have reported the use of
steroids.
 1997 175,000 women reported steroid use.
 15% of NCAA athletes use performance enhancing drugs.
 90% of athletes reported have used some form of
performance enhancing drugs during there career.
3
Daily Dietary %
of Protein
(RDA)
Anabolic Steroid
Use
Days for 10lb
muscle mass
gain
100%
None
450-900
100%
200%
200%
300%
Heavy
450-900
225-300
65-75
225-300
300%
400%
Heavy
None
30-45
225-300
400%
Heavy
30-45
None
Heavy
None
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Testosterone
 Produced by Leydig’s
cells in testes
 Responsible for
secondary sex
characteristics in men
 Sex glands, libido,
reduced body fat
percentage, increased
body hair are all results
from elevated levels
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Estrogen/Aromatase
 Estradiol (estrogen) – primary 
female sex hormone, controls
fertility cycle in women.
Estradiol is beneficial to muscle
growth
Aromatase – any enzyme which
removes the 19 methyl from
AAS and forms 3 double bonds
on the A ring.
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DHT
 Through 5-alpha reductase, testosterone is
converted to a hormone 4X as potent,
dihydrotestosterone
 DHT binds to receptors much more avidly than
testosterone
 5-alpha reductase is present in high amounts in
tissues of the prostate, skin, scalp, liver, and central
nervous system
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What are steroids?
 Fat soluble molecule which contains a system of 4 rings made up of 17
carbon atoms
 E.g. cholesterol, estrogen, testosterone, progesterone, cortisol, etc.
 Anabolic steroid (DEA) – Any hormonal substance, chemically and
pharmacologically, related to testosterone that promotes muscle growth
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Anabolic/Androgenic
 Anabolic – “building”, increased
skeletal muscle mass, bone
density, hemoglobin, nitrogen
retention and protein synthesis
 Androgenic – androgens are sex
hormones that can induce male
traits (e.g. growth of sex organs,
increased body hair, libido, skin
oil, and change in voice)
 Anabolic/Androgenic steroids (AAS) seek to maximize the
anabolic effects while minimizing the androgenic effects.
The ratio of these anabolic/androgenic effects is called the
therapeutic index. Testosterone is the baseline at 1.
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Therapeutic index of common
AAS
Trade Name
Generic name
Therapeutic
Index
Androderm
Testosterone
1
Deca-Durabolin
Nandrolone
Decanoate
11-12
Winstrol
Stanazolol
5-20
Primobolan
Methenolone
7-16
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Basic modifications of
Testosterone
 17 alpha – Remove the H with a methyl or
ethyl group, producing an oral steroid
 17 beta – Add carbon atoms to this position
and increase solubility in lipids
 Other modifications at the carbon 2,3
9, & 19 positions – slow receptor
degradation, increase steroid’s affinity
for binding to receptor sites, inhibit
enzymatic conversion to a weaker
androgen
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Do anabolic steroids work?
 Most research has
shown that anabolic
steroids produce no
effect on muscle
growth. Why?
 Fowler (1965) – Nibal 20mg/day
Results: No increase in muscle
mass (MM)
 Johnson (1968) – D-bol
10mg/day. No increase in MM
 Casner(1971) – Winstrol
6mg/day. No increase in MM
 Hervey (1976) – D-bol
100mg/day. No increase in MM
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AAS Administration
 Oral preparations – 17 methyl alklayted to survive acidic
gastric secretions, short half life (e.g. dianabol, winstrol)
 Injectable solutions – prepared in water or oil. Longer
release times for oil. (e.g. Nandrolone Decanoate)
 Patch and gel – provides steady and constant testosterone
delivery (e.g. Trenbolone)
 Aerosol propellant – rapid effects, very hard to detect in
drug tests
 Sublingual preparations – absorbed directly into blood
stream so avoid digestive system, rapid effects
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Common AAS Practices
 Cycle – period of time
ranging from 1 to 4 months
in which AAS user takes
steroids
 Stacking – combining 2 or
more steroids
 Pyramiding – a gradual
buildup in dosage, and then
tapering off at the end
Wk Deca(mg) D-bol
1
100
10
2
200
15
3
300
15
4
300
