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The developmental origins of chronic adult disease
Abstract
Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin-dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. Coronary heart disease and the disorders related to it arise through a series of interactions between environmental influences and the pathways of development that preceded them. These diseases are the product of branching pathways of development in which the branchings are triggered by the environment before and after birth.
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WEIGHT IN INFANCY AND DEATH FROM ISCHAEMIC HEART DISEASE
Barker, D. J. P., Osmond, C., Winter, P. D., Margetts, B., & Simmonds, S. J. (1989) · The Lancet · doi:10.1016/s0140-6736(89)90710-1 · Cited by 3,574
Fetal origins of coronary heart disease
Barker, D. J. P. (1995) · BMJ · doi:10.1136/bmj.311.6998.171 · Cited by 3,570
Self-citationFetal and infant growth and impaired glucose tolerance at age 64
Hales, C. N., Barker, D. J., Clark, P. M., Cox, L. J., Fall, C., Osmond, C., & Winter, P. D. (1991) · BMJ · doi:10.1136/bmj.303.6809.1019 · Cited by 2,708
Phenotypic Plasticity and the Origins of Diversity
West-Eberhard, M. J. (1989) · Annual Review of Ecology and Systematics · doi:10.1146/annurev.es.20.110189.001341 · Cited by 2,110
Fetal origins of adult disease: strength of effects and biological basis
Barker, D., Eriksson, J., Forsén, T., & Osmond, C. (2002) · International Journal of Epidemiology · doi:10.1093/ije/31.6.1235 · Cited by 2,024
Compensation for a bad start: grow now, pay later?
Metcalfe, N. B., & Monaghan, P. (2001) · Trends in Ecology & Evolution · doi:10.1016/s0169-5347(01)02124-3 · Cited by 1,948
Health consequences of obesity
Reilly, J. J. (2003) · Archives of Disease in Childhood · doi:10.1136/adc.88.9.748 · Cited by 1,652
Calvert, H., Horwich, A., Newlands, E. S., Beǵent, R. H. J., Rustin, G. J. S., Kaye, S. B., Harris, A. L., Williams, C. J., & Slevin, M. L. (1988) · The Lancet · doi:10.1016/s0140-6736(88)92709-2 · Cited by 1,183
Nephron Number in Patients with Primary Hypertension
Keller, G., Zimmer, G., Mall, G., Ritz, E., & Amann, K. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa020549 · Cited by 1,102
The role of size at birth and postnatal catch-up growth in determining systolic blood pressure
Huxley, R., Shiell, A. W., & Law, C. (2000) · Journal of Hypertension · doi:10.1097/00004872-200018070-00002 · Cited by 1,046
Research works printed but not linked: 1
- Bateson P, 1999, Design for a life: how behaviour develops
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Maternal Perinatal Undernutrition Attenuates T-Cell Function in Adult Male Rat Offspring
Badr, G., & Mohany, M. (2011) · Cellular Physiology and Biochemistry · doi:10.1159/000327964 · Cited by 43
Clifton, V. L., Cuffe, J. S. M., Moritz, K. M., Cole, T. J., Fuller, P. J., Lu, N. Z., Kumar, S., Chong, S., & Saif, Z. (2016) · Placenta · doi:10.1016/j.placenta.2016.12.017 · Cited by 46
Logan, C. A., Bornemann, R., Köenig, W., Reister, F., Walter, V., Fantuzzi, G., Weyermann, M., Brenner, H., Genuneit, J., & Rothenbacher, D. (2017) · Scientific Reports · doi:10.1038/srep41847 · Cited by 48
Seabrook, J. A., Smith, A. C. H., Clark, A. F., & Gilliland, J. (2018) · Environmental Research · doi:10.1016/j.envres.2018.12.068 · Cited by 47
A prediction model for short-term neonatal outcomes in severe early-onset fetal growth restriction
Sharp, A., Jackson, R., Cornforth, C., Harrold, J. A., Turner, M. A., Kenny, L. C., Baker, P. N., Johnstone, E., Khalil, A. A., von Dadelszen, P., et al. (2019) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2019.08.007 · Cited by 43
Do neurotrophins regulate the feto-placental development?
Mayeur, S., Lukaszewski, M.-A., Breton, C., Storme, L., Vieau, D., & Lésage, J. (2011) · Medical Hypotheses · doi:10.1016/j.mehy.2011.02.008 · Cited by 44
“The developmental origins of adult health and diseases hypothesis describes the abilities of the fetus to put in place strategies to respond to deleterious in utero conditions that will induce the appearance of chronic diseases in adulthood [1].”
BackgroundMinh, H. V., Huong, D. L., & Giang, K. B. (2008) · Scandinavian Journal of Public Health · doi:10.1177/1403494807086977 · Cited by 42
“women than among better-off women could possibly be explained by Barker’s hypothesis about infant origins of chronic adult diseases [23–25].”
