Despite the burgeoning research in the aetiology of bulimic pathology, bulimia nervosa (BN) remains a serious eating disorder (ED) condition characterized by severe comorbid psychopathology, psychosocial impairment, and significant rates of medical complications [1,2,3,4,5,6,7,8], underscoring the need for successful treatment options [2, 4]. Several systematic and meta-analytic reviews of the literature have given an important update on the extant treatments of BN [2, 9,10,11], also outlining the evidence about predictors of treatment outcome [11,12,13]. These valuable reviews can possibly be complemented by recent empirical evidence on the severity of BN, as defined by the most recent (fifth) edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [14], and its impact on treatment outcome.

BN is characterized by substantial within-diagnosis phenotypical heterogeneity, such that different individuals with the same disorder may exhibit variation in terms of symptom severity, underscoring the need for reliable indicators of disease severity [3, 15]. Importantly, the DSM-5 introduced a new disorder-specific severity rating (ranging from mild to extreme) for BN [14], whose reliability, validity, and clinical utility have recently been established [15, 16], to address within-diagnosis heterogeneity, inform clinicians and patients about disease severity, and allow severity fluctuation and treatment progress to be tracked. Specifically, four BN severity groups based on the weekly frequency of episodes of inappropriate weight compensatory behaviours–IWCBs (e.g., self-induced vomiting, diuretic misuse, fasting, laxative misuse, and excessive exercise) were defined in the DSM-5 [14] as follows: mild (1–3 episodes/week), moderate (4–7 episodes/week), severe (8–13 episodes/week), and extreme (>14 episodes/week).

The informative systematic and meta-analytic reviews of the extant treatment literature [2, 9,10,11] and the (UK) National Institute for Health and Care Excellence (NICE) guidelines (released in 2017) [17] concur in suggesting cognitive-behavioural therapy (CBT) as the best-supported treatment option for people with BN. Nevertheless, the convergent findings from both meta-analytic and systematic reviews of the treatment literature highlight that, although CBT is the treatment of choice for BN (the NICE identified it with a methodological grade “A” [17]), a substantial proportion of patients (≥50%) does not achieve symptom abstinence [2, 9,10,11, 18]. This picture represents only a general tendency if further refined by recent research [15] that contributes to gaining insight into the severity-dependent response to (therapist-led) CBT. Specifically, significant differences were observed in symptom abstinence (treatment outcome) achieved by 0, 10.6, 36.1, and 79.6% of adult outpatients who were classified with DSM-5 extreme, severe, moderate, and mild severity of BN [14] (see above) based on their pre-treatment clinician-rated (weekly) frequency of episodes of IWCBs [15]. Comparable findings have also been reported in a more recent independent study performed with adult patients with BN who received CBT [19]. While, according to the earlier literature, the overvaluation of shape and weight signals greater severity and is a significant predictor of treatment outcome [12], factors external to the ED features addressed in CBT [3], such as comorbid depressive psychopathology and mood intolerance (i.e., deficits in coping with aversive emotional states), have recently emerged as the most relevant variables distinguishing the DSM-5 defined severity groups of BN [15] that, as noted, showed a differential treatment outcome [15, 19], paralleling other relevant reviewed findings in this area [13]. These findings, in accordance with the contents of the practice guideline of the American Psychiatric Association [20], suggest that treatment of BN should ideally address ED and co-occurring psychopathology. In their systematic review of randomized controlled trials of medications for the World Federation of Societies of Biological Psychiatry, Aigner and colleagues reported that Grade A evidence exists for fluoxetine with a good risk–benefit ratio [21]. The rationale to treat BN with antidepressants is evidence of dysfunction in the serotonergic system and psychopathological overlap with psychiatric comorbid conditions (see [10, 21] for details). Although the (UK) NICE guidelines also see some evidence that antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), contribute to the cessation of the behavioural symptoms of BN, pharmacotherapy is not seen as first choice for this condition but is mentioned as an adjunct to psychological therapies for treating comorbid problems such as depression [17]. Nevertheless, the “clinically logical” strategy of adding antidepressant medication (e.g., SSRIs) in an attempt to enhance outcomes in BN patients who have limited response to CBT alone, and/or comorbid psychopathology has received extremely limited attention [10, 20] up to now. According to some past trial evidence (e.g., [22]), fluoxetine (the only drug approved by the US Food and Drug Administration drug for bulimic pathology [23]) is a useful intervention for people with BN (and co-occurring psychopathology) who have not responded adequately to CBT treatment. However, the severity of BN patients (e.g., [22]) was moderate (based on the pre-treatment frequency of IWCBs—see the DSM-5 severity definitions above) and the ability to generalize these findings in BN cases with severe-to-extreme severity remains to be seen. Future research needs to address this issue and take account of the notion of dose–response in therapy, examining, for example, whether (or not) a curvilinear relationship between the fluoxetine dosage and percentage of improving patients with different (DSM-5 defined) degrees of BN severity [15] and comorbid psychopathology [20, 23].