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9 Typing It All Together 251
For example, an article currently under review by this author (RFB)
and her Ph.D. student (Y. Umar) examined a large pool of demo-
graphics, symptoms/states (e.g. anxiety, depression), disorders (e.g. over-
weight/obesity), and sleep-disrupting behaviour (e.g. sedentary lifestyle,
electronic device use, night-eating, binge-eating, substance use, etc.) as
predictors of sleep quality over time, in a large community-derived sam-
ple. Results showed that the strongest predictor of poor sleep quality at 3-
months was late night-eating. Poor sleep quality also predicted late night-
eating at 3-months; night-eating was the strongest statistical mediator of
the stress-sleep relationship over time; and it was the only mediator of
the BMI-sleep relationship over time. Taken together, the results suggest
that of all the sleep-disrupting behaviour examined, night-eating parsi-
moniously explained the impaired sleep in community-well individuals.
Additionally, the results suggest that night-eating increased the risk of
impaired sleep and weight gain over time; although this is not to say that
other sleep-disrupting behaviour were not relevant (or significant in the
analyses).
One interpretation of these longitudinal bidirectional and mediational
results is that a so-called vicious cycle can arise in some individuals; such
that night-eating interferes with the onset of sleep, and while the person
waits for sleep to come, they tend to eat more food, which over time,
contributes to weight gain. Thus, a single risk factor may contribute to
two or more conditions, and it might also possibly explain any concurrent
affective distress (e.g. depression). However, it is alternately possible that
other related risk factors (e.g. electronic device use, alcohol use) interacted
with late night-eating to contribute to comorbidity, but such an assertion
remains to be tested empirically.
As detailed in Chapter 3, eating tends to be synchronised to limit noc-
turnal food ingestion in people who observe a normal circadian rhythm
[45]. It is unclear exactly how food intake and sleep cycles become desyn-
chronised, but it is likely that the timing of food intake interferes with
sleep onset via an increase in nocturnal BT [20] and/or a change in eating-
related hormones [46]. Night-eating can also disrupt the sleep-wake cycle
and circadian rhythm functioning, by moving a person from a conven-
tional diurnal (daytime) rhythm to a delayed (evening) rhythm; and as a
252 R. Brown and E. Thorsteinsson
consequence, it may lead to metabolic dysfunction [47] and possibly dia-
betes mellitus type-II. Therefore, in total, the effects of late night-eating
may be similar to that exerted by sleep problems. However, it is also
possible that late night-eating and impaired sleep aggravate each other,
that is, they may interact with each other to worsen comorbidities (e.g.
overweight/obesity); suggesting that the phenomena should be considered
together in future studies [48], along with diabetes mellitus type-II.
Thus, an additional focus of attention in this book is the consider-
able overlap that exists between the risk factors for different-but-related
conditions; for example, night-eating, binge-eating, electronic device use,
and physical inactivity are all risk factors for overweight/obesity and also
insomnia/impaired sleep, as detailed in Chapters 3 and 7. As discussed in
Chapter 2, it is possible that these overlapping (or shared) risk factors or the
interactions between them play a key role in contributing to comorbid-
ity; although the assertion has rarely been tested. In fact, most prior risk
analysis studies have only computed the odds ratios (or hazard ratios) for
individual risk factors, separately for each condition of interest. In con-
trast, odds ratios have rarely been computed for highly linked clusters of
risk factors in relation to single or comorbid disorders. Further, few longi-
tudinal risk studies have evaluated a large pool of potential risk factors to
determine which of them are most likely to be pertinent to the disorder/s.
As a consequence, it is often unclear which risk factors are likely to be the
strongest drivers towards disease development. Moreover, we know little
about the manner in which different (but related) risk factors interact
with each other to contribute to comorbid conditions. Thus, future stud-
ies should endeavour to conduct complex risk analyses on linked clusters
of risk factors and multiple conditions, psychological and medical, rather
than on single risk factors and single conditions.
