Download PDF
CC BY-NC-ND 4.0 · Am J Perinatol
DOI: 10.1055/a-2260-5051
Review Article

Trauma and Posttraumatic Stress Disorder as Important Risk Factors for Gestational Metabolic Dysfunction

Mariana Rocha
1   Graduate Program in Neuroscience, Emory University, Atlanta, Georgia
,
Keziah Daniels
2   Emory University School of Medicine, Atlanta, Georgia
,
Suchitra Chandrasekaran
3   Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
,
Vasiliki Michopoulos 
3   Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
4   Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, Georgia
› Author Affiliations Funding Supported by the National Institute of Health: MH115174 (V.M.).
› Further Information
   Permissions and Reprints

Abstract

Gestational metabolic diseases adversely impact the health of pregnant persons and their offspring. Pregnant persons of color are impacted disproportionately by gestational metabolic disease, highlighting the need to identify additional risk factors contributing to racial-ethnic pregnancy-related health disparities. Trauma exposure and posttraumatic stress disorder (PTSD) are associated with increased risk for cardiometabolic disorders in nonpregnant persons, making them important factors to consider when identifying contributors to gestational metabolic morbidity and mortality health disparities. Here, we review current literature investigating trauma exposure and posttraumatic stress disorder as psychosocial risk factors for gestational metabolic disorders, inclusive of gestational diabetes, low birth weight and fetal growth restriction, gestational hypertension, and preeclampsia. We also discuss the physiological mechanisms by which trauma and PTSD may contribute to gestational metabolic disorders. Ultimately, understanding the biological underpinnings of how trauma and PTSD, which disproportionately impact people of color, influence risk for gestational metabolic dysfunction is critical to developing therapeutic interventions that reduce complications arising from gestational metabolic disease.

Key Points

  • Gestational metabolic diseases disproportionately impact the health of pregnant persons of color.

  • Trauma and PTSD are associated with increased risk for cardiometabolic disorders in nonpregnant per.

  • Trauma and PTSD impact physiological cardiometabolic mechanisms implicated in gestational metabolic.

Keywords

trauma - PTSD - stress - metabolic disorders during pregnancy - gestational diabetes mellitus - hypertensive disorders of pregnancy - fetal growth restriction


Publication History

Received: 31 August 2023

Accepted: 28 January 2024

Accepted Manuscript online:
02 February 2024

Article published online:
06 March 2024

© 2024. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA

 

