Can CBD help with anemia, and if so, how?

Anemia occurs when the body lacks enough healthy red blood cells to carry adequate oxygen to the tissues. Having anemia can make one feel weak and tired.

There are many forms of anemia, and each has a different cause. The condition can be temporary or long term, and it can range from mild to severe.

Anemia can also manifest as a warning sign of a severe illness. When left untreated, anemia can cause severe fatigue, pregnancy complications, heart problems, or death.

Treatments for anemia can range from taking supplements, such as iron, folate, vitamin B12, and vitamin C, to undergoing medical procedures. 

Individuals may be able to prevent some types of anemia by eating a healthy diet consistently high in iron, vitamin B-12, and folate(1). 

CBD for Anemia: What The Research Says 

CBD has been shown to possess therapeutic benefits that might help with symptoms or conditions linked to some types of anemia.

Although further longitudinal research is needed to validate the results of those studies, the potential benefits of CBD as an alternative for managing symptoms cannot be overlooked.

CBD Oil and Sickle Cell Anemia

Sickle cell anemia is a disorder that affects hemoglobin, the molecule in red blood cells that delivers oxygen to cells throughout the body(2). 

People with this disorder have atypical hemoglobin molecules called hemoglobin S, which can distort red blood cells into a sickle, or crescent, shape.

Sickle cell anemia can cause the pain linked to an accumulation of misshapen red blood cells in the microscopic capillaries. Also, pain can occur from poor oxygenation of the tissues.

In some cases, individuals with sickle cell anemia are prompted to take potent opioid painkillers to manage the pain.

Unfortunately, opioid therapy, often used for this condition, can lead to dependence or addiction, as indicated in a study published in the Journal of the Royal Society of Medicine(3). 

A questionnaire study published in the British Journal of Haematology examined cannabis use in sickle cell disease(4).

52% of those who used marijuana to treat symptoms of the disorder used it to reduce the pain associated with the condition. Meanwhile, 77% said they used it for relaxation or sedation purposes.

A study used an animal model to look at how cannabinoids can be effective at treating the pain from sickle cell anemia(5). 

In the said study, cannabinoids were shown to reduce neuropathic or nerve-related inflammation involved with sickle cell disease.

Although the studies did not focus on CBD use, the results can be used to develop oral cannabinoids in treating acute sickle cell pain. 

CBD Oil and Iron Deficiency Anemia

CBD itself has little effect on iron deficiency anemia. However, hemp seed oil that is often used as a carrier oil in these products is a natural source of vitamin E and minerals, such as phosphorus, potassium, sodium, magnesium, sulfur, calcium, iron, and zinc(6).

Typically, the doses of hemp seed oil used for CBD oil are only a few milliliters per day. For instance, in 100 mL of hemp seed oil, there may be about 8 mg of iron.

The National Institute Of Health says the daily requirements for iron in adults between 19 and 50 years old is 8 mg/day for men, and 18 mg/day in women(7).

The American Society of Hematology recommends taking 150-200 mg of iron each day, or 2 to 5 mg of iron for every kilogram of body weight per day(8).

That much iron is the equivalent of about 1.9 L of hemp seed oil per day, which is an outrageous and unreasonable amount for an individual to take in a day.

Thus, given the modest amounts of iron that can be obtained from hemp seed oil, it is best to stick to iron supplements and other highly-concentrated sources of iron, such as dark leafy vegetables, tofu, and red meat.

CBD for Anemia Symptoms

Iron deficiency anemia can be very mild that, oftentimes, it goes unnoticed. However, as the body becomes deficient in iron and anemia worsens, the signs and symptoms intensify.

Iron deficiency anemia symptoms include:(9)

  • Fast heartbeat, shortness of breath, or chest pain
  • Headache, dizziness or lightheadedness
  • Inflammation or soreness of the tongue
  • Unusual cravings for non-nutritive substances
  • Poor appetite

Meanwhile, studies have shown that CBD can help with these symptoms.

According to a study published in the British Journal of Pharmacology, drastic cannabidiol or CBD administration suppressed irregular heartbeat caused by ischemia-induced heart arrhythmias (inadequate blood supply in the heart)(10). Thus, CBD provides the heart with protection.

A 2014 review from the European Journal of Pharmacology established the potential of cannabis to limit or prevent nausea and vomiting from a wide range of causes(11).

