Statins reduce plasma plant sterol concentrations and, less consistently, their ratios to cholesterol in short-term studies. They most likely accomplish this by decreasing their transport protein levels. In long-term treatment with large doses of effective statins, serum plant sterol concentrations and frequently their ratios to cholesterol are consistently increased, especially with high, as opposed to low, baseline ratios. Enhanced intestinal absorption, decreased biliary secretion, and reversed cholesterol and plant sterol transport could explain these findings. However, statin treatment increases plant sterol ratios in serum and also in arterial plaques of endarterectomized patients. No trials of functional foods with plant sterols or stanols are available for coronary heart disease, even though their combination with statins effectively reduces low-density lipoprotein cholesterol. Plant sterols increase and plant stanols decrease serum plant sterols. Long-term statin treatment lowers coronary heart disease events only in patients with low baseline plant sterols who have high cholesterol synthesis. No convincing evidence is available that statin-induced phytosterolemia worsens atherosclerosis.