20
5
200
15
6
100
15
7
100
10
14
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Why AAS produce muscle
 Activation of rRNA resulting in protein synthesis
 Anticatabolic effect – block action of natural
cortisone
 Increase free testosterone levels
 Stimulates activity of IGF-1 (Insulin-like growth
factor)
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Positive side effects of AAS
 Enhanced muscle mass/strength
 Enhanced blood volume and hemoglobin
concentration
 Enhanced bone density and strength
 Hastened healing of muscular injuries
 Decreased body fat
 Increased immune response
 Elevated mood
17
Clinical Applications
 Bone metabolism conditions – osteoporosis
 Testosterone deficiency conditions – male
hypogonadism, andropause
 Cardiovascular conditions – reduces angina
pectoris, hypertension, coronary artery disease
 AIDS – reduces AIDS wasting
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Common AAS
 Approved in U.S.
 Illegal in U.S.
-Testosterone Cypionate
-Nandrolone Decanoate
-Fluoxyymesterone
-Stanozolol
-Testosterone enanthate
-Methandrostenolone
-Oxandrolone
-Oxymesterone
Veterinary Steroids
-Equipoise (Boldenone undecyclate)
-Trenbolone
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Deca Durabolin
 Nandrolone decanoate Long acting ester
 Most widely used
 Side effects: Water
retention, endogenous test.
suppression, other mild
effects
 Detectable for over 1 year
in drug screenings
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Dianabol (methandrostenolone)
 Easy to use, very effective
 C17 alpha alkylated
 Can show extreme side
effects due to its tendency
to break down into 17alpha
methylestradiol, a form of
estrogen that is much more
active in the body
 Short half life (3-5 hrs.)
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Winstrol (stanozolol)
 Not capable of converting
into estrogen due to
modifications at the 9th C
position
 Prepared in both oral and
injectable forms
 Aside from C17
methylation, relatively few
side effects.
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Side Effects
Hypertension, acne, fluid retention,
hypogonadism, gynecomastia, sleep
disturbances, increased aggression, epistaxis
(nose bleeds), withdrawal depression,
prostate enlargement, heart enlargement,
virilization, abnormal blood clotting, libido
reduction, appetite stimulation, benign
prostate enlargement
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Acne and hair loss
 Acne
 Hair loss
 Sebaceous glands
(responsible for oil
secretion) are
stimulated by
androgens
 Bad acne may develop
on the shoulders, back,
and face
 Highly androgenic
steroids that convert to
DHT will aggravate
balding.
 DHT chokes the hair
follicle, eventually
killing it
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Gynecomastia
 Female breast tissue resulting from high levels of
estrogen
 Estrogen acts upon receptors in the breast and
stimulates the growth of mammary tissue
 Removed only by surgery
25
Stunted Growth
 If taken during adolescence or before, AAS may
halt growth. This occurs because they stimulate
epiphyseal plates on long bones to fuse
prematurely. Once fused, no growing can occur
 Stunted growth caused not by AAS, but the
conversion of AAS to estrogen. AAS that do not
convert to estrogen will actually promote height
growth
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Cardiovascular disease
 AAS have a strong effect
on LDL and HDL levels
 HDL is the “good”
cholesterol because it
removes cholesterol
deposits from the arteries
 LDL has the opposite
effect
 AAS increase LDL levels
and lower HDL levels.
 Oral compounds much
more likely to promote this
adverse effect.
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Testosterone and Aggression
 Testosterone associated
with social dominance
 Test. exacerbates “fight or
flight” response
 Studies indicate an increase
in aggression in animals
treated with AAS
 Prison studies, situational
studies
AAS - pronounced effects on
the limbic system
 AAS can act as
neurotransmitters
 In supraphysiologic doses,
AAS can alter function of
and increase the number of
receptors
 Can also modulate other
NT in the brain
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Permanent Steroid-Induced
Rage Behavior?
 Animal studies show alterations to the test. receptors in the