BackgroundChurch, M. W., Jen, K. ‐. C., Jackson, D. A., Adams, B. R., & Hotra, J. W. (2008) · Neurotoxicology and Teratology · doi:10.1016/j.ntt.2008.09.001 · Cited by 44
“Such findings are consistent with Barker's hypothesis that adverse prenatal and/or postnatal conditions can program the offspring for health disorders in adulthood [4,22,54].”
Huang, C., Guo, C., Nichols, C., Chen, S., & Martorell, R. (2014) · International Journal of Epidemiology · doi:10.1093/ije/dyu193 · Cited by 42
Early-life origins of schizotypal traits in adulthood
Lahti, J. M. T., Räikkönen, K., Sovio, U., Miettunen, J., Hartikainen, A., Pouta, A. M., Taanila, A. M., Joukamaa, M. I., Järvelin, M., & Veijola, J. (2009) · The British Journal of Psychiatry · doi:10.1192/bjp.bp.108.054387 · Cited by 42
Developmental Origins of Disease: Emerging Prenatal Risk Factors and Future Disease Risk
Aris, I. M., Fleisch, A. F., & Oken, E. (2018) · Current Epidemiology Reports · doi:10.1007/s40471-018-0161-0 · Cited by 44
“In humans, exposure to PFASs can occur through dietary intake of contaminated food or drinking water, and are widespread; detectable levels were found in 95% of Americans who participated in the US National Health and Nutrition Examination Survey between 1999 and 2008 [51]. During pregnancy, certain PFASs can cross th…”
InfluentialMonteagudo, A., Sánchez-Delgado, M., Mora, J. R. H., Santamaría, N. T., Gratacós, E., Esteller, M., de Heredia, M. L., Nunes, V., Choux, C., Fauque, P., et al. (2019) · Clinical Epigenetics · doi:10.1186/s13148-019-0630-4 · Cited by 42
Early famine exposure and adult disease risk based on a 10-year prospective study of Chinese adults
Meng, R., Yu, C., Guo, Y., Bian, Z., Si, J., Nie, J., Yang, L., Chen, Y., Du, H., Zhou, L., et al. (2019) · Heart · doi:10.1136/heartjnl-2019-315750 · Cited by 42
Bergamini, M., Simeone, G., Verga, M. C., Doria, M., Cuomo, B., D’Antonio, G., Iacono, I. D., Mauro, G. D., Leonardi, L., Miniello, V. L., et al. (2022) · Nutrients · doi:10.3390/nu14132646 · Cited by 41
“industrialized countries, where the almost unlimited availability of food can expose even children to the risk of developing non-communicable diseases (NCDs) [19,20].”
BackgroundCasavant, S. G., Cong, X. S., Moore, J., & Starkweather, A. R. (2019) · Early Human Development · doi:10.1016/j.earlhumdev.2019.03.003 · Cited by 44
Pregnancy-Induced Hypertension in Women Who Were Born Small
Rasmussen, S., & Irgens, L. M. (2007) · Hypertension · doi:10.1161/01.hyp.0000259924.74947.aa · Cited by 41
High Folate Intake Is Related to Better Academic Achievement in Swedish Adolescents
Nilsson, T. K., Yngve, A., Böttiger, A. K., Hurtig‐Wennlöf, A., & Sjöstróm, M. (2011) · PEDIATRICS · doi:10.1542/peds.2010-1481 · Cited by 41
Epigenetic inheritance of PCOS by developmental programming and germline transmission
Stener‐Victorin, E., & Deng, Q. (2024) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2024.12.002 · Cited by 40
Can Proopiomelanocortin Methylation Be Used as an Early Predictor of Metabolic Syndrome?
Yoo, J. Y., Lee, S., Lee, H. A., Park, H., Park, Y. J., Ha, E., & Kim, Y. J. (2013) · Diabetes Care · doi:10.2337/dc13-1012 · Cited by 39
“It may be that low birth weight predisposes individuals to type 2 diabetes and metabolic syndrome, called “fetal programming” or the “Barker hypothesis” (8,27).”
BackgroundGlucocorticoid programming of neuroimmune function
Walker, D. J., & Spencer, K. A. (2017) · General and Comparative Endocrinology · doi:10.1016/j.ygcen.2017.07.016 · Cited by 42
“The concept of programming proposes that early life events can permanently influence later physiological and behavioural phenotypes in a way that impacts on the health of both the afflicted individual and its offspring (Welberg and Seckl, 2001; Barker, 2004).”
