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Journal articles on the topic 'Barker hypothesis'

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Author: Grafiati

Published: 4 June 2021

Last updated: 25 January 2023

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1

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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2

Daniels, Stephen R. "The Barker hypothesis revisited." Journal of Pediatrics 151, no. 6 (December 2007): A3. http://dx.doi.org/10.1016/j.jpeds.2007.10.036.

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3

Daniels, Stephen R. "The Barker hypothesis revisited." Journal of Pediatrics 173 (June 2016): 1–3. http://dx.doi.org/10.1016/j.jpeds.2016.04.031.

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4

Wilson, John. "The Barker Hypothesis An Analysis." Australian and New Zealand Journal of Obstetrics and Gynaecology 39, no. 1 (February 1999): 1–7. http://dx.doi.org/10.1111/j.1479-828x.1999.tb03432.x.

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5

Wang, Yan Qiu, Hui Juan Zhang, and Martin J. Quinn. "Fetal Hypertension and the “Barker Hypothesis”." Angiology 71, no. 1 (August 29, 2019): 92–93. http://dx.doi.org/10.1177/0003319719870952.

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6

Young, Lorraine E. "Imprinting of Genes and the Barker Hypothesis." Twin Research 4, no. 5 (October 1, 2001): 307–17. http://dx.doi.org/10.1375/1369052012632.

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7

Lumbers, Eugenie R., Ze-Yan Yu, and Karen J. Gibson. "The Selfish Brain And The Barker Hypothesis." Clinical and Experimental Pharmacology and Physiology 28, no. 11 (November 2001): 942–47. http://dx.doi.org/10.1046/j.1440-1681.2001.03554.x.

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8

Gram, I. T., B. Straume, M. L. Lochen, B. K. Jacobsen, E. Arnesen, and E. Lund. "Earlier published work supports the "Barker hypothesis"." BMJ 310, no. 6992 (June 3, 1995): 1468. http://dx.doi.org/10.1136/bmj.310.6992.1468b.

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9

Young, Lorraine E. "Imprinting of Genes and the Barker Hypothesis." Twin Research 4, no. 5 (October 1, 2001): 307–17. http://dx.doi.org/10.1375/twin.4.5.307.

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AbstractSeveral common adult diseases appear to be related to impaired fetal growth and this may be caused either by nutritional inadequacies at particular stages of pregnancy or by variation in alleles at specific growth loci. Little is known about the genes involved in the underlying mechanism. This review proposes that at least some of the effects have their origins at imprinted loci, genes that are unusual because they are expressed from only one parental allele. Many imprinted genes are crucial for fetal growth and determine birthweight. They can be disrupted in the early embryo by environmental influences and these disruptions can be inherited through many cell cycles into adult tissues. Their disruption can affect specific organs during fetal development and disruption could affect adult disease in a variety of direct and indirect means. Imprinted genes may be particularly vulnerable to disruption as they are functionally haploid and their expression is regulated by different means from the rest of the genome. Thus many imprinted genes provide plausible candidates for programming adult disease and warrant further study in this context.

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10

Poulter, Neil R. "Birthweights, maternal cardiovascular events, and Barker hypothesis." Lancet 357, no. 9273 (June 2001): 1990–91. http://dx.doi.org/10.1016/s0140-6736(00)05131-x.

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11

DE BOO, Hendrina A., and Jane E. HARDING. "The developmental origins of adult disease (Barker) hypothesis." Australian and New Zealand Journal of Obstetrics and Gynaecology 46, no. 1 (February 2006): 4–14. http://dx.doi.org/10.1111/j.1479-828x.2006.00506.x.

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12

Ferrucci, Luigi. "Aging Across the Lifespan: Rethinking the David Barker Hypothesis." Innovation in Aging 5, Supplement_1 (December 1, 2021): 32. http://dx.doi.org/10.1093/geroni/igab046.118.

