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Research Article

Prenatal paternal stress predicts infant parasympathetic functioning above and beyond maternal prenatal stress

ORCID Icon, ORCID Icon, ORCID Icon, ORCID Icon & ORCID Icon
Pages 563-576 | Received 19 Jan 2021, Accepted 02 Jun 2021, Published online: 26 Jun 2021
 

ABSTRACT

Background

Paternal stress is often assessed by maternal report and is posited to influence infant development indirectly by contributing to a mother’s stress and experiences during pregnancy. Far less is known about how direct effects of prenatal paternal stress, as described by fathers themselves, are related to an infant’s physiological functioning. We assessed fathers’ own experiences of stress and examined its direct impact on infant respiratory sinus arrhythmia (RSA), a biological index of self-regulation, at seven-month postpartum.

Method

During the third trimester of pregnancy, the UCLA Life Stress Interview was conducted to assess chronic stress in mothers and fathers (N = 90). Infant baseline RSA and RSA reactivity in response to the Still-Face paradigm were assessed at seven-month postpartum.

Results

Infants of fathers with high prenatal stress showed lower baseline RSA, possibly reflective of poor infant psychophysiological regulation. The predictive role of paternal stress remained significant after controlling for maternal stress.

Conclusions

Our findings provide emerging empirical evidence to support the influence of prenatal paternal stress on infant RSA, highlighting the important role of fathers for child development.

Acknowledgments

We would like to thank all of the families who generously donated their time to participate in our study. We would also like to thank Mike Varner and Bob Silver for their support of the BABY study and for providing their dedicated OBGYN Research Network staff to help with screening and recruitment. We thank Connie Hammen for her assistance with training and scoring the UCLA Life Stress Interview. We would also like to thank the University of Utah Vice President’s Clinical Translational Research Scholars program for their mentorship and grantsmanship assistance. Last but not the least, we thank Celine Saenz and Sarah Terrell for their hard work on recruitment, coordination, and study management.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

Part of the data (i.e. infant physiological measure) that support the findings of the study will be available on the National Institute of Mental Health (NIMH) Data Archive (https://nda.nih.gov/edit_collection.html?id=3240). Other parts of the data are available from the corresponding author upon reasonable request.

Additional information

Funding

This study was funded by the National Institute of Mental Health R01MH119070 and R21MH109777 (to S.C. and E.C.), a Career Development Award from the National Institute on Drug Abuse 7K08DA038959-02 (to E.C.), and grants from the University of Utah Consortium for Families and Health Research and Interdisciplinary Research Pilot Program.

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