The problem has been explaining how the process works at the level of the nervous and immune systems.
For many years, experts in psychoneuroimmunology have searched for the explanation. Now, Steve Cole, Ph.D., from the Cousins Center for Psychoneuroimmunology at the University of California, Los Angeles, has uncovered at least part of the mystery.
In his studies, Cole uses genome-wide transcriptional analysis to observe broad patterns of gene expression in cells. This has led to a series of published studies on the link between negative mental states (such as stress or loneliness) and the behavior of the immune system, driven by altering patterns of gene expression.
In one study, his team focused on loneliness. They analyzed genome-wide activity in 14 “people who chronically experienced high or low levels of subjective social isolation.”
This identified 209 genes that were expressed differently in the lonely or non-lonely individuals, including genes that oversee immune activation and blood cell function. Certain genes that dampen bodily inflammation were less effective in lonely people, while pro-inflammatory genes were overexpressed.
“This data provides the first indication that human genome-wide transcriptional activity is altered in association with a social epidemiological risk factor,” writes the research team in the journal Genome Biology. This provides “a functional genomic explanation for elevated risk of inflammatory disease in individuals who experience chronically high levels of subjective social isolation.”
They add, “One of the most robust social risk factors involves the number and quality of an individual’s close personal relationships. People who are socially isolated have increased risk of death from all causes, and several specific infectious, cancerous, and cardiovascular diseases.”
The biological basis of these health risks is poorly understood, the team says, partly because it is unknown whether the lack of social support or the biological effects of loneliness are to blame. Their study confirms that the biological effect clearly plays a major role.
“The data provides the first evidence that social-environmental risk factors are linked to global alterations in human gene transcription,” they write, “and establishes a molecular context for understanding the increased risk of inflammatory disease observed in human beings who experience a chronic sense of subjective social isolation (loneliness).”
And since then, the researchers have replicated the results in a larger group of 93 people.
Various studies over the last three decades have also showed that the brain is linked to the immune system. For example, parts of the nervous system have connections to organs including the thymus and bone marrow, which help fight of disease, and there are specific receptors for neurotransmitters on the surface of immune cells.
In 2003, Dr. Richard Davidson and colleagues at the University of Wisconsin-Madison investigated the impact of emotions on flu risk. They asked 52 participants to recall the best and the worst times of their lives while having a brain scan. Next, the volunteers were given a flu vaccine and had their flu-antibody levels measured six months later.
Those who experienced particularly intense negative emotions (according to their brain activity) had fewer antibodies. In fact, the subjects who felt the worst made 50 percent fewer antibodies than those who were less upset by their painful memories.
Said Davidson, “It’s absolutely likely that positive emotions can improve your immune function. People with negative emotional styles would be more likely to develop the flu.”
The risk of catching a cold has also been linked to emotions. Psychologist Dr. Sheldon Cohen and colleagues at Carnegie Mellon University in Pennsylvania studied over 300 healthy volunteers. Each was interviewed over two weeks to gauge his or her emotional state, with scores for positive categories (happy, pleased, or relaxed) and negative categories (anxious, hostile, and depressed).
Then the rhinovirus, which causes colds, was squirted into each participant’s nose, and they were interviewed daily for five days about any symptoms. This showed that those scoring in the bottom third for positive emotions were three times more likely to catch a cold that those in the top third.
Said Cohen, ”People who express more positive emotions are less susceptible to upper respiratory tract infections than people with a negative emotional style.”
Cole and his team are now moving on to focus on the protective effects of happiness and well-being, a science still in its infancy, but potentially groundbreaking.
“I have spent most of my career and personal life trying to avoid or overcome bad things,” Cole said. “I spend a lot more time now thinking about what I really want to do with my life, and where I’d like to go with whatever years remain.”
Marchant, J. Immunology: The pursuit of happiness. Nature, Volume 503, 27 November 2013, pp. 458-60, doi: 10.1038/503458a
Cole, S. W. et al. Social regulation of gene expression in human leukocytes. Genome Biology, Volume 8, 13 September 2007, doi: 10.1186/gb-2007-8-9-r189
Rosenkranz, M. A. et al. Affective style and in vivo immune response: Neurobehavioral mechanisms. PNAS, Volume 100, pp. 11148-52, doi: 10.1073/pnas.1534743100
Cohen, S. et al. Emotional style and susceptibility to the common cold. Psychosomatic Medicine, Volume 65, July-August 2003, pp. 652-7.