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Journal articles on the topic 'Fetal origins of adult disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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1

Morley, Ruth, and Terence Dwyer. "Fetal Origins of Adult Disease Fetal Origins Of Adult Disease?" Clinical and Experimental Pharmacology and Physiology 28, no. 11 (November 2001): 962–66. http://dx.doi.org/10.1046/j.1440-1681.2001.03557.x.

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2

Bora, Rishabh, and Neharika Malhotra Bora. "Fetal Origin of Adult Disease." Donald School Journal of Ultrasound in Obstetrics and Gynecology 8, no. 2 (2014): 164–77. http://dx.doi.org/10.5005/jp-journals-10009-1352.

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ABSTRACT Fetal origins of adult disease, a concept first popularized by Dr David Barker, has subsequently led to many studies which have provided the evidence that certain diseases do have links pointing to fetal origins—adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood. Links that are well-established are—reduced birth weight and increased risk of coronary heart disease, hypertension and stroke in adulthood. The concept of a fetal origin of adult disease have been extended well-beyond coronary heart disease and being a risk factor for coronary heart disease, and now includes investigations of the development of the central nervous system, early origins of adult mental health and cognitive function. By understanding fetal origin of adult disease, health care professionals and policy makers will make this issue a high health care priority and implement preventive measures and treatment for those at higher risk for chronic diseases. How to cite this article Malhotra N, Malhotra J, Bora NM, Bora R, Malhotra K. Fetal Origin of Adult Disease. Donald School J Ultrasound Obstet Gynecol 2014;8(2):164-177.

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3

Simmons, Rebecca. "Fetal Origins of Adult Disease." NeoReviews 5, no. 12 (December 2004): e511-e515. http://dx.doi.org/10.1542/neo.5-12-e511.

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4

Choi, Gyu Yeon. "Fetal origins of adult disease." Korean Journal of Obstetrics and Gynecology 53, no. 6 (2010): 475. http://dx.doi.org/10.5468/kjog.2010.53.6.475.

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5

Morley, Ruth. "Fetal origins of adult disease." Seminars in Fetal and Neonatal Medicine 11, no. 2 (April 2006): 73–78. http://dx.doi.org/10.1016/j.siny.2005.11.001.

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6

Langley-Evans, Simon C. "Fetal origins of adult disease." British Journal of Nutrition 81, no. 1 (January 1999): 5–6. http://dx.doi.org/10.1017/s0007114599000070.

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7

Calkins, Kara, and Sherin U. Devaskar. "Fetal Origins of Adult Disease." Current Problems in Pediatric and Adolescent Health Care 41, no. 6 (July 2011): 158–76. http://dx.doi.org/10.1016/j.cppeds.2011.01.001.

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8

Barker, DJP. "The fetal origins of adult disease." Fetal and Maternal Medicine Review 6, no. 2 (May 1994): 71–80. http://dx.doi.org/10.1017/s0965539500001005.

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Recent studies have shown that babies who are small for dates at birth, or who fail to grow in infancy, have, in adult life, raised blood pressure, impaired glucose tolerance, abnormal serum lipids, raised fibrinogen and high death rates from coronary disease, stroke and obstructive lung disease. This has led to the hypothesis that these diseases are ‘programmed’ in utero in response to an adverse environment.

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9

Hanson, M. "Fetal origins of adult disease: introduction." Heart 91, no. 7 (July 1, 2005): 863. http://dx.doi.org/10.1136/hrt.2004.047357.

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10

Robinson, R. "The fetal origins of adult disease." BMJ 322, no. 7283 (February 17, 2001): 375–76. http://dx.doi.org/10.1136/bmj.322.7283.375.

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11

BARKER, D. J. P. "THE FETAL ORIGINS OF ADULT DISEASE." Nutrition Today 31, no. 3 (May 1996): 108–14. http://dx.doi.org/10.1097/00017285-199605000-00004.

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12

Nguyễn Công, Khanh. "FETAL ORIGIN OF ADULT DISEASE." Tạp chí Nhi khoa 13, no. 6 (June 2, 2021): 1–9. http://dx.doi.org/10.52724/tcnk.v13i6.28.

