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The impact of maternal cortisol concentrations on child arterial elasticity

Published online by Cambridge University Press:  07 December 2010

P. H. C. Rondó*
Affiliation:
Nutrition Department, School of Public Health, University of São Paulo, Avenida Dr Arnaldo 715, São Paulo, SP, Brazil
J. A. Pereira
Affiliation:
Nutrition Department, School of Public Health, University of São Paulo, Avenida Dr Arnaldo 715, São Paulo, SP, Brazil Nutrition Department, Federal University of Piauí, Campus Senador Helvídio Nunes de Barros, Rua Cícero Eduardo s/n, Bairro Junco, Picus, PI, Brazil
J. O. Lemos
Affiliation:
Nutrition Department, School of Public Health, University of São Paulo, Avenida Dr Arnaldo 715, São Paulo, SP, Brazil
R. F. Ferreira
Affiliation:
Nutrition Department, School of Public Health, University of São Paulo, Avenida Dr Arnaldo 715, São Paulo, SP, Brazil
*
*Address for correspondence: Dr P. H. C. Rondó, Nutrition Department, School of Public Health, University of São Paulo, Avenida Dr Arnaldo 715, São Paulo, SP, CEP: 64600-000, Brazil. (Email: phcrondo@usp.br)

Abstract

Epidemiological studies suggest that glucocorticoid excess in the fetus may contribute to the pathophysiology of cardiovascular diseases in adulthood. However, the impact of maternal glucocorticoid on the cardiovascular system of the offspring has not been much explored in studies involving humans, especially in childhood. The objective of this study was to assess the influence of maternal cortisol concentrations on child arterial elasticity. One hundred and thirty pregnant women followed from 1997 to 2000, and respective children 5–7 years of age followed from 2004 to 2006 were included in the study. Maternal cortisol was determined in saliva by an enzyme immunoassay utilizing the mean concentration of nine samples of saliva. Arterial elasticity was assessed by the large artery elasticity index (LAEI; the capacitive elasticity of large arteries) by recording radial artery pulse wave, utilizing the equipment HDI/PulseWave CR-2000 Cardiovascular Profiling System®. The nutritional status of the children was determined by the body mass index (BMI). Insulin concentration was assessed by chemiluminescence, and insulin resistance by the homeostasis model assessment. Blood glucose, total cholesterol and fractions (LDL-c and HDL-c) and triglyceride concentrations were determined by automated enzymatic methods. The association between maternal cortisol and child arterial elasticity was assessed by multivariate linear regression analysis. There was a statistically significant association between maternal cortisol and LAEI (P = 0.02), controlling for birth weight, age, BMI and HDL-c of the children. This study suggests that exposure to higher glucocorticoid concentrations in the prenatal period is associated to lower arterial elasticity in childhood, an earlier cardiovascular risk marker.

