Birth weight and cardiovascular risk factors in a cohort followed until 80 years of age: the study of men born in 1913

Eriksson, Margaretha; Wallander, Mari‐Ann; Krakau, Ingvar; Wedel, Hans; Svärdsudd, Kurt

doi:10.1046/j.1365-2796.2003.01289.x

Cited by 56 publications

(43 citation statements)

References 55 publications

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“…However, in macrosomic newborns of nondiabetic and nonobese mothers, serum lipid and apolipoprotein values did not differ significantly from those in AGA newborns (8,11). A population study in Uppsala, Sweden, of adult men showed a significantly positive correlation between birth weight and HDL cholesterol levels when adjusted for BMI (27). A study in 8-year-old Indian children also demonstrated a trend for rising HDL cholesterol concentrations with increasing birth weight, which was not, however, statistically significant (28).…”

Section: Results -The Mean (ϯSd) Anthropometric Indexes Of the 37mentioning

confidence: 87%

Lipid Profile, Glucose Homeostasis, Blood Pressure, and Obesity-Anthropometric Markers in Macrosomic Offspring of Nondiabetic Mothers

et al. 2006

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OBJECTIVE -The study was to determine whether being the macrosomic offspring of a mother without detected glucose intolerance during pregnancy has an impact on lipid profile, glucose homeostasis, and blood pressure during childhood.RESEARCH DESIGN AND METHODS -Plasma total, HDL, and LDL cholesterol; triglycerides; apolipoprotein (Apo) A-1, -B, and -E; lipoprotein (a); fasting glucose and insulin; homeostasis model assessment of insulin resistance (HOMA-IR) index; blood pressure; BMI; and detailed anthropometry were evaluated in 85 children aged 3-10 years old, born appropriate for gestational age (AGA; n ϭ 48) and large for gestational age (LGA; n ϭ 37) of healthy mothers.RESULTS -At the time of the assessment, body weight, height, skinfold thickness, BMI, waist circumference, and blood pressure did not differ between the LGA and AGA groups with the exception of head circumference (P Ͻ 0.01). There were no significant differences in plasma total or LDL cholesterol; triglycerides; Apo A-1, -B, or -E; lipoprotein (a); Apo B-to-Apo A-1 ratio; or glucose levels between the groups. The LGA group had significantly higher HDL cholesterol levels (P Ͻ 0.01), fasting insulin levels (P Ͻ 0.01), and HOMA-IR index (P Ͻ 0.01) but lower values of the glucose-to-insulin ratio (P Ͻ 0.01) as compared with the AGA group. CONCLUSIONS -Children bornLGA of mothers without confirmed impaired glucose tolerance during pregnancy show higher insulin concentrations than AGAs. Diabetes Care 29:1197-1201, 2006F etal growth is a complex process involving the interaction of mother, placenta, and fetus (1). Growth and development of the fetus depends upon nutrients such as glucose, lipids, and amino acids (1). Genetic factors, in addition to the maternal and fetal status, are reported to play a role (1,2). Epidemiological, clinical, and experimental findings indicate that gestational diabetes mellitus (GDM), as well as maternal obesity or excessive weight gain during pregnancy, are significant risk factors for fetal overnutrition and macrosomia (1,2). Maternal hyperglycemia leads to fetal hyperglycemia, which in turn stimulates pancreatic islet cells and causes hyperinsulinemia (2,3). This intrauterine hyperinsulinemic state results in increased amounts of fat tissue, liver glycogen content, and total body size (2,3). Macrosomic infants of diabetic mothers are prone to glucose intolerance, obesity, and diabetes during childhood and adulthood (2,4 -6). Disturbances not only in the metabolism of carbohydrates but also in lipids observed at birth in newborns of diabetic mothers may influence the metabolic profile later in life (2,5,7-10).There is limited data regarding the metabolic profile of macrosomic offspring of healthy mothers. Moreover, these studies refer to neonatal or infantile agegroups and pay only restricted attention to childhood (8,11,12). It is important to determine whether being the macrosomic offspring of a mother without detected glucose intolerance during pregnancy has an impact on the lipid profile, insulin secretion, and glu...

