Cross-breeding experiments between large and small strains of mammals have shown the powerful influence of the maternal organism on the control of fetal growth. The prepotency of a maternal regulator has also been demonstrated in humans. Our earlier studies indicated that this regulator acts by means of constraint; there is no equivalent accelerating mechanism. Data on 1092 siblings and 5207 paternal and maternal relatives of 986 probands show different patterns of birthweight among families ascertained, respectively, through very large and very small babies. When constraint is relaxed the Mendelian laws of inheritance are clearly followed. At the lower extreme there is evidence for the transmission of constraint through the female line only. This could be due to the maternal genotype, but our data suggest that a non-Mendelian path might also be involved. Such a process would be adaptive, facilitating fairly fast changes in fetal growth rate as the conditions under which a population lives deteriorate or improve.

Analysis of Variance↗

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Constrained and unconstrained fetal growth: associations with some biological and pathological factors.

Data are presented on the birthweights of 1092 siblings and 5207 maternal and paternal relatives of 986 probands. Previous analyses had demonstrated the potency of a maternal regulator constraining fetal growth. Different patterns of birthweights were found in families ascertained, respectively, through very large and very small babies (Ounsted, Scott and Ounsted 1986). When the data were reanalyzed in respect of other biological and pathological factors affecting fetal growth rate the following findings emerged: (1) When pathological factors were associated with the proband pregnancy the typical patterns of pedigree birthweights were not so clearly manifest; (2) general associations were found between the mothers' own birthweights and their size as adults; (3) low maternal birthweight was the biological factor showing the highest risk associated with small babies. When the babies were large the risks associated with high maternal adult weight and parity were similar to those associated with high birthweight. Paternal factors also made a contribution to fast fetal growth rate when pathological factors were absent. These findings confirm our hypothesis that at the lower extreme of fetal growth rate maternal constraint is pre-potent. At the upper extreme, relaxation of constraint allows other biological factors to take up more of the variance.

Adult↗