What this means

SCN9A codes for the Nav1.7 sodium channel, which is essential for sending pain signals from peripheral neurons to the brain. Rare loss-of-function mutations cause complete inability to feel pain; rare gain-of-function mutations cause severe pain disorders. The common rs6746030 variant studied here has a much smaller effect — it shifts average pain ratings by a few percent, not by an order of magnitude. Day-to-day pain perception is dominated by attention, mood, sleep, and context.

SCN9A makes a channel called Nav1.7 — basically a wire that carries pain signals from your nerves to your brain. Very rare DNA changes can break the wire entirely (people who can't feel pain at all) or jam it on (people with severe pain disorders). This common DNA change is much milder — it shifts average pain ratings by a few percent in experiments, nothing dramatic. Day-to-day pain has way more to do with sleep, mood, and what's grabbing your attention than with this spot.

Caveats

• Effect sizes are small. This is not a pain disorder marker.
• Pain perception varies enormously day-to-day for reasons unrelated to genetics.
• Published associations have not always replicated cleanly.
• This variant should not be used to make clinical decisions about analgesia.

References

• Reimann et al. — Pain perception is altered by a nucleotide polymorphism in SCN9A (PNAS, 2010)
• Cox et al. — An SCN9A channelopathy causes congenital inability to experience pain (Nature, 2006)