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• W2103802743 abstract "HomeCirculationVol. 117, No. 3Impaired Fetal Growth, Cardiovascular Disease, and the Need to Move on Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBImpaired Fetal Growth, Cardiovascular Disease, and the Need to Move on Wulf Palinski, MD and Claudio Napoli, MD, PhD, MBEth Wulf PalinskiWulf Palinski From the Department of Medicine, University of California San Diego, La Jolla (W.P.), and the Department of General Pathology and Excellence Research Center on Cardiovascular Diseases, 1st School of Medicine, II University of Naples, Naples, Italy (C.N.). Search for more papers by this author and Claudio NapoliClaudio Napoli From the Department of Medicine, University of California San Diego, La Jolla (W.P.), and the Department of General Pathology and Excellence Research Center on Cardiovascular Diseases, 1st School of Medicine, II University of Naples, Naples, Italy (C.N.). Search for more papers by this author Originally published22 Jan 2008https://doi.org/10.1161/CIRCULATIONAHA.107.750133Circulation. 2008;117:341–343The final step in the acceptance of a new medical hypothesis is often the approval of significant funding to investigate it. In the case of developmental programming (ie, the notion that the in utero environment determines susceptibility to many diseases later in life), this has recently come in the form of support by the US Congress for the National Children’s Study, a $3 billion project to follow the impact of environmental factors before, during, and after pregnancy on disease manifestation in some 100 000 children up to the age of 25 years.1 This initiative will, no doubt, yield a wealth of correlative data and identify many new factors potentially affecting developmental programming.Article p 405Much of the concept underlying the National Children’s Study stems from the pioneering work of Barker and colleagues,2 whose epidemiological observation of increased cardiovascular risk in children with low birth weight has spurred a large number of retrospective studies during the past 30 years. Despite some conflicting results, most of these studies support the notion that reduced birth weight is indeed associated with increased hypertension, diabetes mellitus, and cardiovascular disease. However, the strong correlation between birth weight and duration of gestation, plus the fact that a short gestation also may be associated with cardiovascular risk,3 poses the question to what extent low birth weight is truly responsible. In this issue of Circulation, an article by Kaijser and coworkers4 at the Karolinska Institute in Stockholm provides a convincing answer. By scanning 250 000 records of birth at 4 major delivery units in Sweden between 1925 and 1949, they identified a cohort of 6437 subjects, which included 2937 children born preterm (<37 weeks of gestation) and 2181 with a birth weight <2000 g for girls or <2100 g for boys. During the follow-up period (1987 to 2002), 617 of these subjects were treated for or died of ischemic heart disease. Statistical analysis of these prospectively collected data indicated a strong negative correlation between birth weight adjusted for gestational duration and ischemic heart disease (P=0.002). Similarly, fetal growth (expressed as SD from the mean weight for gestational age indicated by fetal growth curves) was strongly associated with cardiovascular risk. In contrast, gestational duration adjusted for birth weight showed a positive association with risk (ie, children born before the 37th week had lower risk than term or postterm children, provided that they were not growth retarded). These results are consistent with those of previous, more limited studies and clearly indicate that the increased risk of coronary heart disease is associated with fetal growth restriction rather than premature birth, at least in subjects born before the advent of modern care for very premature births.The Barker postulate—that impaired in utero growth is associated with increased cardiovascular risk later in life—can therefore be considered proven. But what has it taught us about the underlying pathogenic mechanisms, and what are its translational benefits? Ah, there’s the rub, for we ignore not only the pathogenic mechanisms of fetal programming but also its evolutionary significance, if any. It has been proposed that developmental programming constitutes an attempt by the fetus to prospectively adapt to detrimental conditions in utero such as undernutrition. Such “predictive adaptive programming” would be protective if the same conditions are encountered after birth