While humans are able to remain active in the late hours of the night, for some individuals this ability is genetically programmed. To some this may seem like a beneficial skill, however, Night Owl Syndrome — also known as Delayed Sleep Phase Syndrome — is a sleep disorder with potentially severe consequences.
Sleeping consists of two phases: rapid eye movement (REM) and non-REM sleep. REM sleep is so named due to the activity of the eyes and brain during this period. Brain activity measured during REM sleep is similar to the brain’s activity during waking hours. REM sleep also occurs later in the night.
Non-REM sleep has three stages: the transition between wakefulness and sleep, being fully asleep, and deep sleep or slow-wave sleep, named after a particular pattern that appears when measuring brain activity. More time is usually spent in stage three early in the night.
The cycle between REM and non-REM starts over every 80 to 100 minutes. Usually there are four to six cycles per night.
This process for sleep is normally regulated by a biological “clock” that sets the timing for many bodily functions. This clock is driven by a 24-hour circadian rhythm that resets every day according to the sun’s light-dark cycle.
However, this biological timing can sometimes be disrupted. An example of this is Delayed Sleep Phase Syndrome (DSPS) — or night owl syndrome — a disorder in which a person’s sleep is delayed by two hours or more beyond what is considered an acceptable or conventional bedtime. Individuals affected by DSPS normally go to bed between 1 a.m. and 4 a.m. and wake up later in the morning, between 8 a.m. and 11 a.m. DSPS is responsible for 10% of all chronic insomnia cases.
As a result, sleep disorders such as DSPS can pose a serious threat to an individual’s daily life. During sleep, the body is working to support healthy brain function and maintain physical health. In children and teens, sleep also helps support growth and development. Getting inadequate sleep over time can raise the risk for chronic health problems. It can also affect how well someone thinks, reacts, works, learns and gets along with others.
Treatments for DSPS include bright light therapy and melatonin supplements. Bright light therapy consists of a 30-minute treatment where the patient sits near a light box immediately after waking up. The aim of this exposure is to manipulate the patient’s circadian clock, ensuring that they will go to sleep sooner. Melatonin is a hormone that helps control the sleep-wake cycle. It can be prescribed by a doctor.
While these proposed treatment methods have shown some promise, ultimately there is no cure for DSPS. Many treatments have proven ineffective and as a result, patients have had to adjust their personal and professional schedules to accommodate their irregular sleeping patterns.
Much research has been conducted to address the problems that DSPS poses. One such study done by a collaboration of colleges in New York and Turkey in 2017 discovered a hereditary form of DSPS that affected people of European descent. This form of DSPS was associated with a mutation in the gene for the circadian clock, called CRY1. This mutation affected a core protein, enhancing its affinity to certain circadian-related proteins, such as Clock and Bmal1, and resulting in the circadian clock running longer.
The specific interaction between the proteins had yet to be visualized, but this knowledge gap was finally filled in 2020, when researchers at the University of California, Santa Cruz discovered that the protein tail — a chain of proteins — of CRY1 played a significant role in the circadian cycle. The study determined that the mutated CRY1 had a shortened tail, preventing CRY1 from periodically disconnecting with circadian-related proteins, leading to longer cycles for the circadian clock.
These two studies have produced significant findings within the field of sleep research. Mutations known to alter the circadian clock are rare and are important to scientists as clues to understanding the mechanisms behind the body’s clock. Sleep behavior is complex and disorders can be hard to diagnose, so the discoveries of a genetic variation associated with DSPS was a substantial development.
Additionally, these studies provide a biological explanation for why some patients do not have success with certain treatments for DSPS. If the root cause of a problem is genetic, then methods that manipulate environmental factors, such as light therapy, will be ineffective.
The UCSC study also provided suggestions for alternative treatments, such as manipulating circadian-related proteins involved in sleep and regulated alternative splicing (a process by which portions of regions within a pre-mRNA strand are joined or skipped) of the CRY1 gene.
Originally thought to be incurable, those with night owl syndrome can now have hope for a more restful night. These studies have laid the groundwork for future potential, and possibly more effective, treatments.