PRENATAL AND NEONATAL NUTRITION

PEDIATRICS ◽  
1962 ◽  
Vol 30 (1) ◽  
pp. 145-156
Author(s):  
Clement A. Smith
Keyword(s):  
Maternal Diet ◽  
Maternal Blood ◽  
Fetal Life ◽  
Critical Periods ◽  
Prenatal Nutrition ◽  
Base Camp ◽  
Neonatal Nutrition ◽  
Special Information ◽  
The Many ◽  
Newborn Animals

MOST AWARD RECIPIENTS have made carefully planned and masterfully executed investigations of some unexplored nutritional territory, which they could fully describe at such a time as this. I can report only a few disconnected explorations which discovered some useful points of view and uncovered some awkward pitfalls for future travellers. While thanking the Borden Company for the honor of being here, I should like also thank the many colleagues who did most of the work of our explorations, the Boston Lying-in Hospital, which has been such a comfortable base camp, and the Association for the Aid of Crippled Children, whose financial backing has been so necessary and so generous. PRENATAL NUTRITION Our thinking about unborn and newborn babies seems to have dealt so much with other problems than their nutrition and growth that prenatal nutrition was often studied not by first intention but because of some special opportunity. Perhaps the most fortunate of these came when a maternal blood volume study by our medical and obstetrical colleagues provided us with babies whose prenatally acquired iron molecules could be identified throughout infancy, but that was an interesting side trip on a trail we have not pursued further. Another journey began with Mrs. Bertha Burke's investigations of maternal dietary histories, which afforded the chance to examine a series of infants with much special information attached. The results of our attempts to correlate particular deficiencies in what mothers had eaten during pregnancy with the condition of their infants at birth were disappointing to those so recently stirred by the demonstrations of Dr. Warkany, that specific malformations of newborn animals resulted when maternal diet was restricted in certain nutrients at critical periods of fetal life.

scholarly journals The Role of Fetal, Infant, and Childhood Nutrition in the Timing of Sexual Maturation

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 419
Author(s):  
Valeria Calcaterra ◽  
Hellas Cena ◽  
Corrado Regalbuto ◽  
Federica Vinci ◽  
Debora Porri ◽  
...  
Keyword(s):  
Sexual Maturation ◽  
Pubertal Development ◽  
Endocrine System ◽  
Metabolic Adaptation ◽  
Fetal Life ◽  
Critical Periods ◽  
Important Indicator ◽  
Prenatal Growth ◽  
Adaptation Response ◽  
Healthy Growth

Puberty is a crucial developmental stage in the life span, necessary to achieve reproductive and somatic maturity. Timing of puberty is modulated by and responds to central neurotransmitters, hormones, and environmental factors leading to hypothalamic-pituitary-gonadal axis maturation. The connection between hormones and nutrition during critical periods of growth, like fetal life or infancy, is fundamental for metabolic adaptation response and pubertal development control and prediction. Since birth weight is an important indicator of growth estimation during fetal life, restricted prenatal growth, such as intrauterine growth restriction (IUGR) and small for gestational age (SGA), may impact endocrine system, affecting pubertal development. Successively, lactation along with early life optimal nutrition during infancy and childhood may be important in order to set up timing of sexual maturation and provide successful reproduction at a later time. Sexual maturation and healthy growth are also influenced by nutrition requirements and diet composition. Early nutritional surveillance and monitoring of pubertal development is recommended in all children, particularly in those at risk, such as the ones born SGA and/or IUGR, as well as in the case of sudden weight gain during infancy. Adequate macro and micronutrient intake is essential for healthy growth and sexual maturity.

scholarly journals When a Neonate Is Born, So Is a Microbiota

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 148
Author(s):  
Alessandra Coscia ◽  
Flaminia Bardanzellu ◽  
Elisa Caboni ◽  
Vassilios Fanos ◽  
Diego Giampietro Peroni
Keyword(s):  
Bacterial Colonization ◽  
Perinatal Period ◽  
Delivery Mode ◽  
Fetal Life ◽  
Assisted Reproduction Techniques ◽  
Neonatal Nutrition ◽  
Short And Long Term ◽  
Number Of Bacteria

In recent years, the role of human microbiota as a short- and long-term health promoter and modulator has been affirmed and progressively strengthened. In the course of one’s life, each subject is colonized by a great number of bacteria, which constitute its specific and individual microbiota. Human bacterial colonization starts during fetal life, in opposition to the previous paradigm of the “sterile womb”. Placenta, amniotic fluid, cord blood and fetal tissues each have their own specific microbiota, influenced by maternal health and habits and having a decisive influence on pregnancy outcome and offspring outcome. The maternal microbiota, especially that colonizing the genital system, starts to influence the outcome of pregnancy already before conception, modulating fertility and the success rate of fertilization, even in the case of assisted reproduction techniques. During the perinatal period, neonatal microbiota seems influenced by delivery mode, drug administration and many other conditions. Special attention must be reserved for early neonatal nutrition, because breastfeeding allows the transmission of a specific and unique lactobiome able to modulate and positively affect the neonatal gut microbiota. Our narrative review aims to investigate the currently identified pre- and peri-natal factors influencing neonatal microbiota, before conception, during pregnancy, pre- and post-delivery, since the early microbiota influences the whole life of each subject.