As discussed in Chapter 7, sleep-disrupting behaviour often occur in
the context of stress/affective distress, including stress-related night-eating,
binge-eating, substance use (e.g. alcohol use), and electronic device use.
In particular, school-aged children and university students often report
high stress, affective distress (e.g. anxiety, depression), impaired sleep, and
fatigue [49], and they often engage in stress-related eating. For exam-
ple, in a recent study, female high stress eaters were more likely to con-
sume sugar-free soft drinks, chocolate, and sweets, and be obese than
9 Typing It All Together 253
non-stressed eaters, whereas male adolescent stress eaters were more likely
to binge-eat [49]. Results suggest that, in addition to disrupting sleep,
stress-related eating can contribute to overweight/obesity. Thus, it is pos-
sible that stress/affective distress and stress-related behaviour can com-
bine to contribute to sleep problems and other comorbidities (e.g. over-
weight/obesity). Furthermore, it is possible that stress/affective distress,
disordered eating, overweight/obesity, and impaired sleep are functionally
related to each other, as suggested in Chapters 3 and 7.
Finally, and more broadly, the research presented in this book has sug-
gested that if we observe the daily rhythms of the natural world (e.g.
ambient light & temperature) and our own nocturnal behaviour and
body clocks, we can provide ourselves with the best opportunity for good
quality sleep and the maintenance of good physical and mental health;
including potentially, the avoidance of comorbidities. In contrast, if we
engage in sleep-disrupting behaviour, this will tend to interfere with sleep;
potentially resulting in the development of one or more medical and/or
psychological disorders. Given the ready availability of electricity in the
modern world, there are myriad different activities that we can engage in
at night that could potentially disrupt our sleep.
So is there any evidence that our sleep has changed in modern times?
Is our sleep different to the way we slept in antiquity? The sleep historian
Ekirch [50] has speculated that the structure and organisation of sleep
have substantially changed in modern times; in particular, he suggests that
we have moved away from polyphasic sleep. For example, in antiquity,
we likely slept for several hours early in the night, woke up at around
midnight to perform certain activities (e.g. urinate, stoke the fire), then
returned to sleep until morning; paralleling the lack of available light and
colder ambient temperature at night. This assertion is consistent with the
results of several recent human studies showing that sleep does tend to
become polyphasic when it is manipulated in certain ways; for example,
when the photoperiod (i.e. length of exposure to light) is restricted from
16 hours to 10 hours. In this case, participants’ sleep tends to occur in
two discrete periods with a 1–3-hour gap between them, and melatonin
is secreted for a longer time during the night [51]. Taken together, the
results suggest that shortening the photoperiod (such as occurs on a long
254 R. Brown and E. Thorsteinsson
winter’s night) may temporarily change the circadian rhythm of melatonin
secretion, potentially changing the structure of sleep.
However, a recent evaluation of preindustrial communities has shown
that members do not tend to exhibit sleep patterns that are significantly
different from those of people living in modern societies. For instance,
Yetish and colleagues [52] examined the sleep patterns of people living in
Tanzanian, Namibian, and Bolivian communities, and noted that on aver-
age, their sleep duration ranged from 5.7–7.1 hours; sleep onset occurred
an average of 3-hours after sunset; and sleep duration was approximately
1-hour longer in the wintert ime relative to the summertime. In contrast,
Samson and colleagues [53, 54] reported that sleep patterns tended to
be heterogeneous across cultures; for example, Hadza hunter-gatherers
tended to sleep during the night and took an afternoon nap; Malagasy
villagers slept in two phases during the night, separated by a short period
of wakefulness, and they took afternoon naps; whereas preindustrial West-
ern Europeans likely engaged in polyphasic sleep with a short period of
wakefulness between the two sleep episodes at night.
