Hyperaggressive immune cells parked in arterial plaque and feasting on glucose appear to spur coronary artery disease, according to senior author Cornelia Weyand, MD, Stanford professor and chief of immunology and rheumatology, in research published in February in the Journal of Experimental Medicine.
Weyand and colleagues compared the blood of 140 patients who had experienced at least one heart attack with samples from 105 healthy, demographically matched control subjects. They found that the patients with coronary artery disease had immune cells that were much more likely to differentiate into damaging M1 macrophages and to carry a defect predisposing these cells to slurp up glucose. When the scientists later blocked glucose metabolism within those macrophages, their production of interleukin-6 — an immune-signaling protein infamous for driving inflammation throughout the body — dropped off considerably. “Something in there is leading to excessive IL-6 production,” Weyand says, “and that something is our old friend sugar.” She says the discovery could lead to new ways to prevent or treat coronary artery disease, the leading cause of death in America.