healthcare

Understanding Cholesterol: LDL, HDL, and Triglycerides

For Patients

Your doctor orders a lipid panel to measure cholesterol levels in your blood. This test provides crucial information about your cardiovascular risk and helps guide treatment decisions.

Cholesterol is a waxy, fat-like substance your body needs to build cell membranes, produce hormones, and synthesize vitamin D. Your liver makes most of the cholesterol your body needs. The rest comes from animal-based foods you eat.

The Lipid Panel: What Each Number Means

A complete lipid panel measures four key values. Understanding each component helps you interpret your cardiovascular risk profile.

Total Cholesterol

This number combines all cholesterol types in your blood. While useful as a general indicator, total cholesterol alone does not tell the full story. You need to know the breakdown between beneficial and harmful types.

Optimal: Less than 200 mg/dL

Borderline high: 200-239 mg/dL

High: 240 mg/dL and above

LDL Cholesterol (Low-Density Lipoprotein)

Often called "bad cholesterol," LDL carries cholesterol from your liver to cells throughout your body. When LDL levels get too high, excess cholesterol deposits in your artery walls, forming plaque.

This process (atherosclerosis) narrows arteries and restricts blood flow to your heart and brain.

Plaque buildup increases your risk for:

  • Coronary artery disease

  • Heart attack

  • Stroke

  • Peripheral artery disease

For patients with existing heart disease or diabetes, doctors often recommend LDL levels below 70 mg/dL. Some high-risk patients benefit from levels below 55 mg/dL.

Optimal: Less than 100 mg/dL

Near optimal: 100-129 mg/dL

Borderline high: 130-159 mg/dL

High: 160-189 mg/dL

Very high: 190 mg/dL and above

HDL Cholesterol (High-Density Lipoprotein)

Known as "good cholesterol," HDL transports excess cholesterol from your arteries back to your liver for disposal.

Think of HDL as your cardiovascular cleaning system. Higher HDL levels protect against heart attack and stroke by removing cholesterol before it can form dangerous plaque.

Low HDL increases heart disease risk even when total cholesterol appears normal.

Optimal (MEN): 40 mg/dL or higher

Optimal (WOMEN): 50 mg/dL or higher

Protective: 60 mg/dL and above

Triglycerides

Unlike cholesterol, triglycerides store unused calories as fat. Your body converts excess carbohydrates, alcohol, and calories into triglycerides.

Elevated triglycerides may indicate:

  • Metabolic syndrome

  • Insulin resistance or Type 2 diabetes

  • Hypothyroidism

  • Kidney disease

  • Excessive alcohol consumption

High triglyceride levels often accompany low HDL and high LDL, creating a particularly dangerous combination for cardiovascular health.

Normal: Less than 150 mg/dL

Borderline high: 150-199 mg/dL

High: 200-499 mg/dL

Very high: 500 mg/dL and above

Non-HDL Cholesterol: An Important Calculation

Your doctor may discuss non-HDL cholesterol, calculated by subtracting HDL from your total cholesterol. This number includes all cholesterol types that promote plaque formation (LDL, VLDL, and other atherogenic particles).

Many cardiologists consider non-HDL cholesterol a better predictor of cardiovascular risk than LDL alone.

Optimal: Less than 130 mg/dL

Borderline: 130-159 mg/dL

High: 160-189 mg/dL

Very high: 190 mg/dL and above

Apolipoprotein B (ApoB): Advanced Testing

Standard lipid panels measure cholesterol content, but ApoB testing counts the actual number of atherogenic particles in your blood.

Your doctor may order ApoB testing if:

  • Your LDL appears normal but you have other risk factors

  • You have metabolic syndrome or diabetes

  • Your triglycerides are very high (which interferes with accurate LDL calculation)

  • You have a family history of early heart disease

Each LDL and VLDL particle contains one ApoB molecule, making this test highly accurate for assessing cardiovascular risk.

Optimal ApoB: Less than 90 mg/dL

Lipoprotein(a): The Genetic Factor

Lipoprotein(a), or Lp(a), is a genetic variant of LDL cholesterol. High Lp(a) levels significantly increase heart attack and stroke risk, even when other cholesterol numbers look good.

Testing makes sense if you have:

  • Family history of premature heart disease

  • Personal history of cardiovascular events despite normal cholesterol

  • Parents or siblings with high Lp(a)

Unlike other lipid values, diet and exercise do not affect Lp(a) levels.

