Maternal Vitamin Deficiencies Research Articles

Vitamin D Status during Pregnancy versus the Anthropometric Parameters of Two- and Four-Year-Olds: A Pilot Study.

Apart from being associated with a well-documented risk for adverse pregnancy outcomes, maternal deficiency of vitamin D may also negatively affect the physical development of their children. The aim of the study was to evaluate the relationship between maternal as well as umbilical cord blood levels of vitamin D and the weight and height values of two- and four-year-olds. The study was conducted in a group of 52 ‘mother–child’ pairs. On the day of the delivery, total 25(OH)D concentration in blood was measured using immunological tests (LIAISON). Weight and height values were obtained from the database of routine health checks for children aged two and four, which are obligatory in Poland. Multiple regression analysis was used for statistical analysis. No association was detected between maternal-neonatal concentrations of vitamin D and weight and height values of the investigated two- and four-year-olds despite extreme differences in maternal (4.0–37.7 ng/mL) and neonatal (5.9–46.6 ng/mL) concentrations and the fact that vitamin D deficiency was detected in almost 54% of the mothers and 37% of the newborns. Therefore, no relationship between maternal-fetal vitamin D concentrations and the anthropometric parameters of the investigated children up to the age of four was found.

Maternal vitamin D-restricted diet has consequences in the formation of pancreatic islet/insulin-signaling in the adult offspring of mice.

The maternal deficiency of vitamin D can act on organogenesis in mice offspring, being a risk factor for chronic diseases in adulthood. This study investigates the effects of maternal deficiency of vitamin D on structural islet remodeling and insulin-signaling pathway in the offspring. We studied male C57Bl/6 offspring at 3-month old (n=10/group) from mother fed one of the two diets: control diet (C) or vitamin D-restricted diet (VitD-). After weaning, offspring only fed the control diet ad libitum. In the offspring, we studied insulin production, islet remodeling, and islet protein expression of the insulin-signaling pathway (Western blotting, isolated islet, n=5/group). VitD- offspring showed greater glycemia (P=0.012), smaller beta-cell mass (P=0.014), and hypoinsulinemia (P=0.024) than C offspring. Comparing VitD- offspring with C offspring, we observed lower protein levels in islet of insulin (P=0.003), insulin receptor substrate-1 (P=0.025), phosphatidylinositol-3-kinases (P=0.045), 3-phosphoinositide-dependent protein kinase 1 (P=0.017), protein kinase B (P=0.028), with reduced expression of pancreas/duodenum homeobox-1 (PDX-1) (P=0.016), glucose transporter-2 (P=0.003), and glucokinase (P=0.045). The maternal vitamin D-restricted diet modifies the development of the pancreas of the offspring, leading to islet remodeling and altered insulin-signaling pathway. The decrease of PDX-1 is probably significant to the changes in the beta-cell mass and insulin secretion in adulthood.

Maternal vitamin K deficient embryopathy: Association with hyperemesis gravidarum and Crohn disease

Chondrodysplasia punctata (CDP) is an etiologically heterogeneous disorder characterized by the radiographic finding of stippled epiphyses (punctate calcifications). It is often accompanied by a characteristic facial appearance, known as the Binder phenotype, which is attributed to hypoplasia of the nasal cartilages; abnormal distal phalanges (brachytelephalangy) are a common component manifestation as well. We report eight patients with a Binder phenotype with or without CDP who all shared a known or suspected maternal deficiency of vitamin K. We suspect that this phenotype is probably under recognized, and we hope to increase awareness about the maternal risk factors, especially hyperemesis gravidarum, which lead to nutritional deficiency.

