|Causes and Consequences of Intrauterine Growth Retardation, Proceedings of an IDECG workshop, November 1996, Baton Rouge, USA, Supplement of the European Journal of Clinical Nutrition (International Dietary Energy Consultative Group - IDECG, 1996, 100 pages)|
|Biological mechanisms of environmentally induced causes of IUGR|
Biologically, maternal weight and nutritional status are determinants of the environment in which conception is to occur, a certain amount of body fat being required for normal reproductive function. Epidemiological data show associations between early menarche, low pre-pregnancy weight, low pre-pregnancy height, and short inter-pregnancy interval on the one hand, and downward shifts in growth curves or increased risk for growth retardation in subsequent pregnancies on the other (Schell and Hodges, 1985; Cnattingius S et al, 1984; Miller and Merritt, 1979; Tanner and Thomson, 1970; Ferraz et al, 1988; Miller, 1989; Yang et al, 1989). Mothers born with low birth weight are more likely to produce low birth weight infants (Klebanoff et al, 1989).
The role of genetic determinants
Maternal genetic variations are likely to affect fetal growth. There are differences in growth curves in different geographic regions and among different racial groups in the United States. Kessel et al (1988) and Myers and Ferguson (1989) reported that, after correction for social and demographic factors, blacks still have a higher rate of fetal death and are at increased risk for delivering premature and SGA infants. However, it is extremely difficult to separate environmental factors from true genetic differences, and these data should be interpreted cautiously.
Growth in utero is the result of cell multiplication and tissue organization; the effects of genetic endowment on size at birth are small. This is demonstrated by the calculated correlation coefficient between length at birth and adult stature, which is 0.3. In the two-year-old the correlation coefficient between height and adult stature is quite high, 0.8 (Battaglia and Meschia, 1986). It then declines again in the early teenage years with the pubertal growth spurt. Continued decline of percentiles after the age of two years, even in apparently healthy children, should be cause for further investigation.