but constitute a misadaptation to the conditions of excessive caloric and fat consumption prevalent in most Western countries.5 It would also be difficult to correct after birth. Although many early indicators of cardiovascular risk encountered in childhood correlate with adult risk such as endothelial dysfunction and early atherosclerotic lesions6 and therefore constitute promising targets for intervention, compensating for low birth weight does not appear to be beneficial. In fact, accelerated growth during childhood seems to increase, not decrease, long-term risk,7 in particular in prematurely born children, in whom rapid early weight gain enhances insulin resistance and hypertension later in life.8 Thus, it appears that until the mechanisms of programming are better understood, little can be done after birth to reduce the effect of pathogenic in utero programming, except for a more rigorous avoidance of conventional cardiovascular risk factors. At least the need for earlier and more aggressive treatment of high-risk children is now beginning to be recognized in the latest guidelines.9The focus on outcome parameters such as low birth weight or impaired fetal growth also has not been helpful in identifying specific maternal risk factors responsible for developmental programming. Low birth weight may result from a broad range of pathogenetically diverse maternal conditions, including mechanical obstructions of the uterine artery, severe maternal undernutrition or dysnutrition, corticosteroid treatment, and a number of metabolic diseases, most notably diabetes.10 It appears unlikely that these conditions would cause uniform pathogenic programming. Indeed, maternal diabetes may result not only in reduced birth weight but more frequently in macrosomia. Even if the maternal conditions were to influence birth weight in a consistent manner, sibling competition leads to wide disparities in birth weight, complicating the search for the factors responsible for developmental programming and enhanced disease susceptibility in offspring. Finally, it is now well recognized that maternal overnutrition, not undernutrition, will be the main health threat in the coming decades. The call to shift the emphasis away from birth weight and to focus on specific maternal risk factors and outcome parameters contributing to cardiovascular disease is therefore growing louder.11 We also should keep in mind that correlative epidemiological studies cannot establish causal relationships. Now that the influence of developmental programming has been established beyond doubt and the translational need is becoming more urgent, we need to go beyond epidemiology and put greater emphasis on experimental models suitable to investigate the mechanisms and causal relationships.In contrast to animal models of low birth weight, which have yielded inconsistent results, much progress has been made recently in modeling some maternal conditions enhancing atherogenesis in human progeny such as maternal hypercholesterolemia.12,13 It has been established experimentally that maternal hypercholesterolemia and the ensuing increased oxidative stress not only accelerate atherosclerosis, as they do in humans,14,15 but also that they affect early predictors of cardiovascular disease in offspring such as arterial gene expression, endothelial function, and vascular reactivity.14–17 More important, multiple interventions in mothers have been shown to reduce or prevent this form of developmental programming.18,19 Programming by pregestational or gestational diabetes is more difficult to mimic, given the complexity of metabolic changes involved, and work on the role of maternal obesity and insulin resistance is only in its infancy. Increased inflammatory stress associated with these conditions, as well as with maternal hypercholesterolemia18,19 and smoking,20 is likely to be of central importance, as are immune mechanisms.5 Even mild inflammation may modulate immune responses in both the mother and fetus. In fact, evidence in animal models and humans indicates that maternal adaptive immunity programs B- or T-cell–dependent IgM responses in offspring.19,21 Similar programming of offspring IgA by maternal exposure to allergens also has been reported, but in contrast to allergic responses, an enhancement of postnatal immune defenses against cardiovascular, diabetic, or infectious antigens would be desirable, and maternal immunizations have already been shown to protect against postnatal atherogenesis, even in the absence of gestational hypercholesterolemia or hyperglycemia.19In addressing causal relationships, mechanisms, and preventive