Brave Girl Eating_A Family's Struggle with Anorexia

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. 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: 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 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.
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.
Another study compared brain activity in women who were recovering from anorexia with brain activity in healthy women. The participants played a computer game where they won money for guessing correct answers. In healthy women, areas of the brain tied to emotional responses lit up differently when they won money than when they lost. In women with a history of anorexia, there were fewer differences; winning and losing felt very much the same. Kaye suspects this neurological effect applies to eating, too. “For anorexics, perhaps it is difficult to appreciate immediate pleasure if it does not feel much different from a negative experience,” he told a BBC interviewer. By contrast, the part of the brain that links actions to outcomes and planning lit up far more in the recovering anorexics than in the healthy women, reflecting high levels of anxiety about making mistakes and worries about negative consequences.
“There are positive aspects to this kind of temperament,” Kaye points out. “Paying attention to detail and making sure things are done as correctly as possible are constructive traits in careers like medicine or engineering.” Taken too far, though, such traits can hurt more than they can help.
The language of neurobiology describes the nexus between brain chemistry and behavior. It’s observational and nonjudgmental, a far cry from the pronouncements of Minuchin, Bruch, and so many others. What it boils down to, in Kaye’s words, is that “circuit-based abnormalities” lead to changes “related to appetite, emotionality, and cognitive control.” Cause and effect (though it’s hardly that simple), seen as a series of system malfunctions, glitches in the hardware that affect the software. There’s no blame or shame attached, just descriptions of where the system gets wonky or goes astray.
On the other end of the spectrum from Walt Kaye, some researchers are investigating parallels between anorexia and autism. Nancy Zucker, a psychologist at Duke University Medical Center in Chapel Hill, North Carolina, believes that both people with anorexia and people with autism show impairments in what scientists call social cognition—attachment, anxieties, and interpersonal relationships. She published a paper in 2007 suggesting that looking at the social deficits of people with anorexia might help researchers devise better treatments for the illness. But since so many of the “social impairments” seen in anorexia are a function of long-term malnutrition (think of the volunteers in Ancel Keys’s study, who became depressed, anxious, withdrawn, and aggressive), I’m not sure how useful this line of research can be. And I don’t see how comparing anorexia to autism helps people with either disease. The last thing people with anorexia need is another stigmatizing label slapped on them.


One of the most intriguing theories about what causes anorexia comes from Shan Guisinger, a psychologist in Missoula, Montana. Guisinger wondered why anorexia nervosa developed in the first place, what biological function it fulfilled, and why it’s persisted, given its high mortality rate. She came up with what she calls the adapted-to-flee-famine hypothesis, which explains the illness in terms of evolutionary biology.
According to Guisinger, the symptoms of anorexia—the inability to see one’s own extreme thinness, the hyperactivity and restlessness, the aversion to eating, the ability to function on very little food—make sense if you think of them as strategies for surviving famine. Thousands of years ago, she suggests, before humans started farming, they were nomadic, often traveling great distances to find food. In times of famine, malnourishment made people lethargic, weak, and depressed—unable to forage successfully. Guisinger theorizes that the whole group benefited from having a few members who reacted paradoxically to starvation. These evolutionary outliers stayed energetic, becoming restless rather than lethargic during times of scarcity. They didn’t see themselves as dangerously thin and, therefore, stayed optimistic and motivated to survive. All of these qualities made them natural leaders in times of food shortage, leading the drive to find greener pastures. In this context, says Guisinger, the characteristic abilities of anorexics to work hard, delay gratification, and ignore suffering to achieve a goal would have been essential to the group.
To support her theory, Guisinger points to a number of factors: The fact that anorexia nervosa appears across cultural, ethnic, and socioeconomic lines, which suggests that it is biological rather than cultural. The fact that anorexia seems most common in peoples who were more recently nomadic—Hispanics, Caucasians, and Native Americans—and least common among Asians and African Americans; in Africa over the last hundred thousand years, Guisinger argues, “it was probably better for starving people to stay put, conserve energy, and keep searching locally for food, as traveling could result in encounters with hostile neighbors.” Finally, the fact that anorexia affects primarily women. In other primate species, says Guisinger, males who wander from their own territory are typically killed, but females are often accepted and integrated into a new group. So females make the best migrators, in a way.
