The diagnostic workup typically includes complete medical and psychosocial history and follows a rational and formulaic approach to the diagnosis. Neuroimaging using fMRI, MRI, PET and SPECT scans have been used to detect cases in which a lesion, tumor or other organic condition has been either the sole causative or contributory factor in an eating disorder. "Right frontal intracerebral lesions with their close relationship to the limbic system could be causative for eating disorders, we therefore recommend performing a cranial MRI in all patients with suspected eating disorders" (Trummer M "et al." 2002), "intracranial pathology should also be considered however certain is the diagnosis of early-onset anorexia nervosa. Second, neuroimaging plays an important part in diagnosing early-onset anorexia nervosa, both from a clinical and a research prospective".(O'Brien "et al." 2001).

After ruling out organic causes and the initial diagnosis of an eating disorder being made by a medical professional, a trained mental health professional aids in the assessment and treatment of the underlying psychological components of the eating disorder and any comorbid psychological conditions. The clinician conducts a clinical interview and may employ various psychometric tests. Some are general in nature while others were devised specifically for use in the assessment of eating disorders. Some of the general tests that may be used are the Hamilton Depression Rating Scale and the Beck Depression Inventory. longitudinal research showed that there is an increase in chance that a young adult female would develop bulimia due to their current psychological pressure and as the person ages and matures, their emotional problems change or are resolved and then the symptoms decline.

Medical tests to check for signs of physical deterioration in anorexia nervosa may be performed by a general physician or psychiatrist, including:

- Complete Blood Count (CBC): a test of the white blood cells, red blood cells and platelets used to assess the presence of various disorders such as leukocytosis, leukopenia, thrombocytosis and anemia which may result from malnutrition.

- Urinalysis: a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health

- Chem-20: Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes such as potassium, chlorine and sodium and tests specific to liver and kidney function.

- Glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycystic ovary syndrome.

- Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition.

- Liver Function Test: A series of tests used to assess liver function some of the tests are also used in the assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, and Crohn's Disease.

- Lh response to GnRH: Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH): Tests the pituitary glands' response to GnRh a hormone produced in the hypothalamus. Hypogonadism is often seen in anorexia nervosa cases.

- Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatine kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).

- Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabolism first formed in the liver then removed from the body by the kidneys. The BUN test is primarily used to test kidney function. A low BUN level may indicate the effects of malnutrition.

- BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various conditions. A high BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, and intestinal bleeding. A low BUN/creatinine ratio can indicate a low protein diet, celiac disease, rhabdomyolysis, or cirrhosis of the liver.

- Electrocardiogram (EKG or ECG): measures electrical activity of the heart. It can be used to detect various disorders such as hyperkalemia

- Electroencephalogram (EEG): measures the electrical activity of the brain. It can be used to detect abnormalities such as those associated with pituitary tumors.

- Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3)

Previously considered a topic for further research exploration, binge eating disorder was included in the "Diagnostic and Statistical Manual of Mental Disorders" in 2013. Until 2013, binge eating disorder was categorized as an Eating Disorder Not Otherwise Specified, an umbrella category for eating disorders that don't fall under the categories for anorexia nervosa or bulimia nervosa. Because it was not a recognized psychiatric disorder in the "DSM-IV" until 2013, it has been difficult to obtain insurance reimbursement for treatments. The disorder now has its own category under "DSM-5", which outlines the signs and symptoms that must be present to classify a person's behavior as binge eating disorder. Studies have confirmed the high predictive value of these criteria for diagnosing BED.

According to DSM-5, the following criteria must be present to make a diagnosis of binge eating disorder. Studies have confirmed the high predictive value of these criteria for diagnosing BED.

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

1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than what most people would eat in a similar period of time under similar circumstances.

2. 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).

B. The binge-eating episodes are associated with three (or more) of the following:

1. Eating much more rapidly than normal.

2. Eating until feeling uncomfortably full.

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

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

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

C. Marked distress regarding binge eating is present.

D. The binge eating occurs, on average, at least once a week for 3 months.

E. The binge eating is not associated with the recurrent use of inappropriate compensatory behavior as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa.