BackgroundLow-protein diet in puberty impairs testosterone output and energy metabolism in male rats
de Oliveira, J. C., de Moura, E. G., Miranda, R. A., de Moraes, A. M. P., Barella, L. F., da Conceição, E. P. S., Gomes, R. M., Ribeiro, T. A., Malta, A., Martins, I. P., et al. (2018) · Journal of Endocrinology · doi:10.1530/joe-17-0606 · Cited by 41
Endocrinology of Human Pregnancy and Fetal-Placental Neuroendocrine Development
Mesiano, S. A. (2019) · Elsevier eBooks · doi:10.1016/b978-0-323-47912-7.00011-1 · Cited by 42
Obesity and Maternal-Placental-Fetal Immunology and Health
Monaco-Brown, M., & Lawrence, D. A. (2022) · Frontiers in Pediatrics · doi:10.3389/fped.2022.859885 · Cited by 39
“The effect of maternal obesity on the adult phenotype of offspring is a common example of Barker’s hypothesis of fetal origins of adult disease (13).”
BackgroundRehan, V. K., Sakurai, R., Li, Y., Karadag, A., Corral, J., Bellusci, S., Xue, Y., Belperio, J. A., & Torday, J. S. (2011) · Pediatric Pulmonology · doi:10.1002/ppul.21532 · Cited by 38
Młynarczyk, M., Chauhan, S. P., Baydoun, H., Wilkes, C. M., Earhart, K. R., Zhao, Y., GOODIER, C. G., Chang, E., Plenty, N., Mize, E. K., et al. (2017) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2017.04.020 · Cited by 38
“We also did not collect data on serial sonographic examinations and thus cannot comment on growth velocity and adverse outcomes.(40,76) We did not collect any data”
BackgroundThe ‘Skinny’ on Childhood Obesity: How Our Western Environment Starves Kids’ Brains
Lustig, R. H. (2006) · Pediatric Annals · doi:10.3928/0090-4481-20061201-08 · Cited by 37
Delahaye, F., Lukaszewski, M., Wattez, J.-S., Cissé, O., Dutriez-Casteloot, I., Fajardy, I., Montel, V., Dickès-Coopman, A., Laborie, C., Lésage, J., et al. (2010) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00604.2009 · Cited by 41
“These findings have led to the developmental origin of health and disease hypothesis, which states that an adverse perinatal environment programs or imprints the development of several tissues, permanently determining physiological responses and ultimately producing dysfunction and diseases later in life (5, 18, 46, 4…”
BackgroundProtein metabolism in preterm infants with particular reference to intrauterine growth restriction
de Boo, H. A., & Harding, J. E. (2007) · Archives of Disease in Childhood Fetal & Neonatal · doi:10.1136/adc.2006.099697 · Cited by 38
“and the risk for adult-onset diseases, such as hypertension and type 2 diabetes.”
Human cortical neurogenesis is altered via glucocorticoid-mediated regulation of ZBTB16 expression
Krontira, A. C., Cruceanu, C., Dony, L., Kyrousi, C., Link, M.-H., Rek, N., Pöhlchen, D., Raimundo, C., Penner-Goeke, S., Schowe, A. M., et al. (2024) · Neuron · doi:10.1016/j.neuron.2024.02.005 · Cited by 43
Church, M. W., Hotra, J. W., Holmes, P. A., Anumba, J. I., Jackson, D. A., & Adams, B. R. (2011) · Alcoholism Clinical and Experimental Research · doi:10.1111/j.1530-0277.2011.01594.x · Cited by 37
“Maternal undernutrition and handling stress are known to elevate maternal and fetal corticosteroid levels and thereby cause fetal programming effects (Barker, 2004).”
BackgroundInfluentialDiabetic and Metabolic Programming: Mechanisms Altering the Intrauterine Milieu
Eberle, C., & Ament, C. (2012) · ISRN Pediatrics · doi:10.5402/2012/975685 · Cited by 38
“An epidemiological key work connecting poor fetal growth and subsequent development of impaired glucose tolerance and non-insulin-dependent diabetes, as well as hypertension and cardiovascular disease, for example, was presented by Hales and Barker (“Fetal Origin Hypothesis”) [3, 4].”
Epigenetics and fetal adaptation to perinatal events: Diversity through fidelity1
Joss‐Moore, L. A., Metcalfe, D. B., Albertine, K. H., McKnight, R. A., & Lane, R. H. (2009) · Journal of Animal Science · doi:10.2527/jas.2009-2352 · Cited by 37
“…by a long-term cost, and it is now well established that fetal insults are associated with an increased susceptibility to several adult-onset metabolic disorders, including cardiovascular disease, insulin resistance, and obesity (Eriksson et al., 2002; Barker, 2004; Fattal-Valevski et al., 2005).”
