Atherogenic Dyslipidemia: Why Triglycerides and HDL Matter More Than LDL Alone
- David S. Klein, MD FACA FACPM

- 2 hours ago
- 3 min read
Many patients are reassured that their cholesterol is “under control” because LDL cholesterol falls within guideline targets. Yet myocardial infarction, stroke, and progressive atherosclerosis continue to occur—often in patients without overt diabetes.
The explanation frequently lies in atherogenic dyslipidemia, a lipid pattern driven by insulin resistance and hyperinsulinemia that is poorly captured by LDL alone.
What Is Atherogenic Dyslipidemia?

Atherogenic dyslipidemia is characterized by a triad¹:
Elevated triglycerides
Reduced HDL cholesterol
Increased small, dense LDL particles
This pattern reflects disordered lipid trafficking, not simply excess cholesterol. It is most commonly seen in insulin-resistant states, even when fasting glucose and HbA1c remain normal.
The Central Role of Insulin Resistance
Insulin resistance alters hepatic lipid metabolism in predictable ways:
Increased hepatic VLDL production²
Impaired clearance of triglyceride-rich lipoproteins
Cholesteryl ester transfer protein (CETP)–mediated depletion of HDL³
Conversion of LDL into smaller, denser, more atherogenic particles
The result is a lipid profile that accelerates atherosclerosis despite “acceptable” LDL values.
Why Small Dense LDL Is More Dangerous
Not all LDL particles are equivalent. Small dense LDL particles:
Penetrate the arterial wall more easily⁴
Are more susceptible to oxidation
Bind less effectively to LDL receptors
Persist longer in circulation
These properties make them disproportionately atherogenic compared with larger LDL particles, even at the same LDL-C concentration.
Triglycerides and HDL: The Ratio That Matters

The triglyceride-to-HDL ratio is one of the most clinically useful markers of insulin resistance and cardiovascular risk⁵.
A higher ratio correlates with:
Increased small dense LDL burden
Endothelial dysfunction
Higher coronary plaque volume
Greater incident cardiovascular events
This ratio often outperforms LDL-C as a predictor of cardiometabolic risk.

A Link to Fatty Liver and Metabolic Hypertension
Atherogenic dyslipidemia rarely occurs in isolation. It commonly coexists with:
Metabolic dysfunction–associated steatotic liver disease (MASLD)⁶
Insulin-mediated sodium retention and hypertension⁷
Visceral adiposity and systemic inflammation
All share the same upstream driver: chronic hyperinsulinemia.
Why Statins Don’t Fully Solve the Problem
Statins effectively reduce LDL-C, but they do not directly address insulin resistance or hyperinsulinemia. As a result:
Triglycerides may remain elevated
HDL often remains low
Residual cardiovascular risk persists⁸
This explains why cardiovascular events continue to occur despite “optimal” LDL lowering.
Detecting Atherogenic Dyslipidemia Early
More informative assessments include:
Fasting triglycerides and HDL
Triglyceride-to-HDL ratio
Advanced lipoprotein testing (particle number and size)
Integration with insulin-based metabolic markers
Early identification reframes treatment toward metabolic correction rather than cholesterol suppression alone.
Clinical Takeaway
Atherogenic dyslipidemia is a metabolic signal, not merely a lipid abnormality. Elevated triglycerides and low HDL often reveal insulin resistance years before diabetes and long before cardiovascular events occur. Addressing the root metabolic disturbance changes the trajectory of heart disease and aging.
Concerned about cardiovascular risk despite “good” cholesterol numbers?
Advanced lipid and metabolic testing is available at Stages of Life Medical Institute, allowing earlier detection and targeted prevention.
REFERENCES
¹ Grundy SM. Small LDL, atherogenic dyslipidemia, and the metabolic syndrome. Circulation. 1997;95(1):1–4.https://pubmed.ncbi.nlm.nih.gov/8994415/
² Adiels M, et al. Overproduction of VLDL1 driven by insulin resistance. Diabetologia. 2006;49(4):755–765.https://pubmed.ncbi.nlm.nih.gov/16525843/
³ Tall AR. CETP inhibitors to increase HDL cholesterol levels. N Engl J Med. 2007;356(13):1364–1366.https://pubmed.ncbi.nlm.nih.gov/17392497/
⁴ Austin MA, et al. Small, dense LDL as a risk factor for ischemic heart disease. JAMA. 1988;260(13):1917–1921.https://pubmed.ncbi.nlm.nih.gov/3418853/
⁵ McLaughlin T, et al. Triglyceride-to-HDL cholesterol ratio as a marker of insulin resistance. Metabolism. 2005;54(3):345–350.https://pubmed.ncbi.nlm.nih.gov/15736109/
⁶ Fabbrini E, et al. Hepatic steatosis and dyslipidemia. J Clin Endocrinol Metab. 2010;95(10):4791–4799.https://pubmed.ncbi.nlm.nih.gov/20660054/
⁷ Hall JE, et al. Obesity-induced hypertension. Hypertension. 2015;65(6):1005–1011.https://pubmed.ncbi.nlm.nih.gov/25855790/
⁸ Ridker PM, et al. Residual inflammatory risk after statin therapy. Lancet. 2018;391(10118):139–148.https://pubmed.ncbi.nlm.nih.gov/29137811/
The medical references cited in this article are provided for educational purposes only and are intended to support general scientific discussion. They are not a substitute for individualized medical advice, diagnosis, or treatment. Clinical decisions should always be made in consultation with a qualified healthcare professional who can account for a patient’s unique medical history, medications, and circumstances.
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