measures in experimental models, it is important to remember that maternal risk factors are not necessarily the same as those affecting the fetus. In addition to factors crossing the placental barrier by passive diffusion or active transport mechanisms (eg, maternal cholesterol), the placenta is both the target and a source of pathogenic factors reaching the fetus (the Figure). It can, for example, protect against or contribute to fetal oxidative stress induced by maternal hypercholesterolemia and/or vascular inflammation.22 The mechanisms shielding the placenta from recognition by the maternal immune system also may play a role in mediating inflammatory stress from mother to fetus. Another issue to be considered is the extent to which in utero programming is continued in the immediate postnatal period or during childhood. In humans, drastic changes in diet or exposure to environmental risk factors at birth are unlikely. We will therefore have to treat in utero programming, effects of lactation, and early postnatal programming as a single pathogenic entity. Download figureDownload PowerPointFigure. Developmental programming of cardiovascular disease. Note that many of the maternal conditions and pathogenic factors are still hypothetical.The National Children’s Study will investigate some of the maternal conditions thought to enhance cardiovascular risk in offspring, in particular maternal diabetic conditions, oxidative stress, and inflammation, but it will focus on outcomes that are most prevalent in childhood such as diabetes mellitus, not on cardiovascular risk, which can only be extrapolated from the early consequences of developmental programming (the Figure).23 Even under the most optimistic conditions, it will not be feasible to carry out large-scale clinical trials for each putative maternal risk factor and to extend them to the onset of clinical manifestations. The contribution of the Barker hypothesis and the extensive epidemiological work validating it has been to prove, in principle, that developmental programming matters for cardiovascular disease. It is now time to complement human epidemiology by studies focusing on intervention and mechanistic studies in experimental models. This should enable us not only to elucidate the in utero programming mechanisms but also to identify potential new targets for prevention that go beyond the standard advice to treat preexisting maternal conditions. After all, interventions targeting developmental programming are most appealing because they may yield lifelong benefits yet involve very little risk for the fetus when effected before pregnancy.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Sources of FundingWe thank the National Institutes of Health for grant HL-067792 (Fetal Determinants of Atherosclerosis), the Ellison Medical Foundation for a Senior Investigator award (Dr Palinski), and the Fondation Jerome Lejeune (Dr Napoli).DisclosuresNone.FootnotesCorrespondence to Wulf Palinski, University of California San Diego, Department of Medicine, 0682, 9500 Gilman Dr, La Jolla, CA 92093–0682. E-mail [email protected] References 1 National Children’s Study. Available at: http://www.nationalchildrenstudy.gov. Accessed December 17, 2007.Google Scholar2 Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet. 1989; 2: 577–580.CrossrefMedlineGoogle Scholar3 Johansson S, Iliadou A, Bergvall N, Tuvemo T, Norman M, Cnattingius S. Risk of high blood pressure among young men increases with the degree of immaturity at birth. Circulation. 2005; 112: 3430–3436.LinkGoogle Scholar4 Kaijser M, Bonamy AE, Akre O, Cnattingius S, Granath F, Norman M, Ekbom A. Perinatal risk factors for ischemic heart disease: disentangling the roles of birth weight and preterm birth. Circulation. 2007; 117: 405–410.Google Scholar5 Gluckman PD, Hanson MA. Living with the past: evolution, development, and patterns of disease. Science. 2004; 305: 1733–1736.CrossrefMedlineGoogle Scholar6 McMahan CA, Gidding SS, Malcom GT, Tracy RE, Strong JP, McGill HC Jr. Pathobiological determinants of atherosclerosis in youth risk scores are associated with early and advanced atherosclerosis. Pediatrics. 2006; 118: 1447–1455.CrossrefMedlineGoogle Scholar7 Barker DJ, Osmond C, Forsen TJ, Kajantie E, Eriksson JG. Trajectories of growth among children who have coronary events as adults. N Engl J Med. 2005; 353: 1802–1809.CrossrefMedlineGoogle Scholar8 Stettler N, Stallings VA, Troxel AB, Zhao J, Schinnar R, Nelson SE, Ziegler EE, Strom BL. Weight gain in the first week of life and overweight in adulthood: a cohort study of European American subjects fed infant formula. Circulation. 