xlvii. Distribution of early and late types

7 November 2009 at 02:23 | Posted in Circadian rhythm | 7 Comments
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Distribution, early and late types

The illustration above is adapted from Till Roenneberg et al., the team who invented the Munich Chronotype Questionnaire, MCTQ.  The MCTQ is a modern version of the Morningness-eveningness Questionnaire, MEQ, and it is considered to give the best estimate of morningness and eveningness chronotypes.  They have chosen to consider sleep onset at 00:30 and 01:00 as “normal” for the adult population.  Their results are 46.5% early types, 28.5% normal types and 25% late types — as shown in this table:

According to the illustration from MCTQ Percentage of population

Chronotype sleep time    % SUM
       
   EARLY TYPE  EXTREME> 2.0 % 20.30 – 04.30 < 0.5     46.5 %
21.00 – 05.00 < 0.5
21.30 – 05.30 < 0.5
22.00 – 06.00    2.0
     
MODERATE13.0 % 22.30 – 06.30    3.5
23.00 – 07.00    9.5
     
SLIGHT31.5 % 23.30 – 07.30  14.5  
00.00 – 08.00  17.0
         
         
NORMAL TYPE 00.30 – 08.30  16.0     28.5 %
01.00 – 09.00  12.5
         
         
   LATE TYPE 

 

SLIGHT15.0 % 01.30 – 09.30    9.0        

 

 

    25.0 %

02.00 – 10.00    6.0
     
MODERATE6.5 % 02.30 – 10.30    4.0
03.00 – 11.00    2.5
     
EXTREME> 3.5 % 03.30 – 11.30    2.0
04.00 – 12.00    1.0
04.30 – 12.30    0.5
05.00 – 13.00 < 0.5
05.30 – 13.30 < 0.5
         
SUM         100.0 %

But isn’t 1 AM rather late at night to be considered a “normal” bedtime?  In my opinion, normal sleepy time would be no later than 11:30 PM, midnight and perhaps 12:30 AM. 

Using my own idea of what is normal, I’ve reconstructed the table to show these results:  15% early types, 47.5% normal types and 37.5% late types, as shown here:

In my opinion, based upon their figures:

percentage of population

Chronotype sleep time    % SUM
       
   EARLY TYPE  EXTREME< 1.0 % 20.30 – 04.30 < 0.5     15 %
21.00 – 05.00 < 0.5
21.30 – 05.30 < 0.5
     
MODERATE5.5 % 22.00 – 06.00    2.0
22.30 – 06.30    3.5
     
SLIGHT9.5 % 23.00 – 07.00    9.5
         
         
NORMAL TYPE 23.30 – 07.30  14.5       47.5 %
00.00 – 08.00  17.0
00.30 – 08.30  16.0
         
         
   LATE TYPE 

 

SLIGHT21.5 % 01.00 – 09.00  12.5        

 

 

 

    37.5 %

01.30 – 09.30    9.0
     
MODERATE10.0 % 02.00 – 10.00    6.0
02.30 – 10.30    4.0
     
EXTREME6.0 % 03.00 – 11.00    2.5
03.30 – 11.30    2.0
04.00 – 12.00    1.0
04.30 – 12.30    0.5
05.00 – 13.00 < 0.5
05.30 – 13.30 < 0.5
         
SUM         100.0 %

So I’ve also redone the figure at the top of this page to reflect my opinion of what is early and late: 

 Distribution, early and late types

What time do you think “normal types” go to sleep at night?

See the Roenneberg 2007 review: Epidemiology of the human circadian clock.  See also the 5th comment below for an UPDATE.

Posted by Delayed2Sleep (aka “D”).

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Next: Guest blogger:  Breann (again)

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xlii. Researchers mentioned here

13 June 2009 at 18:05 | Posted in Circadian rhythm | 6 Comments
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Several researchers have been mentioned / cited here, and there’ll surely be more.  They are listed below. 

Bjorvatn, Bjørn (in post vii.), is a sleep researcher at the University in Bergen, Norway, and a co-founder of Bergen Sleep Center.

Czeisler, Charles A. (in post xliii.) has been researching circadian rhythms for several decades.

