A banned bronchodilator in the U.S. and by the Olympics, clenbuterol remains readily available through the Internet.
Clenbuterol first came to my attention through an e-mail question. The few claims I found of clenbuterol being an asthma medication seemed little more than a thinly veiled attempt to increase the acceptability of this banned drug.
Clenbuterol is a Beta-2 Agonist, this places it in the same classification as Albuterol and Terbutaline. Clenbuterol is associated with the same type of side effects as well; tremor, increased heart rate, nervousness, and cardiac arrhythmias in those with underlying heart disease. Those side effects seem to be significantly more pronounced than in medications now used for asthma today.
Banned in the U.S. for use in humans and animals, it’s still readily available through several Internet based suppliers. Primarily used in veterinary medicine, clenbuterol is becoming increasingly popular as a anabolic steroid substitute. Clenbuterol’s claim to fame is a supposed anabolic effect similar to anabolic steroids but to a much lesser effect and without steroid associated side effects.
Clenbuterol made itself known to the general public during the Barcelona Summer Olympics in 1992. Two athletes were banned from the games due to this drug. The Olympics isn’t the only place where clenbuterol is being used to cheat. Bodybuilders, weight trainers, and dieters are using it to build muscle and reduce body fat. Unfortunately, this drug is also making its way to teens as well due to its availability.
Another problem with clenbuterol is its use in animals, both show and livestock. Animals are given clenbuterol for reasons similar to those of athletes, to increase muscle mass and leanness. Unfortunately, clenbuterol and its metabolites end up in the muscles and organs. When eaten these animal products have cause illness in human with symptoms familiar to anyone that has used a rescue inhaler or nebulizer. There have been hundreds of documented clenbuterol poisonings in the U.S. and Europe due to eating contaminated meat. Symptoms such as muscle pain, shaking, rapid heart beat, and headache have been known to last as long as 6 days.
Clenbuterol is one of the most popular illegal drugs used in livestock in the United States today
Clenbuterol Toxicology and Scandals:
Clenbuterol is one of the most popular illegal drugs used in livestock in the United States today. It is a legal and also very popular drug in Europe and Canada for cattle and horses. The illegal use of powerful and potentially deadly drugs is endemic within the veal industry.
Clenbuterol is used to make confined calves and lambs gain muscle mass even though they get no exercise. Strong antibiotics are used to try to curb the chronic inflections and diarrhea that afflict calves and lambs who never go outside and may not even get colostrum from their mothers’ milk. Clenbuterol is also often illegally used as a fat partitioning agent to improve the aesthetic appearance of show animals.
The problem of clenbuterol is not just confined to animals. Livestock are usually fed a high amount of clenbuterol up until slaughter. While much of the clenbuterol will be excreted or metabolized, there is still a considerable amount retained by the animals especially in the liver, muscles, and retina.
Clenbuterol is a potent stimulant that is broken down in the liver. A recent article from Spain reports 113 cases of people who developed nervousness, rapid heart rate, muscle shaking, muscle pain and headache 15 minutes to 6 hours after eating veal liver (Public Health Reports, May-June 1995.) Their symptoms lasted from 90 minutes to 6 days. Interestingly, blood levels of clenbuterol were very low, while urine levels from the affected people were very high.
Clenbuterol has found popularity in bodybuilding and other sports where lean mass is desired. Athletes generally take a 20 mcg dose 3 times a day for 2 days then go off it for 2 days. They repeat this cycle for 6-8 weeks. The most prominant short term toxic effects athletes experience is heart palpatations, insomnia, and muscle cramping. The long term side effect would include destruction of the adrenergic receptors; permanant impairment of thyroid activity, making the athlete unable to regulate his/her metabolism and be intolerable to cold temperatures; death. The amount used by athletes are far less than what livestock are fed, and still less than the residual clenbuterol found in meat from animals that were fed clenbuterol.
A total of 1,074 samples taken in Great Britain in 1992 under the statutory and non-statutory surveillance programs were analyzed for residues of clenbuterol. These included 203 ox liver samples purchased from retail outlets. Only two of these retail samples were found to contain clenbuterol, at concentrations of 0.4 Вg/kg and 3.3 Вg/kg respectively. Neither of these residues would have likely posed any threat to human health. However, one of them was above the statutory maximum residue limit (MRL) of 0.5 Вg/kg, which applies to residues arising from licensed uses of clenbuterol. The results of this surveillance were given in response to a written Parliamentary Question on 2 March 1993.