106 The Effects of Fetal Programming on Offspring Pancreas DNA Methylation

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 54-55
Author(s):  
Maria L Hoffman
Keyword(s):  
Dna Methylation ◽  
Fetal Programming ◽  
Maternal Nutrition ◽  
Maternal Diet ◽  
Multiple Generations ◽  
Livestock Species ◽  
Maternal Programming ◽  
Genome Bisulfite Sequencing ◽  
The Many ◽  
Methylation Patterns

Abstract It has been well documented that fetal programming, caused by changes to the maternal environment during pregnancy, can impact the overall health and growth of the offspring in livestock and non-livestock species alike. These effects are observed in the F1 offspring as well as across subsequent generations; however, the mechanisms by which this occurs are still poorly understood. Epigenetics is one of the many mechanisms that is hypothesized to have a role in fetal programming and may be mediating the observed effects across multiple generations. It has been demonstrated by others that DNA methylation patterns can be altered by an individuals’ diet and that the pancreas is vulnerable to the effects of fetal programming. Therefore, we evaluated the effects of poor maternal nutrition during gestation on the pancreas tissue of lambs. We have demonstrated that maternal under- or overnutrition during gestation alters the DNA methylation patterns of the offspring pancreas tissue with these effects being diet dependent and sex specific. We have also begun evaluating the effects of maternal diet in murine models using whole-genome bisulfite sequencing to compare species differences and determine if there are any changes conserved across species. This will allow us to focus on a smaller number of critical factors in individuals as they age and across multiple generations in livestock species such as sheep and cattle. From these data we will be able to elucidate the role DNA methylation has in mediating the effects of maternal programming in the pancreas tissue.

scholarly journals Maternal Intake of Cow’s Milk during Lactation Is Associated with Lower Prevalence of Food Allergy in Offspring

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3680
Author(s):  
Mia Stråvik ◽  
Malin Barman ◽  
Bill Hesselmar ◽  
Anna Sandin ◽  
Agnes E. Wold ◽  
...  
Keyword(s):  
Food Allergy ◽  
Breast Milk ◽  
Maternal Diet ◽  
Maternal Blood ◽  
Cow’S Milk ◽  
Lower Prevalence ◽  
Food Frequency ◽  
Lactating Women ◽  
Cow's Milk ◽  
Pregnancy And Lactation

Maternal diet during pregnancy and lactation may affect the propensity of the child to develop an allergy. The aim was to assess and compare the dietary intake of pregnant and lactating women, validate it with biomarkers, and to relate these data to physician-diagnosed allergy in the offspring at 12 months of age. Maternal diet during pregnancy and lactation was assessed by repeated semi-quantitative food frequency questionnaires in a prospective Swedish birth cohort (n = 508). Fatty acid proportions were measured in maternal breast milk and erythrocytes. Allergy was diagnosed at 12 months of age by a pediatrician specialized in allergy. An increased maternal intake of cow’s milk during lactation, confirmed with biomarkers (fatty acids C15:0 and C17:0) in the maternal blood and breast milk, was associated with a lower prevalence of physician-diagnosed food allergy by 12 months of age. Intake of fruit and berries during lactation was associated with a higher prevalence of atopic eczema at 12 months of age. Our results suggest that maternal diet modulates the infant’s immune system, thereby influencing subsequent allergy development.

scholarly journals Epigenetics and developmental origins of diabetes: correlation or causation?

2018 ◽  
Vol 315 (1) ◽  
pp. E15-E28 ◽  
Author(s):  
Amita Bansal ◽  
Rebecca A. Simmons
Keyword(s):  
Animal Studies ◽  
Metabolic Diseases ◽  
Epigenetic Modification ◽  
Developmental Origins ◽  
Critical Periods ◽  
Metabolic Outcome ◽  
Health And Disease ◽  
Founding Principle ◽  
The Many