BackgroundWells, J. C. K. (2019) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2018.0122 · Cited by 37
Sedaghat, K., Zahediasl, S., & Ghasemi, A. (2015) · Europe PMC (PubMed Central) · Cited by 39
Grafodatskaya, D., Cytrynbaum, C. S., & Weksberg, R. (2013) · EMBO Reports · doi:10.1038/embor.2012.222 · Cited by 37
Dodic, M., McAlinden, A. T., Jefferies, A. J., Wintour, E. M., Cock, M. L., May, C. N., Evans, R. G., & Moritz, K. M. (2006) · The Journal of Physiology · doi:10.1113/jphysiol.2005.102186 · Cited by 37
“There is substantial epidemiological evidence suggesting that long-term adult health can be influenced by an adverse prenatal environment (Osmond & Barker, 2000; Barker, 2004).”
BackgroundBhaumik, S., Lockett, J., Cuffe, J. S. M., & Clifton, V. L. (2023) · Biology · doi:10.3390/biology12081104 · Cited by 42
Hrudey, J., Reynolds, R. M., Oostvogels, A. J. J. M., Brouwer, I. A., & Vrijkotte, T. G. M. (2015) · PLoS ONE · doi:10.1371/journal.pone.0133313 · Cited by 36
“Exposure to certain nutritional factors in utero, such as insufficient maternal 25-hydroxyvitamin D (25OHD), may be related to adverse cardio-metabolic outcomes in offspring [1, 2].”
BackgroundMaternal Lipids and Small for Gestational Age Birth at Term
Kramer, M. S., Kahn, S. R., Dahhou, M., Otvos, J. D., Genest, J. J., Platt, R. W., & Evans, R. G. (2013) · The Journal of Pediatrics · doi:10.1016/j.jpeds.2013.05.014 · Cited by 36
Global Health: Chronic Diseases and Other Emergent Issues in Global Health
Koehlmoos, T. P., Anwar, S., & Cravioto, A. (2011) · Infectious Disease Clinics of North America · doi:10.1016/j.idc.2011.05.008 · Cited by 38
“very little that can be done about some risk factors, such as age and genetic inheritance, and increasing evidence suggests that what happens before a person is born and during early childhood plays a key role in the onset of adult chronic disease, demonstrated by the proven association between low birth weight and in…”
BackgroundDecreased STAT3 in human idiopathic fetal growth restriction contributes to trophoblast dysfunction.
Borg, A., Yong, H., Lappas, M., Degrelle, S., Keogh, R., Costa, F. D. S., Fournier, T., Abumaree, M., Keelan, J., Kalionis, B., et al. (2015) · Reproduction · doi:10.1530/rep-14-0622 · Cited by 32
“FGR affects up to 5% of all pregnancies and is associated with a number of significant perinatal complications, including stillbirth and prematurity, and is associated with an increased risk of cardiovascular disease and glucose intolerance in adult life (Barker 2004).”
BackgroundEpigenetic Programming Effects of Early Life Stress: A Dual-Activation Hypothesis
Lux, V. (2018) · Current Genomics · doi:10.2174/1389202919666180307151358 · Cited by 40
“This indicates an epigenetic programming mechanism in stress-related neural networks during a critical period of stress response development (developmental window) [75, 76].”
BackgroundHanieh, S., Braat, S., Simpson, J. A., Hà, T. T. T., Tran, T. D., Tran, T., Fisher, J., & Biggs, B. (2019) · BMJ Global Health · doi:10.1136/bmjgh-2019-001801 · Cited by 36
Yang, H., Kühn, C., Kolben, T., Ma, Z., Lin, P., Mahner, S., Jeschke, U., & von Schönfeldt, V. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21155175 · Cited by 37
“According to the ’developmental origins of adult disease’ (DOHaD) hypothesis [5], environmental exposures in early life can exert a long-lasting influence on health and lead to adult-onset chronic non-communicable diseases (NCDs) such as hypertension [6], cardiovascular diseases (CVDs) [7], and type 2 diabetes mellitu…”
BackgroundCoall, D. A., & Chisholm, J. S. (2009) · American Journal of Human Biology · doi:10.1002/ajhb.20965 · Cited by 35
Stage-specific nutritional management and developmental programming to optimize meat production
Zhao, L., Liu, X., Gomez, N. A., Gao, Y., Son, J. S., Chae, S. A., Zhu, M. J., & Du, . (2023) · Journal of Animal Science and Biotechnology/Journal of animal science and biotechnology · doi:10.1186/s40104-022-00805-0 · Cited by 39
“For example, maternal nutrient deficiency during the fetal stage results in impaired fetal development with longterm consequences on offspring performance, referred to as “fetal developmental programming” [18].”