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Abstract For many years, the scope of geriatric medicine has been the care of older persons affected by multiple disease with the aim of improving their functional status and optimize quality of life. As our knowledge of the mechanisms of aging grows rapidly, it is becoming clear that accomplishing this scope requires taking a life-course perspective. Research have failed to establish a clear-cut distinction between normal aging and pathology leading to the hypothesis that aging is at the root of chronic diseases, and difference in health can be ascribed to different aging rates. Research in model organisms, suggest that aging can be modified with consequent changes on healthspan and longevity. Interventions that modulate aging may ultimately prevent most-age-associated diseases and their consequences. From this perspective, geriatric medicine is the leading and most promising branch of biomedical science. Challenges remain: first, demonstrating that certain interventions slow down the aging rate requires the valid measure of aging, and while many tools were developed, “epigenetic clocks” being the most promising, the underline mechanism that drive their changes with aging and validity in clinical applications are unclear. We do not know whether variability in the rate of biological aging assessed in old age are already detectable in younger individuals and person-specific rates remain constant during life. In 1986, David Barker stated the hypothesis that the period of gestation, characterized by a strong epigenetic imprinting, affects health and wellbeing across life, perhaps by setting the aging rate. Perhaps pediatric and geriatric medicine are more connected than previously believed.

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13

Fraser, Robert, and Janet Cresswell. "What should obstetricians be doing about the Barker hypothesis?" BJOG: An International Journal of Obstetrics and Gynaecology 104, no. 6 (June 1997): 645–47. http://dx.doi.org/10.1111/j.1471-0528.1997.tb11972.x.

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14

Scott, R. "Sociology and the Barker Hypothesis: Transdisciplinary approaches to obesity." Canadian Journal of Diabetes 35, no. 2 (January 2011): 176. http://dx.doi.org/10.1016/s1499-2671(11)52140-9.

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15

Paneth, N., and M. Susser. "Early origin of coronary heart disease (the "Barker hypothesis")." BMJ 310, no. 6977 (February 18, 1995): 411–12. http://dx.doi.org/10.1136/bmj.310.6977.411.

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16

Rogers, John M. "The Barker hypothesis: implications for future directions in toxicology research." Current Opinion in Endocrinology and Diabetes 13, no. 6 (December 2006): 536–40. http://dx.doi.org/10.1097/med.0b013e328010d23b.

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17

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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18

Kilby, M. D. "Placental glucocorticoid metabolism: An endocrine link with the barker hypothesis." International Journal of Gynecology & Obstetrics 70 (2000): C8. http://dx.doi.org/10.1016/s0020-7292(00)81410-1.

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19

Almond, Douglas, and Janet Currie. "Killing Me Softly: The Fetal Origins Hypothesis." Journal of Economic Perspectives 25, no. 3 (August 1, 2011): 153–72. http://dx.doi.org/10.1257/jep.25.3.153.

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In the epidemiological literature, the fetal origins hypothesis associated with David J. Barker posits that chronic, degenerative conditions of adult health, including heart disease and type 2 diabetes, may be triggered by circumstances decades earlier, particularly, by in utero nutrition. Economists have expanded on this hypothesis, investigating a broader range of fetal shocks and circumstances and have found a wealth of later-life impacts on outcomes including test scores, educational attainment, and income, along with health. In the process, they have provided some of the most credible observational evidence in support of the hypothesis. The magnitude of the impacts is generally large. Thus, the fetal origins hypothesis has not only survived contact with economics, but has flourished.

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20

Walters, E., and RG Edwards. "Further thoughts regarding evidence offered in support of the ‘Barker hypothesis’." Reproductive BioMedicine Online 9, no. 2 (January 2004): 129–31. http://dx.doi.org/10.1016/s1472-6483(10)62121-9.

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21

Scott Yoshizawa, Rebecca. "The Barker hypothesis and obesity: Connections for transdisciplinarity and social justice." Social Theory & Health 10, no. 4 (September 5, 2012): 348–67. http://dx.doi.org/10.1057/sth.2012.11.

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22

Armelagos, George J., Alan H. Goodman, Kristin N. Harper, and Michael L. Blakey. "Enamel hypoplasia and early mortality: Bioarcheological support for the Barker hypothesis." Evolutionary Anthropology: Issues, News, and Reviews 18, no. 6 (November 2009): 261–71. http://dx.doi.org/10.1002/evan.20239.

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23

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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24

Barker, Mary, Caroline H. Fall, Clive Osmond, Cyrus Cooper, Tom P. Fleming, Kent L. Thornburg, and Graham J. Burton. "David James Purslove Barker. 29 June 1938—27 August 2013." Biographical Memoirs of Fellows of the Royal Society 67 (August 7, 2019): 29–57. http://dx.doi.org/10.1098/rsbm.2019.0021.