  • References

  • 1 Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest 2005; 115 (05) 1111-1119
    Google Scholar
  • 2 Sheehy S, Aparicio HJ, Xu N. et al. Hypertensive disorders of pregnancy and risk of stroke in US black women. NEJM Evid 2023; 2 (10) EVIDoa2300058
    Google Scholar
  • 3 Miller EC, Zambrano Espinoza MD, Huang Y. et al. Maternal race/ethnicity, hypertension, and risk for stroke during delivery admission. J Am Heart Assoc 2020; 9 (03) e014775
    Google Scholar
  • 4 Ben-Haroush A, Yogev Y, Hod M. Epidemiology of gestational diabetes mellitus and its association with Type 2 diabetes. Diabet Med 2004; 21 (02) 103-113
    Google Scholar
  • 5 Zhang C, Ning Y. Effect of dietary and lifestyle factors on the risk of gestational diabetes: review of epidemiologic evidence. Am J Clin Nutr 2011; 94 (6, suppl): 1975S-1979S
    Google Scholar
  • 6 Cunningham F. Fetal growth disorders. In: Williams Obstetrics. New York USA: McGraw-Hill Professional Publishing; 2010: 881-910
    Google Scholar
  • 7 Albu AR, Anca AF, Horhoianu VV, Horhoianu IA. Predictive factors for intrauterine growth restriction. J Med Life 2014; 7 (02) 165-171
    Google Scholar
  • 8 Ross KM, Dunkel Schetter C, McLemore MR. et al. Socioeconomic status, preeclampsia risk and gestational length in black and white women. J Racial Ethn Health Disparities 2019; 6 (06) 1182-1191
    Google Scholar
  • 9 Kessler RC, Chiu WT, Demler O, Merikangas KR, Walters EE. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005; 62 (06) 617-627
    Google Scholar
  • 10 Noushad S, Ahmed S, Ansari B, Mustafa UH, Saleem Y, Hazrat H. Physiological biomarkers of chronic stress: a systematic review. Int J Health Sci (Qassim) 2021; 15 (05) 46-59
    Google Scholar
  • 11 Boen CE, Hummer RA. Longer—but harder—lives?: The Hispanic health paradox and the social determinants of racial, ethnic, and immigrant–native health disparities from midlife through late life. J Health Soc Behav 2019; 60 (04) 434-452
    Google Scholar
  • 12 Gillespie CF, Bradley B, Mercer K. et al. Trauma exposure and stress-related disorders in inner city primary care patients. Gen Hosp Psychiatry 2009; 31 (06) 505-514
    Google Scholar
  • 13 Pole N, Best SR, Metzler T, Marmar CR. Why are hispanics at greater risk for PTSD?. Cultur Divers Ethnic Minor Psychol 2005; 11 (02) 144-161
    Google Scholar
  • 14 Schwartz AC, Bradley RL, Sexton M, Sherry A, Ressler KJ. Posttraumatic stress disorder among African Americans in an inner city mental health clinic. Psychiatr Serv 2005; 56 (02) 212-215
    Google Scholar
  • 15 Farr OM, Sloan DM, Keane TM, Mantzoros CS. Stress- and PTSD-associated obesity and metabolic dysfunction: a growing problem requiring further research and novel treatments. Metabolism 2014; 63 (12) 1463-1468
    Google Scholar
  • 16 Michopoulos V, Vester A, Neigh G. Posttraumatic stress disorder: a metabolic disorder in disguise?. Exp Neurol 2016; 284 (Pt B): 220-229
    Google Scholar
  • 17 Russell G, Lightman S. The human stress response. Nat Rev Endocrinol 2019; 15 (09) 525-534
    Google Scholar
  • 18 McCorry LK. Physiology of the autonomic nervous system. Am J Pharm Educ 2007; 71 (04) 78
    Google Scholar
  • 19 Herman JP, McKlveen JM, Ghosal S. et al. Regulation of the hypothalamic-pituitary-adrenocortical stress response. Compr Physiol 2016; 6 (02) 603-621
    Google Scholar
  • 20 Magomedova L, Cummins CL. Glucocorticoids and metabolic control. Handb Exp Pharmacol 2016; 233: 73-93
    Google Scholar
  • 21 Tapp ZM, Godbout JP, Kokiko-Cochran ON. A tilted axis: maladaptive inflammation and HPA axis dysfunction contribute to consequences of TBI. Front Neurol 2019; 10: 345
    Google Scholar
  • 22 Sapolsky RM, Romero LM, Munck AU. How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions. Endocr Rev 2000; 21 (01) 55-89
