Study Sheds New Light on Effects of Emotional Isolation and Alzheimer’s Risk

Kristin Casady, MA, Editorial Director, Geriatrics & Aging.

Yes: in the sea of life enisled,
With echoing straits between us thrown.
Dotting the shoreless watery wild,
We mortal millions live alone.
The islands feel the enclasping flow,
And then their endless bounds they know.

–Matthew Arnold

That humans are social creatures who require meaningful interactions with others for happiness is a truism; however, recent research suggests that relating is valuable for more than emotional well-being. Older adults who are persistently lonely, and who perceive themselves as lacking connection and outlets for meaningful interaction, may be more vulnerable to the effects of age-related neuropathology.

A recently published study has linked the development of Alzheimer’s disease with loneliness. The study, published in the Archives of General Psychiatry, has found that lonely people may be at least twice as likely to develop the type of dementia linked to Alzheimer’s disease than individuals who do not report loneliness in advanced age (Arch Gen Psychiatr 2007;64:234-40).

Previous studies have identified a link between social isolation in old age and the risk of cognitive decline and dementia, but the risk associated with perceived isolation, or loneliness, is not well understood. Social isolation refers to connectedness with one’s social environment. Such isolation can be assessed by measuring the extent and quality of social contact and relationships--whether one is married, or has friendships and other social relationships experienced as meaningful, for example. Loneliness is measured more subjectively, and is assessed by asking people about how alone, empty, or abandoned they feel. In other words, the key distinction is between being alone and feeling alone.

In order to test their hypothesis that loneliness may be associated with increased risk of Alzheimer’s disease (AD), researchers conducted a longitudinal clinicopathologic cohort study with up to 4 years of annual in-home follow-up. They analyzed 823 older Caucasian persons free of dementia at enrollment who were recruited from seniors’ facilities in the Chicago area. Loneliness was assessed with a 5-item scale at baseline (mean ± SD, 2.3 ± 0.6) and annually thereafter. Participants underwent evaluations including assessments of loneliness, classifications of dementia and Alzheimer’s disease, and testing of thinking, learning, and memory abilities. Loneliness was measured on a scale of one to five, the score increasing with the degree experienced. At death, uniform postmortem brain examinations were conducted to quantify AD pathology in multiple brain regions and the presence of cerebral infarctions.

During the follow-up period 76 of the recruits developed clinically defined Alzheimer’s. Risk of AD was more than doubled in lonely persons (score 3.2, 90th percentile) compared with persons who were not lonely (score 1.4, 10th percentile). Researchers controlled for indicators of social isolation and other covariates, which did not affect the finding. Loneliness was associated with lower level of cognition at baseline and with more rapid cognitive decline during follow-up. There was no significant change in loneliness, and mean degree of loneliness during the study was strongly associated with cognitive decline and development of AD. Of the 90 participants who died and in whom autopsy of the brain was performed, loneliness was not related to pathological findings.
Loneliness was associated with impaired cognitive function at baseline, the authors noted. The basis for the association between loneliness, AD and cognitive decline is not yet known. Their results did not suggest that changes in cognition itself produced behaviours that might create impressions of loneliness, and loneliness did not increase in their study with reported levels of altered cognition. Pathological findings also failed to link amyloid plaques to rates of reported loneliness. In other words, their data do not support the hypothesis that loneliness is a reaction to impaired cognition.

Alternately, the authors offer the possibility that loneliness could compromise neural systems underlying cognition and memory, increasing individuals’ vulnerability to the effects of age-related neuropathology. They propose that neural systems underlying social behaviour may be less varied and elaborate in lonely people and thus less able to compensate for other neural systems under insult from age-related pathology. Given that neither AD pathology nor cerebral infarction could account for the association between loneliness and cognitive decline, they suggest that “novel neurobiological mechanisms” may be involved.
Further findings included data indicating that the association of loneliness and AD-related decline is at least partly independent of depressive symptomatology.
Given these data, the authors concluded that loneliness is a risk factor for, not an early sign of, Alzheimer’s disease. They noted that independent replication of their findings is necessary and would optimally involve longer follow-up and greater diversity of participants.