distance. They go around and around the room like that.” It’s like a dance.
In public places, where the interaction is not as close and personal, the need for space still exists. Elliot Aronson is a social psychologist at the University of California, Santa Cruz. He says that Greeks and Americans have very different ideas about how to distribute themselves on an empty stretch of beach. “On an American beach,” says Aronson, “three people arrive and sit as far away from one another as they can. As more people arrive, they fill in, leaving space between strangers. On a Greek beach, three people arrive and immediately sit close together. You can see how Americans would be annoyed by a family of Greeks setting their towels down right next to them with ‘room’ available!”
There are also very different norms about whether you should look people in the eye, according to Ellsworth. “We think that it’s the right thing to do,” she says. “We take it as a sign of sincerity; we assume that if somebody is not looking us in the eye, maybe the person is lying. Yet many other cultures think it’s rude to look somebody right in the eye.”
She has observed this with many of her foreign students at the University of Michigan. Some of them have described to her the experience of driving a car and having their passengers try to make eye contact with them. She says they find it not only annoying but downright scary.
Ellsworth says that significant consequences can result from this cultural misunderstanding. A foreign visitor’s discomfort with making eye contact with an immigration official or a security officer could arouse suspicion in an official who is untrained in these cultural norms.
Ellsworth has been trying to find out when these patterns of behavior emerge. She has begun a comparative analysis of American and Japanese children’s books. As you might expect, the American books tell stories of individuals triumphing over adversity, whereas Japanese stories are more about fitting in and getting along. Ellsworth doubts that these patterns of behavior are something we’re born with—she thinks it must be the result of early childhood experiences.
So, if we Americans as a culture have a narcissistic, self-assured swagger as we strut through the world, and if we are annoyed when our will is thwarted and events we can’t control drive us nuts, we come by these attitudes honestly. Like so many of life’s woes (and joys), it’s all our parents’ fault.
Chris Furbee spent most of his childhood in Philippi, a town on the banks of the Tygart River in central West Virginia. After Chris’s parents got divorced, his mother couldn’t afford their house in nearby Lake Floyd, so Chris and his mom moved into his grandparents’ trailer in Philippi.
Quarters were tight. Chris remembers slinking past his grandfather as the old man lurched down the narrow hallways. “He’d lose balance and bump into me occasionally,” Chris says. “I had a real hard time with it. I hate to say that, but I was a teenager. I felt like it was almost like he had a contagious disease.” Chris’s grandfather did have a disease, but it wasn’t contagious: he was dying of Huntington’s disease (HD).
The lurching is a symptom of the illness, caused by the degeneration of the brain, particularly the basal ganglia, which plays a role in motor function. The movement tics are called
Losing control of your muscles is only one symptom of Huntington’s disease. You also slowly lose your mind: HD patients have difficulty recollecting words, reading emotions in others, learning new things, and remembering old information. Yet these symptoms appear later. Early on—even before the chorea—researchers have found that the symptoms are often more subtle personality changes. One hallmark of the early disease is a feeling of being uncontrollably annoyed.
Although the symptom is defined as irritability, there is no standard clinical definition of the term. Irritability has been largely neglected by psychiatry, according to neuropsychiatrist David Craufurd of the University of Manchester School of Medicine in the United Kingdom. It’s not particularly well studied, well measured, or even well defined. Although irritability is a symptom of other mental illnesses—Tourette’s syndrome, autism, and personality disorders—Huntington’s disease is one of the few illnesses in which the behavior has been systematically studied.
Understanding the brain changes that occur in Huntington’s patients may reveal something about what triggers people to become annoyed and why some people are more prone than others to be irritable.
For healthy people, irritability could be thought of as a person’s propensity to get annoyed. Craufurd, who has thought about irritability in Huntington’s patients perhaps as much as anyone, says, “In common parlance in England, we say that somebody has a short fuse. Irritability is the length of your fuse, so to speak.”
Another way to think about a short fuse, says Kevin Craig, a psychiatrist based in Cambridge, United Kingdom, is as a lens or a mood. Craig distinguishes emotions from moods. “The idea is that emotions have an object. So, if you’re annoyed or surprised or disgusted, it’s always at something or about something that’s external to yourself.” Surprise, happiness, and anger are emotions. The feeling of being annoyed might fit into the emotion category—it’s often short-lived and prompted by something external. “Whereas with moods, it’s more like a lens or a filter,” Craig says.
For psychiatrists who treat Huntington’s patients, it’s not so much the irritable filter that’s the problem, it’s the expression of the irritability. “As psychiatrists, we don’t deal as much in Huntington’s with the internal state as we do with the external,” says Karen Anderson, who runs the Huntington’s clinic at the University of Maryland. It’s not the
HD patients with this symptom punch walls and damage property, kick over their children’s bikes, and throw plates at their spouses because dinner was too salty. This is annoyance to the point of dysfunction. This is annoyance as a disease.
Chris Furbee remembers being aware of his mother’s symptoms when he was thirteen and she was in her late thirties. She had movement tics—a subtler version of his grandfather’s swaying. Huntington’s symptoms usually start to appear at this age—around forty. He also remembers his mother acting annoyed: “This is all in hindsight. She seemed to be angry a lot. Back then, I just thought it was my mom being mean. But I think what happened was the disease affected her to the point where she was very irritable.”
Yet Chris says it’s hard to separate the disease from the circumstances. “A lot of that could have been the fact that she was living with her own parents, in this trailer in Philippi, West Virginia—it’s not ideally where she wanted to be,” he says. This is one of the difficulties with measuring irritability as a symptom of a disease. The details of your life make a difference. “It’s easy not to be very irritable if you live in an environment where people don’t impinge on you too much,” says David Craufurd. “Somebody who lives alone, on the whole, tends to be less irritable than somebody who lives with teenage children, shall we say.”
Chris left his mother when he was a teenager. At eighteen, he relocated to the San Francisco Bay area. His grandfather had died. His mom was still driving, showing only mild symptoms, he remembers. He went back a few times, and then years passed without a visit.
Huntington’s is an inherited disease. Your likelihood of having it is written on the short arm of chromosome four. If one of your parents has the disease, you have a 50 percent chance of inheriting it. If you do not inherit the disease, you cannot pass it on—Huntington’s in your family ends with you.
The gene that causes the disease, technically called IT15, holds the instructions for making the huntingtin protein. What, exactly, the protein does is still a mystery, but it appears to play an important role in nerve cell function. The disease occurs when instructions for the protein are screwed up. Specifically, the gene carrying the instructions includes a sequence of repeating base pairs—cyotosine-adenine- guanine (CAG). Ten to thirty-five CAG repeats on that gene is normal. Thirty-six to thirty-nine puts one at risk for developing the disease. Forty or more repeats, and you will get Huntington’s, with no ambiguity in the prognosis. There is no cure or approved treatment
