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Try out PMC Labs and tell us Looking for my personal muscular female adult lonely you think. Learn More. Department of Psychology, University of Chicago, E. As a social species, humans rely on a safe, secure social surround to survive and thrive.
Perceptions of social isolation, or loneliness, increase vigilance for threat and heighten feelings of vulnerability while also raising the desire to reconnect. Implicit hypervigilance for social threat alters psychological processes that influence physiological functioning, diminish sleep quality, and increase morbidity and mortality. The purpose of this paper is to review the features and consequences of loneliness within a comprehensive theoretical framework that informs interventions to reduce loneliness. We review physical and mental health consequences of loneliness, mechanisms for its effects, and effectiveness of extant interventions.
Features of a loneliness regulatory loop are employed to explain cognitive, behavioral, and physiological consequences of loneliness and to discuss interventions to reduce loneliness. Loneliness is not simply being alone. Interventions to reduce loneliness and its health consequences may need to take into its attentional, confirmatory, and memorial biases as well as its social and behavioral effects.
Loneliness is synonymous with perceived social isolation, not with objective social isolation. People can live relatively solitary lives and not feel lonely, and conversely, they can live an ostensibly rich social life and feel lonely nevertheless.
Each of us is capable of feeling lonely, and loneliness is an equal opportunity tenant for good reason. We have posited that loneliness is the social equivalent of physical pain, hunger, and thirst; the pain of social disconnection and the hunger and thirst for social connection motivate the maintenance and formation of social connections necessary for the survival of our genes [ 89 ]. Feelings of loneliness generally succeed in motivating connection or reconnection with others following geographic relocation or bereavement, for instance, thereby diminishing or abolishing feelings of social isolation.
Left untended, loneliness has serious consequences for cognition, emotion, behavior, and health. Here, we review physical and mental health consequences of perceived social isolation and then introduce mechanisms for these outcomes in the context of a model that takes into consideration the cognitive, emotional, and behavioral characteristics of loneliness. A growing body of longitudinal research indicates that loneliness predicts increased morbidity and mortality [ 12 — 19 ]. The effects of loneliness seem to accrue over time to accelerate physiological aging [ 20 ].
For instance, loneliness has been shown to exhibit a dose—response relationship with cardiovascular health risk in young adulthood [ 12 ]. The greater the of measurement occasions at which participants were lonely i. Similarly, loneliness was associated with increased systolic blood pressure in a population-based sample of middle-aged adults [ 21 ], and a follow-up study of these same individuals showed that a persistent trait-like aspect of loneliness accelerated the rate of blood pressure increase over a 4-year follow-up period [ 22 ].
Loneliness accrual effects are also evident in a study of mortality in the Health and Retirement Study; all-cause mortality over a 4-year follow-up was predicted by loneliness, and the effect was greater in chronically than situationally lonely adults Looking for my personal muscular female adult lonely 17 ]. Penninx et al. Sugisawa et al. Depressive symptoms have been associated with loneliness and with adverse health outcomes, but loneliness continued to predict CHD in these women after also controlling for depressive symptoms.
Finally, loneliness has also been shown to increase risk for cardiovascular mortality; individuals who reported often being lonely exhibited ificantly greater risk than those who reported never being lonely [ 14 ]. In sum, feelings of loneliness mark increased risk for morbidity and mortality, a phenomenon that arguably reflects the social essence of our species.
The impact of loneliness on cognition was assessed in a recent review of the literature [ 9 ]. Perhaps, the most striking finding in this literature is the Looking for my personal muscular female adult lonely of emotional and cognitive processes and outcomes that seem susceptible to the influence of loneliness. The causal nature of the association between loneliness and depressive symptoms appears to be reciprocal [ 32 ], but more recent analyses of five consecutive annual assessments of loneliness and depressive symptoms have shown that loneliness predicts increases in depressive symptoms over 1-year intervals, but depressive symptoms do not predict increases in loneliness over those same intervals [ 36 ].
In addition, experimental evidence, in which feelings of loneliness and social connectedness were hypnotically induced, indicates that loneliness not only increases depressive symptoms but also increases perceived stress, fear of negative evaluation, anxiety, and anger, and diminishes optimism and self-esteem [ 8 ]. These data suggest that a perceived sense of social connectedness serves as a scaffold for the self—damage the scaffold and the rest of the self begins to crumble.