Desirable: Less than 30 mg/dL (or less than 75 nmol/L, depending on the assay used).

When to Get Tested

The American Heart Association recommends adults age 20 and older check cholesterol every four to six years.

More frequent testing applies if you have:

  • High cholesterol or triglycerides

  • Family history of heart disease

  • Diabetes, high blood pressure, or obesity

  • Heart disease or previous cardiac events

Children with family history of high cholesterol or premature heart disease should have their first screening between ages 9 and 11.

Treatment Targets: Individualized Approach

Your doctor determines your target cholesterol levels based on your overall cardiovascular risk, not just your numbers.

Risk assessment considers:

  • Age and sex

  • Blood pressure

  • Diabetes status

  • Smoking history

  • Family history of early heart disease

  • Presence of existing cardiovascular disease

High-risk patients need more aggressive LDL lowering than those at lower risk, even if their starting numbers are similar.

Improving Your Lipid Profile

Lifestyle modifications:

  • Reduce saturated fat intake (found in red meat, full-fat dairy, tropical oils)

  • Eliminate trans fats (partially hydrogenated oils)

  • Increase soluble fiber consumption (oats, beans, apples, citrus fruits)

  • Add plant sterols and stanols (fortified foods, supplements)

  • Exercise at least 150 minutes weekly at moderate intensity

  • Achieve and maintain healthy weight

  • Stop smoking

  • Limit alcohol consumption

Medication options: When lifestyle changes prove insufficient, several medication classes effectively lower cholesterol

  • Statins reduce LDL production in the liver and remain the first-line treatment for high cholesterol. They lower LDL by 30-50% and reduce cardiovascular events by approximately 25-35%.

  • PCSK9 inhibitors block a protein that interferes with LDL removal, lowering LDL by 50-60% when added to statin therapy.

  • Ezetimibe prevents cholesterol absorption in the intestine, reducing LDL by about 18% and providing additional benefit when combined with statins.

  • Bempedoic acid inhibits cholesterol synthesis through a different pathway than statins, offering an alternative for statin-intolerant patients.

  • Fibrates primarily lower triglycerides and modestly increase HDL, making them useful for patients with severely elevated triglycerides.

  • Omega-3 fatty acids (prescription-strength EPA) reduce triglycerides and cardiovascular events in high-risk patients.

Understanding Your Results:

Your lipid panel provides essential information about cardiovascular health, but numbers tell only part of the story.

Work with your healthcare provider to interpret results in context of your complete risk profile and develop an appropriate treatment strategy.

Regular monitoring and consistent management of cholesterol levels significantly reduce your risk of heart attack, stroke, and cardiovascular death.

What Makes This Effective Patient Education:

  • Explains the "why" before the "what": Opens by clarifying what cholesterol is and why the body needs it, giving context before diving into numbers

  • Uses helpful analogies: "Think of HDL as your cardiovascular cleaning system" makes abstract concepts concrete and memorable

  • Organizes by patient journey: Structured around what happens at the doctor's office: test ordered, results explained, treatment discussed

  • Provides actionable number ranges: Gives specific targets (LDL less than 100 mg/dL, HDL above 60 mg/dL) so patients can understand their own results

  • Balances technical accuracy with accessibility: Uses medical terms like "atherosclerosis" but immediately explains it in plain language ("narrows arteries")

  • Addresses individual variation: Explains that treatment targets depend on personal risk factors, not one-size-fits-all numbers

  • Includes lifestyle modifications first: Emphasizes what patients can control (diet, exercise, smoking) before discussing medications

  • Explains medication options clearly: Describes how each drug class works and typical results without overwhelming detail

  • Practical testing guidance: Tells patients when they should get tested and what conditions warrant more frequent monitoring

  • Acknowledges complexity without creating anxiety: "Numbers tell only part of the story" validates that cholesterol management requires professional interpretation

  • Empowers informed conversations: Arms patients with enough knowledge to ask good questions and understand their doctor's recommendations

  • Clear visual hierarchy: Bold headers, indented lists, and organized sections make it easy to scan and find specific information quickly

Managing Treatment-Resistant Acne:

A Pillar-Based Approach to Systemic Therapy

For Dermatology and Primary Care Providers

The updated 2024 American Academy of Dermatology guidelines emphasize limiting systemic antibiotic use while maximizing targeted treatment of acne's underlying pathophysiology.