    Google Scholar
  • 23 Rohleder N. Stress and inflammation - The need to address the gap in the transition between acute and chronic stress effects. Psychoneuroendocrinology 2019; 105: 164-171
    Google Scholar
  • 24 Borges SW. Stress Science: Neuroendocrinology. Elsevier Science; San Diego CA: 2010: 306-312
    Google Scholar
  • 25 Herman JP, McKlveen JM, Solomon MB, Carvalho-Netto E, Myers B. Neural regulation of the stress response: glucocorticoid feedback mechanisms. Braz J Med Biol Res 2012; 45 (04) 292-298
    Google Scholar
  • 26 Morris MC, Rao U. Psychobiology of PTSD in the acute aftermath of trauma: integrating research on coping, HPA function and sympathetic nervous system activity. Asian J Psychiatr 2013; 6 (01) 3-21
    Google Scholar
  • 27 Azulay N, Olsen RB, Nielsen CS. et al. Reduced heart rate variability is related to the number of metabolic syndrome components and manifest diabetes in the sixth Tromsø study 2007-2008. Sci Rep 2022; 12 (01) 11998
    Google Scholar
  • 28 Williams DP, Koenig J, Carnevali L. et al. Heart rate variability and inflammation: a meta-analysis of human studies. Brain Behav Immun 2019; 80: 219-226
    Google Scholar
  • 29 Dennis PA, Kimbrel NA, Sherwood A. et al. Trauma and autonomic dysregulation: episodic–versus systemic–negative affect underlying cardiovascular risk in posttraumatic stress disorder. Psychosom Med 2017; 79 (05) 496-505
    Google Scholar
  • 30 Freaney PM, Harrington K, Molsberry R. et al. Temporal trends in adverse pregnancy outcomes in birthing individuals aged 15 to 44 years in the United States, 2007 to 2019. J Am Heart Assoc 2022; 11 (11) e025050
    Google Scholar
  • 31 Furtado JM, Almeida SM, Mascarenhas P. et al. Anthropometric features as predictors of atherogenic dyslipidemia and cardiovascular risk in a large population of school-aged children. PLoS One 2018; 13 (06) e0197922
    Google Scholar
  • 32 Risser HJ, Hetzel-Riggin MD, Thomsen CJ, McCanne TR. PTSD as a mediator of sexual revictimization: the role of reexperiencing, avoidance, and arousal symptoms. J Trauma Stress 2006; 19 (05) 687-698
    Google Scholar
  • 33 Cohen S, Janicki-Deverts D, Miller GE. Psychological stress and disease. JAMA 2007; 298 (14) 1685-1687
    Google Scholar
  • 34 Pitman RK, Orr SP, Forgue DF, de Jong JB, Claiborn JM. Psychophysiologic assessment of posttraumatic stress disorder imagery in Vietnam combat veterans. Arch Gen Psychiatry 1987; 44 (11) 970-975
    Google Scholar
  • 35 Barateiro A, Mahú I, Domingos AI. Leptin resistance and the neuro-adipose connection. Front Endocrinol (Lausanne) 2017; 8: 45
    Google Scholar
  • 36 Canale MP, Manca di Villahermosa S, Martino G. et al. Obesity-related metabolic syndrome: mechanisms of sympathetic overactivity. Int J Endocrinol 2013; 2013: 865965
    Google Scholar
  • 37 Thorp AA, Schlaich MP. Relevance of sympathetic nervous system activation in obesity and metabolic syndrome. J Diab Res 2015; 2015: 341583
    Google Scholar
  • 38 Furay AR, Bruestle AE, Herman JP. The role of the forebrain glucocorticoid receptor in acute and chronic stress. Endocrinology 2008; 149 (11) 5482-5490
    Google Scholar
  • 39 Tsigos C, Chrousos GP. Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. J Psychosom Res 2002; 53 (04) 865-871
    Google Scholar
  • 40 Keen-Rhinehart E, Ondek K, Schneider JE. Neuroendocrine regulation of appetitive ingestive behavior. Front Neurosci 2013; 7: 213
    Google Scholar
  • 41 Kyrou I, Chrousos GP, Tsigos C. Stress, visceral obesity, and metabolic complications. Ann N Y Acad Sci 2006; 1083 (01) 77-110
    Google Scholar
  • 42 McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia. Crit Care Clin 2001; 17 (01) 107-124
    Google Scholar
