Maternal nutrition and later disease risk

2005 ◽  
pp. 17-27
Author(s):  
Jane Harding ◽  
Frank Bloomfield ◽  
Mark Oliver
2018 ◽  
Vol 9 (3) ◽  
pp. 253-259 ◽  
Author(s):  
M. Oyamada ◽  
A. Lim ◽  
R. Dixon ◽  
C. Wall ◽  
J. Bay

AbstractEvidence in support of the Developmental Origins of Health and Disease (DOHaD) hypothesis has reached the level where it can appropriately be used to inform practice. DOHaD informed interventions supporting primary noncommunicable disease risk reduction should target the pre- and periconceptional periods, pregnancy, lactation, childhood and adolescence. Such interventions are dependent on a health workforce (including dietitians, nurses, midwives, doctors, and nutrition teachers), that has a deep understanding of DOHaD concepts. This study assessed development of awareness of DOHaD concepts during undergraduate health professional training programs. Using a cross-sectional design, a standardized questionnaire was completed by Year 1–4 undergraduate students studying nutrition in Japan (n=309) and Year 1–3 nursing students in New Zealand (n=151). On entry to undergraduate study, most students had no awareness of the terms ‘DOHaD’ or ‘First 1000 Days’. While awareness reached 60% by Year 3 in courses that included DOHaD-related teaching, this remains inadequate. More than 95% of Year 1 undergraduates in both countries demonstrated an appreciation of associations between maternal nutrition and fetal health. However, awareness of associations between parental health status and/or nutritional environment and later-life health was low. While levels of awareness increased across program years, overall awareness was less than optimal. These results indicate evidence of some focus on DOHaD-related content in curricula. We argue that DOHaD principles should be one pillar around which health training curricula are built. This study indicates a need for the DOHaD community to engage with faculties in curriculum development.


2017 ◽  
Vol 70 (3) ◽  
pp. 191-200 ◽  
Author(s):  
Karen L. Lindsay ◽  
Claudia Buss ◽  
Pathik D. Wadhwa ◽  
Sonja Entringer

Background: Several studies about humans and animals have separately examined the effects of prenatal nutrition and stress on fetal development, pregnancy, and birth outcomes, and subsequent child health and disease risk. Although substantial evidence from non-pregnant literature supports the presence of bidirectional interactions between nutrition and stress at various psychological, behavioral, and physiological levels, such interaction effects have not yet been systematically examined in the context of pregnancy. Summary: This paper discusses the multifaceted and multilevel relationship between nutrition and stress. It then reviews the currently available observational and experimental evidence in animals and humans regarding the interplay between maternal psychosocial stress, dietary intake, and nutritional state during pregnancy, and implications for maternal and child health-related outcomes. Key Messages: During pregnancy, maternal psychosocial stress, dietary behavior, and nutritional state likely regulate and counter-regulate one another. Emerging evidence suggests that omega-3 fatty acids may attenuate maternal psychosocial stress, and that high maternal pre-pregnancy body mass index exacerbates unhealthy dietary behaviors under high-stress conditions. Longitudinal studies are warranted in order to understand the interplay between prenatal psychosocial stress, diet, and stress- and nutrition-related biomarkers to obtain further insight and inform the development and design of future, more effective intervention trials for improved maternal and child health outcomes.


2019 ◽  
Vol 11 (3) ◽  
pp. 222-227 ◽  
Author(s):  
Sally A. V. Draycott ◽  
Zoe Daniel ◽  
Raheela Khan ◽  
Beverly S. Muhlhausler ◽  
Matthew J. Elmes ◽  
...  

AbstractEvidence suggests that sub-optimal maternal nutrition has implications for the developing offspring. We have previously shown that exposure to a low-protein diet during gestation was associated with upregulation of genes associated with cholesterol transport and packaging within the placenta. This study aimed to elucidate the effect of altering maternal dietary linoleic acid (LA; omega-6) to alpha-linolenic acid (ALA; omega-6) ratios as well as total fat content on placental expression of genes associated with cholesterol transport. The potential for maternal body mass index (BMI) to be associated with expression of these genes in human placental samples was also evaluated. Placentas were collected from 24 Wistar rats at 20-day gestation (term = 21–22-day gestation) that had been fed one of four diets containing varying fatty acid compositions during pregnancy, and from 62 women at the time of delivery. Expression of 14 placental genes associated with cholesterol packaging and transfer was assessed in rodent and human samples by quantitative real time polymerase chain reaction. In rats, placental mRNA expression of ApoA2, ApoC2, Cubn, Fgg, Mttp and Ttr was significantly elevated (3–30 fold) in animals fed a high LA (36% fat) diet, suggesting increased cholesterol transport across the placenta in this group. In women, maternal BMI was associated with fewer inconsistent alterations in gene expression. In summary, sub-optimal maternal nutrition is associated with alterations in the expression of genes associated with cholesterol transport in a rat model. This may contribute to altered fetal development and potentially programme disease risk in later life. Further investigation of human placenta in response to specific dietary interventions is required.


