Key result
Greater affect regulation variability linked to ~54% higher all-cause mortality risk.
Why the study?
Although distinct affect regulation strategies predict mortality risk, the biological processes involved remain understudied.
Does affect regulation variability predict all-cause mortality risk in adults?
Cohort (n=1,941)
Does affect regulation variability predict all-cause mortality risk in adults?
Effect estimate: HR 1.54 (95% CI 1.11-2.14)
Greater affect regulation variability is associated with higher all-cause mortality risk, an effect that may be modified by allostatic load.
Affect regulation variability was associated with mortality; hypothesis-generating in this cohort, prospective validation needed before clinical consideration.
OBJECTIVE: Although growing evidence indicates that distinct affect regulation strategies (eg, positive reappraisal, anger suppression) predict mortality risk, the biological processes involved remain understudied. We investigated the association of various affect regulation exposures with mortality risk while examining the role of allostatic load. METHODS: From 2004 to 2006, 1941 participants from the Midlife in the United States longitudinal study completed validated scales assessing the use of 9 general and emotion-specific regulatory strategies (eg, denial, anger expression). An SD-based algorithm was also used to characterize how flexibly participants regulate their affect (lower, moderate, or greater variability). Participants further provided data on relevant covariates and 24 allostatic load biomarkers (eg, cortisol, glucose). Cox regressions modeled hazard ratios (HRs) and 95% CIs examined associations of affect regulation variables and all-cause mortality risk until 2022. The confounding, mediating, and moderating role of allostatic load was examined in subsequent models. RESULTS: In fully adjusted models, only greater versus lower affect regulation variability (HR=1.54; 95% CI=1.11-2.14) significantly predicted a higher mortality risk. Associations were relatively unchanged with further inclusion of allostatic load in models and allostatic load did not mediate affect regulation-mortality relationships. Yet, when evaluating moderation effects, greater versus lower and moderate variability, as well as denial, were marginally or significantly related to higher mortality risk among adults with lower allostatic load only. CONCLUSIONS: Allostatic load may modify rather than confound or mediate the association between some dimensions of affect regulation and mortality risk. Future work should evaluate the potential roles of allostatic load among diverse samples.
No takes yet. Share an insight, caveat, or question.
Ng et al. (2025) reported a cohort. Greater affect regulation variability vs. Lower affect regulation variability was evaluated on All-cause mortality (HR 1.54, 95% CI 1.11-2.14). Greater versus lower affect regulation variability significantly predicted a higher all-cause mortality risk (HR 1.54; 95% CI 1.11-2.14).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: