Maternal Licorice Consumption and Detrimental Cognitive and Psychiatric Outcomes in Children

K. Raikkonen, A. K. Pesonen, K. Heinonen, J. Lahti, N. Komsi, J. G. Eriksson, J. R. Seckl, A. L. Jarvenpaa, T. E. Strandberg

Research output: Contribution to journalArticlepeer-review

Abstract

Overexposure to glucocorticoids may link prenatal adversity with detrimental outcomes in later life. Glycyrrhiza, a natural constituent of licorice, inhibits placental 11-beta-hydroxysteroid dehydrogenase type 2, the feto-placental "barrier" to higher maternal levels of cortisol. The authors studied whether prenatal exposure to glycyrrhiza in licorice exerts detrimental effects on cognitive performance (subtests of the Wechsler Intelligence Scale for Children III as well as the Children's Developmental Neuropsychological Assessment and the Beery Developmental Test of Visual-Motor Integration) and psychiatric symptoms (Child Behavior Checklist) in 321 Finnish children 8.1 years of age born in 1998 as healthy singletons at 35-42 weeks of gestation. In comparison to the group with zero-low glycyrrhiza exposure (0-249 mg/week), those with high exposure (>= 500 mg/week) had significant decrements in verbal and visuospatial abilities and in narrative memory (range of mean differences in standard deviation units, -0.31 to -0.41; P < 0.05) and significant increases in externalizing symptoms and in attention, rule-breaking, and aggression problems (range of odds ratios, 2.15 to 3.43; P < 0.05). The effects on cognitive performance appeared dose related. Data are compatible with adverse fetal "programming" by overexposure to glucocorticoids and caution against excessive intake of licorice-containing foodstuffs during pregnancy.

Original languageEnglish
Pages (from-to)1137-1146
Number of pages10
JournalAmerican Journal of Epidemiology
Volume170
Issue number9
DOIs
Publication statusPublished - Nov 2009

Keywords

  • child
  • cognition
  • glucocorticoids
  • glycyrrhiza
  • glycyrrhizic acid
  • mental disorders
  • 11-beta-hydroxysteroid dehydrogenase type 2

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