xlvii. Distribution of early and late types
7 November 2009 at 02:23 | In Circadian rhythm | Leave a CommentTags: Chronotype, Eveningness, MEQ, Morningness, Prevalence

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:
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According to the illustration from MCTQ Percentage of population |
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| 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 | |||
| EXTREME
6.0 % |
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:

What time do you think “normal types” go to sleep at night?
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Next: ~coming soon~
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xlvi. Guest Blogger: Breann Hays
11 October 2009 at 21:15 | In Circadian rhythm | Leave a CommentTags: DSPS, Guest blogger
This post was written in response to one whose author also lives on a very strict schedule and thereby feels that he has “defeated” his circadian rhythm disorder. Breann feels a bit differently about it. Thanks, Breann, for letting me use this!
I wouldn’t say that I’ve beaten DSPS. I know that as soon as I stop doing everything right all the time, things will go back to the way they were. I’ve been on the early morning schedule for about four months now, and my friends and family are really happy for me because they’ve never seen me do it for this long before. (Sad but true :p)
But they also seemed to think that I would somehow have cured myself doing it … conveniently around the time they are getting sick of the unyielding restrictions on my time.
One recently asked how much longer I would have to keep it up. I said I was looking for new chromosomes, but they didn’t seem to have any at the store :( Then I felt bad for being mean, but it made me mad that she seemed to think that just because I was doing things differently it was going to really change anything.
Like I haven’t tried doing things differently a million times… I have to keep reminding people that I have known how to operate an alarm clock for a long time, that’s not the part I had to learn… and none of this changes anything REALLY.
DSPS is a condition, not a habit.
Then she got kind of depressed and said it seems like a lot of work for nothing, then I got kind of depressed because it is… But, oh well, at least I can say that I have a much better chance of at least graduating school.
I haven’t beaten anything… I am just able to cope a lot better now. And it took 3 years to get it down, too!
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xlvii. coming soon
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xliv. Rods and cones and the “new” ipRGC
30 July 2009 at 20:16 | In Circadian rhythm | 2 CommentsTags: Melanopsin, Retina, Retinal ganglion cells, Retinohypothalamic tract, Rods and cones, SCN, Suprachiasmatic nuclei, Suprachiasmatic nucleus
We learned in middle school that there are two, and only two, types of light sensitive cells in the retina, rods and cones, right? Right, that’s what we learned. Could be the science teachers are still saying that, since the third type was discovered within the last decade.

Mammalian retina
The mammalian retina consists of many layers. One might think that light would first strike the rods and cones, the photosensitive cells we use for vision. But our retina is “inside out” compared to the more logical layout found in the octopus and its relatives; light in our eyes must travel through the many retinal layers to reach our rods and cones.
One of the first layers the light reaches is composed of the one and a half million ganglion cells, most of which are involved in processing visual (image forming) information. Fewer than 25000, some say just a couple thousand, of these cells are themselves sensitive to light. They function as light meters and they function much more slowly than the rods and cones, not registering abrupt fluctuations in light intensity. These cells project their axons to several brain centers including the suprachiasmatic nuclei, SCN, the “body clock” through the retinohypothalamic tract. They thus provide the major clue for the adjustment of the body clock. The incoming information about light intensity is also used to adjust pupil size (narrowing of pupils in bright light) and to regulate physical activity and melatonin synthesis.
Newly discovered, they are called by many names:
- intrinsically photosensitive Retinal Ganglion Cells (ipRGC, also pRGC)
- photosensitive ganglion cells
- melanopsin-containing retinal ganglion cells
- melanopsin-expressing retinal ganglion cells (mRGC)

Late in the previous century, scientists weren’t sure that there existed ipRGCs, and those who thought that they do exist were arguing about what opsin, what pigment, they use. Is it melanopsin or one of the cryptochromes, which also respond to blue light? One argument against melanopsin was that it resembles invertebrate opsins and differs from other opsin photopigments found in vertebrates.
Again, as with our hormone melatonin, it was research on specialized light-sensitive cells of frog skin which provided answers.
It has been known for a while that even when vision is lost, the light-sensitive ganglion cells may function perfectly. Recent research on mice at Salk Institute shows that the opposite also is true. A way was found to knock out the ipRGCs while leaving the rods and cones alone. The mice became arrhythmic, but still could see.
One of the researchers speculates: “It is entirely possible that in many older people a loss of this light sensor is not associated with a loss of vision, but instead may lead to difficulty falling asleep at the right time.”
Update: I’ve just discovered a wonderful post, Why can’t human eyes detect all wavelengths?, on the blog of Xenophilius Lovegood (!?). Xeno, claiming to be “a slightly mad scientist”, explains the physical / chemical / electrical changes in the rods and cones as they react to light. He also has a bit about the ipRGCs. Recommended.
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Next: (coming soon)
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xliii. Blindfolding the blind
9 July 2009 at 00:54 | In Circadian rhythm | Leave a CommentTags: Body clock, Circadian rhythm, Core body temperature, Melatonin