A particularly devastating consequence of feeling socially isolated is cognitive decline and dementia. This finding does not rule out a reverse causal direction; cognitive impairments may hamper social interactions, prompt social withdrawal, and thus lead to loneliness. Other studies, however, have indicated that loneliness is a precursor of cognitive decline. For instance, the cognitive functioning of 75—year-olds as assessed by the Mini-Mental State Examination did not differ as a function of loneliness at baseline but diminished to a greater extent among those high than low in loneliness over a year follow-up [ 28 ].
In a prospective study by Wilson et al. Moreover, loneliness at baseline was associated with a faster decline in cognitive performance on most of these measures over a 4-year follow-up. This was not true of the converse: cognitive status at baseline did not predict changes in loneliness.
Overall, it appears that something about our sense of connectedness with others penetrates the physical organism and compromises the integrity of physical and mental health and well-being. Our model of loneliness [ 89 ] posits that perceived social isolation is tantamount to feeling unsafe, and this sets off implicit hypervigilance for additional social threat in the environment. Unconscious surveillance for social threat produces cognitive biases: relative to nonlonely people, lonely individuals see the social world as a more threatening place, expect more negative social interactions, and remember more negative social information.
This self-reinforcing loneliness loop is accompanied by feelings of hostility, stress, pessimism, anxiety, and low self-esteem [ 8 ] and represents a dispositional tendency that activates neurobiological and behavioral mechanisms that contribute to adverse health outcomes. One of the consequences of loneliness and implicit vigilance for social threat is a diminished capacity for self-regulation. Feeling socially isolated impairs the capacity to self-regulate, and these effects are so automatic as to seem outside of awareness.
In a dichotic listening task, for instance, right-handed individuals quickly and automatically attend preferentially to the pre-potent right ear. Latency to respond to stimuli presented to the non-dominant ear can be enhanced, however, by instructing participants to attend to their left ear. Among young adults who were administered this task, the lonely and nonlonely groups did not differ in performance when directed to attend to their pre-potent right ear, but the lonely group performed ificantly worse than the nonlonely group when directed to shift attention to their non-prepotent left ear [ 30 ].
In other words, automatic attentional processes may be unimpaired, but effortful attentional processes are compromised in lonely relative to socially connected individuals. Of relevance for health is the capacity for self-regulation in the arena of lifestyle behaviors. Regulation of emotion can enhance the ability to regulate other self-control behaviors [ 38 ], as is evident from research showing that positive affect predicts increased physical activity [ 39 ].
In middle-aged and older adults, greater loneliness was associated with less effort applied to the maintenance and optimization of positive emotions [ 31 ]. Compromised regulation of emotion in lonely individuals explained their diminished likelihood of performing any physical activity, and loneliness also predicted a decrease in physical activity over time [ 31 ]. Physical activity is a well-known protective factor for physical health, mental health, and cognitive functioning [ 40 ], suggesting that poorer self-regulation may contribute to the greater health risk associated with loneliness via diminished likelihood of engaging in health-promoting behaviors.
A related literature shows that loneliness is also a risk factor for obesity [ 41 ] and health-compromising behavior, including a greater propensity to abuse alcohol [ 42 ]. To the extent that self-regulation s for poorer health behaviors in lonely people, better health behaviors may be more easily accomplished in the actual or perceived company of others.
Interestingly, animal research has shown that social isolation dampens the beneficial effects of exercise on neurogenesis [ 43 ], implying that health behaviors may better serve their purpose or have greater effect among those who feel socially connected than those who feel lonely. This hypothesis remains to be tested, but research on the restorative effects of sleep is consistent with this notion.
Countering the physiological effects of the challenge of daily emotional, cognitive, and behavioral experiences, sleep offers physiological restoration. Experimental sleep deprivation has adverse effects on cardiovascular functioning, inflammatory status, and metabolic risk factors [ 44 ]. In addition, short sleep duration has been associated with risk for hypertension [ 45 ], incident coronary artery calcification [ 46 ], and mortality [ 47 ].
Nonrestorative sleep i. We have noted that loneliness heightens feelings of vulnerability and unconscious vigilance for social threat, implicit cognitions that are antithetical to relaxation and sound sleep. Indeed, loneliness and poor quality social relationships have been associated with self-reported poor sleep quality and daytime dysfunction i.
In young adults, greater daytime dysfunction, a marker of poor sleep quality, was accompanied by more nightly micro-awakenings, an objective index of sleep continuity obtained from Sleep-Caps worn by participants during one night in the hospital and seven nights in their own beds at home [ 53 ]. The conjunction of daytime dysfunction and micro-awakenings is consistent with polysomnography studies showing a conjunction, essentially an equivalence, between subjective sleep quality and sleep continuity [ 54 ], and substantiates the hypothesis that loneliness impairs sleep quality.
