Genes' Grip on IQ Changes With Age, Study of 6,495 Kids Finds

What did they actually find?

• Polygenic scores explained about 11 percent of IQ variation at age 4, rising to 14 percent at 16.
• The overall common-variant share rose from 46 to 56 percent — but that increase was not statistically significant. Keep that caveat close.
• Gene-disabling mutations showed a negative association with IQ 3.2 times larger than protein-altering mutations. Harmless control mutations showed no link.
• Inherited rare variants explained 3.5 times more childhood IQ variation than new mutations; 12 percent of children carried an inherited variant versus 1.8 percent with a new one.
• The strengthening common-variant link concentrated in the upper half of the IQ distribution — above roughly IQ 125 — with no significant change at the bottom 5th percentile.
• At age 4, rare mutations' negative association was 3.9 times greater at the 5th percentile than the 95th; by 16, those differences vanished.

Even high-burden children mostly escaped severe impairment: among the top 5 percent of rare variant burden, about 7 percent had an IQ below 70 at age 8, versus roughly 3 percent of other children.

Rare variants explained 1.40 percent of IQ variation at age 4 — four to eight times more than premature birth (0.35 percent) or maternal pregnancy illness (0.18 percent). The child's educational polygenic score carried an association similar in size to the mother's or father's actual education level.

What are the weaknesses?

Plenty. And the authors admit most of them. Roughly 9 in 10 age-4 scores (5,794 of 6,495) were statistical estimates, not real tests; when researchers hid known scores and re-estimated them, the match was only moderate, with a median correlation of 0.61. Imputation also altered some age-4 percentile patterns. Children with lower polygenic scores completed fewer tests.

"Confidence in the results is somewhat limited by the analyses involving substantial imputation related to missing data, which in some cases altered the results, leaving me with some uncertainty about the interpretation," Liana Machado, a University of Otago psychologist uninvolved in the study, told PsyPost. "However, the thorough analysis approaches boosted my confidence in the reported results."

The sample was limited to Britons of European ancestry, so nothing here supports comparisons between ethnic groups. The scores describe population trends, not individual destinies. And because common- and rare-variant scores are built differently, strong conclusions about their opposite trajectories aren't warranted.

So what does this change for families?

Right now, nothing clinical. The authors suggest early delays in some mutation carriers might stem from treatable physical problems — congenital heart conditions, vision or hearing impairments — or from the developing brain compensating for a broken gene. Machado agreed access to healthcare is worth testing next, since confirmation "would highlight a pathway to better outcomes via targeted interventions." Larger whole-genome cohorts will need to settle it first.