When second grader Jacqueline Olds arrived home from school one afternoon in 1955, she found the atmosphere charged with excitement. Her parents pointed to a headline on the front page of the Montreal Star: “McGill opens vast new research field with brain ‘pleasure area’ discovery.”
Olds, now an HMS associate clinical professor of psychiatry at Massachusetts General Hospital, had only vague notions back then of what her father, James Olds, then a postdoctoral researcher at McGill University, did during the day, yet she knew it had something to do with the brains of rats.
The elder Olds had just published a paper in the Journal of Comparative and Physiological Psychology describing how the rat brain was suffused with desire when a particular region of it was electronically stimulated. The rat would do whatever it could to relive the cerebral voltage regardless of cost, like a jilted lover seeking intimacy anew, or a gambler circling back to the roulette wheel. James Olds’s discovery of the brain’s “pleasure center” has held up for more than half a century, and no scientific discussion on the phenomenon of human love can avoid it.
Most of us, even those disciplined to interpret the world through the lens of evidence–based science, can’t help but imagine love as a ghost in the machine. St. Paul’s famous meditation on the patience and kindess of love, recited in a seemingly nonstop wedding loop, personifies love as an entity embodying what we crave most in others. Love as a spiritual value has so permeated Western culture that even a science–drenched modern fable like the film Eternal Sunshine of the Spotless Mind couldn’t help but bust it out of its neurophysiologic sheathing.
But the scientific evidence is unmistakable: Whatever this thing called love is, we humans need it. Deep attachments to others—and the pleasure–center stimulation those links cause—are as vital to our bodies and minds as food and sleep. Their absence carries catastrophic risk to our health and well–being.
I Feel Your Pain
While many drugs, including antibiotics and certain chemotherapies, gradually lose effectiveness over time, one treatment has manifested a steady rise in potency during the past few decades: the placebo.
Much to the vexation of pharmaceutical companies trying to get antidepressants and pain medications approved for use, clinical trials conducted over the years have revealed the increasing power of the placebo effect. Our efforts to understand that trend throws light on the healing power of doctor/patient connectedness.
Carl Marci ’97, an HMS assistant professor of psychiatry at Massachusetts General Hospital, began paying attention to the placebo effect in the early 1990s, while still a medical student. During a course on alternative therapies, he was struck by the amount of time these practitioners of homeopathy, Reiki, and acupuncture spent with their patients.
“Data showed that, with the exception of intense psychotherapy, people were spending far more time each year with alternative practitioners than they were with other health care providers,” says Marci. “That got me thinking about the relationship.” He began to suspect that the success of these providers had less to do with their therapeutic approach than it did with the time they invested in their patients. He has since spent most of his professional life studying the doctor/patient relationship, using empathy as his framework.
What is empathy, and why does it matter? The term, coined by a contemporary of Freud, goes back to the German word meaning “feeling into.” The English novelist Ian McEwan once wrote, “Imagining what it is like to be someone other than yourself is at the core of our humanity. It is the essence of compassion, and it is the beginning of morality.”
A slightly more scientific paraphrase might describe empathy as the ability of the brain to accurately mirror the emotions it perceives in another. Marci’s contribution to this field is the discovery that most empathy occurs at an unconscious level, evidence that our brains are hardwired for it.
Several years ago Marci conducted a study in which he sought to quantify empathy. Taking 20 patient/therapist pairs, he and colleagues measured the rate at which skin conducted electrical impulses in these subjects, as determined through their sweat production during sessions.
“Skin sweat marks arousal coming from the brain’s emotion center, and it accurately measures the depth of emotional response,” says Marci. “It can’t indicate what you’re feeling, but it indicates the depth and the curve, the trajectory, of your emotion.”
Marci found that at the moments when the rate of electrical conductivity on the skin of patients and therapists synchronized into matched lines of peaks and gullies, the patients reported feeling most understood. (Interestingly, conductivity was most disjointed precisely at those moments in which the therapists monopolized the conversation.)
Since the mid–1990s, when a group of Italian researchers first proposed the idea of “mirror neurons,” researchers have come to grasp that our brains contain dedicated neuronal networks that reflect the world around us. These networks, which reside primarily in the prefrontal cortex—the corner office of cerebral executive function—imitate motions and emotions in a neurobiological monkey see, monkey do. When you witness someone waving, the very part of your brain that activates arm motion and wrist action lights up, even if you jam your hands into your pockets. And despite your efforts to keep your visage impassive, the neurons that animate faces to form beaming smiles flare the nanosecond you glimpse a Cheshire grin. “Our brains are so wired for empathy,” Marci says, “that there’s zero lag time.”
As far as the placebo effect goes, Marci suggests that one explanation for its steady rise is the increasing complexity of clinical trials. The tighter the regulations, the more interactions patients have with a team of providers. The deeper human interaction that presumably results may help explain the increase in the placebo effect.
Which leads us back to the brain’s pleasure center, or reward center. Empathy triggers dopamine and serotonin, neurochemicals associated with the reward center’s conjoined twin, the brain’s emotion center. If, as the scientific literature indicates, mere laughter stimulates the reward center, how much more stimulating would be the act of immersing yourself in the world of another?
From an evolutionary perspective, this makes perfect sense. “Human babies have the most postnatal neuronal growth of any species,” says Marci. “Without empathy, there is no attachment, and attachment is essential for survival.”
What happens when empathy is absent? While Marci’s model is the doctor/patient relationship, Karlen Lyons–Ruth, an HMS associate professor of psychology at Cambridge Health Alliance, studies the physiological effects of human interactions in a relationship far more primordial: the one between mothers and infants.