Short Bowel Syndrome Causing Bleeding Diathesis and Profound Vitamin Deficiency in Pregnancy

Extensive bowel resection may lead to a state of inadequate nutrient absorption and malnutrition known as short bowel syndrome. Deficiencies in fat-soluble vitamins may occur from this condition, with sequelae such as a bleeding diathesis. Maternal vitamin deficiencies also have been associated with fetal anomalies. A young gravid patient with a history of neonatal bowel resection presented with bleeding diathesis. She subsequently was found to have profound vitamin deficiencies and delivered a newborn with multiple anomalies. Preconceptional counseling, nutritional status evaluation, and concomitant management with a gastroenterologist are essential to optimize pregnancy outcome for patients with a history of extensive bowel resection.

Maternal dietary folate and/or vitamin B12 restrictions alter body composition (adiposity) and lipid metabolism in Wistar rat offspring

Maternal vitamin deficiencies are associated with low birth weight and increased perinatal morbidity and mortality. We hypothesize that maternal folate and/or vitamin B12 restrictions alter body composition and fat metabolism in the offspring. Female weaning Wistar rats received ad libitum for 12 weeks a control diet (American Institute of Nutrition-76A) or the same with restriction of folate, vitamin B12 or both (dual deficient) and, after confirming vitamin deficiency, were mated with control males. The pregnant/lactating mothers and their offspring received their respective diets throughout. Biochemical and body composition parameters were determined in mothers before mating and in offspring at 3, 6, 9 and 12 months of age. Vitamin restriction increased body weight and fat and altered lipid profile in female Wistar rats, albeit differences were significant with only B12 restriction. Offspring born to vitamin-B12-restricted dams had lower birth weight, while offspring of all vitamin-restricted dams weighed higher at/from weaning. They had higher body fat (specially visceral fat) from 3 months and were dyslipidemic at 12 months, when they had high circulating and adipose tissue levels of tumor necrosis factor α, leptin and interleukin 6 and low levels of adiponectin and interleukin 1β. Vitamin-restricted offspring had higher activities of hepatic fatty acid synthase and acetyl-CoA-carboxylase and higher plasma cortisol levels. In conclusion, maternal and peri-/postnatal folate and/or vitamin B12 restriction increased visceral adiposity (due to increased corticosteroid stress), altered lipid metabolism in rat offspring perhaps by modulating adipocyte function and may thus predispose them to high morbidity later.

Effect of Maternal Vitamin B-6 Deficiency on Specific Regions of Developing Rat Brain: Amino Acid Metabolism

Amino acid metabolism may be adversely affected by vitamin B-6 deficiency. The effects of a maternal deficiency of vitamin B-6 on concentrations of amino acids in substantia nigra (SN), caudate nucleus/putamen (C/P) and cortex (CORT) in progeny were studied. Female albino rats were fed diets containing either 0.6 (deficient) or 7.0 (control) mg pyridoxine·HCl (PN·HCl) per kilogram diet ad libitum throughout growth, gestation and lactation. Paralleling a significant decrease in body weight, pups in the deficient groups began to show gross neurological symptoms of the deficiency at approximately 11 days of age. Analysis of brain regions at 15 days of age showed that the deficiency resulted in increased concentrations of cystathionine, glycine, leucine, isoleucine and valine and decreased concentrations of alanine and serine in SN, C/P and CORT. Often these changes were more pronounced in one or two of the regions analyzed. At 1 and 3 hours after an intraperitoneal injection of 100 mg PN·HCl per kilogram body weight into deficient pups, concentrations of cystathionine, leucine, isoleucine, valine, alanine and serine in brain regions remained similar to preinjection values. However, within 3 hours postinjection, glycine concentrations had decreased and were similar to control levels in SN and C/P.

Perinatal Metabolism of Vitamin D: Transition from Fetal to Neonatal Life

Recent advances in the understanding of the metabolism of vitamin D are outlined: vitamin D metabolism during pregnancy, vitamin D and the placenta, vitamin D metabolism in the fetus, maternal deficiency of vitamin D, vitamin D and the neonate, osteopenia and rickets of prematurity, and vitamin D and lactation.

