Delayed sleep phase disorder
Delayed sleep phase disorder, more often known as delayed sleep phase syndrome and also as delayed sleep–wake phase disorder, is the delaying of a person's circadian rhythm compared to those of social norms. The disorder affects the timing of biological rhythms including sleep, peak period of alertness, core body temperature, and hormonal cycles. People with this disorder are often called "night owls". It is considered to be a category of circadian rhythm sleep disorder.
The diagnosis of this disorder is currently a point of contention among specialists of sleep disorders. Many insomnia-related disorders can present significantly differently between patients, and circadian rhythm disorders and melatonin-related disorders are not well understood by modern medical science. The orexin system was only identified in 1998, yet it appears intimately implicated in human sleep-wake systems.
Evidence for the plasticity of human circadian rhythm cycles has been provided by multiple studies. In one example, 15 volunteers spent 40 days and nights underground in a French cave while researchers monitored their periods of waking and sleeping. Their results found significant divergence between individuals, with most participants settling upon a rhythm of hours. Researchers have speculated that the lack of exposure to natural sunrise/sunset cycles relates many of the symptoms of these circadian disorders to modern habits of humans spending extended periods indoors, without sunlight exposure and with artificial light.
Symptom management may be possible with therapeutic drugs such as orexin antagonists or melatonin receptor agonists, as well as regular outdoor exercise. There may be a genetic component to the syndrome.
Signs and symptoms
DSPD is responsible for 7–13% of patient complaints of chronic insomnia. However, since many doctors are unfamiliar with the condition, it often goes untreated or is treated inappropriately; DSPD is often misdiagnosed as primary insomnia or as a psychiatric condition.People with DSPD generally fall asleep some hours after midnight and have difficulty waking up in the morning.
Affected people often report that while they do not get to sleep until the early morning, they do fall asleep around the same time every day. Unless they have another sleep disorder such as sleep apnea in addition to DSPD, patients can sleep well and have a normal need for sleep. However, they find it very difficult to wake up in time for a typical school or work day. If they are allowed to follow their own schedules, e.g. sleeping from 4:00 am to 1:00 pm, their sleep is improved and they may not experience excessive daytime sleepiness. Attempting to force oneself onto daytime society's schedule with DSPD has been compared to constantly living with jet lag; DSPD has been called "social jet lag".
Comorbidity
Depression
In the DSPD cases reported in the literature, about half of the patients have had clinical depression or other psychological problems, about the same proportion as among patients with chronic insomnia. According to the ICSD:A direct neurochemical relationship between sleep mechanisms and depression is another possibility.
It is conceivable that DSPD has a role in causing depression because it can be such a stressful and misunderstood disorder. A 2008 study from the University of California, San Diego found no association of bipolar disorder with DSPD and states that
The fact that half of DSPD patients are not depressed indicates that DSPD is not merely a symptom of depression. Sleep researcher Michael Terman has suggested that those who follow their internal circadian clocks may be less likely to have depression than those trying to live on a different schedule.
DSPD patients with depression may be best served by seeking treatment for both problems. There is some evidence that effectively treating DSPD can improve the patient's mood and make antidepressants more effective.
Vitamin D deficiency has been linked to depression. As it is a condition which comes from lack of exposure to sunlight, anyone who does not get enough sunlight exposure during daylight hours could be at risk, without adequate dietary sources or supplements.
Attention deficit hyperactivity disorder
DSPD is genetically linked to attention deficit hyperactivity disorder, according to genetic polymorphism studies that have linked genes involved in ADHD to genes involved in circadian rhythm. A high proportion of people with ADHD have DSPD.Overweight
A 2019 study from Boston showed a relationship of evening chronotypes and greater social jet lag with greater body weight / adiposity in adolescent girls, but not boys, independent of sleep duration.Obsessive–compulsive disorder
People with obsessive–compulsive disorder are also diagnosed with DSPD at a much higher rate than the general public.Head injury
There have been several documented cases of DSPD and non-24-hour sleep–wake disorder developing after traumatic head injury. There have been cases of DSPD developing into non-24-hour sleep–wake disorder, a severe and debilitating disorder in which the individual sleeps later each day.COVID-19
, caused by the SARS-CoV-2 virus, has been observed to act as a comorbidity or aggravating factor in DSPD. Post-acute sequelae of COVID-19 often include neurological and autonomic dysregulation, which can interfere with circadian timing systems. These effects may involve delayed melatonin release, disrupted cortisol rhythms, and autonomic nervous system instability, all of which can exacerbate or prolong DSPD symptoms.Patients recovering from COVID-19 may also experience fatigue, reduced exposure to natural light, and irregular daily routines, which further contribute to circadian disruption. In individuals with pre-existing DSPD, COVID-19 can delay recovery and complicate treatment by reinforcing maladaptive sleep-wake cycles and reducing responsiveness to conventional circadian therapies such as bright light exposure and melatonin.
