Despite the negative stigma courtesy of pharmaceutical companies, LDL particles are necessary for human existence. LDL is made in the liver and carries “passengers” around the body. The passengers include cholesterol, triglycerides, vitamins like A/D/E/K, CoQ10 and so much more. 

The problem occurs when LDLs become damaged from a process known as oxidative stress. As the LDL becomes oxidized, it is not taken out of circulation by the liver. The particles get smaller and smaller, eventually winding up in arteries, thus leading to heart attacks. 

Oxidative stress is from too much of the bad stuff (pro-oxidative forces) and not enough of the good stuff (antioxidant forces). 

Let’s discuss the levels of oxidative damage, why disease occurs, and how to test yourself for oxidative stress. 

Levels of Oxidative Damage in LDL

1. Minimal Oxidation:
   
   
   • Initial lipid peroxidation: In the early stages, polyunsaturated fatty acids (PUFAs) in the phospholipid layer of LDL are oxidized.
   • Result: This can lead to slight structural changes but may not yet trigger a strong inflammatory response.
   • Protection: Antioxidants like vitamin E in LDL can sometimes stop the oxidation process at this stage.
2. Moderate Oxidation:
   
   
   • Propagation phase: As lipid peroxidation progresses, more PUFAs in the LDL particle become oxidized, and the oxidation spreads across the lipid layer.
   • Protein modifications: Oxidation can affect the apolipoprotein B-100 (the protein component of LDL), altering its structure and function.
   • Result: This form of oxidized LDL (ox-LDL) begins to signal danger and is more likely to be taken up by scavenger receptors on macrophages, leading to foam cell formation and plaque buildup.
3. Severe Oxidation:
   
   
   • Extensive damage: At this stage, LDL is heavily oxidized, with significant damage to its lipid, cholesterol, and protein components.
   • Structural breakdown: Severely oxidized LDL is highly inflammatory and cytotoxic.
   • Immune activation: This form of LDL strongly stimulates an immune response, promoting endothelial dysfunction, foam cell formation, and progression of atherosclerosis.

What Determines the Level of Oxidative Damage?

1. Antioxidant Defense:
   
   
   • Adequate levels of antioxidants like vitamin E, vitamin C, beta-carotene, and CoQ10 within the LDL particle or in the surrounding environment help limit oxidative damage.
2. Oxidative Stress:
   
   
   • High levels of ROS from sources like smoking, chronic inflammation, poor diet, or pollution increase LDL’s exposure to oxidative damage.
3. LDL Composition:
   
   
   • LDL particles with a higher proportion of polyunsaturated fatty acids (PUFAs) are more prone to oxidation.
   • Small, dense LDL particles are more susceptible to oxidation than larger, buoyant LDL particles.
4. Enzymatic Defense:
   
   
   • Enzymes associated with HDL (e.g., paraoxonase-1) can help reduce LDL oxidation by neutralizing peroxidized lipids.

Test, Don’t Guess

My best recommendation is for our urinary oxidative stress test. It is included inside our Heart Attack Risk Test package: 

1. Urine test kit for oxidative stress
2. Heart Attack Risk questionnaire
3. Review call with an NHD professional

Learn more about the Heart Attack Risk Test here.