Author Identifier

ORCID: 0000-0003-0035-5680

Date of Award

2019

Document Type

Thesis

Publisher

Edith Cowan University

Degree Name

Master of Science (Human Biology)

School

School of Medical and Health Sciences

First Supervisor

Associate Professor Peter Roberts

Second Supervisor

Dr David Coall

Abstract

The uterine environment in which a fetus grows and develops is now recognised as a risk factor for the development of adult diseases such as cardiovascular disease (CVD). A fetus relies on the nutrients and conditions delivered via the placenta, and as such the placenta plays a vital role in the establishment and maintenance of appropriate uterine conditions. Unfavourable uterine conditions such as an inadequate resource flow from the placenta can lead to diminished growth of the fetus and may ultimately result in both short and long-term increases in risk of CVD for the baby. This has been demonstrated in large observational cohort studies and has been corroborated in animal experiments. Despite these findings, there remains significant variability in the association between the fetal environment and adult disease risk in observational data across human populations. Moreover, the size of the association between the placenta, as master of the uterine environment, and CVD is yet to be quantified. In order to bridge this knowledge gap, the present study conducted a systematic literature search and meta-analysis of published data examining the effects of the placenta on cardiovascular outcomes across the life course.

A systematic search was carried out and results were collated and assessed, with records which met the selection criteria then entered in to a meta-analytical process which included a funnel plot, calculation of Egger’s Regression Intercept and estimation of effect size. The results of the search indicated that the association between placental weight and CVD risk had been investigated in a total of 109,721 participants across eight countries. The meta-analytical process initially indicated that higher blood pressure was related to a lighter placenta. On further inspection of the funnel plot, a distinct outlier was detected. This outlier was removed and the remaining records were analysed again. This second analysis indicated that higher blood pressure was related to a heavier placenta. This process demonstrated that a single large study can substantially alter the results of a meta-analysis. Further, the variety of confounding variables which a study can adjust for demonstrates that placental weight cannot be viewed in isolation. None of the placenta studies relating placental weight to cardiovascular outcomes (such as mortality and morbidity) were comparable in this meta-analysis, indicating that there needs to be some guide to uniformity in the data collection and analysis. Such a guide would lead to better reporting and comparability between studies enabling new knowledge to build on previous research in this field. Ultimately, improved comparability of these studies, along with the transition of this field towards more complex measures of the placenta such as thickness, circumference and volume as well as the use of real-time imaging of the placenta, as the fetus develops in-utero, will contribute another dimension to our understanding of the relationship between placental function and adult disease risk.

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