In the light of these results, a further study of retail ox liver was undertaken. A total of 55 samples of ox liver were purchased from retail outlets throughout the UK in February and March 1993 (Table 1). No samples contained residues of clenbuterol, using an analytical method with a limit of determination of 0.2 Вg/kg.
TABLE 1: Surveillance for residues of clenbuterol in liver, February – March 1993
|Species||Drugs||MRL (Вg/kg)||No. of samples analyzed||No. of sampleswith residues above MRL|
Because of the continuing evidence of abuse of clenbuterol outside Great Britain, surveillance has been stepped up in 1993. A total of 2,264 samples of home-produced, imported and retail bovine tissues will be analyzed for clenbuterol under MAFF’s statutory and non-statutory surveillance schemes.
Clenbuterol is very hard to detect, until the recent development of a test that finds traces in a slaughtered animal’s retinas, the amount of clenbuterol residues in meat can be lethal to humans.
Clenbuterol is also very popular for show animals too. It was an all-American moment — grinning 16-year-old Ryan Rash resting his head on his grand champion steer Badger after winning the blue ribbon at the National Western Stock Show.
The lumbering, black steer fetched $37,500 at auction, and Ryan and his parents couldn’t be more proud. But within days, the ribbon had been stripped, the money forfeited and Ryan banned for life from the Denver show. The reason? Cheating. Badger had been illegally fed clenbuterol that beefed him up, giving him the straight lines and muscular physique of a champion.
Scott McEldowney, who admitted feeding clenbuterol to his 10-year-old daughter’s steer Barney, says he had to cheat to compete on a national level. “It’s like anything in life, either racing cars or anything,” said McEldowney, who has a small farm in Ansonia, Ohio, near Dayton. “If you’re going to play on the same level, let’s play on the same level.”
He and seven others at the Ohio State Fair were caught either drugging their animals with clenbuterol or injecting oil under their skin to give them a better appearance. His daughter, Jessica, was banned for life from showing at the state fair and had to return the $4,000 paid for her steer.
An Ohio Agriculture Department investigation led to the convictions of 10 people for either selling clenbuterol or tampering with livestock, and two Wisconsin veterinarians and one in Iowa have been indicted in the drug distribution scheme.
At the Tulsa State Fair in Oklahoma, six of the top animals tested positive for the drug. And in Louisville, Ky., clenbuterol was found last fall in the grand champion lamb at the North American International Livestock Expo.
The drug is most often smuggled in through Canada, where it is legally used to treat horse respiratory problems, FDA official George “Bert” Mitchell said. No human health problems have been reported domestically, however; only small amounts of drug residue have been detected in the eyeballs of the show animals.
McEldowney estimates 30 percent or more of exhibitors have used clenbuterol on their show animals. Barbara Wood, livestock director for the Tulsa State Fair that disqualified the six cheaters last year, puts the number at about 20 percent.
“At this time a year ago, I tried to deny we had a big problem, but I’ve changed my mind. It’s a serious problem,” said Eddie Smith, Oklahoma state supervisor of agricultural education and adviser to the Future Farmers of America. “I’m sure there’s always been a little fudging here and fudging there, but it’s definitely gotten a lot worse.
Among the newly revealed cases:
В� Clenbuterol was found in a blackfaced lamb exhibited by Brian Wade Johnson, 22, of Gotebo, Oklahoma, who was named the Future Farmer Association’s American Star Farmer of 1994 even as. The lamb was Grand Champion at the North American International Livestock Expo, held last November in Louisville, Kentucky.
В� Two other winning entrants at that fair tested positive for clenbuterol, including the reserve champion steer exhibited by Hilary Wise, 17, of Brownwood, Texas. Wise, who had the grand champion steer at the American Royal fair in Kansas City in 1993, had a steer disqualified at the Royal this year because the animal’s leg had been cosmetically improved with twine, glue, and paint.
В� 15 people, including five professional livestock exhibition groomers, have now been indicted, and nine to date convicted, in connection with clenbuterol-related tampering at the Ohio State fair last August.
В� Clenbuterol was found in six of the 38 animals tested after the Tulsa State Fair last September.