CBD’s potent anti-inflammatory properties were also demonstrated in a 2018 study published in the Journal of Pharmacology and Experimental Therapeutics(12). 

In the said study, CBD has been shown to work directly with the cannabinoid receptors of the body to help suppress inflammation.

In an animal study published in the PLOS One Journal, it was shown that CBD inhibits a receptor in the brain so that ghrelin, which stimulates the appetite, is unable to act(13).

Meanwhile, a study on the relationship between cannabinoids and food intake suggested that endocannabinoids could impact energy balance and food intake within the brain(14).

Conclusion

To date, there has been no study that says CBD can directly help improve anemia conditions. 

Most of CBD’s benefits for anemia is only for the alleviation of the symptoms linked to anemia, rather than the condition itself. 

CBD is non-addictive, says Nora Volkow, director of the National Institute on Drug Abuse (NIDA) in a 2015 article(15). This characteristic makes CBD safe for daily intakes, like a supplement.

Still, before using CBD as a source of iron, or as an adjunct therapy, consult with a doctor experienced in cannabis use for advice.


  1. Mayo Clinic. (2019, Aug 16). Anemia. Retrieved from https://www.mayoclinic.org/diseases-conditions/anemia/symptoms-causes/syc-20351360.
  2. NIH. (2020, March 31). Sickle cell disease. Retrieved from https://ghr.nlm.nih.gov/condition/sickle-cell-disease.
  3. Okpala I, Tawil A. Management of pain in sickle-cell disease. J R Soc Med. 2002;95(9):456–458. DOI:10.1258/jrsm.95.9.456.
  4. Howard J, Anie KA, Holdcroft A, Korn S, Davies SC. Cannabis use in sickle cell disease: a questionnaire study. Br J Haematol. 2005;131(1):123–128. DOI:10.1111/j.1365-2141.2005.05723.x.
  5. Vincent L, Vang D, Nguyen J, Benson B, Lei J, Gupta K. Cannabinoid receptor-specific mechanisms to alleviate pain in sickle cell anemia via inhibition of mast cell activation and neurogenic inflammation. Haematologica. 2016;101(5):566–577. DOI:10.3324/haematol.2015.136523.
  6. Mihoc M, Pop G, Alexa E, Radulov I. Nutritive quality of romanian hemp varieties (Cannabis sativa L.) with special focus on oil and metal contents of seeds. Chem Cent J. 2012;6(1):122. Published 2012 Oct 23. DOI:10.1186/1752-153X-6-122.
  7. NIH. (2020, Feb 28). Iron. Retrieved from https://ods.od.nih.gov/factsheets/Iron-HealthProfessional/.
  8. American Society of Hematology. Iron-Deficiency Anemia. Retrieved from https://www.hematology.org/education/patients/anemia/iron-deficiency.
  9. Mayo Clinic. (2019, Oct 18). Iron deficiency anemia. Retrieved from https://www.mayoclinic.org/diseases-conditions/iron-deficiency-anemia/symptoms-causes/syc-20355034.
  10. Walsh SK, Hepburn CY, Kane KA, Wainwright CL. Acute administration of cannabidiol in vivo suppresses ischaemia-induced cardiac arrhythmias and reduces infarct size when given at reperfusion. Br J Pharmacol. 2010;160(5):1234–1242. DOI:10.1111/j.1476-5381.2010.00755.x.
  11. Sharkey KA, Darmani NA, Parker LA. Regulation of nausea and vomiting by cannabinoids and the endocannabinoid system. Eur J Pharmacol. 2014;722:134–146. DOI:10.1016/j.ejphar.2013.09.068.
  12. Petrosino S et al. Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic Cannabinoid, in Experimental Allergic Contact Dermatitis. Journal of Pharmacology and Experimental Therapeutics June 2018, 365 (3) 652-663; DOI: https://doi.org/10.1124/jpet.117.244368.
  13. Kola B, Farkas I, Christ-Crain M, Wittmann G, Lolli F, Amin F, et al. (2008) The Orexigenic Effect of Ghrelin Is Mediated through Central Activation of the Endogenous Cannabinoid System. PLoS ONE 3(3): e1797. https://doi.org/10.1371/journal.pone.0001797.
  14. Fride E, Bregman T, Kirkham TC. Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood. Exp Biol Med (Maywood). 2005;230(4):225–234. DOI:10.1177/153537020523000401.
  15. Nora Volkow. NIDA. Researching Marijuana for Therapeutic Purposes: The Potential Promise of Cannabidiol (CBD). National Institute on Drug Abuse website. https://www.drugabuse.gov/about-nida/noras-blog/2015/07/researching-marijuana-therapeutic-purposes-potential-promise-cannabidiol-cbd. July 20, 2015. Accessed January 31, 2020. 

