Brave Girl Eating (13 page)

I don't know if we can save her. Tonight I don't know anything.

Emma takes off her glasses, turns out the light, and climbs into bed, snuggling into her blue-and-green quilt as she does every night, until only her thick dark hair is visible. I lie down beside her, ducking to avoid the top bunk. “I hate the anorexia,” she says. I expect tears, but instead there's an edge to her voice.

“Me too,” I say. “How much do you hate it?”

Part of our bedtime ritual has been a kind of call-and-response:
How much do you love me? More than bread loves salt.
This inversion of the usual question makes Emma giggle. “Come on, how much do you hate it?” I ask.

“I'd like to poison it,” she answers. “No, wait. Stab it in the heart!”

“That sounds sufficiently evil,” I say. “Maybe we could put a noose around its neck and hang it.”

“I've got it,” she says. “Burn it to death!”

She starts to laugh, and I smile too. Then she says, “I want to put anorexia in the blender, grind it up, and feed it to the cats!” And suddenly we're both roaring with laughter, rolling around on the bed, breathing in great gulps. “The blender!” she says hysterically, and we're both off again.

“But the poor cats,” I say at last. “They don't deserve it either.”

“They can't catch it!” Emma announces triumphantly.

“So it's just like cat food for them?” I ask. “Crunch crunch, yum yum?”

We're off again, laughing in the face of the worst thing that's ever happened to our family.

I hate the fact that Emma, too, has to deal with this illness. Mealtimes have gotten a little easier, but they're still tense and often explosive. Jamie and I are preoccupied with taking care of Kitty. I wish there was somewhere I could send Emma for a week or two, just to get out of the house. I feel guilty for putting her through this.

Not long ago, another mother told me about a conversation with her younger son, when she told him she was sorry he had to go through his sister's anorexia too, sorry that mealtimes had become so painful for the whole family.

“And you know what he said?” she told me. “He said, ‘Mom, the worst part was before.' I said, ‘Before what?' And he said, ‘Before you started helping her eat, when we were all pretending.'”

That story comforts me now. Maybe Emma will benefit by seeing Jamie and me tackle Kitty's illness. Maybe in the long run she'll feel safer because she'll know that no matter what happens, we'll take it on. That we'd do our best to protect her, too.

I shuffle downstairs to turn out the lights and find Jamie lying on the living room couch. For the first time in months, we're awake and both of our children are asleep. I nudge him over and lie down beside him, and we don't say a word. We don't confer about logistics: who's shopping where, what's for snack or dinner, who's taking Kitty to the doctor or psychiatrist. We don't go over how this happened, when it happened, why we didn't see it coming and stop it. We don't talk about hard it is to walk around feeling so raw, to take in Kitty's terror and rage, to stay present for Emma.

We've done all that, and no doubt will do a lot more of it, though it's usually me who needs to talk things out, perseverate, go over and over events and feelings and worries about the future. But not tonight. Tonight I lie beside my husband, feel the warmth
of him through his clothes and my own. Kitty is built like him, long and angular, muscled but not obviously so—more Clark Kent than Superman.

I look into my husband's face. His eyes are tired; his face is lined. He needs a haircut. But he is still handsome to me. Eighteen years ago I had the great good fortune to marry a man who believes in showing up. He might not always know what to do. He might not always have the words to describe how he feels. But no matter how awkward or terrible the situation, no matter how bad things get with Kitty, he will be there. I don't have to do this alone.

At the moment, I can't imagine anything more romantic.

 

By the end of
the week, we have worked out a plan, along with Ms. Susan: Kitty will start high school, going part-time, at least for the fall semester. I worry that the school will give us a hard time about asking for accommodations—this school district, like many others, makes a practice of saying no to parents—but Ms. Susan suggests we use the words
medical necessity
in talking about what Kitty needs. Sure enough, when I put it that way, Kitty's guidance counselor, Mr. C., becomes extremely helpful. He arranges for Kitty to attend the first and last two periods of the day. In between she'll come home to eat lunch with one of us; we live three blocks from school, which makes this schedule workable. In theory, anyway.

I hope classes and friends will distract Kitty from the misery of recovery. I hope the stress of performing academically—a stress she puts on herself; we've told her many times the world won't come to an end if she gets a B—won't prove too much for her. Kitty wants to go to school because she wants desperately to be “normal.” She hates being sick, hates us thinking of her as sick. Most of all,
she can't stand the idea that people will pity her, because she can't bear the idea that she messed up, that she made mistakes or is in any way less than perfect.

“Everyone makes mistakes,” I tell her. “We're
supposed
to mess up. We learn and grow by trial and error. That's part of what makes us human.”

Kitty shakes her head. “I'm supposed to be smarter than this,” she says. “I'm supposed to be able to figure things out without screwing up.”

I try another tactic. “You've seen me make mistakes, right?” She shakes her head. “Come on,” I say. “I screw up all the time. Remember the bread I made without salt? Disgusting. Remember how I used to get lost in the car when we first moved here? I told you we were having ‘adventures,' but really I was trying to find our way home.”

I'm hoping for at least the hint of a smile; instead, Kitty frowns. “That's different,” she says.

“Why?” I ask. “Because it's me and not you?”

She nods, slowly.

“So you think you're supposed to be better than everyone else in the world?” I ask, smiling so she knows I'm making a joke. Clearly I am no comedian, because she hears my words as criticism and stalks off.

The answer is yes, she really does believe she's supposed to be perfect in a superhuman way. I wonder if somehow we've given her the impression that we expect perfection. I don't
think
so. But what if I'm wrong?

I'm not usually defensive about my parenting. I know I make plenty of mistakes. Like missing the early signs of anorexia—that was a mistake I wish like hell I'd avoided. And I know other people, including my children, make mistakes. It's part of being human. I
think
Jamie and I have given them the message that we love them the way they are.

So why does Kitty hold herself to such an unrealistic, inhuman standard—yet not expect that from other people too? This emotional blind spot feels analogous to her perceptual blind spot about her body: when she looks in the mirror, she sees rolls of fat rather than ribs and hollows. Yet she sees other people's bodies accurately.

Neurologists talk about interoceptive information, data that flows from the body into a part of the brain called the insula—things like taste, touch, temperature, and other visceral sensations. The insula helps transform this physiological input into both self-awareness and emotions. For instance, if you eat something that tastes bitter, you might feel disgust or aversion; the chemical stimulus of
bitterness
becomes the emotional and physical response of
disgust
in the insula. According to Walter Kaye, anorexia symptoms like distorted body image might be related to glitches in the body's interoceptive system.

Maybe someday information like that will lead to better treatments for anorexia. In the meantime, we're stuck with slogging through this, one meal—sometimes one spoonful—at a time.

On the first day of ninth grade, I plan to meet Kitty in Mr. C.'s office and eat lunch with her there, because it's a short day and there's not enough time for her to walk home and eat. When I wake her that morning, the first thing she says is, “I don't want to go! I want to stay home with you!” But she gets dressed in the new clothes we bought last week—a silver T-shirt and plain dark jeans—which I insisted on buying a size larger than necessary; even so, the jeans, which came from a children's store, look painfully tiny. She spends ten long minutes straightening her hair, so now it hangs to her shoulders in a clean blond sheet. Most important, she
eats breakfast with Jamie while I walk Emma to her school. By the time I get back, Kitty is losing her nerve; she takes one look at me and her face starts to crumple. I'm afraid she's going to fall apart in a big way. But miracle of miracles, the phone rings; it's a friend asking if she'd like a ride to school.

“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.

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. During 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: perfection
ism, 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 disturbances 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.