Within the field of developmental psychology, Lyons–Ruth is a leading expert on attachment, with a particular focus on attachment gone wrong. “In a sense,” she says, “I’m most interested in what happens when love goes awry.”
Empathy and mirroring of the infant’s states by the parent is a powerful regulator of normal development, says Lyons–Ruth. The biomarker she uses to measure the quality of a mother–infant relationship is cortisol. This steroid hormone has a number of functions, such as increasing blood sugar and helping the body metabolize fats and carbohydrates. It is also released in response to stress to help the body mobilize to meet a challenge. Yet too much cortisol can lead to health problems.
Combat soldiers in particular are likely to experience long periods of extreme stress. Such prolonged stress keeps the hormone jacked up, but the human organism’s capacity to tolerate such a powerful chemical is limited, so an emergency system clicks in and dams the hormone’s flow. This check can result in an individual who goes through life with a blunted stress response system and attenuated emotional engagement.
Normal cortisol levels and stress responses are essential for healthy attachment, says Lyons–Ruth. When a mother’s cortisol levels are normal, she acts as an external regulator by being attuned to her baby’s fear and discomfort and acting to relieve these negative states. As a result, the baby experiences minimal stress. But when a mother’s cortisol response is blunted, her ability to act as an attuned external regulator for the infant may fail.
“We still have much work to do to understand this model of attachment,” says Lyons–Ruth. “But our research has shown that mothers whose interactions with their infants are the most disrupted have the lowest cortisol levels.” She and her colleague Bjarne Holmes have also observed that the infants of low–cortisol mothers present with low cortisol levels as well. When low–cortisol infants are stressed, though, their cortisol levels fly off the charts. “These babies lack the ability to modulate their stress responses,” Lyons–Ruth says. Because antisocial children and adults also show blunted cortisol responses, low cortisol levels among mothers with very young infants set off alarm bells about these babies’ future development.
Infants reared in orphanages may be most at risk for blunted stress responses and associated disturbances in their ability to form deep emotional bonds. As Megan Gunnar and her colleagues at the University of Minnesota have shown, many children adopted from orphanages show abnormally low hormone levels similar to those of combat veterans and antisocial adults. But instead of acting antisocial, some of these children exhibit what Lyons–Ruth calls indiscriminate friendliness. They lack the “stranger danger” instinct that is recognized as a healthy component of early development. Indiscriminate behavior often persists throughout childhood, even after adoption into healthy and stable homes.
“The work that Charley Zeanah has done at Tulane is pointing to a possible critical period for the formation of attachment bonds,” says Lyons–Ruth. “Despite good care later, unless responsive care is provided before the end of toddlerhood, blunted cortisol and attachment problems can persist.”
Lonely Hearts Club
Richard Schwartz has the distinction of being both an HMS associate clinical professor of psychiatry at McLean Hospital and the husband of Jacqueline Olds, the psychiatrist whose father discovered the brain’s reward center. Together Schwartz and Olds have carved out a niche as experts in the study not only of love and marriage, but of loneliness as well.
They had already written one book on loneliness when a University of Chicago survey found, in 2004, that 24.7 percent of respondents had not spoken to anyone over the prior six months on issues that were important to them. Most striking was that nearly two decades earlier, only 10 percent of respondents taking the survey had reported this circumstance. This finding spurred Schwartz and Olds to tackle a second book on the subject, The Lonely American. Their thesis is straightforward: The United States is suffering from a loneliness epidemic, and the feeling is leading to physical and mental stress. “To put it simply,” says Schwartz, “loneliness is bad for you.”
And there’s plenty of evidence to support this notion. In 1988, University of Michigan sociologist James House published a seminal review article in Science that detailed a link between loneliness and premature death. Even when circumstances such as accidents were factored out, socially isolated individuals were twice as likely to die within a ten–year period as were non–isolated people.
Maintaining contact with others seems to be hardwired into our biology, such that our bodies become stressed when these connections are threatened. Loneliness, in short, is a form of low–level chronic stress.
“When you’re disconnected, your immune system goes to hell,” Schwartz observes, citing another landmark study, this one published in Genome Biology in 2007 by Steve Cole of the University of California at Los Angeles. In this study, researchers found that chronic loneliness alters the expression of a network of genes associated with inflammation. “If we know that loneliness affects our immune response,” Schwartz says, “it’s not surprising that it would happen at the level of DNA expression.”
As therapists, Schwartz and Olds constantly encounter patients who suffer from chronic loneliness, yet most are hesitant to label it as such. As diagnoses go, depression and anxiety are less embarrassing. But it’s hard to overestimate the psychic pain that loneliness can cause. Think of the nibbling feelings you had as a child (or an adult!) when you suspected you were being purposely left out. Then try to imagine the pain of ostracism or, taken to extremes, the outright torture of solitary confinement.
“Few higher mammals are solitary,” observes Schwartz. “Humans are relatively helpless as individuals in the natural world. Part of what makes us so powerful is that we’ve banded together in small groups. And part of the pain of loneliness is the recognition that without other people we simply can’t survive.”
Nor surprisingly, loneliness and substance abuse often go hand in hand. “Many drugs, particularly stimulants, trigger the dopaminergic reward center,” Olds says. “But we now know that social connectedness and the feeling of being loved also activate that same reward center. If you lack the relationships needed to stimulate that part of your brain, you’ll likely find it in a drug.”
Blanche DuBois’s legendary line in A Streetcar Named Desire, “I have always depended on the kindness of strangers,” is evolutionarily and neurologically true. Empathy and attachment are at the core of human relatedness, and a small section of our prefrontal cortex drives us to find it one way or another. Without it, we’re lost.
“Attachment to others,” says Olds, “is the original reward.”
David Cameron is the Director of Science Communications at Harvard Medical School.