2018 ◽  
Vol 76 (7) ◽  
pp. 497-511 ◽  
Author(s):  
Sarah E McKee ◽  
Teresa M Reyes

Abstract Pregnancy represents a critical period in fetal development, such that the prenatal environment can, in part, establish a lifelong trajectory of health or disease for the offspring. Poor nutrition (macro- or micronutrient deficiencies) can adversely affect brain development and significantly increase offspring risk for metabolic and neurological disease development. The concentration of dietary methyl-donor nutrients is known to alter DNA methylation in the brain, and alterations in DNA methylation can have long-lasting effects on gene expression and neuronal function. The decreased availability of methyl-donor nutrients to the developing fetus in models of poor maternal nutrition is one mechanism hypothesized to link maternal malnutrition and disease risk in offspring. Animal studies indicate that supplementation of both maternal and postnatal (early- and later-life) diets with methyl-donor nutrients can attenuate disease risk in offspring; however, clinical research is more equivocal. The objective of this review is to summarize how specific methyl-donor nutrient deficiencies and excesses during pre- and postnatal life alter neurodevelopment and cognition. Emphasis is placed on reviewing the current literature, highlighting challenges within nutrient supplementation research, and considering potential strategies to ensure robust findings in future studies.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1644
Author(s):  
Victoria Arija ◽  
Josefa Canals

The intrauterine environment and, specifically, the nutritional status of the mother are crucial factors that can have short and long-term consequences on the health and disease risk of an unborn child [...]


2009 ◽  
Vol 87 (3) ◽  
pp. 161-179 ◽  
Author(s):  
Caroline Le Clair ◽  
Tina Abbi ◽  
Heather Sandhu ◽  
Paramjit S. Tappia

Epidemiological, clinical, and experimental observations have led to the hypothesis that the risk of developing chronic diseases in adulthood is influenced not only by genetic and adult lifestyle factors, but also by environmental factors during early life. Low birth weight, a marker of intrauterine stress, has been linked to predisposition to cardiovascular disease (CVD) and diabetes. The compelling animal evidence and significant human data to support this conclusion are reviewed. Specifically, the review discusses the role of maternal nutrition before and during pregnancy, placental insufficiencies and epigenetic changes in the increased predisposition to diabetes and CVD in adult life. The impact of low birth weight and catch-up growth as they pertain to risk of disease in adult life is also discussed. In addition, adult disease risk in the overnourished fetus is also mentioned. Reference is made to some of the mechanisms of the induction of diabetes and CVD phenotype. It is proposed that fetal nutrition, growth and development through efficient maternal nutrition before and during pregnancy could constitute the basis for nutritional strategies for the primary prevention of diabetes and CVD.


Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2678
Author(s):  
Nahal Habibi ◽  
Jessica A. Grieger ◽  
Tina Bianco-Miotto

A healthy pregnancy is important for the growth and development of a baby. An adverse pregnancy outcome is associated with increased chronic disease risk for the mother and offspring. An optimal diet both before and during pregnancy is essential to support the health of the mother and offspring. A key mediator of the effect of maternal nutrition factors on pregnancy outcomes is the placenta. Complicated pregnancies are characterized by increased oxidative stress in the placenta. Selenium and iodine are micronutrients that are involved in oxidative stress in placental cells. To date, there has been no comprehensive review investigating the potential synergistic effect of iodine and selenium in the placenta and how maternal deficiencies may be associated with increased oxidative stress and hence adverse pregnancy outcomes. We undertook a hypothesis-generating review on selenium and iodine, to look at how they may relate to pregnancy complications through oxidative stress. We propose how they may work together to impact pregnancy and placental health and explore how deficiencies in these micronutrients during pregnancy may impact the future health of offspring.


2015 ◽  
Vol 6 (5) ◽  
pp. 415-424 ◽  
Author(s):  
A. J. Kermack ◽  
B. B. Van Rijn ◽  
F. D. Houghton ◽  
P. C. Calder ◽  
I. T. Cameron ◽  
...  

The recognition of ‘fetal origins of adult disease’ has placed new responsibilities on the obstetrician, as antenatal care is no longer simply about ensuring good perinatal outcomes, but also needs to plan for optimal long-term health for mother and baby. Recently, it has become clear that the intrauterine environment has a broad and long-lasting impact, influencing fetal and childhood growth and development as well as future cardiovascular health, non-communicable disease risk and fertility. This article looks specifically at the importance of the developmental origins of ovarian reserve and ageing, the role of the placenta and maternal nutrition before and during pregnancy. It also reviews recent insights in developmental medicine of relevance to the obstetrician, and outlines emerging evidence supporting a proactive clinical approach to optimizing periconceptional as well as antenatal care aimed to protect newborns against long-term disease susceptibility.


2004 ◽  
Vol 91 (3) ◽  
pp. 459-468 ◽  
Author(s):  
Rachel R. Huxley ◽  
H. Andrew W. Neil

The fetal-origins hypothesis suggests that maternal and fetal nutrition can have a profound and sustained impact on the health of the offspring in adult life. Although there is abundant literature reporting on the associations between birth weight and disease risk factors, only a handful of studies have been able to examine the relationship between maternal nutrition in pregnancy with the health of offspring in adult life directly. Between 1942 and 1944, nearly 400 pregnant women were recruited into a dietary study to determine whether the wartime dietary rations were sufficient to prevent nutritional deficiencies. Detailed biochemical and clinical assessments were conducted for each of the women, who were followed-up until after delivery. More than 50 years later, approximately one-quarter of the adult offspring were recruited into a study to explore the possible impact of maternal nutrition in pregnancy on CHD risk factors, including glucose tolerance, blood pressure and components of the lipid profile. Results from the present study provide no evidence to support the hypothesis that birth weight or maternal nutrition in pregnancy are associated with CHD risk factors in adult life.


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