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Professor David James Purslove Barker was a physician and one of the most influential medical scientists of our time. His fetal programming hypothesis (known as the Barker Hypothesis) transformed thinking about what causes chronic diseases that are the scourge of modern society: cancer, cardiovascular disease and diabetes. The Barker Hypothesis proposed that the environment of the fetus and infant determined by maternal nutrition and exposure to infection subsequently predisposes the pathologies of later life. He challenged the idea that chronic diseases result from a combination of bad genes and unhealthy adult lifestyle. The environment of the fetus and infant, he suggested, permanently set or ‘programmed’ the body's metabolism and growth, and thereby pathologies of old age. His initially controversial, but now widely accepted, ideas have produced an explosion of research worldwide into the complex processes of nutrition and growth during intrauterine and early post-natal life and how these cause adult diseases. His discoveries created a new field of research, developmental origins of health and disease (DOHaD), influencing global scientific thinking. David believed that ‘the poorer health of people in lower socio-economic groups or living in impoverished places was linked to past and present neglect of the welfare of mothers and babies’. Tackling the epidemics of diabetes and heart disease in the Western world and in developing countries would require, he said, a shift in focus to prioritize the health and nutrition of adolescent girls, pregnant women and infants. This focus has subsequently been enshrined in global health policies and priorities.

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25

Mann, Philippa, Janet Green, and Karen Walker. "Twin-to-twin transfusion syndrome and potential applicability to the Barker hypothesis." Journal of Neonatal Nursing 22, no. 5 (October 2016): 223–27. http://dx.doi.org/10.1016/j.jnn.2016.03.002.

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26

Ryznar, Rebecca Jean, Lacie Phibbs, and Lon J. Van Winkle. "Epigenetic Modifications at the Center of the Barker Hypothesis and Their Transgenerational Implications." International Journal of Environmental Research and Public Health 18, no. 23 (December 2, 2021): 12728. http://dx.doi.org/10.3390/ijerph182312728.

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Embryo/fetal nutrition and the environment in the reproductive tract influence the subsequent risk of developing adult diseases and disorders, as formulated in the Barker hypothesis. Metabolic syndrome, obesity, heart disease, and hypertension in adulthood have all been linked to unwanted epigenetic programing in embryos and fetuses. Multiple studies support the conclusion that environmental challenges, such as a maternal low-protein diet, can change one-carbon amino acid metabolism and, thus, alter histone and DNA epigenetic modifications. Since histones influence gene expression and the program of embryo development, these epigenetic changes likely contribute to the risk of adult disease onset not just in the directly affected offspring, but for multiple generations to come. In this paper, we hypothesize that the effects of parental nutritional status on fetal epigenetic programming are transgenerational and warrant further investigation. Numerous studies supporting this hypothesis are reviewed, and potential research techniques to study these transgenerational epigenetic effects are offered.

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27

Cooper, C., D. Phillips, C. Osmond, C. Fall, and J. Eriksson. "David James Purslove Barker: clinician, scientist and father of the ‘Fetal Origins Hypothesis’." Journal of Developmental Origins of Health and Disease 5, no. 3 (March 3, 2014): 161–63. http://dx.doi.org/10.1017/s2040174414000099.

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28

Stapleton, Phoebe A., Valerie C. Minarchick, Jinghai Yi, Kevin Engels, Carroll R. McBride, and Timothy R. Nurkiewicz. "Maternal engineered nanomaterial exposure and fetal microvascular function: does the Barker hypothesis apply?" American Journal of Obstetrics and Gynecology 209, no. 3 (September 2013): 227.e1–227.e11. http://dx.doi.org/10.1016/j.ajog.2013.04.036.

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29

Heaney, Robert P. "Is Vitamin D Inadequacy in Early Life an Instance of the “Barker Hypothesis”?" Nutrition Today 51, no. 1 (2016): 14–17. http://dx.doi.org/10.1097/nt.0000000000000138.

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30

Lalonde, Christine, Douglas Boreham, and T. C. Tai. "Fetal Programming of Brain and Behavior through Ionizing Radiation." Stresses 3, no. 1 (January 13, 2023): 198–209. http://dx.doi.org/10.3390/stresses3010015.

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For decades, the Barker hypothesis and thrifty phenotype hypothesis have driven researchers to explore the development of metabolic syndrome through fetal programming. In this short review, we provide peer-reviewed support for the fetal programming of neural genetic activity and behavior in multiple neural regions: the prefrontal cortex, the cerebral cortex, the hippocampus, the cerebellum, and the hypothalamic–pituitary–adrenal axis. We also introduce ionizing radiation as a purported indirect driver of phenotypical changes. The predisposition of brain and behavioral phenotypes after gestational exposure to stressors can lead to aversive and harmful outcomes, rather than protective adaptations.

