At the Eating Disorders Unit at the Maudsley Hospital in London, anorexia is not seen as a social disorder — or even primarily a psychological one. While most American treatment providers blame perfection-seeking parents and the media’s idealization of hollow-cheeked actresses for eating disorders (among other dysfunctional behaviors), researchers at Maudsley believe the root cause has little to do with social pressure. Rather, they think anorexia is better explained by heredity — perhaps by some of the same genes associated with autism.
The London researchers have been studying the commonalities between these two conditions for several years. On the surface, they appear entirely different — in autism, patients have difficulty connecting with people in the outside world, while in anorexia, sufferers seem consumed by other people’s perceptions — but Maudsley researchers point out that the salient characteristics of each illness are similar.
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For example, both anorexic and autistic patients have a tendency to behave obsessively and suffer from rigid ways of thinking. Tic disorders, which commonly affect people with autism, are found in 27% of people with severe anorexia. And in both conditions, patients have difficulty with “set-shifting,” or changing course mentally.
“Both autism-spectrum conditions and anorexia share a narrow focus of attention, a resistance to change and excellent attention to detail,” says Simon Baron-Cohen, director of the Autism Research Centre at Cambridge University, who is not involved in the Maudsley research.
In addition, says Janet Treasure, director of the Maudsley Eating Disorders Unit, past research suggests that about 15% to 20% of patients with anorexia may also have Asperger’s syndrome, an autism-spectrum disorder. Research also shows that the conditions occur together in families more often than they would by chance. It’s possible, she says, that the same genetic predisposition for autism and anorexia may be expressed differently depending on gender.
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About 15 times as many boys are given a diagnosis of Asperger’s syndrome as are girls, and nearly 10 times as many girls develop anorexia as boys. It’s easy to see how an outsized sense of perfectionism in a female might lead to an unhealthy obsession with thinness — given society’s preoccupation with physical appearance — while a male might end up obsessing about cars or trains, which is typical in autistic boys. “The reason [Asperger’s] is usually diagnosed less often in females may be because it takes a different form — anorexia may be just one of the forms,” says Baron-Cohen, adding that there are likely multiple routes leading to anorexia and that autistic features may not factor in all of them.
Treasure has found that starvation itself intensifies autistic characteristics like rigidity and obsession — a phenomenon that applies to all people, but particularly those with anorexia. “When they are underweight, people with anorexia get even more like people with autism,” says Treasure. “They can’t interpret other people’s emotions, they can’t regulate their own emotions, and they get overwhelmed when they are frightened or angry.”
In fact, in a study published this month in the journal Clinical Psychology and Psychotherapy, Treasure and colleagues found that underweight anorexics performed poorly on a classic test of understanding others’ emotions that was devised by Baron-Cohen to study such defects in people with autism-spectrum disorders. The theory is that hunger focuses the brain so sharply on the task of getting food that, as with other stressors, it shuts down higher cognitive functions, like reading other people’s emotions.
And according to Dr. Eric Hollander, an attending psychiatrist at Montefiore Medical Center in New York City and an expert on autism, there is evidence that the “repetitive thoughts and behaviors, rigid routines and rituals and perfectionism” that characterize both autism and anorexia may be traced to the same regions in the brain. Imaging studies of patients with either condition have found variations in the activity of brain regions like the anterior cingulate cortex, for example, where disruptions contribute to obsessive-compulsive behavior and aberrant social behaviors.
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“[Anorexia is] highly heritable, it runs in families, and it’s clear now that it’s affected by a cluster of [early life] vulnerabilities like anxiety and perfectionism. If you don’t have those vulnerabilities, you are very unlikely to develop anorexia,” says Dr. Walter Kaye, director of the eating-disorders program at the University of California, San Diego.
Practically speaking, that means researchers may be able to pinpoint specific early risk factors to help identify kids who are vulnerable to developing anorexia — much the same way specialists can now recognize signs of autism as early as 12 months. “We are where autism was 20 years ago. There were the same discussions about the mother causing kids to be autistic, and most of the theory and treatment was based on that,” says Kaye, referring to the outdated notion that autism was caused by cold, neglectful “refrigerator” mothers. “I think that anorexia is as biological as autism. It’s just 20 years behind in terms of research.”
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Treasure’s colleagues at the Maudsley Hospital say current treatments are equally obsolete. In the late 1980s, the British researchers published the earliest studies describing what has become known as the Maudsley method of treating anorexia in teens — and it remains the only therapy that has proved effective in controlled trials. Unlike traditional treatment, which assumes that anorexia is caused by environmental factors and low self-esteem and often involves intense therapy at residential treatment centers, the outpatient Maudsley method does not focus on psychological therapies or on “parent-ectomy” — removing the teen from the home.
Instead, researchers encourage patients and families to regard food as medicine, and caregivers are instructed to use rewards and positive pressure to restore patients’ weight. Use of the car and access to other activities desired by teens are offered as incentives for regularly completing meals, for example. Antidepressant medications, like Prozac, which affect serotonin levels and reduce obsessive thinking among anorexics, may later be prescribed, but not until patients have reached a healthy weight — without enough nutrients in the brain, medications can’t work.
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Essentially, Treasure and her colleagues have abandoned the idea that family dysfunction causes eating disorders and instead enlist the family to help guide patients’ recovery. Most recently, the Maudsley method has also incorporated a new type of cognitive behavioral therapy, based on the autism connection, which aims to broaden the narrow thinking routines of people with anorexia. “We try to get them be more flexible,” she says, “They want to have these rigid habits and we try to get them to break out of that and see the bigger picture.”
The treatment worked for Laura Collins’ 14-year-old daughter, who developed anorexia in 2002. “She ate an apple and thought she could see her arm growing,” says Collins, who says it was clear that her daughter’s condition was more than an obsession with being fashionably thin. Collins read about the Maudsley method in a newspaper article and sought clinicians who were willing to try it. “In the U.S., almost all treatment is predicated on blaming or marginalizing the parents,” Collins says. Today, her daughter is thriving in college, and Collins runs a group called FEAST, which is dedicated to helping families find evidence-based treatment for eating disorders.
Meanwhile, researchers like Kaye have launched a six-site National Institutes of Health–funded clinical trial to compare the Maudsley method to more traditional family therapies. At U.C. San Diego, Kaye’s group also provides affected families a weeklong intensive introduction to the Maudsley method. “At first,” he says, he thought it was “preposterous” that such a short period of treatment would help at all, but “now I’m a believer. It doesn’t work for everyone, but it does work.”
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