Prader–Willi syndrome (PWS) is a rare genetic disorder caused by a loss of function of specific genes on chromosome 15.

[2] Often, affected individuals have a narrow forehead, small hands and feet, short height, and light skin and hair.

[2] PWS is not generally inherited, but rather the genetic changes happen during the formation of the egg, sperm, or in early development.

[10] More aspects seen in a clinical overview include hypotonia and abnormal neurologic function, hypogonadism, developmental and cognitive delays, hyperphagia and obesity, short stature, and behavioral and psychiatric disturbances.

They are often strong in visual organization and perception, including reading and vocabulary, but their spoken language (sometimes affected by hypernasality) is generally poorer than their comprehension.

[19] PWS is frequently associated with a constant insatiable appetite, which persists no matter how much the patient eats, often resulting in morbid obesity.

[21] Currently, no consensus exists as to the cause for this symptom, although genetic abnormalities in chromosome 15 disrupt the normal functioning of the hypothalamus.

In the hypothalamus, nerve cells that produce oxytocin, a hormone thought to contribute to satiety, are believed to be abnormal in people with PWS.

[22] People with PWS have high ghrelin levels, which are thought to contribute directly to the increased appetite, hyperphagia and obesity seen in this syndrome.

[23] 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.

[29][30][31][32] This so-called PWS/AS region in the paternal chromosome 15 may be lost by one of several genetic mechanisms, which in the majority of instances occurs through chance mutation.

Other, less common mechanisms include uniparental disomy, sporadic mutations, chromosome translocations, and gene deletions.

[citation needed] The risk to the sibling of an affected child of having PWS depends upon the genetic mechanism which caused the disorder.

[34] Studies of human and mouse model systems have shown deletion of the 29 copies of the C/D box snoRNA SNORD116 (HBII-85) to be the primary cause of PWS.

Like autism, PWS is a spectrum disorder and symptoms can range from mild to severe and may change throughout the person's lifetime.

GH supports linear growth and increased muscle mass, and may lessen food preoccupation and weight gain.

[20] Physical activity in individuals with PWS for all ages is needed to optimize strength and promote a healthy lifestyle.

GH supports linear growth and increased muscle mass, and may lessen food preoccupation and weight gain.

[45][46][47] Because of severe obesity, obstructive sleep apnea is a common sequela, and a positive airway pressure machine is often needed.

[49] Despite its rarity, PWS has been often referenced in popular culture, partly due to curiosity surrounding the insatiable appetite and the obesity symptomatic of the syndrome.

[53] In July 2007, Channel 4 aired a 2006 documentary called Can't Stop Eating, surrounding the everyday lives of two people with PWS, Joe and Tamara.

[55] In a 2012 episode of Mystery Diagnosis on the Discovery Health channel, Conor Heybach, who has Prader–Willi syndrome, shared how he was diagnosed with it.