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Nandrolone
1. NAME
1.1 Substance
1.2 Group
1.3 Synonyms
1.4 Identification numbers
1.4.1 CAS number
1.4.2 Other numbers
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
2.2 Summary of clinical effects
2.3 Diagnosis
2.4 First aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
3.3 Physical properties
3.3.1 Colour
3.3.2 State/form
3.3.3 Description
3.4 Other characteristics
3.4.1 Shelf-life of the substance
3.4.2 Storage conditions
4. USES
4.1 Indications
4.1.1 Indications
4.1.2 Description
4.2 Therapeutic dosage
4.2.1 Adults
4.2.2 Children
4.3 Contraindications
5. ROUTES OF EXPOSURE
5.1 Oral
5.2 Inhalation
5.3 Dermal
5.4 Eye
5.5 Parenteral
5.6 Other
6. KINETICS
6.1 Absorption by route of exposure
6.2 Distribution by route of exposure
6.3 Biological half-life by route of exposure
6.4 Metabolism
6.5 Elimination by route of exposure
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
7.1.2 Pharmacodynamics
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
7.2.1.2 Children
7.2.2 Relevant animal data
7.2.3 Relevant in vitro data
7.3 Carcinogenicity
7.4 Teratogenicity
7.5 Mutagenicity
7.6 Interactions
7.7 Main adverse effects
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their interpretation
8.5 Overall Interpretation of all toxicological analyses and toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
9.1.2 Inhalation
9.1.3 Skin exposure
9.1.4 Eye contact
9.1.5 Parenteral exposure
9.1.6 Other
9.2 Chronic poisoning
9.2.1 Ingestion
9.2.2 Inhalation
9.2.3 Skin exposure
9.2.4 Eye contact
9.2.5 Parenteral exposure
9.2.6 Other
9.3 Course, prognosis, cause of death
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
9.4.2 Respiratory
9.4.3 Neurological
9.4.3.1 Central nervous system
9.4.3.2 Peripheral nervous system
9.4.3.3 Autonomic nervous system
9.4.3.4 Skeletal and smooth muscle
9.4.4 Gastrointestinal
9.4.5 Hepatic
9.4.6 Urinary
9.4.6.1 Renal
9.4.6.2 Other
9.4.7 Endocrine and reproductive systems
9.4.8 Dermatological
9.4.9 Eye, ear, nose, throat: local effects
9.4.10 Haematological
9.4.11 Immunological
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
9.4.12.2 Fluid and electrolyte disturbances
9.4.12.3 Others
9.4.13 Allergic reactions
9.4.14 Other clinical effects
9.4.15 Special risks
9.5 Other
9.6 Summary
10. MANAGEMENT
10.1 General principles
10.2 Life supportive procedures and symptomatic/specific treatment
10.3 Decontamination
10.4 Enhanced elimination
10.5 Antidote treatment
10.5.1 Adults
10.5.2 Children
10.6 Management discussion
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
12. Additional information
12.1 Specific preventive measures
12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

Nandrolone

International Programme on Chemical Safety
Poisons Information Monograph 910
Pharmaceutical

This monograph does not contain all of the sections completed. This
mongraph is harmonised with the Group monograph on Anabolic Steroids
(PIM G007).

1. NAME

1.1 Substance

Nandrolone

1.2 Group

ATC Classification:
A14 (Anabolic Agents for Systemic Use)
A14A (Anabolic steroids)

1.3 Synonyms

Nor-19-testosterone; Norandrostenolone; Nortestosterone;
Nortestrionate; Oestrenolone

1.4 Identification numbers

1.4.1 CAS number

434-22-0

1.4.2 Other numbers

1.5 Main brand names, main trade names

1.6 Main manufacturers, main importers

2. SUMMARY

2.1 Main risks and target organs

There is no serious risk from acute poisoning, but
chronic use can cause harm. The main risks are those of
excessive androgens: menstrual irregularities and
virilization in women and impotence, premature cardiovascular
disease and prostatic hypertrophy in men. Both men and women
can suffer liver damage with oral anabolic steroids
containing a substituted 17-alpha-carbon. Psychiatric changes
can occur during use or after cessation of these
agents.

