Trans and nonbinary people who were assigned female at birth face a higher cardiovascular risk than the general population. The usual explanation points to the testosterone many of them take as part of gender-affirming hormone therapy. But another hypothesis tends to stay in the background: the physiological toll of the stress that comes with belonging to a minority. An international team has put both forces head to head in the laboratory, and the results are published in American Journal of Physiology-Heart and Circulatory Physiology. The conclusion is that neither of the two explains blood pressure on its own: testosterone and social stress pull in opposite directions, and the difference only becomes visible when the body responds to psychological stress.
Twenty-four people and two stress tests
The study recruited 24 trans and nonbinary adults assigned female at birth, split into two equal groups: 12 who were using testosterone and 12 who were not. All of them had total testosterone measured in blood by radioimmunoassay and were given a composite gender minority stress score built from seven standardised psychosocial scales — discrimination, rejection, identity concealment, among others.
Their blood pressure was then recorded in three situations: at rest, during a physical stress test (putting a hand in very cold water, the so-called cold pressor test) and during a psychological stress test (naming as fast as possible the ink colour of a printed word, the Stroop test).
At rest, nobody stands out
The first result overturns a widespread intuition. Resting blood pressure was almost identical in both groups: 115/68 mmHg whether or not they were using testosterone. In this sample, hormone therapy did not translate into higher baseline pressure.
Two signals pointing in opposite directions
The difference appeared once the system was stressed. During the psychological test, greater minority stress was associated with a blunter blood pressure response (systolic: beta = -0.589, p = 0.002; diastolic: beta = -0.492, p = 0.006), while higher total testosterone levels were associated with a stronger response (diastolic: beta = 0.422, p = 0.013; systolic: beta = 0.301, p = 0.079, just at the edge of statistical significance). The model accounted for about half of the variability between participants: 43% for systolic and 55% for diastolic pressure.
With the cold pressor test, by contrast, no relationship appeared: neither minority stress nor testosterone predicted the physical reaction of blood pressure.
What the two directions mean
That social stress dampens the rise in pressure during a mental task fits the pattern already described in people under chronic stress: the system desensitises or responds with less vigour. That testosterone amplifies it is consistent with its known effect on cardiovascular reactivity. What matters is that both effects show up in the same experiment and for the same kind of stimulus, which forces us to look at them together rather than as separate compartments.
The authors put it plainly: cardiovascular risk in trans and nonbinary people probably reflects an interaction between psychosocial and hormonal factors, and psychological stress pathways are a possible target for prevention and intervention.
The cautions worth keeping
The study is small — 24 participants —, cross-sectional and from a single centre, and testosterone was measured only once. That rules out claims about causes and clinical outcomes: nobody was followed up to see whether those short-term differences in reactivity turn into cardiovascular events years later. Nor does the Stroop test reproduce real life, and the minority stress measure, though built on validated scales, is a psychosocial summary rather than a biological quantity.
Even with those limits, the work carries an idea that goes beyond hormones: measuring cardiovascular risk in this population requires putting the social environment into the equation, not just the treatment. The question it leaves open — whether intervening on social stress improves the cardiovascular profile — will have to be answered by a longitudinal study.
Source: Gender minority stress, testosterone, and blood pressure responses to stress in transgender and nonbinary adults. Turino Miranda et al. American Journal of Physiology-Heart and Circulatory Physiology 2026;331(4):H1267-H1276. DOI: 10.1152/ajpheart.00548.2026.
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