“Oh, why not,” says Kitty with some of her old spirit, and two minutes later she’s out the door without time to worry or fret. It’s a miraculous exit for us, too, as we try to walk the line between acknowledging her anxiety and neediness on one hand and encouraging her glimmers of independence on the other.
Lunch goes all right, considering Kitty has only about twenty-five minutes in Mr. C.’s office to eat. And—another miracle—she tumbles in the door at the end of the day with three friends in tow, girls she’s known for years. She’s animated and laughing, as relaxed as I’ve seen her in months. It’s so good to see her like this, like her old self, I think as I make milk shakes for all of them.
Kitty even cracks a joke. “At our house, we know which ice creams have the most calories,” she says, catching my eye and grinning. It’s true; I’ve made a science out of packing as many calories as possible into everything Kitty eats, both to make it easier for her to get it all down and to speed up the very slow process of gaining weight.
The fact that she’s made a joke about food—about how much food she has to eat—makes me giddy with happiness. That’s my Kitty—funny, observant, alive to nuance and language.
Of course, the joke’s for me. Her friends prove sadly unable to understand it.
“We want to know which ice creams have the least calories!” says one.
“Yeah, because we have a problem over here!” says another, patting her flat stomach.
The third chimes in. “My thighs are enormous,” she says, glancing down at her legs, encased in narrow boot-cut jeans and looking absolutely ordinary.
Kitty, I notice, has gone silent.
I dither for a minute: stay out of the conversation, or jump in? I can’t keep quiet. “Wait a minute,” I say. “There’s nothing wrong with any of your thighs or butts. You’re all beautiful and healthy and strong. Thinking there’s something wrong with you—that’s the problem.”
I might as well be talking to myself. I’ve heard girls this age refer to fat-bashing as a bonding experience, and I can see that as a kind of process of establishing social hierarchy—like the submissive behaviors dogs engage in to find their place in the pack. Saying “I’m so fat!” can be a coded way of expressing social submission, or at least the urge to be accepted, to conform.
But I can’t believe these girls are joking about being too fat in front of someone who’s struggling with anorexia. Of course, they’re only fourteen years old, an age not exactly known for sensitivity to other people’s feelings. And, I remind myself, they have no idea of the hell Kitty’s going through. They know only that she’s been “sick” and is doing better now; a few know it’s anorexia, but some likely don’t. They probably envy her slenderness, though no one says that out loud.
I wonder what would happen if one of them said, “I like the way I look.” In today’s girl culture, would she lose status, become an outsider? Or might she start something positive? Teenagers are herd creatures; at this age, and in this society, it will take more than one voice of reason to start to turn things around.
At least they drink their milk shakes. Kitty, too.
{ chapter five }
The Trouble Is Now
If the case for somatogenesis [an organic, physical cause] were conclusive, our view of the patient would have to change: anorexia nervosa would then be an involuntary disease, perhaps even inheritable, and best treated by purely medical rather than psychotherapeutic techniques.
—JOAN JACOBS BRUMBERG, Fasting Girls: The History of Anorexia Nervosa
Eating disorders are familial and highly heritable in twin studies—50 to 80 percent.
—WALTER KAYE, M.D., professor of psychiatry at University of California San Diego and director of its Eating Disorders Treatment and Research Program
Anorexia nervosa is one of medicine’s biggest mysteries. Doctors have been trying to make sense of it for hundreds of years. From the outside, anorexia seems inexplicable. More than that—it’s a perversion and a denial of the force that animates every living creature. We’ve come to understand suicide as the urge of a moment, with permanent consequences. But anorexia plays out over weeks, months, years. It’s not a single moment of despair, an impulsive turn of the wheel that sends you headfirst into traffic. You need to be determined and stoic to suffer the slow whittling of flesh into bone, the painful alchemies of the starving body. Anorexia makes no sense as suicide; it’s too indirect. Its bizarre and ritualistic elements seem like they must have some purpose beyond death.
