Skip to main content Accessibility help
×
Hostname: page-component-cd9895bd7-fscjk Total loading time: 0 Render date: 2024-12-27T23:53:57.989Z Has data issue: false hasContentIssue false

Chapter 17 - Hormones in Pregnancy and the Developmental Origins of Health and Disease

from Section II - Hormones and Gestational Disorders

Published online by Cambridge University Press:  09 November 2022

Felice Petraglia
Affiliation:
Università degli Studi, Florence
Mariarosaria Di Tommaso
Affiliation:
Università degli Studi, Florence
Federico Mecacci
Affiliation:
Università degli Studi, Florence
Get access

Summary

The Developmental Origins of Health and Disease (DOHaD), also termed developmental programming, refers to adaptations during development that predispose an individual or a population towards later life noncommunicable disease (NCD) conditions or chronic diseases. The developmental trajectory of an individual is determined broadly by the interaction between that individual’s genes and the environment. “Environment” in this sense may include maternal or paternal factors, influences such as nutritional status before or during pregnancy, stress and exposure to contaminants, drugs or alcohol; and maternal diseases of pregnancy that influence transport of substrates and nutrients across the placenta (e.g., preeclampsia, placental insufficiency); and pre-term birth; factors that occur before or around the time of conception, during gestation or in the period after birth; the so-called First 1,000 Days. The interactions between genes and environment determine not only the developmental processes of the fetus and placenta leading to short term morbidity (low birth weight) and mortality, but also long term morbidity of multiple systems including neurodevelopmental disorders such as learning difficulties, poor developmental trajectories and cognitive development, mental health and behavioral disorders in children, and metabolic disorders such as obesity and diabetes. In later life, developmental programming contributes to heart disease such as hypertension and coronary heart disease, type II diabetes, obesity, immune, behavioral, and neurological disorders.

The mechanisms underlying developmental programming can result from structural changes in tissues or organs, effects on germ cells or stem cells, alterations in the microbiome, or in core inflammatory and immunological processes. There are clear sex differences in these responses, strong intergenerational effects, and variable vulnerability across the life course. Many adjustments occur as adaptive fetal responses to adversity or stress, such as hypoxemia or inappropriate nutrient supply, to ensure survival. The placenta plays a critical role in developmental programming, both in regulating the impact of maternal influences on the fetus, and through its direct impact on fetal development.

Type
Chapter
Information
Hormones and Pregnancy
Basic Science and Clinical Implications
, pp. 189 - 198
Publisher: Cambridge University Press
Print publication year: 2022