Dagan, Yaron  (in post xxxviii.) in Israel, often publishing together with Judith Abadi, stated in 2001: “Certain sleep-wake schedule disorders (SWSDs) cannot be successfully managed clinically (…).  …we propose new medical terminology for such cases–SWSD disability. SWSD disability is an untreatable pathology of the circadian time structure…  It is imperative that physicians recognize the medical condition of SWSD disability in their patients and bring it to the notice of the public institutions responsible for vocational and social rehabilitation.”  In almost all of his papers, he emphasizes that people with circadian rhythm disorders often are misdiagnosed because physicians don’t know (enough) about such disorders.  Here is a case study (abstract) about a 14-year-old boy whose other diagnoses fell as soon as his sleep disorder was diagnosed.  It should perhaps be obvious that I appreciate Dagan’s work and his opinion. 

DeCoursey, Patricia (in post xix.), is the grand old, grand old of the field of chronobiology.  In 1960 she invented the Phase Response Curve when the “daily” activity rhythms of her flying squirrels, kept in constant darkness, responded to pulses of light exposure. The response varied according to the time of day — that is, the animals’ subjective “day” — when light was administered. When DeCoursey plotted all her data relating the quantity and direction (advance or delay) of phase-shift on a single curve, she created the PRC. It has since been a standard tool in the study of biological rhythms.

Dijk and Lockley (in post v.).  Derk-Jan Dijk and Steven W. Lockley often publish together.  Dijk, who studies the regulation of sleep and circadian rhythms in humans, is director of the Surrey Sleep Research Centre in the UK.  Lockley, Assistant Professor of Medicine, Harvard Medical School, and Associate Neuroscientist in Sleep Medicine, Brigham and Women’s Hospital in the USA, is particularly interested in the effects of light on the circadian pacemaker in humans.

Horne and Östberg (in post xxxviii.) published their Morningness-Eveningness Questionnaire (MEQ) in 1976.   It is based on O. Öquist’s 1970 thesis at the Department of Psychology, University of Göteborg, Sweden: ”Kartläggning av individuella dygnsrytmer”, “Charting Individual Circadian Rhythms”.  This marks the beginning of modern research into chronotypes.  Olov Östberg modified Öquist’s questionnaire and, together with J. A. (Jim) Horne, he published the MEQ (pmid 1027738, abstract ) which still is used and referred to in virtually all research on this topic. 

Roenneberg, Till (in post xxxvii. and in post xlvii.), professor at the University of Munich, is one of the best-known chronobiologists in Europe, having received international prizes for both his research and his teaching.  He has built up the Centre for Chronobiology at the Munich Medical School with its database on the sleep of over 50 000 Europeans.  In 2008 in India he collaborated with and directed a project in Mangalore chronotyping the south Indian population, with data covering nearly 75 000 participants.  Roenneberg’s work ranges from the cellular/molecular mechanisms of the circadian clock to the consequences of shift work and, as mentioned, huge surveys.

Thorpy, Michael J. (post xxxii.), board certified in sleep medicine, is a sleep researcher and a professor of clinical neurology at the Albert Einstein College of Medicine in New York.  He has held high office in the National Sleep Foundation and in the Sleep Section of the American Academy of Neurology.  Thorpy was for many years editor of The International Classification of Sleep Disorders: Diagnostic and Coding Manual (ICSD) and has been publishing books and articles since the 1980s.

Uchiyama, Makoto (in posts xxxviii. and xxvii.), professor at the Nihon University School of Medicine in Tokyo and managing editor of Sleep and Biological Rhythms, the official English language journal of the Japanese Society of Sleep Research (JSSR), is a prolific co-author of studies on sleep, particularly on DSPS and Non-24, often in cooperation with Masako Okawa, chair of the Asian Sleep Research Society. (ASRS).  This research field is very active in Japan, where study subjects often are people with these disorders.  In the west, in contrast, studies are more often done on healthy, normal people with results extrapolated to effects in people with the disorders.  The Japanese researchers have shown, for example, that the interval between the lowest core body temperature and spontaneous awakening is much longer in people with Non-24 and DSPS than the “about two hours” which is considered normal.