There’s no shortage of theories about anorexia’s essential nature, what causes it, what its symptoms mean, whether and how it can be cured. And there’s no shortage of doctors and therapists who will say with great certainty that they know what anorexia is (and isn’t) “about.” Such definitive pronouncements astound me, in part because they can’t all be right: anorexia can’t be “about” lack of boundaries in the family and “negative family food-related experiences” and “problems with communication.”* More important, none of these pronouncements takes into account what we’ve learned in the last decade or so about eating disorders—most of which contradicts these closely held beliefs.
We now know, for instance, that many of the cognitive and emotional symptoms associated with anorexia are actually physical by-products of starvation. In the mid-1940s, at the tail end of World War II, Ancel Keys, a physiologist at the University of Minnesota, became interested in the experiences of the millions of malnourished people in Europe, including concentration camp victims. Keys devised a yearlong study, known as the Minnesota Experiment, to explore the effects of both starvation and refeeding. He recruited thirty-six healthy young conscientious objectors and, starting in November 1944, fed them normally for three months, observing and recording the most minute details of their personalities, eating patterns, vitals, and behavior (the full study results run well over a thousand pages). For the next six months, Keys and his researchers cut the men’s rations in half; most volunteers lost about a quarter of their weight, putting them well under the physical cutoff point for anorexia. For the last three months of the experiment, the men’s rations were gradually increased until they were eating at or above prestudy levels.
During the months of starvation, the volunteers showed all the physical signs of malnutrition. Their heart rates and metabolisms slowed; they felt cold even in hot weather. They lost so much fat and muscle that sitting, and sometimes walking, became painful. Their feet shrank; their knees, ankles, and faces swelled. Their hair fell out and their muscles cramped. Cuts and wounds bled less and took longer to heal. Hands and feet often went to sleep. The volunteers suffered vertigo and had trouble focusing their eyes, but, interestingly, their hearing improved. Toward the end of the six months, the men had trouble with certain physical actions, including laughing, sneezing, and blushing.
Despite feeling weak, tired, and uncoordinated, some of the men exercised compulsively. They lost interest in sex. They became irritable and depressed. Some of them reported no hunger after a while; others remained ravenous. All of them developed obsessive thoughts and behaviors around eating. They became possessive about their rations, putting their arms around meal trays at the table. They toyed with food to make meals last longer and used large quantities of salt and other spices. They licked their plates to get every crumb and ate everything with enthusiasm, even foods they’d disliked before the experiment began.
Food became, as Keys later wrote, “the principal topic of conversation, reading, and daydreams.”* The volunteers pored over cookbooks and collected coffeepots, hot plates, and other cooking utensils. They took vicarious pleasure in watching other people eat. They fantasized about restaurant careers; three of them actually went on to become cooks, though they’d had no interest in cooking before the experiment.
Keys and his colleagues evaluated psychological and personality changes by giving the volunteers the Minnesota Multiphasic Personality Inventory (MMPI) before, during, and after the experiment. Dur
ing the six months of starvation, the men’s levels of hypochondria, depression, phobias, obsessions and compulsions, and schizophrenia went up. After three months of refeeding, their scores on those scales were still higher than they’d been at the start of the study; it took eight months of refeeding for their profiles to return to normal.
Some of the most interesting data was collected during those first three months of refeeding. Some volunteers lost weight, especially at the beginning; the rest gained weight slowly. Some didn’t gain for weeks, despite the increased calories. Some became more depressed, anxious, impatient, and aggressive toward themselves and others; one man deliberately cut off three of his own fingers.
As the men’s calories increased, so did their appetites. A dozen of the volunteers agreed to stay on after the twelve-week refeeding period, so Keys’s team could observe them. They ate prodigious amounts of food and found it hard to stop eating, saying they still felt hungry even when they couldn’t physically eat another bite.
