Loneliness is gene deep, its molecular signature is reflected in the lonely person’s DNA. This was the conclusion of a new US study by scientists at the University of California Los Angeles (UCLA) and other US academic centres.

The study is published in the latest issue of the journal Genome Biology.

The researchers discovered a distinct pattern of gene expression in immune cells of people who are chronically extremely lonely.

Study author Steve Cole, associate professor of medicine at the Division of Hematology and Oncology at the David Geffen School of Medicine at UCLA, member of the Cousins Center for Psychoneuroimmunology, and member of UCLA’s Jonsson Comprehensive Cancer Center said in a press release that:

“What this study shows is that the biological impact of social isolation reaches down into some of our most basic internal processes: the activity of our genes.”

Cole and colleagues suggest that feelings of isolation are linked to changes in gene expression that drive inflammation, one of the first responses of the immune system.

They hope the study gives a framework for understanding how social factors and increased risk of heart disease, viral infections and cancer are linked.

Scientists already know that social environments affect health. People who are lonely and socially isolated die earlier.

What they don’t know is if the higher rate of death among lonely people is because of reduced social resources or because of the effect of isolation on their bodily functions, or perhaps both.

However, Cole and the other researchers found that changes in the way immune cells express their genes were directly linked to the “subjective experience of social distance”.

The differences were independent of other known risk factors like health status, weight, age and use of medication, they said.

“The changes were even independent of the objective size of a person’s social network,” said Cole.

Cole and colleagues enrolled 14 participants from the Chicago Health, Aging, and Social Relations Study and scanned their DNA using a chip technology called DNA microarrays that allowed them to survey all known human genes in the samples.

6 of the participants scored in the top 15 per cent of a well known psychological test for loneliness that was developed in the 70s called the UCLA Loneliness Scale.

The remaining 8 participants scored in the bottom 15 per cent of the Loneliness Scale.

The DNA survey showed that 209 gene transcripts (where the gene gets its code ready to start making proteins) were expressed differently between the two groups. All the genes coded for leucocytes, agents of the immune system.

78 of the gene transcripts were “over expressed” (resulting in too much protein) and 131 were “under expressed” (not enough protein) in the lonely individuals compared to the others.

The over expressed genes included many that control immune system functions like inflammation.

However, it was also interesting that the under expressed genes were those involved in antiviral responses and production of antibodies.

The study concluded that:

“These data provide the first indication that human genome-wide transcriptional activity is altered in association with a social epidemiological risk factor. 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 subjective social isolation.”

Distinguishing between the various aspects of loneliness that are closely linked to these changes in gene expression, the scientists discovered that:

“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,” said Cole.

He added that the findings could identify molecular targets for blocking the negative health impact of social isolation.

“Effects of loneliness on gene expression.”

Cole SW, Hawkley LC, Arevalo JM, Sung CY, Rose RM, Cacioppo JT.

Genome Biology 2007, 8:R189.

doi:10.1186/gb-2007-8-9-r189

Published online 13 September 2007 (provisional version).

Click here for Abstract (provisional).

Written by: Catharine Paddock