شرح روابط زمانی بین اختلالات تغذیه ای افتراقی و اضطراب های خاص

This study examined the temporal sequencing of eating and anxiety disorders to delineate which anxiety disorders increase eating disorder risk and whether individuals with eating disorders are at greater risk for particular anxiety disorders. The sample was drawn from the Oregon Adolescent Depression Project. Temporal relations between specific eating and anxiety disorders were examined after controlling for relevant variables (e.g., mood disorders, other anxiety disorders) over 14 years. After excluding those with anorexia nervosa (AN) in adolescence (T1), OCD was the only T1 anxiety disorder to predict AN by age 30 (T4). No T1 anxiety disorder was associated with T4 bulimia nervosa (BN). Although T1 AN did not increase risk of any T4 anxiety disorder, T1 BN appeared to increase risk for social anxiety and panic disorders. Evidence that eating disorders may have differential relations to particular anxiety disorders could inform prevention and treatment efforts.

There are high rates of comorbidity between anxiety and eating disorders. To illustrate, 55–60% of those with anorexia nervosa (AN) and 57–68% of people with bulimia nervosa (BN) have experienced an anxiety disorder (Bulik et al., 1997 and Kaye et al., 2004). Relatives of those with AN also have a higher prevalence of anxiety disorders compared to relatives of controls (Strober et al., 2007). Further, eating disorders (ED) and anxiety disorders may share a genetic link (Keel et al., 2005, Kendler et al., 1995, Rowe et al., 2002 and Silberg and Bulik, 2005). There may also be differential relations between particular anxiety disorders and particular ED. For instance, compared to individuals without ED, individuals with AN exhibit higher rates of overanxious disorder (OAD), separation anxiety, panic disorder, and obsessive–compulsive disorder (OCD) whereas those with BN exhibit higher rates of OAD and social anxiety disorder (SAD) (Bulik et al., 1997). Anxiety disorders are posited to be a risk factor for ED (Bulik et al., 1997). Yet, it remains unclear whether ED increase anxiety disorder vulnerability. The identification of sequelae to ED is not trivial because although ED risk may peak in adolescence and early 20’s (Heatherton et al., 1997) individuals with ED may be vulnerable to developing other types of psychopathology such as anxiety disorders. We know of no studies directly testing whether particular anxiety disorders are in fact risk factors for ED and whether particular ED increase anxiety disorder risk. Garber and Hollon (1991) outline three criteria for causal attribution that have traditionally been recognized in psychopathology risk research. First, the proposed risk factor must be correlated with the outcome. Second, the proposed risk factor must demonstrate temporal precedence. Third, the relation between the risk factor and outcome variable must be non-spurious (i.e., not due to a third variable or set of variables).