2005; 111: 1897–1903.LinkGoogle Scholar9 McCrindle BW, Urbina EM, Dennison BA, Jacobson MS, Steinberger J, Rocchini AP, Hayman LL, Daniels SR. Drug therapy of high-risk lipid abnormalities in children and adolescents: a scientific statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in Youth Committee, Council of Cardiovascular Disease in the Young, with the Council on Cardiovascular Nursing. Circulation. 2007; 115: 1948–1967.LinkGoogle Scholar10 Curhan GC, Willett WC, Rimm EB, Spiegelman D, Ascherio AL, Stampfer MJ. Birth weight and adult hypertension, diabetes mellitus, and obesity in US men. Circulation. 1996; 94: 3246–3250.CrossrefMedlineGoogle Scholar11 Gillman MW. Developmental origins of health and disease. N Engl J Med. 2005; 353: 1848–1850.CrossrefMedlineGoogle Scholar12 Napoli C, Palinski W. Maternal hypercholesterolemia during pregnancy influences the later development of atherosclerosis: clinical and pathogenic implications. Eur Heart J. 2001; 22: 4–9.CrossrefMedlineGoogle Scholar13 Palinski W, Napoli C. The fetal origins of atherosclerosis: maternal hypercholesterolemia, and cholesterol-lowering or antioxidant treatment during pregnancy influence in utero programming and postnatal susceptibility to atherogenesis. FASEB J. 2002; 16: 1348–1360.CrossrefMedlineGoogle Scholar14 Napoli C, D’Armiento FP, Mancini FP, Postiglione A, Witztum JL, Palumbo G, Palinski W. Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholesterolemia: intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions. J Clin Invest. 1997; 100: 2680–2690.CrossrefMedlineGoogle Scholar15 Napoli C, Glass CK, Witztum JL, Deutsch R, D’Armiento FP, Palinski W. Influence of maternal hypercholesterolaemia during pregnancy on progression of early atherosclerotic lesions in childhood: Fate of Early Lesions in Children (FELIC) study. Lancet. 1999; 354: 1234–1241.CrossrefMedlineGoogle Scholar16 Napoli C, de Nigris F, Welch JS, Calara FB, Stuart RO, Glass CK, Palinski W. Maternal hypercholesterolemia during pregnancy promotes early atherogenesis in LDL receptor–deficient mice and alters aortic gene expression determined by microarray. Circulation. 2002; 105: 1360–1367.CrossrefMedlineGoogle Scholar17 Khan I, Dekou V, Hanson M, Poston L, Taylor P. Predictive adaptive responses to maternal high-fat diet prevent endothelial dysfunction but not hypertension in adult rat offspring. Circulation. 2004; 110: 1097–1102.LinkGoogle Scholar18 Palinski W, D’Armiento FP, Witztum JL, de Nigris F, Casanada F, Condorelli M, Silvestre M, Napoli C. Maternal hypercholesterolemia and treatment during pregnancy influence the long-term progression of atherosclerosis in offspring of rabbits. Circ Res. 2001; 89: 991–996.CrossrefMedlineGoogle Scholar19 Yamashita T, Freigang S, Eberle C, Pattison J, Gupta S, Napoli C, Palinski W. Maternal immunization programs postnatal immune responses and reduces atherosclerosis in offspring. Circ Res. 2006; 99: E51–E64.LinkGoogle Scholar20 Yang Z, Knight CA, Mamerow MM, Vickers K, Penn A, Postlethwait EM, Ballinger SW. Prenatal environmental tobacco smoke exposure promotes adult atherogenesis and mitochondrial damage in apolipoprotein E−/− mice fed a chow diet. Circulation. 2004; 110: 3715–3720.LinkGoogle Scholar21 Rastogi D, Wang C, Mao X, Lendor C, Rothman PB, Miller RL. Antigen-specific immune responses to influenza vaccine in utero. J Clin Invest. 2007; 117: 1637–1646.CrossrefMedlineGoogle Scholar22 Liguori A, D’Armiento FP, Palagiano A, Balestrieri ML, Williams-Ignarro S, de Nigris F, Lerman LO, D’Amora M, Rienzo M, Fiorito C, Ignarro LJ, Palinski W, Napoli C. Effect of gestational hypercholesterolaemia on omental vasoreactivity, placental enzyme activity and transplacental passage of normal and oxidised fatty acids. BJOG. 2007; 114: 1547–1556.CrossrefMedlineGoogle Scholar23 Charakida M, Deanfield JE, Halcox JP. Childhood origins of arterial disease. Curr Opin Pediatr. 2007; 19: 538–545.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Pedersen J, Mortensen E, Meincke R, Petersen G, Budtz-Jørgensen E, Brunnsgaard H, Sørensen H and Lund R (2019) Maternal infections during pregnancy and offspring midlife inflammation, Maternal Health, Neonatology and Perinatology, 10.1186/s40748-019-0099-3, 5:1, Online publication date: 1-Dec-2019. Crispi F and Gratacós E (2018) Fetal Cardiac Function in Fetal Growth Restriction Placental-Fetal Growth Restriction, 10.1017/9781316181898.020, (164-177) Bhatnagar A (2017) Environmental Determinants of Cardiovascular Disease, Circulation Research, 121:2, (162-180), Online publication date: 7-Jul-2017. 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