Eating Disorders 449
if data from different groups (such as people with the restricting type of anorexia
and people with the binge-eating/purging type) are averaged together, characteristics
that are unique to one of the groups will not be detected. Thus, some research has
focused specifi cally on particular groups, such as patients with the restricting type of
anorexia. In one study, for example (Kojima et al., 2005), researchers examined the
effects of weight gain in this one group. They found that some parts of the brain, in
particular, the parietal lobes, became more active after these patients gained weight.
The parietal lobes represent spatial properties, including size, and may be involved
in representing the body image, which includes information about how large a per-
son feels herself to be. However, other parts of the brain, such as the basal ganglia
and the cerebellum, became less active after the patients gained weight—and the de-
creases in activation in both brain areas were larger for the patients who gained
more weight. Both the basal ganglia and the cerebellum may be critical in control-
ling repetitive behaviors, such as those that underlie recurrent bingeing. The lower
activation in these areas may indicate that the patients were less actively controlling
their eating after gaining weight. However, even after gaining weight, the patients in
this study still had less activity in the anterior cingulate cortex than did the control
participants. As noted earlier, this brain area is involved in monitoring for confl icts
either in actual responses or stored information. These patients may not be able to
monitor accurately confl icts between different responses (such as eating versus not
eating) or among stored information (such as about apearance versus health)—and
this problem persists even after they have gained weight.
Neuroimaging studies not only have documented many abnormalities in thefunctioning of different parts of the brain in people who have eating disorders, but
also have shown that the structure of the brain itself changes with these disorders.
In fact, anorexia is associated with loss of both gray matter (cell bodies of neurons)
and white matter (myelinated axons of the neurons) in the brain (see Chapter 2;
Addolorato et al., 1997; Frank et al., 2004; Herholz, 1996). The gray matter carries
out various sorts of cognitive and emotion-related processes (such as those involved
in learning and in fear responses). Defi cits in white matter may imply that different
parts of the brain are not communicating appropriately, which could contribute to
the problems patients with anorexia have when they try to convert an intellectual un-
derstanding of their disorder into changes in their behavior. Many of these structural
defi cits improve when the patient recovers, although they do not necessary disappear
completely (Frank et al., 2004; Herholz, 1996). Thus, an eating disorder may have
long-term consequences for a person’s cognitive abilities and emotional responses.
Neural Communication: Serotonin
Losing large amounts of weight (as occurs in anorexia) and the associated malnutri-
tion clearly change the amounts of serotonin and other neurotransmitters. We will
focus here on serotonin because it is involved in regulating a wide variety of behav-
iors and characteristics that are associated with eating disorders, including binge
eating and irritability (Hollander & Rosen, 2000; McElroy et al., 2000).
Neuroimaging research has shown that serotonin receptors function abnormallyin patients with anorexia and bulimia (Kaye, Bailer et al., 2005; Kaye, Frank, et al.,
2005). However, such research does not show that either eating disorder causes
these abnormalities; the abnormalities in the serotonin receptors could be produced
by the eating disorder itself or, instead, could be related to specifi c symptoms or
characteristics (such as the impulsivity that is associated with bulimia). Thus, it is
important that evidence seems to imply that the serotonin receptors are abnormal
before patients develop anorexia. As discussed in Chapters 6 and 7, serotonin is
related to mood and anxiety. Prior to developing anorexia, patients tend to be anx-
ious and obsessional, and these traits persist even after recovery, which suggests a
biologically based anxious temperament; this temperament may be related to sero-
tonin levels or functioning (Kaye et al., 2003). Consistent with this view, researchers
have found that people with anorexia are less responsive to serotonin than normal
(Kaye, Bailer, et al., 2005).
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