Endothelial function is impaired in fit young adults of low birth weight

Goodfellow, Jonathan; Bellamy, Michael; Gorman, Sharon; Brownlee, M.; Ramsey, Mike; Lewis, Malcolm J.; Davies, David; Henderson, A R

doi:10.1016/s0008-6363(98)00197-7

Cited by 153 publications

(114 citation statements)

References 56 publications

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“…For example, adult lifestyle factors, such as smoking, could not have confounded the results. Our findings are in line with those of other studies in which conventional cardiovascular risk factors, including blood lipids, showed little if any relationship with endotheliumdependent vasodilation in 9-to 11-year-old children 15 and fit young adults, 16 whereas LBW did. We have previously reported impaired microvascular endothelium-dependent vasodilation in LBW infants, even at birth.…”

Section: Discussionsupporting

confidence: 92%

“…[11][12][13] The first studies on the prevalence of these markers in LBW children have recently been presented. The aortic elasticity in prepubertal schoolchildren with intrauterine growth retardation was normal, 14 whereas endothelium-dependent brachial artery dilation in LBW children and young adults 15,16 and endothelium-dependent microvascular vasodilation in LBW neonates 17 were impaired. We tested the hypothesis that the impairment of vasodilation in LBW newborn infants persists and can be detected in healthy, prepubertal children.…”

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confidence: 98%

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Impaired Endothelial Function and Increased Carotid Stiffness in 9-Year-Old Children With Low Birthweight

et al. 2000

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Background-Low birthweight (LBW) has been associated with an increased incidence of adult cardiovascular disease.Endothelial dysfunction and loss of arterial elasticity are early markers of hypertension and atherosclerosis. We studied the prevalence of these markers in 44 healthy, prepubertal (age 9Ϯ1.3 years) children, 22 with LBW for age. Methods and Results-Endothelial function in skin was tested with the local application of acetylcholine (inducing endothelium-dependent vasodilation) and nitroglycerin (endothelium-independent vasodilation), and local perfusion changes were measured with the laser Doppler method. The elastic properties of the abdominal aorta and common carotid artery were measured with an ultrasonic vessel-wall tracking system. Endothelium-dependent vasodilation was lower in children with LBW (88Ϯ33 perfusion units [PU]) than in normal-birthweight controls (133Ϯ34 PU, PϽ0.001).There was no difference in aortic or carotid elasticity between the 2 groups, but a negative correlation was found between birthweight and stiffness of the carotid artery wall (rϭϪ0.45, PϽ0.01). Endothelium-independent vasodilation and blood pressure were similar in the 2 groups. Conclusions-Schoolchildren with a history of LBW show impaired endothelial function and a trend toward increased carotid stiffness. These findings may be early expressions of vascular compromise, contributing to susceptibility to disease in adult life.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 98%

Impaired Endothelial Function and Increased Carotid Stiffness in 9-Year-Old Children With Low Birthweight

et al. 2000

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“…14 This finding was replicated in a small, independent study of subjects without risk factors in the second decade of life. 32 Because the risk factor burden in these populations was low, it is likely that the effect of birth weight on endothelial function was not dependent on the presence of adverse cardiovascular risk factors at this early stage.…”

Section: Discussionmentioning

confidence: 99%

Impact of Low Birth Weight and Cardiovascular Risk Factors on Endothelial Function in Early Adult Life

Leeson

Kattenhorn²,

Morley³

et al. 2001

Circulation

330

210

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Background-Low birth weight is related to increased risk of coronary heart disease in adults and recently has been associated with vascular endothelial dysfunction in children. We investigated whether the relation between birth weight and endothelial function was still present in early adult life and whether there was an interaction with emerging risk factors. Methods and Results-In 315 adults (165 women, 150 men, aged 20 to 28 years), high-resolution ultrasound was used to determine endothelium-dependent and -independent vascular responses of the brachial artery. Vascular measures were related to classic risk factors (smoking history, lipid profile, blood pressure, fasting insulin, exercise capacity, body mass index, and combined risk score) and birth weight. Low birth weight was associated with reduced flow-mediated dilation (coefficientϭ0.18 kg

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“…Several studies have shown that endothelial-dependant and -independent vasodilation is impaired and flow-mediated dilation is decreased in low-birthweight individuals at 3 months of age, in later childhood and in early adult life. [63][64][65] In rats that were undernourished during the first 18 days of gestation, increased blood pressure at 60 days after birth was noted, and the maximal vasoconstriction response to phenylephrine and norepinephrine was reduced in isolated femoral arteries, 66 although other maternal nutrient restricted diets 67,68 showed no effect on vasoconstrictor responses.…”

Section: Hypertensionmentioning

confidence: 99%

Adult Sequelae of Intrauterine Growth Restriction

Ross

Beall

2008

Seminars in Perinatology

159

115

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Fetal intrauterine growth restriction has been associated with adult disease in both human epidemiologic studies and in animal models. In some cases, intrauterine deprivation programs the fetus to develop increased appetite and obesity, hypertension and diabetes as an adult. Although the mechanisms responsible for fetal programming remain poorly understood, both anatomic and functional (cell signaling) changes have been described in affected individuals. In some animal models, aspects of fetal programming can be reversed postnatally, however at the present time the best strategy for avoiding the adult consequences of fetal growth restriction is prevention.Fetal intrauterine growth restriction (IUGR) occurs in humans as a consequence of poor maternal nutrition, placental insufficiency and diminished fetal oxygenation, or exposure to teratogens, among other causes. In animals, and in some cases in humans, IUGR from these causes has been associated with the development of adult diseases; this phenomenon is called "fetal programming". The association of maladaptive programming with adult disease has been termed the "Barker hypothesis". In general, the Barker hypothesis 1 contends that the malnourished fetus is programmed to exhibit a "thrifty phenotype" with increased food intake and fat deposition and possibly decreased energy output. Faced with ample available calories, such individuals develop obesity and other manifestations of the metabolic syndrome as adults due to alterations in homeostatic regulatory mechanisms. 2-4The issue of fetal programming is not merely of intellectual interest. Currently, 65% of adults in the United States are overweight and almost one in three are obese (BMI>30 kg/m 2 ), representing a modern health crisis. 5 Obesity and its related diseases are the leading cause of death in Western society, with associated risks of hypertension, coronary heart disease, stroke, diabetes, and breast, prostate and colon cancer. Evidence indicates a striking 25 to 63% of adult diabetes, hypertension and coronary heart disease can be attributed to the effects of low birthweight with accelerated newborn-to-adolescent weight gain. 2 therefore gestational programming of low birth weight/ IUGR has contributed importantly to the population shift towards obesity. In Western societies, the incidence of low birth weight infants has increased since the mid-twentieth century. Low birth weight infants are now being born to women with chronic diseases who would previously have had limited survival and reproductive capacity, while assisted reproductive technologies and increasing numbers of multiple gestations have resulted in both preterm and low birth weight offspring. When combined with improved

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Endothelial function is impaired in fit young adults of low birth weight

Abstract: The findings suggest that endothelial dysfunction is a consequence of foetal malnutrition, consistent with contributing to the clinical features of the 'Small Baby Syndrome' in later adult life.

Cited by 153 publications

References 56 publications

Impaired Endothelial Function and Increased Carotid Stiffness in 9-Year-Old Children With Low Birthweight

Impaired Endothelial Function and Increased Carotid Stiffness in 9-Year-Old Children With Low Birthweight

Impact of Low Birth Weight and Cardiovascular Risk Factors on Endothelial Function in Early Adult Life

Adult Sequelae of Intrauterine Growth Restriction

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