CPED1, variants, traits, and what the research shows

CPED1 - what this gene does

Variants catalogued under this gene are linked to metabolic traits in population-level genetic research. Based on the data available here, the strongest signals cluster within the metabolic trait theme.

Key takeaways

• Two variants - rs10261386 and rs6971407 - carry the highest magnitude scores (4.50) and represent the strongest available signals in this gene.
• rs10261386 is explicitly tagged to a metabolic trait and has a published research page.
• 378 variants are tracked across this gene, with 55 having prior published research summaries.
• Most catalogued variants carry a magnitude of 3.00; detailed trait annotations for this tier are not yet available.
• All associations here are population-level statistical signals from genome-wide studies - not guaranteed outcomes for any individual.

Notable variants

The two highest-magnitude entries are rs10261386 and rs6971407, each scoring 4.50. rs10261386 is the only variant in the current dataset with an explicit metabolic trait tag and a published research page. Among the magnitude-3.00 group, rs1010372698, rs1381284878, rs138420997, rs139684091, and rs144800578 are representative entries - though trait details for this tier are pending fuller annotation.

Trait associations

The dominant trait theme across the catalogued variants is metabolic. rs10261386 carries the clearest metabolic label at magnitude 4.50. rs6971407 matches the same magnitude, though its specific trait annotation is not yet available in this dataset. Among the magnitude-3.00 entries, rs1381284878, rs146098402, rs148690363, rs149346746, and rs200638100 await detailed annotation before their trait connections can be described.

Evidence quality

Of the 378 variants tracked in this gene, 55 carry prior published research summaries - a moderate evidence footprint. The strongest available signal is rs10261386 at magnitude 4.50, tagged to a metabolic trait. The current dataset does not include specific effect sizes (such as odds ratios or beta coefficients) or cohort sample sizes, which limits direct assessment of effect magnitude and replication status across studies. These variants are consistent with GWAS - genome-wide association studies (large scans of many people's genomes for statistical links to a trait) - and should be treated as population-level findings rather than confirmed functional mechanisms.

What this is NOT

These variants are population-level statistical signals, not deterministic predictors of health outcomes for any individual. This content does not constitute medical advice, a diagnosis, or a recommendation to take any action.