QUESTION OF THE MONTH: MAY 2000.
Considering that the idea of fetal (intra-uterine) programming of future adult's diseases is getting strong support from several epidemiological studies (hypertension, cardiovascular disease, insulin resistance, some types of diabetes mellitus, small kidneys) as possible results of protracted intra-uterine adverse conditions at some critical points of development, grossly signalled by restricted fetal growth.
And, in view of the fact that early severe pre-eclampsia is clearly associated with these adverse conditions at the feto-maternal interface (biochemical, hormonal, hematological, immunological, nutritional, etc.), would not the children of eclamptic and pre-eclamptic pregnancies be ideal subjects for the study of this mechanism of disease ? would the mothers transmit to some extent their pre-eclamptic phenotype ? would this phenotype fade away or be reinforced in future generations ? How could we separate these influences from those of a genetic susceptibility locus ?