A review suggests a possible link between testosterone and atrial fibrillation, but mixed findings do not establish a new treatment target.
On October 24, 2026, ScienceAlert reported on a review in the Journal of the Endocrine Society examining testosterone and atrial fibrillation (AF). Led by Anand Reddy Maligireddy of the University of Kansas Medical Center, the review considered existing human studies and laboratory research on this irregular heartbeat.
This article is for informational purposes only and is not medical advice. Personal decisions about hormone testing or testosterone treatment belong with a qualified clinician.
The review summarized by ScienceAlert describes evidence consistent with a possible U-shaped relationship between testosterone and AF risk. In that proposed pattern, risk is higher at both lower and higher testosterone levels. The lowest risk may sit near the middle of the normal range.
The shape matters because it challenges a simple assumption that more testosterone must always be better or worse. A U-shaped relationship would instead suggest different associations at different hormone levels. However, the studies reviewed do not all show that same pattern.
The report describes AF symptoms that can include a fluttering heartbeat, fatigue and dizziness. Some people have no symptoms. That makes the research relevant to heart health as well as to questions about hormone levels.
According to ScienceAlert, one observational study followed 4,570 older men without prior cardiovascular disease. During a median follow-up of 4.4 years, 286 developed AF.
Men in the two highest testosterone groups had roughly twice the AF risk of men in the middle group. The study did not find a statistically significant increase at the low end.
This finding supports the higher-testosterone side of the proposed curve more clearly than the lower-testosterone side. It is therefore more precise to describe the actual comparison than to say this study demonstrated a complete U-shaped relationship.
A separate UK Biobank analysis reported in the World Journal of Men’s Health included 179,988 men without a history of AF. It recorded 13,847 new AF cases over a median follow-up of 11.8 years.
That analysis associated lower total testosterone with higher AF risk. Its reported findings did not establish the same increased risk at the higher end.
Read alongside the older-men study, this result shows why the overall picture is mixed. One study highlighted higher testosterone groups. Another linked lower total testosterone with later AF. Combining those observations into a single curve is an interpretation of different findings rather than a pattern consistently demonstrated across studies.
The review also discussed TRAVERSE, a randomized trial involving 5,246 men with low testosterone and existing cardiovascular disease or increased cardiovascular risk.
As reported by ScienceAlert, AF occurred in 3.5% of participants assigned testosterone gel and 2.4% assigned placebo gel. These figures describe the treatment groups in that trial. They are distinct from the comparisons between naturally measured testosterone levels in the observational studies.
TRAVERSE also assessed a main combined cardiovascular outcome. It combined cardiovascular death with nonfatal heart attack and nonfatal stroke. According to the report, that combined outcome was not increased in the testosterone group.
These results concern different outcomes. The finding for the main combined outcome does not erase the separate AF difference. Equally, reporting the AF difference should not turn the trial’s overall cardiovascular findings into a claim that every outcome worsened with testosterone treatment.
The review proposed biological explanations for associations at both ends of the testosterone range. According to ScienceAlert, laboratory research suggests that low testosterone could affect calcium regulation in heart cells. Higher testosterone could alter potassium currents involved in electrical signaling.
These are proposed mechanisms rather than demonstrated explanations for the AF cases recorded in the human studies. They give researchers questions to test: whether different hormone levels affect electrical behavior through different pathways and whether those effects explain clinical outcomes.
Several boundaries matter when interpreting these findings. They concern cause and effect, study populations and the difference between a research hypothesis and a treatment target.
The observational findings do not establish that testosterone itself caused AF. Men grouped by hormone levels may also differ in other ways relevant to heart health.
ScienceAlert notes that excess body fat is linked to lower testosterone. That makes body fat a potential complicating factor when interpreting an association between lower testosterone and AF. The hormone measurement may be part of a broader health picture rather than an isolated explanation for the outcome.
This is one reason that reading a testosterone result in context is more useful than treating it as a stand-alone verdict. In this research, a testosterone result is not an AF risk score.
The higher-testosterone association came from a study of older men without prior cardiovascular disease. TRAVERSE enrolled men with low testosterone who already had cardiovascular disease or increased cardiovascular risk.
Those populations answer different questions. The TRAVERSE percentages should not be treated as a direct estimate for every man using testosterone or for men with different health profiles. Comparing measured hormone levels is also a different question from comparing assignment to testosterone gel or placebo.
ScienceAlert also describes a 2024 analysis of 106 randomized trials. When trials other than TRAVERSE were considered together, that analysis did not find a statistically significant increase in AF.
That result complicates a claim that testosterone treatment has a firmly established AF effect. It does not prove that treatment carries no AF risk. The distinction is between an effect that has been established consistently and a signal that still needs clarification.
The authors’ suggestion that risk may be lowest near the middle of the normal range is not a demonstrated treatment goal. As ScienceAlert reports, aiming for that midpoint has not been shown to reduce AF. Further trials are needed.
An observed comparison between hormone groups and a tested strategy for preventing disease are different kinds of evidence. The review offers the former as a possible pattern. It does not establish the latter as a clinical intervention.
The immediate clinical implication is to include cardiovascular context in a testosterone conversation. The review is not a new clinical guideline and does not support an automatic change to current medical practice.
According to ScienceAlert, the researchers recommend considering heart health and relevant risk factors before treatment. These include obesity, high blood pressure, alcohol use and sleep apnea. For men considering or receiving testosterone, those subjects belong in a discussion with a qualified clinician rather than in a self-directed plan to adjust hormone levels.
A useful clinical conversation can keep several questions separate:
Keeping those questions separate helps avoid turning a heart-rhythm headline into an explanation for every symptom. For readers researching questions about a possible low-testosterone diagnosis, this review adds cardiovascular context rather than a personal diagnostic answer.
The most useful distinction is between noticing a research signal and acting as though it has already settled a treatment decision. The studies provide reasons for a careful discussion. A qualified clinician remains responsible for applying that evidence to an individual’s symptoms and health history.
Bottom line: This review warrants attention to AF within testosterone safety discussions. It does not justify men starting, stopping or changing testosterone treatment on their own. Current decisions should remain individualized and clinician-led rather than driven by the proposed shape of a risk curve.
Identifying whether an AF study measured hormone levels or assigned treatment gives readers a concrete way to assess its claims, and Testostra explains those evidence distinctions. For men uncertain about possible low testosterone symptoms, its coverage adds context about potential causes and testing without assigning a diagnosis or recommending a personal treatment plan.
Testostra follows testosterone research, clinical guidance and emerging evidence without turning general information into personal treatment advice.
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