LDL cholesterolLDL-C
The principal cardiovascular risk lipoprotein; treatment target in primary and secondary prevention.
What it measures
LDL particles deliver cholesterol to peripheral tissues. ApoB on each particle mediates binding to the LDL-receptor. Particle number (apoB) is the proximate causal factor — LDL-C is a concentration surrogate.
Why we order it
Primary lipid target in ASCVD risk reduction.
Interpretation by lens
ACC/AHA 2018 + 2022: secondary prevention LDL-C <70 (often <55); primary prevention statin if 10-year ASCVD risk ≥7.5% with risk-enhancing features.
Functional clinicians emphasize apoB and Lp(a) over LDL-C alone — particularly in lean PCOS or insulin-resistant patients with discordant LDL-C / apoB.
Mendelian randomization confirms causal LDL effect on ASCVD across the lifespan; cumulative LDL-years is the key exposure.
Causes of abnormal values
- ↑Diet (saturated/trans fats)
- ↑Familial hypercholesterolemia (LDL >190 with family history)
- ↑Hypothyroidism (always rule out before treating)
- ↑Nephrotic syndrome
- ↑Cholestasis
- ↑Drugs: thiazides, glucocorticoids, cyclosporine, atypical antipsychotics
- ↓Severe liver disease
- ↓Malabsorption
- ↓Hyperthyroidism
- ↓PCSK9 loss-of-function variants
Pre-analytic & interpretation traps
- !Friedewald equation is invalid when triglycerides >400; use direct LDL or Martin/Hopkins.
- !Statin trials measured LDL-C, but apoB is the more accurate causal exposure.
Logical next-step labs
What the data says
Primary literature
- 2018 ACC/AHA cholesterol guideline — Grundy SM et al., Circulation 2019
- Cholesterol Treatment Trialists' meta-analysis — Lancet 2010