This study replicates and extends a growing body of prospective research showing that loneliness has adverse consequences for health and mortality. In a large, population-based national sample of older Americans, we replicated prior research by showing that feelings of loneliness are associated with increased mortality risk. Net of sociodemographic characteristics, social relationships, and health behaviors, older adults with the highest levels of loneliness were 1.96 times more likely to die within six years than those with the lowest levels of loneliness.
Several studies exist on the mechanisms that may explain the association between loneliness and mortality. Sugisawa et al. (1994)
reported that the effect of loneliness on mortality over a 3-year period among older adults in Japan was fully explained by chronic diseases, functional status, and self-rated health. Patterson & Veenstra (2010)
found that the relationship between loneliness and mortality fell to non-significance when social relationships and health behaviors were taken into account. Shiovitz-Ezra & Ayalon (2010)
found that the effect of loneliness on mortality remained statistically significant after controlling for medical status, functional impairment, and depression. The apparent inconsistencies may be attributable to differences in the mechanisms that were investigated and the measures that were included. Shiovitz-Esra & Ayalon (2010)
, for instance, did not include health behaviors or social relationships in their analysis. In the present study, we included measures of each of these mechanisms. In addition, we used a time sensitive model for survival analysis while some previous studies used a simple “died-didn’t die” dichotomy (e.g., Patterson & Veenstra, 2010
). Moreover, unlike other studies, we explicitly tested the significance of mediated (i.e., indirect) effects and the resulting change in the magnitude of the direct effect of loneliness. Our results showed that the three health outcomes combined to affect changes in the risk of dying later, and that taking the health variables into account resulted in a small decline in the association between loneliness and mortality. The results of the mediational analyses further indicated that functional status and self-rated health, but not depressive symptoms, constitute proximal mechanisms through which loneliness affects later mortality.
Mortality analysis showed that health outcomes assessed at the same time as loneliness helped explain the effect of loneliness on mortality, but did not permit evaluation of the causal direction between loneliness and health. Using cross-lagged models, we found that loneliness predicted increases in depressive symptoms, modest decreases in self-rated health and increases in functional limitations over two years even when the reciprocal effects of these health measures on loneliness were taken into account. These findings are consistent with a causal direction that implicates decrements in emotional and physical health as mechanisms through which loneliness leads to increases in mortality risk.
Possessing a richness of social attachments and friends protects against mortality (House et al., 1988
), and generally signifies lower levels of loneliness (Hawkley et al., 2008
; Pinquart & Sorenson, 2003
). Ancillary analyses confirmed that respondents who were married and who had more friends living nearby were less lonely (not shown), but these objective characteristics of respondents’ social lives did not explain much of the effect of loneliness on mortality risk. This is consistent with Patterson and Veenstra (2010)
which, in a much larger sample of more than 6,500 adults followed over a 34-year period, found only a modest effect of marital status and no effect of number of close friends and relatives on mortality risk independent of a significant effect of loneliness.
We posited that social relationships may influence mortality to the extent that family and friends exert social control by encouraging and supporting salubrious health behaviors. At the same time, we noted that health behaviors are insufficient to account for the mortality effects of the existence (or not) of social relationships in humans and are not plausible explanations for mortality effects in socially isolated non-human social animals. The effects of loneliness on self-control (Cacioppo & Hawkley, 2009
), on the other hand, suggest that health behaviors may differ as a function of loneliness and help explain mortality differences. This reasoning did not find support, however. Although health behaviors influenced mortality as expected, health behaviors (physical exercise, smoking) did not explain loneliness differences in mortality.
The fact that loneliness continues to predict health outcomes when health behaviors are held constant suggests that loneliness alters physiology at a more fundamental level. The sizeable remaining effect of loneliness on mortality in our final model allows for additional explanatory mechanisms. Prior research indicates that loneliness increases vascular resistance (Hawkley et al., 2003
), increases SBP (Hawkley et al., 2010b
), alters hypothalamic pituitary adrenocortical activity (Adam et al., 2006
), diminishes sleep salubrity (Hawkley et al., 2010a
), alters gene transcription (Cole et al., 2007
), and diminishes immunity (Pressman et al., 2005
). Future research should include efforts to examine how these physiological processes contribute to the effect of loneliness on mortality.
This study used a 3-item composite index of loneliness which has been shown to have good validity and reliability (Hughes et al., 2004
). This measure is an important improvement over previous studies on the loneliness-mortality relationship that measured loneliness with a single item asking respondents whether and/or how often they felt lonely. Specifically, our 3-item measure avoids use of the term “lonely” or “loneliness” and thus avoids much of the stigma associated with and consequent underestimation of loneliness. Nevertheless, the fact that mean loneliness levels were higher in 2006 than in 2002 and 2004, and that this difference corresponded to a change from an interview-based to a self-administered questionnaire leaves open the possibility that stigma may have resulted in an underestimation of loneliness in the interview-based data. Future waves of HRS, in which loneliness will continue to be assessed by self-administered questionnaire, will allow testing the degree to which the relationships reported in this study are robust to questionnaire format.
Furthermore, even though we analyzed the reciprocal associations of loneliness with depressive symptoms, self-rated health, and functional limitations, arguably other factors, such as sleep quality and physical activities, could be both cause and effect of loneliness and health. Future research needs to construct more complex models to gain a better understanding of the dynamics of these relationships.
Our study contributes to a growing literature indicating that loneliness is a risk factor for morbidity and mortality and it points to potential mechanisms through which this process works. Whether loneliness has similar health effects and operates through similar mechanisms in non-Western countries as was observed in the U.S. remains to be studied, and the importance of such research is highlighted by the fact that loneliness is as or more prevalent in non-Western countries as in the United States. In China, for example, a national survey conducted in 2000 found that 29.8% of older adults were lonely (Yang & Victor, 2008
); in rural China, as many as 78.1% of the older adults were reportedly moderately or intensely lonely (Wang et al., 2011
). The potential implications for health and longevity are great in a world characterized by societal unrest and threats to the integrity of people’s sense of interpersonal and collective connectedness.