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“Fetal origins of adult disease”, often called the “Barker hypothesis” after a large proportion data of Barker and colleagues in Southampton over the last decade, that adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in structure, physiology, metabolism, which result in increased disease risk in adulthood. Many further studies have provided evidence for the hypothesis that size at birth is related to the risk of developing disease in later life. In particular, links are well established between reduced birthweight and increased risk of coronary heart disease, diabetes, hypertension and stroke in adulthood. The most widely accepted mechanisms thought to underlie these relationship are those of altered fetal nutrition, genetic–epigenetic links, fetal programming and fetal excess glucocorticoid exposure. It is suggested that the fetus makes physiological adaption in response to changes in its environment to prepare itself for posnatal life. The “Fetal origin of adult disease” hypothesis is attractive. It suggests that these diseases could be prevented by improving maternal health and fetal development

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13

van Ginneken, Vincent, and Clemens Löwik. "“Extension of the “Fetal Origin Hypothesis of Barker” towards the “Fetal Origin Hypothesis of Mental Diseases”." Psychology and Mental Health Care 2, no. 3 (July 6, 2018): 01–07. http://dx.doi.org/10.31579/2637-8892/033.

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In this editorial we will first describe most common information about the intriguing “traditional” fetal origin hypothesis of Barker for physiological, endocrine and cardiovascular diseases (CVDs). The ‘developmental origins of adult disease’ hypothesis, often called the ‘Barker hypothesis’, states that adverse inﬂuences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood.

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14

Paraskevas, Kosmas I., Despina D. Briana, Ariadne Malamitsi-Puchner, and Dimitri P. Mikhailidis. "Fetal/Infant Origins of Adult Vascular Disease." Current Vascular Pharmacology 18, no. 4 (June 4, 2020): 418–20. http://dx.doi.org/10.2174/1570161118999200304123040.

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15

Hales, C. N. "Fetal and infant origins of adult disease." Journal of Clinical Pathology 50, no. 5 (May 1, 1997): 359. http://dx.doi.org/10.1136/jcp.50.5.359.

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16

Becker, Genevieve. "Fetal and Infant Origins of Adult Disease." Journal of Human Lactation 11, no. 1 (March 1995): 62. http://dx.doi.org/10.1177/089033449501100134.

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17

KAJANTIE, E. "Fetal Origins of Stress-Related Adult Disease." Annals of the New York Academy of Sciences 1083, no. 1 (November 1, 2006): 11–27. http://dx.doi.org/10.1196/annals.1367.026.

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18

Smith, G. D. "Fetal and infant origins of adult disease." Heart 69, no. 5 (May 1, 1993): 467–68. http://dx.doi.org/10.1136/hrt.69.5.467.

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19

ARTMAN, M. "Fetal and Infant Origins of Adult Disease." Cardiovascular Research 27, no. 6 (June 1, 1993): 1137. http://dx.doi.org/10.1093/cvr/27.6.1137a.

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20

Barker, D. J. P. "1.W04.1 Fetal origins of adult disease." Atherosclerosis 134, no. 1-2 (October 1997): 11. http://dx.doi.org/10.1016/s0021-9150(97)88154-3.

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21

Barker, D. J. P. "Fetal and infant origins of adult disease." Monatsschrift Kinderheilkunde 149 (June 1, 2001): S2—S6. http://dx.doi.org/10.1007/s001120170002.

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22

Williams, R. "Fetal and Infant Origins of Adult Disease." Journal of Epidemiology & Community Health 47, no. 4 (August 1, 1993): 337. http://dx.doi.org/10.1136/jech.47.4.337.

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23

Bradley, P. "Fetal and infant origins of adult disease." BMJ 302, no. 6768 (January 12, 1991): 113. http://dx.doi.org/10.1136/bmj.302.6768.113-a.

