# Acute blood biomarker responses to consensual sexual choking/strangulation in young adult women: a randomized crossover study

**Authors:** Sage H. Sweeney, Grace O. Recht, Giselle Lima-Cooper, Dibyadyuti Datta, Claire V. Buddenbaum, Harper Day, Bella Buehler, Megan E. Huibregtse, Debby Herbenick, Keisuke Kawata

PMC · DOI: 10.3389/fgwh.2025.1717361 · 2026-01-08

## TL;DR

This study found that consensual sexual choking in young women temporarily increases blood markers linked to brain injury and inflammation.

## Contribution

The study is the first to show acute biomarker changes in humans after consensual sexual strangulation.

## Key findings

- Neurofilament light (NfL) increased significantly after choking-involved sex.
- CCL-2 and VEGF-A also showed acute increases after choking, suggesting hypoxia-related inflammation.
- Other neural and inflammatory markers remained unchanged between conditions.

## Abstract

Sexual strangulation, commonly referred to as “choking”, has become increasingly common among young adults, yet its neurobiological consequences remain poorly understood. Preclinical and clinical evidence suggests strangulation may trigger axonal injury, neuroinflammation, and blood–brain barrier dysfunction. Blood biomarkers of neural injury and inflammation provide a sensitive means to detect subtle effects.

To examine whether consensual sexual choking/strangulation acutely alters blood biomarkers of neural injury and inflammation compared to non-choking sexual activity in young adult women.

In a randomized crossover study, 29 women (mean age 21.5 ± 2.7) completed three laboratory visits: baseline (≥24 h abstinence), post-choking sex, and post-non-choking sex. Blood was collected within 24 h of sexual events. Neural injury biomarkers (NfL, tau, GFAP, UCH-L1, S100B) and inflammatory markers (IL-1ra, TNF-R1, CCL-2, VEGF-A, VCAM-1) were analyzed using Quanterix and Luminex multiplex immunoassays. Mixed-effects regression models tested exposure-by-time interactions, adjusting for age and brain trauma history.

Neurofilament light (NfL) significantly increased after choking-involved sex but remained unchanged after non-choking, which resulted in a statistically significant exposure-by-time interaction [β = −0.21, 95% CI (−0.38, −0.03), p = 0.021]. Other neural biomarkers did not differ by exposure. Among inflammatory markers, CCL-2 and VEGF-A demonstrated a similar pattern as NfL, with acute increases after choking-involved sex, but not following non-choking sex, yielding in exposure-by-time interaction effects (CCL-2: β = −14.60, 95% CI [−25.70, −3.43, p = 0.011; VEGF-A: β = −9.29 (−19.71, 1.13), p = 0.079]. IL-1ra, TNF-R1, and VCAM-1 remained stable.

Consensual sexual strangulation elicited acute increases in NfL and CCL-2, with VEGF-A showing a similar pattern, suggesting transient axonal stress and hypoxia-related inflammatory signaling. These findings indicate that sexual choking/strangulation, even in consensual contexts, may have subtle, yet detectable cellular burden. Future studies with larger samples, refined temporal sampling, and multimodal outcomes are needed to clarify short- and long-term implications.

## Linked entities

- **Proteins:** NEFL (neurofilament light chain), MAPT (microtubule associated protein tau), GFAP (glial fibrillary acidic protein), UCHL1 (ubiquitin C-terminal hydrolase L1), S100B (S100 calcium binding protein B), IL1R1 (interleukin 1 receptor type 1), TNFRSF1A (TNF receptor superfamily member 1A), CCL2 (C-C motif chemokine ligand 2), VEGFA (vascular endothelial growth factor A), VCAM1 (vascular cell adhesion molecule 1)

## Full-text entities

- **Genes:** MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, IL1RN (interleukin 1 receptor antagonist) [NCBI Gene 3557] {aka CRMO2, DIRA, ICIL-1RA, IL-1RN, IL-1ra, IL-1ra3}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, S100B (S100 calcium binding protein B) [NCBI Gene 6285] {aka NEF, S100, S100-B, S100beta}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, NEFL (neurofilament light chain) [NCBI Gene 4747] {aka CMT1F, CMT2E, CMTDIG, NF-L, NF68, NFL}, UCHL1 (ubiquitin C-terminal hydrolase L1) [NCBI Gene 7345] {aka HEL-117, HEL-S-53, NDGOA, PARK5, PGP 9.5, PGP9.5}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, TNFRSF1A (TNF receptor superfamily member 1A) [NCBI Gene 7132] {aka CD120a, FPF, TBP1, TNF-R, TNF-R-I, TNF-R55}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}
- **Diseases:** Neural injury (MESH:D014947), hypoxia (MESH:D000860), inflammation (MESH:D007249), brain trauma (MESH:D000070642), neuroinflammation (MESH:D000090862), axonal injury (MESH:D001480)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12823983/full.md

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Source: https://tomesphere.com/paper/PMC12823983