Zivkovic, Bora, aka “Coturnix (in posts xxxvii.xxxiii.xviii. and  xv.), should have had his PhD by now but the ideal job came along and his dissertation isn’t getting done.  He tells about that and about chronobiology and about lots more at ScienceBlogs

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Next:  xliii. Blindfolding the blind

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xxxviii. Eveningness vs. DSPS

10 November 2007 at 07:00 | Posted in Circadian rhythm | 4 Comments
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“Well, I don’t like getting up before seven either,

but I have to, and I do.”

Implication: and you can, too.

But, is that true?

The article on Wikipedia about Chronotypes, morningness/eveningness, reports what researchers know so far about these normal variations, which have been studied since about 1970 and are measured by the Horne-Östberg questionnaire, the MEQ, a short version of which can be found online at Bruce Logie’s interesting site.

 
It can be interesting to compare normal evening types with what we know about people with Delayed Sleep-Phase Syndrome.

 
Normal, healthy sleepers can be morning types (up to 25%), intermediate types (50% or more) or evening types (up to 25%). Any of them can be classified as long sleepers or short sleepers in normal distribution. They have normal “sleep architecture”, as do most people with DSPS. 
 
Normal night owls who are good sleepers:
 
  • like to sleep in and don’t like to go to bed early.
  • are more alert in the evening than just after awakening, as opposed to morning types.
  • can take a nap at 10 a.m. or noon after a night with less sleep than usual, while morning types generally don’t want a nap until 2 p.m. or later.
  • experience both Dim-Light Melatonin Onset (DLMO) and the minimum of the daily cortisol rhythm later (clock time) than morning types.

So far, it sounds like people with DSPS are evening types, as the properties above apply to both groups. However, normal evening types:

  • after starting a new routine requiring them, for example, to start work earlier than before, will adjust their sleep-wake schedules to the new times within a few days.
  • awaken spontaneously earlier in their circadian phase than morning people; that is, the interval between the low point of the body temperature and wake time is shortest in evening types. In people with DSPS, it’s notably much longer than average.

People with DSPS do not adjust to a new schedule easily, if at all.

CRSD [circadian rhythm sleep disorders] patients differ from night or morning type people … in the rigidity of their maladjusted biological clock. While “owls” and “larks” prefer morning or evening, they are flexible and can adjust to the demands of the environmental clock. CRSD patients, on the other hand, appear to be unable to change their clock by means of motivation or education,” according to Dagan, 2002 (PDF, page 3).
 
Or, as Wikipedia puts it: Attempting to force oneself through 9 – 5 life with DSPS has been compared to constantly living with 6 hours of jet lag.”
 
Uchiyama et al, 1999, found that people with DSPS do not evidence normal recovery sleep after sleep deprivation. They conclude that “[t]his suggests that DSPS may involve problems related to the homeostatic regulation of sleep after sleep deprivation.
 
Some of the characteristics of normal evening types may or may not also be characteristic of people with DSPS. If these points have been reported in the literature about DSPS, I haven’t seen them:
  • Evening types have a core body temperature which is a bit lower than average, both day and night. Is this also true for people with DSPS?
  • Evening types have a melatonin profile which declines much more slowly after midpoint, as compared with morning types. Is this also true for people with DSPS?
  • Evening types take a long time to “get going” after awakening. In relation to the timing of spontaneous awakening, the following points contribute to this for evening types, and possibly also for people with DSPS:
  • the timing of lowest body temperature,
  • the timing of the cortisol minimum,
  • the timing of melatonin offset, and
  • the slower decline of blood levels of melatonin.  

We have a disorder which, without treatment, forces us to fall asleep even later than evening types. Simply trying to enforce conventional sleep and wake times does not advance the circadian markers. It seems almost impossible to wake us much earlier than our pre-programmed wake time (as my siblings will attest). The disorder is chronic, changing little or not at all after the age of 20.  

When normal chronotypes shift their schedules, all the body’s rhythms catch up and are synchronized to each other within a few days. In DSPS, the dissynchrony may continue as long as the shifted, “unnatural” schedule lasts, even for years or decades, leading to physical and psychological disorders.

