Be happy: Your genes may thank you for it

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.

In the present study, the researchers drew blood samples from 80 healthy adults who were assessed for hedonic and eudaimonic well-being, as well as potentially confounding negative psychological and behavioral factors. The team used the CTRA gene-expression profile to map the potentially distinct biological effects of hedonic and eudaimonic well-being.

And while those with eudaimonic well-being showed favorable gene-expression profiles in their immune cells and those with hedonic well-being showed an adverse gene-expression profile, "people with high levels of hedonic well-being didn't feel any worse than those with high levels of eudaimonic well-being," Cole said. "Both seemed to have the same high levels of positive emotion. However, their genomes were responding very differently even though their emotional states were similarly positive.

"What this study tells us is that doing good and feeling good have very different effects on the human genome, even though they generate similar levels of positive emotion," he said. "Apparently, the human genome is much more sensitive to different ways of achieving happiness than are conscious minds."

Other authors on the study included Jesusa M.G. Arevalo and Jeffrey Ma, both of UCLA, and Karen M. Grewen, Kimberly A. Coffey, Sara B. Algoe and Ann M. Firestine of the University of North Carolina.

The research was supported by National Institutes of Health grants R01NR012899, R01CA116778 and P30AG107265.