  • 43 Kang W, Tong T, Park T. Corticotropin releasing factor-overexpressing mouse is a model of chronic stress-induced muscle atrophy. PLoS One 2020; 15 (02) e0229048
    Google Scholar
  • 44 Morris T, Moore M, Morris F. Stress and chronic illness: the case of diabetes. J Adult Dev 2011; 18 (02) 70-80
    Google Scholar
  • 45 Spruill TM. Chronic psychosocial stress and hypertension. Curr Hypertens Rep 2010; 12 (01) 10-16
    Google Scholar
  • 46 Jovanovic T, Ressler KJ. How the neurocircuitry and genetics of fear inhibition may inform our understanding of PTSD. Am J Psychiatry 2010; 167 (06) 648-662
    Google Scholar
  • 47 Dunlop BW, Wong A. The hypothalamic-pituitary-adrenal axis in PTSD: Pathophysiology and treatment interventions. Prog Neuropsychopharmacol Biol Psychiatry 2019; 89: 361-379
    Google Scholar
  • 48 Kolassa I-T, Eckart C, Ruf M, Neuner F, de Quervain DJ, Elbert T. Lack of cortisol response in patients with posttraumatic stress disorder (PTSD) undergoing a diagnostic interview. BMC Psychiatry 2007; 7 (01) 54
    Google Scholar
  • 49 Matić G, Milutinović DV, Nestorov J. et al. Lymphocyte glucocorticoid receptor expression level and hormone-binding properties differ between war trauma-exposed men with and without PTSD. Prog Neuropsychopharmacol Biol Psychiatry 2013; 43: 238-245
    Google Scholar
  • 50 Yehuda R, Boisoneau D, Lowy MT, Giller Jr EL. Dose-response changes in plasma cortisol and lymphocyte glucocorticoid receptors following dexamethasone administration in combat veterans with and without posttraumatic stress disorder. Arch Gen Psychiatry 1995; 52 (07) 583-593
    Google Scholar
  • 51 Rasmusson AM, Schnurr PP, Zukowska Z, Scioli E, Forman DE. Adaptation to extreme stress: post-traumatic stress disorder, neuropeptide Y and metabolic syndrome. Exp Biol Med (Maywood) 2010; 235 (10) 1150-1162
    Google Scholar
  • 52 Beck B. Neuropeptide Y in normal eating and in genetic and dietary-induced obesity. Philos Trans R Soc Lond B Biol Sci 2006; 361 (1471): 1159-1185
    Google Scholar
  • 53 Whitehead JP, Richards AA, Hickman IJ, Macdonald GA, Prins JB. Adiponectin–a key adipokine in the metabolic syndrome. Diabetes Obes Metab 2006; 8 (03) 264-280
    Google Scholar
  • 54 Muhie S, Gautam A, Meyerhoff J, Chakraborty N, Hammamieh R, Jett M. Brain transcriptome profiles in mouse model simulating features of post-traumatic stress disorder. Mol Brain 2015; 8 (01) 14
    Google Scholar
  • 55 Miller AH, Maletic V, Raison CL. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biol Psychiatry 2009; 65 (09) 732-741
    Google Scholar
  • 56 Elenkov IJ. Neurohormonal-cytokine interactions: implications for inflammation, common human diseases and well-being. Neurochem Int 2008; 52 (1–2): 40-51
    Google Scholar
  • 57 Busillo JM, Azzam KM, Cidlowski JA. Glucocorticoids sensitize the innate immune system through regulation of the NLRP3 inflammasome. J Biol Chem 2011; 286 (44) 38703-38713
    Google Scholar
  • 58 Bellinger DL, Millar BA, Perez S. et al. Sympathetic modulation of immunity: relevance to disease. Cell Immunol 2008; 252 (1–2): 27-56
    Google Scholar
  • 59 Pal M, Febbraio MA, Whitham M. From cytokine to myokine: the emerging role of interleukin-6 in metabolic regulation. Immunol Cell Biol 2014; 92 (04) 331-339
    Google Scholar
  • 60 Yang J-J, Jiang W. Immune biomarkers alterations in post-traumatic stress disorder: a systematic review and meta-analysis. J Affect Disord 2020; 268: 39-46
    Google Scholar
  • 61 Nance DM, Sanders VM. Autonomic innervation and regulation of the immune system (1987-2007). Brain Behav Immun 2007; 21 (06) 736-745
    Google Scholar
  • 62 Maes M, Lin AH, Delmeire L. et al. Elevated serum interleukin-6 (IL-6) and IL-6 receptor concentrations in posttraumatic stress disorder following accidental man-made traumatic events. Biol Psychiatry 1999; 45 (07) 833-839
