Key Benefits

• Understand your heart risk by mapping cholesterol and artery-clogging particle number and size.
• Spot plaque-building particle burden with ApoB and LDL-P, beyond LDL cholesterol.
• Flag high triglycerides that raise pancreatitis risk and signal insulin resistance.
• Guide therapy choices and intensity to cut plaque risk and prevent events.
• Clarify HDL quality with HDL-P and size when triglycerides run high.
• Detect small, dense LDL patterns linked to faster plaque growth in insulin resistance.
• Support pregnancy planning by flagging lipid patterns tied to preeclampsia and gestational diabetes.
• Track progress from diet, exercise, and medications through particle and triglyceride changes.

What are Dyslipidemia

Dyslipidemia biomarkers are blood measures that reveal how your body packages, moves, and clears fats. They track the traffic of energy fats and cholesterol from the intestine and liver to tissues and back to the liver for recycling. This testing shows whether the system that loads, delivers, and retrieves these fats is in balance or drifting toward artery-clogging buildup. Core markers capture the fats themselves (cholesterol, triglycerides) and the particles that carry them (lipoproteins: LDL, HDL, VLDL, remnants). They also include the protein “tags” that define these particles (apolipoproteins: ApoB, ApoA-I) and a genetically driven variant that heightens stickiness in arteries (lipoprotein(a)). Some tests quantify how many cholesterol-carrying particles are in circulation and how they’re built (particle number and size; LDL-P). Together, these biomarkers reflect production by the liver, release from the gut, remodeling in the bloodstream, and clearance by cell receptors. They enable early detection of imbalance, indicate which pathways are off, and guide prevention and treatment to reduce atherosclerosis risk.

Why are Dyslipidemia biomarkers important?

Dyslipidemia biomarkers track how your body packages and moves fats through the bloodstream—information that touches every system that relies on energy, hormones, and vessel health. They signal how well the liver, intestines, and endocrine network load cholesterol and triglycerides into particles, and whether those particles are likely to nourish tissues or deposit in artery walls.

In most people, lower LDL, triglycerides, ApoB, and LDL particle number are favorable, because fewer atherogenic particles means less plaque formation. Higher HDL and higher HDL particle number tend to be protective, while larger LDL size (fewer small, dense LDL) and mid‑to‑larger HDL size reflect healthier metabolism. Women typically have higher HDL than men; children and teens usually have lower atherogenic profiles, and pregnancy naturally raises triglycerides and LDL as fuel for the placenta.

When values are low, the meaning depends on which marker is low. Low LDL, ApoB, or LDL‑P can reflect efficient clearance or, if very low, point to malabsorption, hyperthyroidism, or chronic illness. Very low triglycerides often mirror good insulin sensitivity, but can also occur with undernutrition or malabsorption. Low HDL or HDL‑P suggests reduced reverse cholesterol transport, commonly seen with insulin resistance—more frequent in men and in women with PCOS—often accompanied by central weight gain and fatty liver. Smaller LDL size (a “low” size) signals more small, dense LDL, a pattern linked to metabolic syndrome.

High LDL, ApoB, LDL‑P, and triglycerides mean more cholesterol‑rich or remnant particles that infiltrate arterial walls; this is usually silent until vascular disease develops. Very high triglycerides can inflame the pancreas. Extremely high HDL is uncommon and may be dysfunctional rather than protective.

Big picture: these markers integrate liver output, thyroid tone, insulin action, kidney function, and inflammation. Their long‑term patterns forecast atherosclerotic risk, pancreatitis risk, and metabolic health, tying daily energy handling to heart, brain, and liver outcomes.

What Insights Will I Get?

Dyslipidemia biomarkers map how the body packages and traffics fats and cholesterol that power cells, build membranes, and signal hormones; imbalances drive atherosclerosis and influence insulin signaling, hepatic metabolism, brain, reproduction, and immunity. At Superpower, we test LDL, HDL, Triglycerides, ApoB, LDL-P, HDL-P, LDL Size, HDL Size.

LDL delivers cholesterol to tissues; HDL returns it to the liver (reverse transport). Triglycerides are energy-rich fats in VLDL/chylomicrons; higher levels suggest remnant accumulation and hepatic insulin resistance. ApoB enumerates atherogenic particles (one per VLDL, IDL, LDL, Lp(a)). LDL-P is LDL particle number; more particles raise arterial wall exposure. HDL-P (HDL particle number) reflects transport capacity better than HDL-C. LDL size separates small, dense from larger, buoyant LDL; smaller is more atherogenic. HDL size gauges HDL maturation; very small or very large patterns can indicate less functional HDL.

Lower ApoB and LDL-P with adequate HDL-P support steady lipid delivery without excess arterial deposition. Moderate triglycerides imply efficient fat clearance and metabolic flexibility. Larger-average LDL with fewer small, dense particles reduces endothelial entry and oxidation, while balanced HDL size with sufficient particle number signals active cholesterol efflux and anti-inflammatory tone.

Notes: Interpretation shifts with age, sex hormones, pregnancy, menopause, acute illness, thyroid/liver/kidney disease, and medications (statins, estrogens, retinoids, steroids). Fasting status, recent alcohol, and strenuous exercise alter triglycerides and particle measures. Different assays yield modestly different particle counts and size cutoffs.