The incidence of metabolic disorders like type 2 diabetes (T2D) and obesity continue to increase. Although it is evident that the increasing incidence of diabetes confers a global societal and economic burden, the mechanisms responsible for the increased incidence of T2D are not well understood. Extensive efforts to understand the association of early-life perturbations with later onset of metabolic diseases, the founding principle of developmental origins of health and disease, have been crucial in determining the mechanisms that may be driving the pathogenesis of T2D. As the programming of the epigenome occurs during critical periods of development, it has emerged as a potential molecular mechanism that could occur early in life and impact metabolic health decades later. In this review, we critically evaluate human and animal studies that illustrated an association of epigenetic processes with development of T2D as well as intervention strategies that have been employed to reverse the perturbed epigenetic modification or reprogram the naturally occurring epigenetic marks to favor improved metabolic outcome. We highlight that although our understanding of epigenetics and its contribution toward developmental origins of T2D continues to grow, whether epigenetics is a cause, consequence, or merely a correlation remains debatable due to the many limitations/challenges of the existing epigenetic studies. Finally, we discuss the potential of establishing collaborative research efforts between different disciplines, including physiology, epigenetics, and bioinformatics, to help advance the developmental origins field with great potential for understanding the pathogenesis of T2D and developing preventive strategies for T2D.

scholarly journals Epigenetics, Maternal Diet and Metabolic Programming

2019 ◽  
Vol 7 (1) ◽  
pp. 45-51
Author(s):  
Karina Ramírez-Alarcón ◽  
Ángela Sánchez-Agurto ◽  
Liliana Lamperti ◽  
Miquel Martorell
Keyword(s):  
Metabolic Diseases ◽  
Maternal Diet ◽  
Metabolic Programming ◽  
Methyl Groups ◽  
Fetal Life ◽  
Methyl Donors ◽  
Lysine Residues ◽  
Adenosyl Methionine ◽  
Health And Disease ◽  
B Complex Vitamins

Background: The maternal environment influences embryonic and fetal life. Nutritional deficits or excesses alter the trajectory of fetus/offspring’s development. The concept of “developmental programming” and “developmental origins of health and disease” consists of the idea that maternal diet may remodel the genome and lead to epigenetic changes. These changes are induced during early life, permanently altering the phenotype in the posterior adult stage, favoring the development of metabolic diseases such as obesity, dyslipidemia, hypertension, hyperinsulinemia, and metabolic syndrome. In this review, it is aimed to overview epigenetics, maternal diet and metabolic programming factors and determine which of these might affect future generations. Scope and Approach: Nutrients interfere with the epigenome by influencing the supply and use of methyl groups through DNA transmethylation and demethylation mechanisms. They also influence the remodeling of chromatin and arginine or lysine residues at the N-terminal tails of histone, thus altering miRNA expression. Fats, proteins, B vitamins and folates act as important cofactors in methylation processes. The metabolism of carbon in the methyl groups of choline, folic acid and methionine to S-Adenosyl Methionine (SAM), acts as methyl donors to methyl DNA, RNA, and proteins. B-complex vitamins are important since they act as coenzymes during this process. Key Findings and Conclusion: Nutrients, during pregnancy, potentially influence susceptibility to diseases in adulthood. Additionally, the deficit or excess of nutrients alter the epigenetic machinery, affecting genes and influencing the genome of the offspring and therefore, predisposing the development of chronic diseases in adults.

scholarly journals Supplementation of a maternal low-protein diet in rat pregnancy with folic acid ameliorates programming effects upon feeding behaviour in the absence of disturbances to the methionine–homocysteine cycle

2009 ◽  
Vol 103 (7) ◽  
pp. 996-1007 ◽  
Author(s):  
Sarah F. Engeham ◽  
Andrea Haase ◽  
Simon C. Langley-Evans
Keyword(s):  
Folic Acid ◽  
Feeding Behaviour ◽  
Dna Methyltransferase ◽  
Maternal Diet ◽  
Regulation Of Gene Expression ◽  
Later Life ◽  
Protein Restriction ◽  
Fetal Life ◽  
Folate Supplementation ◽  
Low Protein

Maternal protein restriction in rat pregnancy is associated with altered feeding behaviour in later life. When allowed to self-select their diet, rats subject to prenatal undernutrition show an increased preference for fatty foods. The main aim of the present study was to evaluate the contribution of folic acid in the maternal diet to programming of appetite, since disturbances of the folate and methionine–homocysteine cycles have been suggested to impact upon epigenetic regulation of gene expression and hence programme long-term physiology and metabolism. Pregnant rats were fed diets containing either 9 or 18 % casein by weight, with folate provided at either 1 or 5 mg/kg diet. Adult male animals exposed to low protein (LP) in fetal life exhibited increased preference for high-fat food. Providing the higher level of folate in the maternal diet prevented this effect of LP, but offspring of rats fed 18 % casein diet with additional folate behaved in a similar manner to LP-exposed animals. Among day 20 gestation fetuses, it was apparent that both protein restriction and maternal folate supplementation could have adverse effects upon placental growth. Examination of methionine–homocysteine and folate cycle intermediates, tissue glutathione concentrations and expression of mRNA for methionine synthase, DNA methyltransferase 1 and methyltetrahydrofolate reductase revealed no gross disturbances of folate and one-carbon metabolism in either maternal or fetal tissue. The present findings indicated that any role for DNA methylation in programming of physiology is not related to major perturbations of folate metabolism, and is likely to be gene-specific rather than genome-wide.

