More than few people believe heart disease is purely a modern health problem caused by fast food, stress, and lack of exercise. While these factors certainly play a role, the truth runs deeper and is much older. The arteries carry a hidden “design flaw” that traces back millions of years, long before processed foods or sedentary jobs existed. Understanding this flaw not only explains why coronary artery disease (CAD) is so common but it also points to steps that can be taken to protect our cardiovascular health, generally, and arteries, specifically.
The Strength and Fragility of Our Arteries
The human circulatory system is a marvel of biological engineering. It is flexible, self-repairing, and remarkably efficient at delivering oxygen and nutrients throughout the body. The arteries, which carry oxygen-rich blood under high pressure, are lined with a single-cell-thick layer called the endothelium. This thin but vital barrier regulates vascular tone, prevents inappropriate clotting, and maintains a smooth surface for unobstructed blood flow (Deanfield et al., 2007). However, unlike the lower-pressure systems of some other animals, the human arterial system is constantly subjected to high mechanical stress. The natural curves, bends, and branch points in arteries, particularly in the coronary vessels, create turbulent blood flow. This turbulence exerts uneven shear stress on the endothelium, making certain sites more vulnerable to microscopic injury (Libby, 2021).
The Paradox of Arterial Repair: When Healing Becomes Harmful
When the endothelium is injured, the body initiates a highly coordinated repair process. Immune cells, platelets, and lipoproteins, especially low-density lipoprotein (LDL) particles, arrive to seal and stabilize the damaged area. Over time, small dense LDL cholesterol particles become trapped and oxidized in the innermost layer of an artery (i.e., tunica intima), triggering an inflammatory cascade that draws in more immune cells, including macrophages. These macrophages engulf oxidized LDL, becoming foam cells, and over time form fatty streaks the earliest visible sign of atherosclerosis.
As the process continues, layers of fibrous tissue, more immune cells, calcium deposits, and lipid material accumulate, producing atherosclerotic plaque, a complex lesion consisting of lipids, inflammatory cells, smooth muscle cells, extracellular matrix, and calcification (Libby, 2021). Initially, this fibrous “patch” is protective. It reinforces the weakened arterial wall. Yet as it thickens and stiffens, it begins to narrow the artery, restrict blood flow, and increase the risk of rupture. A ruptured plaque can trigger a clot that blocks blood supply to the heart muscle, causing a heart attack.
This repair response is adaptive in the short term. However, with repeated or chronic injury from high blood pressure, smoking, persistent inflammation, a cardiogenic diet constituted of highly processed foods loaded with salt, sugar and fat or elevated blood sugar and insulin levels, this repair process becomes paradoxically maladaptive, meaning the repair mechanism itself begins to contribute to disease progression.
The Evolutionary Trade-Off
From an evolutionary standpoint, our arterial structure was “good enough” for survival in ancestral environments. Early humans were physically active and rarely lived long enough for atherosclerosis to cause problems (Finch & Crimmins, 2004). Evolution selects traits that enhance reproductive success, not post-reproductive longevity. Hence, there was little evolutionary pressure to design arteries resistant to age-related plaque buildup (Libby, 2021). In fact, certain cardiovascular traits may have been advantageous earlier in life, for example:
- Robust clotting systems would have reduced the risk of fatal bleeding from injury but increase the risk of clot-related heart attacks later in life.
- Elevated inflammatory responses would have enhanced survival against infections but now promote chronic inflammation (“inflammaging”) and atherosclerosis.
- Higher LDL cholesterol levels may have supported hormone production and immune defense in early adulthood but predispose to plaque formation in later decades.
These trade-offs, while beneficial in a high-injury, pathogen-rich environment, become liabilities in our current era of longer lifespans and different chronic disease health challenges.
What We Can Do Now
While we are unable to change our evolutionary blueprint, we can protect our arteries by minimizing the stress and damage that promote maladaptive plaque formation:
- Maintain healthy blood pressure to reduce mechanical strain on artery walls.
- Reduce chronic inflammation through a balanced diet rich in vegetables, fruits, omega-3 fatty acids, and low-glycemic whole foods.
- Support nitric oxide production with foods like beets, leafy greens, and pomegranate (Machha et al., 2022).
- Incorporate circulation-supportive botanicals such as aged garlic extract, hawthorn, cayenne, European mistletoe, motherwort, and bilberry (among others), which have been studied for their ability to enhance endothelial function, reduce arterial stiffness, and support vascular health (Ried et al., 2016; Tadi et al., 2022).
Conclusion
Built to Last, But Not Forever
Our arteries are an evolutionary marvel—strong enough to sustain life for decades, yet inherently vulnerable because of their structure and the evolutionary trade-offs that shaped them. The single-cell-thick endothelium, constant high-pressure circulation, and turbulent flow at vessel branch points create opportunities for microscopic injury. Over time, the body’s natural repair response can shift from protective to maladaptive, leading to the buildup of complex atherosclerotic plaque.
These vulnerabilities were rarely an issue for our ancestors, who lived shorter, more physically demanding lives. But in today’s world where we live longer, move less, and face chronic low-grade inflammation this design flaw becomes a leading cause of illness and death. Robust clotting, strong immune reactivity, and higher cholesterol levels once helped humans survive but now, they contribute to heart disease risk.
The good news is that we can work with our biology. By controlling blood pressure, reducing inflammation, supporting nitric oxide production, and embracing both nutrient-rich foods and circulation-supportive botanicals, we can protect our arteries well beyond their original evolutionary “warranty period.”
Looking Ahead
Understanding the design flaw is the first step in reducing its impact. In the next part of this series, we’ll explore how a mismatch between our ancient biology and the modern inflammatory burden further fuels the risk of CAD. We’ll look at how changes in diet, environment, and lifestyle have amplified this vulnerability and outline practical, science-based steps you can take to tip the balance toward lifelong cardiovascular health.
References
Deanfield, J. E., Halcox, J. P., & Rabelink, T. J. (2007). Endothelial function and dysfunction: Testing and clinical relevance. Circulation, 115(10), 1285–1295. https://doi.org/10.1161/CIRCULATIONAHA.106.652859
Finch, C. E., & Crimmins, E. M. (2004). Inflammatory exposure and historical changes in human life-spans. Science, 305(5691), 1736–1739. https://doi.org/10.1126/science.1092556
Libby, P. (2021). The changing landscape of atherosclerosis. Nature, 592, 524–533. https://doi.org/10.1038/s41586-021-03392-8
Machha, A., Schechter, A. N., & Gladwin, M. T. (2022). Dietary nitrate and the nitric oxide pathway: Implications for cardiovascular health. Annual Review of Nutrition, 42, 69–94. https://doi.org/10.1146/annurev-nutr-071721-025015
Ried, K., Travica, N., & Sali, A. (2016). The effect of aged garlic extract on blood pressure and other cardiovascular risk factors in uncontrolled hypertensives: The AGE at Heart trial. Integrative Blood Pressure Control, 9, 9–21. https://doi.org/10.2147/IBPC.S97413
Tadi, P., Mohiuddin, S. S., & Sharma, S. (2022). Hawthorn. In StatPearls. StatPearls Publishing.