BackgroundHuman placental uptake of glutamine and glutamate is reduced in fetal growth restriction
McIntyre, K. R., Vincent, K., Hayward, C. E., Li, X., Sibley, C. P., Desforges, M., Greenwood, S. L., & Dilworth, M. R. (2020) · Scientific Reports · doi:10.1038/s41598-020-72930-7 · Cited by 35
Peng, H., Xu, H., Wu, J., Li, J., Zhou, Y., Ding, Z., Siwko, S. K., Yuan, X., Schalinske, K. L., Alpini, G. D., et al. (2021) · Liver International · doi:10.1111/liv.14811 · Cited by 36
Prediction of pre-eclampsia: a protocol for systematic reviews of test accuracy
Cnossen, J. S., van der Post, J., Mol, B. W., Khan, K. S., Meads, C., & ter Riet, G. (2006) · BMC Pregnancy and Childbirth · doi:10.1186/1471-2393-6-29 · Cited by 35
“In the long term, women and foetuses affected by these disorders may be prone to cardiovascular disease in adult life [24-28].”
Life course body size and lipid levels at 53 years in a British birth cohort
Skidmore, P. M. L., Hardy, R., Kuh, D. J., Langenberg, C., & Wadsworth, M. E. J. (2007) · Journal of Epidemiology & Community Health · doi:10.1136/jech.2006.047571 · Cited by 34
Diet, behavior and immunity across the lifespan
Hale, M. W., Spencer, S. J., Conti, B., Jasoni, C. L., Kent, S., Radler, M. E., Reyes, T. M., & Sominsky, L. (2014) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2014.12.009 · Cited by 34
Shao, X., Cheng, H. M., Zhou, J., Zhang, J., Zhu, Y., Yang, C., Narzo, A. D., Yu, J., Shen, Y., Li, Y., et al. (2020) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2020.110726 · Cited by 34
“This phenomenon is referred as the Developmental Origins of Health and Diseases (DOHaD) paradigm (Barker, 1997; Barker, 2004; Barker and Godfrey, 2001).”
BackgroundEndothelial caveolar subcellular domain regulation of endothelial nitric oxide synthase
Ramadoss, J., Pastore, M. B., & Magness, R. R. (2013) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.12136 · Cited by 34
“hypertensive disease, Type 2 diabetes, adiposity and other diseases, as described by the Barker hypothesis.(1)”
BackgroundEndocrinology of Fetal Development
Dattani, M., Hindmarsh, P. C., & Fisher, D. A. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4377-0324-5.00022-5 · Cited by 34
Birthweight and feeding practices are associated with child growth outcomes in South Asia
Harding, K. L., Aguayo, V. M., & Webb, P. (2018) · Maternal and Child Nutrition · doi:10.1111/mcn.12650 · Cited by 34
“, 2013), while also being identified as a risk factor for chronic disease later in life (Barker, 2004).”
BackgroundThe Effects of Early Prenatal Alcohol Exposure on Epigenome and Embryonic Development
Wallén, E., Auvinen, P., & Kaminen‐Ahola, N. (2021) · Genes · doi:10.3390/genes12071095 · Cited by 33
Low-protein diet in adult male rats has long-term effects on metabolism
Malta, A., de Oliveira, J. C., Ribeiro, T. A., Tófolo, L. P., Barella, L. F., Prates, K. V., Miranda, R. A., Elmhiri, G., Franco, C. C. D. S., Agostinho, A. R., et al. (2014) · Journal of Endocrinology · doi:10.1530/joe-13-0473 · Cited by 35
“Many metabolic diseases with high worldwide prevalence such as obesity, type 2 diabetes, and hypertension can have their etiology during fetal development (Barker 2004).”
BackgroundJones‐Smith, J. C., Fernald, L. C. H., & Neufeld, L. M. (2007) · Journal of the American Dietetic Association · doi:10.1016/j.jada.2007.09.011 · Cited by 33
Meta-analysis of sex difference in testosterone levels in umbilical cord blood
Barry, J. A., Hardiman, P. J., Siddiqui, M., & Thomas, M. (2011) · Journal of Obstetrics and Gynaecology · doi:10.3109/01443615.2011.614971 · Cited by 33
Leeuwerke, M., Eilander, M. S., Pruis, M. G. M., Lendvai, Á., Erwich, J. J., Scherjon, S. A., Plösch, T., & Eijsink, J. J. H. (2016) · Biology of Reproduction · doi:10.1095/biolreprod.115.131698 · Cited by 33
“Apart from these direct adverse outcomes, low birth weight of the fetus is also associated with health problems later in life like hypertension, coronary heart disease and diabetes [7].”
BackgroundWattez, J.-S., Delahaye, F., Barella, L. F., Dickès-Coopman, A., Montel, V., Breton, C., Mathias, P. C. D. F., Foligné, B., Lésage, J., & Vieau, D. (2014) · Journal of Developmental Origins of Health and Disease · doi:10.1017/s2040174413000548 · Cited by 32
LIFE HISTORY AND REAL LIFE: AN EXAMPLE OF NEUROANTHROPOLOGY IN ABORIGINAL AUSTRALIA
Burbank, V. K. (2012) · Annals of Anthropological Practice · doi:10.1111/j.2153-9588.2012.01097.x · Cited by 32
The Association of Maternal Age with Birth Weight and Gestational Age: A Cross-Cohort Comparison.
