SLC39A8 rs13107325: What Your Genotype Means
The rs13107325 variant is a genetic change located in the SLC39A8 gene, which encodes a protein responsible for transporting essential metals like manganese into cells. Research suggests this variant is associated with variations in blood manganese levels and has been studied for its potential influence on neurodevelopmental outcomes.
What each genotype means
Typical metal transporter function
This genotype represents the most common version of the SLC39A8 gene found in the general population. It is associated with standard cellular uptake of essential metals like manganese and zinc. No specific health risks are attributed to this genotype based on current research.
This is the major allele genotype and is the most common configuration observed across global populations.
Altered metal transport association
This genotype includes one copy of the A391T variant (rs13107325). Research indicates this variant is associated with various human traits, including differences in body mass index, lipid levels, and blood pressure. Because this gene regulates essential metal homeostasis, you should discuss any concerns regarding metabolic health or nutrition with your healthcare provider.
This heterozygous genotype is found at varying frequencies depending on ancestry, being more common in certain populations than others.
Variant metal transport profile
Carrying two copies of the A391T variant may result in more pronounced differences in how your cells transport manganese and zinc compared to the typical genotype. Studies have linked this variant to shifts in metabolic markers such as cholesterol and body mass index. Please consult with a clinician or nutritionist to discuss how your metabolic health profile relates to your overall wellness.
This homozygous genotype is less common than the heterozygous form and varies significantly by ancestral background.
Understanding the SLC39A8 Gene
The SLC39A8 gene provides instructions for creating a protein known as ZIP8. This protein functions as a transmembrane transporter, acting like a gatekeeper on the surface of cells to regulate the influx of divalent metal ions, including manganese, zinc, iron, and selenium. Because these metals are essential cofactors for various enzymes and biological processes, the proper function of ZIP8 is critical for maintaining cellular health. The gene is expressed ubiquitously throughout the body, including in the brain, liver, and intestinal epithelium, where it helps manage the distribution and uptake of these vital nutrients. Disruptions in this transporter can lead to imbalances in metal homeostasis, which may impact physiological functions ranging from protein glycosylation to the development of specific brain regions.
What is the rs13107325 Variant?
The rs13107325 variant is a specific single nucleotide polymorphism (SNP) found within the SLC39A8 gene. In genetic studies, this variant is often identified by the substitution of one DNA base for another, typically denoted as a C/T change. Scientists track this specific location to understand how it correlates with measurable biological traits, such as the concentration of manganese in the blood. Because this variant sits within a gene that is highly conserved across vertebrates, researchers are particularly interested in how even minor changes in the genetic code might alter the efficiency of the ZIP8 transporter. By studying this SNP, investigators aim to map the relationship between genetic architecture and the body's ability to maintain the delicate balance of trace metals required for normal development and metabolic health.
Research and Evidence Strength
Current evidence linking rs13107325 to clinical outcomes is considered limited and primarily observational. Studies, such as those involving pediatric cohorts, have observed that individuals carrying the minor allele (T) may exhibit lower blood manganese concentrations compared to those with the common allele. While some research has explored potential associations between these genetic differences and neurodevelopmental markers—such as motor function or cognitive performance—these findings are based on statistical correlations rather than direct causation. Furthermore, while severe mutations in SLC39A8 are known to cause rare, serious conditions like congenital disorders of glycosylation or Leigh-like syndrome, the rs13107325 variant is a common polymorphism and should not be conflated with these rare, pathogenic mutations. The scientific community continues to investigate how this variant might influence long-term health, but current data is insufficient to predict individual health outcomes.
Interpreting Your Genetic Information
It is important to understand that genetic variants like rs13107325 represent only one small piece of a complex biological puzzle. Many factors, including diet, environmental exposure, and other genetic influences, play a much larger role in determining your manganese levels and overall health. Because the evidence for this variant is limited, it cannot be used to diagnose any condition or predict specific health risks. If you have concerns about your nutritional status, neurological health, or developmental milestones, you should consult with a qualified healthcare professional. They can provide appropriate testing and clinical guidance based on your personal medical history. Never use information from genetic databases to make decisions about your health or to alter your diet or medication regimen without professional medical supervision.
How common is this variant?
The rs13107325 variant is considered rare in many populations, though frequency can vary significantly by ancestry. Detailed frequency data is available through the gnomAD database for those interested in specific population statistics.
Frequently asked questions
Can this variant cause manganese deficiency?
While the variant is associated with lower blood manganese levels in some studies, it is not a direct cause of clinical manganese deficiency. Severe deficiency is typically linked to rare, pathogenic mutations in the SLC39A8 gene, not common polymorphisms.
Should I take manganese supplements if I have this variant?
No. You should never start or change supplementation based on genetic results. Consult your doctor to determine if you have a nutritional deficiency through blood testing before considering any supplements.
Is this variant linked to neurological diseases?
Some research has explored associations between SLC39A8 variants and neurodevelopmental outcomes, but the evidence for rs13107325 is limited. It is not a diagnostic marker for any neurological disease.
Where can I find more information about my specific genotype?
You can look up your rsID on the NCBI dbSNP database or the GWAS Catalog. These resources provide summaries of published research and the current scientific understanding of the variant.
Sources & further reading
Educational information only, last refreshed 10/27/2026. Not medical advice — these associations describe population statistics, not individual predictions.
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Missense variant (p.Ala391Thr) in SLC39A8 linked to differences in HDL cholesterol, body mass index, blood pressure, and risk of schizophrenia.
A pleiotropic missense variant (p.Ala391Thr) affecting cellular manganese and zinc transport, linked across GWAS to lipid profiles, blood pressure, and inflammatory bowel disease risk.
Missense variant (p.Ala391Thr) robustly associated with sleep duration and daytime sleepiness in recent large-scale UK Biobank sleep health genome-wide scans.