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58 R. Brown and Y. Umar
covered in this book are not only highly concurrent with each other; but
a similar range of risk factors tends to exist for each of the comorbid
conditions. That said, it is not exactly clear what this pattern of over-
lapping risk factors really means. It might indicate that a similar array
of risk factors can contribute to the development of multiple different
comorbid conditions. However, myriad different potentially bidirectional
linkages may exist between the various risk factors and the disorders in
different individuals. Alternately, the same risk factors may exert d iffer-
ential effects on the different disorders, due to interactions between the
various risk factors and protective factors. For example, night-eating may
contribute to impaired sleep over time, but it may only contribute to
overweight/obesity if the eating is more akin to binge-eating, in terms of
the quantity of food that is consumed at night. Alternately, it is possible
that night-eating tends to occur in the context of stress/affective distress,
whereas binge-eating is more strongly linked to perceptions of body image
and feelings of affective distress. However, irrespective of the cause/s, there
is a pressing need to better understand the complex dynamics that likely
underpin the relationship between sleep problems, disordered eating, and
overweight/obesity.
3.4 Overweight/Obesity, Disordered Eating,
Sleep, and Body Temperature
As detailed above, overweight/obesity is highly concurrent with disor-
dered eating (e.g. binge-eating and night-eating) and impaired sleep, but
the precise mechanism/s underpinning the relationship are unclear. How-
ever, it is evident that obese people are more likely to eat late at night
than normal-weight individuals [57, 89], thus, late night-eating may at
least partly explain the observed relationship between overweight/obesity
and impaired sleep in affected individuals. Late night-eating (and binge-
eating) are known to be linked to impaired sleep (e.g. longer sleep onset
latency) [84, 101] and weight gain in obese people [91, 100], and clin-
ically, obese people are at an increased risk of a BED diagnosis [112]
and/or NES diagnosis [113]. A similar profile of sleep deficits is also
evident in overweight/obese people, binge-eaters, and night-eaters, and
3 Overweight/Obesity and Concurrent Disorders… 59
impaired sleep (e.g. short sleep duration) is reported to be associated with
overweight/obesity, night-eating, and binge-eating [18, 69] including a
longer sleep onset latency [84]. However, the sleep problems appear to
resolve after the person has lost weight, suggesting that they are function-
ally related to the person’s weight [114].
Thus, it is possible that the sleep problems experienced by over-
weight/obese people are at least in part due to the indirect effects of late
night-eating and/or binge-eating, but it is less clear exactly how this might
occur. Yeh and Brown [89] evaluated the relationship between night-
eating, binge-eating, sleep quality, and BMI in a community-derived sam-
ple. The results showed that binge-eating partly mediated the relationship
between poor sleep quality to high BMI, whereas night-eating mediated
the relationship between high BMI to poor sleep quality; although the
results were only cross-sectional. Nevertheless, the results suggest that late-
night eating may impair a person’s ability to fall asleep and while they wait
for sleep to come, if they engage in binge-eating, then this might lead
to weight gain over time, although other interpretations are possible, as
detailed below.
Several biological mechanisms have been proposed to explain the rela-
tionship between disordered eating, overweight/obesity, and impaired
sleep, including an elevated BT. For example, perturbations in BT have
been shown to be linked to overweight/obesity, although the results tend
to be contradictory. Some studies show that overweight/obesity (or proxy
measures of it) is positively correlated with BT; for instance, high BMI was
associated with high tympanic temperature [115]. Similarly, in another
study, mean BT was 36.1 ± 0.4, 36.4 ± 0.4, and 36.3 ± 0.4 °C in
men, premenopausal, and postmenopausal women, respectively; and BT
was positively correlated with BMI, waist, waist-to-hip ratio, body area,
resting heart rate, glucose and insulin levels, in men and postmenopausal
women, but in premenopausal women, BT was positively correlated only
with restingheart rate and insulin and the factorswere nolonger significant
after multivariable adjustment [115]. Further, Obermeyer and colleagues
[116] showed, based on 243,506 temperature measurements obtained
from 35,488 patients who had not received an infection diagnosis and
were not prescribed antibiotics, that the mean BT was 36.6°C, although
it was lower in older people and higher in women. High BT was also
60 R. Brown and Y. Umar
linked to higher BMI and cancer diagnosis, whereas low BT was detected
in patients with hypothyroidism. Interestingly, the unexplained variation
in BT predicted later mortality risk; specifically, an increase of 0.15°C was
linked to an 8.4% increase in mortality risk 1 year later. Taken together,
the results suggest that overweight/obesity is associated with higher BT.