If the adapted-to-flee-famine theory is true, says Guisinger, maybe one reason anorexia recovery rates are so low in our culture is that the illness was designed to be “switched off,” so to speak, in a social context that no longer exists. “In the radically individualistic western culture, it may be hard to imagine the social pressure that is brought to bear on deviant individuals in tribal cultures,” she writes. Once the tribe settled into a new area where food was more abundant, ritual prayers, thanksgiving celebrations, and food sharing might have pushed anorexics to begin eating again. She points to the fact that recovered anorexics in our culture often say that support from friends and family helped them beat the illness.
By contrast, many therapists and eating-disorders specialists still believe that psychodynamics cause eating disorders. Much of the literature emphasizes the way starvation unsexes a teenage girl, shrinks the budding breasts, damps down new sexual feelings. Therapists like Hilde Bruch wrote about girls (and boys) with anorexia who are afraid of the complexities of adult sexual relationships and so choose to starve themselves back into childhood to avoid them.
To me this feels awfully contrived. Primitive people observed lightning and thunder and came up with a story to explain them: the gods were angry. They looked for intention and meaning in the world around them because that’s what humans do; our brains seek to make order out of chaos, narrative out of random occurrences. Theories like Bruch’s are equally unscientific; they conflate correlation—things that happen at the same time—with causation. It’s true that eating disorders often start at adolescence, but we could come up with a dozen theories that “explain” that correlation—say, eating disorders are physiologically triggered by hormones. It’s just as likely as the ambivalent-about-growing-up theory, to my mind.
Guisinger’s theory seeks meaning in the illness too, but her conclusions seem more genuinely aligned with reality—though it’s a reality that no longer literally applies.
At the end of the day, of course, no one knows what causes anorexia, and no one is likely to know for a long time, if ever, which is yet another reason why family-based treatment appeals to me: in the clamor of competing theories and hypotheses, the Maudsley approach says simply, “We don’t need to know in order to treat the illness.” FBT emphasizes recovery over etiology, results over theories. Human lives over intellectual jousting.
As a journalist, I want to know what’s behind this deadly disease, what makes young women and men starve themselves, what are the causes and risk factors. I follow the research, collecting scientific articles the way some people collect baseball cards. I go to conferences, look up medical terminology, try to teach myself the essentials of anatomy so I can understand what the insula does, why tryptophan is important, how ketosis works. I read and reread descriptions of metabolism and appetite, hunger and satiety. My curiosity is piqued by the mystery that is anorexia.
As a mother, I care about only one thing: my daughter. The dead look in her eyes makes me feel dead inside. What drives me is the terror that she will never come back. That her life will be a wasteland without landmarks or topography. That Kitty’s face, more known to me than my own, will harden and set into the mask of Not-Kitty, and that when I look into her eyes years from now I’ll see the demon looking back.
Or worse: I’ll see nothing, because she’ll be gone.
One night I sit at the computer and explore a Web site called somethingfishy, which is dedicated to people with eating disorders. I read some of the threads in the chat room for families and feel ill at the despair and hopelessness expressed there. But the most disturbing part of the site is a page of memorials to people who have died from eating disorders. I scroll through screen after screen of candles, each marked with a name, a date, a fragment of a story:
Christy Henrich, died July 26, 1994, from anorexia. Number 2 gymnast in the USA in 1989.
Jane, died December 26, 1995, from anorexia and bulimia; she is survived by her husband, Andy, and their 14-month-old son.
This is in prayer to light a candle for Baby Angella Hope, born September 17, died December 2, 1996. She is the result of a practicing bulimic.
Heidi Guenther, age 22. Died of a sudden fatal heart attack on June 30, 1997, in California on her way to Disneyland.
Deborah Simone Fradin. Debbie died from anorexia nervosa after battling this disease with every fiber in her being for 18 years. The disease ravaged her body, but not her gentle soul.
Candle after candle. Name after name. Story after story. She struggled with this disease for a year, for five years, for twenty-five years. Bright shining girls who should be giggling with friends in the halls of high schools and colleges, studying Latin and microbiology and dance. Girls who should have been walking through fields of light and dark, who instead fell into shadow. They died of heart attacks in bathrooms, in beds, in hospital rooms. They died at home, at school, alone. They died with their parents crying over them, their friends confused. They died before they had a chance to live, because once the demon moves in they’re not really living. I know. Believe me, I know.
Tears stream down my face, tears I haven’t been able to shed for my own bright shining daughter because I haven’t been able to face the fact that she might have died this summer. She still might die. I hope she’s on the road to recovery, that she’ll have to walk this particular stretch only once. But the numbers are against her. The statistics say she’ll come back this way again and again, her body getting weaker and more adapted to starvation until it comes to feel natural and right to her, until her very cells learn the pattern and shape and feeling of constant gnawing hunger. Until that skull face in the mirror looks like her face. Until it is her face. Until it has obliterated her real face not only in her own eyes but in ours.
