Placental weight, birth measurements, and blood pressure at age 8 years.

Moore, Vivienne; Miller, Alison; Boulton, T. J. C.; Cockington, Richard A.; Craig, Ian H.; Magarey, A. M.; Robinson, Jeffrey S.

doi:10.1136/adc.74.6.538

Cited by 118 publications

(70 citation statements)

References 23 publications

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“…The increased ratio of placental/fetal weight observed in this study is similar to that described in human IVF pregnancies, where IVF offspring were associated with hypertension later in life (Barker et al 1990, Moore et al 1996, Koudstaal et al 2000. The reasons for the increased ratio of placental/fetal weight are likely complicated; one possible explanation involves a compensatory process for the depressed fetal growth or the impaired function of the placenta itself (Feuer et al 2014, Chen et al 2015.…”

Section: Discussionsupporting

confidence: 68%

IVF affects embryonic development in a sex-biased manner in mice

Tan¹,

Wang²,

Zhang³

et al. 2016

Reproduction

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Increasing evidence indicates that IVF (IVF includes in vitro fertilization and culture) embryos and babies are associated with a series of health complications, and some of them show sex-dimorphic patterns. Therefore, we hypothesized that IVF procedures have sex-biased or even sex-specific effects on embryonic and fetal development. Here, we demonstrate that IVF-induced side effects show significant sexual dimorphic patterns from the pre-implantation to the prenatal stage. During the pre-implantation stage, female IVF embryos appear to be more vulnerable to IVF-induced effects, including an increased percentage of apoptosis (7.22G1.94 vs 0.71G0.76, P!0.01), and dysregulated expression of representative sex-dimorphic genes (Xist, Hprt, Pgk1 and Hsp70). During the mid-gestation stage, IVF males had a higher survival rate than IVF females at E13.5 (male:femaleZ1.33:1), accompanied with a female-biased pregnancy loss. In addition, while both IVF males and females had reduced placental vasculogenesis/angiogenesis, the compensatory placental overgrowth was more evident in IVF males. During the late-gestation period, IVF fetuses had a higher sex ratio (male:femaleZ1.48:1) at E19.5, and both male and female IVF placentas showed overgrowth. After birth, IVF males grew faster than their in vivo (IVO) counterparts, while IVF females showed a similar growth pattern with IVO females. The present study provides a new insight into understanding IVF-induced health complications during embryonic and fetal development. By understanding and minimizing these sex-biased effects of the IVF process, the health of IVF-conceived babies may be improved in the future.

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Section: Discussionsupporting

confidence: 68%

IVF affects embryonic development in a sex-biased manner in mice

Tan¹,

Wang²,

Zhang³

et al. 2016

Reproduction

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“…score. Other studies, but not all, have shown a negative relationship between birth size and blood pressure 23,24 and a positive relationship between birth size and insulin resistance 11 in prepubertal children. This apparent inconsistency could be due to the small number of low weight babies (seven children had a birth weight < 2.50 kg) and the higher mean birth weight (3.47 AE 0.49 kg) in this study compared to others.…”

Section: Discussionmentioning

confidence: 99%

Abdominal fat and birth size in healthy prepubertal children

et al. 2001

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BACKGROUND: Studies examining the foetal origins hypothesis suggest that small birth size may be a marker of foetal adaptations that programme future propensity to adult disease. We explore the hypothesis that birth size may relate to fat distribution in childhood and that fat distribution may be a link between birth size and adult disease. OBJECTIVE: To investigate the relationship between birth size and abdominal fat, blood pressure, lipids, insulin and insulin:glucose ratio in prepubertal children. DESIGN: Cross-sectional study, based on a birth cohort of consecutive full-term births. SUBJECTS: Two hundred and fifty-five (137 females) healthy, 7-and 8-y-old children. MEASUREMENTS: Body composition and abdominal fat was measured by dual energy X-ray absorptiometry. Lipid, glucose and insulin profiles were measured after an overnight fast and an automated BP monitor was used for blood pressure measurements. RESULTS: There was a negative association between abdominal fat and birth weight s.d. score across a range of normal birth weights (b ¼ 70.18; 95% CI ¼ 70.31 to 70.04, P ¼ 0.009) and a positive association with weight s.d. score at 7=8 y (b ¼ 0.35; 95% CI ¼ 0.24 to 0.46, P < 0.001). Children who were born with the lowest weight s.d. score and had the greatest weight s.d. score at 7=8 y had significantly more (P < 0.001) abdominal fat, as a percentage of total fat (6.53 AE 1.3%) than those who had the highest birth weight s.d. score and the lowest weight s.d. score at 7=8 y (4.14 AE 0.5%). Similar results were seen if head circumference, but not ponderal index, was used as an indicator of birth size. Increased abdominal fat was associated with higher total cholesterol:HDL cholesterol, higher triglyceride concentration and increased diastolic blood pressure. CONCLUSIONS: Birth weight independently predicted abdominal fat. Children with the highest amount of abdominal fat were those who tended to be born lighter and gained weight centiles. Increased abdominal fat was associated with precursor risk factors for ischaemic heart disease.

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“…Subjects with a mean systolic pressure of 150 mm Hg or more, a level sometimes used to define hypertension in clinical practice, comprise a group who as babies were relatively small in relation to the size of their placentas. A rise in blood pressure with increasing placental weight was also found in 4-year-old children in Salisbury, UK, and among 8-yearold children in Adelaide, Australia (37,39). However, in studies of children and adults the association between placental enlargement and raised blood pressure has been inconsistent (40).…”

Section: Possible Mechanismsmentioning

confidence: 96%

Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women

Osmond¹,

Barker²

2000

Environmental Health Perspectives

145

130

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Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension and noninsulindependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies.

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Placental weight, birth measurements, and blood pressure at age 8 years.

Cited by 118 publications

References 23 publications

IVF affects embryonic development in a sex-biased manner in mice

IVF affects embryonic development in a sex-biased manner in mice

Abdominal fat and birth size in healthy prepubertal children

Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women

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