Posted by: Chris Maloney | November 7, 2011

Time: A Consensus Rather Than a Fact. But Is It Unhealthy?

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With the abrupt switch of an hour, I am again reminded with the sheer arbitrariness of this thing we call time.  Oh, and by the way, it isn’t based on anything.   Really, it’s a convention.  Keep reading.

I read that we’re considering a move to atomic time rather than Greenwich mean timeA bit of a to-do in Greenwich, and some hand wringing over the loss of “Victorian Superpowerhood,” in England.  I think that ship has sailed, gents.

Right now, we adjust the atomic clocks to human time, whatever that may mean.  It seems very fluid, almost as fluid as flipping our clocks around to give ourselves more light.

So if you are late, the next time someone yells out:  “Do you know what time it is?”  Simply shrug and say:  “None of us really knows what time it is.”  That ought to get you either a good slap or a metaphysical discussion.

It made me curious about the whole concept of time and how healthy it is.  We already know that shift workers and night shift people in particular have health problems.  What is the true circadian rhythm of a human being?

It depends.  The rhythm is approximately twenty four hours, and is judged by checking various hormone levels.  The trouble is that even a single night’s sleeplessness is enough to disrupt those hormones.  So the rhythm of an individual’s CLOCK gene expression (their real, scientific name) is both a cause and effect of hormonal expression.

Variations in sleep definitely affect hormones, which in turn affect the immune system and the body’s abilities to make decisions.  So moving an entire country by an hour is both foolish and probably unhealthy.  Might I suggest the half-hour hop in two parts?  Or do away with it entirely and -gasp- have people schedule things according to when the sun rises.  Isn’t that what we’re trying to do anyway, and not really succeeding?

Here’s the data on time:

Chronobiol Int. 2011 Apr;28(3):204-15.

Hepatic, duodenal, and colonic circadian clocks differ in
their persistence under conditions of constant light and in their entrainment
by restricted feeding.

Polidarová L, Sládek M, Soták M, Pácha J, Sumová A.

Source

Departments of Neurohumoral Regulations, Institute of
Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic.

Abstract

Physiological functions of the gastrointestinal tract (GIT)
are temporally controlled such that they exhibit circadian rhythms. The
circadian rhythms are synchronized with the environmental light-dark cycle via
signaling from the central circadian clock located in the suprachiasmatic
nucleus (SCN) of the hypothalamus, and by food intake. The aim of the study was
to determine the extent to which disturbance in the SCN signaling via prolonged
exposure to constant light affects circadian rhythms in the liver, duodenum,
and colon, as well as to determine whether and to what extent food intake can
restore rhythmicity in individual parts of the GIT. Adult male rats were
maintained in constant light (LL) for 30 days and fed ad libitum throughout the
entire interval or exposed to a restricted feeding (RF) regime for the last 14
days in LL. Locomotor and feeding behaviors were recorded throughout the
experiment. On the 30th day, daily expression profiles of clock genes (Per1,
Per2, Rev-erbα, and Bmal1) and of clock-controlled genes (Wee1 and Dbp) were
measured by real-time reverse transcriptase-polymerase chain reaction (RT-PCR)
in the duodenum, colon, and liver. By the end of the LL exposure, rats fed ad
libitum had completely lost their circadian rhythms in activity and food
intake. Daily expression profiles of clock genes and clock-controlled genes in
the GIT were impaired to an extent depending on the tissue and gene studied,
but not completely abolished. In the liver and colon, exposure to LL abolished
circadian rhythms in expression of Per1, Per2, Bmal1, and Wee1, whereas it
impaired, but preserved, rhythms in expression of Rev-erbα and Dbp. In the
duodenum, all but Wee1 expression rhythms were preserved. Restricted feeding
restored the rhythms to a degree that varied with the tissue and gene studied.
Whereas in the liver and duodenum the profiles of all clock genes and
clock-controlled genes became rhythmic, in the colon only Per1, Bmal1, and
Rev-erbα-but not Per2, Wee1, and Dbp-were expressed rhythmically. The data
demonstrate a greater persistence of the rhythmicity of the circadian clocks in
the duodenum compared with that in the liver and colon under conditions when
signaling from the SCN is disrupted. Moreover, disrupted rhythmicity may be
restored more effectively by a feeding regime in the duodenum and liver
compared to the colon.

PMID: 21452916

Eur J Neurosci. 2009 May;29(9):1820-9. Epub 2009 Apr 28.

Circadian clock genes and sleep homeostasis

Franken P, Dijk DJ.