brain. They’ve also shown modifications to other receptors
 The most bothersome alterations in the brain are the increase
in androgen receptors and the increased binding capacity of
these receptors. After cessation of AAS use, these receptors
are thought to be “hungry” for elevated androgen levels.
Other NT’s recognize this deficit and may remain low
(similar to andropause) resulting in depression, self esteem
problems, and a greater tendency to lash out
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Cancer
 AAS are just a
synthetic version of
hormones that are
already present in the
body, so the stress on
organs is not very high.
 As such, cancer
resulting from AAS is
extremely rare
The only exception to this
is the use of c17 alpha
alkylated compounds
which are liver toxic.
They have been known
to induce liver damage
and cancer
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Sexual Dysfunction
Impotence
Male reproductive system
depends largely on the
level of androgenic
hormones. Rebound
effect occurs after AAS
use in which no
androgens are present
in the body.
Testicular atrophy
Production of test. is
turned off (along with
spermatogenesis)
resulting in a
noticeable change in
size of the testicles.
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Body Dysmorphia
AAS often produce addiction and body image
disorders that have been labeled as
 Megorexia or bigorexia
 Reverse anorexia
 Adonis complex
 Muscle dysmorphia
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Women and AAS
 Large amounts of test.
in women can produce
very noticeable side
effects
Virilization
Women develop masculine
characteristics such as a
deepening of the voice,
changes in skin texture,
acne, libido, hair loss, body
hair, and enlargement of
the clitoris
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AAS & the Gateway Phenomenon
After AAS, over 50% used drugs such as:
• 31% estrogen receptor inhibitors
• 22% HCG
• 17% diuretics and/or “uppers”
• 15% pain killers
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Aromatase inhibitors/Estrogen
Blockers
 Aromatase Inhibitors
 Estrogen Blockers
Blocks the aromatase enzyme,
preventing test. from
converting to estrogen
Slows muscle growth,
suppresses HDL
cholesterol, prevents water
retention
e.g. Arimidex (anastrozole)
Binds to free floating estrogen
molecules, preventing
estrogen from attaching to
androgen receptors
May also stimulate FSH and
LH
endogenous test.
production
e.g. Nolvadex (Tamoxifen
citrate)
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Stimulation of Test. Production
HCG - used clinically to treat
hypo-gonadism. Used postcycle to stimulate
endogenous test. by
mimicking LH
Clomid – used clinically as a
fertility aid. Acts as an
estrogen antagonist,
opposes negative feedback
of estrogens on
hypothalmus
Hypothalamus: GnRH
Pituitary: LH, FSH
Testes
Testosterone
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Insulin
 Regulates glucose levels in the blood , its role in the body is
to control the uptake, utilization, and storage of amino acids,
carbohydrates, and fatty acids in the body.
 Insulin is both anti-catabolic and anabolic because it
stimulates the use and retention of nutrients in muscle cells
(specifically glycogen)
 Cannot be detected in drugs tests
 Hypoglycemia one possible outcome of use. Can also result
in immediate death, coma, or insulin dependent diabetes.
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Cutting compunds
Clenbuterol
• Beta-2 sypathomimetic,
used as a bronchodilator.
• Animal studies indicate
anabolic properties, but
used primarily as a
thermogenic compound by
directly stimulating fat
cells and breaking down
triglycerides. Effects are
temporary due to down
regulation
Thyroid hormone
• Used to treat thyroid
deficiency, obesity, and
other metabolic disorders
• Synthetic version of T3
which stimulates thyroid
gland resulting in;
acceleration of cellular
reactions, increase in
metabolism &
cardiovascular functions.
• Rebound effect
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Steroid Precursors/Prohormones
 Androstenedione
 Androstenediol
 Dehydroepiandrosterone
(DHEA)
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Androstenedione
 Produced by the adrenal glands