Most of the men gradually returned to their prestudy weights and eating habits. A few continued to deliberately limit their food intake. One volunteer restricted his eating to keep himself at 160 pounds, 18 pounds lighter than he’d been at the start of the experiment.
The findings of the Minnesota Experiment were published in 1950 as a two-volume treatise called The Biology of Starvation, which was more or less ignored by eating-disorders specialists until about twenty years ago. But these results are crucial for several reasons. First, they establish the fact that the physical process of starvation also causes psychological symptoms, which can include depression, anxiety, and obsessiveness around food and eating—all of which are hallmarks of anorexia. Psychiatrists commonly diagnose depression or anxiety rather than anorexia; Dr. Newbie diagnosed Kitty with a primary depression, and an eating disorder second. But Keys’s study demonstrates that when these psychological changes start during starvation—that is, when there are no signs of them beforehand—they’re typically caused by malnutrition and resolve along with the physical symptoms. And although some people with anorexia also suffer from other psychiatric disorders (a concept called comorbidity), it’s impossible to diagnose depression or anxiety or OCD while a patient is starving. A better approach might be to feed the patient first, and then see which psychological symptoms persist after physical recovery.
Second, as Keys wrote in his two-volume study results, “Starvation affects the whole organism and its results may be described in the anatomical, biochemical, physiological, and psychological frames of reference.” This rather clinical sentence has profound implications for the way we think about anorexia—and, more important, for how it’s treated. It puts starvation at the heart of the illness rather than considering it an almost secondary symptom. Rather than getting caught up in theories about family dynamics and psychological dysfunction, those who treat anorexia should aim to reverse starvation first—by any means necessary. The idea that a person with anorexia has to “choose” to eat is both irrelevant and dangerous, especially early in treatment, when nearly all sufferers are anosognosic—literally unable to perceive or understand that they’re ill. They can’t “choose” to eat; expecting them to, as we saw with Kitty, is both cruel and counterproductive.
If all treatment for anorexia started with nutritional rehabilitation, I have no doubt that patients would recover faster and suffer less.
Keys’s study doesn’t answer the question of what causes anorexia in the first place. But its findings go a long way toward explaining how malnutrition and starvation affect the human body, and how difficult it can be to reverse those effects.
The men in the study starved for six months and were refed for three. They weren’t anorexic; they didn’t exhibit the same fear of fat or distorted body image that’s common (though not universal) among people with anorexia nervosa. They shared none of the risk factors of anorexia: they were men in their late teens and twenties, not adolescent females. Nor did they set out to diet; their starvation was imposed on them, though they volunteered for the experience.
By contrast, anorexia nearly always starts with a diet or an inadvertent weight loss from illness or exercise. At some point, probably early in the process of restricting, anorexics are overwhelmed by the effects of malnutrition. Their brains as well as their bodies stop working well. They fall down the rabbit hole. And they can’t climb back out until they eat. Not just a little, but a lot. And not just for a week or two but for months and months.
Keys’s findings contributed to what Walter Kaye describes as the neurobiology of eating disorders. Kaye’s current research focuses on using brain imaging to connect physiology and pathology, looking at how brain structures and pathways vary in people with anorexia nervosa. His theory about causation begins with a strand of DNA—specifically, with chromosome 1p, which has been associated with anorexia. “People with anorexia have a relatively large section of a chromosome in common,” says Kaye. “However, there are hundreds of genes in this region, and we don’t know which ones are involved.”
Kaye started studying the genetics of eating disorders in the 1990s. In 2001, the National Institutes of Health gave him funding to create the Genetics of Anorexia Nervosa Collaborative Study, a multisite international study looking at whether and how genetic variations make some people more vulnerable to anorexia. “We don’t expect anorexia to be caused by a single gene,” he explains. “Rather, it’s a complex combination of many genes that, in turn, cause alterations in neural pathways.” Kaye and other researchers from around the world will have to study thousands of people and sequence many genes before they can hope to understand exactly how genetics come into play.
