A Hypothesis About A Mechanism For The Programming Of Blood Pressure And Vascular Disease In Early Life

Authors

  • Cn Martyn,

    1. * MRC Environmental Epidemiology Unit, University of Southampton, Southampton and Institute of Pathology, Royal London Hospital, London, UK
    Search for more papers by this author
  • Se Greenwald

    1. * MRC Environmental Epidemiology Unit, University of Southampton, Southampton and Institute of Pathology, Royal London Hospital, London, UK
    Search for more papers by this author

  • Based on a paper presented at a meeting of the 11th International Congress of Endocrinology, Satellite Meeting on Endocrinology and Development, South Australia, November 2000. This paper has been peer reviewed.

Dr CN Martyn, MRC Environmental Epidemiology Unit, University of Southampton, Southampton SO16 6YD, UK. Email: cnm@mrc.soton.ac.uk

SUMMARY

1. There is now a great deal of evidence that people whose weight at birth was low tend to have higher blood pressure and increased risk of death from cardiovascular disease as adults.

2. We argue that, in fetuses whose growth is impaired, synthesis of elastin in the walls of the aorta and large arteries is deficient and that this deficiency leads to permanent changes in the mechanical properties of these vessels.

3. Over a lifetime, such changes could predispose an individual to higher blood pressure and cardiovascular disease.

Ancillary