Mechanism
DSPD is a disorder of the body's timing system—the circadian clock. Individuals with DSPD might have an unusually long circadian cycle, might have a reduced response to the resetting effect of daylight on the body clock, or may respond overly to the delaying effects of evening light and too little to the advancing effect of light earlier in the day. In support of the increased sensitivity to evening light hypothesis, "the percentage of melatonin suppression by a bright light stimulus of 1,000 lux administered 2 hours prior to the melatonin peak has been reported to be greater in 15 DSPD patients than in 15 controls".The altered phase relationship between the timing of sleep and the circadian rhythm of body core temperature has been reported previously in DSPD patients studied in entrained conditions. That such an alteration has also been observed in temporal isolation supports the notion that the etiology of DSPD goes beyond simply a reduced capacity to achieve and maintain the appropriate phase relationship between sleep timing and the 24-hour day. Rather, the disorder may also reflect a fundamental inability of the endogenous circadian timing system to maintain normal phase relationships among physiological systems, and to properly adjust those internal relationships within the confines of the 24-hour day. In normal subjects, the phase relationship between sleep and temperature changes in temporal isolation relative to that observed under entrained conditions: in isolation, temperature minimum tends to occur toward the beginning of sleep, whereas under entrained conditions, temperature minimum occurs toward the end of the sleep period—a change in phase angle of several hours; DSPD patients may have a reduced capacity to achieve such a change in phase angle in response to entrainment.
Possibly as a consequence of these altered internal phase relationships, that the quality of sleep in DSPD may be substantially poorer than that of normal subjects, even when bedtimes and wake times are self-selected. A DSPD subject exhibited an average sleep onset latency twice that of the 3 control subjects and almost twice the amount of wakefulness after sleep onset as control subjects, resulting in significantly poorer sleep efficiency. Also, the temporal distribution of slow wave sleep was significantly altered in the DSPD subject. This finding may suggest that, in addition to abnormal circadian clock function, DSPD may be characterized by alteration in the homeostatic regulation of sleep, as well. Specifically, the rate with which Process S is depleted during sleep may be slowed. This could, conceivably, contribute to the excessive sleep inertia upon awakening that is often reported by those with DSPD. It has also been hypothesized that, due to the altered phase angle between sleep and temperature observed in DSPD, and the tendency for longer sleep periods, these individuals may simply sleep through the phase-advance portion of the light PRC. Though quite limited in terms of the total number of DSPD patients studied, such data seem to contradict the notion that DSPD is merely a disorder of sleep, rather than a disorder of the sleep system itself.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically help to advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPD have difficulty falling asleep before their usual sleep time, even if they are sleep-deprived. Sleep deprivation does not reset the circadian clock of DSPD patients, as it does with normal people.
Genetic factors
Researchers in 2017 linked DSPD to at least one genetic mutation. The syndrome usually develops in early childhood or adolescence. An adolescent version may disappear in late adolescence or early adulthood; otherwise, DSPD is a lifelong condition. The best estimate of prevalence among adults is 0.13–0.17%. Prevalence among adolescents is as much as 7–16%.In most cases, it is not known what causes the abnormality in the biological clocks of DSPD patients. DSPD tends to run in families, and a growing body of evidence suggests that the problem is associated with the hPer3 gene and the CRY1 gene.
For people who may have a circadian period significantly longer than 24 hours, a differential diagnosis may be warranted.