В� Clenbuterol was found in a champion hog at the American Royal exhibition in Kansas City last November.
Clenbuterol – Food Safety and Inspection Service:
The U.S. Department of Agriculture’s Food Safety and Inspection Service is responsible for ensuring that meat and poultry products are safe, wholesome and accurately labeled. The Agency works in cooperation with the Food and Drug Administration, which is mandated to ensure the safety of all other food products and is responsible for regulating animal drugs and feedstuffs.
In 1991, FDA and FSIS were alerted that the veterinary drug clenbuterol was being illegally used to gain competitive advantage in some show animals such as calves, lambs, and swine. According to USDA officials, show animals comprise less than one percent of the millions of food animals slaughtered in the United States. Nevertheless, the illegal use of clenbuterol could be a public health concern if show animals were to be slaughtered for human food with clenbuterol residues in the liver or in the muscle tissue (meat).
Clenbuterol residues can affect lung and heart function in persons who have eaten liver or meat of animals given the drug. In the United States, no human illnesses have been associated with clenbuterol use in food animals. But, several outbreaks of reversible, short-term illnesses in Europe have been traced to ingesting clenbuterol residues in European beef liver.
To protect the public health, FSIS and FDA are taking enforcement actions against the illegal use of clenbuterol in show animals. While, FDA takes regulatory action against persons involved in the use or distribution of clenbuterol, FSIS tests meat and liver for illegal residues to help keep contaminated meat out of consumer channels. FSIS and FDA coordinate findings with the Justice Department, which handles prosecution of violators of Federal law.
At the same time, FSIS and FDA are working with other organizations to educate the agricultural community about the public health concern and the legal risks. Groups include the Extension Service, producer organizations, state officials, the Future Farmers of America, the 4-H, and livestock show leaders.
Clenbuterol is a growth-promoting drug in the beta-agonist class of compounds. Its illegal use in show animals is linked to its ability to induce weight gain and a greater proportion of muscle to fat. It is not licensed for any use in the United States, but some countries have approved it for use in animals not used for food, and a few countries have approved it for therapeutic uses in food producing animals. The dosages needed for therapeutic purposes are much lower than those required to increase muscle mass. Clenbuterol may be available in the United States through chemical supply houses for laboratory use and the so-called “black market. When used illegally, it is added to animal feed.
Since the first alert in 1991, USDA and FDA have been working with state departments of agriculture and others to avoid contamination of the meat supply. The agencies have alerted them about possible illegal use of clenbuterol. FDA also alerted U.S. Customs to block the illegal import of clenbuterol and is following up with enforcement activities.
For example, in 1994, traces of clenbuterol residues were found in animals at stock shows held in Ohio and Oklahoma. In Tulsa, a clenbuterol test of champion animals disqualified six animals including steers, sheep, and a hog. In 1995, two champion steers were disqualified because residues were found at the National Western Stock Show in Denver. FDA is also undertaking investigations concerning the sale of feed with clenbuterol and its possible use in veal calves in several states.
No deaths were reported in several European incidents involving the consumption of liver with clenbuterol residues. Spain reported two outbreaks of illness in 1990 totaling 135 persons who consumed contaminated beef liver. Samples had clenbuterol concentrations of 160 to 291 parts per billion. The people were hospitalized with reversible symptoms of increased heart rate, muscular tremors, headache, nausea, fever, and chills.
Clenbuterol was suspected, but not confirmed, as the cause of an earlier outbreak of illness, also in Spain. A similar incident with 22 cases, also traced to beef liver, was reported from France. Clenbuterol was also a concern in Ireland in 1991.
Although the toxic effects of clenbuterol residues have been described as mild, FDA considers all unintended effects on humans to be unacceptable. FDA said it is possible that persons being treated with adrenergic agents or who are otherwise sensitive to these drugs, may be far more severely affected by residues of clenbuterol than are normal, healthy individuals.
FDA is also concerned that the illicit use of clenbuterol could lead to illness or death in persons handling the drug. FDA said it is possible that clenbuterol effects on the cardiovascular system may be more hazardous via occupational inhalation exposure than via ingestion in food. But FDA said it has not been able to confirm reports of such reactions.