And that’s when my fury rises. Between our reality—where Kitty’s life hangs in the balance—and the theories about why she is sick and how to help her lies an enormous chasm. I have no idea how to get across it. I don’t even know if it’s possible. And all the research is no help. It exists only on paper, tidy and two-dimensional, disconnected from the messy, dangerous, three-dimensional world we’re trapped in.
Every paper I read, every doctor I talk to, seems to have a different explanation for and approach to anorexia. No wonder the field has such a lousy track record. A higher percentage of people with anorexia die than people with schizophrenia or bipolar disorder or depression or any other mental illness. Of those who survive, only half truly recover.
You’d think numbers like these would inspire a little more soul-searching among the professionals. You’d be wrong.
A heart surgeon who used outmoded techniques would be barred from the operating room. Yet eating-disorders therapists cleave to theories from sixty years ago as if they represented the most up-to-date thinking, and they defend their beliefs with the self-righteous vigor of zealots. Maybe this is because so many of the people who treat eating disorders had (or still have) the illness themselves. On one hand, this gives them great empathy. On the other, it weds them to a particular narrative—their own personal story line. For instance, if they recovered by finding God—which isn’t that unusual; one of the biggest residential treatment chains, Remuda Ranch, offers a twelve-step, Bible-based approach—they’ll push their patients in that direction. If, as is all too common, they themselves still struggle with disordered eating, they’re likely to believe, and to communicate to their patients, that full recovery is impossible, that anorexia is an illness you have to manage for the rest of your life. They will, however inadvertently, convey a sense of hopelessness and resignation based on nothing but their own experience.
What I want is what’s commonplace in every other area of medicine: best practice. Evidence-based treatment, based on the most up-to-date research and clinical practice. It doesn’t seem a lot to ask, to advise patients out of knowledge rather than belief. That’s what doctors do, isn’t it?
Not in the world of eating disorders. Not yet.
When Kitty was four or five, she went through a fairy-tale phase. Every night Jamie and I read her parables about good and evil, usually featuring a young girl in mortal danger who, in the end, lives happily ever after. So I know how fairy tales work. Events unfold according to a formula known or intuited in advance. They have a predictable story line, complete with warnings and foretellings, symbols and metaphors that make them both universal and compelling. Which, now that I think about it, might be why Kitty loved them so much. She’s always been the kind of child who likes rules, who needs to know not just what to do and how to do it but what not to do and how to stay out of trouble.
If our story were a fairy tale, there would be a magic needle, a bridge rising out of the mist, a talking fish that would whisper instructions in my ear about how to trick our way across that chasm. And we would cross that chasm. We would overcome all obstacles, real and supernatural, and make our way to safety.
One of Kitty’s favorite childhood books was a gorgeously illustrated retelling of the Russian firebird myth. The main characters are a dim but handsome young prince named Dmitri and his wise talking horse. Together they face dangers, pass through trials by fire and water, and pit their wits against the machinations of an evil king. Each time they face a seemingly insurmountable obstacle, Dmitri runs crying to the horse, wringing his hands, sure that he’ll fail. And each time the horse says, “The trouble is not now. The trouble is still to come,” and then tells Dmitri what to do. Those phrases—The trouble is not now. The trouble is still to come—become a refrain in the book, and over time they’ve become a kind of family motto for us, a joke we tell each other to remind ourselves that we can handle it, whatever it is.
Toward the end of the book, Dmitri must leap three times into a cauldron of boiling water without getting scalded or drowned. When he runs to the horse, anxious about this final test, the horse replies, “The trouble is now.” It comes as a shock because you’ve been lulled by the reassuring leitmotif: The trouble is not now. The trouble is still to come. Of course, thanks to the horse’s quick thinking, Dmitri passes unscathed through the boiling water, vanquishing the evil king and winning the hand of the woman he loves. Happily ever after for everyone, including the horse.
I want someone to tell us not only what to do and how to do it but that we can do it. I want to live inside a fairy tale, where good triumphs over evil and love overpowers greed, envy, resentment, and fear. Because the one thing I know for sure is that the trouble is now. The water is boiling, the demon is laughing, the young woman’s life is in mortal danger.
If I can’t have a talking horse, I at least want a guide, someone who’s traveled this road and knows how to make it across the chasm. Who will talk us through the scary parts. The trouble is now and the trouble is still to come. And I don’t know if we’ll be all right.