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31

Hoy, Wendy E., Megan Rees, Emma Kile, John D. Mathews, and Zhiqiang Wang. "A new dimension to the Barker hypothesis: Low birthweight and susceptibility to renal disease." Kidney International 56, no. 3 (September 1999): 1072–77. http://dx.doi.org/10.1046/j.1523-1755.1999.00633.x.

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32

Costello, Anthony. "Fetal growth and adult disease: what does the Barker hypothesis mean for developing countries?" Journal of Pediatric Gastroenterology & Nutrition 27, no. 2 (August 1998): 242. http://dx.doi.org/10.1097/00005176-199808000-00026.

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33

Denham, Tim. "Early farming in Island Southeast Asia: an alternative hypothesis." Antiquity 87, no. 335 (March 1, 2013): 250–57. http://dx.doi.org/10.1017/s0003598x00048766.

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Several recent articles in Antiqui (Barker et al. 201 la; Hung et al. 2011; Spriggs 2011), discuss the validity of, and revise, portrayals of an Austronesian farming-language dispersal across Island Southeast Asia (ISEA) during the mid-Holocene (approximately 4000-3000 years ago) . In conventional portrayals of the Austronesian dispersal hypothesis (e.g. Bellwood 1984/85, 1997, 2002, 2005; Diamond 2001; Diamond & Bellwood 2003) , and its Neolithic variant (e.g. Spriggs 2003, 2007), farmer-voyagers migrated out of Taiwan approximately 4500-4000 cal BP to colonise ISEA from 4000 cal BP (Bellwood 2002) and the Mariana Islands and Palau by c. 3500-3400 cal BP (Hung et al. 201 1). The descendants of these voyagers subsequently established the Lapita Cultural Complex in the Bismarck Archipelago by c. 3470-3250 cal BP (Kirch 1997; Spriggs 1997) and became the foundational cultures across most of the Pacific from c. 3250-3100 cal BP (Kirch 2000; Addison & Matisoo-Smith 2010; dates for Lapita in Denham et al. 2012). A major problem with this historical metanarrative is the absence of substantial archaeological evidence for the contemporaneous spread of farming from Taiwan (Bulbeck 2008; Donohue & Denham 2010; Denham 2011 ).

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34

DeCherney, Alan, Micah Hill, and Olivia Carpinello. "Developmental Origins of Health and Disease: The History of the Barker Hypothesis and Assisted Reproductive Technology." Seminars in Reproductive Medicine 36, no. 03/04 (May 2018): 177–82. http://dx.doi.org/10.1055/s-0038-1675779.

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AbstractSince Barker's publication of “The fetal and infant origins of adult disease” in 1990, significant emphasis has been placed on the intrauterine environment and its effect on adult disease. Historical events such as the Dutch Famine and the 1918 Flu Pandemic have provided organic data about the epigenetic changes that can result from famine, infection, and stress. Mechanisms that allow for intrauterine survival may predispose to adult disease states when the fetus enters a world of abundance. As the field of in vitro fertilization (IVF) has developed and evolved, little attention has been paid to subtle yet significant differences in IVF offspring. Offspring of assisted reproductive technology (ART) have been reported to have higher rates of preterm birth, abnormal fetal size, and birth defects. It is clear that epigenetic modifications may begin as early as pre-pregnancy. These differences are likely not attributable to one factor in the IVF process. Each variable likely plays a subtle role in the epigenetic manipulation of the embryo. Thus, moving forward, physicians should practice with heightened determination to follow the long-term outcomes of the offspring of ART in an effort to further modify and perfect the field.

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35

Deocaris, Custer, and Malona Alinsug. "Maternal Diet During Pregnancy and COVID-19 Susceptibility of Offspring: The “Thrifty Phenotype Hypothesis” Connection." Journal of Tropical Life Science 11, no. 1 (February 3, 2021): 53–57. http://dx.doi.org/10.11594/jtls.11.01.07.