A variety of medical and psychological conditions have been misdiagnosed as anorexia nervosa; in some cases the correct diagnosis was not made for more than ten years.

The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make as there is considerable overlap between people diagnosed with these conditions. Seemingly minor changes in a people's overall behavior or attitude can change a diagnosis from anorexia: binge-eating type to bulimia nervosa. A main factor differentiating binge-purge anorexia from bulimia is the gap in physical weight. Someone with bulimia nervosa is ordinarily at a healthy weight, or slightly overweight. Someone with binge-purge anorexia is commonly underweight. People with the binge-purging subtype of AN may be significantly underweight and typically do not binge-eat large amounts of food, yet they purge the small amount of food they eat. In contrast, those with bulimia nervosa tend to be at normal weight or overweight and binge large amounts of food. It is not unusual for a person with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time.

Individuals suffering from BED often have a lower overall quality of life and commonly experience social difficulties.

Early behavior change is an accurate prediction of remission of symptoms later.

Individuals who have BED commonly have other comorbidities such as major depressive disorder, personality disorder, bipolar disorder, substance abuse, body dysmorphic disorder, kleptomania, irritable bowel syndrome, fibromyalgia, or an anxiety disorder. There may also be panic attacks and a history of attempted suicide.

While people of a healthy weight may overeat occasionally, an ongoing habit of consuming large amounts of food in a short period of time may ultimately lead to weight gain and obesity. Binging episodes usually include foods that are high in fat, sugar, and/or salt, but low in vitamins and minerals, as these types of foods tend to trigger greatest emotional reward. The main physical health consequences of this type of eating disorder are brought on by the weight gain resulting from the binging episodes. Up to 70% of individuals with BED may also be obese, and therefore obesity-associated morbidities such as high blood pressure and coronary artery disease type 2 diabetes mellitus gastrointestinal issues (e.g., gallbladder disease), high cholesterol levels, musculoskeletal problems and obstructive sleep apnea may also be present.

NES is sometimes comorbid with excess weight; as many as 28% of individuals seeking gastric bypass surgery were found to suffer from NES in one study. However, not all individuals with NES are overweight. Night eating has been associated with diabetic complications. Many people with NES also experience depressed mood and anxiety disorders.

Night eating syndrome (NES) is an eating disorder, characterized by a delayed circadian pattern of food intake. Although there is some degree of comorbidity with binge eating disorder, it differs from binge eating in that the amount of food consumed in the evening/night is not necessarily objectively large nor is a loss of control over food intake required. It was originally described by Dr. Albert Stunkard in 1955 and is currently included in the other specified feeding or eating disorder category of the DSM-5. Research diagnostic criteria have been proposed and include evening hyperphagia (consumption of 25% or more of the total daily calories after the evening meal) and/or nocturnal awakening and ingestion of food two or more times per week. The person must have awareness of the night eating to differentiate it from the parasomnia sleep-related eating disorder (SRED). Three of five associated symptoms must also be present: lack of appetite in the morning, urges to eat in the evening/at night, belief that one must eat in order to fall back to sleep at night, depressed mood, and/or difficulty sleeping.

NES affects both men and women, between 1 and 2% of the general population, and approximately 10% of obese individuals. The age of onset is typically in early adulthood (spanning from late teenage years to late twenties) and is often long-lasting, with children rarely reporting NES. People with NES have been shown to have higher scores for depression and low self-esteem, and it has been demonstrated that nocturnal levels of the hormones melatonin and leptin are decreased. The relationship between NES and the parasomnia SRED is in need of further clarification. There is debate as to whether these should be viewed as separate diseases, or part of a continuum. Consuming foods containing serotonin has been suggested to aid in the treatment of NES, but other research indicates that diet by itself cannot appreciably raise serotonin levels in the brain. A few foods (for example, bananas) contain serotonin, but they do not affect brain serotonin levels, and various foods contain tryptophan, but the extent to which they affect brain serotonin levels must be further explored scientifically before conclusions can be drawn, and "the idea, common in popular culture, that a high-protein food such as turkey will raise brain tryptophan and serotonin is, unfortunately, false."

