Dyslipidaemia which is characterised by decreased levels of HDL-C and accompanied with increased levels of TG, apo B, and small dense LDL particles, is an important modifiable risk factor for the development of atherosclerosis and CVD. Guidelines for the treatment of lipid disorders recommend initiating treatment with the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins.

In vitro studies showed that polysaccharides and oxygenated triterpenoids from Ganoderma lucidum have a very broad spectrum of biological activities and pharmacological effects. Some types of ganoderic acid might reduce cholesterol by inhibiting HMG-CoA reductase, like the statin drugs. Compounds isolated from fruiting bodies of Ganoderma lucidum including ganolucidic acid eta, ganoderenic acid K, and the farnesyl hydroquinones (ganomycin J and ganomycin B), showed strong inhibitory activity against HMG-CoA reductase.

The cholesterol-lowering properties of Ganoderma lucidum have been exhibited in a series of in vitro and ex vivo studies, and in hamsters and minipigs. The organic fractions containing oxygenated lanosterol derivatives inhibited cholesterol synthesis in T9A4 hepatocytes. The scientiests found that both 2.5 and 5% dried Ganoderma lucidum reduced hepatic microsomal ex-vivo HMG-CoA reductase activity. In hamsters, administration of 5.0% dried Ganoderma lucidum decreased TC and HDL-C but not LDL-C, whereas in minipigs, 2.5% dried Ganoderma lucidum reduced all these parameters.

The improvements in the lipid profile in some diabetic animal models and in patients with T2DM treated with Ganoderma lucidum products may be related to the improvement in glycemic control, rather than a direct effect on lipid metabolism as hyperglycaemia is often related with elevated TG and reduced HDL-C. In a randomised, double-blind, cross-over study in 26 patients with borderline elevations of blood pressure and/or cholesterol, administration of Reishi (1.44g extract/d) for 12weeks produced a non-significant trend for reduction in TG and increase in HDL-C. Those changes could have been related to improvements in insulin resistance as these lipid abnormalities, hypertension, central obesity and insulin resistance cluster together in the metabolic syndrome.