Type
Original Articles
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

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References

1.Seckl, JR, Meaney, MJ. Glucocorticoid programming. Ann N Y Acad Sci. 2004; 1032, 6384.CrossRefGoogle ScholarPubMed
2.Moritz, KM, Boon, WM, Wintour, EM. Glucocorticoid programming of adult disease. Cell Tissue Res. 2005; 322, 8188.CrossRefGoogle ScholarPubMed
3.Drake, AJ, Tang, JI, Nyirenda, MJ. Mechanisms underlying the role of glucocorticoid in the early life programming of adult disease. Clin Sci. 2007; 113, 219232.CrossRefGoogle ScholarPubMed
4.van Zaane, B, Reuwer, AQ, Büller, HR, et al. Hormones and cardiovascular disease: a shift in paradigm with clinical consequences? Semin Throm Hemost. 2009; 35, 478487.CrossRefGoogle ScholarPubMed
5.Whitworth, A, Williamson, PM, Mangos, G, Kelly, JJ. Cardiovascular consequences of cortisol excess. Vasc Health Risk Manag. 2005; 1, 291299.CrossRefGoogle ScholarPubMed
6.Phillips, DI. Programming of the stress response: a fundamental mechanism underlying the log-term effects of the fetal environment? J Intern Med. 2007; 261, 453460.CrossRefGoogle Scholar
7.Morton, NM. Obesity and corticosteroids: 11 beta-hydroxysteroid type 1 as a cause and therapeutic target in metabolic disease. Mol Cell Endocrinol. 2010; 316, 154164.CrossRefGoogle ScholarPubMed
8.Schrot, S, Weidenfeller, C, Chaffer, TE, Robenek, H, Galla, HJ. Influence of hydrocortisone on the mechanical properties of the cerebral endothelium in vitro. Biophys J. 2005; 89, 39043910.CrossRefGoogle ScholarPubMed
9.Kari, MA, Hallman, M, Eronen, M, et al. Prenatal dexamethasone treatment in conjunction with rescue therapy of human surfactant: a randomized placebo-controlled multicenter study. Pediatrics. 1994; 93, 730736.Google ScholarPubMed
10.Berry, LM, Polk, DH, Ikegami, M, et al. Preterm newborn lamb renal and cardiovascular responses after fetal or maternal antenatal betamethasone. Am J Physiol Regul Integr Comp Physiol. 1997; 41, R1972R1979.CrossRefGoogle Scholar
11.Docherty, C, Kalmar-Nagy, J, Engelen, M, et al. Effect of in vivo infusion of dexamethasone at 0.75 gestation on responses to endothelin-1 in isolated fetal ovine resistance arteries. Am J Physiol. 2001; 281, R261R268.Google Scholar
12.Dodic, M, Baird, R, Hantzis, V, et al. Organs/systems potentially involved in one model of programmed hypertension in sheep. Clin Exp Pharmacol Physiol. 2001; 28, 952956.CrossRefGoogle ScholarPubMed
13.Molnar, J, Nijland, MJM, Howe, DC, Nathanielsz, PW. Evidence for microvascular dysfunction after prenatal dexamethasone at 0.7, 0.75, and 0.8 gestation in sheep. Am J Physiol Regul Integr Comp Physiol. 2002; 283, R561R567.CrossRefGoogle ScholarPubMed
14.Moritz, KM, Johnson, K, Douglas-Denton, R, Wintour, EM, Dodic, M. Maternal glucocorticoid treatment programs alterations in the rennin angiotensin system of the ovine fetal kidney. Endocrinology. 2002; 14, 44554463.CrossRefGoogle Scholar
15.Molnar, J, Howe, DC, Nijland, MJ, Nathanielsz, PW. Prenatal dexamethasone leads to both endothelial dysfunction and vasodilatory compensation in sheep. J Physiol. 2003; 547, 6166.CrossRefGoogle ScholarPubMed
16.Singh, RR, Cullen-McEwen, LA, Kett, MM, et al. Prenatal corticosterone exposure results in altered AT1/AT2, nephron deficit and hypertension in the rat offspring. J Physiol. 2007; 579, 503513.CrossRefGoogle ScholarPubMed
17.Rondó, PHC, Ferreira, RF, Nogueira, F, et al. Maternal psychological stress and distress as predictors of low birth weight, prematurity and intrauterine growth retardation. Eur J Clin Nutr. 2003; 57, 266272.CrossRefGoogle ScholarPubMed
18.Rondó, PHC, Lemos, JO, Pereira, JA, Oliveira, JM, Innocente, LR. The relationship between birthweight and arterial elasticity in childhood. Clin Sci. 2008; 115, 317326.CrossRefGoogle ScholarPubMed
19.Kirschbaum, C, Hellhammer, DH. Salivary cortisol in psychoneuroendocrine research: recent developments and applications. Psychoneuroendocrinology. 1994; 19, 313333.CrossRefGoogle ScholarPubMed
20.Rondó, PH, Lemos, JO, Pereira, JA, Souza, JM. The relationship between cortisol concentrations in pregnancy and systemic vascular resistance in childhood. Early Hum Dev. 2010; 86, 127131.CrossRefGoogle ScholarPubMed
