Neuroprotective Effects of Caffeine in Sleep Deprivation - Caffeine: Chemistry, Analysis, Function and Effects - page 291

precursors of crucial neurotransmitters involved in sleep regulation (e.g. 5-
HT). For instance, it has been shown that REM sleep depends on dietary
amino acid and subsequent protein synthesis and metabolism whereas,
restricted food intake increases sleep latency and diminishes NREM sleep
(Karklin et al 1994). These findings suggest that the CNS can sense nutritional
status and alter sleeping patterns accordingly. Increased energy status favors
sleep whereas diminished energy reserves, initially, increases slow wave sleep
(stages 3 and 4 NREM sleep) in order to conserve energy but later leads to
sleep loss and increased vigilance as energy stores approach depletion
(Nicolaidis 2006). The increase in vigilance reflects a shift in priorities for
the brain from conserving energy to actively searching for metabolic fuel to
replenish energy stores. Tryptophan, a 5-HT precursor, seems to plays crucial
role in modulating sleep latency and brain development in infants. In line with
this finding, a-lactalbumin, a type of milk with 80% less casein than whole milk
improves sleep even after 3-4 days of total food restriction by increasing
tryptophan transport and subsequent 5-HT synthesis in the brain. Moreover,
rats deprived of dietary tryptophan show a reorganization of sleep architecture
and diminished sleep circadian rhythm (Lanoir et al 1981). In addition, it has
been shown that SD increases brain serotonin levels which may be responsible
for subsequent sleep rebound (Grossman et al 2000).

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16.4 Sleep Deprivation
Sleep and its function have attracted the attention of scientists and
philosophers throughout history and its influence is pervasive in modern
societies as certain occupations or social constraints demand the prospect of
inadequate sleep. The ability to voluntarily sacrifice sleep for more time awake
is unique to humans and the health implications are far reaching.
Although sleep function is not completely understood at the moment, there
is no doubt that sleep is homeostatically regulated. Thus, the physiological
need for sleep is undoubtedly one of the strongest drives found in animals and
humans. Indeed, such a process must be vital if it is worth the risk of decreased
vigilance and vulnerability to predatory attack. Accordingly, the detrimental
effects of SD on different physiological aspects such as: immunological factors,
body temperature regulation, endocrine secretion patterns and learning and
memory processes reflect the homeostatic imbalance of the organism. As the
organism repeatedly attempts to restore homeostasis throughout the period of
''sleepy'' wakefulness the stress of being continuously awake becomes greater
and an allostatic load develops. The allostatic load represents a change in the
set point for homeostasis and was first characterized in blood pressure
dynamics. Rechstaffen's group were the first to characterize the SD syndrome
in rats that leads to death after 3-4 weeks of SD using the disk-over-water
method (Rechtschaffen et al 1983). After continuous total SD for 2-3 weeks, a
constellation of symptoms appears including an initial increase in body
temperature without a concomitant increase in energy expenditure followed by