Inflammation, Oxidized LDL & the Atherosclerotic Cascade
Prepared by:
Dr. Michel Garko, Ph.D., M.S. M.A.
Inside each of us, our arteries are lined with a delicate, one-cell-thick layer called the endothelium, the body’s “biological Teflon.” It keeps blood flowing smoothly and regulates vascular tone, clotting, and immune responses (Gimbrone & García-Cardeña, 2016).
But this layer isn’t invincible. Over time, it can be damaged by high blood pressure, elevated blood sugar, cigarette smoke, excess LDL cholesterol, chronic stress, insulin resistance, environmental toxins, and even a diet high in processed fats and refined carbohydrates. When injured, the endothelium becomes more permeable, meaning it loses its ability to act as a tight protective barrier. This allows substances that normally stay in the bloodstream such as low-density lipoprotein (LDL) cholesterol particles to slip beneath the endothelial lining into the intima, the innermost layer of the artery (Libby et al., 2019).
Once inside, LDL particles are vulnerable to oxidation by free radicals — unstable molecules generated by poor diet, smoking, chronic stress, and normal metabolism (Stocker & Keaney, 2004). These oxidized LDL (oxLDL) particles are what truly set the stage for inflammation and plaque formation.
When Repairs Become a Problem: The Paradox of Protection
Our immune system detects oxidized LDL as “foreign” and dispatches white blood cells called macrophages to clean up the damage. These macrophages engulf the oxLDL, forming what are known as foam cells, the building blocks of arterial plaque. These cells, along with lingering inflammatory signals, accumulate to form fatty streaks, the earliest visible signs of atherosclerosis. Ironically, the body is trying to heal itself, but in doing so, it sparks a self-reinforcing inflammatory cycle (Ross, 1999).
Plaque isn’t just cholesterol; it’s a complex mixture of foam cells, dead immune cells, calcium, and connective tissue proteins. Over time, this mixture hardens and narrows the arteries, restricting blood flow. Worse yet, unstable plaques can rupture, triggering clots that cause heart attacks or strokes (Bentzon et al., 2014).
At this stage, the paradoxical process of healing is silent. There’s no pain, no symptoms, nothing to warn you. But beneath the surface, the inflammatory cascade continues unabated.
Inflammation: The True Villain Behind the Scenes
For decades, cholesterol was framed as the “villain” of heart disease, but modern science paints a more nuanced picture. It’s chronic, unresolved inflammation that drives the most dangerous changes inside the arteries. Factors such as an atherogenic diet consisting of ultra processed foods, hyperglycemia, sedentary lifestyle, obesity, and chronic stress, among other factors elevate systemic inflammation and amplify vascular damage (Libby, 2021).
Protecting Your Arteries: An Integrate Approach
Supporting arterial health isn’t just about lowering cholesterol or controlling blood pressure. It requires an integrated approach that reduces inflammation, improves endothelial function, and protects against plaque formation and rupture. Alongside diet, exercise, and lifestyle strategies, certain botanicals have been traditionally and scientifically recognized for supporting cardiovascular integrity.
Looking Ahead: Connecting the Dots
The story of coronary artery disease is far more than “too much cholesterol.” It’s about the cascade of events involving endothelial injury, oxidized LDL, chronic inflammation, and immune overactivation — that converge to create an environment where plaques form and rupture.
In Part 3, we’ll explore a powerful molecule your body makes every day, nitric oxide (NO), and how it maintains vascular flexibility, regulates inflammation, and helps keep your arteries youthful. As we’ll see, small changes in diet, movement, and herbal support can significantly boost your NO levels and protect your cardiovascular health.
References
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Bentzon, J. F., Otsuka, F., Virmani, R., & Falk, E. (2014). Mechanisms of plaque formation and rupture. Circulation Research, 114(12), 1852–1866. https://doi.org/10.1161/CIRCRESAHA.114.302721
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Gimbrone, M. A., & García-Cardeña, G. (2016). Endothelial cell dysfunction and the pathobiology of atherosclerosis. Circulation Research, 118(4), 620–636. https://doi.org/10.1161/CIRCRESAHA.115.306301
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Libby, P. (2021). Inflammation in atherosclerosis: From pathophysiology to practice. Journal of the American College of Cardiology, 78(16), 1733–1747. https://doi.org/10.1016/j.jacc.2021.08.011
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Ried, K., Fakler, P., & Stocks, N. P. (2016). Effect of aged garlic extract on blood pressure and other cardiovascular risk factors. Integrated Blood Pressure Control, 9, 9–21. https://doi.org/10.2147/IBPC.S93344
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Ross, R. (1999). Atherosclerosis — an inflammatory disease. New England Journal of Medicine, 340(2), 115–126. https://doi.org/10.1056/NEJM199901143400207
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Stocker, R., & Keaney, J. F. (2004). Role of oxidative modifications in atherosclerosis. Physiological Reviews, 84(4), 1381–1478. https://doi.org/10.1152/physrev.00047.2003
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Tadi, P. P., & Singh, S. K. (2021). Hawthorn: Cardioprotective herb with bioactive compounds. Frontiers in Pharmacology, 12, 641705. https://doi.org/10.3389/fphar.2021.641705