The debate about what causes eating disorders is often framed as “state versus trait”: states refer to a psychological condition—a state of confusion or excitement, for instance. Traits are biological, passed down genetically from parents to children. Certain personality traits are strongly associated with anorexia: perfectionism, obsessionality, negative emotionality, neuroticism, and harm avoidance. These traits often manifest in childhood, long before the eating disorder; run in families (just as eating disorders do; my mother’s sister and several of my cousins struggled with bulimia), turning up in family members who don’t have eating disorders; and persist after recovery. In other words, a tendency toward perfectionism doesn’t disappear when normal weight is restored.
Kaye’s working theory about what causes anorexia goes something like this: Some people are born with a biological predisposition, a genotype that produces personality traits like perfectionism and obsessionality, which typically show up early in childhood, long before any symptoms of an eating disorder. This underlying biology may include irregularities in the neurotransmitter systems, which can lead to a certain rigidity of thinking and personality; people with eating disorders, for instance, often have trouble with what psychologists call set shifting, meaning the ability to change what you’re doing in response to a changing environment. They have trouble being flexible in certain ways.
People with anorexia often believe they should be able to do things perfectly, and they don’t understand that mistakes are part of the normal learning process. They may also have abnormalities of the central nervous system, which controls how much cortisol, a stress hormone, and other hormones are released into the bloodstream. The central nervous system also regulates neuropeptides, molecules that help neurons communicate with one another. Leptin, a substance that modulates appetite and behaviors around eating, is a neuropeptide; so is galanin, which affects waking and sleep as well as eating.
These biological vulnerabilities may be activated by environmental factors; maybe the flood of female hormones around puberty pushes the brain chemistry further out of sync. Stress (or perceived and/or self-induced stress, like the internal pressure to achieve) can exacerbate an already anxious and obsessive temperament.
Starvation may actually represent a kind of self-medicating. People with anorexia have disturb
ances in the 5-HT system, a network that revolves around the neurotransmitter serotonin. Too much 5-HT action causes anxiety and a loss of appetite. In the long run, starvation leads to malnutrition, which triggers anxiety and depression. But in the short term, for some people, not eating lowers the brain’s levels of carbohydrates, which in turn reduces anxiety. When people with anorexia eat after a period of starvation, the 5-HT system revs up, raising anxiety even more and creating negative reinforcement for eating. So people become trapped in a vicious downward spiral of starving and suffering.
Walt Kaye is quick to point out that no one really understands the mechanisms involved in anorexia and other eating disorders. Some of the differences in brain chemistry may be the result of anorexia rather than the cause; since it’s impossible to know who will eventually develop anorexia, how can we distinguish cause from effect?
“Is it physiology that causes you to think in [anorexic] ways, or is it your thinking in these ways that gets you to starve and causes physiological consequences?” asks Daniel le Grange of the University of Chicago. “I would get a handsome award if I could figure out what comes first.” What we know for sure, he says, is that the causes of eating disorders are complex, multifaceted, and hard to tease apart.
But neurobiology clearly plays a role, which is one reason why Kaye’s research uses new technologies like functional MRI and CT scans to literally look into the human brain as it’s working. In one recent study, women who had recovered from anorexia showed different neurological responses to the taste of both sugar and water. Areas of the brain connected with both pleasurable tastes and with rewards lit up far less in recovered anorexics than in a control group. The fact that both of these responses are lower than usual might help explain why people with anorexia tend to avoid high-calorie food that tastes good; they experience it as less rewarding on a physiological level. Or their ability to experience a sense of reward may be impaired. Other recent research suggests that for people with anorexia, the part of the brain that signals punishment lights up along with the rewards center, indicating that reward comes with a sense of guilt or anxiety. Or, says Kaye, the neural shifts might reflect a kind of scarring in the brain, the consequences of past malnutrition and weight loss.
Brave Girl Eating Page 12