Restrepo–Méndez, M. C., Lawlor, D. A., Horta, B. L., Matijasevich, A., Santos, I. S., Menezes, A. M. B., Barros, F. C., & Victora, C. G. (2015) · International Journal of Epidemiology · doi:10.1093/ije/dyv097.281 · Cited by 32
Goldstein, J. M., Cherkerzian, S., Buka, S. L., Fitzmaurice, G. M., Hornig, M., Gillman, M. W., O'Toole, S., & Sloan, R. P. (2011) · Journal of Developmental Origins of Health and Disease · doi:10.1017/s2040174411000651 · Cited by 32
“Birth weight has been found to be inversely associated with coronary heart disease incidence and mortality.(18) Birth weight also appears to be negatively associated with CVD risk factors in adulthood, including BP and glucose intolerance.”
BackgroundRole of Endothelin in Uteroplacental Circulation and Fetal Vascular Function
Paradis, A. N., & Zhang, L. (2013) · Current Vascular Pharmacology · doi:10.2174/1570161111311050004 · Cited by 31
“For most organisms, the most critical point occurs in utero during the fetal development [55].”
BackgroundHow could complementary feeding patterns affect the susceptibility to NCD later in life?
Adair, L. S. (2012) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2012.03.011 · Cited by 32
“A substantial literature relates fetal and early infant nutrition to adult non-communicable disease (NCD) outcomes [1,2], and a strong recent focus has been on the role of rapid weight gain in infancy.”
BackgroundCohort Profile: Stress in Pregnancy (SIP) Study
Finik, J. M., & Nomura, Y. (2017) · International Journal of Epidemiology · doi:10.1093/ije/dyw264 · Cited by 32
The cellularity of offspring's adipose tissue is programmed by maternal nutritional manipulations
Lecoutre, S., & Breton, C. (2014) · Adipocyte · doi:10.4161/adip.29806 · Cited by 31
“These observations have participated in establishing the Developmental Origin of Health and Disease (DOHaD) hypothesis.(2) This concept states that an adverse environment in utero or during infancy, including dysnutrition, can program or imprint the development of several tissues, including the adipose tissue.”
BackgroundRice, M. S., & Valentine, C. J. (2015) · Nutrition in Clinical Practice · doi:10.1177/0884533615578917 · Cited by 31
Anderson, L. N., Knight, J. A., Hung, R. J., Hewko, S. L., Seeto, R. A., Martin, M., Fleming, A. S., Maguire, J. L., Matthews, S. G., Murphy, K. E., et al. (2018) · Paediatric and Perinatal Epidemiology · doi:10.1111/ppe.12473 · Cited by 31
Rahman, M. L., Liang, L., Valeri, L., Su, L., Zhu, Z., Gao, S., Mostofa, G., Qamruzzaman, Q., Hauser, R. B., Baccarelli, A., et al. (2018) · Epigenetics · doi:10.1080/15592294.2018.1481704 · Cited by 31
“Low birthweight is an important population indicator of neonatal mortality and morbidity and an established risk factor for later-life chronic diseases, particularly cardiovascular disease and metabolic syndrome [1, 2].”
BackgroundNutritional, pharmacological, and environmental programming of NAFLD in early life
Galvan-Martinez, D. H., Bosquez-Mendoza, V. M., Ruíz‐Noa, Y., Ibarra‐Reynoso, L. D. R., Barbosa‐Sabanero, G., & Lazo-de-la-Vega-Monroy, M.-L. (2022) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00168.2022 · Cited by 31
Church, M. W., Jen, K. ‐. C., Stafferton, T., Hotra, J. W., & Adams, B. R. (2006) · Neurotoxicology and Teratology · doi:10.1016/j.ntt.2006.10.009 · Cited by 31
“It is well accepted that adverse prenatal conditions can program the fetus for subsequent childhood and adult-onset disorders [3].”
BackgroundGreenwood, P. L., Thompson, A. N., & Ford, S. P. (2009) · Springer eBooks · doi:10.1007/978-90-481-3135-8_1 · Cited by 31
“While these studies initially related to agricultural production, within the last decade or so many studies have used sheep as an experimental model of fetal programming, following widespread recognition that fetal development may have long-term health implications in humans [7, 8 ]. Increasingly, these studies have f…”
BackgroundThe appearance of discretionary income: Influence on the prevalence of under- and over-nutrition
Karp, R. J., Cheng, C. I.-F., & Meyers, A. F. (2005) · International Journal for Equity in Health · doi:10.1186/1475-9276-4-10 · Cited by 31
“A final consideration, deriving from the work of David Barker and colleagues in England [29] is that undernutrition in-utero and during the first months of life is a precursor of obesity and the elements of the metabolic syndrome later in life.”