THE FOUR-PILLAR FRAMEWORK

Effective acne management requires addressing all four pathogenic pillars: excess sebum production, follicular hyperkeratinization, inflammation, and Cutibacterium acnes proliferation.

Treatment failure often results from inadequately targeting multiple mechanisms simultaneously.

Pillar 1: Sebum Production

Topical clascoterone remains the only FDA-approved topical androgen receptor blocker that directly reduces sebum production.

Systemic options include isotretinoin, spironolactone 50 mg daily to twice daily, and oral contraceptive pills.

Pillar 2: Follicular Hyperkeratinization

Topical retinoids address microcomedone formation and follicular plugging. Recent FDA approvals include photostable formulations such as trifarotene and tazarotene 0.045%.

Combination products like Twyneo (tretinoin 0.1%/benzoyl peroxide 3%) and Cabtreo (clindamycin 1.2%/adapalene 0.15%/BPO 3.1%) offer multi-pillar targeting with simplified regimens.

Azelaic acid provides additional benefit for patients experiencing retinoid irritation.

Counsel patients on barrier protection through consistent moisturization to improve retinoid adherence.

Pillar 3: Inflammation

Topical options include retinoids, clindamycin with benzoyl peroxide, topical minocycline 4%, dapsone, and azelaic acid.

Systemic anti-inflammatory agents include doxycycline, minocycline, sarecycline, spironolactone, and oral contraceptives.

Pillar 4: Cutibacterium Acnes

The 2024 AAD guidelines recommend concomitant benzoyl peroxide with all systemic antibiotics to minimize resistance development.

Topical antibiotics should always be combined with benzoyl peroxide. Systemic options include sarecycline, doxycycline, minocycline, and tetracycline.

WHEN TO ESCALATE TO SYSTEMIC THERAPY

The 2024 NICE guidelines on treatment-resistant acne recommend considering systemic agents when topical regimens fail to control new active breakouts, breakouts follow clear hormonal patterns, any degree of scarring is present or developing, or acute triggers cause inflammatory flares.

Isotretinoin remains the most effective single agent, targeting all four pathogenic pillars.

The AAD guidelines strongly recommend isotretinoin for severe acne or for patients who have failed standard treatment with oral or topical therapy.

CLINICAL PEARL

Optimal outcomes require addressing multiple pillars simultaneously with the fewest products possible.

Combination formulations and strategic systemic therapy selection improve adherence while maximizing therapeutic coverage across multiple pathogenic mechanisms.

KEY REFERENCES

Clinical Guidelines

  1. Yeung H, et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2024.

  2. National Institute for Health and Care Excellence. Acne vulgaris: management. NICE guideline NG198. Updated 2024. Pivotal Studies

  3. Miranti S. When to Move from Topical to Systemic Therapy for Acne. Presented at: New Wave Dermatology; May 2025; Aventura, FL.

References

  1. Yeung H, Chen SC, Keri JE, et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2024;91(6):1317-1348.

  2. National Institute for Health and Care Excellence. Acne vulgaris: management. NICE guideline NG198. Published June 2021. Updated December 2024.

  3. Miranti S. When to Move from Topical to Systemic Therapy for Acne. Presented at: New Wave Dermatology; May 2025; Aventura, FL.

WHAT MAKES THIS HCP-APPROPRIATE:

  • Medical terminology without definitions: Uses "follicular hyperkeratinization" and "Cutibacterium acnes" without explanation, assuming clinical knowledge

  • Prescribing-level details: Includes specific dosages (spironolactone 50 mg daily to twice daily), exact formulations (tretinoin 0.1%/BPO 3%), and branded product names

  • Clinical decision framework: Organized around treatment strategy and escalation criteria rather than condition education

  • Mechanism-based structure: Four pillars address pathophysiology (sebum production, comedogenesis) not patient symptoms (oily skin, blackheads)

  • Guideline citations: References 2024 AAD and NICE guidelines as practice standards

  • Provider-to-provider guidance: "Counsel patients on barrier protection" assumes reader is the clinician, not the patient

  • High information density: Multiple drug classes, mechanisms, and FDA approvals packed efficiently without educational preamble

  • No condition basics: Never defines acne, discusses prevalence, or includes emotional reassurance - jumps straight to treatment strategy

  • Evidence-based practice focus: Emphasizes antibiotic stewardship, resistance prevention, and adherence to current clinical guidelines

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