How do frequency and specific sexual practices (e.g., fisting, chemsex) quantitatively change FI risk in longitudinal studies?
Executive summary
Longitudinal and cohort research consistently show that both the frequency of high‑risk sexual practices and participation in chemsex are associated with substantially higher odds of acquiring bloodborne and sexually transmitted infections, with effect sizes in published studies often in the range of roughly twofold or greater (for example, chemsex aOR ≈2.2 for HIV; shared fisting lubricant aOR ≈2.34 for HCV) [1] [2]. However, true causal dose–response—how increasing frequency quantitatively raises individual risk over time—is incompletely documented because many studies are cross‑sectional or limited in follow‑up, and longitudinal datasets routinely flag confounding by network exposure, bleeding, and injection practices [3] [4] [2].
1. The measurable signal: chemsex and elevated odds of infection
Meta‑analyses and cohort summaries report that engagement in chemsex correlates with higher prevalence and incidence of HIV and other STIs, with pooled adjusted odds ratios often around twofold compared with non‑chemsex peers (aOR ≈2.2 for HIV in a large meta‑analysis) [1] [5]. Longitudinal surveillance within sexual health and PrEP cohorts likewise links baseline reports of chemsex or use of specific chemdrugs to subsequent STI/HIV diagnoses, and in one clinic cohort drug use plus group sex or condomless sex predicted incident infection [6] [7].
2. Frequency matters, but longitudinal dose–response is thin
Several cohort and longitudinal analyses observe that higher frequency of risk behaviours clusters with greater incidence—studies report trajectories showing increases in chemsex and linked practices over time and higher STI incidence in those with persistent behaviours—but few studies present a clean per‑episode or per‑month risk increment [3] [2]. The Swiss and other cohort reports emphasize that longitudinal data are scarce and that while repeated engagement (e.g., monthly receptive fisting or regular chemsex sessions) maps to higher population attributable fractions for outcomes like HCV, exact quantitative dose–response curves for individual risk remain under‑specified in the literature [3] [2].
3. Which specific practices carry the largest effect sizes in cohorts?
Among practices repeatedly implicated in longitudinal and case‑control work, frequent anorectal trauma and bleeding show the largest associations with HCV acquisition (frequent anal bleeding aOR = 4.17), frequent anorectal douching is strongly associated (aOR = 3.20), and shared fisting lubricant and receptive fisting are independently associated with increased HCV risk (shared fisting lubricant aOR = 2.34; receptive fisting linked in other cohort follow‑up) [2] [8]. Earlier London cohort data similarly identified fisting as the single practice most strongly associated with sexual HCV seroconversion after controlling for partner numbers [8].
4. Injecting, slamming and drug types amplify risk beyond sexual acts
Injecting during sex (“slamming”) and specific chemsex drugs (mephedrone, GHB/GBL, crystal meth) multiply transmission pathways: injectors in one study had far higher subsequent HIV detection (16% of injectors testing HIV‑positive in a cohort), and slamming has been repeatedly associated with HCV and HIV transmission in multivariable models [7] [2]. Cohort and clinic data show that chemsex is linked with more partners, longer sessions, and mucosal trauma, creating conditions where drug type, route (injection), and frequency of use together produce markedly higher adjusted odds of infection [9] [5] [4].
5. Confounding, causality limits, and publication patterns
Most papers acknowledge that associations do not prove chemsex or a specific act causes infection for a given individual because behaviour clusters (multiple partners, condomless sex, overlapping STI presence), network exposure, and reporting biases complicate causal inference; several reviews and editorial pieces explicitly call for more longitudinal, representative work to untangle temporal ordering and dose–response [10] [4] [3]. Meta‑analyses have detected publication bias for some chemsex associations and cohort authors warn that effect estimates can be inflated when networks with high HIV/HCV prevalence are overrepresented [1] [3].
6. Practical takeaway for public‑health risk quantification
For policymakers and clinicians the evidence is clear enough to treat frequent fisting, shared fisting lubricant, anorectal trauma/bleeding, slamming, and recurrent chemsex as markers of substantially elevated infection risk (aORs commonly >1.8 and in some models >4.0), but the literature cannot yet provide precise per‑episode risk increments or an unconfounded dose–response curve for individuals; filling that gap will require larger prospective cohorts with fine‑grained exposure measurement and network data [2] [3] [1]. Harm‑reduction strategies therefore target both behavioural frequency (screening, counselling, lubricant hygiene) and chemsex‑specific interventions (safer‑use services, injection harm reduction, integrated STI screening) because the convergent evidence shows multiplicative risk when practices and drug use co‑occur [6] [11] [10].