Over a nine-year follow-up in the Atherosclerosis Risk in Communities Study, an age-adjusted SBP increase of approximately 1 mm Hg per year was observed in a sample of 8,555 adults 45–64 years old (Diez Roux et al., 2002
). We tested a much smaller sample of 229 adults 50–68 years old over a shorter follow-up period of four years, and we found a somewhat smaller age-adjusted increase in SBP of approximately 0.6 mm Hg per year. Estimates of SBP change over a longer follow-up period would be expected to provide somewhat different estimates of age-related trends in SBP. In addition, attrition in CHASRS claimed less healthy adults at a higher rate than healthy adults, and the loss of just a few such subjects from our relatively small sample could result in underestimates of change in SBP over time.
Importantly, increases in SBP were not homogeneous across the sample. By way of example, individuals differing by one standard deviation in their loneliness level differed in SBP such that the lonelier individual was predicted to have a 2.3 mm greater increase in SBP over four years on top of a 3.7 mm higher SBP at study onset. Across the full range of loneliness scores (20–80, SD
10), these estimates predict that the most lonely individuals will exhibit SBP increases of 3.6 mm/year (0.6*6 SD
s), or a 14.4 mm greater increase in SBP than their least lonely counterparts over the course of 4 years. Faster rates of increases in SBP translate into higher rates of clinical hypertension at a younger age. Hypertension is the most common primary diagnosis in the U.S., is the primary or contributing cause of about 18% of U.S. deaths, and is estimated to cost $73.4 billion in 2009 (Lloyd-Jones et al., 2009
). Our data indicate that lonelier individuals may be over-represented in the hypertensive segment of the population, and at a younger age. The economic cost of hypertension and the price it exacts in quality and quantity of life suggest that loneliness has significant clinical and public health implications. In addition, special national advisory committees encourage physicians to heed even small differences in SBP because the risk for cardiovascular disease is continuous across the range of SBP from 115 – 185 mm Hg (Chobanian et al., 2003
). We conclude that the risk for high and more rapidly increasing SBP associated with loneliness warrants clinical attention.
Loneliness did not have a significant short-term (i.e., one year) lagged effect of loneliness on SBP, but when the short-term effect of loneliness on SBP was held constant, loneliness was revealed to have a durable influence that was evident in larger increases in SBP over a four-year period. We have posited that the physiological effects of chronic loneliness accrue gradually to accelerate increases in SBP (Cacioppo, Hawkley, Crawford et al., 2002
; Hawkley & Cacioppo, 2007
), and a one-year lag may not be sufficient to capture the effect of this accrual on SBP. High measurement reliability is important when examining long-term influences, so we ensured at each annual assessment that participants were well-habituated to the laboratory setting prior to the initiation of blood pressure readings. SBP was determined by averaging over hundreds of beat-by-beat readings to obtain a reliable and internally consistent measurement. These procedures revealed a cumulative long-term effect of loneliness on SBP in a population-based sample of 50–68 year-old adults.
The long physiological shadow cast by chronic loneliness may begin earlier in life than middle age, however. First, the SBP levels of lonely and nonlonely adults were already distinguishable at study onset. Physiological processes yet to be delineated, but possibly including increases in TPR, could have been operative for years prior to our study for us to observe higher SBP in lonelier 50–68 year-old adults. Second, evidence for an early accrual onset includes the finding that, among 26-year-old adults in the longitudinal Dunedin Multidisciplinary Health and Development Study, chronic social isolation, rejection, and/or feelings of loneliness in early childhood, adolescence, and young adulthood had a dose-response association with number of risk factors for poor cardiovascular health, including elevated blood pressure (Caspi, Harrington, Moffitt, Milne, & Poulton, 2006
The strength of the association between loneliness and SBP could be expected to diminish in the elderly, however. Until the fifth decade of life, total peripheral resistance is the primary determinant of increases in SBP, after which arterial stiffening plays a growing role (Franklin et al., 1997
). In prior research, we observed that lonely young adults exhibited chronically elevated levels of TPR relative to their age-matched nonlonely counterparts (Cacioppo, Hawkley, Crawford et al., 2002
; Hawkley et al., 2003
). Faster rates of increase in TPR and blood pressure foster earlier development of arterial stiffening and further increases in SBP (Franklin et al., 1997
). By this logic, loneliness may be associated with earlier or larger structural changes in resistance arteries that favor collagen deposition and the loss of elastic fiber content, but may no longer be associated with changes in blood pressure that derive from arterial stiffening.
