Eating Disorders: Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder

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Eating Disorders:

Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder

SECTION 1 Basic Prescribing Practices

Essential Concepts

  • The reader should appreciate the commonalities of the genetic heritability and brain functional abnormalities that appear to be common across the DSM-5 eating disorders and should also understand there may be significant symptom overlap.

  • The key is in the detail of the symptom (phenotypic) presentation and, frankly, in the symptom list diagnostic approach provided by the DSM-5 system. Particular attention to this detail may lead to better diagnosis, treatment selection, and outcome.

  • For example, bulimia nervosa (BN) and binge eating disorder (BED) share many symptoms, and even anorexia nervosa (AN) patients may suffer from compensatory activities to avoid weight gain (induced vomiting, excessive exercise, etc.) as well.

  • Eating disorder in adults is often confounded by other psychiatric disorders, such as the existence of an anxiety, depressive, or personality disorder.

  • Anorexia patients often have more rigid, obsessive-compulsive personality types while bulimics tend to be more impulsive and addictive.

  • Women tend to be diagnosed and identified more than men, but men are being increasingly diagnosed and should be screened for eating disorders routinely as well.

  • AN patients may present as medical emergencies and have a higher mortality risk whereas BN and BED do not.

  • There are no approved medications for AN and treatment is largely behavioral and residential.

  • The SSRI antidepressants are approved for BN.

  • Lisdexafetamine is approved for BED.

Phenomenology, Diagnosis, Clinical Interviewing

TIP: Eating Disorder Comorbidity

  • 56.2% of AN, 94.5% of BN, 78.9% of BED patients will meet criteria for at least one other major psychiatric disorder.

  • BN patients have the greatest risk of anxiety disorder at 81%, followed by BED at 65% and AN at 48%.

  • BN patients have the greatest risk of depressive disorder at 70%, followed by BED at 46% and AN at 42%.

  • BN patients have the greatest risk for substance use disorder (SUD) at 37%, followed by AN (27%) and BED (23%).

TIP: Eating Disorders Screening Questions

Anorexia Nervosa

  • How do you feel about your weight? Despite being average to thin, do you feel you need to lose a lot more weight or have a great fear of gaining even a few pounds?

Bulimia Nervosa or Binge Eating Disorder

  • Do you ever go through spells where you feel compelled to eat tons of food over a short period of time? Or have you ever made yourself throw up after eating?


  • Anorexia Nervosa

    • Weight Fear Bothers Anorexics”

      • Weight is low, fear of gaining, and body image distortion are all needed for diagnosis.

  • Bulimia Nervosa

    • Bulimics Consume Bunches

      • Binging episodes, compensatory behavior to avoid weight, body image conscious.

  • Binge Eating Disorder

    • “Bulimia without compensation”

      • The BED criteria are very similar except patients do not engage in self induced vomiting, excessive exercise, etc. to avoid weight gain.

DSM-5 Diagnosis
Anorexia Nervosa

People with AN experience abnormal weight loss or an inability to maintain a normal weight. They suffer from body image distortion and have an intense fear, or phobia, of gaining weight in the future. More formal diagnosis per the DSM-5 suggests that a person with AN must display:

Anorexia Nervosa (AN)

  • Persistent restriction of energy intake leading to significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory, and physical health).

  • Either an intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain (even though significantly low weight).

  • Disturbance in the way one’s body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.

Two subtypes exist where the restricting type patients will not consume enough calories from meals and avoid eating and binge-eating/purging type patients will eat but later will typically vomit their meals to lose weight.
*NOTE: for all eating disorders, psychosocial distress and comorbidity criteria are uniform throughout the DSM-5 similar to other disorders.

Bulimia Nervosa

People with BN experience an acute need to eat in a binging manner, where a high volume of food is eaten in a short amount of time. There is an addictive or compulsive quality to this. These episodes are often followed by compensatory behavior to rid the body of the food or associated weight gain (vomiting, diuretic or laxative abuse, etc.).

Bulimia Nervosa (BN)

  • Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

  • Eating, in a discrete period of time (e.g., within any two-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances.

  • A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating).

  • Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise.

  • The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for three months.

  • Self-evaluation is unduly influenced by body shape and weight.

  • The disturbance does not occur exclusively during episodes of anorexia nervosa.