    Google Scholar
  • 63 Spivak B, Shohat B, Mester R. et al. Elevated levels of serum interleukin-1 β in combat-related posttraumatic stress disorder. Biol Psychiatry 1997; 42 (05) 345-348
    Google Scholar
  • 64 O'Donovan A, Sun B, Cole S. et al. Transcriptional control of monocyte gene expression in post-traumatic stress disorder. Dis Markers 2011; 30 (2–3): 123-132
    Google Scholar
  • 65 Pace TW, Wingenfeld K, Schmidt I, Meinlschmidt G, Hellhammer DH, Heim CM. Increased peripheral NF-κB pathway activity in women with childhood abuse-related posttraumatic stress disorder. Brain Behav Immun 2012; 26 (01) 13-17
    Google Scholar
  • 66 Kathiresan S, Larson MG, Vasan RS. et al. Contribution of clinical correlates and 13 C-reactive protein gene polymorphisms to interindividual variability in serum C-reactive protein level. Circulation 2006; 113 (11) 1415-1423
    Google Scholar
  • 67 Michopoulos V, Rothbaum AO, Jovanovic T. et al. Association of CRP genetic variation and CRP level with elevated PTSD symptoms and physiological responses in a civilian population with high levels of trauma. Am J Psychiatry 2015; 172 (04) 353-362
    Google Scholar
  • 68 Steven S, Frenis K, Oelze M. et al. Vascular inflammation and oxidative stress: major triggers for cardiovascular disease. Oxid Med Cell Longev 2019; 2019: 7092151
    Google Scholar
  • 69 Daniele G, Guardado Mendoza R, Winnier D. et al. The inflammatory status score including IL-6, TNF-α, osteopontin, fractalkine, MCP-1 and adiponectin underlies whole-body insulin resistance and hyperglycemia in type 2 diabetes mellitus. Acta Diabetol 2014; 51 (01) 123-131
    Google Scholar
  • 70 Dinarello CA, Donath MY, Mandrup-Poulsen T. Role of IL-1β in type 2 diabetes. Curr Opin Endocrinol Diabetes Obes 2010; 17 (04) 314-321
    Google Scholar
  • 71 Trøseid M, Seljeflot I, Arnesen H. The role of interleukin-18 in the metabolic syndrome. Cardiovasc Diabetol 2010; 9 (01) 11
    Google Scholar
  • 72 Zeng Z, Liu F, Li S. Metabolic adaptations in pregnancy: a review. Ann Nutr Metab 2017; 70 (01) 59-65
    Google Scholar
  • 73 Herrera E. Metabolic adaptations in pregnancy and their implications for the availability of substrates to the fetus. Eur J Clin Nutr 2000; 54 (1, suppl 1): S47-S51
    Google Scholar
  • 74 Parrettini S, Caroli A, Torlone E. Nutrition and metabolic adaptations in physiological and complicated pregnancy: focus on obesity and gestational diabetes. Front Endocrinol (Lausanne) 2020; 11: 611929
    Google Scholar
  • 75 Stein PK, Hagley MT, Cole PL, Domitrovich PP, Kleiger RE, Rottman JN. Changes in 24-hour heart rate variability during normal pregnancy. Am J Obstet Gynecol 1999; 180 (04) 978-985
    Google Scholar
  • 76 Vegiopoulos A, Herzig S. Glucocorticoids, metabolism and metabolic diseases. Mol Cell Endocrinol 2007; 275 (1–2): 43-61
    Google Scholar
  • 77 Tuckermann JP, Kleiman A, McPherson KG, Reichardt HM. Molecular mechanisms of glucocorticoids in the control of inflammation and lymphocyte apoptosis. Crit Rev Clin Lab Sci 2005; 42 (01) 71-104
    Google Scholar
  • 78 Di Cianni G, Miccoli R, Volpe L, Lencioni C, Del Prato S. Intermediate metabolism in normal pregnancy and in gestational diabetes. Diabetes Metab Res Rev 2003; 19 (04) 259-270
    Google Scholar
  • 79 Catalano PM, Tyzbir ED, Roman NM, Amini SB, Sims EA. Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women. Am J Obstet Gynecol 1991; 165 (6, Pt 1): 1667-1672
    Google Scholar
  • 80 Faas MM, Spaans F, De Vos P. Monocytes and macrophages in pregnancy and pre-eclampsia. Front Immunol 2014; 5: 298
    Google Scholar
  • 81 Brown MB, von Chamier M, Allam AB, Reyes L. M1/M2 macrophage polarity in normal and complicated pregnancy. Front Immunol 2014; 5: 606
    Google Scholar
  • 82 Catalano PM. Trying to understand gestational diabetes. Diabet Med 2014; 31 (03) 273-281
