Polyphagia usually occurs early in the course of diabetic ketoacidosis. However, once insulin deficiency becomes more severe and ketoacidosis develops, appetite is suppressed.

Causes of increased appetite include:

- Anxiety

- Stress

- Depression

- Certain drugs

- Diabetes mellitus

- Hyperthyroidism

- Hypoglycemia

- Fatigue

- Depression

- Premenstrual syndrome

- Prader–Willi syndrome

- Bulimia

- Graves' disease

- Kleine–Levin syndrome

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."

Childhood obesity is a condition where excess body fat negatively affects a child's health or well-being. As methods to determine body fat directly are difficult, the diagnosis of obesity is often based on BMI. Due to the rising prevalence of obesity in children and its many adverse health effects it is being recognized as a serious public health concern. The term overweight rather than obese is often used in children as it is less stigmatizing.

The first problems to occur in obese children are usually emotional or psychological. Obese children often experience bullying by their peers. Some are harassed or discriminated against by their own family. Stereotypes abound and may lead to low self-esteem and depression.

Emotional eating is defined as overeating in order to relieve negative emotions. Thus, emotional eating is considered a maladaptive coping strategy. If an individual frequently engages in emotional eating, it can increase the risk of developing other eating disorders, like bulimia and anorexia nervosa. Research has also shown that the presence of an existing eating disorder increases the likelihood that an individual will engage in emotional eating. Given the relationship between serious eating disorders and emotional eating behavior, it is important for clinical psychologists and nutritionists to recognize the signs of emotional eating and provide individuals with treatment. Since emotional eating is utilized to manage negative emotions, treatment necessitates learning healthy and more effective coping strategies.

Patients with Kleine–Levin syndrome (KLS) experience reoccurring episodes of prolonged sleep (hypersomnia). In most cases, patients sleep 15 to 21 hours a day during episodes.

Excessive appetite (hyperphagia) and unusual cravings are present in half to two thirds of cases. About half of patients, mainly male patients, experience dramatically increased sexual urges (hypersexuality). Several other symptoms usually accompany the syndrome, including marked changes in mood and cognitive ability. Derealization and severe apathy are present in at least 80 percent of cases. About one third of patients experience hallucinations or delusions. Depression and anxiety occur less commonly; one study found them in about 25 percent of patients. Individuals usually cannot remember what happened during episodes. Repetitive behaviors and headaches are commonly reported. Some patients act very childlike during episodes, and communication skills and coordination sometimes suffer.

Sleep studies of KLS show varying results based on the amount of time the patient is observed. Slow wave sleep is often reduced at the beginning of episodes, and REM sleep is reduced near the end. Conversely, REM sleep is often normal at the beginning, and slow wave sleep is often normal by the conclusion. Stage two non-rapid eye movement sleep is often interrupted during KLS. Studies also show that stage one and three non-rapid eye movement sleep become more efficient when the episodes end. The Multiple Sleep Latency Test has yielded inconsistent results when given to KLS patients. In many cases, hours are spent in a withdrawn sleep-like state while awake during episodes. Most sleep studies have been performed while subject are near the end of their episodes. Some patients experience brief insomnia and become very happy and talkative after the episode ends.

The first time a patient experiences KLS, it usually occurs along with symptoms that are similar to those of the flu or encephalitis. In at least 75 percent of cases, symptoms occur after an airway infection or a fever. Viruses observed before the development of the condition include Epstein-Barr virus, varicella zoster virus, herpes zoster virus, Influenza A virus subtypes, and adenovirus. Several days after symptoms first occur, patients become very tired. In cases that occur after an infection, KLS usually starts within three to five days for teenagers and fewer for children. In other cases, alcohol consumption, head injury, or international travel precede symptoms. Lifestyle habits, such as stress, alcohol abuse and lack of sleep and stress, have also been proposed as possible triggers. First episodes of KLS are preceded by a clear event in about 90 percent of cases. Recurrences generally do not have clear triggers; only about 15 percent have a precipitating event.

The condition generally disrupts the social lives and academic or profession obligations of sufferers. Some patients also gain weight during episodes. The most severe cases cause a long-term impact on mood and cognitive attention. In rare cases, patients experience long-term memory problems.