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24

Alberman, E. "Fetal and Infant Origins of Adult Disease." Archives of Disease in Childhood 68, no. 3 (March 1, 1993): 434. http://dx.doi.org/10.1136/adc.68.3.434-c.

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25

Wallace, Helen M. "Fetal and Infant Origins of Adult Disease." JAMA: The Journal of the American Medical Association 269, no. 6 (February 10, 1993): 802. http://dx.doi.org/10.1001/jama.1993.03500060102043.

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26

Byrne, C. D. "Fetal origins of adult disease: epidemiology and mechanisms." Journal of Clinical Pathology 53, no. 11 (November 1, 2000): 822–28. http://dx.doi.org/10.1136/jcp.53.11.822.

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27

Rocchini, Albert P. "Fetal and pediatric origins of adult cardiovascular disease." Current Opinion in Pediatrics 6, no. 5 (October 1994): 591–95. http://dx.doi.org/10.1097/00008480-199410000-00015.

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28

PHILLIPS, D. "Endocrine programming and fetal origins of adult disease." Trends in Endocrinology and Metabolism 13, no. 9 (November 1, 2002): 363. http://dx.doi.org/10.1016/s1043-2760(02)00696-3.

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29

Lucas, A., M. S. Fewtrell, and T. J. Cole. "Fetal origins of adult disease---the hypothesis revisited." BMJ 319, no. 7204 (July 24, 1999): 245–49. http://dx.doi.org/10.1136/bmj.319.7204.245.

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30

Barker, D. J. "The fetal and infant origins of adult disease." BMJ 301, no. 6761 (November 17, 1990): 1111. http://dx.doi.org/10.1136/bmj.301.6761.1111.

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31

Miles, Harriet L., Paul L. Hofman, and Wayne S. Cutfield. "Fetal Origins of Adult Disease: A Paediatric Perspective." Reviews in Endocrine and Metabolic Disorders 6, no. 4 (December 2005): 261–68. http://dx.doi.org/10.1007/s11154-005-6184-0.

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32

Thompson, Joan Nalani. "Fetal Nutrition and Adult Hypertension, Diabetes, Obesity, and Coronary Artery Disease." Neonatal Network 26, no. 4 (July 2007): 235–40. http://dx.doi.org/10.1891/0730-0832.26.4.235.

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The fetal-origins-of-adult-disease hypothesis describes an adaptive phenomenon of in utero reprogramming of the undernourished fetus that predisposes the infant to increased morbidity as an adult. Studies have identified a positive association between indicators of fetal undernutrition such as low birth weight and chronic adult diseases like hypertension, diabetes, obesity, and coronary artery disease. Current research is focusing on determining other factors that may contribute to these chronic adult diseases.

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33

HANSON, M. "Birth Weight and the Fetal Origins of Adult Disease." Pediatric Research 52, no. 4 (September 27, 2002): 473–74. http://dx.doi.org/10.1203/01.pdr.0000028851.79917.4d.

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34

Tunstall-Pedoe, H. "Book Review: Fetal and Infant Origins of Adult Disease." Scottish Medical Journal 39, no. 1 (February 1994): 31. http://dx.doi.org/10.1177/003693309403900114.

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35

Sadler, MICHÈLE. "Fetal origins of adult disease Evidence from animal models." Nutrition Bulletin 21, no. 1 (January 1996): 54–58. http://dx.doi.org/10.1111/j.1467-3010.1996.tb00628.x.

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36

Rinaudo, Paolo, and Julie Lamb. "Fetal Origins of Perinatal Morbidity and/or Adult Disease." Seminars in Reproductive Medicine 26, no. 05 (September 2008): 436–45. http://dx.doi.org/10.1055/s-0028-1087109.

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37

Kimm, Sue Y. S. "Fetal origins of adult disease: the Barker hypothesis revisited???2004." Current Opinion in Endocrinology & Diabetes 11, no. 4 (August 2004): 192–96. http://dx.doi.org/10.1097/01.med.0000140938.39925.4c.

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38

GILLMAN, MATTHEW W. "Epidemiological challenges in studying the fetal origins of adult disease." Paediatric and Perinatal Epidemiology 19, s1 (January 2005): 1. http://dx.doi.org/10.1111/j.1365-3016.2005.00607.x.