    Google Scholar
  • 83 Johns EC, Denison FC, Norman JE, Reynolds RM. Gestational diabetes mellitus: mechanisms, treatment, and complications. Trends Endocrinol Metab 2018; 29 (11) 743-754
    Google Scholar
  • 84 Parsons JA, Brelje TC, Sorenson RL. Adaptation of islets of Langerhans to pregnancy: increased islet cell proliferation and insulin secretion correlates with the onset of placental lactogen secretion. Endocrinology 1992; 130 (03) 1459-1466
    Google Scholar
  • 85 Cousins L. Insulin sensitivity in pregnancy. Diabetes 1991; 40 (Suppl. 02) 39-43
    Google Scholar
  • 86 Nielsen JH. Beta cell adaptation in pregnancy: a tribute to Claes Hellerström. Ups J Med Sci 2016; 121 (02) 151-154
    Google Scholar
  • 87 Alfadhli EM. Gestational diabetes mellitus. Saudi Med J 2015; 36 (04) 399-406
    Google Scholar
  • 88 Shaw JG, Asch SM, Katon JG. et al. Post-traumatic stress disorder and antepartum complications: a novel risk factor for gestational diabetes and preeclampsia. Paediatr Perinat Epidemiol 2017; 31 (03) 185-194
    Google Scholar
  • 89 Mason SM, Tobias DK, Clark CJ, Zhang C, Hu FB, Rich-Edwards JW. Abuse in childhood or adolescence and gestational diabetes: a retrospective cohort study. Am J Prev Med 2016; 50 (04) 436-444
    Google Scholar
  • 90 Schoenaker DAJM, Callaway LK, Mishra GD. The role of childhood adversity in the development of gestational diabetes. Am J Prev Med 2019; 57 (03) 302-310
    Google Scholar
  • 91 Silveira ML, Whitcomb BW, Pekow P. et al. Perceived psychosocial stress and glucose intolerance among pregnant Hispanic women. Diabetes Metab 2014; 40 (06) 466-475
    Google Scholar
  • 92 Mishra S, Shetty A, Rao CR, Nayak S, Kamath A. Effect of maternal perceived stress during pregnancy on gestational diabetes mellitus risk: a prospective case-control study. Diabetes Metab Syndr 2020; 14 (05) 1163-1169
    Google Scholar
  • 93 MacGregor C, Freedman A, Keenan-Devlin L. et al. Maternal perceived discrimination and association with gestational diabetes. Am J Obstet Gynecol MFM 2020; 2 (04) 100222
    Google Scholar
  • 94 Hosler AS, Nayak SG, Radigan AM. Stressful events, smoking exposure and other maternal risk factors associated with gestational diabetes mellitus. Paediatr Perinat Epidemiol 2011; 25 (06) 566-574
    Google Scholar
  • 95 Wilson BL, Dyer JM, Latendresse G, Wong B, Baksh L. Exploring the psychosocial predictors of gestational diabetes and birth weight. J Obstet Gynecol Neonatal Nurs 2015; 44 (06) 760-771
    Google Scholar
  • 96 Goldenberg RL, Culhane JF. Low birth weight in the United States. Am J Clin Nutr 2007; 85 (02) 584S-590S
    Google Scholar
  • 97 Bamfo JE, Odibo AO. Diagnosis and management of fetal growth restriction. J Pregnancy 2011; 2011: 640715
    Google Scholar
  • 98 Cetin I, Alvino G. Intrauterine growth restriction: implications for placental metabolism and transport. A review. Placenta 2009; 30 (suppl A): S77-S82
    Google Scholar
  • 99 Marconi AM, Paolini C, Buscaglia M, Zerbe G, Battaglia FC, Pardi G. The impact of gestational age and fetal growth on the maternal-fetal glucose concentration difference. Obstet Gynecol 1996; 87 (06) 937-942
    Google Scholar
  • 100 Sibley CP, Turner MA, Cetin I. et al. Placental phenotypes of intrauterine growth. Pediatr Res 2005; 58 (05) 827-832
    Google Scholar
  • 101 Hilmert CJ, Dominguez TP, Schetter CD. et al. Lifetime racism and blood pressure changes during pregnancy: implications for fetal growth. Health Psychol 2014; 33 (01) 43-51
    Google Scholar
  • 102 Flom JD, Chiu YM, Hsu HL. et al. Maternal lifetime trauma and birthweight: effect modification by in utero cortisol and child sex. J Pediatr 2018; 203: 301-308
    Google Scholar