Blindfolding blind people sounds like an oxymoronic exercise. But it is clear that some people with no visual light perception, do, in fact, entrain normally. I believe it was Charles A. Czeisler who, about 1980, discovered that some blind people entrain normally to the 24-hour light/dark cycle while others do not.
He and colleagues worked with a number of blind people throughout the 1990s, reporting the results in such papers as this one from 1995 and this one from 1998.
These researchers, as well as others, worked on determining the circadian periods of individuals by the use of forced desynchrony, so-called constant routines. Conditions which are impossible to entrain to, allow mapping of body temperatures and melatonin levels.
The illustration above, from the 1995 paper, shows two days and nights in the lives of a sighted (above) and a blind (below) *person. They call this the “Melatonin Suppression Test”. Circadian phase is determined in the first night: the high point of the level of melatonin in the blood corresponding more-or-less to the low point of the core body temperature. The second night both subjects are submitted to 90 minutes of bright light (the white columns) at the time of their highest melatonin levels the night before. And the melatonin levels go way down in both subjects!
In a repeat of the test with the blind person blindfolded, the light had no effect. Obviously, somehow, the light signal makes it to the body clock in some blind people. More about how this works, for all of us, in the next post.
* (It seems to me to be not-too politically correct to call healthy volunteers “subjects” and healthy blind people “patients”. Czeisler et co will have to answer for that.)
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Next: xliv. Rods and cones and the “new” ipRGC
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xl. The post-lunch dip
6 June 2008 at 16:10 | In Circadian rhythm | Leave a CommentTags: Body clock
Sleep timing, when not manipulated too badly, is controlled by body clock and homeostasis. Homeostasis starts building a need for sleep as soon as we wake up for the day, but at first it’s easy to ignore. For a normal or lark sleeper, that means until sometime between noon and two. At that point the body clock kicks with a need for wake which builds until just before bedtime. The sleep gate, a term used by some researchers, then opens and sleep occurs.
During about the first half of the night, one sleeps away the built-up sleep need (as controlled by homeostasis). Some people wake up for a time at that point, which researchers are starting to see is normal and not a problem.
Then, normally about 2 a.m., the body clock kicks in with an intense sleepiness which dissipates through the next 4 hours.
So a normal lark is sleepy at 10pm (body clock’s need for wake gets turned off). The day’s sleep debt is paid off by about 2am when the body clock turns on a need for four hours more sleep. Happy lark awakens at 6am, raring to go, when neither homeostasis nor body clock craves sleep.
In theory, the body clock should kick in with its need for wake just before a big sleepiness hits at 2pm, but there’s often a bit of a delay, probably culturally encouraged in areas using the siesta, and that included/includes many agrarian cultures far from Iberia. It is known that humans without electric light often experience an hour or two of wake in the middle of the night. (Said to be good for meditating, socializing and sex, not to mention nursing the baby.)
Thus, normal people are most intensely sleepy at 2pm and at 2am.
So! It seems reasonable to me to apply this 12 hour difference to people with Delayed Sleep-Phase Syndrome, at least those who aren’t totally desynchronized internally. Take the classical DSPS example of sleeping 4am to noon. At 8am, the body clock has just turned on its intense need for continued sleep (making it impossible to hear an alarm clock or three). At noon we awaken (not quite as bushy-tailed as the lark was at 8am, perhaps because society has told us all our lives that “sleeping in” is BAD!).
Twelve hours after the intense need for sleep at 8am, we may experience the sleepy “after-lunch dip” at around 8pm. All times are approximate.
This explains, I think, why the long naps I used to take at 6 or 7pm abruptly ended at 10pm or so. Very tired larks may be able to sleep a couple-three hours at siesta time, but they won’t sleep for 8 hours then. Same with me; if I haven’t been up the previous 36+ hours, I won’t sleep longer than about four hours at my “siesta time”.
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Next: xli. Coincidence & update
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xxxix. Guest Blogger
6 December 2007 at 16:42 | In Circadian rhythm | Leave a CommentTags: Guest blogger, Non-24
Every now and then, someone on the mail list for DSPS and Non-24 just says it so well, often in a rant. I fell for this one by J., who has Non-24-hour sleep-wake syndrome. By permission:
I am so sick of people viewing me as crazy and lazy, which, seriously, has been the case since this whole n24 thing hit when I was a teenager.
But now at least I KNOW and can EXPLAIN how maybe I’m not lazy after all. And, no, not a junkie either! In fact the ones feeding me the drugs… who was that?! DOCTORS. My sleep will never be normal. Trying to force it with daily drugs, morning and night, was wrong. Maybe my neurology in general will never be normal. My perception may never be normal.
I have finally started to accept it because that is the right thing to do. The doctors need to get on board with this if they want to “do no harm”.
xxxviii. Eveningness vs. DSPS
10 November 2007 at 07:00 | In Circadian rhythm | 1 CommentTags: Chronotype, Circadian rhythm, Core body temperature, Cortisol, DLMO, DSPS, Eveningness, Jet lag, Melatonin, MEQ, Morningness, Shift work, Sleep architecture, Sleep deprivation

“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?
- 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.
- 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:
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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