# The interplay between thrombosis, stress, and social risk factors in trans persons on gender affirming hormone therapy

**Authors:** Kevin Liang, Carl G. Streed, Pablo Buitron de la Vega, Beth M. Cohen

PMC · DOI: 10.1016/j.rpth.2026.103369 · Research and Practice in Thrombosis and Haemostasis · 2026-01-23

## TL;DR

This paper explores how stress and social risk factors may increase blood clotting risk in trans people undergoing hormone therapy.

## Contribution

The paper introduces a novel framework linking minority stress, socioeconomic disparities, and thrombosis in trans individuals.

## Key findings

- Stress-induced hypercoagulability may be exacerbated by social risk factors in trans persons.
- Gender affirming hormone therapy may compound prothrombotic effects in this population.
- Socioeconomic disparities are theorized to moderate the relationship between stress and thrombosis.

## Abstract

Although the use of exogenous hormone therapy has been the primary focus of transgender and gender diverse (trans) health research, additional factors that contribute to thrombosis warrant further evaluation in this population. Because stress is a trigger of hypercoagulability, disparities in thrombosis experienced by trans persons should be examined through a minority stress lens. Given the high burden of socioeconomic disparities experienced by trans persons and the potential moderating effect of socioeconomic status on minority stress, clinicians and researchers should assess the role of social risk factors in exacerbating stress and thrombosis in this population. Clotting during mental stress is thought to have evolved, in part, as an adaptive response in anticipation of bleeding from injury, acting via 2 hormonal pathways: catecholamine- and glucocorticoid-mediated pathways. Because trans persons face significant socioeconomic disparities, the theorized role of social risk factors in exacerbating stress-induced hypercoagulability should be studied in this population. This is especially relevant for those on gender affirming hormone therapy, which can have compounding prothrombotic effects. We define sex via the genetic complement of chromosomes, including cellular and molecular differences, as well as physical traits such as genitalia and reproductive organs. We define gender as comprising the social, environmental, cultural, and behavioral factors that influence a person's self-identity, health, and well-being.

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, F8 (coagulation factor VIII) [NCBI Gene 2157] {aka AHF, DXS1253E, F8B, F8C, FVIII, HEMA}, SELP (selectin P) [NCBI Gene 6403] {aka CD62, CD62P, GMP140, GRMP, LECAM3, PADGEM}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}, SERPINE1 (serpin family E member 1) [NCBI Gene 5054] {aka PAI, PAI-1, PAI1, PLANH1}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, INSR (insulin receptor) [NCBI Gene 3643] {aka CD220, HHF5}, CYP19A1 (cytochrome P450 family 19 subfamily A member 1) [NCBI Gene 1588] {aka ARO, ARO1, CPV1, CYAR, CYP19, CYPXIX}
- **Diseases:** Thrombosis (MESH:D013927), discrimination (MESH:D010468), VTE (MESH:D054556), hyperinsulinemia (MESH:D006946), hypertension (MESH:D006973), ischemic stroke (MESH:D002544), cardiac output (MESH:D002303), COVID-19 (MESH:D000086382), blood coagulation (MESH:D001778), cardiovascular disease (MESH:D002318), myocardial infarction (MESH:D009203), gender dysphoria (MESH:D000068116), Insulin Resistance (MESH:D007333), endothelial injury (MESH:D057772), Depression (MESH:D003866), hypercholesterolemia (MESH:D006937), disordered eating (MESH:D001068), intimate partner violence (MESH:C563733), MetS (MESH:D024821), hyperglycemia (MESH:D006943), Platelet aggregation (MESH:D001791), inflammatory (MESH:D007249), injury (MESH:D014947), alcohol abuse (MESH:D000437), diabetes (MESH:D003920), endothelial dysfunction (MESH:D014652), GAHT (MESH:D019968), Alzheimer (MESH:D000544), Anxiety (MESH:D001007), bleeding (MESH:D006470), obese (MESH:D009765), tachycardia (MESH:D013610), blood stasis (MESH:D014647), Hypercoagulability (MESH:D019851), overweight (MESH:D050177), pulmonary embolism (MESH:D011655), posttraumatic stress disorder (MESH:D013313), acute limb ischemia (MESH:D000208)
- **Chemicals:** prednisolone (MESH:D011239), GAHT (-), Catecholamine (MESH:D002395), carbohydrate (MESH:D002241), steroids (MESH:D013256), ethinyl estradiol (MESH:D004997), salbutamol (MESH:D000420), Cortisol (MESH:D006854), carvedilol (MESH:D000077261), androstenedione (MESH:D000735), 17-beta estradiol (MESH:D004958), adrenaline (MESH:D004837), adenosine diphosphate (MESH:D000244), triglycerides (MESH:D014280), estrone (MESH:D004970), testosterone (MESH:D013739), noradrenaline (MESH:D009638), cyclic adenosine monophosphate (MESH:D000242)
- **Species:** Homo sapiens (human, species) [taxon 9606], Felis catus (cat, species) [taxon 9685], Canis lupus familiaris (dog, subspecies) [taxon 9615]

## Full text

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## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC12934322/full.md

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Source: https://tomesphere.com/paper/PMC12934322