Delayed sleep-wake phase disorder (DSWPD) is characterised by an inability to fall asleep at a socially acceptable time, and an inability to wake up at conventional early times for school or work.
Dr Gregory Carter from the University of Texas Southwestern Medical Center at Dallas, is conducting research into ‘night owl preference’, and what can be done to realign ones circadian rhythm.
Read more: https://doi.org/10.5664/jcsm.5100
Hello and welcome to Research Pod! Thank you for listening and joining us today.
In this episode we will be looking at the research of Dr Gregory Carter from the University of Texas Southwestern Medical Center at Dallas, into delayed sleep-wake phase disorder.
Delayed sleep-wake phase disorder (DSWPD) is characterised by an inability to fall asleep at a socially acceptable time (known as “night owl” preference), usually for more than two hours, and an inability to wake up at conventional early times for traditional social, school or employment schedules. This results in chronic sleep deprivation and inertia (an inability to fully wake up and stay alert in the morning), which further impairs daytime activity.
DSWPD is often differentiated from chronic insomnia, as patients have improved subjective sleep quality and duration when they are allowed to sleep at their desired times when they do not have to wake up at conventional times. It is the most commonly diagnosed circadian rhythm sleep disorder, estimated to affect 0.2 – 10 percent of the general population.
The feeling of tiredness throughout the day can cause distress for patients and further affect those around them, as they may be tardy or miss school and work days. It is not surprising that anxiety, depression, and personality vulnerabilities are frequently found to be associated with DSWPD. For example, failure to maintain a required schedule increases the risk of interpersonal conflicts, which lower self-esteem and feelings of competence. This further reduces the capacity to enforce self-discipline to strive for achievements.
DSWPD is most commonly observed in adolescents, increases in frequency during an individual’s early 20s, and decreases amongst older populations. However, DSWPD can persist in older individuals who have usually developed adaptations resulting in less distress.
The circadian clock is a 24-hour cycle that is part of the body’s internal mechanism, which generates a 24-hour rhythm in gene expression (the process whereby the DNA instructions are converted into a functional product). This circadian clock regulates rhythms of metabolism, sleep, body temperature, blood pressure, and immune function, to name a few. Different systems of the body follow the circadian clock and these systems are synchronised with a master clock in the brain. The master clock is directly influenced by environmental cues, especially light. Hence, the circadian clock is inherently tied to the cycle of day and night.
The sleep-wake cycle is driven by determinants of the internal circadian rhythm. In the morning, light exposure causes the internal clock to synchronize with the day, generating alertness. This is called ‘process C’ or the circadian drive, which increases over the course of the day or wakefulness to counter ‘process S’ or the drive to sleep. ‘Process S’ becomes stronger the longer an individual is awake, probably due to decreased brain energy reserves from wakefulness. At the onset of sleep, ‘process C’ drops dramatically to allow the onset of sleep. In DSWPD, ‘process C’ is misaligned with the desired sleep/wake cycle and continues to strongly oppose sleep onset at the desired time even in the presence of accumulated sleep deprivation.
The exact cause of DSWPD has remained elusive. Researchers have hypothesised that both genetic and environmental factors play a role in initiating and exacerbating this condition. A family history with the same condition has been found in approximately 40% of individuals.
Polymorphism in the circadian clock gene hPer3, human leukocyte antigen, and Clock are found to be associated with DSWPD onset and progression. A 2017 study published in Cell identified a gene involved in the circadian clock, CRY1, to play a role in DSWPD. A gain-of-function mutation leads to increased CRY1 protein expression and inhibition of target genes: Clock and BMAL1. Altogether, it is associated with increased period of molecular circadian rhythms in cells and delayed sleep onset.
Decreased exposure to bright light in the morning and increased exposure to light late in the evening can exacerbate the delayed circadian phase, which causes individuals to have the desire to fall asleep and arise later than usual times. Furthermore, certain changes in lifestyle can initiate the onset of DSWPD, such as maladjustment to changes in work and social schedules, different time zones, shift work, and activities that continue into late evening.
A 2015 paper published in the Journal of Clinical Sleep Medicine outlines the treatment recommendations from the American Academy of Sleep Medicine for DSWPD according to an extensive systematic literature review and meta-analyses. This is summarised and expanded in a chapter of a 2020 book titled, ‘Circadian Rhythm Sleep-Wake Disorders’, authored by Dr Gregory
Carter from the University of Texas Southwestern Medical Centre at Dallas.
Firstly, melatonin represents a potential therapy avenue, as it is a hormone associated with the internal circadian clock. Three reviewed investigations have contradictory information regarding the effects of melatonin and sleep improvement/circadian rhythm in adult patients. The most definitive results showed a decrease in sleep latency (the amount of time it takes to transition from full wakefulness to onset of sleep) by 43.52 minutes in co-morbid depressed patients and 37.70 minutes in non-depressed DSWPD patients when 5 milligrams of melatonin was administered.
Studies in children aged 6 – 12 years old when given a low dose of melatonin, ranging from 0.05 milligrams per kilogram to 0.15 milligrams per kilogram showed an improvement in sleep latency in comparison to the placebo group. Two randomised, placebo-controlled studies on children and adolescents with various psychiatric comorbidities showed an advancement in sleep onset time when melatonin was administered.
There are no reported serious adverse effects from a daily dose of 10 miligrams of melatonin in healthy adults. However, adverse effects have been observed in higher doses, and in individuals with pre-existing conditions, such as headaches, somnolence, hypotension, hypertension, gastrointestinal upset, and exacerbation of hair loss. Despite low support from studies for the use of melatonin supplements, clinical experience nevertheless supports its use due to inconclusive adverse effects compared to no treatment. It has been suggested that a single dose of melatonin of 0.3 to 3 miligrams should be taken four hours prior to the desired bedtime.
A combination light therapy has also been suggested as a potential treatment option for DSWPD patients. Upon waking up, participants in a 2011 study were exposed to natural sunlight or a 1,000 lux broad-spectrum lamp for 30-120 minutes. In counter-clockwise increments of 30 minutes per day, participants advanced to a target time of 0600 hours. When this time was achieved, light therapy was discontinued and participants were encouraged to maintain the same early rise time. Therefore, the success of therapy requires personal motivation to maintain a rigid schedule. Along with this, sessions of cognitive behaviour therapy were performed. Results showed that total sleep time and initial sleep latency were improved compared to patients who were on the wait list to partake in the investigation. No serious adverse effects have been reported with the use of light therapy.
Due to positive results from limited studies, it has been suggested for patients to undergo bright light therapy at 10,00 0lux 30 minutes to 4 hours after waking up and no later than 8 hours before the desired sleep onset. The light should be placed to the side of the face at a distance of about 24 inches. Alternatively, sunlight exposure in the early mornings or midday for 30 minutes to 4 hours can also be helpful, provided appropriate UV light safeguards are used (but not including darkened glasses).
Both therapies require patients to fix their daily schedule, which would cause initial anxiety. Thus, successful treatment depends on personal motivation to endure sleep deprivation initially and maintain a rigid schedule continuously. Anti-anxiety medication can reduce motivation or complicate successful therapy. Further and continued maladaptive sleep behaviours, such as adolescent after-school jobs, blue light screen exposures from computers, television, and cell phones, stimulating substances consumed within 6 hours of desired sleep onset time, and exciting activities before bedtime, such as family discussions and phone usage, can interfere with successful treatment. Therefore, discipline from both patients and support systems are needed to ensure DSWPD is tackled.
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