  • 103 Xiong X, Harville EW, Mattison DR, Elkind-Hirsch K, Pridjian G, Buekens P. Exposure to Hurricane Katrina, post-traumatic stress disorder and birth outcomes. Am J Med Sci 2008; 336 (02) 111-115
    Google Scholar
  • 104 Rashid HU, Khan MN, Imtiaz A, Ullah N, Dherani M, Rahman A. Post-traumatic stress disorder and association with low birth weight in displaced population following conflict in Malakand division, Pakistan: a case control study. BMC Pregnancy Childbirth 2020; 20 (01) 166
    Google Scholar
  • 105 Rosen D, Seng JS, Tolman RM, Mallinger G. Intimate partner violence, depression, and posttraumatic stress disorder as additional predictors of low birth weight infants among low-income mothers. J Interpers Violence 2007; 22 (10) 1305-1314
    Google Scholar
  • 106 Gelaye B, Sanchez SE, Andrade A. et al. Association of antepartum depression, generalized anxiety, and posttraumatic stress disorder with infant birth weight and gestational age at delivery. J Affect Disord 2020; 262: 310-316
    Google Scholar
  • 107 Rondó PH, Ferreira RF, Nogueira F, Ribeiro MC, Lobert H, Artes R. Maternal psychological stress and distress as predictors of low birth weight, prematurity and intrauterine growth retardation. Eur J Clin Nutr 2003; 57 (02) 266-272
    Google Scholar
  • 108 Brown SJ, Gartland D, Weetra D. et al. Health care experiences and birth outcomes: results of an Aboriginal birth cohort. Women Birth 2019; 32 (05) 404-411
    Google Scholar
  • 109 Brown MA, Buddie ML. The importance of nonproteinuric hypertension in pregnancy. Hypertens Pregnancy 1995; 14 (01) 57-65
    Google Scholar
  • 110 Payne B, Magee LA, von Dadelszen P. Assessment, surveillance and prognosis in pre-eclampsia. Best Pract Res Clin Obstet Gynaecol 2011; 25 (04) 449-462
    Google Scholar
  • 111 Magee LA, Pels A, Helewa M, Rey E, von Dadelszen P. SOGC Hypertension Guideline Committee. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy: executive summary. J Obstet Gynaecol Can 2014; 36 (07) 575-576
    Google Scholar
  • 112 Gestational Hypertension and Preeclampsia. Gestational hypertension and preeclampsia: ACOG Practice Bulletin, Number 222. Obstet Gynecol 2020; 135 (06) e237-e260
    Google Scholar
  • 113 Saudan P, Brown MA, Buddle ML, Jones M. Does gestational hypertension become pre-eclampsia?. Br J Obstet Gynaecol 1998; 105 (11) 1177-1184
    Google Scholar
  • 114 Karrar SA, Hong PL. Preeclampsia. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022
    Google Scholar
  • 115 Stanhope KK, Cammack AL, Perreira KM. et al. Adverse childhood experiences and lifetime adverse maternal outcomes (gestational diabetes and hypertensive disorders of pregnancy) in the Hispanic Community Health Study/Study of Latinos. Ann Epidemiol 2020; 50: 1-6
    Google Scholar
  • 116 Gilliam HC, Howell KH, Paulson JL, Napier TR, Miller-Graff LE. Pregnancy complications and intimate partner violence: the moderating role of prenatal posttraumatic stress symptoms. J Trauma Stress 2022; 35 (05) 1484-1496
    Google Scholar
  • 117 Caplan M, Keenan-Devlin LS, Freedman A. et al. Lifetime psychosocial stress exposure associated with hypertensive disorders of pregnancy. Am J Perinatol 2021; 38 (13) 1412-1419
    Google Scholar
  • 118 Morgan N, Christensen K, Skedros G, Kim S, Schliep K. Life stressors, hypertensive disorders of pregnancy, and preterm birth. J Psychosom Obstet Gynaecol 2022; 43 (01) 42-50
    Google Scholar
  • 119 Marcoux S, Bérubé S, Brisson C, Mondor M. Job strain and pregnancy-induced hypertension. Epidemiology 1999; 10 (04) 376-382
    Google Scholar
  • 120 Klonoff-Cohen HS, Cross JL, Pieper CF. Job stress and preeclampsia. Epidemiology 1996; 7 (03) 245-249
    Google Scholar
  • 121 Schneider S, Freerksen N, Maul H, Roehrig S, Fischer B, Hoeft B. Risk groups and maternal-neonatal complications of preeclampsia--current results from the national German Perinatal Quality Registry. J Perinat Med 2011; May; 39 (03) 257-265
