These markers are single nucleotide polymorphisms (SNPs) in the LDLR gene, which encodes the low-density lipoprotein (LDL) receptor. The LDL receptor sits on cell surfaces and helps remove LDL particles from the bloodstream, a core step in cellular cholesterol handling. Genetic variants like rs688 and rs72658855 are common, inherited differences studied for effects on receptor expression, RNA processing, or protein function. Researchers have examined these specific SNPs in population studies to see how they associate with blood lipid patterns and related biomarkers. While individual variants do not determine outcomes on their own, they provide biological context about inherited tendencies in lipid metabolism and can help explain why two people with similar diets or labs may show different lipid or inflammatory profiles.

Results indicating alleles associated with reduced LDLR activity are often linked to patterns such as higher LDL particle measures, raised ApoB, or other lipid changes; however, this is an association, not a diagnosis. Conversely, alleles associated with preserved or increased LDLR activity tend to align with lower measured LDL particle burden or more favorable lipid profiles in some studies. These genotype signals should be interpreted alongside the Cardio Zoomer’s lipid, inflammation, metabolic, and vascular markers to form a complete picture of cardiovascular biology.

Cardio Zoomer includes LDLR rs688 and rs72658855 to capture inherited influences on LDL receptor biology. Measuring these variants helps clinicians contextualize lipid and biomarker patterns, clarify likely mechanisms behind abnormal labs, and integrate genetic tendency into a personalized cardiovascular profile.