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There is accumulating evidence suggesting that ACE2, the host cell receptor for the spike (S) protein of the SARS-CoV-2, mediates viral entry and infection, is under epigenetic control. Here, we discuss studies suggesting a nutritional strategy for down-regulating ACE2 expression in tissues of offspring through the phenomenon of maternal epigenomic reprogramming mediated by maternal diet. The "thrifty hypothesis" was first proposed by Hales and Barker, which posits that specific genes are programmed based on early-life experience to promote efficient fat deposition and storage in adulthood. Our analysis of the proposed mechanism for "early life programming" in this paper via nutritional modulation of histone acetylation and DNA methylation goes beyond the physiological consequence of boosting the innate cellular resistance to a viral transmission. During the pandemic, where there is still no specific antiviral drug or a widely disseminated vaccine for COVID-19, we hypothesize that an epigenomic nutrition approach may be a practical approach to help mitigate viral transmission offspring.

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36

Arafat, Subhi, and Camelia C. Minică. "Fetal Origins of Mental Disorders? An Answer Based on Mendelian Randomization." Twin Research and Human Genetics 21, no. 6 (December 2018): 485–94. http://dx.doi.org/10.1017/thg.2018.65.

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The Barker hypothesis states that low birth weight (BW) is associated with higher risk of adult onset diseases, including mental disorders like schizophrenia, major depressive disorder (MDD), and attention deficit hyperactivity disorder (ADHD). The main criticism of this hypothesis is that evidence for it comes from observational studies. Specifically, observational evidence does not suffice for inferring causality, because the associations might reflect the effects of confounders. Mendelian randomization (MR) — a novel method that tests causality on the basis of genetic data — creates the unprecedented opportunity to probe the causality in the association between BW and mental disorders in observation studies. We used MR and summary statistics from recent large genome-wide association studies to test whether the association between BW and MDD, schizophrenia and ADHD is causal. We employed the inverse variance weighted (IVW) method in conjunction with several other approaches that are robust to possible assumption violations. MR-Egger was used to rule out horizontal pleiotropy. IVW showed that the association between BW and MDD, schizophrenia and ADHD is not causal (all p > .05). The results of all the other MR methods were similar and highly consistent. MR-Egger provided no evidence for pleiotropic effects biasing the estimates of the effects of BW on MDD (intercept = -0.004, SE = 0.005, p = .372), schizophrenia (intercept = 0.003, SE = 0.01, p = .769), or ADHD (intercept = 0.009, SE = 0.01, p = .357). Based on the current evidence, we refute the Barker hypothesis concerning the fetal origins of adult mental disorders. The discrepancy between our results and the results from observational studies may be explained by the effects of confounders in the observational studies, or by the existence of a small causal effect not detected in our study due to weak instruments. Our power analyses suggested that the upper bound for a potential causal effect of BW on mental disorders would likely not exceed an odds ratio of 1.2.

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37

BARKER, S. C., and A. MURRELL. "Systematics and evolution of ticks with a list of valid genus and species names." Parasitology 129, S1 (October 2004): S15—S36. http://dx.doi.org/10.1017/s0031182004005207.

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In recent years there has been much progress in our understanding of the phylogeny and evolution of ticks, in particular the hard ticks (Ixodidae). Indeed, a consensus about the phylogeny of the hard ticks has emerged which is quite different to the working hypothesis of 10 years ago. So that the classification reflects our knowledge of ticks, several changes to the nomenclature of ticks are imminent or have been made. One subfamily, the Hyalomminae, should be sunk, while another, the Bothriocrotoninae, has been created (Klompen, Dobson & Barker, 2002). Bothriocrotoninae, and its sole genus Bothriocroton, have been created to house an early-diverging (‘basal’) lineage of endemic Australian ticks that used to be in the genus Aponomma. The remaining species of the genus Aponomma have been moved to the genus Amblyomma. Thus, the name Aponomma is no longer a valid genus name. The genus Rhipicephalus is paraphyletic with respect to the genus Boophilus. Thus, the genus Boophilus has become a subgenus of the genus Rhipicephalus (Murrell & Barker, 2003). Knowledge of the phylogenetic relationships of ticks has also provided new insights into the evolution of ornateness and of their life cycles, and has allowed the historical zoogeography of ticks to be studied. Finally, we present a list of the 899 valid genus and species names of ticks as of February 2004.

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38

Whitaker, C. J., A. J. Dubiel, and O. P. Galpin. "Social and geographical risk factors inHelicobacter pyloriinfection." Epidemiology and Infection 111, no. 1 (August 1993): 63–70. http://dx.doi.org/10.1017/s0950268800056685.