2.2 Summary of clinical effects

Acute overdosage can produce nausea and gastrointestinal
upset. Chronic usage is thought to cause an increase in
muscle bulk, and can cause an exageration of male
characteristics and effects related to male hormones.
Anabolic steroids can influence sexual function. They can
also cause cardiovascular and hepatic damage. Acne and male-
pattern baldness occur in both sexes; irregular menses,
atrophy of the breasts, and clitoromegaly in women; and
testicular atrophy and prostatic hypertrophy in men.

2.3 Diagnosis

The diagnosis depends on a history of use of oral or
injected anabolic steroids, together with signs of increased
muscle bulk, commonly seen in “body-builders”. Biochemical
tests of liver function are often abnormal in patients who
take excessive doses of oral anabolic steroids.

Laboratory analyses of urinary anabolic steroids and their
metabolites can be helpful in detecting covert use of these
drugs.

2.4 First aid measures and management principles

Supportive care is the only treatment necessary or
appropriate for acute intoxication. Chronic (ab)users can be
very reluctant to cease abuse, and may require professional
help as with other drug misuse.

3. PHYSICO-CHEMICAL PROPERTIES

3.1 Origin of the substance

Naturally-occuring anabolic steroids are synthesised in
the testis, ovary and adrenal gland from cholesterol via
pregnenolone. Synthetic anabolic steroids are based on the
principal male hormone testosterone, modified in one of three
ways:

alkylation of the 17-carbon
esterification of the 17-OH group
modification of the steroid nucleus

(Murad & Haynes, 1985).

3.2 Chemical structure

Chemical name:
Estr-4-en-3-one, 17-hydroxy-, (17b)-

Molecular formula
C18H26O2

3.3 Physical properties

3.3.1 Colour

3.3.2 State/form

3.3.3 Description

3.4 Other characteristics

3.4.1 Shelf-life of the substance

3.4.2 Storage conditions

Protect from light.

Vials for parenteral administration should be stored
at room temperature (15 to 30°C). Visual inspection
for particulate and/or discoloration is
advisable.

4. USES

4.1 Indications

4.1.1 Indications

Anabolic agent; systemic
Anabolic steroid
Androstan derivative; anabolic steroid
Estren derivative; anabolic steroid
Other anabolic agent
Anabolic agent for systemic use; veterinary
Anabolic steroid; veterinary
Estren derivative; veterinary

4.1.2 Description

The only legitimate therapeutic indications for
anabolic steroids are:

(a) replacement of male sex steroids in men who have
androgen deficiency, for example as a result of loss
of both testes

(b) the treatment of certain rare forms of aplastic
anaemia which are or may be responsive to anabolic
androgens.

(ABPI Data Sheet Compendium, 1993)

(c) the drugs have been used in certain countries to
counteract catabolic states, for example after major
trauma.

4.2 Therapeutic dosage

4.2.1 Adults

4.2.2 Children

Not applicable

4.3 Contraindications

Known or suspected cancer of the prostate or (in men)
breast.
Pregnancy or breast-feeding.
Known cardiovascular disease is a relative contraindication.

5. ROUTES OF EXPOSURE

5.1 Oral

Anabolic steroids can be absorbed from the
gastrointestinal tract, but many compounds undergo such
extensive first-pass metabolism in the liver that they are
inactive. Those compounds in which substitution of the 17-
carbon protects the compound from the rapid hepatic
metabolism are active orally (Murad and Haynes, 1985).
There are preparations of testosterone that can be taken
sublingually.

5.2 Inhalation

Not relevant

5.3 Dermal

No data available

5.4 Eye

Not relevant

5.5 Parenteral

Intramuscular or deep subcutaneous injection is the
principal route of administration of all the anabolic
steroids except the 17-alpha-substituted steroids which are
active orally.

5.6 Other

Not relevant

6. KINETICS

6.1 Absorption by route of exposure

The absorption after oral dosing is rapid for
testosterone and probably for other anabolic steroids, but
there is extensive first-pass hepatic metabolism for all
anabolic steroids except those that are substituted at the
17-alpha position.

The rate of absorption from subcutaneous or intramuscular
depots depends on the product and its formulation. Absorption
is slow for the lipid-soluble esters such as the cypionate or
enanthate, and for oily suspensions.