In patients with KLS, MRI and CT scans show normal brain morphology. When SPECT is performed, hypoperfusion can often be observed in the brain, particularly in the thalamic and frontotemporal areas. The hypoperfusion is significantly diminished between episodes. Serum biology, c-reactive proteins and leptins, the hormonal pituitary axis, and protein in the cerebral spinal fluid (CSF) are normal in KLS patients.

Emotional eating is a form of disordered eating and is defined as "an increase in food intake in response to negative emotions" and can be considered a maladaptive strategy used to cope with difficult feelings. More specifically, emotional eating would qualify as a form of emotion-focused coping, which attempts to minimize, regulate and prevent emotional distress. Interestingly, a study conducted by Bennett et al. found that emotional eating sometimes does not reduce emotional distress but instead enhances emotional distress by sparking feelings of intense guilt after an emotional eating session. Not only is emotional eating a poor way to cope, but those individuals who frequently utilize emotional eating to cope with social or psychological stressors are at an increased risk of developing eating disorders. Emotional eaters are at an especially high risk of developing binge-eating disorder. 2.8% of Americans struggle with binge-eating disorder, which increases their risk of developing cardiovascular disease and high blood pressure. At the same time, the presence of other eating disorders increases the risk of an individual engaging in emotional eating. In a clinical setting, emotional eating disorders can be diagnosed by the Dutch Eating Behavior Questionnaire which contains a scale for restrained, emotional and external eating. While therapists may use positive psychology as a way to reduce the negative emotions that trigger emotional eating, reappraisal is often a complementary treatment with the primary treatment being focused on developing alternative coping strategies.

The variable presentation of ROHHAD includes the following main symptoms:

- Hyperphagia and obesity by age of 10 years - (median age 3 years);

- Respiratory Manifestations:

- Alveolar Hypoventilation (median onset age 6.2 years);

- Cardiorespiratory arrest;

- Reduced Carbon Dioxide Ventilatory Response;

- Obstructive sleep apnea.

- Thermal or other hypothalamic dysregulations, with autonomic dysregulation by median age 3.6 years:

- Failed Growth Hormone Stimulation;

- Adipsic hypernatremia (inability to feel thirst to keep normal hydration);

- Hypernatremia;

- Hyperprolactinemia;

- Hyperphagia;

- Diabetes insipidus;

- Ophthalmologic Manifestations;

- Thermal Dysregulation;

- Gastrointestinal dysmotility;

- Altered Perception of Pain;

- Altered Sweating;

- Cold Hands and Feet.

- Neurobehavioral disorders;

- Tumors of neural crest origin.

Clinically overlapping cases exist because CCHS phenotype can also include autonomic nervous system dysregulation, or tumors of neural crest origin.

Currently there are no official tests or treatments for ROHHAD. Each child has the symptoms above at different ages, yet most symptoms are eventually present. Many children are misdiagnosed or are never diagnosed until alveolar hypoventilation occurs.

Kleine–Levin syndrome (KLS), also known as Sleeping Beauty syndrome, is a rare sleep disorder characterized by persistent episodic hypersomnia and cognitive or mood changes. Many patients also experience hyperphagia, hypersexuality and other symptoms. Patients generally experience recurrent episodes of the condition for more than a decade and may return at a later age. Individual episodes generally last more than a week, some times lasting for months. The condition greatly affects the personal, professional, and social lives of sufferers. The severity of symptoms and the course of the syndrome vary between sufferers. Patients commonly have about 20 episodes over about a decade. Several months generally elapse between episodes. The onset of the condition usually follows a viral infection; several different viruses have been observed to trigger KLS. It is generally only diagnosed after similar conditions have been excluded; MRI, CT scans, lumbar puncture, and toxicology tests are used to rule out other possibilities. The syndrome's mechanism is not known, but the thalamus is thought to possibly play a role. SPECT has shown thalamic hypoperfusion of patients during episodes.

KLS is very rare, occurring at a rate of one in 14 million, which limits research into genetic factors. The condition primarily affects adolescent males, though females can also be affected and the age of onset varies. There is no known cure, and there is little evidence supporting drug treatment. Lithium has been reported to have limited effects in case reports, decreasing the length of episodes and duration between them in some patients. Stimulants have been shown to promote wakefulness during episodes, but they do not counteract cognitive symptoms or decrease the duration of episodes. The condition is named after Willi Kleine and Max Levin, who described cases of the disease in the early 20th century. It was added to the International Classification of Sleep Disorders in 1990.