In 1991, FSIS announced it would condemn meat that tests positive for clenbuterol residues. When an animal shows a positive clenbuterol urine screening test, the animal is identified for tracking during transport to slaughter plants. At the plant, the carcasses are held for FSIS testing, as are carcasses from all animals suspected of having illegal drug residues. FSIS inspectors collect liver and muscle tissue samples and send them to the FSIS Midwestern Laboratory in St. Louis for analysis. Testing is done using an FSIS-developed test for clenbuterol in liver. The test is sensitive to one part per billion (1 ppb).
Also, both eyes from the carcass are sent to an FDA laboratory for testing of the retinas. Although the eyeballs are not used to make disposition of retained carcasses, they are extremely helpful in assisting FDA in identifying and investigating violators because residues can remain in the retinas for months.
In addition to testing carcasses after live animals have tested positive at shows, FSIS expanded testing for clenbuterol in 1994 to include an exploratory two tier program. In Tier I, for one year, FSIS collected and tested more than 1,800 tissue samples taken at random from normal animals (not necessarily show animals). At the end of Tier I testing, in early 1995, there were no positive findings. During Tier II, FSIS samples show animal carcasses at the slaughter plant. TierII is ongoing and targets approximately eight show animals in each of the agency’s five regions every month.
Clenbuterol begins to show in the urine and body organs within a day of administration and can remain in the liver for several days. Because the body begins eliminating the drug immediately, it is possible for residues to be depleted from urine and edible tissues if sufficient time elapses before slaughter. But, exposure can be detected by testing retinal tissue from the eyes because residues remain there for at least five months. Retina testing has revealed residues in show animals in Ohio, Oklahoma, and Colorado.
Local Action Is Essential
Prevention of clenbuterol residues in human food from show animals is most effective at the source, which is at the time of sale or administration of the drug. State regulations for residue testing of show animals vary widely. For example, the State of Texas requires testing of show animals at fairs and livestock shows for antibiotics, hormones, diuretics, and steroids. Betaagonists are also included, but other states may not have such regulations.
To help stop use of clenbuterol in show animals and other livestock used for food, since 1991 FSIS, FDA, and USDA’s Extension Service have been working with others, including state agriculture and inspection officials, slaughterhouse managers, as well as leaders of livestock shows, 4-H groups, and the Future Farmers of America.
Clenbuterol in the Horse:
Confirmation and Quantitation of Serum Clenbuterol by *** after Oral and Intratracheal Administration
A.F. Lehner1, J.D. Harkins1, W. Karpiesiuk1, W.E. Woods1, N.E. Robinson2, L. Dirikolu1, M. Fisher3, and T. Tobin1
1 Maxwell H. Gluck Equine Research Center and the Department of Veterinary Science, University of Kentucky, Lexington, Kentucky 40506;
2 Department of Large Animal Clinical Sciences, Veterinary Medical Center, Michigan State University, East Lansing, Michigan; and
3The Kentucky Racing Commission, Lexington, Kentucky 40506
Clenbuterol and Anabolic Steroids: A Previously Unreported Cause of Myocardial Infarction With Normal Coronary Arteriograms
Daniel R. Goldstein, MD, Thomas Dobbs, MD, Barbara Krull, MD, Vance J. Plumb, MD, Department of Medicine, Division of Cardiology, University of Alabama at Birmingham.
[South Med J 91(8) 780-784, 1998. © 1998 Southern Medical Association]
During the last 10 years, several cases of myocardial infarction associated with anabolic steroid use have been reported. Postulated mechanisms to explain this association have included changes in lipid levels, the fibrinolytic system, and platelet aggregation. Clenbuterol is a b2-agonist with anabolic properties that has not been seen previously with myocardial infarction. We report a case of myocardial infarction in an otherwise healthy 26-year-old body-builder who recently used clenbuterol and anabolic steroids. In this case, synergistic effects of the two agents seem likely to have played a role in the infarct. The normal coronary arteriograms before any anticoagulant or thrombolytic therapy strongly suggest coronary spasm as the mechanism of the infarct.
Several reports of myocardial infarction associated with anabolic steroid use have been reported over the last 10 years. The mechanism of infarction remains controversial. Clenbuterol is a beta2-agonist that has not been previously associated with myocardial infarction. We report the case of a previously healthy 26-year-old man who had an acute myocardial infarction after taking both clenbuterol and anabolic steroids.
