Man's secret use of synthetic testosterone for cows nearly destroyed his heart

Doctors warn that such life-threatening cases are becoming more common.

For 11 years, a Massachusetts man had an alarming array of health problems, most notably that his heart kept failing. He landed in the hospital over and over again, needed life support at one point, spent years going to specialists, and underwent a barrage of tests along the way.

But through it all, he never revealed a key detail behind his ailments: He was taking powerful, illicit synthetic testosterone derivatives (aka anabolic-androgenic steroids, or AAS). One of the drugs he took was approved only for use in animals; it’s primarily used to beef up cows.

Left in the dark, his doctors had to puzzle this out on their own. In a case report in this week’s issue of the New England Journal of Medicine, they explain how they did it. They also offer a warning: These cases will only become more common, and clinicians need to know what they look like.

“Use of AAS has now become a major international substance use disorder,” they wrote. In the US, it’s estimated that between 2.9 and 4 million people, mostly male athletes, use AAS. To put this in a public health perspective, this is more than the number of people in the US with an HIV infection.

“Clinicians should be prepared to encounter increasing numbers of patients presenting with the long-term effects of AAS exposure, including cardiomyopathy, atherosclerotic disease, and anabolic steroid–induced hypogonadism.”

Patients also need to be prepared for what recovery looks like, which they described as being “lengthy and varied.” The man’s case offers a stark example.

Troubling tale

The problems started when he was 39. He fell ill after returning from a trip to the Caribbean and went to Massachusetts General Hospital in Boston with a fever, chills, and trouble breathing. Tests suggested he had an acute kidney injury, liver damage, and an injured heart. Testing of his heart showed that the left chamber was pumping out just 21 percent of its blood in a beat (a normal amount is above 50 percent). His heart only got worse from there, and within hours, he ended up on a type of life support called ECMO (venoarterial extracorporeal membrane oxygenation), a machine that does the work of both the heart and lungs in dire circumstances. He luckily recovered—and quickly. But doctors were baffled by the cause.

When he was weaned off ECMO a few days later, his heart function normalized. Doctors looked for evidence of anything that could have sparked the sudden cardiac spiral. They found nothing but a mildly elevated level of antibodies against a toxin made by Streptococcus bacteria. In rare instances, an infection with these germs can lead to a condition called poststreptococcal myocarditis, which could potentially explain some of his symptoms. It was their best guess. They prescribed him antibiotics, as well as drugs to lower his blood pressure.

Two years later, he went to another hospital. This time it was for acute pain in his abdomen and legs. Doctors found signs of cell death in his kidneys. The arteries that supply blood to his kidneys appeared narrowed, suggesting a condition called renal-artery stenosis. There were also signs of inflammation in his blood vessels. But the doctors at the hospital couldn’t pinpoint the problem. They prescribed him anti-inflammatory drugs and sent him on his way.

For the next five years, the man started seeing a cadre of specialists to monitor his health, including doctors in primary care, cardiology, nephrology, rheumatology, general medicine, sleep medicine, and psychiatry. When he was about 46, he reported fatigue to his primary care doctor, who found that his testosterone level was low. The man then went to an endocrinologist, reporting not just fatigue but low libido and poor sleep. The endocrinologist recommended treatment for obstructive sleep apnea, which can increase the risk of low testosterone.

A year later, the man added a hematologist to his rotation of care providers. A routine blood test revealed abnormally high levels of red blood cells (erythrocytosis). The hematologist noted the man also had high blood pressure (150/108 mm Hg) but found everything else to be normal. The hematologist ended up attributing the erythrocytosis to the man’s sleep apnea and renal-artery stenosis.

Tangled toxicity

It wasn’t until he arrived again at Mass General in 2026 that doctors finally put it all together. Now 50, the man was once again experiencing heart failure—and he had again just returned from the Caribbean.

In the case report, doctors provided a more complete picture of the man, noting that he lived with his wife and children in eastern Massachusetts, worked as a facilities manager, and described himself as a workout “fanatic.” He used tanning beds and applied spray tans. He told doctors he had erectile dysfunction and reduced libido for several years. They also noticed that he had mildly enlarged breast tissue (a condition called gynecomastia), progressive insulin resistance, decreased levels of “good” cholesterol (HDL or high-density lipoprotein), and fatty liver disease.

When he arrived at the hospital, he reported five days of worsening chest tightness and pressure, fatigue, swelling in his legs, and trouble breathing. His heart was racing at 134 beats per minute. His blood pressure was high at 146/106 mm Hg. Doctors described him as “muscular, tanned, anxious, and in mild distress.” Tests showed his heart was once again failing, with the left chamber pumping out just 20 percent of its blood.

The doctors started reviewing a long list of possible explanations. They ruled out infectious diseases that can cause heart inflammation (myocarditis), as well as autoimmune conditions, medication side effects, and toxins. The explanation they were left with—which also seemed to explain much of his other problems—was high doses of testosterone, or perhaps an AAS.

Illicit use of AAS is clearly linked to the heart problems, including the decreased blood pumping the man had, as well as strain and damage. It could also explain his enlarged breast tissue, fatty liver and signs of liver damage, progressive insulin resistance, kidney injuries, high blood pressure, and high levels of red blood cells (erythrocytosis). The sleep problems, fatigue, and low testosterone levels—which doctors previously guessed were from obstructive sleep apnea—could actually be from a drop in natural hormone production after doses of AAS (a condition called hypogonadism).

In the man’s lengthy medical history, he had never mentioned using AAS or testosterone supplements. Doctors prepared to have a delicate conversation to determine if he was secretly using the drugs. When they finally broached the topic, he confessed; he had been intermittently using high doses of AAS to boost his muscles, taking the most recent dose before his vacation to the Caribbean. The testosterone derivative he used was trenbolone, an AAS only approved for use in veterinary medicine; it’s mostly used in livestock.

Tricky treatment

The doctors then tested his total testosterone level, finding it was so high that the test couldn’t accurately measure it. The assay’s range of detection was 12 to 1,500 nanograms per deciliter of blood. His level was over 1,500 ng/dl. The range considered normal for the test was between 249 and 836 ng/dl. The doctors gave their final diagnosis: androgen excess–related cardiomyopathy.

The primary treatment for his heart is to stop taking AAS. Doctors prescribed him medications for high blood pressure, heart failure, and diabetes. Four months later, heart tests showed his left chamber was pumping 49 percent of its blood, a significant improvement. The state of his liver also improved. But recovery from the AAS-induced hypogonadism was a much longer, more difficult journey. It was made harder because he was over age 35, had taken AAS for more than a decade, and had preexisting dysfunction.

Six months into his recovery, he still had significant hypogonadism symptoms, which include loss of sexual desire, erectile dysfunction, gynecomastia, reduced orgasmic satisfaction, and ejaculatory disorders. He opted to try a drug called clomiphene, which binds to estrogen receptors. It’s often used in women to help with fertility, but in men it is sometimes used to try to jumpstart natural testosterone production. It didn’t work for the man. He moved on to trying topical testosterone-replacement therapy but continued to have erectile dysfunction. Doctors warn that it could take up to three years for the hypogonadism to resolve.

In the last follow-up at eight months, he reported that he was still off AAS and had no symptoms of heart failure.