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Section: Results -The Mean (ϯSd) Anthropometric Indexes Of the 37mentioning

confidence: 87%

Lipid Profile, Glucose Homeostasis, Blood Pressure, and Obesity-Anthropometric Markers in Macrosomic Offspring of Nondiabetic Mothers

et al. 2006

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“…This led to hypothesis that maternal conditions in the prenatal period might have an important impact on the emergence of later vascular disease, and to the use of size at birth as a proxy for prenatal conditions (Barker, Osmond, Golding, Kuh, and Wadsworth, 1989). The relationship between size or relative thinness at birth and the risk of a group of chronic diseases including heart and vascular diseases, adult-onset diabetes, and the cluster of conditions known as the "metabolic syndrome" has since been observed in numerous different populations (Barker, 1995;Eriksson, Forsen, Tuomilehto, Osmond, and Barker, 2000;Eriksson, Wallander, Krakau, Wedel, and Svardsudd, 2004;IsmailBeigi, Catalano, and Hanson, 2006;Rich-Edwards et al, 1999;Rich-Edwards et al, 2005). The effect of birth size is not simply a confounded effect of postnatal conditions, but it does interact with them to influence chronic disease outcomes.…”

Section: Fetal Programming In Human Epidemiologymentioning

confidence: 99%

Fetal programming and fetal psychology

Ellison

2010

Infant and Child Development

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The introduction of the "fetal programming hypothesis," first in epidemiology, subsequently in a broad range of disciplines concerned with developmental biology, has generated new interest in phenotypic plasticity, the mechanisms that govern it, and its place in evolutionary biology. A number of epidemiological studies link small size at birth, assumed to be a consequence of constrained prenatal energy availability, with adverse effects on the risk of chronic diseases later in life. The cluster of chronic diseases associated with the metabolic syndrome and alterations of glucose metabolism are particularly implicated. Recent evidence suggests that epigenetic modification of gene expression affecting the hypothalamic-pituitary-adrenal (HPA) axis may be involved in these effects. In animal studies epigenetic alteration of HPA axis activity and responsiveness is associated with changes in adult behavior and stress responsiveness.The potential for similar effects to contribute to psychological and psychiatric outcomes has been explored in a number of contexts, including famine exposure, observed covariance with birth weight, and prenatal dexamethasone treatment of fetuses at risk of congenital adrenal hyperplasia. While fetal programming effects have now been widely demonstrated across species and human populations, the adaptive significance of these effects is still a matter of debate.Life is integrated, cumulative, and continuous, not episodic, static, or discrete.Behavioral scientists rarely forget this, but biologists often do. Developmental biology is the one domain of the life sciences where the organism as a progressively unfolding phenomenon is a central concept. The reemergence of developmental biology as a vigorous discipline, intersecting in important ways with genetics (Badayev, 2008), evolution (West-Eberhard, 2003), and epidemiology (Barker, 1994;Gluckman and Hanson, 2006;Kuh, Ben-Shlomo, Lynch, Hallqvist, and Power, 2003), has injected new energy and new ideas into all those fields. Within epidemiology a seminal impact of this new attention to developmental biology has been in the formulation of the "fetal programming hypothesis," also known as the "fetal origins hypothesis," or, more generally, as the "developmental origins of health and disease" (DOHaD). Simply put, this hypothesis suggests that conditions very early in development, even in utero, can leave lasting imprints of an organism's physiology, imprints that may affect susceptibility to diseases with onsets that may occur many decades later (Barker, Eriksson, Forsen, and Osmond, 2002;.The concept of fetal programming is, of course, not new. Behavioral endocrinologists and neuroscientists, for example, have long recognized "organizational effects" of prenatal androgen hormones in "programming" certain aspects of reproductive axis function and reproductive behavior that emerges later in an animal's life (Nelson, 2005). "Critical periods" in development, including fetal development, are familiar