Depressive mixed states occur when patients experience depression and non-euphoric, usually subsyndromal, hypomania at the same time. As mentioned previously, it is particularly difficult to diagnose BP-II when a patient is in this state.

In a mixed state, mood is depressed, but the following symptoms of hypomania present as well:

- Irritability

- Mental overactivity

- Behavioral overactivity

Mixed states are associated with greater levels of suicidality than non-mixed depression. Antidepressants may increase this risk.

It is during depressive episodes that BP-II patients often seek help. Symptoms may be syndromal or subsyndromal. Depressive BP-II symptoms may include five or more of the below symptoms (at least one of them must be either depressed mood or loss of interest/pleasure). In order to be diagnosed, they need to be present only during the same two-week period, as a change from previous hypomanic functioning:

- Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g., appears tearful). (Note: In children and adolescents, can be irritable mood.)

- Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).

- Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. (Note: In children, consider failure to make expected weight gain.)

- Insomnia or hypersomnia nearly every day.

- Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective feelings of restlessness or being slowed down).

- Fatigue or loss of energy nearly every day.

- Feelings of worthlessness or excessive or inappropriate guilt nearly every day (not merely self-reproach or guilt about being sick).

- Diminished ability to think or concentrate, possible irritability or indecisiveness, nearly every day (either by subjective account or as observed by others).

- Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, a suicide attempt, or a specific plan for committing suicide.

Evidence also suggests that BP-II is strongly associated with atypical depression. Essentially, this means that many BP-II patients exhibit reverse vegetative symptoms. BP-II patients may have a tendency to oversleep and overeat, while typically depressed patients sleep and eat less than usual.

Prader–Willi syndrome is frequently associated with a constant, extreme, ravenous insatiable appetite which persists no matter how much the patient eats, often resulting in morbid obesity. Caregivers need to strictly limit the patients' access to food, usually by installing locks on refrigerators and on all closets and cabinets where food is stored. It is the most common genetic cause of morbid obesity in children. There is currently no consensus as to the cause for this symptom, although genetic abnormalities in chromosome 15 disrupt the normal functioning of the hypothalamus. Given that the hypothalamus arcuate nucleus regulates many basic processes, including appetite, there may well be a link. In the hypothalamus of people with PWS, nerve cells that produce oxytocin, a hormone thought to contribute to satiety, have been found to be abnormal.

People with Prader–Willi syndrome have high ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia, and obesity seen in this syndrome. Cassidy states the need for a clear delineation of behavioral expectations, the reinforcement of behavioural limits and the establishment of regular routines.

The main mental health difficulties experienced by people with PWS include compulsive behaviour (usually manifested in skin picking) and anxiety. Psychiatric symptoms, for example, hallucinations, paranoia and depression, have been described in some cases and affect approximately 5–10% of young adults. Patients are also often extremely stubborn and prone to anger. Psychiatric and behavioural problems are the most common cause of hospitalization.

It is typical for to 70–90% of affected individuals to develop behavioral patterns in early childhood. Aspects of these patterns can include stubbornness, temper tantrums, controlling and manipulative behavior, difficulty with change in routine, and compulsive-like behaviors.

There are several aspects of PWS that support the concept of growth hormone deficiency in individuals with PWS. Specifically, individuals with PWS have short stature, are obese with abnormal body composition, have reduced fat free mass (FFM), have reduced lean body mass (LBM) and total energy expenditure, and have decreased bone density.

PWS is characterized by hypogonadism. This is manifested as undescended testes in males and benign premature adrenarche in females. Testes may descend with time or can be managed with surgery or testosterone replacement. Adrenarche may be treated with hormone replacement therapy.

The list of symptoms differs somewhat by source. Generally included are the following:

1. Amnesia. Characterised by an inability to recall memories. Its nature is both anterograde and retrograde, meaning new memories cannot be formed and old memories cannot be recalled. The level of amnesia is considered to be profound.

2. Docility. Characterized by exhibiting diminished fear responses or reacting with unusually low aggression. This has also been termed "" or "tameness".

