Chapter 4. Prevention of Type 1 Diabetes

  1. R. Williams2,
  2. W. Herman3,
  3. A.-L. Kinmonth5 and
  4. N. J. Wareham4
  1. Jay S. Skyler

Published Online: 9 APR 2003

DOI: 10.1002/0470846585.ch4

The Evidence Base for Diabetes Care

The Evidence Base for Diabetes Care

How to Cite

Skyler, J. S. (2002) Prevention of Type 1 Diabetes, in The Evidence Base for Diabetes Care (eds R. Williams, W. Herman, A.-L. Kinmonth and N. J. Wareham), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470846585.ch4

Editor Information

  1. 2

    Nuffield Institute for Health, University of Leeds, 71-75 Clarendon Road, Leeds LS2 9PL, UK

  2. 3

    Department of Internal Medicine and Epidemiology, 1500 East Medical Center Drive, 3920 Taubman Center, Box 0345, Ann Arbor, MI 48109, USA

  3. 4

    Department of Public Health and Primary Care, Institute of Public Health, University Forvie Site, Robinson Way, Cambridge CB2 2SR, UK

  4. 5

    General Practice and Primary Care Research Unit, Dept. of Public Health & Primary Care, Institute of Public Health, University Forvie Site, Robinson Way, Cambridge CB2 2SR, UK

Author Information

  1. Division of Endocrinology, Diabetes and Metabolism, University of Miami, Chairman, NIDDK Type 1 Diabetes TrialNet, 1450 NW 10th Avenue - Suite 3061, Miami, Florida 33136, USA

Publication History

  1. Published Online: 9 APR 2003
  2. Published Print: 27 AUG 2002

ISBN Information

Print ISBN: 9780471988762

Online ISBN: 9780470846582



  • risk;
  • genetics;
  • autoantibody;
  • metabolic change;
  • pharmacological intervention;
  • nicotinamide;
  • insulin;
  • milk protein;
  • cyclosporine;
  • azathioprine


Type 1 diabetes is characterized by immune-mediated pancreatic islet β-cell destruction and absolute insulin deficiency. The disease process involves a genetic predisposition, environmental factors and the activation of immune mechanisms targeted against the β-cells. The goal of intervention prior to disease onset is to arrest immune destruction and thus delay or prevent clinical disease. The goal of intervention at disease onset is to halt the destruction of β-cells, perhaps allowing residual β-cells to recover function, thereby lessening the severity of clinical manifestations. Studies aimed at delay or prevention of clinical type 1 diabetes are dependent on the ability to identify individuals at risk. Most have focused on relatives, since they have a 10-20-fold increased risk, while evidence suggests the disease process is the same in sporadic cases. This chapter reviews the evidence concerning interventions designed to interdict the type 1 diabetes disease process.