Binge Eating Disorder

BED is more similar to BN than AN. These patients essentially binge eat, but often to a less severe level in regard to frequency and carry less symptom burden than BN. More formal diagnosis is as follows:

Binge Eating Disorder (BED)

  • Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

    • Eating, in a discrete period of time (e.g., within any two-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances.

    • A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating).

  • The binge eating episodes are associated with three or more of the following:

    • Eating much more rapidly than normal.

    • Eating until feeling uncomfortably full.

    • Eating large amounts of food when not feeling physically hungry.

    • Eating alone because of feeling embarrassed by how much one is eating.

    • Feeling disgusted with oneself, depressed, or very guilty afterward.

  • Marked distress regarding binge eating is present.

  • Binge eating occurs, on average, at least once a week for three months.

  • Binge eating not associated with the recurrent use of inappropriate compensatory behaviors (e.g., self induced vomiting) as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa

Rating Scales

Eating Attitudes Test (EAT-26)

  • A positive score of 20 or greater is likely indicative of an eating disorder. The scale also has subsections to better describe the eating patterns or behaviors that can help further delineate the actual eating disorder (ED) diagnosis and the severity as well.

  • This scale was adapted and validated using a DSM-based ED symptom checklist structure. It is copyrighted but the author graciously grants permission for free use at the following website


TABLE 1: Eating Attitudes Test

Treatment Guidelines


  • For the novice prescriber who attempts to treat an adult with an eating disorder, it is essential to know the basics of the available guidelines that exist to help provide a high level of care.

  • Next, a prescriber must know what psychotropics are specifically approved for each eating disorder

  • It is important to disclose to the patient that the approach being used is approved by the FDA (U.S. Food and Drug Administration). The prescriber and patient should find some comfort knowing that at least two or more large scale clinical trials exist where the drug was able to outperform a placebo and have a distinct safety profile. Imparting this information is the basis for informed consent and should increase patient acceptance to use the medication.

  • In this chapter we discuss three eating disorders (AN, BN, and BED). AN often has its own treatment guidelines as it has a higher mortality rate and also there are no current approved pharmacologic treatments.

  • BN and BED are symptomatically very similar and often may share similar guidelines, but interestingly their pharmacological management may differ as well where an SSRI is approved for the former and a stimulant for the latter.

TIP: AN Approved Medications

  • There are no current FDA approvals for this psychiatric disorder.

  • Pharmacological management is often thwarted by refusal of AN patient to sign consent to take a known weight gain agent or due to a high drop-out rate once initial weight is gained.

  • Typically, clinicians will try to prescribe drugs known to increase weight similar to those used in cancer cachexia management (megestrol) or will frankly choose psychotropics with known weight gain side effects (mirtazapine, olanzapine, etc.).

  • Small trials with the antidepressant mirtazapine (Remeron) and SSRIs were inconclusive. The atypical antipsychotic olanzapine (Zyprexa) may have the most studies and results have been limited and unfounded, but at least some positive data exists.

  • It is generally accepted that the comorbidities associated with AN (ex. major depressive disorder) should be treated with approved medication for the associated comorbidity. Ideally, weight gain side effects would be deemed appropriate and clinically useful in these cases. Unfortunately, it is unclear if this approach lessens AN symptom burden.

TIP: BN Approved Medications

  • Fluoxetine (Prozac) is the only approved medication for BN and is an SSRI antidepressant.

  • Theoretically, other antidepressants that act via serotonin reuptake inhibition (ex. SSRI, SNRI, TCA) might be considered helpful as well.

  • In theoretical practice, BN can be viewed perhaps as obsessive-compulsive, which is why the SSRIs have an advantage.

  • As BN is similar to BED, stimulants may be considered as second-line treatment.

TIP: BED Approved Medications

  • Lisdexamfetamine (Vyvanse) is a stimulant and is the only approved medication for BED.

  • Theoretically, the effeciveness of a stimulant may suggest that BED is an act of impulsivity or poor executive function (inhibition of bevavior).

  • As BED is similar to BN, SSRIs may be warranted as well if the BED patient in question has a relative contraindication to stimulant use (ex. addiction, cardiac condition, etc.).

ED Summary:

  • AN is a difficult illness to treat and is more labor intensive in regard to psychotherapy, inpatient and intensive outpatient programming. There are no bona-fide psychopharmacologic interventions and mortality rates are the highest amongst EDs.

