Both Low and High Testosterone Linked to Irregular Heartbeats

What if the hormone that fuels sex drive and muscle tone also nudges the heart out of rhythm? That question is getting louder after a new review of human and lab studies suggests atrial fibrillation — a common irregular heartbeat — may be more likely at both extremes of testosterone levels.

Both too little and too much testosterone appear to raise the risk of atrial fibrillation, through separate biological mechanisms. The review, published in the Journal of the Endocrine Society and led by Anand Reddy Maligireddy at the University of Kansas Medical Center, sifted through population data, clinical trials and bench research to find a surprisingly consistent pattern: risk seems lowest near the middle of the normal hormone range and rises at either end.

Why would that happen? The mechanisms look different depending on the direction of the imbalance. Laboratory work points to low testosterone disrupting calcium handling inside heart cells — a critical element of the electrical choreography that keeps the atria beating in step. High testosterone, by contrast, appears to alter potassium currents, another electrical lever that can change how impulses travel through cardiac tissue. Two distinct molecular detours. One common outcome.

Real-world studies echo those signals, though they stop short of proving cause and effect. Classic population cohorts such as the Framingham Heart Study linked lower testosterone with higher atrial fibrillation risk in certain age groups. On the other side, an analysis of 4,570 older men without prior cardiovascular disease found that those in the top two testosterone groups had roughly double the risk of developing atrial fibrillation over about 4.4 years compared with men in the middle group.

Clinical trials add nuance. The TRAVERSE trial — a large randomized study of 5,246 men with low testosterone and preexisting cardiovascular disease or elevated cardiovascular risk — assigned participants to testosterone gel or a placebo gel. Atrial fibrillation was reported in 3.5 percent of the testosterone-treated men versus 2.4 percent of controls. Importantly, TRAVERSE did not show an increase in the trial’s primary combined endpoint of cardiovascular death, nonfatal heart attack or nonfatal stroke, but the AF signal remains a puzzle clinicians must weigh.

Not everyone agrees. A 2024 meta-analysis that pooled 106 randomized trials did not find a statistically significant rise in atrial fibrillation when studies other than TRAVERSE were combined. Observational studies, meanwhile, can reveal associations but cannot prove that testosterone itself caused the rhythm disturbance. Confounders — age, obesity, blood pressure, alcohol use, sleep apnea — complicate the picture. Excess fat, for example, lowers testosterone while also creating its own cardiovascular risks.

So what should doctors and patients do right now? The review’s authors recommend careful assessment before starting hormone replacement: look at heart health, weigh other risks, and consider reversible contributors like sleep apnea and uncontrolled hypertension. That pragmatic stance could help clinicians aim for safer, more individualized targets rather than assuming higher levels are automatically better.

We still need more randomized trials specifically designed to test whether adjusting testosterone toward the middle of the normal range actually reduces atrial fibrillation. Until then, the strongest takeaway is humility: testosterone influences more than libido and muscle mass. It touches the heart’s electric conversation in ways we’re only beginning to untangle — and that makes monitoring, not guesswork, the safest path forward.