Few studies to date have examined OSFED prevalence. The largest community study is by Stice (2013), who examined 496 adolescent females who completed annual diagnostic interviews over 8 years. Lifetime prevalence by age 20 for OSFED overall was 11.5%. 2.8% had atypical AN, 4.4% had subthreshold BN, 3.6% had subthreshold BED, and 3.4% had purging disorder. Peak age of onset for OSFED was 18–20 years. NES was not assessed in this study, but estimates from other studies suggest that it presents in 1% of the general population.

A few studies have compared the prevalence of EDNOS and OSFED and found that though the prevalence of atypical eating disorders decreased with the new classification system, the prevalence still remains high. For example, in a population of 215 young patients presenting for ED treatment, the diagnosis of EDNOS to OSFED decreased from 62.3% to 32.6%. In another study of 240 females in the U.S. with a lifetime history of an eating disorder, the prevalence changed from 67.9% EDNOS to 53.3% OSFED. Although the prevalence appears to reduce when using the categorizations of EDNOS vs. OSFED, a high proportion of cases still receive diagnoses of atypical eating disorders, which creates difficulties in communication, treatment planning, and basic research.

DSPD is diagnosed by a clinical interview, actigraphic monitoring, and/or a sleep diary kept by the patient for at least two weeks. When polysomnography is also used, it is primarily for the purpose of ruling out other disorders such as narcolepsy or sleep apnea. If a person can adjust to a normal daytime schedule on her/his own, with just the help of alarm clocks and will-power, the diagnosis is not given.

DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder. DSPD is often confused with: psychophysiological insomnia; depression; psychiatric disorders such as schizophrenia, ADHD or ADD; other sleep disorders; or school refusal. Practitioners of sleep medicine point out the dismally low rate of accurate diagnosis of the disorder, and have often asked for better physician education on sleep disorders.

For those patients who have not been able to stop this disorder on their own, doctors have been working to discover a treatment that will work for everyone. One treatment that Schenck and Mahowald studied consisted of psychotherapy combined with "environmental manipulation". This was usually done separately from the weight-reducing diets. However, during this study only 10 percent of the patients were able to lose more than one third of their initial excess weight, which was not a viable percentage. In addition, they reported that many of the patients experienced "major depression" and "severe anxiety" during the attempted treatments. This was not one of the most successful attempts to help those with NSRED.

However, Dr. R. Auger reported on another trial treatment where patients were treated utilizing pramipexole. Those conducting the treatment noticed how the nocturnal median motor activity was decreased, as was assessed by actigraphy, and individual progress of sleep quality was reported. Nevertheless, Augur also said, "27 percent of subjects had RLS (restless legs syndrome, a condition known to respond to this medication), and number and duration of waking episodes related to eating behaviors were unchanged." Encouraged by the positive response verified in the above-mentioned trial treatment, doctors and psychiatrists conducted a more recent study described by Auger as "efficacy of topiramate [an antiepileptic drug associated with weight loss] in 17 consecutive patients with NSRED." Out of the 65 percent of patients who continued to take the medication on a regular basis, all confirmed either considerable development or absolute remission of "night-eating" in addition to "significant weight loss" being achieved. This has been one of the most effective treatments discovered so far, but many patients still suffered from NSRED. Therefore, other treatments were sought after.

