Citation

Saarinen A, Keltikangas-Järvinen L, Dobewall H, Ahola-Olli A, Salmi M, Lehtimäki T, Raitakari O, Jalkanen S, Hintsanen M. Dev. Psychobiol. 2021; ePub(ePub): ePub.

Copyright

(Copyright © 2021, John Wiley and Sons)

DOI

10.1002/dev.22070

PMID

unavailable

Abstract

BACKGROUND: Previously, compassion has been found to protect against depressive symptoms, while emotional adversities in childhood are suggested to increase inflammatory responses. The current study investigated (a) whether emotional family environment in childhood predicts levels of such cytokines in adulthood that are previously found to be elevated in depression (interleukin [IL]-2, IL-6, IL-1b, monocyte chemoattractant protein-1, interferon-gamma [IFN-γ], and tumor necrosis factor alpha [TNF-α]) and (b) whether these associations are modified by compassion in adulthood.

METHODS: The participants (N = 1,198-1,523) came from the prospective population-based Young Finns data. Emotional family environment and parental socioeconomic factors were evaluated in 1980; participants' compassion in 2001; and participants' cytokine levels and adulthood covariates in 2007.

RESULTS: Risky emotional family environment in childhood predicted higher levels of IL-2, IL-6, IFN-γ, and TNF-α in adulthood. Additionally, there were significant interaction effects between compassion and emotional risk in childhood, when predicting IL-2, IL-6, and TNF-α. Specifically, individuals who grew up in a risky emotional family environment had on average higher levels of IL-2, IL-6, and TNF-α in adulthood when combined with low compassion.

CONCLUSIONS: In individuals coming from risky emotional family environments, high compassion for others may protect against elevated levels of cytokines previously linked with depression.

Language: en

Keywords

personality; childhood environment; cytokines; emotional environment; family environment; inflammation