THE ÆTIOLOGICAL ROLE OF MATERNAL VITAMIN-B 6 DEFICIENCY IN THE DEVELOPMENT OF ATHEROSCLEROSIS

Lysyl oxidase is the copper-dependent enzyme responsible for the normal crosslinking of both collagen and elastin which is necessary for their functional integrity. There is now strong evidence that this enzyme is vitamin-B 6-dependent. The earliest visible lesion of atherosclerosis, commonly found in human neonatal coronary arteries and probably indicative of the location of future atherosclerotic plaques, is a focal splitting of the internal elastic lamina, the cause of which has hitherto remained unexplained. It is suggested that this lesion is the result of imperfect crosslinking of arterial elastin as well as collagen, and is caused by a maternal deficiency of vitamin B 6 which is commonly found in pregnancy and which could thus impair the function of lysyl oxidase. Prophylactic supplementation of maternal diet with adequate vitamin B 6 is therefore suggested.

Congenital eye defects in rats following maternal folic-acid deficiency during pregnancy

ABSTRACT Malformations of fetal rat eyes result from a variety of maternal vitamin deficiencies employed either transiently or continuously during pregnancy. Thus, eye defects have been produced in rat fetuses as a result of maternal deficiencies of vitamin A (Wilson, Jordan & Brent, 1953), pantothenic acid (Lefebvres-Boisselot, 1951; Nelson, Asling & Evans, 1957), niacin (Chamberlain & Nelson, 1963) and pteroylglutamic acid (PGA or folic acid) (Evans, Nelson & Asling, 1951; Nelson, Asling & Evans, 1952; Giroud & Boisselot, 1951; Giroud, Lefebvres & Dupuis, 1952; Giroud, Delmas, Lefebvres & Prost, 1954). Previous studies on the teratogenic effects of PGA-deficiency on the developing rat eye, although informative, have been concerned mainly with stages after the 15th day of pregnancy (the day of finding sperm in the vagina is considered to be day zero). However, since the eye begins forming between the 9th and 10th days of gestation, it was felt that a study embracing both early and late stages of ocular development in rat embryos from mothers maintained on a PGA-deficient regimen for different lengths of time during gestation would be of more value in understanding the genesis of certain ocular abnormalities. The following account concerns such an investigation and describes the abnormalities en-countered in the visual system.

Disturbance of embryonic development by maternal vitamin deficiencies.

Disturbance of embryonic development by maternal vitamin deficiencies.

The Relation of Vitamin a to Anophthalmos in Pigs

Forty-two pigs (four litters) were born blind at the Texas Agricultural Experiment Station in the course of experiments relating to maternal vitamin-A deficiency. Other defects noted were cleft palate, cleft lip, accessory ears, and arrested ascension of the kidneys. Definite and complete genetic tests were made to determine whether or not an hereditary factor was responsible for the eye anomaly and close matings such as blind brother x blind sister, and normal mother x blind son, produced only normal pigs. These studies leave no reasonable doubt that maternal deficiency of vitamin A will result in a variety of defects in the offspring, including blindness and even a failure of complete development of eye tissue, together with those above-mentioned. The normal mothers of these blind pigs were depleted to a very low state of vitamin A before breeding and were continued on the vitamin-A-free ration for the first 30 days of the gestation period (the time during which the eye develops in the pig embryo). Vitamin-A deficiency is by no means uncommon in human diet and it may easily be that many of the eye weaknesses which we suffer today are due to maternal vitamin-A deficiency, just as Dr. H. M. Taylor has recently discovered that some of the deafness among Southern children is due to quinine taken by the mother during pregnancy. In any case, it is obvious that until we have evidence to the contrary, we should insist on an abundance of vitamin A in the diet of the expectant mother in the early stages of pregnancy when so many of the vital organs of the embryo are being formed. From the Division of Swine Husbandry, Texas Agricultural Experiment Station. Read before the Association for Research in Ophthalmology, Atlantic City, June 11, 1935.