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SummaryA correlation between childhood crowding and the later development of gastric cancer has been demonstrated by Barker and colleagues, who proposed that the relationship was the consequence of infection by an organism such asHelicobacter pylori. In order to test this hypothesis the presence of IgG antibodies toH. pyloriin sera from blood donors in North Wales has been investigated. During donation sessions, donors answered questions relating to social conditions and domicile in childhood (at age 10 years) and adult life (the preceding 2 years).A stepwise logistic regression analysis of the data demonstrated significant independent relationships between seropositivity and the following factors: sharing a bed in childhood, housing density, locality of birth, adult social class and age.

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39

Lamont, Ronald F., Birgitte Møller Luef, and Jan Stener Jørgensen. "Childhood inflammatory and metabolic disease following exposure to antibiotics in pregnancy, antenatally, intrapartum and neonatally." F1000Research 9 (February 25, 2020): 144. http://dx.doi.org/10.12688/f1000research.19954.1.

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Background: There are concerns that the use of antibiotics before, during or immediately after pregnancy may have adverse effects on the neonatal gut microbiome and adversely affect the development of the infant immune system, leading to the development of childhood allergy, asthma, atopic disease and obesity. Methods: In this narrative review, we have explored a number of hypotheses, including the “Barker hypothesis”, the “hygiene hypothesis”, the link between inflammation and metabolic disease, and the influence of the neonatal gut microbiota on the development of the immune system in infants. Results: We found evidence to link the use of antibiotics before, during or immediately after pregnancy with an increased risk of childhood allergy, asthma, atopy and obesity. Conclusions: Although we found robust evidence to link antibiotic use in pregnancy with obesity and an “allergic triad” of asthma, eczema and hay fever, care must be taken when interpreting the findings because of the lack of adjustment for confounding variables in published studies. These may be (i) whether or not the mother had the same outcome variable (for example, asthma) as the infant, for which the mother may have received the antibiotics; (ii) the indication, timing or number of antibiotic courses given; (iii) the use of broad-spectrum or narrow-range antibiotics; (iv) the dose-dependent nature of the effector; and (v) the class of antibiotics used.

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40

Rosenfeld, C. S. "Homage to the ‘H’ in developmental origins of health and disease." Journal of Developmental Origins of Health and Disease 8, no. 1 (August 31, 2016): 8–29. http://dx.doi.org/10.1017/s2040174416000465.

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Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.

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41

Osmond, C., WY Kwong, and TP Fleming. "Statistical analysis of data in support of the Barker hypothesis, advantages of using random effects regression model in hierarchical data." Reproductive BioMedicine Online 10, no. 2 (January 2005): 152–53. http://dx.doi.org/10.1016/s1472-6483(10)60934-0.

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42

Walters, Eurof, and Robert G. Edwards. "On a fallacious invocation of the Barker hypothesis of anomalies in newborn rats due to mothers' food restriction in preimplantation phases." Reproductive BioMedicine Online 7, no. 5 (January 2003): 580–82. http://dx.doi.org/10.1016/s1472-6483(10)62075-5.

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Hockaday, T. D. R., and C. S. Yajnik. "-to: Hales CN, Barker DJP (1992) Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia 35:595–601." Diabetologia 46, no. 2 (February 2003): 303–4. http://dx.doi.org/10.1007/s00125-002-1024-1.

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Dietert, Rodney R. "Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies." Advances in Medicine 2014 (2014): 1–18. http://dx.doi.org/10.1155/2014/867805.

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Developmental immunotoxicity (DIT) is a term given to encompass the environmentally induced disruption of normal immune development resulting in adverse outcomes. A myriad of chemical, physical, and psychological factors can all contribute to DIT. As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations. This review of DIT considers: (1) the history and context of DIT research, (2) the fundamental features of DIT, (3) the emerging role of DIT in risk of noncommunicable diseases (NCDs) and (4) the range of risk factors that have been investigated through human research. The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals). Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds.

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Mcmillen, I. Caroline, and Jeffrey S. Robinson. "Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming." Physiological Reviews 85, no. 2 (April 2005): 571–633. http://dx.doi.org/10.1152/physrev.00053.2003.