Source

Center for Integrative Genomics, University of Lausanne,
Lausanne-Dorigny, Switzerland. paul.franken@unil.ch

Abstract

Circadian and sleep-homeostatic processes both contribute
to sleep timing and sleep structure. Elimination of circadian rhythms through
lesions of the suprachiasmatic nuclei (SCN), the master circadian pacemaker,
leads to fragmentation of wakefulness and sleep but does not eliminate the
homeostatic response to sleep loss as indexed by the increase in EEG delta
power. In humans, EEG delta power declines during sleep episodes nearly
independently of circadian phase. Such observations have contributed to the
prevailing notion that circadian and homeostatic processes are separate but
recent data imply that this segregation may not extend to the molecular level.
Here we summarize the criteria and evidence for a role for clock genes in sleep
homeostasis. Studies in mice with targeted disruption for core circadian clock
genes have revealed alterations in circadian rhythmicity as well as changes in
sleep duration, sleep structure and EEG delta power. Clock-gene expression in
brain areas outside the SCN, in particular the cerebral cortex, depends to a
large extent on prior sleep-wake history. Evidence for effects of clock genes
on sleep homeostasis has also been obtained in Drosophila and humans, pointing
to a phylogenetically preserved pathway. These findings suggest that, while
within the SCN clock genes are utilized to set internal time-of-day, in the
forebrain the same feedback circuitry may be utilized to track time spent awake
and asleep. The mechanisms by which clock-gene expression is coupled to the
sleep-wake distribution could be through cellular energy charge whereby clock
genes act as energy sensors. The data underscore the interrelationships between
energy metabolism, circadian rhythmicity, and sleep regulation.

PMID: 19473235

J Neurosci. 2009 Jun 24;29(25):7948-56.

Functional magnetic resonance imaging-assessed brain
responses during an executive task depend on interaction of sleep homeostasis,
circadian phase, and PER3 genotype.

Vandewalle G, Archer SN, Wuillaume C, Balteau E, Degueldre
C, Luxen A, Maquet P, Dijk DJ.

Source

Cyclotron Research Centre, University of Liège, B-4000
Liège, Belgium.

Abstract

Cognition is regulated across the 24 h sleep-wake cycle by
circadian rhythmicity and sleep homeostasis through unknown brain mechanisms.
We investigated these mechanisms in a functional magnetic resonance imaging
study of executive function using a working memory 3-back task during a normal
sleep-wake cycle and during sleep loss. The study population was stratified
according to homozygosity for a variable-number (4 or 5) tandem-repeat
polymorphism in the coding region of the clock gene PERIOD3. This polymorphism
confers vulnerability to sleep loss and circadian misalignment through its
effects on sleep homeostasis. In the less-vulnerable genotype, no changes were
observed in brain responses during the normal-sleep wake cycle. During sleep
loss, these individuals recruited supplemental anterior frontal, temporal and
subcortical regions, while executive function was maintained. In contrast, in
the vulnerable genotype, activation in a posterior prefrontal area was already
reduced when comparing the evening to the morning during a normal sleep-wake
cycle. Furthermore, in the morning after a night of sleep loss, widespread
reductions in activation in prefrontal, temporal, parietal and occipital areas
were observed in this genotype. These differences occurred in the absence of
genotype-dependent differences in circadian phase. The data show that dynamic
changes in brain responses to an executive task evolve across the sleep-wake
and circadian cycles in a regionally specific manner that is determined by a
polymorphism which affects sleep homeostasis. The findings support a model of
individual differences in executive control, in which the allocation of
prefrontal resources is constrained by sleep pressure and circadian phase.

PMID: 19553435

Am J Physiol. 1998 Aug;275(2 Pt 1):E243-8.

Effect of the shift of the sleep-wake cycle on three robust
endocrine markers of the circadian clock.

Goichot B, Weibel L, Chapotot F, Gronfier C, Piquard F,
Brandenberger G.

Source

Laboratoire des Régulations Physiologiques et des Rythmes
Biologiques chez l’Homme, Institut de Physiologie, 67085 Strasbourg Cedex,
France.

Abstract

To determine the effect of a phase shift in sleep on the
circadian clock, thyroid-stimulating hormone (TSH), cortisol, and melatonin,
three robust markers of the circadian clock, were analyzed using a 10-min blood
sampling procedure. In an initial experiment eight subjects were studied during
two experimental sessions: once under baseline conditions with normal nighttime
sleep from 2300 to 0700 (baseline) and once after a night of sleep deprivation
followed by daytime sleep from 0700 to 1500 (day 1). In a second experiment,
carried out on seven subjects, the 24-h hormone profiles of the first day (day
1) were compared with those of the second day (day 2) of the sleep shift.
During the night of sleep deprivation (day 1) the TSH surge was higher than
during baseline conditions, whereas melatonin and cortisol rhythms remained
unaffected. On day 2 the amplitude of the nocturnal TSH surge was reduced in
comparison to day 1, whereas the amplitudes of melatonin and cortisol rhythms
were unchanged. There was a clear phase shift in the three endocrine rhythms.
Triiodothyronine levels were slightly higher in the morning after the first
night of sleep deprivation. These results demonstrate that 2 consecutive days
of sleep shift are sufficient to affect the timing of the commonly accepted
circadian markers, suggesting the existence of a rapid resetting effect on the
circadian clock. TSH reacts in a distinctive manner to the sleep-wake cycle
manipulation by modulating the amplitude of the nocturnal surge. This amplitude
modulation is probably an integral part of the phase-shifting mechanisms
controlled by the circadian clock.

PMID: 9688625


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