Thus, it is apparent that sleep patterns tend to be shaped by local condi-
tions (e.g. ambient temperature, length of photoperiod) and the manner
in which a person lives (e.g. nocturnal access to electricity/lights, cul-
tural practices). Specifically, if the photoperiod is short and/or ambient
conditions are cold, then there may be a tendency towards polyphasic
sleep; whereas if the photoperiod is long and/or the nights are warm,
this will likely result in shorter episodes of monophasic sleep. However,
there appears to be little evidence suggesting that average sleep duration
has decreased substantially in modern times, and this is probably the case
for people who experience good quality sleep. However, currently, about
one-third or more of the population report experiencing some degree of
impaired sleep, including delayed sleep onset and shorter sleep duration,
and this does likely represent a significant departure from the sleep prac-
tices of old.
9 Typing It All Together 255
9.3 Possible Existing, Repurposed,
and Novel Treatments for Comorbid
Illness
Unravelling the causes of comorbidity currently ranks among the top
priorities in clinical practice [12, 55]. However, there are currently few
protocols and clinical practice guidelines that exist to assist clinicians in
treating comorbid conditions in a coordinated way. Instead, the guide-
lines and protocols tend to focus on single disorders and they generally
fail to take comorbidities into account. This has resulted in the comorbid
disorders being treated as if they are isolated clinical entities, with each
condition managed separately, often by different clinicians. Thus, there
is a clear need to develop new clinical practice guidelines that do take
comorbidity into account; especially in patients with highly prevalent and
highly comorbid disorders. At the least, there is a need to routinely and
systematically investigate the possible presence of comorbidities in indi-
vidual medical patients and psychology clients. Additionally, if evidence
of a comorbidity is detected, at the least, the disorder should be treated
contemporaneously with the other disorder and/or the patient should be
referred to an appropriatehealth or allied health professionalfor treatment.
As a result, existing medical and psychological therapies have not gen-
erally been designed (and have not been tested) for their utility in treating
multiple comorbid conditions; and few novel therapies appear to be on
the horizon that might be used to effectively treat the disorders. As a con-
sequence, there are few available therapies with any demonstrated utility
in effectively treating more than a single disorder in a single patient, either
concurrently or using a sequential therapy approach.
Thus, there is a clear need to go back to first principles to explore
the potential utility of existing and novel therapies. Accordingly, three
broad treatment approaches will be explored in detail in this section. First,
some therapy approaches are already known to effectively treat multiple-
but-related conditions, including Cognitive Behavioural Therapy (CBT).
Second, it might be possible to change, alter, repurpose and/or tailor exist-
ing therapies to treat the comorbidities, by developing new co-therapy or
256 R. Brown and E. Thorsteinsson
sequential therapy protocols or by tailoring therapy protocols to the indi-
vidual needs of patients.Third, our clinical theory will be used to explore a
range of possible new (or repurposed) approaches to therapy; for example,
the use of therapies that can correct circadian rhythm dysfunction.
First, several therapy approaches are known to effectively manage
multiple-related-conditions, including Cognitive Behavioural Therapy
(CBT). CBT has been shown to effectively treat depressed mood, fatigue,
insomnia/sleep problems, and eating disorders; and there are disorder-
specific CBT protocols for the treatment of depression [56], fatigue [57],
insomnia (CBT-I) [58], and eating disorders (CBT-E) [59]. However, the
CBT protocols do notgenerally provideany specific detail about theway in
which the comorbid conditions should be managed together; for instance,
if the treatments should be concurrent or sequential in a single individ-
ual. For instance, in a client with an eating disorder (e.g. binge-eating
disorder), overweight/obesity, and insomnia, it is unclear whether the eat-
ing disorder, weight problem or sleep problem should be targeted first;
or if the conditions should be co-managed together. If such a co-therapy
protocol did exist, it could assist clinicians in optimally co-managing a
client’s maladaptive behaviour (e.g. binge-eating) and their weight and
sleep problems.
