The associations between paternal postpartum depressive symptoms and testosterone and cortisol levels in hair over the first two years postpartum.
Level 3 - non-randomized controlled study
Prospective longitudinal observational cohort study.
PubMed 39793750 · doi:10.1016/j.pnpbp.2024.111245
What was done
Researchers evaluated 226 fathers enrolled in the DREAM HAIR sub-study of the longitudinal prospective DREAM cohort study across the first two years postpartum. Paternal postpartum depressive symptoms (PPDS) were assessed at 8 weeks, 14 months, and 24 months after birth using the Edinburgh Postnatal Depression Scale. At each time point, 2 cm scalp-near hair samples were collected to quantify hair testosterone (HairT) and cortisol (HairF) concentrations. Authors performed cross-sectional correlations and longitudinal random intercept cross-lagged panel models to determine bidirectional relationships, controlling for batch and storage time.
What was found
No numerical values or effect sizes were reported in the abstract. Correlation analyses showed a negative cross-sectional association between HairF and paternal PPDS at 14 months postpartum. Random intercept cross-lagged panel modeling showed prospective relationships between PPDS at 8 weeks postpartum and lower HairF at 14 months postpartum, and between 14 months and 2 years postpartum in an exploratory model. HairT showed no significant cross-sectional or longitudinal associations with paternal PPDS.
Why it matters
This longitudinal investigation suggests that paternal postpartum depressive symptoms may precede reductions in cumulative cortisol secretion rather than altered steroid hormone levels acting as causal drivers. It clarifies that hair testosterone is not consistently associated with paternal depression in healthy community samples.
Limits
The abstract reports no numerical statistics, effect sizes, or confidence intervals. The sample was drawn from a relatively healthy cohort with low baseline depressive burden, which may obscure associations present in clinically depressed populations. Key psychosocial, sleep, and lifestyle confounders were not specified.