  • BN is generally treated with an SSRI.

  • BED is now treated with the stimulant lisdexamfetamine.

TIP: Psychopharmacology

  • Initiate all at the lowest possible dose (even lower than FDA suggested).

  • Dosing information is readily available electronically and in print from a myriad of resources. It is also located in the Prescribing Table in this chapter.

  • Stimulants allow for therapeutic effects within a single dose and can be measured over a few days. The dose may be systematically titrated upward every 1–2 weeks until BED symptoms resolve or side effects occur.

  • SSRIs may take several weeks to show effectiveness comparable to their use in depressive and anxiety disorders.

  • The full specific dose range of each drug should be used before a drug treatment failure occurs. If side effects occur, the dose can be lowered and titration slowed.

  • As EDs tend to be chronic and relapsing, once an effective regimen is established, remission of symptoms should be the goal. Perhaps after a few years of remission, effective agents may be slowly removed.

TIP: BN Prescribing

  • Fluoxetine (Prozac) is the only approved medication and is an SSRI. It should be started at low dose (10mg) and escalated every few weeks towards 60mg/day.

  • If this is not effective, then another SSRI may be tried off-label, and if this fails, moving to an SSRI-Plus, SNRI, or TCA antidepressant may be warranted in order. Readers are referred to the depressive disorders chapter for more information on these off-label agents.

  • If serotonergic antidepressants fail, use of noradrenergic-dopaminergic agents such as the NDRI bupropion (WellbutrinXL) or even stimulants may be warranted. The difficulty with bupropion is that it carries warnings against use in those with an eating disorder.

TIP: BED Prescribing

  • Lisdexamfetamine (Vyvanse) is the only approved medication and is a prodrug amphetamine stimulant product. Readers are referred to the ADHD chapter for further information.

  • Labeling suggests starting at 30mg but to avoid side effects it is recommended to start at 10mg and titrate as needed to full dose 70mg. It can be increased 10–20mg every week.

  • If this is not effective, then another amphetamine stimulant may be tried off-label. If addiction or cardiac side effects are a concern, than bupropion may be considered as it is the next best agent for increaseing the dopamine and norepinephrine monoamines when compared to the stimulants. The prescriber would have to balance the risk of weight loss and seizure side effects when using this product off-label.

  • If these approaches fail or cannot be tolerated, then moving to an SSRI, SNRI-Plus, SNRI, or TCA antidepressant may be warranted in order. Readers are referred to the depressive disorders chapter for more information on these agents.

SECTION 2 Advanced Prescribing Practices

In Section 1, the premise was to convince the reader that they must make an accurate diagnosis and pick an approved agent with well-defined dosing guidelines and expected clinical outcomes. This approach is largely one of pattern recognition: (1) identify the pattern of phenotypic symptoms, (2) choose from a finite list of available, proven effective drugs, (3) start dosing low and escalate through an approved dosing range, (4) assess for effectiveness, and (5) continue medication if effective or cross-titrate to a new drug if ineffective or not tolerated. This is a methodical, mathematical approach that can improve the standard of care and, ideally, patient outcomes when treated by the novice psychopharmacologist.
Section 2 is designed to provide a greater depth of neuroscience and pharmacodynamic knowledge to the reader and is written for prescribers who are knowledgeable and competent in those skills outlined in Section 1. The section is generally intended for those patients who are felt to be treatment resistant and comorbid with other disorders.
Eating disorder diagnoses appear mutually exclusive where anorexia nervosa (AN) patients are felt to restrict food and bulimia nervosa (BN) patients tend to inappropriately binge on food. This is actually a spectrum where some BN may restrict food and some patients who do not meet BN criteria may meet binge eating disorder (BED) criteria. Using specific DSM-5 criteria, prevalence rates are outlined below:


Table 2: Epidemiology and Lifetime Prevalences


  • In regard to AN, family members of those suffering from AN have a 10-fold greater risk of developing AN themselves.

  • Twin studies suggest a heritability of 0.56. Linkage analyses suggest chromosome 1 may be a site for risk genes for AN. Here, the 5HT-1d serotonin receptor and the delta opioid receptor have been implicated as possible risk genes.

  • Behavioral drive for thinness and obsessiveness may link to chromosomes 1, 3, and 13. Purging type behavior associated with AN may actually be related to risks in the mutation of COMT genes. This enzyme is involved in the breakdown of NE and DA.