17alpha-hydroxyprogesterone & DHEA.
 Once produced it is one step away from
testosterone and estrogen
 Missing the a hydrogen atom in the 17th
position.
 Processed by the liver where the hydrogen
atom is added.
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Steroid Chart
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Estrogen or Testosterone?
 Testosterone

Androstenedione is converted into testosterone
by 17beta-hydroxysteroid dehydrogenase, which
is activated by luteinizing hormone secreted by
the hypothalamus and pituitary gland
 Estrogen

Androstenedione may also be converted to the
estrogen, by the enzyme aromatase.
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Estrogen or Testosterone?
44
Androstenediol
 Similar to Androstenedione
 Lacks a 3-keto group that enables the
conversion into estrogen
 A much more androgenic compound
(produces much more male based effects)
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Why Androstenediol?
 Has higher conversion rates to testosterone.
 Doesn’t convert into estrogen.
 Does not convert into DHT (cause of
balding).
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DHEA
 2 steps away
 A precursor to testosterone that is produced
in the adrenal glands.
 Aids in producing Androstenedione which
produces testosterone and estrogen
 DHEA>Andro>Testosterone/Estrogen
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Why Take a Steroid Precursor
 Increase lean muscle mass?
 Decrease body fat?
 Increase strength ?
 Increase libido?

Only temporarily increases blood levels of
testosterone, does not cause body to naturally
produce testosterone.
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Negative Side Effects








Balding
Acne
Enlarged prostate
Reduced sperm count
Increased aggression
Kidney & Liver damage
Disrupt the menstrual cycle
Decrease levels of HDL cholesterol
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Creatine
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What is Creatine?
 An amino acid taken into the body through
meats and animal products.
51
What does Creatine do in the
body?
 Once ingested creatine is synthesized into
phosphocreatine in the kidneys, liver, and the
pancreas.
 Creatine is synthesized by the three amino acids
arginine, glycine, and methionine.
 Once synthesized into phosphocreatine it is
transported to skeletal muscles, the heart, and the
brain for energy usage.
52
What Does Creatine do in the
Body Cont.?
 Assists with the production of ATP, which is
used for short term energy exertion.
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What is ATP?
 Adenosine triphosphate (ATP).
 ATP is used during short-term high intensity
energy output.
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55
How Does Creatine Assist with
the Production of ATP?
 When ATP is broken down during exercise, energy
is produced with the loss of a phosphate ion.
 During high intensity exercise, ATP is constantly
broken down to ADP and Phosphorous and
reproduced to provide maximum energy output.
 When this occurs, phosphocreatine donates one of
its phosphate ions to facilitate the resynthesis of
ATP.
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Results of this Process.
 Reduced muscle fatigue - the rate at which
ATP is broken down does not exceed the rate
at which it can be resynthesized.
 Decreased Lactic Acid
 Faster Recovery
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Side Effects
 There is no pure evidence that creatine causes
actual physical harm.
 Possible Risks





Weight gain of 1-2kgs, due to the increase of fluid stores.
Increased risk for muscle cramps, and tears due to the
increased water retention
Damage to kidneys.
Usage may lead to cancer causes cancer.
Excessive use may decrease the bodies natural ability to
produce creatine.
58
How is Creatine Taken?
 Powder form
 Pill
 Serum
59
Typical Dosage
 5g daily – regular usage
 20g daily – During loading period to build up
creatine supply in the body
60
Growth Hormone (GH)
 A naturally occurring hormone in the body.
 Signaled release from the hypothalamus.
 Release from the pituitary gland regulated by two
hormones.