Cross-lagged panel analyses of the three consecutive days indicated potentially reciprocal causal roles for loneliness and daytime dysfunction: lonely feelings predicted daytime dysfunction the following day, and daytime dysfunction exerted a small but ificant effect on lonely feelings the following day [ 55 ], effects that were independent of sleep duration.
In other words, the same amount of sleep is less salubrious in individuals who feel more socially isolated and, ironically, less salubrious sleep feeds forward to further exacerbate feelings of social isolation. This recursive loop operates outside of consciousness and speaks to the relative impenetrability of loneliness to intervention. The association between loneliness and cardiovascular disease and mortality [ 131419 ] may have its roots in physiological changes that begin early in life. In our study of young adults, loneliness was associated with elevated levels of total peripheral resistance TPR [ 4956 ].
TPR is the primary determinant of SBP until at least 50 years of age [ 57 ], which suggests that loneliness-related elevations in TPR in early to middle-adulthood may lead to higher blood pressure in middle and older age. Consistent with this hypothesis, loneliness was associated with elevated SBP in an elderly convenience sample [ 49 ], and in a population-based sample of 50—year-old adults in the Chicago Health, Aging, and Social Relations Study [ 21 ].
The association between loneliness and elevated SBP was exaggerated in older relative to younger lonely adults in this sample [ 21 ], suggesting an accelerated physiological decline in lonely relative to nonlonely individuals.
Our recent study of loneliness and SBP in these same individuals over five annual assessments supported this hypothesis. Short-term i. These increases were cumulative such that higher initial levels of loneliness were associated with greater increases in SBP over a 4-year period. Elevated SBP is a well-known risk factor for chronic cardiovascular disease, and these data suggest that the effects of loneliness accrue to accelerate movement along a trajectory toward serious health consequences [ 20 ].
The physiological determinants responsible for the cumulative effect of loneliness on blood pressure have yet to be elucidated. TPR plays a critical role in determining SBP in early to mid-adulthood, but other mechanisms come into play with increasing age. Candidate mechanisms include age-related changes in vascular physiology, including increased arterial stiffness [ 58 ], diminished endothelial cell release of nitric oxide, enhanced vascular responsivity to endothelial constriction factors, increases in circulating catecholamines, and attenuated vasodilator responses to circulating epinephrine due to decreased beta-adrenergic sensitivity in vascular smooth muscle [ 59 — 61 ].
In turn, many of these mechanisms are influenced by lifestyle factors such as diet, physical inactivity, and obesity—factors that alter blood lipids and inflammatory processes that have known consequences for vascular health and functioning [ 6263 ].
Changes in TPR levels are themselves influenced by a variety of physiological processes, including activity of the autonomic nervous system and the hypothalamic-pituitary adrenocortical HPA axis. The sympathetic branch of the autonomic nervous system plays a major role in maintaining basal vascular tone and TPR [ 6465 ] and elevated sympathetic tone is responsible for the development and maintenance of many forms of hypertension [ 66 ].
To date, loneliness has not been shown to correlate with SNS activity at the myocardium i. Activation of the HPA axis involves a cascade of als that in release of ACTH from the pituitary and cortisol from the adrenal cortex. Vascular integrity and functioning are beholden, in part, to well-regulated activity of the HPA axis. Dysregulation of the HPA axis contributes to inflammatory processes that play a role in hypertension, atherosclerosis, and coronary heart disease [ 67 — 69 ].
Loneliness has been associated with urinary excretion of ificantly higher concentrations of cortisol [ 70 ], and, in more recent studies, with higher levels of salivary or plasma cortisol [ 7172 ]. Pressman et al.
In our study of middle-aged and older adults, day-today fluctuations in feelings of loneliness were associated with individual differences in the cortisol awakening response. For this study, diary reports of daily psychosocial, emotional, and physical states were completed at bedtime on each of three consecutive days, and salivary cortisol levels were measured at wakeup, 30 min after awakening, and at bedtime each day.
Parallel multilevel causal models revealed that prior-day feelings of loneliness and related feelings of sadness, threat, and lack of control were associated with a higher cortisol awakening response the next day, but morning cortisol awakening response did not predict experiences of these psychosocial states later the same day [ 73 ]. Social evaluative threat is known to be a potent elicitor of cortisol [ 74 ], and our theory that loneliness is characterized by chronic threat of and hypervigilance for negative social evaluation [ 9 ] is consistent with the finding that loneliness predicts increased cortisol awakening response.
