SleepChart: Phase shift graph

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This text is part of: "Science of sleep" by Piotr Wozniak (2017)

Phase shift graph

The phase shift graph may be used by people in free running sleep suffering from ASPS or DSPS. This graph shows the degree of phase-shift as well as its dependence on the time of day. The graph can be used to see the expected bedtime given a specific natural waking time:

Phase shift graph shows the degree of phase-shift as well as its dependence on the time of day and can be used to see the expected bedtime given a specific natural waking time

Blue line shows the bedtime (vertical axis) for days with a given waking hour (horizontal axis). Red line shows the next day's waking hours (which are shifted by 1-2 hours in DSPS). Fuchsia and gray lines indicate the siesta period. Even though the red waking line begins at the origin of the graph, it shows a substantial phase shift at later hours (DSPS). From the presented exemplary graph one can read that for the waking time equal to 7 am (horizontal axis), the expected time to go to bed, as indicated by the blue line, is 1 am (vertical axis), while optimum siesta time occurs between 15:00 and 16:00. However, if the wake time is 11 am, the bedtime is likely to come only at 5 am the next day.

Remember! Each individual will have a his or her own unique graph. Moreover, the graph will look differently if it is taken at times of work or at times of summer vacation. It will be affected by stresses at work and at home. It may even change when you move from one house to another, or when you change the climate zone. The graph will accurately reflect your rhythm only if you adhere to free running sleep. If you use an alarm clock, this graph will be meaningless!

Correlates of sleep phase syndromes

It is not known which are the predominant underlying physiological factors that result in sleep phase disorders. Family clusters show that genes may affect the length of the circadian period. The lifestyle will affect the levels of neurotransmitters and via their impact on the sleep phase will affect the period of the circadian clock as well. Lifestyle also affects the timing of zeitgebers (e.g. late night web surfing in DSPS). Conversely, the level of neurotransmitters may select for a specific lifestyle choices. Age may have a direct impact on the clock circuits, it may affect neurotransmitters, or it can affect the lifestyle. Last but not least, sleep phase disorders will affect the mood and the levels of neurotransmitters in varying ways depending on whether free running sleep is used to remedy the disorder, or whether the individual attempts to fit a predetermined desirable sleep schedule.

Subsets of circadian rhythm sleep disorders (CRSDs) are strongly correlated with certain personality characteristics, and may have a strong genetic background. DSPS is more prevalent among adolescents, while ASPS is more frequently observed in an aging population. Women prevail in ASPS, while a slightly larger proportion of males suffer from DSPS (Sack et al. 2007[1]). Impaired vision often leads to DSPS due to a lesser impact of light on the circadian clock.

DSPS is by far more frequent among students, programmers, avid readers, passionate artists, writers, computer game addicts, etc. It is possible that the same characteristics that help individual's creativity may also lead to problems with falling asleep early. ASPS seems more likely in individuals whose life is deprived of intense stimulation (esp. in the evening), who meet fewer new challenges, who are less passionate about their job or hobbies, or who are not facing information overload and the related stress, etc. Perhaps this is why ASPS is more prevalent in the elderly. For hormonal reasons, its prevalence also shows a sharp increase around the time of menopause in women. ASPS tends to run in families. A number of genes have been identified to be involved in FASPS (familial ASPS)(see: Clock genes and mutations affecting the clock period(Golombek and Rosenstein 2010[2]).

There is a complex relationship between DSPS/ASPS and psychiatric disorders. 25% of people who could not maintain their 24h sleep-wake cycle were suffering from a psychiatric disorder (Hayakawa et al. 1998[3]). Some psychiatric disorders or the prescribed medication may induce DSPS, while, at the same time, DSPS conversely may cause various psychiatric symptoms. On one hand, there may be a link between DSPS and manic personalities. Anti-depressants tend to increase the period of the body clock (e.g. clorgyline, imipramine). On the other, paradoxically, DSPS individuals may be more likely to suffer from depression (e.g. when suffering from persistent insomnia, sleep deprivation, and the resulting social problems, etc.). Dr Daniel Kripke concluded that DSPS phenotype is familial and is associated with unipolar depression (Kripke et al. 2008[4]). However, the epidemic of DSPS in creative individuals suggests that those correlates need further investigation. Perhaps some contradictions can be explained by the fact that the state of mind of a DSPS sufferer depends largely on his or her ability to get sufficient and properly timed sleep? Thus more on a naturally manic side when sleep-satisfied, e.g. on a free running sleep schedule, and more on the depressed side when in circadian trouble (e.g. when forced to an early waking schedule)?

Similarly, low-stress tolerance depressed individuals are more likely to suffer from ASPS. Again, when they are forced to adapt to "normal" life, their symptoms of depression tend to weaken either due to a sense of higher productivity or due to the fact that mild sleep deprivation counteracts the depression. The cause-effect relationship between sleep phase disorders and mood disorders is complex. Understanding it will contribute substantially to mitigating the escalating epidemic of sleep problems.

References

  1. Sack R., Auckley D., Auger R.R., Carskadon M.A., Wright K.P., Vitiello M.V., Zhdanova I.V., "Circadian rhythm sleep disorders: Part II, advanced sleep phase disorder, delayed sleep phase disorder, free-running disorder, and irregular sleep-wake rhythm," SLEEP / Volume 30 / Issue 11 (2007):1484-1501
  2. Golombek D.A. and Rosenstein R.E., "Physiology of Circadian Entrainment," Physiological Reviews / Volume 90 / Issue 3 (July 2010): 1063-1102, doi: 10.1152/physrev.00009.2009
  3. Hayakawa T., Kamei Y., Urata J., Shibui K., Ozaki S., Uchiyama M., and Okawa M., "Trials of bright light exposure and melatonin administration in a patient with non-24 hour sleep-wake syndrome," Psychiatry and Clinical Neurosciences / Volume 52 / Issue 2 (261–262): 261-262
  4. Kripke D.F., Rex K.M., Ancoli-Israel S., Nievergelt C.M., Klimecki W., and Kelsoe J.R., "Delayed sleep phase cases and controls," Journal of Circadian Rhythms / Volume 6 / Issue 6 (2008), doi:10.1186/1740-3391-6-6