Somatostatin (SS) – decreases GH output.
Growth Hormone-Releasing Hormone (GHRH) –
Increase GH output.
Can also be regulated by the amount of GH and Insulin
Like Growth Factor 1 (ILGF-1) that is circulated back
through the body.
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GH in the Body
62
Other Factors that Increase GH
 Decreased blood glucose during exercise and sleep
trigger the release of GH.
 High protein increase small amounts GH release.
 Some amino acids such as L-arginine can increase
GH by decreasing the release SS from the
hypothalamus.
 Niacin has been shown to increase exercise induced
GH release by 300- 600% (Murray, 1995).
63
Theories about GH
 Somatomedin hypothesis (Daughaday,
1972).
1. GH is released from the pituitary gland.
2. Travels to the liver where it is converted
into ILGF.
3. ILGF enters the blood stream and
stimulates muscle growth.
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Theory 2
 Dual Effector Theory - Similar to the
Somatomedin hypothesis except it is
believed that GH alone has anabolic effects
without ILGF.
 Studies in mice have shown that mice
injected with GH are significantly larger than
those that were solely injected with ILGF.
65
How does GH Cause Muscle
Growth?
 Once converted into ILGF, ILGF stimulates
the production of, and the conversion of
satellite cells into muscle cells.
 Satellite cells – Cells that lie dormant around
muscle tissue until stimulated by ILGF.
Have the ability to replicate the genetic
makeup of muscle cells.
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Side Effects
 One of the most common side effects of GH
abuse is acromegaly.

overgrowth of bone and connective tissue which
leads to a change in physical appearance such as
a protruding jaw and eyebrow bones.
 Metabolic dysfunction

Glucose intolerance
67
How is GH Administered
 Must have a prescription.
 IM injections.
 Dosage - A weekly dosage of 0.30 mg/kg of
body weight.
 Very expensive!

Can be over $20,000 for an annual supply of
Growth Hormone.
68
Beta Blockers
 Medically used to:





Reduce blood pressure
Migraine headaches
Heart arrhythmia
Alcohol withdrawals
Anti-anxiety
69
Athletic Uses
 Reduces anxiety, jitters, and slows the heart rate.
 Commonly used in sports that require a steady
hand.






Golf
Archery
Bowling
Pool
Biathlon
Rifle shooting
70
Physiological Effects
1. During heightened arousal adrenaline is
produced
2. Heart rate increases and blood pressure is
increased
3. Beta Blockers block the beta receptor on
the muscles of the heart which reduces
these effects.
71
Side Effects
 Impotence
 Low Blood Pressure
 Insomnia
 Cardiac failure
 Poor circulation
 May reduce performance capacity
72
Diuretics
 Increase the amount of urine formation and the rate
at which it is excreted.
 Used in sports that require reduced weight such as:



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Wrestling
Horse racing
Bodybuilding
Boxing
 Also used to mask the use of other performance
enhancing drugs.
73
Side Effects
 Dehydration
 Decreased circulation of blood volume
 Muscle cramps
 Renal disorders
 Dizziness
 Disrupted Heart rhythm
74
Blood Doping/Erythropoietin
 Blood Doping


Adding additional blood to the system to
increase the amount of red blood cells in the
system.
Increased red blood cells increases the amount of
oxygen that the body can carry.


Thus, increasing the performance during endurance
sports.
Illegal, but hard to detect!
75
Erythropoietin
 A naturally occurring hormone released from
the kidneys.
 Causes increased production of red blood
cells.


Increased oxygen capacity
Increased tolerance to lactic acid.
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Side Effects

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



Can be very dangerous
Bacterial infection
Induce shock
Hypertension
Stroke
May receive the wrong blood type
Increased blood viscosity



Increased workload
Increased risk for blood clots
Increased risk for heart attack
77
Additional Performance
Enhancing Drugs
 GHB

Enables athlete to reach deeper state when
sleeping


Body produces more growth hormone
Highly abused among athletic community as a
recreational drug because it produces similar
intoxication to alcohol without the caloric intake
and hangover.
78
Additional Performance
Enhancing Drugs
 GHB

Enables athlete to reach deeper state when
sleeping


Body produces more growth hormone
Highly abused among athletic community as a
recreational drug because it produces similar
intoxication to alcohol without the caloric intake
and hangover.
79