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Barker, DJP, Winter, PD, Osmond, C, et al. Weight in infancy and death from ischaemic heart disease. Lancet. 1989, 8663:577580.Google Scholar
Barker, DJP, Bull, AR, Osmond, C, et al. Fetal and placental size and the risk of hypertension in adult life. Br Med J. 1990, 301:259262.Google Scholar
Rich-Edwards, JW, Stampfer, MJ, Manson, JE, et al. Birthweight and risk of cardiovascular disease in a cohort of women followed up since 1976. Br Med J. 1997, 315:396400.Google Scholar
Langley-Evans, SC, Gardner, D, and Jackson, AA. Maternal protein restriction influences the programming of the rat hypothalamic-pituitary adrenal axis. J Nutrition. 1996, 126:15781585.CrossRefGoogle ScholarPubMed
Lillycrop, KA, Phillips, ES, Jackson, AA, et al. Dietary protein restriction of pregnant rats induces, and folic acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring. J. Nutrition. 2005, 135:13821386.Google Scholar
Meaney, MJ, S Zyf, M, and Seckl, JR. Epigenetic mechanisms of perinatal programming of hypothalamic-pituitary adrenal function and health. Trends Mol Med. 2007, 2007:269277.Google Scholar
Langley-Evans, SC. Hypertension induced by foetal exposure to a maternal low-protein diet, in the rat, is prevented by pharmacological blockade of maternal glucocorticoid synthesis. J. Hypertension. 1997, 15:537544.Google Scholar
Reynolds, RM, Labad, J, Buss, C, et al. Transmitting biological effects of stress in utero: Implications for mother and offspring. Psychoneuroendocrinology. 2013, 38:18431849.Google Scholar
Meaney, MJ. Maternal care, gene expression and the transmission of individual differences in stress reactivity across generations. Ann Rev Neurosci. 2001, 24:11611192.Google Scholar
Roseboom, TJ, van der Meulen, JH, Osmond, C, et al. Coronary heart disease after prenatal exposure to the Dutch famine, 1944–45. Heart. 2000, 84:595598.Google Scholar
Eriksson, JG. Early growth, and coronary heart disease and type 2 diabetes: Experiences from the Helsinki birth cohort. Int J Obesity. 2006, 30:S18–S22.Google Scholar
Ozanne, SE, and Hales, NC. Peer fetal growth followed by rapid catch-up growth leads to premature death. Mech Ageing Dev. 2005, 126:852854.Google Scholar
Gluckman, PD, Hanson, MA, Beedle, AS, et al. Predictive adaptive responses in perspective. Trends Endocrinol Metab. 2008, 19:109110.Google Scholar
Gluckman, PD, Hanson, MA, and Low, FM. Evolutionary and developmental mismatches are consequences of adaptive developmental plasticity in humans and have implications for later disease risk. Phil Trans Royal Society B. 2019. https://doi.org/10.1098/rstb.2018.0109.Google Scholar
Braun, T, Challis, JR, Newnham, JP, et al. Early life glucocorticoid exposure: The hypothalamic-pituitary-adrenal axis, placental function and long-term disease risk. Endocr Rev. 2013, 34:885916.CrossRefGoogle ScholarPubMed
Seckl, JR, Benediktssion, R, Linsay, RS, et al. Placental 11b-hydroxysteroid dehydrogenase and the programming of hypertension. J Steroid Biochem Mol Biol. 1995, 55:447450.Google Scholar
Connor, KL, Kibschull, M, Matysiak-Zablocki, E, et al. Maternal malnutrition impacts placental morphology and transporter expression: An origin for poor offspring growth. J Nutr Biochem. 2020, 78:108329.CrossRefGoogle ScholarPubMed
Regnault, TR, Friedman, JE, Wilkening, RB, et al. Fetoplacental transport and utilization of amino acids in IUGR – A review. Placenta. 2005. Suppl A; S52S62.CrossRefGoogle ScholarPubMed
Audette, MC, Challis, JRG, Jones, RL, et al. Antenatal dexamethasone treatment in mid-gestation reduces system A transporter activity in the late gestation murine placenta. Endocrinology. 2011. 152: 35613570.Google Scholar
Challis, JRG, Matthews, SG, Gibb, W, et al. Endocrine and paracrine regulation of birth at term and preterm. Endocr Rev. 2000. 21:514550.Google Scholar
Challis, JRG, and Brooks, AN. Maturation and activation of hypothalamic-pituitary-adrenal function in fetal sheep. Endocr Rev. 1989, 10:182204.Google Scholar
Braun, T, Li, S, Sloboda, DM, et al. Effects of maternal dexamethasone treatment in early pregnancy on pituitary-adrenal axis in fetal sheep. Endocrinology. 2009 150:54665477.Google Scholar