Second, pharmaceutical treatment for high blood pressure increases with age. Some evidence suggests that loneliness motivates people to visit their physician (Cheng, 1992
) and the emergency department (Geller, Janson, McGovern, & Valdini, 1999
), perhaps for the social contact as much if not more than for medical reasons, and this may result in a greater probability of being prescribed medications. To the extent that SBP is more likely to be treated by medication in lonely than nonlonely individuals, loneliness may exhibit an attenuated association with SBP in elderly adults. A treatment effect would depend on comparable adherence to medication regimens across the range of loneliness feelings, and in support of this assumption, compliance was not associated with loneliness in an earlier study of the CHASRS sample (Kudielka, Hawkley, Adam, & Cacioppo, 2007
). Future research should examine whether differential healthcare utilization and treatment explain loneliness differences in SBP.
Finally, loneliness and high blood pressure have been associated with higher rates of mortality (Penninx et al., 1997
). If poor health or death result in earlier attrition of lonely than nonlonely individuals, the association between loneliness and SBP will diminish with time. Indeed, in older adults, loneliness-related attrition may have already occurred if poor health compelled individuals to discontinue participation, or if it prevented their participating in the study in the first place. Attrition in our sample was not associated with loneliness, but we cannot rule out loneliness-related recruitment failures. Additional longitudinal research on older adults is needed to evaluate the extent to which differential experimental mortality attenuates the association between loneliness and SBP.
We note that high BMI, smoking, and lack of physical activity, factors that are typically considered risk factors for elevated SBP, did not explain the effects of loneliness on SBP over the 4-year follow-up period. Our dichotomous measure of physical activity is rudimentary, however, and measures of activity duration and frequency may be more relevant to changes in SBP over time. In supplementary analyses of a subset of the sample with activity duration data, we found no change in the pattern of results when we substituted activity duration for the dichotomous measure of activity. Additional research is needed to replicate this effect and determine the role of alternative measures of physical activity in explaining loneliness differences in the rate of increase in SBP over time. There may be other unmeasured or omitted covariates that account for the prospective influence of loneliness on SBP. Dietary intake is one possibility. In supplementary analyses, we failed to find an association between caloric intake and SBP either at study onset or prospectively. Intake of specific nutrients or non-nutritive food may nevertheless contribute to SBP, and it remains an open question whether loneliness influences food choices that affect SBP. A second example is alcohol consumption. Although we controlled for differences between drinkers and non-drinkers, the prospective effect of loneliness on SBP may be better explained by taking into consideration the amount of alcohol consumed and the effects of binge drinking. A third example is access to healthcare. Health insurance coverage is uneven in the U.S., and to the extent that loneliness is associated with a lower probability of having health insurance, this factor may contribute to loneliness differences in healthcare utilization relevant to SBP. Future research should consider the role not only of health insurance, but also of neighborhood factors that influence access to healthcare resources (e.g., location of healthcare facilities, public transportation) in explaining loneliness differences in rates of SBP increase over time.
The effects of loneliness on SBP may differ as a function of chronic disease status, cardiovascular medication use, hypertension, and obesity. In supplementary analyses of subsets of participants who were initially healthy (i.e., no chronic conditions), unmedicated (i.e., no anti-hyperlipidemic or cardiovascular medications), and normotensive (i.e., not on cardiovascular medications and SBP <140), loneliness persisted in its lagged effects on SBP two, three, and four years later. In initially healthy individuals and unmedicated individuals, the long-lagged effects of loneliness were comparable to that observed in the full sample (B = 0.136 and B = 0.165, respectively, vs. 0.152). In initially normotensive participants, the long-lagged effect of loneliness was larger in magnitude, B = 0.243, SE = 0.144, p < .1, one-tailed, than in the full sample. On the other hand, in initially non-obese participants (i.e., BMI below the 80th percentile within each racial/ethnic group), the long-lagged effect of loneliness was reduced from B = 0.152 to B = 0.115. Additional research is needed to examine whether health status, medication use, hypertension, and obesity moderate the prospective effect of loneliness on SBP.
What physiologic mechanisms might explain loneliness differences in age-related SBP increases? As reviewed above, we hypothesize that elevated levels of total peripheral resistance contribute to loneliness-related SBP increases at least until 50 years of age. This hypothesis would ideally be tested in a study of individuals from young adulthood to age 55 or more to establish TPR as a contributor to loneliness differences in SBP later in life. Physiologic pathways leading to elevated TPR may involve increased activation of the sympathetic nervous system. We have observed an association between loneliness and epinephrine concentrations in overnight urine samples (Hawkley et al., 2006
) that is consistent with this possibility. Loneliness has also been associated with increased activity of the hypothalamic-pituitary-adrenocortical axis as reflected in higher levels of circulating cortisol (Pressman et al., 2005
) and an elevated salivary cortisol response to awakening (Adam et al., 2006
; Steptoe et al., 2004
). Cortisol operates through the vascular nitric oxide system to affect blood pressure, and we posit that loneliness may influence TPR and SBP through its influence on cortisol and vascular endothelial function. Additional research is needed to determine the degree to which neuroendocrine pathways and endothelial function contribute to loneliness-related increases in SBP.