However, in several studies, overweight/obesity (or proxy measures of
it) was shown to be negatively correlated with BT; for example, high body
mass was correlated with low oral temperature [117], whereas h igh BMI
was correlated with low tympanic temperature in men [118]. In contrast,
core BT was similar in overweight/obese adults vs. normal-weight adults,
using wireless temperature-sensing capsules to continuously monitor core
BT [119]. Nevertheless, a larger study of 18,630 adults aged 20–98 years
showed that obesity was correlated with high mean BT in every age group,
after controlling for sex, BMI, and white cell count. BT tended to decrease
with advancing age (0.3°F lower in oldest vs. youngest) and it was slightly
higher in females than in males [120]. Taken together, the results for BT
and overweight/obesity are somewhat contradictory, but in most studies,
and in the largest studies, obesity (or proxy measures of it) was linked to
higher BT. Furthermore, it is noteworthy that people with low BT tend
to live longer than those with an elevated BT, as shown in the Baltimore
Longitudinal Study of Aging Men [121].
So what might explain the conflicting results for BT and over-
weight/obesity? As suggested by Bastardot et al. [115], the disparate results
may be due to differences in the study samples (e.g. gender, menopausal
status, autonomic arousal, and/or hormonal secretion). However, themost
compelling explanation is related to eating behaviour, in particular, late-
night eating [72]. Quite simply, eating is thermogenic; that is, it increases
BT regardless of the time of day that the food is consumed, whether
it is during the day or night. For example, normal-weight unrestrained
eaters showed an elevated liver temperature (0.8–1.5°C) from the start of
a meal to 60–90 minutes later, whereas overweight and normal-weight
restrained eaters showed a lack of a change in their post-lunch BT [122].
This result suggests that eating naturally leads to the production of body
heat, although the rate and pattern of the food intake (e.g. restrained eat-
ing) may affect the person’s post-meal thermogenesis. Taken together, the
results suggest that BT increases in anticipation of eating, remains elevated
3 Overweight/Obesity and Concurrent Disorders… 61
during a meal, and then declines an hour or so after eating, but this may
be different in overweight/obese individuals or those who tend to restrict
their eating.
In this regard,the Islamicpractice ofabstaining fromfood anddrink (i.e.
fasting) during daylight hours, and consuming food in the evening during
Ramadan, has provided a unique opportunity to examine the potential
effects of late night-eating on BT and sleep. For example, BaHammam
and colleagues [123] showed that during Ramadan, bedtime and wakeup
times were delayed and there was a significant reduction in total sleep
time (which slightly decreased from the first to third weeks of fasting)
in Muslims but not non-Muslims, but there was no increase in daytime
sleepiness. In a smaller study, BaHammam [124] showed that fasting dur-
ing the first three-weeks of Ramadan in healthy Muslim medical students
was related to the delayed onset of bedtime, a significant delay in wakeup
time, greater daytime sleepiness, and a (non-significant) shortening of
sleep, relative to baseline. Similarly, BaHammam and colleagues [125]
reported a significant reduction in the proportion of REM sleep during
fasting, but there was no significant change in daytime sleepiness, sleep
onset latency, NREM sleep percentage, arousal index or sleep efficiency;
whereas Roky and colleagues [126] showed that fasting was related to
longer sleep onset latency and shorter total sleep time by 40 minutes, at
the beginning and end of Ramadan as well as a decrease in slow-wave sleep
and REM sleep duration.
Mechanistically, Roky and colleagues [127] showed that sleep onset
latency and an increase in subjective daytime sleepiness were associated
with an increase in rectal temperature, suggesting that night-time food
intake and its thermogenic effects are sufficient to impair a person’s sleep.
Similarly, BaHammam and colleagues [124, 128] detected a delay in the
peak of energy expenditure during the first two-weeks of fasting and a
delay in the acrophase of skin temperature, indicating that a phase-shift
had likely occurred in the circadian rhythm of BT. Taken together, the
results suggest that daytime fasting andconsuming food late in the evening
may lead to a change in the circadian rhythm of BT thereby potentially
interfering with sleep onset.
Thus, if a person eats late at night, their BT will likely increase, and
in turn, this may interfere with the normal evening decline in BT which
62 R. Brown and Y. Umar
is thought to cue the onset of sleep [129, 130], as discussed in detail in
Sect. 2.2. Thus, disordered eating (e.g. night-eating) may interfere with
the ability to fall sleep by increasing a person’s nocturnal BT, which poten-
tially results in a phase-shift in the sleep-wake cycle, thereby interfering
with sleep onset [128] and the circadian rhythm of core BT. In support
of this assertion, adherents typically show a delay in the acrophase of
skin temperature during Ramadan, indicating that a phase-shift has likely
occurred in the circadian rhythm of core BT [128], and the high BT is
linked to a longer sleep onset latency [127].