6.2 Distribution by route of exposure

The anabolic steroids are highly protein bound, and is
carried in plasma by a specific protein called sex-hormone
binding globulin.

6.3 Biological half-life by route of exposure

The metabolism of absorbed drug is rapid, and the
elimination half-life from plasma is very short. The duration
of the biological effects is therefore determined almost
entirely by the rate of absorption from subcutaneous or
intramuscular depots, and on the de-esterification which
precedes it (Wilson, 1992).

6.4 Metabolism

Free (de-esterified) anabolic androgens are metabolized
by hepatic mixed function oxidases (Wilson, 1992).

6.5 Elimination by route of exposure

After administration of radiolabelled testosterone,
about 90% of the radioactivity appears in the urine, and 6%
in the faeces; there is some enterohepatic recirculation
(Wilson, 1992).

7. PHARMACOLOGY AND TOXICOLOGY

7.1 Mode of action

7.1.1 Toxicodynamics

The toxic effects are an exaggeration of the
normal pharmacological effects.

7.1.2 Pharmacodynamics

Anabolic steroids bind to specific receptors
present especially in reproductive tissue, muscle and
fat (Mooradian & Morley, 1987). The anabolic steroids
reduce nitrogen excretion from tissue breakdown in
androgen deficient men. They are also responsible for
normal male sexual differentiation. The ratio of
anabolic (“body-building”) effects to androgenic
(virilizing) effects may differ among the members of
the class, but in practice all agents possess both
properties to some degree. There is no clear evidence
that anabolic steroids enhance overall athletic
performance (Elashoff et al, 1991).

7.2 Toxicity

7.2.1 Human data

7.2.1.1 Adults

No data available.

7.2.1.2 Children

No data available.

7.2.2 Relevant animal data

No data available.

7.2.3 Relevant in vitro data

No data

7.3 Carcinogenicity

Anabolic steroids may be carcinogenic. They can
stimulate growth of sex-hormone dependent tissue, primarily
the prostate gland in men. Precocious prostatic cancer has
been described after long-term anabolic steroid abuse(Roberts
& Essenhigh, 1986). Cases where hepatic cancers have been
associated with anabolic steroid abuse have been reported
(Overly et al, 1984).

7.4 Teratogenicity

Androgen ingestion by a pregnant mother can cause
virilization of a female fetus (Dewhurst & Gordon,
1984).

7.5 Mutagenicity

No data available.

7.6 Interactions

No data available.

7.7 Main adverse effects

The adverse effects of anabolic steroids include weight
gain, fluid retention, and abnormal liver function as
measured by biochemical tests. Administration to children can
cause premature closure of the epiphyses. Men can develop
impotence and azoospermia. Women are at risk of
virilization.

8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids

8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations

8.4 Other biomedical (diagnostic) investigations and their
interpretation

8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations

Biomedical analysis
The following tests can be relevant in the investigation of
chronic anabolic steroid abuse:
a) full blood count
b) electrolytes and renal function tests
c) hepatic function tests
d) testosterone
e) Lutenizing hormone
f) prostatic acid phosphatase or prostate related antigen
g) blood glucose concentration
h) cholesterol concentration

Toxicological analysis
-urinary analysis for anabolic steroids and their
metabolites

Other investigations
-electrocardiogram

8.6 References

9. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

Nausea and vomiting can occur.

9.1.2 Inhalation

Not relevant

9.1.3 Skin exposure

Not relevant

9.1.4 Eye contact

Not relevant

9.1.5 Parenteral exposure

Patients are expected to recover rapidly after
acute overdosage, but there are few data. “Body-
builders” use doses many times the standard
therapeutic doses for these compounds but do not
suffer acute toxic effects.

9.1.6 Other

Not relevant

9.2 Chronic poisoning

9.2.1 Ingestion

Hepatic damage, manifest as derangement of
biochemical tests of liver function and sometimes
severe enough to cause jaundice; virilization in
women; prostatic hypertrophy, impotence and
azoospermia in men; acne, abnormal lipids, premature
cardiovascular disease (including stroke and
myocardial infarction), abnormal glucose tolerance,
and muscular hypertrophy in both sexes; psychiatric
disturbances can occur during or after prolonged
treatment (Ferner & Rawlins, 1988; Kennedy, 1992; Ross
& Deutch, 1990; Ryan, 1981; Wagner, 1989).

