Many epidemiological studies have now shown a strongly increased risk of developing type 2 diabetes and the metabolic syndrome in adults who as neonates showed signs of poor early (fetal and early postnatal) growth. The thrifty phenotype hypothesis was proposed to provide a conceptual and experimentally testable basis of these relationships. We have used protein restriction of rat dams, as a means to test this hypothesis. In vivo and in vitro studies of the growth-restricted offspring of such pregnancies have provided findings showing remarkable parallels with the human conditions.
The intrauterine environment is a major contributor to normal physiological growth and development of an individual. Disturbances at this critical time can affect the long-term health of the offspring. Low birth weight individuals have strong correlations with increased susceptibility to type 2 diabetes and cardiovascular disease in later-life. These observations led to the Thrifty Phenotype Hypothesis which suggested that these associations arose because of the response of a growing fetus to a suboptimal environment such as poor nutrition.
We posit that maternal prenatal nutrition can influence offspring schizophrenia risk via epigenetic effects. In this article, we consider evidence that prenatal nutrition is linked to epigenetic outcomes in offspring and schizophrenia in offspring, and that schizophrenia is associated with epigenetic changes. We focus upon one-carbon metabolism as a mediator of the pathway between perturbed prenatal nutrition and the subsequent risk of schizophrenia.
BACKGROUND: It is well established that obesity tends to track from early childhood into adult life. Studies in experimental animals have suggested that changes in the peri- and early postnatal intake of n-3 (omega-3) polyunsaturated acids can affect the development of obesity in adult life. OBJECTIVE: The aim of the current study was to investigate the effect of daily supplementation with 2.7 g long-chain n-3 fatty acids during the third trimester of pregnancy on adiposity in 19-y-old offspring.
BACKGROUND: We examined whether hypospadias was associated with several aspects of the diet, including intake of animal products, intake of several nutrients and food groups related to a vegetarian diet and oestrogen metabolism, and diet quality. METHODS: The study included deliveries from 1997 to 2005 that were part of the National Birth Defects Prevention Study. Diet was assessed by food frequency questionnaire during maternal telephone interviews, and two diet quality indices were developed based on existing indices.
BACKGROUND: In infants, vitamin B12 deficiency may be due to an inborn error of absorption and metabolism, or nutritional problems. CASE PRESENTATION: An exclusively breastfed 5-month-old Italian male infant, who was born after a normal full-term pregnancy to a vegan mother who was apparently daily treated with a multivitamin oral preparation during the second and third trimester, was hospitalised because of poor weight gain, feeding difficulties, severe pallor, muscle hypotonia and somnolence.
Nutrient requirements increase during periods of growth and development such as pregnancy and lactation. In response, many clinicians recommend dietary supplements during these important periods of the life cycle. Although there exist some recommendations concerning the need for a limited number of nutrients in supplemental form (eg, iron, folic acid, and iodine), there is a relative paucity of data concerning the use of dietary supplements during pregnancy and lactation. Limited data suggest, however, that usage is dependent on demographic, sociologic, and economic factors.
There are periods during perinatal development in which specific nutrients are required for optimal development, and there is growing evidence that optimal dietary intake of these nutrients, which include iodine, docosahexaenoic acid, choline, and folate, is important. Lessons in how these nutrient effects were identified can help us to broaden our approaches for finding other critical nutrients: we are looking for nutrients for which there is a wide range of dietary intake, that have no or marginal pathways for biosynthesis, and that are needed by dividing progenitor cells.
Although vitamin D deficiency is common at birth, the consequences to growth and bone mass by weaning are unclear. This study was designed to determine whether maternal dietary vitamin D deficiency in pregnancy has a negative impact on the bone mass of full-term neonates and if postnatal supplementation could restore bone mass. Forty guinea pigs were randomized to receive a control (C) or deficient (D) diet (0.03 microg vs. 0.00 microg cholecalciferol/g) during pregnancy.
This study aimed to examine the association of fetal growth and elevated third trimester maternal serum folate due to folic acid (FA) supplement intake. Dietary intake, use of FA supplements, weight, and blood biomarkers of B-vitamins (serum folate, pyridoxal, vitamin B(12), and plasma total homocysteine) were observed in 33 healthy pregnant women at the third trimester (average gestational age 35 wk). Birth outcomes were assessed through hospital birth records. Infant anthropometry and maternal blood biomarkers were followed up at 1 mo postpartum.