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“…Caloric supplementation of pregnant women, as well as folic acid and iron supplements, reduced the incidence of low birth weight (22,28,30), whereas a diet rich in vegetables and fruits (important sources of folate, carotenoids, and antioxidants) was strongly associated with increased birth weight in rural India (122). Risk factors for cardiovascular disease, such as smoking, diet, a sedentary lifestyle, social status, and alcohol consumption, do not affect the relationship between low birth weight and cardiovascular disease (44,63,79,123). The most frequently studied association is between low birth weight (or IUGR) and hypertension (68,88).…”

Section: The Barker Hypothesismentioning

confidence: 99%

Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon

Racasan¹,

Braam²,

Koomans³

et al. 2005

American Journal of Physiology-Renal Physiology

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Racasan, Simona, Branko Braam, Hein A. Koomans, and Jaap A. Joles. Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon. Am J Physiol Renal Physiol 288: F626 -F636, 2005. First published November 16, 2004 doi:10.1152/ ajprenal.00314.2004.-The "programming hypothesis" proposes that an adverse perinatal milieu leads to adaptation that translates into cardiovascular disease in adulthood. The balance between nitric oxide (NO) and reactive oxygen species (ROS) is disturbed in cardiovascular diseases, including hypertension. Conceivably, this balance is also disturbed in pregnancy, altering the fetal environment; however, effects of perinatal manipulation of NO and ROS on adult blood pressure (BP) are unknown. In spontaneously hypertensive rats (SHR), NO availability is decreased and ROS are increased compared with normotensive Wistar-Kyoto rats, and, despite the genetic predisposition, the perinatal environment can modulate adult BP. Our hypothesis is that a disturbed NO-ROS balance in the SHR dam persistently affects BP in her offspring. Dietary supplements, which support NO formation and scavenge ROS, administered during pregnancy and lactation resulted in persistently lower BP for up to 48 wk in SHR offspring. The NO donor molsidomine and the superoxide dismutase mimic tempol-induced comparable effects. Specific inhibition of inducible nitric oxide synthase (NOS) reduces BP in adult SHR, suggesting that inducible NOS is predominantly a source of ROS in SHR. Indeed, inducible NOS inhibition in SHR dams persistently reduced BP in adult offspring. Persistent reductions in BP were accompanied by prevention of proteinuria in aged SHR. We propose that in SHR the known increase in ANG II type 1 receptor density during development leads to superoxide production, which enhances inducible NOS activity. The relative shortage of substrate and cofactors leads to uncoupling of inducible NOS, resulting in superoxide production, activating transcription factors that subsequently again increase inducible NOS expression. This vicious circle probably is perpetuated into adult life. spontaneously hypertensive rat; nitric oxide; inducible nitric oxide synthase; molsidomine; tempol; proteinuria THERE IS NOW A LARGE BODY of epidemiological data proving that environmental factors acting early in life, in particular in the intrauterine and postnatal period, correlate with chronic cardiovascular diseases. From these observations, Barker (10) developed the "programming hypothesis," which proposes that fetal adaptation to adverse environmental factors in the perinatal period results in permanent structural and physiological changes that manifest as disease in adult life. As such, fetal programming is a form of phenotypic plasticity (10), which has conveyed an evolutionary advantage in the past but now has adverse effects because of relatively rapid changes in the environment in which we live (58). An example of this may be the explosion of hyperten...

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Birth weight and cardiovascular risk factors in a cohort followed until 80 years of age: the study of men born in 1913

Cited by 56 publications

References 55 publications

Lipid Profile, Glucose Homeostasis, Blood Pressure, and Obesity-Anthropometric Markers in Macrosomic Offspring of Nondiabetic Mothers

Lipid Profile, Glucose Homeostasis, Blood Pressure, and Obesity-Anthropometric Markers in Macrosomic Offspring of Nondiabetic Mothers

Fetal programming and fetal psychology

Programming blood pressure in adult SHR by shifting perinatal balance of NO and reactive oxygen species toward NO: the inverted Barker phenomenon

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