A previously healthy 26-year-old man with no known risk factors for coronary artery disease came to the internal medicine outpatient clinic with dull, central chest pain of 3 hours’ duration. The patient said that he was a competitive body builder who had used anabolic steroids over the previous 3 years. Specifically, he had used intermittent, intramuscular depot injections of testosterone propionate, cypionate, and enanthate, in addition to oral methandrostenolone and stanozolol. He had not used any steroid preparation for 4 weeks before presentation but had since started using oral clenbuterol. The patient was unable to give details of dosing regimes concerning any of the these medications. His only other symptoms were occasional palpitations, tremors, and nervousness over the past 2 weeks.
His medical history was unremarkable, and he denied using tobacco, cocaine, or any other substances of abuse. On examination, the patient was a lean, muscular man in no acute distress, with a blood pressure of 140/90 mm Hg and a pulse rate of 90/min. The remainder of the physical examination was unremarkable. An electrocardiogram revealed 1-mm ST segment elevation in leads II, III, AVF, and V4 to V6 (Fig 1). Echocardiogram showed dyskinesias of the inferior and posterior wall, normal global ejection fraction, and evidence of left ventricular hypertrophy, with the left ventricular posterior wall measuring 12 mm. After receiving aspirin and nitroglycerin, the patient was sent emergently to the cardiac catheterization laboratory where his coronary angiograms were normal (Figs 2 and 3). The left ventriculogram showed a mildly dilated left ventricle with dyskinesias in the same areas as the echocardiogram.
The patient’s cardiac enzymes confirmed a myocardial infarction with a peak creatinine kinase of 1,060 IU/L (normal range, 25 to 190) and MB fraction of 54 ng/mL (normal range, 0.0 to 5.0). His lipid panel was within the normal range. Testing for hypercoagulability with a protein C, S, antithrombin III levels, and factor V Leyden was normal. The remainder of the laboratory data, including a homocysteine level and a urine illicit drug screen, was unrevealing. The patient had an uneventful hospital course. Two weeks after discharge, he was asymptomatic, and an echocardiogram showed resolution of the areas of dyskinesias.
It is estimated that in the United States approximately one million people use anabolic steroids each year. Over the past decade, there have been an increasing number of reports of anabolic steroid use associated with cardiovascular entities, including sudden death, ventricular arrhythmia, dilated cardiomyopathy, stroke, arterial thrombosis, and myocardial infarction.
To our knowledge, since 1988 eight cases have been reported in the English language literature regarding myocardial infarction associated with anabolic steroid use. The reported patients were young men, generally with a paucity of cardiac risk factors. The timing of steroid use varied from 5 weeks before presentation to use on the day of admission. In one case, high doses of amphetamines were believed to be responsible for the myocardial infarction. No other substances of abuse were identified in the other cases. Evidence of dyslipidemia was found in three patients who had markedly high low-density lipoprotein (LDL) and low high-density lipoprotein (HDL). Thrombolytics were given to four patients. Six patients had cardiac catheterizations; normal angiograms were noted in two. No patients had primary angioplasty or cardiac catheterization before anticoagulant or thrombolytic therapy. One patient had cardiogenic shock, and another was found to have a dilated cardiomyopathy. Long-term follow-up information is lacking, but there were no deaths during hospitalization.
Various mechanisms have been proposed to account for the association between anabolic steroids and myocardial infarction, though there is no direct evidence. First, there have been several studies that showed anabolic steroids can cause dyslipidemias — notably an increase in LDL and reduction in HDL. Hence, the use of anabolic steroids could be a risk factor for the development of coronary artery disease. Second, anabolic steroids may cause a hypercoagulable state by altering components of the coagulation and fibrinolytic system. This was suggested by a recent study that showed activation of the hemostatic system in body builders who used anabolic steroids compared with controls who did not use steroids. Specifically, anabolic steroid users had higher concentrations of thrombin/antithrombin complexes, prothrombin fragments, and d-dimers. Additional evidence has suggested that anabolic steroids can increase platelet aggregation and thereby promote thrombosis. Third, anabolic steroids may cause a reduction in nitric oxide synthesis and may alter vasodilator properties. This disruption in endothelial function may lead theoretically to coronary artery spasm. Finally, there is evidence from case reports and echocardiographic studies that anabolic steroids can cause ventricular hypertrophy. Hypertrophy may promote ischemia and infarction in predisposed patients.
