Higher Maternal Intake Research Articles

Neurodevelopmental effect of aluminum in mice: Fostering studies

In order to determine sensitive periods for induction of neurodevelopmental effects of aluminum (Al), mice were fed either 25 (control) or 1000 (high Al) μg Al/g diet (as Al lactate) from conception through lactation and litters were fostered either within or between groups at birth. Birth parameters were not influenced by Al intake. Food intake and body weight were 10%–12% lower during lactation in dams fed the high Al diets. Both gestation and lactation high Al exposure led to growth retardation in offspring beginning on day 10 postnatal; combined gestation and lactation exposure led to the biggest weight differential at weaning (23%). For neurobehavioral measures obtained at weaning, forelimb grasp strength was influenced by gestation high Al exposure, whereas negative geotaxis was influenced by lactation exposure, and hindlimb grasp and temperature sensitivity were influenced by both gestation and lactation exposure. Pup liver and brain manganese (Mn) and liver iron (Fe) concentrations at weaning were lower after high Al lactation exposure than in controls. Pup brain and liver Al concentrations were similar among the groups. These data show that mice are susceptible to neurodevelopmental effects of high maternal dietary Al intake during both gestation and lactation, and that high maternal intake can result in altered essential trace element metabolism in the offspring.

Abnormal fetal behavioural state regulation in a case of high maternal alcohol intake during pregnancy

In the near term human fetus disturbed behavioural state organization has been found in cases of intra-uterine growth retardation or maternal type-1-diabetes. The present case report describes abnormal fetal behavioural state organization found in combination with maternal alcohol abuse during pregnancy. The abnormalities included frequent interruptions of the periods of concordant association of 2F-parameters, reflected by a high proportion of no-coincidence, and spontaneous awakenings (State 4F), always following stable periods of State 1F. The latter phenomenon was not found thus far by us or others, neither in normal nor in complicated pregnancies. After birth normal state organization was found. It is suggested that the abnormalities in fetal behaviour might have been due to maternal alcohol abuse, whereas a possible withdrawal effect might have occurred in utero.

Effects of Maternal Intake of Ascorbic Acid on the Postnatal Metabolism of This Vitamin in the Guinea Pig

Guinea pigs were fed diets containing 0.04% (control), 0.56% (E-1) or 0.86% (E-2) ascorbic acid during the last half of pregnancy. Levels of ascorbic acid in serum and various organs of the mother and fetuses were higher in the animals receiving the E-1 diet than in controls. Between 5 and 10 days after birth ascorbic acid catabolism was measured in the offspring of the various groups by determining the rate of excretion of 14CO2 after an injection of l-[1-14C] ascorbic acid. Compared with controls, pups from the E-1 and E-2 groups had similar increased ascorbic acid catabolism. Animals in the E-1 group, fed a 0.006% (MDR) ascorbic acid diet from day 11 after birth, had markedly decreased ascorbic acid catabolism after ten days on the MDR diet. After 20 days on this diet ascorbic acid catabolism was similar to controls fed the MDR diet. By contrast, catabolism values remained elevated in pups maintained on the E-1 diet. Similarly, tissue ascorbic acid levels among all groups of offspring reflected comparable changes. Prolonged high maternal intake of ascorbic acid during pregnancy increases the metabolism of this vitamin in the neonatal period. Additional postnatal effects depend on dietary manipulation and may either be lasting or transient.vitamin C guinea pigs maternal-fetal exchange