9.2.2 Inhalation

Not relevant

9.2.3 Skin exposure

Not relevant

9.2.4 Eye contact

Not relevant

9.2.5 Parenteral exposure

Virilization in women; prostatic hypertrophy,
impotence and azoospermia in men; acne, abnormal
lipids, premature cardiovascular disease (including
stroke and myocardial infarction), abnormal glucose
tolerance, and muscular hypertrophy in both sexes.
Psychiatric disturbances can occur during or after
prolonged treatment. Hepatic damage is not expected
from parenteral preparations.

9.2.6 Other

Not relevant

9.3 Course, prognosis, cause of death

Patients with symptoms of acute poisoning are expected
to recover rapidly. Patients who persistently abuse high
doses of anabolic steroids are at risk of death from
premature heart disease or cancer, especially prostatic
cancer. Non-fatal but long-lasting effects include voice
changes in women and fusion of the epiphyses in children.
Other effects are reversible over weeks or months.

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

Chronic ingestion of high doses of anabolic
steroids can cause elevations in blood pressure, left
ventricular hypertrophy and premature coronary artery
disease (McKillop et al., 1986; Bowman, 1990; McNutt
et al., 1988).

9.4.2 Respiratory

Not reported

9.4.3 Neurological

9.4.3.1 Central nervous system

Stroke has been described in a young
anabolic steroid abuser (Frankle et al.,
1988).

Pope & Katz (1988) described mania and
psychotic symptoms of hallucination and
delusion in anabolic steroid abusers. They
also described depression after withdrawal
from anabolic steroids. There is also
considerable debate about the effects of
anabolic steroids on aggressive behaviour
(Schulte et al., 1993) and on criminal
behaviour (Dalby, 1992). Mood swings were
significantly more common in normal
volunteers during the active phase of a trial
comparing methyltestosterone with placebo (Su
et al., 1993).

9.4.3.2 Peripheral nervous system

No data available

9.4.3.3 Autonomic nervous system

No data available

9.4.3.4 Skeletal and smooth muscle

No data available

9.4.4 Gastrointestinal

Acute ingestion of large doses can cause nausea
and gastrointestinal upset.

9.4.5 Hepatic

Orally active (17-alpha substituted) anabolic
steroids can cause abnormalities of hepatic function,
manifest as abnormally elevated hepatic enzyme
activity in biochemical tests of liver function, and
sometimes as overt jaundice.

The histological abnormality of peliosis hepatis has
been associated with anabolic steroid use (Soe et al.,
1992).

Angiosarcoma (Falk et al, 1979) and a case of
hepatocellular carcinoma in an anabolic steroid user
has been reported (Overly et al., 1984).

9.4.6 Urinary

9.4.6.1 Renal

Not reported

9.4.6.2 Other

Men who take large doses of anabolic
steroids can develop prostatic hypertrophy.
Prostatic carcinoma has been described in
young men who have abused anabolic steroids
(Roberts & Essenhigh, 1986).

9.4.7 Endocrine and reproductive systems

Small doses of anabolic steroids are said to
increase libido, but larger doses lead to azoospermia
and impotence. Testicular atrophy is a common clinical
feature of long-term abuse of anabolic steroids, and
gynaecomastia can occur (Martikainen et al., 1986;
Schurmeyer et al., 1984; Spano & Ryan, 1984).

Women develop signs of virilism, with increased facial
hair, male pattern baldness, acne, deepening of the
voice, irregular menses and clitoral enlargement
(Malarkey et al., 1991; Strauss et al., 1984).

9.4.8 Dermatological

Acne occurs in both male and female anabolic
steroids abusers. Women can develop signs of virilism,
with increased facial hair and male pattern
baldness.

9.4.9 Eye, ear, nose, throat: local effects

Changes in the larynx in women caused by
anabolic steroids can result in a hoarse, deep voice.
The changes are irreversible.

9.4.10 Haematological

Anabolic androgens stimulate erythropoesis.

9.4.11 Immunological

No data available

9.4.12 Metabolic

9.4.12.1 Acid-base disturbances

No data available.

9.4.12.2 Fluid and electrolyte disturbances

Sodium and water retention can
occur, and result in oedema; hypercalcaemia
is also reported (Reynolds, 1992).