  • For BN, initial studies seemed to implicate that the serotonin transporter gene and the 5HT-2a receptor gene may convey risk to develop BN. Larger and meta-analytic studies have often failed to replicate these findings. Mutations in the ghrelin gene have more recently been implicated as a possible link to BN symptom development.

  • The long allele of the serotonin transporter has been recently noted to promote risk of developing BED. D2 receptor gene mutations have been linked to BED in other studies. Similar to BN, grehlin gene mutations have also been found to be significant.

Neuroanatomy of Eating Disorders


  • Decreased activity in inferior parietal and occipital lobes have been noted when patients are presented with food cues. There is an inverse overactivation in the frontal cortex.

  • AN patients, when presented with images of themselves, will preferentially activate the insular cortex or attentional networks when compared to controls.


  • BN who are faced with conflict tend to not activate frontostriatal circuits (including the right inferolateral and dorsolateral prefrontal cortices and putamen). This may be seen as a loss of self-regulatory control.

  • Insular activity has been seen to increase in BN patients who are more dissatisfied with their body size. Also, during tasks of assessing their body size, BN patients tend to overestimate their size while activating the medial frontal gyrus and underactivating to occipital cortex.


  • BED patients tend to show diminished activity in the ventromedial prefrontal cortex (vmPFC), inferior frontal gyrus (IFG), and insula. Additionally, dietary restraint scores are often negatively correlated with right IFG and vmPFC activation. These findings appear different to those noted above for BN.

  • BED individuals appear to have a diminished ability to recruit impulse control–related brain regions, which may explain a loss of control seen in binge episodes.

TIP: Functional Neuroanatomical Findings in Eating Disorders

  • Insula—generally increased activity across all ED

  • DLPFC—decreased activity in AN and BN

  • VMPFC—decreased activity in BED

Neuroscientific Background and Rationale for Medication Use
In treating eating disorders, there are two classes of medications that are frequently used. (SSRI and stimulants for BN and BED respectively.) (See Prescribing Table.):

  1. SSRI

Mechanism of Action

Fluoxetine (Prozac)

  • All SSRIs are similar in that they block serotonin reuptake pumps. More scientifically, this is called inhibition of the serotonin transporter (SERT). The net effect is an increase in serotonin (SR or sometimes abbreviated “5HT”) availability in BOTH the frontal cortex and in the limbic system.

  • The frontal cortex may govern higher levels of emotional processing and emotional thinking, especially in the vmPFC. The limbic system is likely in charge of more primitive functions, such as threat assessment, fight or flight responses, reward-driven behavior, etc. This system evolutionarily functions in a self-preservation manner, often scanning the environment looking for threats to be evaded or conquered. It also helps look for immediately rewarding situations. These functional neuroanatomic concepts were covered in the anxiety and depressive disorders chapters.

  • If BN is conceptualized as an obsessive-compulsive state (i.e., the repetetive drive to compulsively binge and purge), then use of an SSRI is akin to its use in OCD. Increasing serotonergic tone may normalize these neuroanatomic circuits in a similar manner. Additionally, some depressives seem compelled, and lose control over their impulsives, to hurt themselves or commit suicide.

  • Similarly, those with BN or BED, may have an inability to prevent responses to their urge to binge. Normalizing activity in the insula or vmPFC may help in this case. These brain areas seem to have many serotonergic projections and may respond preferentually to SSRIs.

  • Functional brain PET studies have implicated both serotonergic pathways and dysfunction of SERT systems and certain receptors.

  • Theoretically, any agent known to increase serotonergic tone (SNRIs, TCAs, MAOIs, SSRI-Plus, SGAs) might be utilized in an off-label fashion to help BN patients. Given the similar binging activity between BN and BED, serotonergic agents may be utilized for either.

  1. Stimulants

Mechanism of Action

Lisdexamfetamine (Vyvanse)

  • As discussed in the ADHD Chapter and Section 1 above, stimulants generally increase both noradrenergic tone (NET inhibition) and dopaminergic tone (DAT inhibition and/or reversal).

  • For ADHD, stimulants are felt to strengthen cortical tone, possibly through the glutamateric system. Stimulants seem to allow the DLPFC to provide for greater exective fuctioning and the ACC to provide greater vigilance.