Thyrotropin releasing hormone does not stimulate prolactin release in the preterm human fetus

1990 ◽  
Vol 122 (4) ◽  
pp. 462-466 ◽  
Author(s):  
Elio Roti ◽  
Eliana Gardini ◽  
Roberta Minelli ◽  
Lina Bianconi ◽  
Alessandro Alboni ◽  
...  
Keyword(s):  
Cord Blood ◽  
Maternal Blood ◽  
Inhibitory Effect ◽  
Maternal Serum ◽  
Fetal Life ◽  
Prolactin Release ◽  
Cord Blood Serum ◽  
Trh Stimulation ◽  
Saline Administration ◽  
Serum Tsh

Abstract. Previous studies have suggested that fetal PRL secretion does not respond to stimuli such as TRH, metoclopramide, and cimetidine. It was postulated that the lack of response to TRH could be due to the possibility that, in the term fetus, lactotropes secrete PRL maximally and would be unresponsive to further stimulation. In order to study this hypothesis, 200 μg TRH or saline were administered to preterm pregnant women in labor. Maternal blood was obtained before TRH and saline administration. Maternal and cord blood were obtained at parturition. PRL, TSH, T4 and T3 concentrations were measured in all sera. TRH administration induced a significant increase in maternal serum PRL, TSH and T3 concentrations. In the cord blood of newborns whose mothers received TRH, serum TSH, T4 and T3 concentrations were significantly higher than in cord blood of newborns whose mothers received saline. Cord blood serum PRL concentrations were unchanged after TRH administration. This latter finding suggests that fetal lactotropes do not respond to TRH in the preterm fetus. Desensitization of fetal PRL secreting cells to TRH stimulation and/or the inhibitory effect of elevated fetal circulating corticosteroids on TRH-induced PRL secretion may explain the absent PRL response to TRH during fetal life.

scholarly journals Critical periods and growth patterns from fetal life onwards associated with childhood insulin levels

Diabetologia ◽  
2016 ◽  
Vol 60 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Ellis Voerman ◽  
Vincent W. V. Jaddoe ◽  
Oscar H. Franco ◽  
Eric A. P. Steegers ◽  
Romy Gaillard
Keyword(s):  
Growth Patterns ◽  
Fetal Life ◽  
Critical Periods ◽  
Insulin Levels

scholarly journals Nutritional anaemia dysregulates endocrine control of fetal growth

2008 ◽  
Vol 100 (2) ◽  
pp. 408-417 ◽  
Author(s):  
S. Mahajan ◽  
R. Aalinkeel ◽  
P. Shah ◽  
S. Singh ◽  
N. Kochupillai
Keyword(s):  
Birth Weight ◽  
Maternal Blood ◽  
Severe Anaemia ◽  
Abdominal Circumference ◽  
Control Group ◽  
Critical Periods ◽  
Anthropometric Parameters ◽  
Endocrine Control ◽  
Anthropometric Measures ◽  
Fetal Origins

Severe anaemia is associated with increased low birth weight and Barker's hypothesis of ‘fetal origins’ proposes that a nutritional insult during critical periods of development results in adaptations that predispose individuals to adult onset diseases. We hypothesize that endocrine alterations may occur in the maternal–fetal milieu as a consequence of nutritional anaemia during pregnancy. We examined the quantitative variations in hormonal profiles in paired maternal and cord blood samples obtained from mothers and their neonates who were classified based on maternal anaemia status. Our results show that: (1) 74·6 % of the mothers enrolled in the study were anaemic, of which 85·2 % had moderate anaemia and 14·7 % had severe anaemia; (2) anthropometric parameters measured in the mothers indicate that severely anaemic mothers had a significantly low pre- and post-pregnancy weight, a significantly decreased maternal fundal height and abdominal circumference; (3) anthropometric measures in the neonates born to severely anaemic mothers show a significant reduction in ponderal index, birth weight and placental weight; (4) significant increase in both maternal, fetal insulin-like growth factor 1, ferritin levels and increased maternal erythropoietin levels were observed with an increase in severity of anaemia; (5) decreased T3and increased prolactin levels were observed in the maternal blood of severely anaemic mothers as compared with the control group. An insight into the endocrine modulation to overcome a growth disadvantage due to nutritional anaemia in pregnancy may lead to a better understanding of fetal adaptations invoked when the maternal-placental nutrient supply fails to meet the fetal nutrient demand.

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