Colloca · Pain 2019 · experimental laboratory cohort study · n=160

OPRM1 rs1799971, COMT rs4680, and FAAH rs324420 genes interact with placebo procedures to induce hypoalgesia.

Cited 48 times in the scientific literature.

Level 3 - non-randomized controlled study

Controlled experimental laboratory study assessing genetic associations and epistasis in healthy human volunteers.

PubMed 31335650 · doi:10.1097/j.pain.0000000000001578 · record verified 2026-08-29

What was done

Researchers examined whether three single nucleotide polymorphisms involved in opioid, dopamine, and endocannabinoid signaling—OPRM1 rs1799971, COMT rs4680, and FAAH rs324420—and their three-way interaction influenced placebo hypoalgesia. The study tested 160 healthy participants using two experimental placebo procedures: verbal suggestion and a conditioning/learning paradigm. Genotypes and procedure types were analyzed individually and in combination to predict placebo responsiveness.

What was found

Placebo hypoalgesia occurred significantly in individuals with the combined OPRM1 AA and FAAH Pro/Pro genotypes, as well as those carrying COMT met/met combined with FAAH Pro/Pro. Participants carrying the COMT met/val genotype exhibited significant placebo effects regardless of their OPRM1 or FAAH alleles. Combining the specific placebo procedure with genotype data predicted placebo responder status with an area under the curve (AUC) of 0.773, outperforming models based on genetic variants alone.

Why it matters

This study demonstrates that placebo analgesia is shaped by epistatic interactions across multiple neurotransmitter pathways rather than single genes in isolation. It highlights that genetic predisposition interacts with the psychological context and induction method to determine placebo responsiveness.

Limits

The total sample size was modest (n = 160) for testing three-way genetic interactions, meaning specific multi-allele subgroup counts were likely very small. The study was conducted in healthy volunteers exposed to experimental pain, limiting direct generalizability to clinical chronic pain populations.

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