    Google Scholar
  • 122 Leeners B, Neumaier-Wagner P, Kuse S, Stiller R, Rath W. Emotional stress and the risk to develop hypertensive diseases in pregnancy. Hypertens Pregnancy 2007; 26 (02) 211-226
    Google Scholar
  • 123 Vollebregt KC, van der Wal MF, Wolf H, Vrijkotte TG, Boer K, Bonsel GJ. Is psychosocial stress in first ongoing pregnancies associated with pre-eclampsia and gestational hypertension?. BJOG 2008; 115 (05) 607-615
    Google Scholar
  • 124 Hammer F, Stewart PM. Cortisol metabolism in hypertension. Best Pract Res Clin Endocrinol Metab 2006; 20 (03) 337-353
    Google Scholar
  • 125 Kang J, Chang Y, Kim Y, Shin H, Ryu S. Ten-second heart rate variability, its changes over time, and the development of hypertension. Hypertension 2022; 79 (06) 1308-1318
    Google Scholar
  • 126 Kivioja A, Toivonen E, Tyrmi J. et al. Increased risk of preeclampsia in women with a genetic predisposition to elevated blood pressure. Hypertension 2022; 79 (09) 2008-2015
    Google Scholar
  • 127 Nilsson E, Salonen Ros H, Cnattingius S, Lichtenstein P. The importance of genetic and environmental effects for pre-eclampsia and gestational hypertension: a family study. BJOG 2004; 111 (03) 200-206
    Google Scholar
  • 128 Kiecolt-Glaser JK. Stress, food, and inflammation: psychoneuroimmunology and nutrition at the cutting edge. Psychosom Med 2010; 72 (04) 365-369
    Google Scholar
  • 129 Dolsen EA, Crosswell AD, Prather AA. Links between stress, sleep, and inflammation: are there sex differences?. Curr Psychiatry Rep 2019; 21 (02) 8
    Google Scholar
  • 130 Ramakrishnan U. Nutrition and low birth weight: from research to practice. Am J Clin Nutr 2004; 79 (01) 17-21
    Google Scholar
  • 131 Soto E, Bahado-Singh R. Fetal abnormal growth associated with substance abuse. Clin Obstet Gynecol 2013; 56 (01) 142-153
    Google Scholar
  • 132 Bovin MJ, Marx BP. The problem with overreliance on the PCL–5 as a measure of PTSD diagnostic status. Clin Psychol Sci Pract 2023; 30 (01) 122-125
    Google Scholar
  • 133 Powers A, Woods-Jaeger B, Stevens JS. et al. Trauma, psychiatric disorders, and treatment history among pregnant African American women. Psychol Trauma 2020; 12 (02) 138-146
    Google Scholar
  • 134 Weathers FW, Keane TM, Davidson JR. Clinician-administered PTSD scale: a review of the first ten years of research. Depress Anxiety 2001; 13 (03) 132-156
    Google Scholar
  • 135 Su S, Jimenez MP, Roberts CT, Loucks EB. The role of adverse childhood experiences in cardiovascular disease risk: a review with emphasis on plausible mechanisms. Curr Cardiol Rep 2015; 17 (10) 88
    Google Scholar
  • 136 Huffhines L, Noser A, Patton SR. The link between adverse childhood experiences and diabetes. Curr Diab Rep 2016; 16 (06) 54
    Google Scholar
  • 137 Chandan JS, Okoth K, Gokhale KM, Bandyopadhyay S, Taylor J, Nirantharakumar K. Increased cardiometabolic and mortality risk following childhood maltreatment in the United Kingdom. J Am Heart Assoc 2020; 9 (10) e015855
    Google Scholar
  • 138 Goncalves Soares A, Zimmerman A, Zammit S, Karl A, Halligan SL, Fraser A. Abuse in childhood and cardiometabolic health in early adulthood: evidence from the Avon longitudinal study of parents and children. J Am Heart Assoc 2021; 10 (24) e021701
    Google Scholar
  • 139 Gluck RL, Hartzell GE, Dixon HD. et al. Trauma exposure and stress-related disorders in a large, urban, predominantly African-American, female sample. Arch Women Ment Health 2021; 24 (06) 893-901
    Google Scholar
  • 140 Records, Wilson BL, Dyer JM. et al Exploring the Psychosocial Predictors of Gestational Diabetes and Birth Weight. J Obstet Gynecol Neonatal Nurs 2015; 44 (06) 760-771
    Google Scholar