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The “fetal” or “early” origins of adult disease hypothesis was originally put forward by David Barker and colleagues and stated that environmental factors, particularly nutrition, act in early life to program the risks for adverse health outcomes in adult life. This hypothesis has been supported by a worldwide series of epidemiological studies that have provided evidence for the association between the perturbation of the early nutritional environment and the major risk factors (hypertension, insulin resistance, and obesity) for cardiovascular disease, diabetes, and the metabolic syndrome in adult life. It is also clear from experimental studies that a range of molecular, cellular, metabolic, neuroendocrine, and physiological adaptations to changes in the early nutritional environment result in a permanent alteration of the developmental pattern of cellular proliferation and differentiation in key tissue and organ systems that result in pathological consequences in adult life. This review focuses on those experimental studies that have investigated the critical windows during which perturbations of the intrauterine environment have major effects, the nature of the epigenetic, structural, and functional adaptive responses which result in a permanent programming of cardiovascular and metabolic function, and the role of the interaction between the pre- and postnatal environment in determining final health outcomes.

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Trosko, James E., and Brad L. Upham. "A Paradigm Shift is Required for the Risk Assessment of Potential Human Health After Exposure to Low Level Chemical Exposures." International Journal of Toxicology 29, no. 4 (July 2010): 344–57. http://dx.doi.org/10.1177/1091581810371384.

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Chemicals are known to be associated with birth defects, cancer, cardiovascular diseases, immunological, reproductive, and neurological disorders. In response to recent reviews of limitations of current concepts and techniques for toxicity testing, this commentary challenges the paradigm that chemicals are directly responsible for DNA damage in the genomic–nuclear DNA in relevant cells of the human body. This challenge is not that mutations do not play roles in human-inherited or somatic diseases but that chemical exposures bring about disease end points by epigenetic mechanisms or by alterations in adult stem cell numbers in utero (ie, the Barker hypothesis) or postnatally, by selecting preexisting mutated cells. Classic concepts, that is, multistage, multimechanism process of carcinogenesis, stem cell theory of cancer, and newer and ignored concepts, such as cancer stem cells and cell−cell communication, will be used to support the view that the toxic effect of chemicals is mediated by nonmutagenic mechanisms at human relevant exposures.

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Kwong, WY, C. Osmond, and TP Fleming. "Support for Barker hypothesis upheld in rat model of maternal undernutrition during the preimplantation period: application of integrated ‘random effects’ statistical model." Reproductive BioMedicine Online 8, no. 5 (January 2004): 574–76. http://dx.doi.org/10.1016/s1472-6483(10)61105-4.

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Hulanicka, Barbara, Anna Lipowicz, Sławomir Kozieł, and Alicja Kowalisko. "Relationship between early puberty and the risk of hypertension/overweight at age 50: Evidence for a modified Barker hypothesis among Polish youth." Economics & Human Biology 5, no. 1 (March 2007): 48–60. http://dx.doi.org/10.1016/j.ehb.2006.12.001.

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Lamberto, Federica, Irene Peral-Sanchez, Suchitra Muenthaisong, Melinda Zana, Sandrine Willaime-Morawek, and András Dinnyés. "Environmental Alterations during Embryonic Development: Studying the Impact of Stressors on Pluripotent Stem Cell-Derived Cardiomyocytes." Genes 12, no. 10 (September 30, 2021): 1564. http://dx.doi.org/10.3390/genes12101564.

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Non-communicable diseases (NCDs) sauch as diabetes, obesity and cardiovascular diseases are rising rapidly in all countries world-wide. Environmental maternal factors (e.g., diet, oxidative stress, drugs and many others), maternal illnesses and other stressors can predispose the newborn to develop diseases during different stages of life. The connection between environmental factors and NCDs was formulated by David Barker and colleagues as the Developmental Origins of Health and Disease (DOHaD) hypothesis. In this review, we describe the DOHaD concept and the effects of several environmental stressors on the health of the progeny, providing both animal and human evidence. We focus on cardiovascular diseases which represent the leading cause of death worldwide. The purpose of this review is to discuss how in vitro studies with pluripotent stem cells (PSCs), such as embryonic and induced pluripotent stem cells (ESC, iPSC), can underpin the research on non-genetic heart conditions. The PSCs could provide a tool to recapitulate aspects of embryonic development “in a dish”, studying the effects of environmental exposure during cardiomyocyte (CM) differentiation and maturation, establishing a link to molecular mechanism and epigenetics.

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Reynolds, Clare M., and Mark H. Vickers. "The role of adipokines in developmental programming: evidence from animal models." Journal of Endocrinology 242, no. 1 (July 2019): T81—T94. http://dx.doi.org/10.1530/joe-18-0686.

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Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.

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