Fetal origins of adult disease

Manuel RG Carrapato

Künye

Fetal origins of adult disease. Perinatoloji Dergisi 2002;10(3):156-156

Yazar Bilgileri

Manuel RG Carrapato

Hospital S Sebastiao - Santa Maria da Feira PT

Yazışma Adresi

Manuel RG Carrapato, Hospital S Sebastiao - Santa Maria da Feira PT,

Yayın Geçmişi

Çıkar Çakışması

Çıkar çakışması bulunmadığı belirtilmiştir.

Based on epidemiological data from the beginning of the 20th century, David Barker and colleagues have worked to establish a link between intrauterine events and the later development of cardiovascular and related disorders. Their collected observations have become known as the 'Barker I lypothesis' and constitute the basis of 'Programming' - a concept whereby a stimulus or an insult at critical periods of development will determine lifelong effects upon organ structure and/or function. in order to support this thesis ihey have elaborated an ingenious mechanism of 'fetal under-nutrilion operating at different stages in pregnancy with consetjuent differing effects upon body proportions at birth, placental ratios and, eventually, disease patterns later in life. Depending upon the type and timing of fetal nutritional deprivation, intraııterine grovvth and development would be affected leading to altered ponderal indexes (weight/length3) head circumference, placental .size, height and \veight at one ye-ar of age, differently for boys and girls and, subsecjuently, hypertension, coronary disease, stroke and insulin resistant status, ali adapted to fit the circum.stances. Not surprisingly, sııclı intricate mechanisms and explanation.s have met with considerable criticisms and controversy remains as to whether il is the intraııterine millieu or postnatal factors 'imprinting' on the genetic background which have a greater inf-luence upon events later on in life.

Nevertheless, in recent years from animal experiments it has been repeatedly shown that by modifying intrauterine conditions the offspring will be differently affected and, quite interestingly, these changes will be further transferred into future generations. in addition, diabetes in pregnancy serves as the ideal model to illustrate how an adverse intrauterine environment will condition fetal and neona ta 1 morbidity and how fetal determinants will impose upon conditions developing from childhood to later in life. Of greater importance is the fact that tight metabolic control will avoid, or greatly reduce the whole spect-rum of the diabetic embıyofetopathy including the later appearance of adult type 1 and 2 diabetes and their related morbidities.