BackgroundPerinatal Nutrition Programs the Hypothalamic Melanocortin System in Offspring
Wattez, J.-S., Delahaye, F., Lukaszewski, M., Risold, P., Eberlé, D., Vieau, D., & Breton, C. (2013) · Hormone and Metabolic Research · doi:10.1055/s-0033-1357182 · Cited by 32
Marks, K. J., Howards, P. P., Smarr, M. M., Flanders, W. D., Northstone, K., Daniel, J. H., Sjödin, A., Calafat, A. M., & Hartman, T. J. (2021) · Epidemiology · doi:10.1097/ede.0000000000001351 · Cited by 30
Developmental programming and beef production
Greenwood, P. L., Clayton, E. H., & Bell, A. W. (2017) · Animal Frontiers · doi:10.2527/af.2017-0127 · Cited by 30
Analysis of ‘sensitive’ periods of fetal and child growth
Zhang, X., Tilling, K. M., Martin, R. M., Oken, E., Naimi, A. I., Aris, I. M., Yang, S., & Kramer, M. S. (2018) · International Journal of Epidemiology · doi:10.1093/ije/dyy045 · Cited by 30
“In the DOHaD literature, growth in weight, length/height, and body mass index (BMI) have often been studied at birth and during infancy and childhood for their associations with adiposity, obesity, blood pressure, and other cardiometabolic outcomes later in life.(6, 12-16) One of the”
BackgroundAberrant NMDA-dependent LTD after perinatal ethanol exposure in young adult rat hippocampus
Kervern, M., de Ferron, B. S., Alaux‐Cantin, S., Fedorenko, O. A., Antol, J., Naassïla, M., & Pierrefiche, O. (2015) · Hippocampus · doi:10.1002/hipo.22414 · Cited by 33
Vrselja, A., Pillow, J. J., & Black, M. J. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10173896 · Cited by 31
“It is clear that early life events impact organ development and function deleteriously, and thus programme infants for increased vulnerability to developing adulthood disease [28,29].”
BackgroundDeclerck, K., Szic, K. S. V., Palagani, A., Heyninck, K., Haegeman, G., Morand, C., Milenković, D., & Berghe, W. V. (2015) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026615666150825141720 · Cited by 29
Feto-placental vascular dysfunction as a prenatal determinant of adult cardiovascular disease
Pisaneschi, S., Boldrini, A., Genazzani, A. R., Coceani, F., & Simoncini, T. (2013) · Internal and Emergency Medicine · doi:10.1007/s11739-013-0925-y · Cited by 29
“have a disproportionately high fat mass in relation to lean body mass, which will lead to insulin resistance [7].”
BackgroundLv, Y., Fu, L., Zhang, Z., Gu, W., Luo, X., Zhong, Y., Xu, S., Wang, Y., Yan, L., Li, M., et al. (2019) · Journal of the American Heart Association · doi:10.1161/jaha.118.010456 · Cited by 28
“5 on PASMCs in IUGR rats after 2 weeks of hypoxia, causing exaggerated PAH in adults as previously suggested.1 The progression and outcome of PAs underlie PAH following IUGR.”
BackgroundInfluentialDiet and the developing immune system
Langley‐Evans, S. C., & Carrington, L. J. (2006) · Lupus · doi:10.1177/0961203306070001 · Cited by 29
Controversies in the management of hyperglycemia in the ELBW infant.
