Anxiety, alcohol use, drug use and depressive disorders frequently co-occur in patients with eating disorders (Braun et al., 1994, Halmi et al., 1991, Hudson et al., 2007 and McElroy et al., 2005), and also among their family members (Lilenfeld et al., 1998 and Jacobi et al., 2004). The co-morbidity of schizophrenia and eating disorders is currently understudied (Foulon, 2003 and Lyketsos et al., 1985).
Some reports have described cases of patients with schizophrenia who developed eating disturbances undistinguishable from a full-blown syndrome of anorexia nervosa (Cheung and Wilder-Smith, 1995, Korkina et al., 1975, Lyon and Silber, 1989 and Munoz and Ryan, 1997). Conversely, symptoms of psychosis can develop in both anorexia (Dymek and le Grange, 2002, Grounds, 1982, Hsu et al., 1981 and Kiraly and Joy, 2003), and albeit more rarely, in bulimia nervosa (Deckelman et al., 1997 and Shiraishi et al., 1992).
In a recent survey of 2436 female inpatients treated for eating disorders, Blinder and co-workers found schizophrenia/other psychoses to be three times more likely with restricting anorexia, and twice as likely with binge-purge anorexia, compared with bulimia nervosa (Blinder et al., 2006). On the whole, the prevalence of diagnosable schizophrenia in clinical samples of patients with eating disorders is generally calculated as below 10%, with males having a higher risk than females, particularly for the hebephrenia variant of schizophrenia (Foulon, 2003, Korkina et al., 1992 and Striegel-Moore et al., 1999).
More often, symptoms of psychosis in eating disorders co-occur in patients with co-morbid schizoaffective and/or bipolar disorder (Hudson et al., 1984), while bipolar disorder shows higher rates of comorbidity for full- and partial-syndrome eating disorders (McElroy et al., 2006). Eating disturbances in childhood often precede affective psychosis in adulthood (Cannon et al., 2001), while patients who develop psychotic symptoms after the onset of anorexia nervosa may show schizothymic personality traits in the pre-psychotic period (Shiraishi et al., 1992).
Many authors have discussed the possible role of starvation and metabolic disturbances in the etiology of psychosis that may develop concurrently with an eating disorder (Shiraishi et al., 1992, Mavrogiorgou et al., 2001 and Wenokur and Luby, 1997). However, some cases of schizophrenia-like psychosis had their onset after recovery from anorexia nervosa, pointing towards some continuity between the two disorders ( Ferguson and Damluji, 1988 and Hugo and Lacey, 1998). In a survey of 1,017 patients admitted to Danish psychiatric institutions with the diagnosis of eating disorder during the period of 1968–1986, Moller-Madsen and Nystrup (1994) found that up to 6% of them ended up with a diagnosis of a psychosis. In discussing these and other findings, Hugo and Lacey (1998) proposed a role for disordered eating as a defense against psychosis: according to this view, anorexia and bulimia nervosa may exist in a continuum ranging from neurosis to character disorder to psychosis.
Better knowledge of the comorbidity of eating disorders with psychosis is important for treatment: on the one hand, the outcome in patients with eating disorders co-morbid with psychosis is expected to be poor (Shiraishi et al., 1992); on the other hand, patients with anorexia and bulimia nervosa co-morbid with psychosis may be more responsive to therapeutic drugs acting on the dopaminergic system (Bosanac et al., 2005 and Brambilla et al., 2007). Increased dopamine activity at the central dopamine receptors is believed to play a role in the pathophysiology of schizophrenia (Davis et al., 1991 and Kapur, 2003), and some reports also indicate dopaminergic pathway abnormalities in eating disorders (Barbato et al., 2006 and Shinohara et al., 2004).
To date, most of the evidence on the comorbidity of eating disorders with psychosis comes from clinical case studies (Table 1), and no study has investigated the distribution and frequency of symptoms of psychosis in patients with eating disorders in comparison with a control group without significant eating disorder symptoms.
Table 1.
