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7 Arousal States, Symptoms, Behaviour, Sleep … 199
males and females, and older and younger people, tend to use different
electronic devices and/or functions; thus, the effects of these devices may
tend to be different in different individuals.
Mechanistically, the effects ofbright light exposure oncircadian rhythm
functioning have been advanced to explain the tendency of electronic
devices to impair sleep [166, 171, 172]. Even exposure to ordinary indoor
room light has been shown to alter the circadian rhythm of core BT (e.g.
delayedpeakofcoreBT)[173] and to increase a person’s BT, even if they
are sedentary [174]. Thus, exposure to bright lights prior to bedtime may
delay a person’s circadian rhythm of sleep, melatonin secretion, and the
expected nocturnaldecline in BT [166,171, 172], all ofwhich are thought
to underpin the initiation of sleep. However, laptop use has been shown
to be linked to a >1 °C increase in scrotal temperature in men, regardless
of the leg position or use of a lap pad [175]. Thus, electronic device use,
including watching television[176] and laptop computer use[177], is also
associated with an elevated BT. As discussed in detail in Chapter 2,ifa
person practises sleep-disrupting behaviour at night which is linked to an
elevated BT (or reduced melatonin secretion), it may potentially interfere
with the onset of sleep.
Substance use has been shown to interfere with sleep onset and to exert
thermoregulatory effects, including a change in the circadian rhythm of
core BT and altered sleep patterns [178]. For example, alcohol intake leads
to an elevated BT, especially night-time alcohol use, which causes mild
hyperthermia (+0.36 °C) and reduces the circadian amplitude of core BT
by 43% in humans [179]. In contrast, a dose-dependent relationship h as
been shown to exist between morphine use andBT;for example, in a study
of rats, low-dose morphine elevated BT, whereas a high-dose morphine
reduced BT [113]. Thus, the nocturnal use of certain medicinal or non-
medicinal agents may potentially interfere with the onset of sleep, via an
increase in BT and/or an alteration in the sleep-wake cycle.
Antidepressanttherapies including antidepressantdrugs [180]andbright
light therapy have been shown to lower nocturnal BT (e.g. in seasonal
affective disorder patients) [181], whereas bright light therapy normalises
the circadian rhythm of core BT in anorexia and bulimia nervosa patients
[182]. However, thechronic administrationof selective serotoninreuptake
200 R. Brown and E. Thorsteinsson
inhibitors (SSRIs)can lead toan overall increasein BT [183],whereas elec-
troconvulsive therapy increases or decreases BT [184], and amphetamines
consistently elevate it [185]. Thus, it is possible that the chronic adminis-
tration of SSRIs can impair sleep (e.g. reduced slow-wave sleep) [178]via
an increase in BT, although to the author’s knowledge, such a premise has
yet to be examined.
Shift work (e.g. night shift, rotating shift) can impair sleep in shift
workers, relativeto daytime workers [186,187], especially if theytry tofall
asleep during the day at a time when their body is promoting wakefulness
[188, 189]. Shift work is also linked to high stress and affective distress
[190], including greater work stress and role overload [191]. Similarly,
young (but not older) male shift workers showed higher cortisol levels
than day workers [192], and they reported higher anxiety levels [193].
Further, a recent systematic review showed there is preliminary evidence
that shiftwork can contribute to weightgain over time [194]. Additionally,
shift workers are reported to show a smaller BT amplitude relative to day-
shift staff [195, 196], and the amplitude was smaller the more night-shifts
the workers completed over an eight-day period [196]. Finally, night shift
workers are reported to experience a delayed BT acrophase (by 4-hours),
relative today-shift workers, and the changes are linked to sleep disruption
and poor tolerance to shift work [195]. Thus, the nature of night shift
work, which typically involves sleeping during the day and working at
night, appears to conflict with the sleep-wake cycle and the circadian
rhythm of core BT. Circadian rhythm dysfunction is the mechanism by
which shift work is likely to interfere with a worker’s sleep, although some
adaptation may occur in long-term night shift workers.
In summary, a varietyof sleep-disrupting behaviours areknown to inter-
fere with sleep, and in many cases, they are also risk factors for anxi-
ety/depression and overweight/obesity, and they can potentially increase
a person’s BT. As discussed in detail in Chapter 2, if a person practises
sleep-disrupting behaviour at night which is linked to an elevated BT (or
reduced melatonin secretion), it may potentially interfere with the onset
of sleep. However,it is certainly appreciated that detecting a relationship/s
between certainstates, symptoms, disordersand behaviour isnot a demon-
stration of causality, even if the factors are longitudinally related to each
other. That is to say, just because two conditions are highly comorbid with
7 Arousal States, Symptoms, Behaviour, Sleep … 201
each other or concurrent with affective distress or a particular behaviour,
it does not imply that the distress or the behaviour was responsible for the
comorbidities. Furthermore, just because a phenomenon is consistently
linked to an elevated nocturnal BT, this does not necessarily mean that
an elevated BT has caused the observed relationship. However, in many
cases, there issubstantial evidence showing that the aforementioned states,
symptoms, disorders and behaviour are linked to an alteration in circa-
dian rhythm functioning in affected individuals. Such results do tend t o
suggest that the phenomena may, at least in part, be caused by circadian
rhythm dysfunction. There is insufficient space in this section to detail
the methodological and statistical limitations that accrue to correlational
research, in particular, its limited utility in helping us to fully appreciate
the nature of the linkages between comorbid conditions and concurrent
states, symptoms and behaviour, although such a detailed discussion is
provided in Chapters 2 and 8.
Finally, irrespective of these methodological and statistical considera-
tions, we have provided considerable evidence in this chapter which shows
that autonomic arousal (or affective states; e.g. stress, anxiety), symptoms
(e.g. fatigue, chronic pain), sleep-disrupting behaviour (e.g. physical inac-
tivity, electronic device use, TV watching, shift work) and medications
or non-medicinal substances are linked to impaired sleep and, in many
cases, also affective distress and overweight/obesity. In many cases, the
phenomena are also linked to an elevated BT, and in some cases, a high
nocturnal BT, although there is a lack of specific research pertaining to
nocturnal BT, and the relationship between BT and chronic pain. As dis-
cussed in detail in Chapter 2, a relative hyperthermia at night is known
to potentially interfere with sleep onset, possible via a phase-shift in the
sleep-wake cycle.However, anelevated BTcan also leadto activation ofthe
inflammatory response system (e.g. cytokine secretion), which may rep-
resent another possible mechanism by which the aforementioned states,
symptoms, disorders and behaviour can develop.
202 R. Brown and E. Thorsteinsson
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