Loneliness and Social Isolation: Determinants of Cardiovascular Outcomes

Tanya Sharma, Prasad R Padala, Jawahar L Mehta, Tanya Sharma, Prasad R Padala, Jawahar L Mehta

Abstract

One in three Americans report experiencing loneliness in everyday life, a number that has grown exponentially over the last few decades. As we respond to the SARS-COV2 pandemic with quarantine and social distancing, social isolation and feelings of loneliness are increasing among people of all ages. This presents as an opportune time to recognize the public health impact of these important psychosocial determinants. Loneliness and social isolation are associated with a higher incidence of CVD, higher healthcare utilization and worse outcomes even after controlling for conventional risk factors of CVD. In this review, we discuss loneliness and social isolation as determinants of cardiovascular outcomes, the pathophysiology of this association, and its implications in clinical practice. We discuss some of the shortcomings in the assessment of loneliness and social isolation while identifying the most commonly used rating scales for the same. Finally, we suggest modifications to interventions for loneliness and social isolation during the COVID-19 pandemic.

Keywords: COVID-19; Loneliness; cardiovascular outcomes; pathophysiology.; psychosocial risk factors; social isolation.

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Figures

Fig. (1)
Fig. (1)
Hypothesized model of loneliness and social isolation affecting cardiovascular outcomes. Loneliness and social isolation can impact health-related behaviors. It also leads to an exaggerated autonomic response to stress and sympathetic nervous system hyperactivity. These conditions are associated with increased total peripheral resistance (TPR) and reduced heart rate variability (HRV), contributing to hypertension, ischemic heart disease and poor cardiac output. In animal models, social isolation has been associated with higher resting glucocorticoid levels from overactivation of the hypothalamic-pituitary-axis (HPA), leading to chronic inflammation and glucocorticoid resistance (receptor desensitization). It also increases the vasoconstrictive effects of catecholamines and decreases nitric oxide (NO) synthesis at the level of endothelial cells. There is evidence linking renin-angiotensin-aldosterone-system (RAAS) to social isolation, which in turn contributes to increased TPR, platelet activation and endothelial dysfunction. Loneliness has also been associated with increased circulating natural killer (NK) cells, fibrinogen and other inflammatory mediators, e.g. interleukin-6 (IL-6), IL-1β and tumor necrosis factor-alpha (TNF-alpha). This may be due to increased glucocorticoid levels or direct action on myelopoiesis. This state of chronic inflammation, along with endothelial dysfunction and platelet activation, leads to accelerated atherosclerosis. (A higher resolution / colour version of this figure is available in the electronic copy of the article).

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Source: PubMed

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