3. Dietary changes and hyperphagia. Characterized by eating inappropriate objects (pica), or overeating, or both.

4. Hyperorality. This was described by Ozawa et al. as "an oral tendency, or compulsion to examine objects by mouth".

5. Hypersexuality. Characterized by a heightened sex drive or a tendency to seek sexual stimulation from unusual or inappropriate objects.

6. Visual agnosia. Characterized by an inability to recognize familiar objects or people.

While this cluster of syndromes is common to such sources as 1997's "The Neuropsychiatry of Limbic and Subcortical Disorders", 2005's "Functional Neuroanatomy: Text and Atlas" and 1997's "Single-Photon Emission CT and MR Findings in Klüver-Bucy after Reye syndrome", an article in the "American Journal of Neuroradiology", the three vary thereafter.

Inconsistent criteria include:

- Hypermetamorphosis, characterized by Ozawa et al. as "an irresistible impulse to notice and react to everything within sight". This is included under the classification systems described by "The Neuropsychiatry of Limbic and Subcortical Disorders" and "Single-Photon Emission CT and MR Findings in Klüver-Bucy".

- Lack of emotional response, diminished emotional affect. This is a symptom under "The Neuropsychiatry of Limbic and Subcortical Disorders" and is included under "Single-Photon Emission CT and MR Findings in Klüver-Bucy" along with apathy under docility.

In psychology, disinhibition is a lack of restraint manifested in disregard for social conventions, impulsivity, and poor risk assessment. Disinhibition affects motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms similar to the diagnostic criteria for mania. Hypersexuality, hyperphagia, and aggressive outbursts are indicative of disinhibited instinctual drives.

Klüver–Bucy syndrome is a syndrome resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus). Klüver–Bucy syndrome may present with compulsive eating, hypersexuality, insertion of inappropriate objects in the mouth (hyperorality), visual agnosia, and .

Microcephaly is a disorder in which the circumference of the head is smaller than average for the person's age and gender. Most children with microcephaly also have a smaller than typical brain and intellectual disability. Some of the most common signs and symptoms associated with microcephaly are seizures, poor feeding, high pitched cry, intellectual disability, developmental delay, and increased movement of arms and legs.

Puberty in children with 1p36 deletion syndrome can be early, normal, or delayed.

Witzelsucht (from the German "witzeln", meaning to joke or wisecrack, and "sucht", meaning addiction or yearning) is a set of rare neurological symptoms characterized by a tendency to make puns, or tell inappropriate jokes or pointless stories in socially inappropriate situations. A less common symptom is hypersexuality, the tendency to make sexual comments at inappropriate times or situations. Patients do not understand that their behavior is abnormal, therefore are nonresponsive to others' reactions. This disorder is most commonly seen in patients with frontal lobe damage, particularly right frontal lobe tumors or trauma. The disorder remains named in accordance with its reviewed definition by German neurologist Hermann Oppenheim; its first description as the less focused "Moria" ("stupidity"), by German neurologist Moritz Jastrowitz, was in 1888.

Due to similarity of symptoms of the disorder to the mannerisms of Batman's arch-rival Joker, it is sometimes known as 'The Joker Syndrome'

According to Grafman et al. "disinhibition" is a lack of restraint manifested in several ways, affecting motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms e.g. impulsivity, disregard for others and social norms, aggressive outbursts, misconduct and oppositional behaviors, disinhibited instinctual drives including risk taking behaviors and hypersexuality. Disinhibition is a common symptom following brain injury, or lesions, particularly to the frontal lobe and primarily to the orbitofrontal cortex. The neuropsychiatric sequelae following brain injuries could include diffuse cognitive impairment, with more prominent deficits in the rate of information processing, attention, memory, cognitive flexibility, and problem solving. Prominent impulsivity, affective instability, and disinhibition are seen frequently, secondary to injury to frontal, temporal, and limbic areas. In association with the typical cognitive deficits, these sequelae characterize the frequently noted "personality changes" in TBI (Traumatic Brain Injury) patients. Disinhibition syndromes, in brain injuries and insults including brain tumors, strokes and epilepsy range from mildly inappropriate social behavior, lack of control over one's behaviour to the full-blown mania, depending on the lesions to specific brain regions. Several studies in brain traumas and insults have demonstrated significant associations between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices, affecting visuospatial functions, somatosensation, and spatial memory, motoric, instinctive, affective, and intellectual behaviors.