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39

Harding, JE. "The nutritional basis of the fetal origins of adult disease." International Journal of Epidemiology 30, no. 1 (February 2001): 15–23. http://dx.doi.org/10.1093/ije/30.1.15.

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40

Skilton, M. R. "Parity and risk of stroke: Fetal origins of adult disease?" Neurology 74, no. 18 (March 24, 2010): 1408–9. http://dx.doi.org/10.1212/wnl.0b013e3181dd4e20.

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41

Gillman, M. W., and J. W. Rich-Edwards. "The fetal origins of adult disease: from sceptic to convert." Paediatric and Perinatal Epidemiology 14, no. 3 (July 2000): 192–93. http://dx.doi.org/10.1046/j.1365-3016.2000.00265.x.

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42

Burton, Graham J., Abigail L. Fowden, and Kent L. Thornburg. "Placental Origins of Chronic Disease." Physiological Reviews 96, no. 4 (October 2016): 1509–65. http://dx.doi.org/10.1152/physrev.00029.2015.

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Epidemiological evidence links an individual's susceptibility to chronic disease in adult life to events during their intrauterine phase of development. Biologically this should not be unexpected, for organ systems are at their most plastic when progenitor cells are proliferating and differentiating. Influences operating at this time can permanently affect their structure and functional capacity, and the activity of enzyme systems and endocrine axes. It is now appreciated that such effects lay the foundations for a diverse array of diseases that become manifest many years later, often in response to secondary environmental stressors. Fetal development is underpinned by the placenta, the organ that forms the interface between the fetus and its mother. All nutrients and oxygen reaching the fetus must pass through this organ. The placenta also has major endocrine functions, orchestrating maternal adaptations to pregnancy and mobilizing resources for fetal use. In addition, it acts as a selective barrier, creating a protective milieu by minimizing exposure of the fetus to maternal hormones, such as glucocorticoids, xenobiotics, pathogens, and parasites. The placenta shows a remarkable capacity to adapt to adverse environmental cues and lessen their impact on the fetus. However, if placental function is impaired, or its capacity to adapt is exceeded, then fetal development may be compromised. Here, we explore the complex relationships between the placental phenotype and developmental programming of chronic disease in the offspring. Ensuring optimal placentation offers a new approach to the prevention of disorders such as cardiovascular disease, diabetes, and obesity, which are reaching epidemic proportions.

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43

Nobile, Stefano, Chiara Di Sipio Morgia, and Giovanni Vento. "Perinatal Origins of Adult Disease and Opportunities for Health Promotion: A Narrative Review." Journal of Personalized Medicine 12, no. 2 (January 25, 2022): 157. http://dx.doi.org/10.3390/jpm12020157.

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The “developmental origins of health and disease” (DOHaD) hypothesis refers to the influence of early developmental exposures and fetal growth on the risk of chronic diseases in later periods. During fetal and early postnatal life, cell differentiation and tissue formation are influenced by several factors. The interaction between genes and environment in prenatal and early postnatal periods appears to be critical for the onset of multiple diseases in adulthood. Important factors influencing this interaction include genetic predisposition, regulation of gene expression, and changes in microbiota. Premature birth and intrauterine growth restriction (IUGR) are other important factors considered by the DOHaD hypothesis. Preterm birth is associated with impaired or arrested structural or functional development of key organs/systems, making preterm infants vulnerable to cardiovascular, respiratory, and chronic renal diseases during adulthood. Growth restriction, defined as impaired fetal growth compared to expected biological potential in utero, is an additional negative factor increasing the risk of subsequent diseases. Environmental factors implicated in the developmental programming of diseases include exposure to pollution, stress, drugs, toxic agents, nutrition, and exercise. The DOHaD may explain numerous conditions, including cardiovascular, metabolic, respiratory, neuropsychiatric, and renal diseases. Potential antenatal and postnatal preventive measures, interventions, and future directions are discussed.