Painter, RC, Roseboom, TJ, and de Rooij, SR. Long-term effects of prenatal stress and glucocorticoid exposure. Birth Defects Res Embryo Today. 2021, 96:315324.CrossRefGoogle Scholar
Reynolds, RM. Glucocorticoid excess and the developmental origins of disease; two decades of testing the hypothesis. Psychoneuroendocrinology. 2013, 38:111.CrossRefGoogle ScholarPubMed
Waterland, RA, and Jirtle, RL. Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases. Nutrition. 2004, 20:6368.Google Scholar
Bloomfield, F, Oliver, M, Hawkins, P, et al. A periconceptional nutritional origin for non-infectious preterm birth. Science. 2003, 300:606.Google Scholar
Bloomfield, FH, Oliver, MH, Hawkins, P, et al. Periconceptional undernutrition in sheep accelerates maturation of the fetal hypothalamic-pituitary-adrenal axis in late gestation. Endocrinology. 2004, 145:42784285.Google Scholar
Connor, KL, Challis, JRG, vanZijl, P, et al. Do alterations in placental 11beta-hydroxysteroid dehydrogenase (11betaHSD) activities explain differences in fetal hypothalamic-pituitary-adrenal (HPA) function following periconceptional undernutrition or twinning in sheep. Reprod Sci. 2009 16:12011212.Google Scholar
Begum, G, Stevens, A, Connor, K, et al. Epigenetic changes in fetal hypothalamic energy regulating pathways are associated with maternal undernutrition and twinning. FASEB J. 2012, 26:16941703.Google Scholar
Begum, G, Davies, A, Stevens, A, et al. Maternal undernutrition programs tissue-specific epigenetic changes in the glucocorticoid receptor in adult offspring. Endocrinology. 2013, 154:45604569.CrossRefGoogle ScholarPubMed
Johnstone, JF, Godfrey, KM, Zelsman, M, et al. The relationship between placental 11β HSD-2 and maternal body composition, age and dieting status. 2005 Society for Gynecologic Investigation Annual Meeting, Los Angeles, 2005.Google Scholar
Braun, T, Li, S, Sloboda, DM, et al. Effects of maternal dexamethasone treatment in early pregnancy on pituitary-adrenal axis in fetal sheep. Endocrinology. 2009, 150: 54665477Google Scholar
Constantinof, A, Moisiadis, VG, and Matthews, SG. Programming of stress pathways: A transgenerational perspective. J Steroid Biochem Mol Biol. 2016, 160; 175180.CrossRefGoogle ScholarPubMed
Petraglia, F, Imperatore, A, and Challis, JRG, Neuroendocrine mechanisms in pregnancy and parturition. Endocr Rev. 2010, 31:783816.Google Scholar
Sun, K, Yang, K, and Challis, JRG. Differential expression of 11betahydroxysteroid dehydrogenase types 1 and 2 in human placenta and foetal membranes. J. Clin Endocr Metab. 1997, 82:300305.Google Scholar
Alexander, N, Rosenlocher, F, and Stadler, T. Impact of antenatal synthetic glucocorticoid exposure on endocrine stress reactivity in term-born children. J Clin Endocr Metab. 2012, 97:35383544.Google Scholar
Asztalos, EV, Murphy, KE, and Matthews, SG. A growing dilemma: Antenatal corticosteroids and long-term consequences. Am J Perinatol. 2020, https://doi.org/10.1055/s-0040-1718573.Google Scholar
Roseboom, TJ, Ozanne, SE, Godfrey, KM, et al. Unheard, unseen and unprotected: DOHaD Council’s call for action to protect the younger generation from the long-term effects of COVID-19. J. Develop Orig Health Dis. 2021, https://doi.org/10.1017/S2040174420000847.CrossRefGoogle Scholar
Shenk, CE, O’Donnell, KJ, Pokhvisneva, I, et al. Epigenetic age acceleration and risk for posttraumatic stress disorder following exposure to substantiated child maltreatment. J Clin Child Adolesc Psychol. 2021, 111.Google Scholar
Franke, HA. Toxic stress: Effects, prevention and treatment. Children. 2014, 1:390402.Google Scholar
Anda, RF, Felitti, VJ, Bremner, JD, et al. The enduring effects of abuse and related adverse experiences in childhood: A convergence of evidence from neurobiology and epidemiology. Eur Arch Psychiat Clin Neurosci. 2006, 256:174186.Google Scholar
Kuffer, AL, Thoma, MV, and Maercker, A. Transgenerational aspects of former Swiss child laborers: Do second generations suffer from their parents’ adverse early-life experiences. Eur J. Psychotraumatol. 2016, 7: https://doi.org/10.3402/ejptv7.30804.Google Scholar
