Different kinds of happiness - different immune system consequences.

Happiness is usually classified into two main flavors: hedonic and eudaimonic. Hedonic refers mainly to self gratification and eudaimonic to a sense of meaning and purpose beyond that. In a study involving 80 healthy adult subjects, Fredrickson et al. used a questionnaire to asses levels of hedonic and eudaimonic happiness (questions such as 'over the last week, how often did you feel happy or satisfied? (hedonic); or, 'how often in the last week did you feel your life has a sense of purpose, meaning or direction?' (eudaimonic). They also looked at expression of genes associated with immune system responses. The fascinating result was that hedonic happiness correlated with higher expression of genes typically activated by extended periods of stress, activity that increases inflammation and decreases antiviral responses. Higher Eudaimonic happiness correlated with lower activation levels of these genes and strengthened immune function.

Both kinds of happiness make us "feel good." The central point is that our genome may be "more sensitive to qualitative variations in well-being than are our conscious affective experiences." Here is their abstract:

To identify molecular mechanisms underlying the prospective health advantages associated with psychological well-being, we analyzed leukocyte basal gene expression profiles in 80 healthy adults who were assessed for hedonic and eudaimonic well-being, as well as potentially confounded negative psychological and behavioral factors. Hedonic and eudaimonic well-being showed similar affective correlates but highly divergent transcriptome profiles. Peripheral blood mononuclear cells from people with high levels of hedonic well-being showed up-regulated expression of a stress-related conserved transcriptional response to adversity (CTRA) involving increased expression of proinflammatory genes and decreased expression of genes involved in antibody synthesis and type I IFN response. In contrast, high levels of eudaimonic well-being were associated with CTRA down-regulation. Promoter-based bioinformatics implicated distinct patterns of transcription factor activity in structuring the observed differences in gene expression associated with eudaimonic well-being (reduced NF-κB and AP-1 signaling and increased IRF and STAT signaling). Transcript origin analysis identified monocytes, plasmacytoid dendritic cells, and B lymphocytes as primary cellular mediators of these dynamics. The finding that hedonic and eudaimonic well-being engage distinct gene regulatory programs despite their similar effects on total well-being and depressive symptoms implies that the human genome may be more sensitive to qualitative variations in well-being than are our conscious affective experiences.