  • Theoretically, the DLPFC could be strengthened along with the VMPFC and OFC to delay impulsive tendencies as well. If BED is theoretically conceptualized as an impulse control disorder (like ADHD), then improving top-down control of impulsive drives may lower BED activity.

  • Theoretically, any agent known to increase dopaminergic/noradrenergic tone (other stimulants, bupropion products) might be utilized in an off-

  • label fashion to help BED patients. Given the similar binging activity between BN and BED, these agents may be utilized for BN as well.

  • Of note, bupoprion is contraindicated for use in eating disorders. There is a risk of increased seizures for AN, and there is an application-based risk if a drug known to cause weight loss is in fact being given to an eating disorder patient. This is ironic in that bupropion has less mechanistic strength than stimulants in altering dopamine/noradrenergic tone.

  • Interestingly, stimulants have been used cosmetically as anorectics for years, but now one is approved for an eating disorder.

  • There appears to be a double standard where a stimulant can be used anecdotally for BED, but a similarly mechanistic bupropion cannot. Clearly, neither type of agent should be used in AN. The current contraindication states that a current or former diagnosis of AN or BN should exclude a patient from taking bupropion products.

  • Theoretically, if amphetamine-based lisdexamfetamine is helpful in BED then other amphetamine or methylphenidate stimulants may be effective off-label as well.

The following medication options are all considered off-label. They all act by increasing the monoamines. Theoretically, if an approved agent has failed to yield a remission in ED symptoms, use of one of the following agents may be warranted.

  1. SPA (Serotonin Partial Agonists)

Mechanism of Action

Buspirone (BuSpar)

  • Buspirone is a unique anxiolytic that is neither an SSRI nor SNRI. It is only approved to treat GAD, but its ability to facilitate the serotonergic systems through 5HT-1a receptor partial agonism has been shown to help alleviate resistant depression when added to SSRI ro SNRI.

  • It is typically used as an augmentation in BN similar to its use in augmentation of depressive/anxiety disorders.

  • Essentially, adding a SPA will further escalate the level of SR neurotransmission and theoretically lower BN symptoms greater than monotherapy alone.

  1. The SSRI-Plus Agents (Serotonin Partial Agonist Reuptake Inhibitors (SPARIs))

Mechanism of Action

Vilazodone (Viibryd), Vortioxetine (Trintellix)

  • As discussed in the depressive disorder chapter, these two agents are SSRI mechanistically but both enhance serotonergic activity similar to buspirone (5HT-1a receptor partial agonism) and the latter agent may antagonize 5HT-3 and 7 as well.

  • If a BN patient fails an SSRI monotherapy, then switching to one of these in effect increases serotonergic treatment potential.

  • These agents are more extensively discussed in the depressive disorders chapter.

  1. SNRI/TCA Antidepressants

Mechanism of Action

Venlafaxine (EffexorXR), Duloxetine (Cymbalta), Imipramine (Tofranil), etc.

  • All SNRIs and half of the TCAs share a similar mechanism to that of SSRIs, where they inhibit SERT. They are serotonin reuptake inhibitors.

  • The SNRI are called selective as they mainly act at SERT and NET but avoid anticholinergic, anti-alpha adrenergic, and antihistaminergic side effects.

  • Essentially, the TCA can provide SRI and NRI properties to treat anxiety/depression, but unfortunately block, or antagonize, cholinergic muscarinic (ACHm), alpha-1 (A1) and histamine 1 (H1) receptors, causing more remarkable side effects when compared to an SSRI.

  • It is unclear what NET inhibition can accomplish for eating disorders, but if patients cannot tolerate or fail to respond to an SSRI, a switch to an SNRI or TCA could be warranted, similar to the treatment of MDD.

  • Similarly, if a patient cannot tolerate a stimulant they might obtain improved noradrenergic tone with one of these agents.

  • The TCAs, as a class, tend to increase weight gain as a side effect. There may be some application for use in AN, assuming cardiac variables are monitored.

  • These agents are extensively discussed in the depressive disorders chapter.

  1. MAOI (Monoamine Oxidase Inhibitors)

Mechanism of Action

Selegiline (EMSAM), Phenelzine (Nardil), Tranylcypromine (Parnate)

  • The MAOIs are one of the original antidepressant treatments approved for use in major depressive disorder (MDD) but theoretically could be positioned to help BN or BED.