Such treatments include those targeted to associated sleep disorders with the hope that it would play an essential part of the treatment process of NSRED. In Schenck and Mahowald's series, combinations of cardibopa/L-dopa, codeine, and clonazepam were used to treat five patients with RLS and one patient with somnambulism and PLMS (periodic limb movements in sleep). These patients all were suffering from NSRED as well as these other disorders, and they all experienced a remission of their NSRED as a result of taking these drugs. Two patients with OSA (obstructive sleep apnea) and NSRED also reported as having a "resolution of their symptoms with nasal continuous positive airway pressure (nCPAP) therapy." Clonazepam monotherapy was also found to be successful in 50 percent of patients with simultaneous somnambulism. Interestingly, dopaminergic agents such as monotherapy were effective in 25 percent of the NSRED subgroup. Success with combinations of dopaminergic and opioid drugs, with the occasional addition of sedatives, also was found in seven patients without associated sleep disorders. In those for whom opioids and sedatives are relatively contraindicated (e.g., in those with histories of substance abuse), two case reports were described as meeting with success with a combination of bupropion, levodopa, and trazodone. Notably, hypnotherapy, psychotherapy, and various behavioral techniques, including environmental manipulation, were not effective on the majority of the patients studied. Nevertheless, Auger argue that behavioral strategies should complement the overall treatment plan and should include deliberate placement of food to avoid indiscriminate wandering, maintenance of a safe sleep environment, and education regarding proper sleep hygiene and stress management. Even with their extensive studies, Schenck and Mahowald did not find the success as Auger found by treating his patients with topiramate.

Few studies guide the treatment of individuals with OSFED. However, cognitive behavioral therapy (CBT), which focuses on the interplay between thoughts, feelings, and behaviors, has been shown to be the leading evidence-based treatment for the eating disorders of BN and BED. For OSFED, a particular cognitive behavioral treatment can be used called CBT-Enhanced (CBT-E), which was designed to treat all forms of eating disorders. This method focuses not only what is thought to be the central cognitive disturbance in eating disorders (i.e., over-evaluation of eating, shape, and weight), but also on modifying the mechanisms that sustain eating disorder psychopathology, such as perfectionism, core low self-esteem, mood intolerance, and interpersonal difficulties. CBT-E showed effectiveness in two studies (total N = 219) and well maintained over 60-week follow-up periods. CBT-E is not specific to individual types of eating disorders but is based on the concept that common mechanisms are involved in the persistence of atypical eating disorders, AN, and BN.

DSPD is genetically linked to attention deficit hyperactivity disorder by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm and a high proportion of DSPD among those with ADHD.

The "DSM-IV-TR" diagnostic criteria for sleep terror disorder requires:

- recurrent periods where the individual abruptly wakes from sleeping with a scream

- the individual experiences intense fear and symptoms of autonomic arousal, such as increased heart rate, heavy breathing, and increased perspiration

- the individual cannot be soothed or comforted during the episode

- the individual is unable to remember details of the dream or details of the episode

- the occurrence of the sleep terror episode causes "clinically significant" distress or impairment in the individual's functioning

- the disturbance is not due to the effects of a substance or general medical condition

In individuals with autism, schizophrenia, and certain physical disorders (such as Kleine-Levin syndrome), nonnutritive substances may be eaten. In such instances, pica should not be noted as an additional diagnosis.

In most children, night terrors eventually subside and do not need to be treated. It may be helpful to reassure the child and their family that they will outgrow this disorder.

Psychotherapy or counseling can be helpful in many cases. There is some evidence to suggest that night terrors can result from lack of sleep or poor sleeping habits. In these cases, it can be helpful to improve the amount and quality of sleep which the child is getting. If this is not enough, benzodiazepines (such as diazepam) or tricyclic antidepressants may be used; however, medication is only recommended in extreme cases.

Polysomnography is also used to aid in the diagnosis of other sleep disorders such as obstructive sleep apnea (OSA), narcolepsy, and restless leg syndrome (RLS). Normal test results show little to no episodes of sleep apnea and normal electrical activity in the individual's brain and muscles during sleep.

There is no single test that confirms pica. However, because pica can occur in people who have lower than normal nutrient levels and poor nutrition (malnutrition), the health care provider should test blood levels of iron and zinc.

Hemoglobin can also be checked to test for anemia. Lead levels should always be checked in children who may have eaten paint or objects covered in lead-paint dust. The health care provider should test for infection if the person has been eating contaminated soil or animal waste. The Diagnostic and Statistical Manual of Mental Disorders, 5th edition, posits four criteria that must be met for a person to be diagnosed with Pica:

Polysomnography is a study conducted while the individual being observed is asleep. A polysomnograph (PSG) is a recording of an individual's body functions as they sleep. Complete sleep studies are most commonly facilitated at a designated sleep center. Specialized electrodes and monitors are connected to the individual and remain in place throughout study. Video cameras can be used in certain cases to record physical behaviors occurring while the individual is asleep. Typically the unwanted sexual behaviors do not present on film, therefore the majority of information is taken from a sleep study.

