Hyoung Yoon Chang1, Dong In Suh2, Song-I Yang3, Mi-Jin Kang4, So-Yeon Lee3, Eun Lee5, In Ae Choi6, Kyung-Sook Lee7, Yee-Jin Shin8, Youn Ho Shin9, Yoon Hee Kim10, Kyung Won Kim10, Kangmo Ahn11, Hye-Sung Won12, Suk-Joo Choi13, Soo-Young Oh13, Ja-Young Kwon14, Young Han Kim14, Hee Jin Park15, Kyung-Ju Lee15, Jong Kwan Jun16, Ho-Sung Yu4, Seung-Hwa Lee4, Bok Kyoung Jung4, Ji-Won Kwon17, Yoon Kyung Choi18, Namhee Do18, Yun Jin Bae18, Ho Kim19, Woo-Sung Chang20, Eun-Jin Kim20, Jeom Kyu Lee20, Soo-Jong Hong21. 1. Department of Psychiatry, Ajou University School of Medicine, Suwon, Korea; Sunflower Center of Southern Gyeonggi for Women and Children Victims of Violence, Suwon, Korea; Center for Traumatic Stress, Ajou University Medical Center, Suwon, Korea. 2. Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea. 3. Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea. 4. Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea. 5. Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Environmental Health Center, University of Ulsan College of Medicine, Seoul, Korea. 6. Sewon Infant Child Development Center, Seoul, Korea. 7. Department of Rehabilitation, Hanshin University, Osan, Korea. 8. Department of Psychiatry, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. 9. Department of Pediatrics, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Korea. 10. Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea. 11. Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. 12. Department of Obstetrics and Gynecology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. 13. Department of Obstetrics and Gynecology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. 14. Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea. 15. Department of Obstetrics and Gynecology, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Korea. 16. Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea. 17. Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, Korea. 18. Korea Institute of Child Care and Education, Seoul, Korea. 19. Graduate School of Public Health, Seoul National University, Seoul, Korea. 20. Division of Allergy and Chronic Respiratory Diseases, Center for Biomedical Science, Korea National Institute of Health, Cheongju, Korea. 21. Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea; Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Environmental Health Center, University of Ulsan College of Medicine, Seoul, Korea. Electronic address: sjhong@amc.seoul.kr.
Abstract
BACKGROUND: Recent evidence suggests that prenatal maternal distress increases the risk of allergic diseases in offspring. However, the effect of prenatal maternal depression and anxiety on atopic dermatitis (AD) risk remains poorly understood. OBJECTIVE: We investigated whether prenatal maternal distress is associated with AD risk in offspring and whether the mechanism is mediated by reactive oxygen species. METHODS: Two general population-based birth cohorts formed the study. One cohort (Cohort for Childhood Origin of Asthma and Allergic Diseases [COCOA]) consisted of 973 mother-baby dyads, and the other (Panel Study on Korean Children [PSKC]) consisted of 1531 mother-baby dyads. The association between prenatal distress and AD was assessed by using Cox proportional hazards and logistic regression models. In COCOA placental 11β-hydroxysteroid dehydrogenase type 2 and glutathione levels and serum IgE levels in 1-year-old children were measured. RESULTS: In COCOA and PSKC AD occurred in 30.6% (lifetime prevalence) and 11.6% (1 year prevalence) of offspring, respectively. Prenatal maternal distress increased the risk of AD in offspring, both in COCOA (hazard ratio for depression, 1.31 [95% CI, 1.02-1.69]; hazard ratio for anxiety, 1.41 [95% CI, 1.06-1.89]) and PSKC (odds ratio for distress, 1.85 [95% CI, 1.06-3.25]). In COCOA both prenatal maternal depression and anxiety scores were positively related to the predicted probability of AD (P < .001 in both). Prenatal distress decreased placental glutathione to glutathione disulfide ratios (P = .037) and, especially in those who later had AD, decreased placental 11β-hydroxysteroid dehydrogenase type 2 levels (P = .010) and increased IgE levels at 1 year of age (P = .005). CONCLUSION: Prenatal maternal depression and anxiety promote risk of AD in offspring. Maternal distress increases the predicted probability of AD. The mechanism might involve chronic stress, abnormal steroid levels, and reactive oxygen species.
BACKGROUND: Recent evidence suggests that prenatal maternal distress increases the risk of allergic diseases in offspring. However, the effect of prenatal maternal depression and anxiety on atopic dermatitis (AD) risk remains poorly understood. OBJECTIVE: We investigated whether prenatal maternal distress is associated with AD risk in offspring and whether the mechanism is mediated by reactive oxygen species. METHODS: Two general population-based birth cohorts formed the study. One cohort (Cohort for Childhood Origin of Asthma and Allergic Diseases [COCOA]) consisted of 973 mother-baby dyads, and the other (Panel Study on Korean Children [PSKC]) consisted of 1531 mother-baby dyads. The association between prenatal distress and AD was assessed by using Cox proportional hazards and logistic regression models. In COCOA placental 11β-hydroxysteroid dehydrogenase type 2 and glutathione levels and serum IgE levels in 1-year-old children were measured. RESULTS: In COCOA and PSKC AD occurred in 30.6% (lifetime prevalence) and 11.6% (1 year prevalence) of offspring, respectively. Prenatal maternal distress increased the risk of AD in offspring, both in COCOA (hazard ratio for depression, 1.31 [95% CI, 1.02-1.69]; hazard ratio for anxiety, 1.41 [95% CI, 1.06-1.89]) and PSKC (odds ratio for distress, 1.85 [95% CI, 1.06-3.25]). In COCOA both prenatal maternal depression and anxiety scores were positively related to the predicted probability of AD (P < .001 in both). Prenatal distress decreased placental glutathione to glutathione disulfide ratios (P = .037) and, especially in those who later had AD, decreased placental 11β-hydroxysteroid dehydrogenase type 2 levels (P = .010) and increased IgE levels at 1 year of age (P = .005). CONCLUSION: Prenatal maternal depression and anxiety promote risk of AD in offspring. Maternal distress increases the predicted probability of AD. The mechanism might involve chronic stress, abnormal steroid levels, and reactive oxygen species.
Authors: S El-Heis; S R Crozier; E Healy; S M Robinson; N C Harvey; C Cooper; H M Inskip; J Baird; K M Godfrey Journal: Clin Exp Allergy Date: 2017-03-17 Impact factor: 5.018
Authors: María Emilia Solano; Megan C Holmes; Paul R Mittelstadt; Karen E Chapman; Eva Tolosa Journal: Semin Immunopathol Date: 2016-07-28 Impact factor: 9.623
Authors: Emma Puosi; Laura S Korhonen; Linnea Karlsson; Eeva-Leena Kataja; Heikki Lukkarinen; Hasse Karlsson; Minna Lukkarinen Journal: Pediatr Allergy Immunol Date: 2021-12-05 Impact factor: 5.464
Authors: Carmen W H Chan; Bernard M H Law; Yun-Hong Liu; Alexandra R B Ambrocio; Natasha Au; Melody Jiang; Ka Ming Chow Journal: Int J Environ Res Public Health Date: 2018-02-25 Impact factor: 3.390