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.