Clenbuterol is a potent beta2-agonist that is used in Europe as an oral bronchodilator. It has improved oral absorption compared with other beta2-agonists and has a long elimination half-life. This drug has been used in the farming industry for its anabolic and thermogenic effects, which are mediated via beta2-receptors. Body builders use the drug illicitly in this country for these effects.
Cases of accidental clenbuterol poisoning after ingestion of bovine liver have been reported from Europe. Manifestations included palpitations, nervousness, tachycardia, and muscle tremors. These effects are thought to be mediated by beta1-receptors and are propanolol sensitive.
There is little data on the cardiac effects of clenbuterol in patients, and there are no reports of myocardial infarction. One study compared the effect of intravenous clenbuterol with salbutamol in nine patients with a history of myocardial infarction. The study found that clenbuterol had a similar, if not better, safety profile than salbutamol. In a recent publication, two body builders were reported to be using the combination of clenbuterol and anabolic steroids. One patient was asymptomatic and was shown to have left ventricular hypertrophy by echocardiogram. The other patient, who was reportedly using high doses of clenbuterol, had a monomorphic ventricular tachycardia induced by an exercise test. Subsequently, an echocardiogram showed a decreased ejection fraction of 30% with left ventricular hypertrophy and dilatation. Myocardial ischemia and infarction were not thought to play a role in either case.
To our knowledge, this case is the first in which myocardial infarction was associated with a combination of anabolic steroids and clenbuterol. We can only speculate regarding the possible mechanisms of our patient’s myocardial infarction. The patient had no known traditional cardiac risk factors, though his lipid profile could have been falsely lowered in the presence of a myocardial infarction. Additionally, testing of the patient’s coagulation system, as stated previously, was normal. Our patient had a cardiac catheterization within 6 hours of the onset of chest pain, with the intent of primary angioplasty. None of the cases in the literature reported to date have documented such an early cardiac catheterization, and no patient had such a procedure before anticoagulation or thrombolytic therapy. Other than aspirin and nitroglycerin, the patient had no therapeutic manipulations before the coronary angiograms. The fact that the patient had angiographically normal coronary arteries suggests coronary artery spasm as the mechanism of myocardial infarction, though rapidly autolysed coronary thrombus cannot be ruled out. The findings on ventriculography and echocardiography are consistent with transmural ischemia in the distribution of the posterior coronary circulation.
We suspect that there may have been a synergistic role between the anabolic steroid and clenbuterol. Hypothetically, the anabolic steroid may have caused cardiac hypertrophy, coronary artery spasm, or thrombosis. The clenbuterol may have precipitated ischemia by producing intermittent tachycardia. Alternatively, clenbuterol may have contributed primarily to the cardiac hypertrophy by its anabolic effects. Although there is no direct evidence that clenbuterol can cause hypertrophy in humans, recent studies have shown that clenbuterol can cause cardiac hypertrophy in rat models. Supranormal doses of either anabolic steroids or clenbuterol could potentially be more pathogenic. Our patient’s symptoms for 2 weeks before presentation are suggestive of clenbuterol toxicity. However, it is possible that clenbuterol may have had no pathologic effect.
It is likely that the illicit use of drugs like clenbuterol and anabolic steroids with their health-related consequences will become more prevalent in the future. Young adults appear to be the largest user group, and we are concerned that many users are exposed to other illicit drugs like cocaine, potentially creating an even more hazardous combination. We found it alarming that information about clenbuterol and anabolic steroids could be easily obtained through the world wide web .
In this case of a myocardial infarction in a healthy 26-year-old body builder who recently used clenbuterol and anabolic steroids, it is difficult to elucidate the contributing roles of each agent, but synergistic effects seem likely to have played a role in the infarct. The normal coronary arteries before any anticoagulant or thrombolytic therapy strongly suggest coronary spasm as the mechanism of the infarct. We urge physicians to ask about these substances when confronted with young patients who have cardiovascular events such as myocardial infarctions, and we welcome further reports.
Reprint requests to Daniel R. Goldstein, MD, UAB Department of Medicine, Division of Cardiology, 310 Lyons-Harrison Research Bldg, 701 S 19th St, Birmingham, AL 35294-0007.
