Influence of chronic stress in pregnant women on development of eating habits in their offspring in postnatal life
DOI:
https://doi.org/10.15584/medrev.2016.1.7Keywords:
prenatal stress, maternal cortisol, obesityAbstract
Nowadays, stress became an integral part of human life and accompanies it from conception to death. Effects of its influence on human organism are mainly dependent on patterns of reaction programmed already in prenatal period. Negative stimuli lead to activation of hypothalamic– pituitary–adrenal axis and autonomic nervous system. Chronic tension results in significant increase in the level of stress hormones which break natural and enzymatic placental barrier and permeate to fetus’ bloodstream thus contributing to significant disorders in development of eating habits. A consequence of this situation is considerable risk of overweight in postnatal life of children of those mothers who were subjected to chronic stress during pregnancy. Exposition of pregnant woman to stress stimuli also has significant implications on developing central nervous system. Disorders in brain transmission pathways, especially of hypothalamus as an organ which has a major role in central regulation of food intake, may significantly influence amount and calorific value of chosen foods. Attempt to explain complex mechanisms between chronic stress in prenatal period and excessive weight in postnatal period is paramount because of rapidly increasing percentage of people with such affliction, mainly among children and teenagers, and multitude of complications involving all systems of human organism.
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Fairbrother N, Young AH, Janssen P, Antony MM, Tucker E. Depression and anxiety during the perinatal period. BMC Psychiatry 2015;15:206.
Holmes TH, Rahe EK. The social readjustment rating scale. J Psychosom Res 1967;11(2):213-218.
Krzyżanowska-Zbucka J. Problemy emocjonalne kobiet w okresie okołoporodowym. Wydawnictwo Fundacja Rodzić po Ludzku, Warszawa 2008, 7-58.
Sarkar P, Bergman K, Fisk NM, O’Connor TG, Glover V. Ontogeny of foetal exposure to maternal cortisol using midtrimester amniotic fluid as a biomarker. Clin Endocrinol 2007;66(5):636-640.
Grote NK, Bridge JA, Gavin AR, Melville JL, Iyengar S, Katon WJ. A meta-analysis of depression during pregnancy and the risk of preterm birth, low birth weight, and intrauterine growth restriction. Arch Gen Psychiatry 2010;67(10):1012-1024.
Fan JM, Chen XQ, Du JZ. Prenatal stress, anxiety and depression: a mechanism involving CRH peptide family. Neuro Endocrinol Lett 2014;35(6):429-439.
Brunton PJ, Russell JA. Prenatal social stress in the rat programmes neuroendocrine and behavioural responses to stress in the adult offspring: sex-specific effects. J Neuroendocrinol 2010;22(4):258-271.
Jośko-Ochojska J. Wpływ dramatycznych przeżyć i lęków matki ciężarnej na losy jej dziecka. W: Jośko-Ochojska J. Lęk – nieodłączny towarzysz człowieka od poczęcia aż do śmierci. Wydawnictwo Śląski Uniwersytet Medyczny, Katowice 2013;11-35.
Brunst KJ, Enlow MB, Kannan S, Carroll KN, Coull BA, Wright RJ. Effects of Prenatal Social Stress and Maternal Dietary Fatty Acid Ratio on Infant Temperament: Does Race Matter? Epidemiology (Sunnyvale) 2014;4(4):1000167.
World Health Organization. Obesity and Overweight. Geneva: WHO 2014. http://www.who.int/mediacentre/factsheets/fs311/en/ (12.10.2015)
Kuźbicka K, Rachoń D. Bad eating habits as the main cause of obesity among children. Pediatr Ednocrinol Diabetes Metab 2013;19(3):106-110.
Gurnani M, Birken C, Hamilton J. Childhood Obesity: Causes, Consequences, and Management. Pediatr Clin North Am 2015;62(4):821-840.
Mitanchez D, Yzydorczyk C, Siddeek B, Boubred F, Benahmed M, Simeoni U. The offspring of the diabetic mother – short- and long-term implications. Best Pract Res Clin Obstet Gynaecol. 2015;29(2):256-269.
Seremak-Mrozikiewicz A, Barlik M., Drews K. Programowanie wewnątrzmaciczne jako przyczyna chorób przewlekłych wieku dorosłego. Ginekol Pol 2014;85:43-48.
Tamashiro KL, Moran TH. Perinatal environment and its influences on metabolic programming of offspring. Physiol Behav 2010;100(5):560-566.
Calkins K, Devaskar SU. Fetal origins of adult disease. Curr Probl Pediatr Adolesc Health Care 2011;41(6):158-176.
Entringer S, Buss C, Swanson JM et al. Fetal programming of body composition, obesity, and metabolic function: the role of intrauterine stress and stress biology. J Nutr Metab 2012;2012:632548.
Cao-Lei L, Dancause KN, Elgbeili G et al. DNA methylation mediates the impact of exposure to prenatal maternal stress on BMI and central adiposity in children at age 131⁄2 years: Project Ice Storm. Epigenetics 2015;10(8):749-761.
Entringer S. Impact of stress and stress physiology during pregnancy on child metabolic function and obesity risk. Curr Opin Clin Nutr Metab Care 2013;16(3):320-327.
Reynolds RM, Labad J, Buss C, Ghaemmaghami P, Räikkönen K. Transmitting biological effects of stress in utero: implications for mother and offspring. Psychoneuroendocrinology 2013;38(9):1843-1849.
