What does current research say about rates of fecal incontinence in people who practice anal sex versus those who do not?

1. What the major studies measured and what they actually found

Two types of evidence dominate: population surveys and narrative/clinical reviews. The French ERAS survey analyzed 21,762 MSM and reported that frequent receptive anal intercourse (RAI ≥ several times/week) was associated with a 12.7% one‑month FI prevalence versus 5.7% among those not reporting RAI; it also identified higher FI among people reporting chemsex and fisting ^{[2] [1]}. The U.S. analysis of NHANES 2009–2010 (n≈4,170 adults aged 20–69 who answered both sexual behavior and FI questions) found that anal intercourse was associated with greater odds of monthly FI, with a marked effect in men (authors concluded anal intercourse should be assessed as a contributing factor to FI) ^{[3] [4]}.

2. Magnitude of the association—numbers matter

Reported prevalence differences in these datasets are moderate but meaningful: 12.7% vs. 5.7% in the ERAS MSM subgroup for frequent RAI (a roughly twofold increase in one‑month prevalence) ^{[1] [2]}. The NHANES-based paper reported that men who ever had anal intercourse had substantially higher odds of monthly FI compared with men who had not; Reuters reporting summarized this as men’s odds being “almost tripled,” and baseline population FI prevalence in that NHANES sample was about 5.6% for men and 8.3% for women ^{[4] [5]}.

3. What the studies do not prove—limits of causal claims

All cited studies are observational, mostly cross‑sectional surveys, so they show associations not definitive causation. The ERAS study used a large convenience (non‑random) online sample and assessed FI only for the prior month; authors explicitly noted these as limitations ^[2]. NHANES is a representative survey but still cross‑sectional; its authors and subsequent coverage cautioned that frequency and timing of anal intercourse (one or two times vs. regular practice) could not be disentangled for causal inference ^{[3] [5]}.

4. Potential mechanisms and clinical observations

Narrative reviews and smaller physiologic studies hypothesize plausible mechanisms: repeated penetrative anal activity and certain “hard” practices (fisting, vigorous activity) may reduce anal sphincter resting pressure or mucosal sensitivity, which can contribute to FI risk; the 2024 narrative review summarized both the ERAS prevalence differences and older physiologic work showing lower resting pressures after anal intercourse in small samples ^{[6] [2]}. These mechanistic links are credible but not universally quantified across populations ^[6].

5. Heterogeneity by practice, frequency, and population

Risk is not uniform. ERAS and the review highlight higher FI with greater frequency of RAI, with chemsex and fisting showing particularly high associated FI rates (e.g., chemsex: 21.4% vs. 7.2%; fisting: 18.1% vs. 7.2% in ERAS reporting) ^{[1] [2]}. Other studies of women who report anal penetrative intercourse also find associations with anal incontinence symptoms, but prevalence and context differ by study design and sample ^{[7] [8]}.

6. Competing viewpoints and gaps in the record

Sources consistently report associations but differ on interpretation: some emphasize the need to screen for anal intercourse as a risk factor in clinical evaluation ^[4], while authors of ERAS caution about sampling bias and short FI recall window ^[2]. Available sources do not mention long‑term prospective cohort studies definitively proving causation or quantifying absolute lifetime risk attributable solely to consensual anal sex (not found in current reporting).

7. Practical takeaway for clinicians and people who practice anal sex

Current evidence supports asking about anal sexual practices when assessing FI or pelvic‑floor complaints—especially frequency and high‑risk modalities (fisting, chemsex)—and considering pelvic‑floor evaluation and conservative management when symptoms are present ^{[2] [6] [3]}. The literature frames anal intercourse as a modifiable risk context among many (others include childbirth, surgery, neurologic disease), but causal attribution remains unproven by randomized or longitudinal data ^{[2] [3]}.

Limitations: this summary relies only on the provided sources and their cited designs; additional primary studies or long‑term cohorts beyond these reports are not covered here (not found in current reporting).