Testing the fetal origins hypothesis in twins: the Birmingham twin study
Testing the fetal origins hypothesis in twins: the Birmingham twin study
Aims/hypothesis: To test whether the link between birthsize and raised blood pressure or glucose tolerance is due to genetic or intrauterine factors, we studied whether differences in birthweight between pairs of monozygous and dizygous twins are associated with adult differences in blood pressure and glucose tolerance.
Methods: A sample of 58 monozygous and 140 dizygous twins were identified from a register of births in Birmingham, United Kingdom, between 1950 and 1954. The twins had their blood pressure measured and underwent an oral glucose tolerance test.
Results: There were no statistically significant associations between birthweight, length or ponderal index, and either blood pressure or glucose tolerance in the twins. Although there were substantial within-pair differences in birthweight between monozygous and dizygous twin pairs, these differences did not correlate with the adult outcomes. Monozygous correlations, however, for both blood pressure and glucose tolerance were statistically significantly higher than dizygous correlations and a quantitative genetic model suggested statistically significant heritability for these traits. In contrast correlations of birthsize were similar in monozygous and dizygous pairs suggesting only a small genetic component in determining fetal size.
Conclusion/interpretation: Our results show that birthsize in twins does not predict adult blood pressure or glucose tolerance. We also suggest that shared genetic determinants for fetal growth and adult outcomes are not likely to be prevalent or powerful.
fetal growth, birthweight, twins, programming, blood pressure, glucose tolerance, the fetal origins hypothesis
33-39
Baird, J.
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Osmond, C.
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Macgregor, A.
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Snieder, H.
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Hales, C.N.
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Phillips, D.I.W.
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January 2001
Baird, J.
f4bf2039-6118-436f-ab69-df8b4d17f824
Osmond, C.
2677bf85-494f-4a78-adf8-580e1b8acb81
Macgregor, A.
bca7b75b-d04a-404a-8b29-bdabf5269966
Snieder, H.
e6eeab3f-5d42-4ea9-8ba9-859f3ac17ae5
Hales, C.N.
d3056fe8-da77-494b-ab8e-57207e92e0ea
Phillips, D.I.W.
29b73be7-2ff9-4fff-ae42-d59842df4cc6
Baird, J., Osmond, C., Macgregor, A., Snieder, H., Hales, C.N. and Phillips, D.I.W.
(2001)
Testing the fetal origins hypothesis in twins: the Birmingham twin study.
Diabetologia, 44 (1), .
(doi:10.1007/s001250051577).
Abstract
Aims/hypothesis: To test whether the link between birthsize and raised blood pressure or glucose tolerance is due to genetic or intrauterine factors, we studied whether differences in birthweight between pairs of monozygous and dizygous twins are associated with adult differences in blood pressure and glucose tolerance.
Methods: A sample of 58 monozygous and 140 dizygous twins were identified from a register of births in Birmingham, United Kingdom, between 1950 and 1954. The twins had their blood pressure measured and underwent an oral glucose tolerance test.
Results: There were no statistically significant associations between birthweight, length or ponderal index, and either blood pressure or glucose tolerance in the twins. Although there were substantial within-pair differences in birthweight between monozygous and dizygous twin pairs, these differences did not correlate with the adult outcomes. Monozygous correlations, however, for both blood pressure and glucose tolerance were statistically significantly higher than dizygous correlations and a quantitative genetic model suggested statistically significant heritability for these traits. In contrast correlations of birthsize were similar in monozygous and dizygous pairs suggesting only a small genetic component in determining fetal size.
Conclusion/interpretation: Our results show that birthsize in twins does not predict adult blood pressure or glucose tolerance. We also suggest that shared genetic determinants for fetal growth and adult outcomes are not likely to be prevalent or powerful.
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Published date: January 2001
Keywords:
fetal growth, birthweight, twins, programming, blood pressure, glucose tolerance, the fetal origins hypothesis
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Local EPrints ID: 25212
URI: http://eprints.soton.ac.uk/id/eprint/25212
ISSN: 0012-186X
PURE UUID: 40fd84cf-eebc-4704-a79c-a5e0e89bc7e4
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Date deposited: 07 Apr 2006
Last modified: 16 Mar 2024 03:29
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Author:
A. Macgregor
Author:
H. Snieder
Author:
C.N. Hales
Author:
D.I.W. Phillips
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