  • They have a unique mechanism where these drugs irreversibly inhibit and render ineffective monoamine oxidase A and B enzymes. These enzymes serve to destroy serotonin, norepinephrine, and dopamine, but when all are blocked simultaneously, there is an increase in levels of these monoamines in the central nervous system (CNS).

  • The serotonin increases may help BN and BED. Interestingly, the MAOI transdermal patch (Selegline) has active metabolites that may turn urine drug screens positive for methamphetamine.

  • Given the ability of this MAOI to promote stimulant-like activity, it may create a niche for its use in more refractory BN or BED cases as well.

  • MAOIs are more extensively discussed in the depressive disorders chapter.


Table 2: Prescribing Table for Eating Disorders

Practical Applications

TIP: Essential Concepts

  • After identifying the specific eating disorder, pharmacologic treatment is fairly linear.

    • If AN, rely more on behavioral and residential interventions and psychotropics that treat comorbid psychiatric conditions that have a side effect propensity to drive weight gain.

    • If BN, choose an SSRI, and if that fails, progress by using other highly serotonergic treatments similar to treating a depressive disorder. If that fails, attempt to treat BN as if it were BED.

    • If BED, choose a stimulant unless contraindicated. If that fails, progress by using other agents with noradrenergic/dopaminergic propensity. If that fails, attempt to treat BED as if were BN.

  • Polypharmacy of BN and BED makes sense in treatment-resistant patients. Combining medications of different mechanisms to improve serotonin, dopamine, and noradrenergic function makes clinical and theoretical sense similar to that of treating depressive/anxiety disorder.

Good Polypharmacy to be Used for Reaching Remission in Comorbid Patients

ED + Major Depressive Disorder (MDD)


    • NDRI (bupropion (WellbutrinXL)) is contraindicated in ED, but if needed might consider in BED who cannot tolerate stimulants.

    • Stimulants (lisdexamfetamine) has not been proven effective for MDD but may help in some MDD patients.

  • For AN, use sedating antidepressants mirtazapine (Remeron), trazodone (Desyrel), nefazodone (Nefazodone).

  • For AN, use second-generation antipsychotic (SGA) augmentations that have antidepressant properties and tend to promote weight gain (risperidone (Risperdal), olanzapine (Zyprexa), quetiapine(Seroquel)).

ED + Anxiety Disorder

  • For BN, use SSRIs and SNRIs which have approvals for both disorders.

  • For BN, use of SSRIs/SNRIs/etc. using anxiety disorder guidelines is clinically warranted.

  • For BN, use serotonergic-based TCAs: imipramine (Tofranil), amitriptyline (Elavil), clomipramine (Anafranil). All initially have serotonin reuptake inhibition and also have norepinephrine reuptake inhibiting metabolites.

ED + Bipolar Disorder

  • Use second-generation antipsychotics (SGA) as most have serotonergic potential when compared to the mood stabilizing AEDs or lithium.

  • For overweight BN/BED patients, consider using the more metabolically friendly SGA (ziprasidone (Geodon), lurasidone (Latuda), aripiprazole (Abilify), cariprazine (Vraylar), asenapine (Saphris)).

  • For AN patients consider using weigt gain–prone SGAs (risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel)).

ED + Schizophrenia

  • Use second-generation antipsychotics (SGA) as most have serotonergic potential when compared to the mood stabilizing AEDs or lithium.

  • For overweight BN/BED patients consider using the more metabolically friendly SGAs (ziprasidone, lurasidone, aripiprazole, cariprazine, asenapine).

  • For AN patients consider using weight gain–prone SGAs (risperidone, olanzapine, quetiapine).

ED + Substance Abuse

  • For BED, avoid use of stimulants due to addiction risk.

ED + Borderline Personality

  • For BN, use SSRIs and other serotonergic antidepressants.

  • Use second-generation antipsychotics (SGA) as most have serotonergic potential when compared to the mood stabilizing AEDs or lithium.

  • For overweight BN/BED patients consider using the more metabolically friendly SGAs (ziprasidone, lurasidone, aripiprazole, cariprazine, asenapine).

  • For AN patients consider using weight gain–prone SGAs (risperidone, olanzapine, quetiapine).

  • For BED avoid using stimulants given higher abuse potential.

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