DuRant RHO, Rickert VI, Asworth US, et al: Use of multiple drugs among adolescents who use anabolic steroids. N Engl J Med 1993; 328:922-926
Luke JO, Farb A, Virmani R, et al: Sudden cardiac death during exercise in a weight lifter using anabolic steroids: pathological and toxicological findings. J Forens Sci 1990; 35:1441-1447
Niemine MS, Ram MY, Viitasalo M, et al: Serious cardiovascular side effects of large doses of anabolic steroids in weight lifters. Eur Heart J 1996; 17:1576-1583
Laroche GP: Steroid anabolic drugs and arterial complications in an athlete — a case history. Angiology 1990; 41:964-969
McNutt RA, Ferenchick S, Kirklin PA, et al: Acute myocardial infarction in a 22-year-old world class athlete using anabolic steroids. Am J Cardiol 1988; 62:164
Capezzuto A, Achilli A, Suran N: Myocardial infarction in a 21 year old body builder. Am J Cardiol 1989; 63:1530
Bowman SJ, Tanna S, Fernando S, et al: Anabolic steroids and infarction. BMJ 1989; 299:632
Ferenchick GS, Adelman S: Myocardial infarction associated with anabolic steroid use in a previously healthy 37 year old weight lifter. Am Heart J 1992; 124:507-508
Kennedy C: Myocardial infarction in association with misuse of anabolic steroids. Ulster Med J 1993; 63:174-176
Huie MJ: An acute myocardial infarction occurring in an anabolic steroid user. Med Sci Sports Exerc 1994; 26:408-413
Fisher M, Appleby M, Rittoo D, et al: Myocardial infarction with extensive inracoronary thrombus induced by anabolic steroids. Br J Clin Pract 1996; 50:222-223
Glazer G: Atherogenic effects of anabolic steroids on serum lipid levels. Arch Intern Med 1991; 151:1925-1933
Ferenchick GS, Hirokawa S, Mammen EF, et al: Anabolic-androgenic steroid abuse in weight lifters. Am J Hematol 1995; 49:282-288
Ferenchick G, Schwartz D, Ball M, et al: Androgenic-anabolic abuse and platelet aggregation: a pilot study in weight lifters. Am J Med Sci 1992; 303:78-82
Green DJ, Cable NT, Ranklin JM, et al: Anabolic steroids and vascular responses. Lancet 1993; 342:863
De Picoli B, Giada F, Benettin A, et al: Anabolic steroid use in body builders: an echocardiographic study of left ventricular morphology and function. Int J Sports Med 1991; 12:408-412
Martinez-Navarro JF: Food poisoning related to consumption of illicit of beta agonists in liver. Lancet 1990; 336:1311
Maistro S, Chiesa E, Angeletti R, et al: Beta blockers to prevent clenbuterol poisoning. Lancet 1995; 346:180
Pasotti C, Gandolfi P, Capra A, et al: Cardiovascular effects of clenbuterol in comparison with salbutamol in subjects with coronary artery disease. Curr Ther Res 1984; 36:126-132
Petro M, Wynne DG, Boheler KR, et al: Clenbuterol induced hypertrophy of latissimus dorsi muscle and heart in the rat with molecular and phenotypic changes. Circulation 1995; 92:483-488
Clenbuterol Poisoning in Humans
Clenbuterol is a drug that has been used by athletes to grow larger muscles and cattlemen to grow larger cattle. A report from Spain showed that humans can be poisoned by eating veal liver from cattle that had been given clenbuterol.
Clenbuterol belongs to a class of drugs called beta agonists that are used to treat asthma. Training for sports is done by taking a hard workout, waking up the next morning with sore muscles, and then taking easy workouts until the soreness goes away. Clenbuterol hastens recovery so it can shorten the recovery period from three or more days to just one or two. The athlete can do more work and therefore becomes stronger. All beta agonists are banned by the International Olympic Committee. It is also illegal for cattlemen to give clenbuteral or any other beta agonist to cattle.
Beta agonists are potent stimulants and are broken down in the liver. The report from Spain involved 113 cases of people who developed nervousness, rapid heart rate, muscle shaking, muscle pain and headache, 15 minutes to 6 hours after eating veal liver. Their symptoms lasted from 90 minutes to 6 days. Interestingly, blood levels of clenbuteral were very low, while urine levels from affected people were very high. This study shows that humans and animals can get very sick after taking clenbuteral and so can people who eat animals that take that drug.