9.4.12.3 Others

Insulin resistance with a fall in
glucose tolerance (Cohen & Hickman, 1987),
and hypercholesterolaemia with a fall in high
density lipoprotein cholesterol, have been
reported (Cohen et al., 1988; Glazer, 1991;
Webb et al., 1984).

9.4.13 Allergic reactions

No data available

9.4.14 Other clinical effects

No data available

9.4.15 Special risks

Risk of abuse

9.5 Other

No data available

9.6 Summary

10. MANAGEMENT

10.1 General principles

The management of acute overdosage consists of
supportive treatment, with fluid replacement if vomiting is
severe. Chronic abuse should be discouraged, and
psychological support may be needed as in the treatment of
other drug abuse. The possibility of clinically important
depression after cessation of usage should be borne in
mind.

10.2 Life supportive procedures and symptomatic/specific treatment

Not relevant

10.3 Decontamination

Not usually required.

10.4 Enhanced elimination

Not indicated

10.5 Antidote treatment

10.5.1 Adults

None available

10.5.2 Children

None available

10.6 Management discussion

Not relevant

11. ILLUSTRATIVE CASES

11.1 Case reports from literature

A 38-year old man presented with acute urinary
retention, and was found to have carcinoma of the prostate.
He had taken anabolic steroids for many years, and worked as
a “strong-man” (Roberts and Essenhigh, 1986).

A 22-year old male world-class weight lifter developed severe
chest pain awaking him from sleep, and was shown to have
myocardial infarction. For six weeks before, he had been
taking high doses of oral and injected anabolic steroids.
Total serum cholesterol was 596 mg/dL (HDL 14 mg/dL, LDL 513
mg/dL) (McNutt et al., 1988). Values of total cholesterol
concentration above 200 mg/dL are considered undesirable.

A 22-year old body builder took two eight-week courses of
anabolic steroids. He became severely depressed after the
second course, and when the depression gradually receded, he
had prominent paranoid and religious delusions (Pope and
Katz, 1987).

A 19-year old American college footballer took intramuscular
testosterone and oral methandrostenolone over 4 months. He
became increasingly aggressive with his wife and child. After
he severely injured the child, he ceased using anabolic
steroids, and his violence and aggression resolved within 2
months (Schulte et al, 1993).

12. Additional information

12.1 Specific preventive measures

Anabolic steroid abuse amongst athletes, weight
lifters, body builders and others is now apparently common at
all levels of these sports. Not all abusers are competitive
sportsmen.
There is therefore scope for a public health campaign, for
example, based on gymnasia, to emphasize the dangers of
anabolic steroid abuse and to support those who wish to stop
using the drugs.

12.2 Other

No data available.

13. REFERENCES

ABPI Data Sheet Compendium (1993) Datapharm Publications,
London.

Bowman S. (1990) Anabolic steroids and infarction. Br Med J;
300:

Cohen JC & Hickman R. (1987) Insulin Resistance and diminished
glucose tolerance in powerlifters ingesting anabolic steroids. J
Clin Endocrinol Metab 64: 960.

Cohen JC, Noakes TD, & Spinnler Benade AJ. (1988)
Hypercholesterolemia in male power lifters using Anabolic
Androgenic Steroids. The Physician and Sports medicine 16:
49-56.

Dalby JT. (1992) Brief anabolic steroid use and sustained
behavioral reaction. Am J Psychiatry 149: 271-272.

Dewhurst J. & Gordon RR (1984). Fertility following change of
sex: a follow-up. Lancet: ii: 1461-2.

Elashoff JD, Jacknow AD, Shain SG, & Braunstein GD. (1991) Effects
of anabolic-androgenic steroids on muscular strength. Annals Inter
Med 115: 387-393.

Falk H, Thomas LB, Popper H, Ishak KG. (1979). Hepatic
angiosacroma associated with androgenic-anabolic steroids. Lancet
2; 1120-1123.

Ferner RE & Rawlins MD (1988) Anabolic steroids: the power and the
glory? Br Med J 1988; 297: 877-878.

Frankle MA, Eichberg R, & Zacharian SB. (1988) Anabolic Androgenic
steroids and stroke in an athlete: case report. Arch Phys Med
Rehabil 1988; 69: 632-633.

Glazer G. (1991) Atherogenic effects of anabolic steroids on serum
lipid levels. Arch Intern Med 151: 1925-1933.

Kennedy MC. (1992). Anabolic steroid abuse and toxicology. Aust NZ
J Med 22: 374-381.