According to one meta-analysis, the mean prevalence rate for North America and Western Europe is estimated to be 14.5±8.0%. Specifically in the United States, the prevalence of restless leg syndrome is estimated to be between 5 and 15.7% when using strict diagnostic criteria. RLS is over 35% more prevalent in American women than their male counterparts.

Due to rapidly increasing knowledge about sleep in the 20th century, including the discovery of REM sleep in the 1950s and circadian rhythm disorders in the 70s and 80s, the medical importance of sleep was recognized. The medical community began paying more attention than previously to primary sleep disorders, such as sleep apnea, as well as the role and quality of sleep in other conditions. By the 1970s in the USA, clinics and laboratories devoted to the study of sleep and sleep disorders had been founded, and a need for standards arose.

Specialists in Sleep Medicine were originally certified by the American Board of Sleep Medicine, which still recognizes specialists. Those passing the Sleep Medicine Specialty Exam received the designation "diplomate of the ABSM." Sleep Medicine is now a recognized subspecialty within internal medicine, family medicine, pediatrics, otolaryngology, psychiatry and neurology in the United States. Certification in Sleep Medicine shows that the specialist:"has demonstrated expertise in the diagnosis and management of clinical conditions that occur during sleep, that disturb sleep, or that are affected by disturbances in the wake-sleep cycle. This specialist is skilled in the analysis and interpretation of comprehensive polysomnography, and well-versed in emerging research and management of a sleep laboratory."

Competence in sleep medicine requires an understanding of a myriad of very diverse disorders, many of which present with similar symptoms such as excessive daytime sleepiness, which, in the absence of volitional sleep deprivation, "is almost inevitably caused by an identifiable and treatable sleep disorder", such as sleep apnea, narcolepsy, idiopathic hypersomnia, Kleine–Levin syndrome, menstrual-related hypersomnia, idiopathic recurrent stupor, or circadian rhythm disturbances. Another common complaint is insomnia, a set of symptoms which can have a great many different causes, physical and mental. Management in the varying situations differs greatly and cannot be undertaken without a correct diagnosis.

Sleep dentistry (bruxism, snoring and sleep apnea), while not recognized as one of the nine dental specialties, qualifies for board-certification by the American Board of Dental Sleep Medicine (ABDSM). The resulting Diplomate status is recognized by the American Academy of Sleep Medicine (AASM), and these dentists are organized in the Academy of Dental Sleep Medicine (USA). The qualified dentists collaborate with sleep physicians at accredited sleep centers and can provide oral appliance therapy and upper airway surgery to treat or manage sleep-related breathing disorders.

In the UK, knowledge of sleep medicine and possibilities for diagnosis and treatment seem to lag. Guardian.co.uk quotes the director of the Imperial College Healthcare Sleep Centre: "One problem is that there has been relatively little training in sleep medicine in this country – certainly there is no structured training for sleep physicians." The Imperial College Healthcare site shows attention to obstructive sleep apnea syndrome (OSA) and very few other sleep disorders. Some NHS trusts have specialist clinics for respiratory and/or neurological sleep medicine.

In general, there are two broad classes of treatment, and the two may be combined: psychological (cognitive-behavioral) and pharmacological. In situations of acute distress such as a grief reaction, pharmacologic measures may be most appropriate. With primary insomnia, however, initial efforts should be psychologically based, including discussion of good sleep hygiene. Other specific treatments are appropriate for some of the disorders, such as ingestion of the hormone melatonin, correctly timed bright light therapy and correctly timed dark therapy or light restriction for the circadian rhythm sleep disorders. Specialists in sleep medicine are trained to diagnose and treat these disorders, though many specialize in just some of them.