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44

Gillman, Matthew W. "Epidemiological challenges in studying the fetal origins of adult chronic disease." International Journal of Epidemiology 31, no. 2 (April 2002): 294–99. http://dx.doi.org/10.1093/intjepid/31.2.294.

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45

Gillman, M. W. "Epidemiological challenges in studying the fetal origins of adult chronic disease." International Journal of Epidemiology 31, no. 2 (April 1, 2002): 294–99. http://dx.doi.org/10.1093/ije/31.2.294.

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46

Barker, DJP, JG Eriksson, T. Forsén, and C. Osmond. "Fetal origins of adult disease: strength of effects and biological basis." International Journal of Epidemiology 31, no. 6 (December 2002): 1235–39. http://dx.doi.org/10.1093/ije/31.6.1235.

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47

Hall, JG. "The importance of the fetal origins of adult disease for geneticists." Clinical Genetics 72, no. 2 (July 26, 2007): 67–73. http://dx.doi.org/10.1111/j.1399-0004.2007.00842.x.

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48

Phillips, David I. W. "Programming of adrenocortical function and the fetal origins of adult disease." Journal of Endocrinological Investigation 24, no. 9 (October 2001): 742–46. http://dx.doi.org/10.1007/bf03343920.

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49

Guo, Jun, Jue Wu, Qinyuan He, Mengshu Zhang, Hong Li, and Yanping Liu. "The Potential Role of PPARs in the Fetal Origins of Adult Disease." Cells 11, no. 21 (November 2, 2022): 3474. http://dx.doi.org/10.3390/cells11213474.

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The fetal origins of adult disease (FOAD) hypothesis holds that events during early development have a profound impact on one’s risk for the development of future adult disease. Studies from humans and animals have demonstrated that many diseases can begin in childhood and are caused by a variety of early life traumas, including maternal malnutrition, maternal disease conditions, lifestyle changes, exposure to toxins/chemicals, improper medication during pregnancy, and so on. Recently, the roles of Peroxisome proliferator-activated receptors (PPARs) in FOAD have been increasingly appreciated due to their wide variety of biological actions. PPARs are members of the nuclear hormone receptor subfamily, consisting of three distinct subtypes: PPARα, β/δ, and γ, highly expressed in the reproductive tissues. By controlling the maturation of the oocyte, ovulation, implantation of the embryo, development of the placenta, and male fertility, the PPARs play a crucial role in the transition from embryo to fetus in developing mammals. Exposure to adverse events in early life exerts a profound influence on the methylation pattern of PPARs in offspring organs, which can affect development and health throughout the life course, and even across generations. In this review, we summarize the latest research on PPARs in the area of FOAD, highlight the important role of PPARs in FOAD, and provide a potential strategy for early prevention of FOAD.

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50

Magalhães, Elizabeth, Maria Méio, and Maria Moreira. "Hormonal Biomarkers for Evaluating the Impact of Fetal Growth Restriction on the Development of Chronic Adult Disease." Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics 41, no. 04 (April 2019): 256–63. http://dx.doi.org/10.1055/s-0039-1683904.

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AbstractThe hypothesis of fetal origins to adult diseases proposes that metabolic chronic disorders, including cardiovascular diseases, diabetes, and hypertension originate in the developmental plasticity due to intrauterine insults. These processes involve an adaptative response by the fetus to changes in the environmental signals, which can promote the reset of hormones and of the metabolism to establish a “thrifty phenotype”. Metabolic alterations during intrauterine growth restriction can modify the fetal programming. The present nonsystematic review intended to summarize historical and current references that indicated that developmental origins of health and disease (DOHaD) occur as a consequence of altered maternal and fetal metabolic pathways. The purpose is to highlight the potential implications of growth factors and adipokines in “developmental programming”, which could interfere in the development by controlling fetal growth patterns. These changes affect the structure and the functional capacity of various organs, including the brain, the kidneys, and the pancreas. These investigations may improve the approach to optimizing antenatal as well as perinatal care aimed to protect newborns against long-term chronic diseases.

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