It’s clear that people with DSPS who (try to) work days, have much the same set of problems that many shift workers have, whether these always work nights or are on a rotating schedule. However, shift workers’ problems receive sympathy and understanding while people with DSPS are commonly stereotyped as undisciplined and lazy. Dagan again (PDF, page 7), on adolescents, points out that “[f]requently, the patients’ parents, teachers, doctors, or psychologists believe that the patients’ biological sleep-wake problem and the accompanying dysfunction at school are motivational or psychological in nature, a belief that during the years, the patients tend to adapt themselves. This attitude toward CRSD patients, to which [they have] been subjected since early childhood or adolescence, adds psychological distress to the practical difficulties of coping with life.”

Like normal people, we do adjust (entrain) to the earth’s 24-hour rotation, but, without treatment, we don’t “learn” to wake up at a conventional, early time of day.

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Next:  xxxix. Guest Blogger

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xxxvii. Daylight Saving Time / Summer Time

27 October 2007 at 13:33 | Posted in Circadian rhythm | Leave a comment
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In 2005, Kazakhstan stopped using Summer Time (Daylight Saving Time, DST). Dr. Zaira Majitova, MD, said: “A human body has its own biological watch which runs synchronously with nature’s watch. When the human body is forced to readjust artificially, it leads to disturbances in the biological watch.” Doctors reported a long list of health complications resulting from the hour lost in the springtime.

In 2006, Finnish researchers at their National Public Health Institute published their study showing that the transition to daylight saving time reduces sleep duration by over an hour and reduces sleep efficiency by an average of 10%.

Now in 2007, scientists in Germany and Switzerland report: The Human Circadian Clock’s Seasonal Adjustment Is Disrupted by Daylight Saving Time. Two studies are here rolled into one.  First, data from a large survey which examined sleep patterns of 55 000 people in Central Europe were mined. Under standard time, sleep timing on free — usually weekend — days follows the seasonal progression of dawn. Under summer time, it does not.

In the second study, they analyzed the timing of sleep and activity for eight weeks around each of the two annual transitions in 50 people, taking into account each individual’s natural chronotype, ranging from morning larks to night owls. They found that the timing of both sleep and peak activity levels readily adjust to the release from DST in autumn, but that the timing of activity does not adjust to the start of DST in spring. In everyone, but especially in the night owl chronotypes, biological timing stays on standard (winter) time, while our social schedules must be adjusted to the advanced clock time throughout the summer. “When we implement small changes into a biological system which by themselves seem trivial, their effects, when viewed in a broader context, may have a much larger impact than we had thought,” says Till Roenneberg of Ludwig-Maximilian-University in Munich.

Both sleep times and daily activity patterns were tracked. The time of mid-sleep in the large population correlates with dawn under standard time but is widely scattered under DST. In the smaller study, daily activity patterns most clearly show the lack of adjustment to DST; sleep times show the same thing but to a lesser degree.

From the study report: “the human circadian clock tracks dawn under standard time but not under DST. Whereas the human clock … predictably advances from autumn to spring …, it remains locked to the same time between spring and autumn…. These results, in combination with those from the database, suggest that the incomplete adjustment of activity in larks and the nonadjustment in owls continues … throughout the months of DST.”

“Like other animals, humans are seasonal (in birth rates, mortality, suicide rates, etc.). However, seasonality in humans has drastically declined in industrialized countries over the last 60 years. The main reason for this is probably increased shielding from [nature], but DST might constitute an additional factor for the dissociation of human biology from the seasons.” I do so agree. Our circadian rhythms are primarily connected to dawn, not to sundown. A Wikipedia illustration shows very clearly how our exposure to the natural dawn cycle is changed by our use of daylight “saving” time.

Figure 4, “Relationship between Natural and Behavioral Light-Dark Cycles with and without DST” in the 2007 report linked to above, shows and explains the same thing. There, the “enforced delay of seasonal progression” is shown, and it’s pointed out that the “amplitude of the relationships as well as the degree of their perturbations by DST increase with latitude.”

A quarter of the world’s population is subjected to the one-hour time change twice a year, and the impact is still not understood. I’ve never liked DST, but I’ll let Coturnix say it for me: “In this day and age of around-the-clock life, global communications, telecommuting, etc., the clock-shifting twice a year has outlived its usefulness and should go the way of the dodo.”

