<unk> s improve atherogenic dyslipidemia characterized by high triglyceride and/or low HDL-C levels and elevated concentrations of small dense LDL particles, with or without high LDL-C levels.<unk> s may be compared to statin drugs, which reduce LDL-cholesterol (LDL-C) and have only limited effects on other lipid parameters. Clinical trials have shown that the combination of statins and<unk> s results in a significantly greater reduction in LDL-C and triglyceride levels and greater increases in high-density lipoprotein cholesterol (HDL-C) compared with monotherapy with either drug.<unk> s are used in accessory therapy in many forms of hypercholesterolemia, but the combination of some<unk> s (e.g., gemfibrozil) with statins is contraindicated due to an increased risk of rhabdomyolysis.<unk> s stimulate peroxisome proliferator activated receptor (PPAR) alpha, which controls the expression of gene products that mediate the metabolism of triglycerides (TG) and high-density lipoprotein (HDL). As a result, synthesis of fatty acids, TG and VLDL is reduced, whilst that of lipoprotein lipase, which catabolises TG, is enhanced. In addition, production of Apo A1 and ATP binding cassette A1 is up-regulated, leading to increased reverse cholesterol transport via HDL. Consequently,<unk> s reduce TG by up to 50% and increase HDL-C by up to 20%, but LDL-C changes are variable. Fewer large-scale trials have been conducted with<unk> s than with statins and the results are less conclusive, but reduced rates of cardiovascular disease have been reported with<unk>  therapy in the subgroup of patients with low HDL-C levels and elevated TG (e.g. TG > 2.3 mmol/L (200 mg/dL)).<unk> s are usually well tolerated but share a similar side-effect profile to statins. In addition, they may increase the risk of cholelithiasis and prolong the action of anticoagulants. Accumulating evidence suggests that they may also have a protective effect against diabetic microvascular complications. Clinical trials do support their use as monotherapy agents.<unk> s reduce the number of non-fatal heart attacks, but do not improve all-cause mortality and are therefore indicated only in those not tolerant to statins. Although less effective in lowering LDL levels, the ability of<unk> s to increase HDL and lower triglyceride levels seems to reduce insulin resistance when the dyslipidemia is associated with other features of the metabolic syndrome (hypertension and diabetes mellitus type 2). They are therefore used in many hyperlipidemias. Due to a rare paradoxical decrease in HDL-C seen in some patients on fenofibrate, as per US FDA label change, it is recommended that the HDL-C levels be checked within the first few months after initiation of<unk>  therapy. If a severely depressed HDL-C level is detected,<unk>  therapy should be withdrawn, and the HDL-C level monitored until it has returned to baseline.
Fibrate
Clofibrate
Fish oil
Fish oil 
Macrogol
Fruit salt
Empty calories
Iodised salt