Kairamkonda, V., & Khashu, M. (2008) · PubMed · Cited by 29
Predictors of growth velocity in early infancy in a resource-poor setting
Olusanya, B. O., & Renner, J. K. (2011) · Early Human Development · doi:10.1016/j.earlhumdev.2011.05.002 · Cited by 28
de Wijs-Meijler, D. P. M., Duncker, D. J., Tibboel, D., SCHERMULY, R. T., Weißmann, N., Merkus, D., & Reiss, I. K. M. (2016) · Pulmonary Circulation · doi:10.1086/689748 · Cited by 28
Durhan, G., Unverdi, H. G., Deveci, C. D., BÜYÜKŞİRECİ, M., Karakaya, J., Değirmenci, T., Bayrak, A., Koşar, P. N., Hücümenoğlu, S., & Ergün, Y. (2016) · Ultrasound in Medicine & Biology · doi:10.1016/j.ultrasmedbio.2016.08.037 · Cited by 28
Gagné‐Ouellet, V., Breton, É., Thibeault, K., Fortin, C., Cárdenas, A., Guérin, R., Perron, P., Hivert, M., & Bouchard, L. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21010329 · Cited by 30
Metabolic Impact of Growth Hormone Treatment in Short Children Born Small for Gestational Age
Lebl, J., Lebenthal, Y., Koloušková, S., Steensberg, A., Jøns, K., Kappelgaard, A., Ibáñez, L., & Phillip, M. (2011) · Hormone Research in Paediatrics · doi:10.1159/000329729 · Cited by 27
“Although the main aim of GH treatment in short SGA children is to increase height, additional metabolic effects derived from this therapy may modify food intake, appetite and body composition, and potentially result in favourable long-term metabolic benefits. SGA children with spontaneous catch-up growth appear to be…”
BackgroundJohnson, W., Kuh, D. J., Tikhonoff, V., Charakida, M., Woodside, J., Whincup, P. H., Hughes, A. D., Deanfield, J. E., & Hardy, R. (2014) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.113.302572 · Cited by 27
Obesity, Metabolic Syndrome and Disorders of Energy Balance
Han, J. C., & Weiss, R. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-62520-3.00024-5 · Cited by 27
Nutritional genomics: a practical approach by early life conditioning with dietary phosphorus
Ashwell, C. M., & Angel, R. (2010) · Revista Brasileira de Zootecnia · doi:10.1590/s1516-35982010001300030 · Cited by 27
“However, if this ‘programming’ of metabolism during embryonic and fetal development is inappropriate for the long-term nutritional environment it may lead to adverse long term consequences for the offspring (Sayer et al., 2004; Yajnik, 2004; Barker, 2004).”
BackgroundChisaka, T., Mogi, M., Nakaoka, H., Kan‐no, H., Tsukuda, K., Wang, X., Bai, H., Shan, B., Kukida, M., Iwanami, J., et al. (2015) · American Journal of Hypertension · doi:10.1093/ajh/hpv072 · Cited by 26
From Birth to “Immunohealth,” Allergies and Enterocolitis
Houghteling, P. D., & Walker, W. A. (2015) · Journal of Clinical Gastroenterology · doi:10.1097/mcg.0000000000000355 · Cited by 26
Fetal developmental programing: insights from human studies and experimental models
Lopes, G. A. D., Ribeiro, V. L. B., Barbisan, L. F., & Rodrigues, M. A. M. (2016) · The Journal of Maternal-Fetal & Neonatal Medicine · doi:10.1080/14767058.2016.1183635 · Cited by 25
“[9] proposed that the primary programing influence experienced by the human fetus is maternal nutrition.”
BackgroundO’Neill, K. M., Irwin, R. E., Mackin, S.-J., Thursby, S.-J., Thakur, A., Bertens, C., Masala, L., Loughery, J., McArt, D. G., & Walsh, C. P. (2018) · Epigenetics & Chromatin · doi:10.1186/s13072-018-0182-4 · Cited by 25
Racial differences of early vascular aging in children and adolescents
Kruger, R., Gafane-Matemane, L. F., & Kagura, J. (2020) · Pediatric Nephrology · doi:10.1007/s00467-020-04593-5 · Cited by 26
Zander‐Fox, D., Fullston, T., McPherson, N. O., Sandeman, L., Kang, W. X., Good, S. B., Spillane, M., & Lane, M. (2015) · Biology of Reproduction · doi:10.1095/biolreprod.114.123489 · Cited by 27
“In these studies, offspring also displayed changes to glucose homeostasis, insulin resistance, and lipid metabolism; however, whether this resulted from increased adiposity accumulation with age, or vice versa, remains to be elucidated [58–63].”
Background
Metadata
- Authors
- Barker, D.
- Affiliations
- Southampton General Hospital (GB)
- Corresponding author
- Barker, DJP
- Venue
- Acta Paediatrica
- Publisher
- Wiley
- Published
- 2004-11
- Volume
- 93
- Issue
- s446
- Pages
- 26-33
- ISSN
- 0365-1436 (ISSN-L)
- 0803-5253
- 1651-2227
- OpenAlex
- W2143230895
- Cited by
- 790
- References
- 53
- Citations by year
- 2026: 19 · 2025: 38 · 2024: 49 · 2023: 42 · 2022: 36 · 2021: 63 · 2020: 55 · 2019: 42 · 2018: 39 · 2017: 37 · 2016: 33 · 2015: 40 · 2014: 37 · 2013: 40 · 2012: 45
- FWCI
- 17.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Paediatrica (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- developmental origins of health and disease, low birth weight, coronary artery disease, stroke, hypertension, type 2 diabetes, developmental plasticity, fetal growth restriction, gestational age, child weight gain, environmental influences on development
- MeSH terms
- Adult, Birth Weight, Cardiovascular Diseases, Child, Child Development, Child, Preschool, Chronic Disease, Diabetes Mellitus, Type 2, Female, Humans, Infant, Infant, Newborn, Male
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