Antidepressant use during pregnancy and puberty timing in the offspring: results from the Norwegian Mother,…

Abstract

Background: Preclinical studies suggest perinatal antidepressant exposure may alter pubertal timing, but human evidence is lacking.

Objective: To investigate whether maternal antidepressant exposure is associated with pubertal timing in human offspring.

Study design: We used data from the Norwegian Mother, Father, and Child Cohort Study linked with the Medical Birth Registry of Norway, including 1396 singleton births to women with depression/anxiety before pregnancy. Group-based trajectory modeling was used to identify four antidepressant exposure trajectories: continuers (n = 49, 3.5%), early discontinuers (n = 140, 10.0%), late discontinuers (n = 51, 3.7%), and non-exposed (n = 1156, 82.8%). The Pubertal Development Scale with five items assessed at 14 years allowed us to classify the outcome variable as early, normal, and delayed puberty. Modified Poisson regression with generalized overlap weighting was used to estimate weighted risk ratios (wRR) and their 95% confidence interval (CI).

Results: In total, delayed puberty occurred in 17 children (1.2%), mainly in males. Early puberty occurred in 631 (45.2%), more frequently among females. Compared with unexposed children, children born to continuers, early discontinuers, and late discontinuers had lower point estimates of risk of early puberty (wRR range 0.77–0.82). When early discontinuers were the comparator, estimates of early puberty risk were attenuated closer to the null (wRR range 1.00–1.07), with differences observed between males and females. Crude estimates, however, suggested higher risk of delayed puberty.

Conclusion: Children born to mothers who continued antidepressants or discontinued late in pregnancy did not have increased risk of early puberty, but the risk of delayed puberty might be higher.

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BibTeX RIS

BibTeX

@article{riva2026antidepressant,
  title = {{Antidepressant use during pregnancy and puberty timing in the offspring: results from the Norwegian Mother, Father, and Child Cohort Study}},
  author = {Alessandro Riva and Olav Spigset and Hedvig Nordeng and Per Magnus and Nhung T H Trinh},
  journal = {International Journal of Epidemiology},
  year = {2026},
  month = nov,
  doi = {10.1093/ije/dyag240},
  url = {https://doi.org/10.1093/ije/dyag240},
  note = {CC BY 4.0},
}

RIS

TY  - JOUR
TI  - Antidepressant use during pregnancy and puberty timing in the offspring: results from the Norwegian Mother, Father, and Child Cohort Study
AU  - Alessandro Riva
AU  - Olav Spigset
AU  - Hedvig Nordeng
AU  - Per Magnus
AU  - Nhung T H Trinh
PY  - 2026
DA  - 2026/11/04
JO  - International Journal of Epidemiology
DO  - 10.1093/ije/dyag240
UR  - https://doi.org/10.1093/ije/dyag240
AB  - Background: Preclinical studies suggest perinatal antidepressant exposure may alter pubertal timing, but human evidence is lacking.  Objective: To investigate whether maternal antidepressant exposure is associated with pubertal timing in human offspring.  Study design: We used data from the Norwegian Mother, Father, and Child Cohort Study linked with the Medical Birth Registry of Norway, including 1396 singleton births to women with depression/anxiety before pregnancy. Group-based trajectory modeling was used to identify four antidepressant exposure trajectories: continuers (n = 49, 3.5%), early discontinuers (n = 140, 10.0%), late discontinuers (n = 51, 3.7%), and non-exposed (n = 1156, 82.8%). The Pubertal Development Scale with five items assessed at 14 years allowed us to classify the outcome variable as early, normal, and delayed puberty. Modified Poisson regression with generalized overlap weighting was used to estimate weighted risk ratios (wRR) and their 95% confidence interval (CI).  Results: In total, delayed puberty occurred in 17 children (1.2%), mainly in males. Early puberty occurred in 631 (45.2%), more frequently among females. Compared with unexposed children, children born to continuers, early discontinuers, and late discontinuers had lower point estimates of risk of early puberty (wRR range 0.77–0.82). When early discontinuers were the comparator, estimates of early puberty risk were attenuated closer to the null (wRR range 1.00–1.07), with differences observed between males and females. Crude estimates, however, suggested higher risk of delayed puberty.  Conclusion: Children born to mothers who continued antidepressants or discontinued late in pregnancy did not have increased risk of early puberty, but the risk of delayed puberty might be higher.
SN  - 0300-5771
SN  - 1464-3685
ER  -

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