UC Riverside

Empirical research suggests that prosocial behavior (i.e., doing acts of kindness for others) leads to improvements in psychological well-being and physical health, including mortality. However, little work has focused on identifying the underlying biological mechanisms that may mediate the relationship between prosociality and physical health. In this pre-registered experiment, I tested whether a 4-week kindness intervention that has been demonstrated in previous work to elicit changes in pro-inflammatory gene expression (Nelson-Coffey, Fritz, Lyubomirsky, & Cole, 2017) could shift a related psychobiomarker of health – namely, leukocyte telomere length – as well as improve psychological health. Across a diverse community sample (N = 230), participants who performed three kind acts for other people each week for 4 weeks did not demonstrate hypothesized shifts in telomere length (i.e., reduced rates of shortening), nor in well-being and related constructs, relative to those who tracked daily activities (i.e., controls). Exploratory analyses revealed that, relative to controls, participants who performed three self-focused acts (i.e., kindness to the self) also did not demonstrate shifts in telomere length, but did report greater declines in loneliness across the intervention period, relative to controls, although this effect attenuated at the 2-week follow-up. However, participants who performed kind acts for others showed reductions in loneliness through the 2-week follow up, relative to controls. In conclusion, the salubrious effects of prosocial behavior may not likely to be due to the inhibition of cellular aging. However, kindness holds promise as a plausible intervention to alleviate the growing public health crisis of loneliness.