Intrauterine nutrition: long-term consequences for vascular health

International Journal of Women’s Health Dovepress open access to scientific and medical research Review International Journal of Women's Health downloaded from https://www.dovepress.com/ by 88.198.20.149 on 06-Oct-2019 For personal use only. Open Access Full Text Article Intrauterine nutrition: long-term consequences for vascular health This article was published in the following Dove Press journal: International Journal of Women’s Health 11 July 2014 Number of times this article has been viewed Dorota Szostak-Wegierek Department of Human Nutrition, Medical University of Warsaw, Warsaw, Poland Video abstract Point your SmartPhone at the code above. If you have a QR code reader the video abstract will appear. Or use: http://dvpr.es/1pQuMbR Correspondence: Dorota SzostakWegierek Department of Human Nutrition, Medical University of Warsaw, Erazma Ciołka 27, 01-445 Warsaw, Poland Tel +48 608 675 995 Email dorota.szostak-wegierek@wum. edu.pl Introduction There is a growing body of evidence that improper intrauterine nutrition may negatively influence vascular health in later life. It concerns both undernutrition and overnutrition. Fetal undernutrition may result from maternal malnutrition or placental dysfunction that is often related to hypertensive disorders of pregnancy or poorly controlled maternal diabetes. The most common reasons for intrauterine overnutrition are maternal excessive nutrient intake and maternal diabetes. Imbalanced intrauterine nutrition seems to influence vascular health in the offspring by both an increase in their cardiometabolic risk factors and direct influence on vascular structure and function. Maternal malnutrition Inadequate birth weight is regarded as a surrogate measure of poor fetal nutritional status. It has been shown that maternal malnutrition, defined as prepregnancy 647 submit your manuscript | www.dovepress.com International Journal of Women’s Health 2014:6 647–656 Dovepress © 2014 Szostak-Wegierek. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php http://dx.doi.org/10.2147/IJWH.S48751 Powered by TCPDF (www.tcpdf.org) Abstract: There is a growing body of evidence that improper intrauterine nutrition may negatively influence vascular health in later life. Maternal malnutrition may result in intrauterine growth retardation and, in turn, metabolic disorders such as insulin resistance, diabetes, hypertension, and dyslipidemia, and also enhanced risk of atherosclerosis and cardiovascular death in the offspring. Energy and/or protein restriction is the most critical determinant for fetal programming. However, it has also been proposed that intrauterine n-3 fatty acid deficiency may be linked to later higher blood pressure levels and reduced insulin sensitivity. Moreover, it has been shown that inadequate supply of micronutrients such as folate, vitamin B12, vitamin A, iron, magnesium, zinc, and calcium may contribute to impaired vascular health in the progeny. In addition, hypertensive disorders of pregnancy that are linked to impaired placental blood flow and suboptimal fetal nutrition may also contribute to intrauterine growth retardation and aggravated cardiovascular risk in the offspring. On the other hand, maternal overnutrition, which often contributes to obesity and/or diabetes, may result in macrosomia and enhanced cardiometabolic risk in the offspring. Progeny of obese and/or diabetic mothers are relatively more prone to develop obesity, insulin resistance, diabetes, and hypertension. It was demonstrated that they may have permanently enhanced appetites. Their atheromatous lesions are usually more pronounced. It seems that, particularly, a maternal high-fat/junk food diet may be detrimental for vascular health in the offspring. Fetal exposure to excessive levels of saturated fatty and/or n-6 fatty acids, sucrose, fructose and salt, as well as a maternal high glycemic index diet, may also contribute to later enhanced cardiometabolic risk. Keywords: maternal malnutrition, intrauterine growth retardation, maternal overnutrition, macrosomia, adult cardiovascular disease International Journal of Women's Health downloaded from https://www.dovepress.com/ by 88.198.20.149 on 06-Oct-2019 For personal use only. Szostak-Wegierek u nderweight and/or insufficient body mass gain during gestation, may result in intrauterine growth retardation (IUGR).1 This was also confirmed in our study.2 Underweight women gave birth to significantly smaller babies than those whose body mass before pregnancy was normal or excessive. The mean birth weight of the offspring of undernourished mothers was about 300 g lower than that of the progeny of mothers with normal body mass and about 600 g lower than that of babies of overweight mothers. The mean birth weight of newborns of women who did not meet Institute of Medicine recommendations concerning weight gain during pregnancy was about 350 g lower than that of the offspring of mothers with adequate weight gain. In the last three decades many epidemiological studies have documented the association between fetal growth restriction and the prevalence of cardiovascular risk factors, hypertension, insulin resistance, type 2 diabetes, and cardiovascular deaths.3,4 In addition, it was shown that IUGR may be related to such vascular abnormalities as stiffness of abdominal aorta,5 reduced arterial compliance,6 narrower retinal arteriolar caliber,7 and endothelial dysfunction.8–11 Martyn et al12 demonstrated a strong inverse relationship between birth weight and the risk of carotid atherosclerosis in elderly subjects. Also, our investigation confirmed these observations.13 In 110 young males aged 27–32 years we found that those with a higher value of carotid intima media thickness (CIMT) (>0.6 mm versus [vs] 0.6 mm) were born with significantly lower birth weights (median 3,380 g vs 3525 g, P=0.001). This relationship was independent of classic risk factors and the presence of metabolic syndrome, which suggests that the association is more complex. In a recent study, IUGR fetuses demonstrated echocardiographic abnormalities that predicted postnatal hypertension and arterial remodeling already at the age of 6 months.14 The relationship between inadequate maternal diet and enhanced cardiovascular risk in the progeny has been documented in many studies. Subjects who were exposed to severe nutritional restriction during their intrauterine period of life at the time of the Dutch or (...truncated)