I’m writing this blog post at exactly the wrong time of year, of course. All studies show that in the autumn, everyone fully adjusts to standard time within a week. It’s the transition in spring which causes problems.

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Next:  xxxviii. Eveningness vs. DSPS

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xii. Circadian rhythm disorders

27 November 2005 at 11:14 | Posted in Circadian rhythm | 6 Comments
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There are a great many sleep disorders. I read recently that an official list of them had been pared down to about 70. Many have to do with not getting enough sleep, or getting sleep of poor quality by several criteria. Some have obvious causes, such as chronic pain, frequent stops in breathing etc.

My interest is in the timing of sleep as my sleep seems otherwise normal. As the experts put it, I have normal “sleep architecture”. (For a good, short explanation of sleep architecture — stages and brain waves — see this page from Feinberg School of Medicine at Northwestern University in the USA.)

Nearly all of us can reset our clocks daily, adjusting the various rhythms to 24 hours. As much as I’ve read about it, I’ve not found a good enough explanation for being able to adjust to 24 hours while not being able to adjust to sleeping midnight to eight or so.

I’m not immune to the light/dark cycle. I need to get up at noon. I fly 8 hours east or west, go through jet lag like anyone else and within days I need to get up at noon in the new location. This is built in. I’m not the only one. I’d just like to understand it better.

A Japanese paper (2004) suggests these possible mechanisms:

  • reduced sensitivity of the oscillator to photic entrainment,
  • an intrinsic period beyond the range of entrainment to the 24 hour day, and
  • abnormal coupling of the sleep/wake cycle to the circadian rhythm.

 

The least common and most debilitating circadian disorder is the one where body temperature, melatonin secretion, sleep and other rhythms vary several times a day, in and out of phase with one another, so called Irregular Sleep/Wake Disorder. This has been reported in humans who’ve been in accidents and had physical injuries to the hypothalamus. It’s also been provoked by surgery in lab animals.

One of the most rare disorders which occurs naturally is called Non-24. Sufferers simply(?) live on a 23, 25 or 26 hour cycle, getting up one hour later each day for example, thus coming in sync with the earth’s rotation every few weeks. Their rhythms are in sync internally, just not with the light/dark cycle outside. Most, but not all, of these people are blind. 

ASPS, Advanced Sleep-Phase Syndrome, is also rare. These people fall asleep and awaken much earlier than normal. The disorder runs in families, and an American family has been studied intensively the last few years. Research on their genetic mutation was published in 2001. “Detailed sequence studies of the candidate human gene, hPer2, in the affected family members, revealed a key change in a single amino acid — from serine to glycine — at position 662 in the hPer2 protein.” The alteration “occurred in the portion of the hPer2 protein that governed binding to an enzyme called casein kinase one-epsilon (CK1e ).” In animal models, this enzyme regulates “proteins involved in controlling the length of circadian rhythms.”

Now this is beyond me, but it would appear that these disorders may be genetically programmed. Though ASPS is rare, it seems reasonable that researchers start there, since one can compare the DNA of people who are related to one other.

DSPS, Delayed Sleep-Phase Syndrome, is a bit more common. Studies indicate that somewhat more than one in a thousand adults have DSPS (Japan 0.13%, Norway 0.17%). It runs less commonly in families, but it doesn’t seem unreasonable to guess that its cause may be similar to that of ASPS.
 
Clearly, anyone whose health cannot tolerate frequent forced awakening earlier than 10 a.m., will have few real choices in our society. Thus, hardcore (inflexible) DSPS must be considered a disability.

Another disorder which may be related to the others is Seasonal Affective Disorder, SAD. Sufferers are normal in summer, have problems of mood, weight gain etc. when days get shorter and can often be treated successfully by bright light therapy. It seems likely that they may have a mild form of ASPS or DSPS which is “treated” by morning/evening daylight when days are long.

Diurnal preference, spoken of as “morningness”, larks, and “eveningness”, owls, is also a subject of study, the field of chronobiology. This is, reasonably enough, connected to one’s circadian rhythms. However, it does not appear that ASPS is an extreme morningness chronotype nor DSPS an extreme eveningness chronotype. The internal relationships among the various rhythms do not place these conditions on a simple continuum.

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Next post:  xiii. DSPS-sleep

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