e weight is lower than training weight, athletes’ memoirs have described how coaches and players, perhaps unwittingly, elicit AN symptoms (37). The ability to develop AN in response to calorie restriction may have become a de facto requirement for elite competition. Ignorance about the actual cause of AN allows these practices to continue without debate.
The homogeneous phenomenology of AN points towards the biological mechanisms and structures involved in restricting food, hyperactivity and hallucinating body fat. It has been difficult for even the most articulate sufferers to explain the anguish of being asked to eat. People with AN often think obsessively about food and cook elaborate meals for others that they cannot bring themselves to eat. One patient said, “I know if I continue like this I will die, but eating is even more terrifying.”
Endocrinologists were first in noting that some appetite signals in AN are the opposite of normal starvation (38). In 2001 Akio Inui noted that while people with anorexia nervosa have high levels of hunger hormones they also have increased satiety and anorexigenic signaling (39). For example, a potent satiety signal, cholecystokinin, increases rapidly when underweight people with AN begin to eat, leading to queasy satiety along with gnawing hunger. Inui wrote, “This may explain why many anorexics cannot easily reverse their illness in contrast to simple starvation. It is possible that the mixed signals about satiety and desire to feed could contribute to the ambivalence about food, i.e., the dissociation that anorexics often display between reduced caloric intake and obsessive thoughts about food” (39, p. 623). Inui’s conclusions had no discernable impact on psychogenic theories for AN.
In the last decade functional magnetic resonance imaging (fMRI) from independent laboratories reported the same pattern of abnormal activation when subjects were asked to eat or imagine eating. Thinking about food stimulates excessive prefrontal cortical activity (40-43). The prefrontal cortex provides executive control over motivational drives; it is responsible for identifying and carrying out the individual’s goals. All mammals have an executive cortical area sending “top-down” instructions to more primitive deep-brain centers. For example, during breeding it directs the devoted behavior required for successful reproduction, including ignoring hunger and fatigue when necessary. People with AN behave as though it is necessary to ignore hunger and fatigue although starving. Brooks and colleagues found that enhanced working memory (WM) interacted with limbic processes to foster impulse control in AN (44).Normally when hungry people imagine drinking chocolate milk neural activity increases in reward and taste centers. The insula connects and interprets sensory information from the body into self-awareness of the condition of the body, including hunger and pain, thus is important in homeostasis. When hungry people with AN imagine food, activity is inhibited in parts of the insula that evaluate the meaning of hunger signals and anticipate taste (45-47). They pay little attention to food when hungry(48). Reduced activation of somatosensory appetite-related regions is combined with greater activity in the amygdala and the cingulate cortex, emotional centers that evaluate and respond to dangers (45, 49). In other words, thinking about eating silences neural regions that complain of hunger and activates of anxiety and fear centers. One of the most startling symptoms of AN is that victims see fat on their emaciated bodies (1); this body image distortion increases as more weight is lost. Now, brain-imaging researchers have discovered part of the reason. When underweight women with AN look at their own bodies, fMRI images show inhibition of the primary visual and visual association cortex (50). Meanwhile the part of the parietal cortex responsible for body image is hyperactive, filling in a fattened likeness (51). We think that the visual illusion of extra fat stores would have given starving migrators the con