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Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,532
Online ISSN 1827-1715
Cataldi L. 1,2, Buonsenso D. 2
1 Istituto di Clinica Pediatrica Università Cattolica del Sacro Cuore Policlinico Universitario “A. Gemelli”, Roma, Italia
2 Gruppo di Studio di Storia della Pediatria della Società Italiana di Pediatria
The hypothesis of the prenatal programming of adult diseases took on increasing interest from the moment that, in the ‘60s, an epidemiological association was proposed between low birth weight and cardiovascular diseases. In the last 20 years it has been demonstrated that individuals with low weight, low stature and thinness at birth have a higher risk of developing cardiovascular diseases and type 2 diabetes. Animal and clinical studies are casting light on the biological mechanisms underlying the association between modified development in the uterus and diseases, and on how growth in adolescence and in adult life can modulate this initial proneness to disease. One of the mechanisms that has aroused most interest among researchers is the reduced number of nephrons, associated with low birth weight, which predisposes to glomerulosclerosis and increased systemic arterial pressure in adult life. A correlation has also been found between low weight at birth and peripheral resistance to insulin. Nevertheless, it is thought that modified prenatal development is only a predisposing factor, open to profound influences in the course of postnatal development. It has in fact been demonstrated that accelerated development in the period of infancy and adolescence can extend the initial condition of neonatal suffering. Indirectly these studies renew and at the same time extend the concept of prevention, a priority aim of the physician of the third millennium.