Intrauterine Programming of Cardiovascular Disease by Maternal Nutritional Status

Institute of Human Nutrition, University of Southampton, United Kingdom.
Nutrition (Impact Factor: 2.93). 02/1998; 14(1):39-47. DOI: 10.1016/S0899-9007(97)00391-2
Source: PubMed


The origins of cardiovascular disease are related to genetic factors, postnatal environmental and behavioral influences, and also the environment experienced in utero. Patterns of disproportionate fetal growth consistent with maternal undernutrition appear to be predictive of later hypertension and coronary heart disease. These findings from epidemiologic studies are strongly supported by animal studies. Experimental models are suggestive of a role for glucocorticoid hormones in the intrauterine programming of cardiovascular function. New understanding of the relationships between maternal diet and the development and maturation of fetal tissues may enable prevention of cardiovascular disease by intervention in early life.

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Available from: David S Gardner, Aug 14, 2014
    • "For two decades it has been recognised in animal studies that exposure to excessive glucocorticoid levels in utero, by bypassing or overwhelming placental 11b-HSD2, causes short-term effects such as foetal growth restriction and long-term effects that include increased risk of cardiovascular disease when the offspring reach adulthood (Benediktsson et al. 1993, Nyirenda et al. 1998). Maternal nutritional restriction, which prematurely activates the foetal HPA axis (Cottrell et al. 2012), also increases foetal glucocorticoid levels and 'programmes' greater risk of cardiovascular disease once adult (Langley-Evans et al. 1998, Roseboom et al. 2001), as does maternal stress, probably through increased maternal glucocorticoid levels (Seckl & Holmes 2007, Bingham et al. 2013). Glucocorticoid and/or nutritional programming of adult disease has been extensively reviewed (for recent reviews see Seckl & Holmes (2007), Langley-Evans (2013) and Reynolds (2013)). "

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    • "There are several studies relating the gestational environment to the late effects on the body composition of animals, evidencing this phase as a critical period for the genesis of diseases. These studies support the concept of "fetal programming", which suggests that, during intrauterine development, the fetus may be programmed to develop diseases during adulthood [2,3]. According to this paradigm, the susceptibility to diseases (including reproductive diseases and dysfunctions) is influenced by diet, environmental exposure to toxic agents and stress during the fetal and neonatal periods [4]. "
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    ABSTRACT: Recent studies have supported the concept of "fetal programming" which suggests that during the intrauterine development the fetus may be programmed to develop diseases in adulthood. The possible effects of in utero protein restriction on sexual development of rat male offspring were evaluated in the present study. Pregnant Wistar rats were divided into two experimental groups: one group treated with standard chow (SC, n = 8, 17% protein) and the other group treated with hypoproteic chow (HC, n = 10, 6% protein) throughout gestation. After gestation the two experimental groups received standard chow. To evaluate the possible late reproductive effects of in utero protein restriction, the male offspring of both groups were assessed at different phases of sexual development: prepubertal (30 days old); peripubertal (60 days old); adult (90 days old). Student's t-test and Mann-Whitney test were utilized. Differences were considered significant when p < 0.05. We found that in utero protein restriction reduced the body weight of male pups on the first postnatal day and during the different sexual development phases (prepubertal, peripubertal and adult). During adulthood, Sertoli cell number, sperm motility and sperm counts in the testis and epididymal cauda were also reduced in HC. Furthermore, the numbers of sperm presenting morphological abnormalities and cytoplasmic drop retention were higher in HC. In conclusion, in utero protein restriction, under these experimental conditions, causes growth delay and alters male reproductive-system programming in rats, suggesting impairment of sperm quality in adulthood.
    Full-text · Article · Jun 2011 · Reproductive Biology and Endocrinology
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    • "The altered in vitro vascular responses reported by Holemans et al. (1999) would appear to oppose one another, in that NO would increase vascular resistance whilst bradykinin promotes vasodilatation. This illustrates the previously-observed point that just as the dietary stimuli that programme hypertension are varied, there are a number of different hormonal mechanisms operating in fetal life which appear to promote adult disease (Langley-Evans et al. 1998). With regard to the development of hypertension, intra-uterine environment-induced alterations to these responses may require further postnatal influences to elicit significant and permanent elevations of blood pressure. "

    Full-text · Article · Feb 1999 · British Journal Of Nutrition
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