What this means

OPRM1 codes for the mu-opioid receptor — the target of endorphins, morphine, and most opioid analgesics. The A118G variant changes one amino acid (N40D) in the receptor's extracellular region. Carriers show small but consistent differences in pain processing and in responses to social acceptance and rejection (this same receptor is thought to underlie part of how we experience social warmth). G carriers sometimes need somewhat different doses of opioid medications, which is mostly relevant in clinical anaesthesia.

OPRM1 makes the receptor that endorphins, morphine, and most opioid painkillers latch onto. A common DNA change tweaks one tiny part of this receptor. People with the tweaked version show small but consistent differences in how they feel pain — and in how they experience social warmth and rejection (this same receptor seems to be part of how that registers in the brain). The medical relevance is mainly around opioid painkillers in hospitals: people with the tweaked version sometimes need different doses, which anaesthetists already factor in.

Caveats

• Clinical effects on analgesia exist but are modest.
• The "social sensitivity" finding is interesting but small and not always replicated.
• Allele frequency varies sharply between populations.
• This is informational only and should not be used to self-direct opioid dosing.

References

• Bond et al. — Single-nucleotide polymorphism in the human mu opioid receptor gene alters beta-endorphin binding and activity (PNAS, 1998)
• Way et al. — Variation in the mu-opioid receptor gene (OPRM1) is associated with dispositional and neural sensitivity to social rejection (PNAS, 2009)