Summary
The Barker hypothesis states that size at birth is negatively associated with disease risk later in life. Numerous studies have tested and confirmed this hypothesis in singletons. Using twin (or sibling) data, several extensions of the Barker hypothesis may be considered:
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1.
Within pairs, is the smallest twin also the one with the highest disease risk later in life? Since twins (or siblings) come from the same family, this test controls for any shared family effects, such as maternal nutrition, parental education or socio-economic status.
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A second extension compares associations of differences in size at birth with differences in disease risk in monozygotic (MZ) and dizygotic (DZ) twin pairs. If associations of difference scores are larger in DZ than in MZ twin pairs, this is taken as evidence that the association is mediated by genetic factors.
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These two methods can be considered as alternative approaches to the full bivariate analysis of MZ and DZ twin data. Using a bivariate structural equation model, the correlation between two traits can be decomposed into genetic and environmental correlations.
We address some statistical questions regarding the relation of difference scores (within MZ and DZ pairs) and genetic and environmental correlations. We show that the comparison of associations between MZ and DZ difference scores does not necessarily provide clear-cut answers to the question of how the relation of size at birth and later outcome is mediated.
We present an empirical application to data on stature, birth weight and height assessed in a large sample of Dutch adult MZ and DZ twin pairs. There is a significant association between size at birth (both weight and length) and later stature. Within MZ and DZ twin pairs, the largest/heaviest twin at birth is the one who is tallest later in life. Using a bivariate structural equation model, we show that the association of birth length/weight and adult stature is explained by shared genes as well as by correlated common family and unique environmental influences.
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References
Abuzzahab MJ, Schneider A, Goddard A, Grigorescu F, Lautier C, Keller E, Kiess W, Klammt J, Kratzsch J, Osgood D, Pfaffle R, Raile K, Seidel B, Smith RJ, Chernausek SD; Intrauterine Growth Retardation (IUGR) Study Group (2003) IGF-I receptor mutations resulting in intrauterine and postnatal growth retardation. N Engl J Med 349:2211–2222
Allison DB, Paultre F, Heymsfield SB, Pi-Sunyer FX (1995) Is the intra-uterine period really a critical period for the development of adiposity? Int J Obes Relat Metab Disord 19:397–402
Barker DJP (1995) Fetal origins of coronary heart disease. BMJ 311:171–174
Barker DJ (ed) (1998) Mothers, babies and health in later life. Sidcup. Kent: Churchill Livingstone
Barker DJ (2002) Fetal programming of coronary heart disease. Trends Endocrinol Metab 13:364–368
Barker DJ (2003) The developmental origins of adult disease. Eur J Epidemiol 18:733–736
Barker DJ, Osmond C, Golding J, Kuh D, Wadsworth ME (1989). Growth in utero, blood pressure in childhood and adult life, and mortality from cardiovascular disease. BMJ 298:564–567
Boomsma DI, Koopmans JR, Doornen LJP van, Orlebeke JF (1994) Genetic and social influences on starting to smoke: a study of Dutch adolescent twins and their parents, Addiction 89:219–226
Boomsma DI, Geus EJC de, Baal GCM van, Koopmans JR (1999) Religious upbringing reduces the influence of genetic factors on disinhibition: Evidence for interaction between genotype and environment, Twin Res 2:115–125
Boomsma DI, Vink JM, van Beijsterveldt TC, de Geus EJ, Beem AL, Mulder EJ, Derks EM, Riese H, Willemsen GA, Bartels M, van den Berg M, Kupper NH, Polderman TJ, Posthuma D, Rietveld MJ, Stubbe JH, Knol LI, Stroet T, van Baal GC (2002a) Netherlands Twin Register: a focus on longitudinal research. Twin Res 5: 401–406
Boomsma DI, Busjahn A, Peltonen L (2002b) The classical twin study and beyond. Nat Genet Rev 3:872–882
Doyle D, Leon D, Morton S, de Stavola B (1999) Twins and the fetal origins hypothesis. Patterns of growth retardation differ in twins and singletons. BMJ 319:517–518
