Kumar and Singh in those processes, the attention of bench and clinical researchers, the pharmaceutical industry, and treatment providers has been focused on acellular elements for several decades. The major acellular elements are cholesterol, cholesterol esters, and phospholipids. Whereas the human body produces the majority of its daily requirement of cholesterol, most Americans now exceed that requirement with additional intake through their diet. Because cholesterol is insoluble when it enters the circulatory system it is transported as a lipoprotein. The major lipoprotein entities in a fasting individual are LDL-C, HDL-C, and very low-density lipoprotein cholesterol (VLDL-C). Measuring serum fasting lipid levels assists in evaluating and treating excessive serum lipid levels which are associated with increased morbidity and mortality from CHD. A fasting serum lipid panel consists of total cholesterol (TC), LDL-C, HDL-C, and triglyceride concentrations. While each of the aforementioned parameters have been shown to be independent risk factors for developing CHD, further analysis has shown that the aim of treatment should be reduction of the concentration of LDL-C particles because these are highly atherogenic and constitute 60%–70% of TC.6 In fact, the atherogenic nature of LDL-C, even when considered low-risk for developing CHD, has the potential to raise CHD risk, especially when combined with other elements. This overall combination, borderline high-risk LDL-C (130–159 mg/dL), high-normal triglycerides (150–250 mg/dL), presence of small LDL-C particles, and low HDL-C (,35 mg/dL) is what defines “atherogenic dyslipidemia”.7 However, as per the Third Report of the National Cholesterol Education Program – Adult Treatment Panel (NCEP-ATP) III, atherogenic dyslipidemia is defined as the triad of elevated triglycerides, low HDL-C, and small LDL-C particles. This triad is most commonly found in individuals with an atherogenic phenotype and/or type 2 diabetes mellitus (DM), and treatment involves lowering triglycerides and increasing HDL-C by diet modification, increased exercise, and pharmacologic therapy with fibrates or nicotinic acid.6 Scope of the problem The risk of developing atherosclerotic disease is increased two- to three-fold in people with diabetes.9 The WHO estimate of worldwide diabetic prevalence of 171 million in 2000 is expected to grow substantially to 366 million by 2030.10 In the US alone, the WHO estimates that the prevalence will increase from 17,702,000 in 2000 to 30,312,000 by 2030.11 For the year 2007, the Centers for Disease Control and 666 submit your manuscript | www.dovepress.com Dovepress Dovepress Prevention estimates that the prevalence of diagnosed DM in individuals of all ages in the US was 23.6 million, which is close to the WHO 2030 estimate. DM is categorized as type 1, type 2, gestational, and other, with type 2 being the most frequently diagnosed category.12 In terms of financial costs, Haung and Basu et al projected that annual spending on DM over the next 25 years will grow to $336 billion per year, with Medicare slightly exceeding 50% of its total yearly expenditure on the disease by 2034.13 It is clear that aggres- sive medical and financial management is needed for type 2 DM and atherogenic dyslipidemia. Management strategies As evidenced by the Scandinavian Simvastatin Survival Study (4S),14 Cholesterol And Recurrent Events (CARE),15 and Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID)16 secondary prevention trials, as well as the primary and secondary trials Heart Protection Study (HPS),17 Antihypertensive and Lipid-Lowering Treatment to prevent Heart Attack Trial (ALLHAT),18 and Anglo-Scandinavian Cardiac Outcome Trial-Lipid Lowering Arm (ASCOT-LLA),19 and the most recent and only primary prevention study, the Col- laborative Atorvastatin Diabetes Study (CARDS),20 the use of statins in type 2 diabetics has been shown to decrease CVD out- comes significantly (see Figure 1). Furthermore, a meta-analysis of 18,686 diabetics on a statin in the Cholesterol Treatment Trialists’ (CTT) collaborators study found that, after a mean follow-up of 4.3 years there was a proportional 9% decrease in all-cause mortality per mmol/L reduction in LDL-C, and a proportional 21% reduction per mmol/L decrease in LDL-C in major vascular events, compared with nondiabetics, indicating that all diabetics should start an HMG-CoA reductase inhibitor if they are at high risk for vascular events.36 This is consistent with current treatment recommendations from the NCEP-ATP III, which addresses the management of atherogenic dyslipidemia, and makes recommendations for weight reduction, increased exercise, and lipid-lowering therapies (ie, HMG-CoA reductase inhibitors, fibrates, and nicotinic acid).6 In terms of atherogenic dyslipidemia and DM, specifically those with type 2 DM, the NCEP-ATP III and the American Diabetes Association (ADA) both recommend life- style modification and HMG-CoA reductase inhibitor therapy regardless of baseline LDL-C for those with overt CVD and those without CVD who are age .40 years with one or more CVD risk factors. For those who do not have overt CVD or age ,40 years, statin therapy should be considered, along with lifestyle modification if LDL-C is .100 mg/dL or the patient has multiple CVD risk factors. Treatment goals for LDL-C Vascular Health and Risk Management 2010:6