Over the past thirty years, several studies have found that those afflicted with NSRED all have different symptoms and behaviors specific to them, yet they also all have similar characteristics that doctors and psychologists have identified to distinguish NSRED from other combinations of sleep and eating disorders such as night eating syndrome. Winkelman says that typical behaviors for patients with NSRED include: "Partial arousals from sleep, usually within 2 to 3 hours of sleep onset, and subsequent ingestion of food in a rapid or 'out of control' manner." They also will attempt to eat bizarre amalgamations of foods and even potentially harmful substances such as glue, wood, or other toxic materials. In addition, Schenck and Mahowald noted that their patients mainly ate sweets, pastas, both hot and cold meals, improper substances such as "raw, frozen, or spoiled foods; salt or sugar sandwiches; buttered cigarettes; and odd mixtures prepared in a blender."

During the handling of this food, patients with NSRED distinguish themselves, as they are usually messy or harmful to themselves. Some eat their food with their bare hands while others attempt to eat it with utensils. This occasionally results in injuries to the person as well as other injuries. After completing their studies, Schenck and Mahowald said, "Injuries resulted from the careless cutting of food or opening of cans; consumption of scalding fluids (coffee) or solids (hot oatmeal); and frenzied running into walls, kitchen counters, and furniture." A few of the more notable symptoms of this disorder include large amounts of weight gain over short periods of time, particularly in women; irritability during the day, due to lack of restful sleep; and vivid dreams at night. It is easily distinguished from regular sleepwalking by the typical behavioral sequence consisting of "rapid, 'automatic' arising from bed, and immediate entry into the kitchen." In addition, throughout all of the studies done, doctors and psychiatrists discovered that these symptoms are invariant across weekdays, weekends, and vacations as well as the eating excursions being erratically spread throughout a sleep cycle. Most people that suffer from this disease retain no control over when they arise and consume food in their sleep. Although some have been able to restrain themselves from indulging in their unconscious appetites, some have not and must turn to alternative methods of stopping this disorder. It is important for trained physicians to recognize these symptoms in their patients as quickly as possible, so those with NSRED may be treated before they injure themselves.

Rumination syndrome is diagnosed based on a complete history of the individual. Costly and invasive studies such as gastroduodenal manometry and esophageal Ph testing are unnecessary and will often aid in misdiagnosis. Based on typical observed features, several criteria have been suggested for diagnosing rumination syndrome. The primary symptom, the regurgitation of recently ingested food, must be consistent, occurring for at least six weeks of the past twelve months. The regurgitation must begin within 30 minutes of the completion of a meal. Patients may either chew the regurgitated matter or expel it. The symptoms must stop within 90 minutes, or when the regurgitated matter becomes acidic. The symptoms must not be the result of a mechanical obstruction, and should not respond to the standard treatment for gastroesophageal reflux disease.

In adults, the diagnosis is supported by the absence of classical or structural diseases of the gastrointestinal system. Supportive criteria include a regurgitant that does not taste sour or acidic, is generally odourless, is effortless, or at most preceded by a belching sensation, that there is no retching preceding the regurgitation, and that the act is not associated with nausea or heartburn.

Patients visit an average of five physicians over 2.75 years before being correctly diagnosed with rumination syndrome.

Purging disorder is an eating disorder characterized by recurrent purging (self-induced vomiting, misuse of laxatives, diuretics, or enemas) to control weight or shape in the absence of binge eating episodes.

Purging disorder differs from bulimia nervosa (BN) because individuals with purging disorder do not consume a large amount of food before they purge. In current diagnostic systems, purging disorder is a form of Other specified feeding or eating disorder (OSFED). Research indicates that purging disorder may be as common as bulimia nervosa or anorexia nervosa in women, that the syndrome is associated with clinically significant levels of distress, and that it appears to be distinct from bulimia nervosa on measures of hunger and ability to control food intake. Some of the signs of purging disorder are frequent trips to the bathroom directly after a meal, frequent use of laxatives, and obsession over one's appearance and weight. Other signs include swollen cheeks, popped blood vessels in the eyes, and clear teeth which are all signs of excessive vomiting.