NAMA, variants, traits, and what the research shows

NAMA - what this gene does

Variants near NAMA have been linked to traits spanning neurological, hormonal, cardiovascular, immune, liver, and metabolic domains. The specific molecular function of this gene in these processes is not yet characterized in the available data.

Key takeaways

• Two variants at this locus carry the highest association scores in this dataset, with one linked to neurological traits
• Three separate variants point to hormonal traits, suggesting a consistent signal in that domain
• Immune system phenotypes appear across three separate variants, adding further weight to that association
• Variants at this locus span six trait categories, an unusually broad range for a single gene region
• Fifty total variants have been catalogued here, with 19 carrying published research records

Notable variants

The two highest-magnitude variants in this dataset are rs118082100 and rs150424154, both scoring 4.50 on the association magnitude scale; rs150424154 carries a neurological trait label. Among magnitude-2.20 variants, the hormonal domain is covered by three separate signals - rs10512264, rs10988820, and rs10988865 - a pattern that lends some within-gene weight to that association. rs10760685 carries a cardiovascular label, rs11788118 an immune label, and rs12346763 a liver trait label.

Trait associations

The variant data at this locus spans at least six trait domains. The neurological domain is anchored by rs150424154. Three variants - rs10512264, rs10988820, and rs10988865 - point independently to hormonal phenotypes, representing the strongest multi-variant signal in the current dataset. Cardiovascular associations appear in rs10760685. Immune phenotypes are linked to rs10760693, rs10819689, and rs11788118, again showing three variants converging on a single domain. Liver traits appear in rs12346763 and metabolic traits in rs12551906. The remaining variants on file carry no trait annotation in the current data.

Evidence quality

The strongest individual signals are rs118082100 and rs150424154 at magnitude 4.50, while all other annotated variants sit at magnitude 2.20. No effect sizes (such as odds ratios or beta coefficients), sample sizes, or replication status are available in the current data, limiting the ability to assess evidence strength beyond the magnitude score. The spread of trait categories across 20 listed variants is notable but may partly reflect genomic linkage disequilibrium, a statistical phenomenon where nearby variants on the same chromosome tend to be inherited together and can appear correlated without being independently causal. All findings should be treated as preliminary associations until mechanistic or multi-cohort replication data become available.

What this is NOT

These variants represent population-level statistical signals from GWAS (genome-wide association studies, which scan many people's genomes for variants statistically associated with a trait), not deterministic predictors of outcomes for any individual. This content does not constitute medical advice, a diagnosis, or a recommendation of any kind.