Malarkey WB, Strauss RH, Leizman DJ, Liggett M, & Demers LM.
(1991). Endocrine effects in femal weight lifters who self-
administer testosterone and anabolic steroids. Am J Obstet Gynecol
165: 1385-1390.

Martikainen H, Alen M, Rahkila P, & Vihko R. (1986) Testicular
responsiveness to human chorionic gonadotrophin during transient
hypogonadotrophic hypogondasim induced by androgenic/anabolic
steroids in power athletes. Biochem 25: 109-112.

McKillop G, Todd IC, Ballantyne D. (1986) Increased left
ventricular mass in a body builder using anabolic steroids. Brit J
Sports Med 20: 151-152.

McNutt RA, Ferenchick GS, Kirlin PC, & Hamlin NJ. (1988) Acute
myocardial infarction in a 22 year old world class weight lifter
using anabolic steroids. Am J Cardiol 62: 164.

Mooradian JE, Morley JE, Korenman SG. (1987) Biological actions of
androgens. Endocrine Reviews 8:1-27.

Murad F, & Haynes RC. (1985). Androgens. in. Ed: Goodman Gilman
A, Goodman L S, Roll T W, Murad F. The Pharmacological Basis of
Therapeutics, 7th edition, Macmillan, New York: 1440-1458

Overly WL et al. (1984). Androgens and hepatocellular carcinoma in
an athlete. Ann Int Med 100: 158-159.

Pope GR, & Katz DL. (1988). Affective and psychotic symptoms
associated with anabolic steroid use. Am J Psychiatry 145:
487-490.

Reynolds Ed. (1992) Martindale-The Extra Pharmacopeia. The
Pharmaceutical Press. London.

Roberts JT, & Essenhigh DM. (1986) Adenocarcinoma of prostate in
40-year old body builder. Lancet 2: 742.

Ross RB, & Deutsch S I.(1990) Hooked on hormones. JAMA 263:
2048-2049.

Ryan A J. (1981) Anabolic steroids are fool’s gold. Fed Proc 40:
2682-2688.

Schurmeyer T, Belkien L, Knuth UA, & Nieschlag E. (1984)
Reversible azoospermia induced by the anabolic steroid
19-nortestosterone. Lancet i: 417-420.

Soe KL. Soe M. & Gluud C. (1992). Liver pathology associated
with the use of anabolic-androgenic steroids. Liver 12:
73-9.

Schulte HM, Hall MJ, & Boyer M. (1993). Domestic violence
associated with anabolic steroid abuse. Am J Psychiatr 150:
348.

Spano F, & Ryan W G. (1989) Tamoxifen for gynecomastia induced by
anabolic steroids? New Engl J Med 311: 861-862.

Strauss RH, Liggett MT, & Lanese RR. (1984) Anabolic steroid use
and perceived effects in 10 weight-trained women athletes JAMA
253: 2871-2873.

Su T-P, Pagliaro M, Schmidt PJ, Pickar D, Wolkowitz O, & Rubinow
DR. (1993) Neuropsychiatric effects of anabolic steroids in male
normal volunteers. JAMA 269: 2760-2764.

Wagner JC (1989). Abuse of drugs used to enhance athletic
performance. Am J Hosp Pharm 46: 2059-2067

Webb O L, Laskarzewski P M, & Glueck, CJ. (1984) Severe depression
of high-density lipo protein cholesterol levels in weight lifters
and body builders by self-administered exogenous testerone and
anabolic-andorgenic steroids. Metabolism 33: 971-975.

Wilson J D. (1992). Androgens. In: Goodman Gilman A., Rall T W,
Nies A S, & Taylor P. Goodman and Gilman’s Pharmacological Basis
of Therapeutics. McGraw-Hill, Toronto. Pages 1413-1430.

14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)

Author: Dr R. E. Ferner,
West Midlands Centre for Adverse Drug Reaction
Reporting,
City Hospital Dudley Road,
Birmingham B18 7QH
England.
Tel: +44-121-5074587
Fax: +44-121-5236125
Email: [email protected]

Date: 1994

Peer review: INTOX Meeting, Sao Paulo, Brazil, September 1994
(Drs P.Kulling, R.McKuowen, A.Borges, R.Higa,
R.Garnier, Hartigan-Go, E.Wickstrom)

Editor: Dr M.Ruse, March 1998

See Also:
Nandrolone Phenylpropionate (PIM 909)

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