However, few studies have examined late night-eating in non-fasting
individuals. Only one study [131] has shown that food intake late at
night can lead to an increase in mental alertness at bedtime. Nonetheless,
several studies have examined the relationship between specific types of
food intake and sleep. For example, eating spicy food in the evening was
shown to impact upon sleep by increasing sleep onset, reducing slow-wave
sleep and Stage2 sleep, and increasing total awake time [132]. Similarly, in
a review, a low-fibre, high-fat, and sugar diet was reported to be associated
with less restorative sleep and more sleep arousals [133], whereas fast-
food intake partly mediated the relationship between later bedtime and
higher BMI [134]. Taken together, the results suggest that certain types
of food (e.g. high in fat, sugar, and spices) may be most likely to interfere
with a person’s sleep, although the mechanism/s by which this occurs is
unknown, and the effects may vary depending on how accustomed the
person is to certain types of foods (e.g. spicy food).
In sharp contrast, caloric restriction (CR) has consistently been shown
to be linked to lower BT. For example, a recent randomised controlled
trial of 25% CR in 150 people who dieted for ≥6-years showed that their
core BT was lower than those who were not on the diet, by about 0.4°F
after 6 months of CR therapy [135]. Similarly, in another study, mean 24-
hour, daytime, and night-time core BT were lower in people on CR diets,
relative to those who were on a western diet [136]. Thus, it is apparent
that eating can result in an increase in BT, whereas prolonged CR reliably
reduces BT [135, 136].
Nevertheless, several other mechanisms have been proposed to explain
the relationship between disordered eating, overweight/obesity, and
impaired sleep. For example, some researchers posit that shorter sleep
3 Overweight/Obesity and Concurrent Disorders… 63
duration over time tends to promote a positive energy balance, which
in turn, may lead to significant weight gain [137]. Alternately, a longer
sleep onset latency and shorter sleep duration may provide additional
time during which a person can consume food at night, thus, contribut-
ing to weight gain over time [137, 138]. However, other researchers have
suggested that neuroendocrine and metabolic pathways are involved in
mediating the effects of binge-eating on sleep and weight or vice versa.
For example, a change in leptin and ghrelin secretion after sleep depriva-
tion has been suggested to indirectly lead to binge-eating by promoting
food intake [103, 139], as detailed below.
Finally, impaired sleep is suggested to result in dysregulation of eating
regulation hormones, which in turn, may lead to weight gain [137]. Sleep
deprivation can alter leptin and ghrelin secretion; hormones that assist in
the initiation and restriction of food intake [139]. Leptin is released from
adipocytes to restrict hunger and produce satiation [140, 141], whereas
ghrelin, a peptide secreted from the stomach, increases appetite [142],
opposing the effects of leptin. As a result, during periods of positive energy
balance, ghrelin levels decrease in the body, whereas the levels tend to
increase after fasting [143]. In contrast, appetite is reported to increase
in people who experience long-term sleep deprivation via a change in
leptin and ghrelin secretion. In particular, shorter sleep duration (≤ 7.7-
hours/night) is linked to a decrease in leptin and an increase in ghrelin
secretion, which results in an overall increase in appetite [144]. As lit-
tle as two consecutive nights of sleep restriction (i.e. 4-hours total sleep
loss) has been reported to be linked to an 18% decrease in leptin and
a 28% increase in ghrelin during the day, which corresponded to a 24%
increase inhunger and a 23% increase in appetite. Specifically, participants
reported an increase in their specific appetite (33–45%) for high-calorie
carbohydrate-containing foodssuch as sweets, salty food,and starchyfood,
whereas their appetite for fruits, vegetables, and high-protein food did not
change after sleep restriction [139]. Taken together, the results suggest that
a change in metabolic and neuroendocrine hormones may at least partly
explain the comorbidity between overweight/obesity, disordered eating,
and impaired sleep.
64 R. Brown and Y. Umar
In summary, we examined the premise that overweight/obesity, insom-
nia/impaired sleep, and disordered eating (e.g. night-eating) are function-
ally linked to an elevated nocturnal BT. Taken together, the results suggest
that if a person engages in disordered eating at night, this may lead to a
phase-shift in the circadian rhythm ofcore BT, which potentially interferes
with the onset of sleep. Furthermore, once a person’s sleep has become dis-
turbed, they may tend to engage in this sleep-disrupting behaviour more
often, while they wait for sleep to come, which may result in additional
weight gain over time [138]. In this way, disturbed sleep may contribute
to the development of a ne w condition (e.g. overweight/obesity) and the
worsening or perpetuation of existing behaviour (e.g. night eating). Addi-
tionally, impaired sleep may be the result of this behaviour, which is com-
monly practised by overweight/obese individuals. Thus, it is possible that
an elevated nocturnal BT that interferes with sleep onset can underpin the
development and/or perpetuation of concurrent symptoms and disorders,
including insomnia/impaired sleep, overweight/obesity, and disordered
eating. That is to say, sleep problems may play a pivotal and bidirectional
role in contributing to the causation, worsening and/or perpetuation of
other symptoms, disorders, and behaviour, via an increase in nocturnal
BT, as well as potentially being caused by the same bio-behavioural mech-
anism/s, see Figs. 2.1–2.3 in Chapter 2.
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