Eriksson JG, Forsen TJ, Osmond C, Barker DJ (2003) Pathways of infant and childhood growth that lead to type 2 diabetes. Diab Care 26:3006–3010
Huxley R, Neil A, Collins R (2002) Unravelling the fetal origins hypothesis: is there really an inverse association between birthweight and subsequent blood pressure? Lancet 360:659–665
Ijzerman RG, Stehouwer CD, Boomsma DI (2000) Evidence for genetic factors explaining the birth weight-blood pressure relation: analysis in twins. Hypertension 36:1008–1012
Ijzerman RG, Stehouwer CDA, Weissenbruch MM van, Geus EJC de, Boomsma DI (2001a) Intra-uterine and genetic influences on the relationship between size at birth and height in later life: analysis in twins. Twin Res 4:337–343
Ijzerman RG, Stehouwer CD, van Weissenbruch MM, de Geus EJ, Boomsma DI (2001b) Evidence for genetic factors explaining the association between birth weight and LDL cholesterol, and possible intrauterine factors influencing the association between birth weight and HDL cholesterol: analysis in twins. J Clin Endocrinol Metab 86:5479–5484
Kendler KS, Eaves LJ (1986) Models for the joint effect of genotype and environment on liability to psychiatric illness. Am J Psychiat 143:279–289
Martin N, Boomsma D, Machin G. (1997) A twin-pronged attack on complex traits. Nature Genet 17:387–392
McCarron P, Okasha M, McEwen J, Smith GD (2002) Height in young adulthood and risk of death from cardiorespiratory disease: a prospective study of male former students of Glasgow University, Scotland. Am J Epidemiol 155:683–687
Miura K, Nakagawa H, Tabata M, Morikawa Y, Nishijo M, Kagamimori S (2001) Birth weight, childhood growth, and cardiovascular disease risk factors in Japanese aged 20 years. Am J Epidemiol 153:783–789
Neale M, Cardon L (1992) Methodology for genetic studies of twins and families. Dordrecht: Kluwer Academic Publishers
Neale MC, Boker SM, Xie G, Maes, HH (2003) Mx: Statistical modeling. 6th Edition. Richmond, VA, Department of Psychiatry
Paneth N, Susser M (1995) Early origins of coronary heart disease (the "Barker hypothesis"). BMJ 310:411–412
Phillips D (2002) Endocrine programming and fetal origins of adult disease. Trends Endocrinol Metab 13:363
Pietilainen KH, Kaprio J, Rasanen M, Winter T, Rissanen A, Rose RJ (2001) Tracking of body size from birth to late adolescence: contributions of birth length, birth weight, duration of gestation, parents’ body size, and twinship. Am J Epidemiol 154:21–29
Pietilainen KH, Kaprio J, Rasanen M, Rissanen A, Rose RJ (2002) Genetic and environmental influences on the tracking of body size from birth to early adulthood. Obes Res 10:875–884
Plomin, R, DeFries JC, McClearn GE, McGuffin P (2001) Behavioral genetics. 4th Edition. New York: Worth Publishers
Rich-Edwards JW, Manson JE, Stampfer MJ, Colditz GA, Willett WC, Rosner B, Speizer FE, Hennekens CH (1995) Height and the risk of cardiovascular disease in women. Am J Epidemiol 142:909–917
Silventoinen K, Sammalisto S, Perola M, Boomsma DI, Cornes BK, Davis C, Dunkel L, De Lange M, Harris JR, Hjelmborg JV, Luciano M, Martin NG, Mortensen J, Nistico L, Pedersen NL, Skytthe A, Spector TD, Stazi MA, Willemsen G, Kaprio J (2003) Heritability of adult body height: a comparative study of twin cohorts in eight countries. Twin Res 6:399–408
Song YM, Smith GD, Sung J (2003) Adult height and cause-specific mortality: a large prospective study of South Korean men. Am J Epidemiol 158:479–485
Vaessen N, Janssen JA, Heutink P, Hofman A, Lamberts SW, Oostra BA, Pols HA, van Duijn CM (2002) Association between genetic variation in the gene for insulin-like growth factor-I and low birthweight. Lancet 359:1036–1037
Yarnell JW, Limb ES, Layzell JM, Baker IA (1992) Height: a risk marker for ischaemic heart disease: prospective results from the Caerphilly and Speedwell Heart Disease Studies. Eur Heart J 13:1602–1605
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Boomsma, D. et al. (2005). Twins and the fetal origins hypothesis: An application to growth data. In: Kordon, C., Gaillard, RC., Christen, Y. (eds) Hormones and the Brain. Research and Perspectives in Endocrine Interactions. Springer, Berlin, Heidelberg. https://doi.org/10.1007/3-540-26940-1_2
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DOI: https://doi.org/10.1007/3-540-26940-1_2
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