تحليل الدهون في الدم: دليل شامل لفهم أرقام الكوليسترول

A lipid panel provides a snapshot of blood fat levels that influence cardiovascular risk:

• Total cholesterol: Sum of all cholesterol fractions. Desirable: below 200 mg/dL. Less useful than individual components for risk assessment.
• LDL-C (low-density lipoprotein cholesterol): The primary driver of atherosclerosis. Optimal: below 100 mg/dL. For high-risk patients: below 70 mg/dL. For very-high-risk: below 55 mg/dL (2019 ESC/EAS guidelines).
• HDL-C (high-density lipoprotein cholesterol): Often called "good cholesterol" — removes cholesterol from artery walls. Optimal: above 60 mg/dL for cardiovascular protection; below 40 mg/dL (men) or 50 mg/dL (women) is a risk factor.
• Triglycerides: Blood fats from dietary intake and liver production. Normal: below 150 mg/dL. Borderline: 150-199 mg/dL. High: 200-499 mg/dL. Very high: 500+ mg/dL (pancreatitis risk).
• Non-HDL cholesterol: Total cholesterol minus HDL. May be a better predictor of cardiovascular risk than LDL alone because it includes VLDL and remnant particles. Target: LDL goal + 30 mg/dL.

Upload your lipid panel to WAYJET's Medical Report Analyzer for personalized risk interpretation.

Cholesterol levels are influenced by both modifiable and non-modifiable factors:

Non-modifiable:

• Genetics: Family history accounts for 40-60% of cholesterol variability. Familial hypercholesterolemia affects 1 in 250 people, causing very high LDL (above 190 mg/dL) from birth.
• Age and sex: LDL increases with age. Women often see a jump in LDL after menopause due to declining estrogen.

Modifiable factors:

• Diet: Saturated fat intake is the strongest dietary determinant of LDL. Each 1% reduction in saturated fat calories reduces LDL by approximately 1-2 mg/dL. Trans fats are even more harmful — they raise LDL and lower HDL simultaneously.
• Weight: Each 10 kg of weight loss reduces LDL by approximately 8 mg/dL and raises HDL by 3-5 mg/dL.
• Exercise: Regular aerobic exercise raises HDL by 5-15% and modestly reduces triglycerides. The effect on LDL is minimal without dietary changes.
• Alcohol: Moderate intake raises HDL but also raises triglycerides. Not recommended as a cardiovascular strategy.
• Smoking: Lowers HDL by 5-10 mg/dL. Cessation improves HDL within weeks.

Current guidelines (AHA/ACC 2018) recommend statin therapy for four primary groups:

• Clinical ASCVD: Anyone with established cardiovascular disease (prior heart attack, stroke, peripheral artery disease) — high-intensity statin regardless of LDL level
• LDL above 190 mg/dL: High-intensity statin regardless of other risk factors (likely familial hypercholesterolemia)
• Age 40-75 with diabetes: Moderate-intensity statin; high-intensity if 10-year ASCVD risk exceeds 7.5%
• Age 40-75 with elevated risk: 10-year ASCVD risk 7.5%+ by pooled cohort equations — moderate-to-high intensity statin after risk discussion

Statin efficacy is well-established: a 2019 Lancet meta-analysis of 27 major trials found each 1 mmol/L (39 mg/dL) reduction in LDL decreased major cardiovascular events by 22% and all-cause mortality by 10%.

Lifestyle alternatives for borderline cases include the portfolio diet (plant sterols, nuts, viscous fiber, soy protein), which reduces LDL by 25-35% — approaching low-dose statin levels. Red yeast rice contains natural lovastatin but has variable potency and the same interaction profile as statins.