良好的心态能影响基因

A good state of mind -- that is, your happiness -- affects your genes, scientists say. In the first study of its kind, researchers from UCLA's Cousins Center for Psychoneuroimmunology and the University of North Carolina examined how positive psychology impacts human gene expression. What they found is that different types of happiness have surprisingly different effects on the human genome.

People who have high levels of what is known as eudaimonic well-being -- the kind of happiness that comes from having a deep sense of purpose and meaning in life (think Mother Teresa) -- showed very favorable gene-expression profiles in their immune cells. They had low levels of inflammatory gene expression and strong expression of antiviral and antibody genes.

However, people who had relatively high levels of hedonic well-being -- the type of happiness that comes from consummatory self-gratification (think most celebrities) -- actually showed just the opposite. They had an adverse expression profile involving high inflammation and low antiviral and antibody gene expression.

The report appears in the current online edition of the journal Proceedings of the National Academy of Sciences.

For the last 10 years, Steven Cole, a UCLA professor of medicine and a member of the UCLA Cousins Center, and his colleagues, including first author Barbara L. Fredrickson at the University of North Carolina, have been examining how the human genome responds to stress, misery, fear and all kinds of negative psychology.

In this study, though, the researchers asked how the human genome might respond to positive psychology. Is it just the opposite of stress and misery, or does positive well-being activate a different kind of gene expression program?

The researchers examined the biological implications of both hedonic and eudaimonic well-being through the lens of the human genome, a system of some 21,000 genes that has evolved fundamentally to help humans survive and be well.

Previous studies had found that circulating immune cells show a systematic shift in baseline gene-expression profiles during extended periods of stress, threat or uncertainty. Known as conserved transcriptional response to adversity, or CTRA, this shift is characterized by an increased expression of genes involved in inflammation and a decreased expression of genes involved in antiviral responses.

This response, Cole noted, likely evolved to help the immune system counter the changing patterns of microbial threat that were ancestrally associated with changing socio-environmental conditions; these threats included bacterial infection from wounds caused by social conflict and an increased risk of viral infection associated with social contact.

"But in contemporary society and our very different environment, chronic activation by social or symbolic threats can promote inflammation and cause cardiovascular, neurodegenerative and other diseases and can impair resistance to viral infections," said Cole, the senior author of the research.