S-allyl cysteine (SAC) is the primary bioavailable active component of AGE. SAC supports nitric oxide bioavailability (improving endothelial function and vasodilation), inhibits ACE (angiotensin-converting enzyme - similar to ACE inhibitor BP medications, though weaker), and provides antioxidant activity.
Plaque modulation: AGE may slow progression of coronary artery calcification (CAC) and promote regression of unstable, lipid-rich heterogeneous plaque. Mechanisms include endothelial protection, anti-inflammatory effects, and reduced LDL oxidation. The LARRY (Los Angeles Atherosclerosis) trials and subsequent LANCER trial demonstrated reduced CAC progression with AGE.
BP reduction: Mild ACE inhibition + improved NO availability + reduced oxidative stress in vasculature contribute to modest BP reduction (~5-10 mmHg systolic in hypertensive individuals).
Antioxidant: AGE contains potent antioxidants that reduce LDL oxidation (the atherogenic form of LDL) and protect endothelium from oxidative damage.
Anti-inflammatory: Reduces inflammatory markers (CRP, IL-6, TNF-alpha) relevant to atherosclerosis progression.
Platelet function: Modest antiplatelet effect (mild reduction in platelet aggregation) - contributes to cardiovascular benefit but rare bleeding risk at typical doses.
Lipid modulation: Modest reductions in total cholesterol, LDL, and triglycerides (effect smaller than statins or BPF).
Immune support: AGE enhances NK cell activity, T-cell function, and macrophage activity. May reduce cold/flu duration.