The relevance of the association between loneliness and HPA regulation is particularly noteworthy given recent evidence that loneliness-related alterations in HPA activity may occur at the level of the gene, a topic to which we turn next. Cortisol regulates a wide variety of physiological processes via nuclear hormone receptor-mediated control of gene transcription. Cortisol activation of the glucocorticoid receptor, for instance, exerts broad anti-inflammatory effects by inhibiting pro-inflammatory aling pathways. Given that loneliness is associated with elevated cortisol levels, loneliness might be expected to reduce risk for inflammatory diseases.
However, as we have noted above, feelings of loneliness and social isolation are associated with increased risk for inflammatory disease. We found evidence consistent with glucocorticoid insensitivity in Looking for my personal muscular female adult lonely examination of gene expression rates in chronically lonely versus socially connected older adults [ 75 ].
Genome-wide microarray analyses revealed that transcripts, representing distinct genes, were differentially expressed in these two groups. Markers of immune activation and inflammation e. The net functional implication of the differential gene transcription favored increased cell cycling and inflammation in the lonely group [ 75 ]. Bioinformatic analyses also indicated a possible decrease in glucocorticoid receptor-mediated transcription in the lonely group, despite the fact that there were no group differences in circulating glucocorticoid levels.
These suggest that feelings of loneliness may exert a unique transcriptional influence that has potential relevance for health. In an extension of this work, a recent study showed that feelings of social isolation were associated with a proxy measure of functional glucocorticoid insensitivity [ 76 ]. The composition of the leukocyte population in circulation is subject to the regulatory influence of glucocorticoids; high cortisol levels increase circulating concentrations of neutrophils and simultaneously decrease concentrations of lymphocytes and monocytes.
In a study of older Taiwanese adults, this relationship was reflected in a positive correlation between cortisol levels and the ratio of neutrophil percentages relative to lymphocyte or monocyte percentages. However, in lonely individuals, this correlation was attenuated and nonificant, consistent with a diminished Looking for my personal muscular female adult lonely of cortisol at the level of leukocytes.
The precise molecular site of glucocorticoid insensitivity in the pro-inflammatory transcription cascade has yet to be identified, and additional longitudinal and experimental research are needed to determine the degree to which chronic feelings of social isolation play a causal role in differential gene expression.
However, the association between subjective social isolation and gene expression corresponds well to gene expression differences in animal models of social isolation e. Impaired transcription of glucocorticoid response genes and increased activity of pro-inflammatory transcription control pathways provide a functional genomic explanation for elevated risk of inflammatory disease in individuals who experience chronically high levels of loneliness.
Loneliness differences in immunoregulation extend beyond inflammation processes. Loneliness has been associated with impaired cellular immunity as reflected in lower natural killer NK cell activity and higher antibody titers to the Epstein Barr Virus and human herpes viruses [ 7080 — 82 ]. In addition, loneliness among middle-age adults has been associated with a smaller increase in NK cell s in response to the acute stress of a Stroop task and a mirror tracing task [ 71 ].
In young adults, loneliness was associated with poorer antibody response to a component of the flu vaccine [ 72 ], suggesting that the humoral immune response may also be impaired in lonely individuals. However, in the latter study, loneliness predicted a slower rate of decline in levels of CD4 T-lymphocytes over a 3-year period [ 84 ]. These data suggest that loneliness protects against disease progression, but no association was observed between loneliness and time to AIDS diagnosis or AIDS-related mortality [ 84 ].
Additional research is needed to examine the role of loneliness chronicity, age, life stress context, genetic predispositions, and interactions among these factors to determine when and how loneliness operates to impair immune functioning. Six qualitative reviews of the loneliness intervention literature have been published since [ 85 — 90 ], and all explicitly or implicitly addressed four main types of interventions: 1 enhancing social skills, 2 providing social support, 3 increasing opportunities for social interaction, and 4 addressing maladaptive social cognition.
All but one of these reviews concluded that loneliness interventions have met with success, particularly interventions which targeted opportunities for social interaction. Findlay [ 87 ] was more cautious in his review, noting that only six of the 17 intervention studies in his review employed a randomized group comparison de, with the remaining 11 studies subject to the shortcomings and flaws of pre-post and nonrandomized group comparison des.
We recently completed a meta-analysis of loneliness intervention studies published between and September to test the magnitude of the intervention effects within each type of study de and to determine whether the intervention target moderated effect sizes Masi et al.
Of the 50 studies eligible for inclusion in the meta-analysis, 12 were pre-post studies, 18 were non-randomized group comparison studies, and 20 were randomized group comparison studies.Looking for my personal muscular female adult lonely
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