Hyoung Yoon Chang, MD, PhD, MPHa, b, c, *, Dong In Suh, MDd, *, Song-I. Yang, MD, PhDe, Mi-Jin Kang, MSf, So-Yeon Lee, MD, PhDe, Eun Lee, MDg, In Ae Choi, MSh, Kyung-Sook Lee, PhDi, Yee-Jin Shin, MD, PhDj, Youn Ho Shin, MDk, Yoon Hee Kim, MDl, Kyung Won Kim, MD, PhDl, Kangmo Ahn, MD, PhDm, Hye-Sung Won, MD, PhDn, Suk-Joo Choi, MD, PhDo, Soo-Young Oh, MD, PhDo, Ja-Young Kwon, MD, PhDp, Young Han Kim, MD, PhDp, Hee Jin Park, MD, PhDq, Kyung-Ju Lee, MD, PhDq, Jong Kwan Jun, MD, PhDr, Ho-Sung Yu, MSf, Seung-Hwa Lee, MSf, Bok Kyoung Jung, MSf, Ji-Won Kwon, MDs, Yoon Kyung Choi, PhDt, Namhee Do, PhDt, Yun Jin Bae, PhDt, Ho Kim, PhDu, Woo-Sung Chang, PhDv, Eun-Jin Kim, PhDv, Jeom Kyu Lee, PhDv, Soo-Jong Hong, MD, PhDf, g
a Department of Psychiatry, Ajou University School of Medicine, Suwon, Korea
b Sunflower Center of Southern Gyeonggi for Women and Children Victims of Violence, Suwon, Korea
c Center for Traumatic Stress, Ajou University Medical Center, Suwon, Korea
d Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea
r Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea
e Department of Pediatrics, Hallym Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea
f Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea
g 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
n Department of Obstetrics and Gynecology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
h Sewon Infant Child Development Center, Seoul, Korea
i Department of Rehabilitation, Hanshin University, Osan, Korea
j Department of Psychiatry, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
l Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea
p Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea
k Department of Pediatrics, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Korea
m Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
o Department of Obstetrics and Gynecology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
q Department of Obstetrics and Gynecology, CHA Gangnam Medical Center, CHA University School of Medicine, Seoul, Korea
s Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, Korea
t Korea Institute of Child Care and Education, Seoul, Korea
u Graduate School of Public Health, Seoul National University, Seoul, Korea
v Division of Allergy and Chronic Respiratory Diseases, Center for Biomedical Science, Korea National Institute of Health, Cheongju, Korea
Corresponding author: Soo-Jong Hong, MD, PhD, Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Environmental Health Center, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea.
*These authors contributed equally to this work as co-first authors.
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.
Key words : Anxiety; depression; atopic dermatitis; prenatal; psychological stress; cohort; reactive oxygen species