Strobel, NA, Richardson, A, Shepherd, CCJ, et al. Modelling factors for Aboriginal and Torres Strait Islander child neurodevelopment outcomes: A latent class analysis. Paediatr Perinat Epidemiol. 2019, 00:112. https://doi.org/10.1111/ppe.12616.Google Scholar
Boyce, WT, and Kobor, MS. Development and the epigenome: The ‘synapse’ of gene – Environment interplayDevelop Sci. 201518:123.CrossRefGoogle ScholarPubMed
Chen, L, Pan, H, Tuan, TA, et al. GUSTO Study Group. Brain-derived Neurotrophic Factor (BDNF) val66met polymorphism influences the association of the methylome with maternal anxiety and neonatal brain volumesDevelop Psychopathol. 2015271:137150.Google Scholar
Meaney, MJ. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Ann Rev Neurosci. 2001, 24:11611192.Google Scholar
Moisiadis, VG, and Matthews, SG. Glucocorticoids and fetal programming part1: Outcomes. Nat Rev Endocrinol. 2014, 10:391402.Google Scholar
Moisiadis, VG, and Matthews, SG. Glucocorticoids and fetal programming part 2: Mechanisms. Nat Rev Endocrinol. 2014, 10:403411.Google Scholar
Ibanez, L, Potau, N, Ferrer, A, et al. Reduced ovulation rate in adolescent girls born small for gestational age. J Clin Endocrinol Metab. 2002, 87:33913393.Google Scholar
Sloboda, DM, Hickey, M, and Hart, R. Reproduction in females: The role of early life environment. Hum Reprod Update. 2011, 17:210227.Google Scholar
Sloboda, DM, Hart, R, Doherty, DA, et al. Age at menarche: Influences of prenatal and postnatal growth. J Clin Endocrinol Metab. 2007, 92:4650.Google Scholar
. Sloboda, DM, Howie, GJ, Gluckman, PD, et al. Pre-and postnatal nutritional histories influence reproductive maturation and ovarian function in the rat. PLoS ONE. 2009, 4:e6744.Google Scholar
Jazwiec, P, and Sloboda, DM. Nutritional adversity, sex and reproduction: Thirty years on from Barker and what have we learned? J Endocrinol. 2019, 242:T51T68.Google Scholar
Tsoulis, M, Chang, P Moore, CJ, et al. Maternal high fat diet induced loss of fetal oocytes is associated with compromised follicle growth in adult offspring. Biol Reprod. 2016, 94:94.Google Scholar
Vannuccini, S, Lazzeri, L, Orlandini, C, et al. Potential influence of in utero and early neonatal exposures on the later development of endometriosis. Fertil Steril. 2016 105:9971002.Google Scholar
Liu, S, Cui, H, Zhang, Q, et al. Influence of early-life factors on the development of endometriosis. Eur J Contracept Reprod Health Care. 2019, 24:216221.Google Scholar
Borghese, B, Sibiude, J, Santulli, P, et al. Low birth weight is strongly associated with the risk of deep infiltrating endometriosis: Results of a 743 case-control study. PLoS ONE. 2015, 10:e0117387.Google Scholar
Dumesic, DA, Goodarzi, MO, Chazenbalk, GD, et al. Intrauterine environment and polycystic ovary syndrome. Semin Reprod Med. 2014, 32:159165.Google Scholar
Flint, HJ, Scott, KP, Louis, P, et al. The role of gut microbiota in nutrition and health. Nat Rev Gastroenterol Hepatol. 2012, 9:577589.CrossRefGoogle ScholarPubMed
Gohir, W, Ratcliffe, EM, and Sloboda, DM. Of the bugs that shape us: Maternal obesity, the gut microbiome and longterm disease risk. Pediatr Res. 2014, 77:196204.Google Scholar
Gohir, W, Whelan, FJ, Surette, MG, et al. 2015. Pregnancy-related changes in the maternal gut microbiota are dependent upon the mother’s periconceptional diet. Gut Microbiobes. 6:310320.Google Scholar
Finlay, BB, Amato, KR, Azad, M, et al. The hygiene hypothesis, the COVID pandemic, and consequences for the human microbiome. Proc Natl Acad Sci. 2021, 118:e2010217118.Google Scholar
Abdul-Hussein, A, Kareem, A, Tewari, S, et al. Early life risk and resiliency factors and their influences on developmental outcomes and disease pathways: A rapid evidence review of systematic reviews and meta-analyses. J Develop Orig Health Dis. 2021 (in press).Google Scholar
Britto, PR, Lye, SJ, Proulx, K, et al. Nurturing care: Promoting early childhood development. Lancet. 2017, 389:91102.Google Scholar
Daelmans, B, Darmstadt, GL, Lombardi, J, et al. Early childhood development, the foundation of sustainable development. Lancet. 2017, 389:911.Google Scholar

Save book to Kindle

To save this book to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×