21.Cohn, JN, Finkelstein, S, McVeigh, G, et al. Noninvasive pulse wave analysis for the early detection of vascular disease. Hypertension. 1995; 26, 503508.CrossRefGoogle ScholarPubMed
22.Jelliffe, DB, Jelliffe, EFP (eds.). Community Nutritional Assessment with Special Reference to Less Technically Developed Countries, 2nd edn, 1989. Oxford University Press: London.Google Scholar
23. Centers for Disease Control and Prevention – CDC & National Center for Health Statistics. CDC Growth Charts. Atlanta, USA. Retrieved 31 July 2010 from http://www.cdc.gov/growthchartsGoogle Scholar
24.American Diabetes Association Position Statement. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2004; 27(Suppl 1), 510.CrossRefGoogle Scholar
25.Matthews, DR, Hosker, JP, Rudenski, AS, et al. Homeostasis model assessment: Insulin resistance and beta cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28, 412419.CrossRefGoogle ScholarPubMed
26.Valerio, G, Licenziati, MR, Iannuzzi, A, et al. Insulin resistance and impaired glucose tolerance in obese children and adolescents from Southern Italy. Nutr Metab Cardiovasc Dis. 2006; 16, 279284.CrossRefGoogle ScholarPubMed
27.D'Annunzio, G, Vanelli, M, Meschi, F, et al. The SIEDP Study Group. Valori normali di- HOMA-IR in bambini e adolescenti: studio multicentrico italiano. Quad Pediatr. 2004; 3, 44.Google Scholar
28.Friedewald, WT, Levy, RI, Fredrickson, DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultra centrifuge. Clin Chem. 1972; 18, 499502.CrossRefGoogle Scholar
29.Back Giuliano I de, C, Caramelli, B, Pellanda, L, et al. I Guideline for preventing atherosclerosis in childhood and adolescence. Int J Atheroscler. 2006; 1, 130.Google Scholar
30.Fantidis, P. The role of the stress-related anti-inflammatory hormones ACTH and cortisol in atherosclerosis. Curr Vasc Pharmacol. 2010; 8, 517525.CrossRefGoogle ScholarPubMed
31.Evensen, L, Micklem, DR, Blois, A, et al. Mural cell associated VEGF is required for organotypic vessel formation. PLoS One. 2009; 4, e5798.CrossRefGoogle ScholarPubMed
32.Xiao, D, Huang, X, Xu, Z, Yang, S, Zhang, L. Prenatal cocaine exposure differentially causes vascular dysfunction in adult offspring. Hypertension. 2009; 53, 937943.CrossRefGoogle ScholarPubMed
33.Muszkat, M, Kurnik, D, Sofowora, GG, et al. Desensitization of vascular response in vivo: contribution of genetic variation in the [alpha] 2B-adrenergic receptor subtype. J Hypertens. 2010; 28, 278284.CrossRefGoogle ScholarPubMed
34.Huh, SY, Andrew, R, Rich-Edwards, JW, et al. Association between umbilical cord glucocorticoids and blood pressure at age 3 years. BMC Med. 2008; 6, 25.CrossRefGoogle ScholarPubMed
35.Davis, EP, Glynn, LM, Waffarn, F, Sandman, CA. Prenatal maternal stress programs infant stress regulation. J Child Psychol Psychiatry. 2010; September 20 [Epub ahead of print].Google ScholarPubMed
36.Brand, SR, Engel, SM, Canfield, LR, Yehuda, R. The effect of maternal ptsd following in utero trauma exposure on behavior and temperament in the 9-month-old infant. Ann N Y Acad Sci. 2006; 1071, 454458.CrossRefGoogle ScholarPubMed
37.Yehuda, R, Engel, SM, Brand, SR, et al. Transgenerational effects of posttraumatic stress disorder in babies of mothers exposed to the World Trade Center attacks during pregnancy. J Clin Endocrinol Metab. 2005; 90, 41154118.CrossRefGoogle Scholar
38.Boyne, MS, Woollard, A, Phillips, DI, et al. The association of hypothalamic-pituitary-adrenal axis activity and blood pressure in an Afro-Caribbean population. Psychoneuroendocrinology. 2009; 34, 736742.CrossRefGoogle Scholar
39.Drake, AJ, Walker, BR. The intergenerational effects of fetal programming: non-genomic mechanisms for the inheritance of low birth weight and cardiovascular risk. J Endocrinol. 2004; 180, 116.CrossRefGoogle ScholarPubMed
40.Drake, AJ, Walker, BR, Seckl, JR. Intergenerational consequences of fetal programming by in utero exposure to glucocorticoids in rats. Am J Physiol Regul Integr Comp Physiol. 2005; 288, R34R38.CrossRefGoogle ScholarPubMed
41.Bassareo, PP, Marras, AR, Pasqualucci, D, Mercuro, G. Increased arterial rigidity in children affected by Cushing's syndrome after successful surgical cure. Cardiol Young. 2010; 21, 15.Google Scholar