There is a heavy burden of metabolic disease in hepatitis C infected populations Allison et al (1994) were the first to identify an interaction between chronic hepatitis C virus (HCV) infection and diabetes, demonstrating an increase in the prevalence of type 2 diabetes among HCV-infected patients with cirrhosis compared to patients with cirrhosis from other causes (50% versus 9%, respectively).1 Subsequent studies have found the prevalence of type 2 diabetes among this population to range between, 7.6% to 50%.2 The presence of insulin resistance and type 2 diabetes in HCV has been associated with poor HCV antiviral treatment response,3,4 acceleration of liver fibrosis,5 increased risk for hepatocellular carcinoma (HCC),6 higher transplant complication rates7 and possibly increased morbidity from cardiovascular and metabolic complications.8 Early intervention with lifestyle modification and/or metformin in patients with pre-diabetes can delay or prevent the onset of type 2 diabetes in high risk populations. It is unknown whether this benefit extends to those infected with HCV.9 [see Appendix I for definitions of insulin resistance, impaired fasting glucose, and diabetes] There is lack of agreement on how to manage insulin resistance in HCV-infected patients. There may be risks with some diabetes medications in this population. Sulfonylureas and insulin may be associated with an increased risk of developing HCC in this population. Additional evaluation of the risks and benefits of diabetic medications in HCV are required.10 HCV is also known to induce changes in lipid metabolism. The HCV life cycle is dependent on the VLDL pathway. Viral replication involves the formation of complexes termed lipoviral particles resulting in decreased secretion of VLDL. The assembly of these lipoviral particles is believed to facilitate binding with LDL receptor and considered a mechanism by which HCV gains entry to the hepatocyte. Numerous studies have demonstrated lower total cholesterol, triglycerides (TG), HDL-C and LDL-C levels in patients with chronic hepatitis C infection. Lower lipid levels correlate with higher HCV viral load,11 decreased antiviral virological cure rates12 [A.K.A Sustained Virological Response (SVR)] and increased hepatic steatosis.13,14 Successful treatment of HCV with IFN/Ribavirin is typically associated with the reversal of hypolipidemia yet in some patients lipid levels may increase to levels associated with increased cardiovascular risk.15,16