LPL rs13702: Understanding the Genetic Link to Lipid Metabolism
The rs13702 variant is a single-nucleotide polymorphism located in the LPL gene, which encodes the lipoprotein lipase enzyme. Research suggests this variant may influence how the body processes fats and cholesterol by altering the regulation of the LPL gene through microRNA interactions.
What each genotype means
Typical lipid metabolism
You carry two copies of the common T allele at the LPL rs13702 locus. In functional studies, transcripts with this allele allow binding by microRNA-410, which moderately represses lipoprotein lipase translation. Research links this genotype to typical baseline levels of triglycerides and HDL cholesterol, with average dietary fat responsiveness.
Carried by approximately 60% to 70% of individuals of European and American ancestry, making it the most common genotype.
Favorable lipid response
You carry one copy of the minor C allele, which disrupts a microRNA-410 binding site in the 3-prime untranslated region of the LPL gene. Large-scale association studies indicate this allele is linked to modest reductions in circulating triglycerides and slight increases in HDL cholesterol. Research also suggests your lipid profile may show enhanced sensitivity to dietary fat quality, such as unsaturated fatty acid intake.
Carried by approximately 25% to 35% of individuals across European, American, and Arab populations.
Enhanced lipoprotein lipase activity
You carry two copies of the functional C allele, leading to loss of microRNA-410-mediated suppression and increased lipoprotein lipase expression. Population studies observe an additive beneficial pattern for this genotype, characterized by lower fasting triglycerides and higher HDL cholesterol. While these lipid associations are consistently replicated, clinical implications remain limited and dietary interactions continue to be investigated.
Found in approximately 2% to 6% of individuals in European and American populations.
What is the rs13702 Variant?
The rs13702 variant is a specific change in the DNA sequence of the LPL gene, which sits on chromosome 8. In genetic terms, this SNP is located in the 3' untranslated region (3' UTR) of the gene. This region does not code for the protein itself but acts as a regulatory area that controls how much of the LPL protein is produced. Specifically, the rs13702 variant is thought to disrupt a binding site for a molecule called microRNA-410. MicroRNAs are small molecules that typically bind to messenger RNA to silence or reduce gene expression. By altering this binding site, the rs13702 variant may change how effectively the cell can regulate the production of the lipoprotein lipase enzyme, potentially leading to differences in enzyme activity levels between individuals.
The Role of the LPL Gene
The LPL gene provides instructions for making the lipoprotein lipase enzyme. This enzyme is essential for breaking down fats in the form of triglycerides, which are carried in the blood by lipoproteins. Lipoprotein lipase acts like a gatekeeper, helping to clear triglycerides from the bloodstream and allowing cells to use them for energy or store them for later use. Because of its central role in lipid metabolism, the activity of this enzyme directly influences the levels of circulating triglycerides and high-density lipoprotein (HDL) cholesterol, often referred to as 'good' cholesterol. Variations in the LPL gene can lead to differences in how efficiently an individual clears fats from their blood, which is why researchers study these variants to better understand the genetic underpinnings of cardiovascular health and lipid profiles.
Research Associations and Evidence
Scientific studies have investigated the association between the rs13702 variant and lipid traits. Meta-analyses have observed that carriers of the minor allele (C) often show lower levels of triglycerides and higher levels of HDL cholesterol compared to those with the major allele (T). Some research also suggests that this variant may interact with dietary fat intake, potentially influencing how an individual's lipid levels respond to different types of fats, such as polyunsaturated fatty acids. While these statistical associations are significant in large population studies, the evidence is considered limited in terms of clinical application. It is important to note that these findings are based on population-level data and do not predict an individual's specific health outcomes. Further research is needed to fully understand the biological mechanisms and the extent to which this variant influences long-term health.
What You Can and Cannot Do With This Information
Understanding your genetic variants can be an interesting way to learn about your biology, but it is not a substitute for professional medical advice. You cannot use the rs13702 genotype to diagnose a health condition or predict your personal risk for cardiovascular disease. Genetic markers are only one piece of a very complex puzzle that includes diet, lifestyle, environment, and other genetic factors. If you are concerned about your cholesterol or triglyceride levels, the most effective approach is to consult with a healthcare provider or a registered dietitian. They can perform standard blood tests to assess your actual lipid levels and provide personalized guidance on diet and lifestyle changes. Never make changes to your diet or health regimen based solely on genetic information without first discussing it with your clinician or pharmacist.
How common is this variant?
The minor allele (C) of rs13702 has a frequency of approximately 0.15 to 0.25 in European and American populations.
Frequently asked questions
Does the rs13702 variant mean I have high cholesterol?
No, having a specific genotype for rs13702 does not mean you have high cholesterol. Lipid levels are influenced by many factors, including your diet, physical activity, and overall genetic makeup.
Can I change my diet based on my rs13702 genotype?
While some studies suggest gene-diet interactions, you should not make significant dietary changes based on this variant alone. Always consult with a healthcare provider or a registered dietitian before altering your diet for health reasons.
Is rs13702 a diagnostic test for heart disease?
No, rs13702 is not a diagnostic test. It is a genetic variant studied in research settings to understand biological pathways and is not used to diagnose or predict heart disease in a clinical setting.
Where can I get my rs13702 genotype tested?
This variant is often included in direct-to-consumer genetic testing panels. However, these results are for informational purposes only and should not be used for medical decision-making.
Sources & further reading
Educational information only, last refreshed 10/19/2026. Not medical advice — these associations describe population statistics, not individual predictions.
Curious what your genotype is for rs13702?
Upload a raw DNA file from 23andMe, AncestryDNA, MyHeritage, or FamilyTreeDNA and see this variant — plus thousands more — interpreted in your full report.
Get my report — $29Related variants in LPL
Missense variant in the lipoprotein lipase gene (Asn291Ser) associated with altered lipid profiles, increased risk of ischemic heart disease, and multivariate aging-related healthspan traits.
Lipoprotein lipase S447X (often referred to as S474X in older literature) variant affects triglyceride clearance.
A common variant in the LPL gene that helps lower triglyceride levels and provides protection against heart disease.
This variant in the lipoprotein lipase gene is studied for its interaction with diet and lifestyle interventions in the context of obesity management.
