Genomic data could alleviate health impact of loneliness
heart disease and infection but a new study could point to new ways
of reducing its impact on health.
Dr Steven Cole and colleagues at University of California Los Angeles (UCLA) and the University of Chicago have generated a genetic 'signature' of loneliness that helps to explain how a feeling of isolation can lead to an increased risk of diseases where inflammation plays a negative role. People who are socially isolated suffer from higher all-cause mortality, and higher rates of cancer, heart disease and infection. Although there are also likely to be social factor that account for some of the impact on health, such as reduced physical or economic assistance, or perceptions of threat and uncertainty leading to the activation of neuroendocrine stress responses, Cole believes his study proves this doesn't provide the whole answer. "What this study shows us, is that the biological impact of social isolation reaches down into some of our most basic internal processes - the activity of our genes," said Cole. The impact of such diseases on health care costs is monumental and any drugs that could reduce their occurrence would not only be welcomed by potential patients but could also save billions. The scientists used DNA microarrays to measure the activity of all known genes in the white blood cells of 14 individuals. Six of those were medically classified as chronically lonely - they were in the top 15 per cent of the UCLA Loneliness scale, a widely used measure developed in the 1970s - and the remaining eight subjects acted as a control and were in the bottom 15 per cent of the scale. Of the genes surveyed, levels of some 209 transcripts were different between the two groups with 78 genes being over-active and 131 under-expressed. In the first group were many involved in immune system activation and inflammation, while those genes under-expressed included key genes in antiviral responses and antibody production. An analysis of the data identified some of the biological pathways involved, including reduced activity in the anti-inflammatory glucocorticoid pathway and increased gene levels in the pro-inflammatory nuclear factor kappa B (NF-kB)/Rel pathway. Other modulated pathways include CREB/ATF, JAK/STAT, IRF1, C/EBP, Oct, and GATA. "These findings provide molecular targets for our efforts to block the adverse health effects of social isolation," said Cole. The data, set out in an article in the journal Genome Biology, could be used as a biomarker to monitor interventions designed to reduce the impact of loneliness on health. Perhaps one of the most surprising results of the study is that changes in gene expression appear to be linked to the "subjective experience of social distance", according to Cole. "The differences we observed were independent of other known risk factors for inflammation, such as health status, age, weight, and medication use. The changes were even independent of the objective size of a person's social network. What counts, at the level of gene expression, is not how many people you know, it's how many you feel really close to over time," he said. Cole acknowledged that the study needed to be repeated with a larger group of subjects and using other cell types.
