Nearly two and a half millennia ago, Aristotle triggered a revolution in happiness. At the time, Greek philosophers were trying hard to define precisely what this state of being was. Some contended that it sprang from hedonism, the pursuit of sensual pleasure. Others argued from the perspective of tragedy, believing happiness to be a goal, a final destination that made the drudge of life worthwhile. These ideas are still with us today, of course, in the decadence of Instagram and gourmet-burger culture or the Christian notion of heaven. But Aristotle proposed a third option. In his Nicomachean Ethics, he described the idea of eudaemonic happiness, which said, essentially, that happiness was not merely a feeling, or a golden promise, but a practice. “It’s living in a way that fulfills our purpose,” Helen Morales, a classicist at the University of California, Santa Barbara, told me. “It’s flourishing. Aristotle was saying, ‘Stop hoping for happiness tomorrow. Happiness is being engaged in the process.’ ” Now, thousands of years later, evidence that Aristotle may have been onto something has been detected in the most surprising of places: the human genome.
The finding is the latest in a series of related discoveries in the field of social genomics. In 2007, John Cacioppo, a professor of psychology and behavioral neuroscience at the University of Chicago, and Steve Cole, a professor of medicine at the University of California, Los Angeles, among others, identified a link between loneliness and how genes express themselves. In a small study, since repeated in larger trials, they compared blood samples from six people who felt socially isolated with samples from eight who didn’t. Among the lonely participants, the function of the genome had changed in such a way that the risk of inflammatory diseases increased and antiviral response diminished. It appeared that the brains of these subjects were wired to equate loneliness with danger, and to switch the body into a defensive state. In historical and evolutionary terms, Cacioppo suggested, this reaction could be a good thing, since it helps immune cells reach infections and encourages wounds to heal. But it is no way to live. Inflammation promotes the growth of cancer cells and the development of plaque in the arteries. It leads to the disabling of brain cells, which raises susceptibility to neurodegenerative disease. In effect, according to Cole, the stress reaction requires “mortgaging our long-term health in favor of our short-term survival.” Our bodies, he concluded, are “programmed to turn misery into death.”
In early 2010, Cole spoke about his work at a conference in Las Vegas. Among the audience members was Barbara Fredrickson, a noted positive psychologist from the University of North Carolina at Chapel Hill, who had attended graduate school with Cole. His talk made her wonder: If stressful states, including loneliness, caused the genome to respond in a damaging way, might sustained positive experiences have the opposite result? “Eudaemonic and hedonic aspects of well-being had previously been linked to longevity, so the possibility of finding beneficial effects seemed plausible,” Fredrickson told me. The day after the conference, she sent Cole an e-mail, and by autumn of that year they had secured funding for a collaborative project. Fredrickson’s team would profile a group of participants, using questionnaires to determine their happiness style, then draw a small sample of their blood. Cole would analyze the samples and see what patterns, if any, emerged.