The Barker Hypothesis

Malnutrition in early pregnancy may result in symmetrically small babies with LBW. Mid-pregnancy malnutrition, the time of maximal placental growth, may result in a small baby and placental hypertophy. Final trimester malnutrition, the time of maximal fetal weight gain, may produce thin babies. Thus, there are a variety of markers of intra-uterine malnutrition: low birth weight, low birth weight relative to placental weight or low ponderal index (birth weight / length3) [12].

A retrospective study among 5,664 men born in Hertfordshire, UK between 1911 and 1930 demonstrated an association between those of lowest birth weight, or lowest weight at age 1 year and deaths from ischaemic hear disease. This suggested a link between intra-uterine environment and cardiovascular disease [4] and this study also demonstrated that low ponderal index (abnormal thinness) was associated with cardiovascular disease in adulthood.

A further series of retrospective studies using a cohort on 449 men and women born between 1935 and 1942 in Preston, Lancashire, UK who still lived in the area were studied because there were extremely detailed maternity records for these people. Systolic and diastolic blood pressure, were strongly associated with placental weight at birth in both men and women [2]. An association between the development of both impaired glucose tolerance and Type 2 diabetes mellitus and LBW was also demonstrated [3].

Changes in hormone levels occur during fetal life [13]. Extensive research has focused upon changes in maternal glucocorticoids [14, 15] to explain the association between LBW and hypertension. It is hypothesised that dysfunction of the placental glucocorticoid barrier results in increased fetal exposure to maternal glucocorticoids which, in turn, effects the development of fetal vessels and thus increases the risk of adulthood hypertension [14].

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