Jonczyk P. Symptomatologia zespołu Cushinga. Endokrynol. Ped 2014;1(46):41-54.
Reynolds RM. Glucocorticoid excess and the developmental origins of disease: two decades of testing the hypothesis-2012 Curt Richter Award Winner. Psychoneuroendocrinology 2013;38(1):1-11.
Hohwü L, Henriksen TB, Grønborg TK, Hedegaard M, Sørensen TIA, Obel C. Maternal salivary cortisol levels during pregnancy are positively associated with overweight children. Psychoneuroendocrinology 2015;52:143-152.
Hohwü L, Zhu JL, Graversen L, Li J, Sørensen TIA, Obel C. Prenatal parental separation and body weight, including development of overweight and obesity later in childhood. PLoS One 2015;10(3):e0119138.
Boersma GJ, Moghadam AA, Cordner ZA, Tamashiro KL. Prenatal stress and stress coping style interact to predict metabolic risk in male rats. Endocrinology 2014;155(4):1302-1312.
Tamashiro KL, Terrillion CE, Hyun J, Koenig JI, Moran TH. Prenatal stress or high-fat diet increases susceptibility to diet-induced obesity in rat offspring. Diabetes 2009;58(5):1116-1125.
Sominsky L, Spencer SJ. Eating behavior and stress: a pathway to obesity. Front Psychol 2014;5:434.
Nagalski A, Kiersztan A. Fizjologia i molekularny mechanizm działania glikokortykoidów. Postepy Hig Med Dosw 2010;64:133-145.
Mina TH, Reynolds RM. Mechanisms Linking In Utero Stress to Altered Offspring Behaviour. W: Pariante CM, Lapiz-Bluhm MD. (red.) Behavioral Neurobiology of Stress-related Disorders. Wydawnictwo Springer, Verlag Berlin Heidelberg 2014;93-122.
Kohno D, Sone H, Tanaka S, Kurita H, Gantulga D, Yada T. AMP-activated protein kinase activates neuropeptide Y neurons in the hypothalamic arcuate nucleus to increase food intake in rats. Neurosci Lett 2011;499(3):194-198.
Pietrzak P, Kotunia A, Godlewski MM, Zabielski R. Wpływ greliny na przewód pokarmowy. Prz Gastroenterol 2007;2(4):185–191.
Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev 2007;8(1):21-34.
Korek E, Krauss H, Piątek J, Chęcińska Z. Regulacja hormonalna łaknienia. Medycyna Ogólna i Nauki o Zdrowiu 2013;19(2):211–217.
Haleem DJ, Inam QU, Haider S, Perveen T, Haleem MA. Serum Leptin and Cortisol, Related to Acutely Perceived Academic Examination Stress and Performance in Female University Students. Appl Psychophysiol Biofeedback 2015;40(4):305-312.
Baranowska-Bik A, Zgliczyński W. Zespół Cushinga a choroby układu sercowo-naczyniowego. Postępy Nauk Medycznych 2012;889-894.
Peckett AJ, Wright DC, Riddell MC. The effects of glucocorticoids on adipose tissue lipid metabolism. Metabolism 2011;60(11):1500-1510.
Anagnostis P, Athyros VG, Tziomalos K, Karagiannis A, Mikhailidis DP. Clinical review: The pathogenetic role of cortisol in the metabolic syndrome: a hypothesis. J Clin Endocrinol Metab 2009;94(8):2692-2701.
Entringer S, Wadhwa PD. Developmental programming of obesity and metabolic dysfunction: role of prenatal stress and stress biology. Nestle Nutr Inst Workshop Ser 2013;74:107-120.
Campbell JE, Peckett AJ, D’Souza AM, Hawke TJ, Riddell MC. Adipogenic and lipolytic effects of chronic glucocorticoid exposure. Am J Physiol Cell Physiol 2011;300:C198–209.
McEwen BS. Effects of Stress on the Developing Brain. Cerebrum 2011;2011:14.
Buss C, Entringer S, Swanson JM, Wadhwa PD. The Role of Stress in Brain Development: The Gestational Environment’s Long-Term Effects on the Brain. Cerebrum: the Dana Forum on Brain Science 2012;2012:4.
Cassidy-Bushrow AE, Peters RM, Johnson DA, Templin TN. Association of depressive symptoms with inflammatory biomarkers among pregnant African-American women. J Reprod Immunol 2012;94(2):202-209.
Paternain L, Batlle MA, De la Garza AL, Milagro FI, Martínez JA, Campión J. Transcriptomic and epigenetic changes in the hypothalamus are involved in an increased susceptibility to a high-fat-sucrose diet in prenatally stressed female rats. Neuroendocrinology 2012;96(3):249-260.
Yau YH, Potenza MN. Stress and eating behaviors. Minerva Endocrinol 2013;38(3):255-267.
George SA, Khan S, Briggs H, Abelson JL. CRH-stimulated cortisol release and food intake in healthy, non-obese adults. Psychoneuroendocrinology. 2010;35(4):607-612.
Portella AK, Kajantie E, Hovi P et al. Effects of in utero conditions on adult feeding preferences. J Dev Orig Health Dis 2012;3(3):140-152.
Boersma GJ, Tamashiro K. Individual differences in the effects of prenatal stress exposure in rodents. Neurobiol Stress 2015;1:100-108.
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