C ardiovascular disease (CVD) constitutes the major cause of mortality and morbidity in both type 1 (T1D) and type 2 (T2D) diabetes patients. Although the microvascular complications of T1D are well studied, macrovascular CVD, its treatment, and link to diabetes have been investigated primarily in T2D patients. On April 27 and 28, 2003, the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) sponsored a meeting to identify ways to close gaps in our knowledge about CVD in T1D to improve prevention and treatment. Participants were asked to: (1) Evaluate opportunities for studying the pathogenesis of CVD in T1D patients. Risk factors unique to these patients were of particular interest, as well as studies of the cause of CVD in T1D with respect to existing databases or cohorts and involving partnerships between basic and clinical investigators. (2) Evaluate opportunities for intervention studies to treat or prevent CVD in T1D. Because of practical obstacles (recruitment, duration, and cost of interventional studies with hard clinical end points), identification of reliable methods and markers that enable efficient intervention were a high priority.The meeting included 3 sessions: (1) current understanding of T1D and CVD; (2) opportunities to expand our understanding of the pathogenesis and clinical course of CVD in T1D; and (3) opportunities for intervention studies to reduce cardiovascular complications in T1D. This report summarizes the presentations made and concludes with recommendations drawn from the presentations and discussion among the participants. Current Understanding of T1D and CVDThe epidemic of T2D in the United States has focused renewed attention on its complications. The complication causing greatest mortality and expense is CVD, responsible for 65% to 75% of deaths in the T2D population. T1D is comparatively uncommon and usually has its onset in younger populations. Although not associated with many of the CVD risk factors recognized in T2D, the age-adjusted relative risk for CVD in T1D may even exceed that in T2D. 1 Relatively little is known about risks for CVD specific to T1D, except the substantial risk imparted by renal disease. 1 The mechanism(s) by which glycemia affects CVD through microvascular complications, secondary metabolic changes, or some direct effect requires further exploration. Such effects may be best appreciated in T1D, isolated from risk factors commonly accompanying T2D.Studies in T2D have demonstrated benefits of blood pressure control, lipid lowering, and aspirin on CVD. No study has conclusively addressed the effects of glycemic control on CVD events in T1D patients. However, the Epidemiology of Diabetes Interventions and Complications (EDIC) study, a long-term follow-up of the Diabetes Control and Complications Trial (DCCT), used ultrasonographic measurements of carotid intimal-medial thickness (IMT), a marker for atherosclerosis that correlates with clinical events. The group that received ...

Emerging evidence suggests that components of the metabolic syndrome either in isolation or in aggregate may impact the onset or severity of neurodegenerative processes, including those physiologic changes that lead to Alzheimer's Disease (AD). Several animal models that were originally designed to interrogate the metabolic syndrome are readily available. These models can now be used to support studies that may provide new mechanistic links between the metabolic syndrome and neurodegeneration. In addition, animal strains currently being generated and phenotyped through the efforts of an array of NIDDK-supported projects are likely to provide novel and better tools to advance Alzheimer's disease research in the near future.