Disinhibition syndromes have also been reported with mania-like manifestations in old age with lesions to the orbito-frontal and basotemporal cortex involving limbic and frontal connections (orbitofrontal circuit), especially in the right hemisphere. Behavioral disinhibition as a result of damage to frontal lobe could be seen as a result of consumption of alcohol and central nervous system depressants drugs, e.g. benzodiazepines that disinhibit the frontal cortex from self-regulation and control. It has also been argued that ADHD, hyperactive/impulsive subtype have a general behavioural disinhibition beyond impulsivity and many morbidities or complications of ADHD, e.g. conduct disorder, anti-social personality disorder. substance abuse and risk taking behaviours are all consequences of untreated behavioural disinhibition.

ONH can be unilateral (in one eye) or bilateral (in both eyes), although it presents most often bilaterally (80%). Because the unilateral cases tend to have better vision, they are typically diagnosed at a later age than those with bilateral ONH. Visual acuity can range from no light perception to near-normal vision.

Children diagnosed with ONH generally present with vision problems which include nystagmus (involuntary movement of the eyes), which tends to develop at 1 to 3 months and/or strabismus (inability to align both eyes simultaneously), manifested during the first year of life.

The majority of children affected experience improvement in vision during the first few years of life, though the reason for this occurrence is unknown. There have been no reported cases of decline in vision due to ONH.

Dysfunction of the hypothalamus results in loss of regulation over behavior and function of the pituitary gland (master gland). Hypopituitarism is present in 75% to 80% of patients with ONH. The anterior pituitary gland contributes to growth, metabolism, and sexual development. The most common pituitary endocrinopathies are growth hormone (GH) deficiency (70%), hypothyroidism (43%), adrenal insufficiency (27%), and diabetes insipidus (5%).

Absence of GH may often be indicated by short stature, although this is not always the case. Other indicators of GH deficiency may include hypoglycemic events (including seizures), prolonged jaundice, micropenis in boys, and delayed dentition. Testing for GH may involve blood tests (IGF-1 and IGFBP-3), growth hormone stimulation test, or bone age x-ray of the hand or wrist (or body for children younger than 2 years).

A poorly functioning pituitary gland may also cause a lack of thyroid hormone, leading to central hypothyroidism. Thyroid hormone is critical for growth and brain development, especially during the first few weeks to months of life. Children with untreated hypothyroidism are at high risk of mental retardation; thus, early detection is crucial. Central hypothyroidism can be diagnosed by a low or normal thyroid-stimulating hormone (TSH) in the presence of a low level of free T4. Free T-4 should be checked annually for at least four years.

Cortisol is made in times of stress. Approximately one-quarter of patients with ONH have adrenal insufficiency, meaning they do not produce enough cortisol on a daily basis or in stressful situations.

Imbalances in sex hormone may result in a delay in sexual development (puberty) or precocious puberty. Sex hormones may be tested from birth to 6 months of age (during a mini-puberty).

Hyperprolactinemia (an excess of prolactin) often occurs in conjunction with ONH and indicates either dysfunction of the hypothalamus or a disconnect between the hypothalamus and pituitary gland. Hyperprolactinemia often correlates with development of obesity in children with ONH.

The posterior pituitary gland produces anti-diuretic hormone (ADH), which controls outflow of water from the body by urine. ADH deficiency, also known as diabetes insipidus (DI), results in dehydration and high sodium levels in the body from excessive urination. Testing for DI involves blood and urine testing, including water deprivation tests, to determine ADH creation levels by the body. DI may be treated with a medication called desmopressin acetate (DDAVP).

Oxytocin is also produced in the posterior pituitary gland. Though best known for its role in childbirth and lactation, oxytocin has also been found to have a role in human bonding, increase in trust, and decrease in fear.

Hypothalamic dysfunction may also result in problems with feeding, sleep, and body temperature regulation. Feeding behaviors in children with ONH often include hyperphagia (overeating), resulting in obesity; or hypophagia (reduced food intake) with or without weight loss. Children also frequently experience aversion to specific textures of food. Disturbance of circadian sleep rhythm, resulting in abnormal sleep-wake cycles, is noted in one-third of children with ONH. This disturbance could result in behavioral problems and disruption of family life.