Among possible psychosocial mediators of the effect of loneliness, we found no evidence that depressive symptoms, perceived stress, hostility, or low social support accounted for the influence of loneliness on SBP. Another potential mediator is inhibited temperament. Loneliness is correlated with shyness, and in our sample, the correlation was r
(210) = .39, p < .001. However, we saw no correlation between shyness and SBP, r(206) = −.03, p > .6. It is worth noting that temperament is not as stable across the life course as is often assumed. For instance, a recent meta-analysis found decreases in one aspect of introversion (i.e., social submission) across the life course (Roberts, Walton, & Viechtbauer, 2006
). This is not to say that inhibited temperament does not influence physiology and health over the long term. To the best of our knowledge, however, evidence for an association between inhibited temperament and blood pressure in the extant literature is limited to a single study that found higher SBP in high- than low-shy older adults (Bell, et al., 1993
). Whereas shyness is often characterized by avoidance of social interactions due to lack of confidence and awkwardness, loneliness is characterized by a motivational impulse to connect with others but also a fear of negative evaluation, rejection, and disappointment. We hypothesize that threats to one’s sense of safety and security with others are the toxic component of loneliness, and that hypervigilance for social threat (conscious or unconscious) may contribute to alterations in physiological functioning, including elevated blood pressure.
Do effective interventions for loneliness exist? We recently completed a meta-analysis examining the effectiveness of interventions for loneliness published between 1970 and April 2009 (Masi, Chen, Hawkley, & Cacioppo, under review
). Our assumption when we began the study was that our analyses would support the general conclusion found in qualitative reviews, namely that group interventions (i.e., providing people with opportunities to interact and form relationships with others) effectively reduce loneliness. To our surprise, our quantitative literature review revealed that studies with the highest quality design (randomized control group design) showed absolutely no intervention effect, regardless of intervention type and numerous other potential moderators. We believe the failure of prior interventions is based in part on a faulty understanding of loneliness; loneliness is not synonymous with being alone or isolated. We are in the process of designing an intervention based on our theory that loneliness is a subjective state of perceived isolation that, without our awareness, colors attention, cognition, and behavior in self-defeating ways (Cacioppo & Hawkley, 2009
). Accordingly, an effective intervention would be expected to include cognitive-behavioral training and practice in (1) extending oneself socially, (2) increasing one’s awareness of qualities of good relationships, (3) selecting relationship partners carefully to optimize synergies, (4) being more optimistic and expecting the best from relationship partners, and (5) synchronizing affect and behavior with a relationship partner (Cacioppo & Patrick, 2008
Most medical practitioners have neither the time nor the training to follow-up on psychosocial risk factors for high blood pressure or health more generally. However, a simple assessment of loneliness by questionnaire or interview could be sufficient to determine whether the patient should be referred to a clinical psychologist for therapy. Although no effective therapy for loneliness has yet been documented, a cognitive-behavioral therapist should be able to identify and address specific sources of problems in patients’ social experiences. Of course, even if loneliness is reduced, we have no evidence that blood pressure will also be reduced. Given that the physiological changes that lead to high blood pressure are often irreversible (e.g., arteriosclerosis), a reasonable goal may be to attenuate the subsequent rate of SBP increase. The more important goal may be to detect and treat loneliness early in life, before it has an opportunity to take a toll on physical and mental health and well-being.
Patterns of social integration have been transformed in late modern United States, and the implications for loneliness and its role in health and well-being are profound. Dramatic changes in the family have been noted in higher divorce rates and a higher proportion of adults living alone (Casper & Bianchi, 2002
). Greater heterogeneity in life paths, increasing income inequality, and a more diverse population may be eroding the basis for feeling connected with others (Hughes & O'Rand, 2004
). A recent study supports this view, finding that Americans’ discussion networks shrank significantly between 1985 and 2004, with the modal number of confidants reported by Americans across the past two decades declining from three to zero
(McPherson, Smith-Lovin, & Brashears, 2006
). Social isolation has been linked to broad-based morbidity and mortality (House, Landis, & Umberson, 1988
), but perceived social isolation (i.e., loneliness) has received less attention. Our results show that loneliness, not social network size, predicts changes in SBP. Moreover, independent of social network size, age, gender, race/ethnicity, traditional cardiovascular risk factors (BMI, poor health behaviors), cardiovascular medications, chronic health conditions, and a set of related psychosocial variables (depressive symptoms, perceived stress, social support, hostility), loneliness appears to be a unique risk factor for elevated SBP and increases in SBP over time.