For example, CBT-I principles could be integrated with CBT to address
the propensity of overweight clients to engage in disordered eating, which
interferes with sleepand contributes to substantial weight gain; thus, treat-
ing the person’s eating, weight, and sleep problems together. A coordinated
therapy approach might interrupt the vicious cycle between a client’s late
night-eating, weight gain, and impaired sleep, thereby, potentially result-
ing in the dovetailing of the therapy response. That is, improvement in
one health problem may result in additional improvements in other health
problems. For instance, if a client’s sleep problem is treated early, they will
not be awake late at night to engage in dysfunctional thinking or eat-
ing (e.g. depressive rumination, binge-eating) which could interfere with
their sleep or lead to weight gain over time; and as a result, they may lose
additional weight over time [60]. In other words, the client’s comorbid-
ity burden may improve by living a conventional lifestyle (e.g. observing
the appropriate times for eating and sleeping) and appreciating that when
9 Typing It All Together 257
they compromise their sleep this can lead to physical and mental health
problems.
However, only a few CBT co-therapy protocols have been developed
and tested for their efficacy; for instance, in treating comorbid insomnia,
depressed mood, and fatigue, using CBT-Insomnia (CBT-I). For exam-
ple, in a recent meta-analytic study [61], individual face-to-face CBT-I
that incorporated sleep restriction therapy was shown to effectively treat
sleep and depressive symptoms in patients with insomnia, but not the
fatigue. Similarly, Wu et al. [62]. showed that CBT-I effectively treated
clients’ insomnia symptoms, normalised sleep parameters, and assisted
in managing the coexisting psychiatric conditions, including depression.
Thus, at least in the case of CBT-I, which is typically used to treat insom-
nia, it might also be able to effectively treat comorbid depressed mood,
but not fatigue. However, there is still a lot of work to be done to more
fully integrate these variants of CBT together into complex co-therapy
(or sequential therapy) protocols which might be used to more effectively
treat comorbid conditions.
However, there may be at least several potential pitfalls in using a co-
therapy orsequential therapy approach. Forexample, the concurrent use of
several co-therapies could result in unanticipated drug (or other therapy)
interactions, which could lead to significant therapeutic side effects at
a lower than expected dose and/or offset other clinical improvements
in individual patients. For instance, antidepressants have been examined
for their utility in concurrently treating insomnia and depressed mood,
but there is a lack of clarity as to whether the drug actually improves
or worsen sleep [63, 64]. Further, co-therapy-related problems and the
more general potential to do harm has yet to be explored in any detail in
the psychological literature, although we do know much more about the
nature of specific drug interactions and the need to avoid the concurrent
use of certain medications in some patients.
A secondbroad therapyapproach mightbe to change, alter, orrepurpose
existing therapies to treat a number of comorbid conditions, including
the tailoring of existing therapies. For example, a possibility suggested by
Obermeyer et al. [65] is that individualised ‘precision temperatures’ could
be used to tailor the decisions about testing and therapy to a patient’s
specific physiology; that is, the therapeutic approach might be different
258 R. Brown and E. Thorsteinsson
depending on the patient’s BT (i.e. euthermic, hypothermic or hyperther-
mic). For instance, an elevated BT is used as a prognostic indicator for
acute stroke. In a study of 725 stroke patients admitted to an acute stroke
unit within 6-hours of stroke onset, the mean BT was typically normal
upon admission, but it increased in major stroke patients 4–6 hours after
stroke onset. An elevated BT 10–12 hours after stroke onset was linkedto a
poor clinicaloutcome; although, in mild to moderate stroke patients, there
was no significant rise in BT. In particular, severe infarcts and intracerebral
haemorrhage led to an increase in BT, whereas initial BT > 37.5 °C was
unrelated to stroke severity or stroke outcome [66]. Similar results have
been reported in a small study, showing that peak hyperthermia occurred
1.5–2 days after stroke onset. The researchers suggested that the results
reflected the need to consider therapeutic hypothermia in the treatment
of severe stroke patients [67], suggesting that the tailoring of the therapy
to the thermal characteristics of patients might potentially be useful.
Alternately, existing therapy protocols could be changed or repurposed
to treat the comorbidities, for example, by developing and testing co-
therapy or sequential therapy protocols, using existing medical and psy-
chological treatments. Such an approach—involving the coordinated use
of co-therapies and/or sequential therapies in the multidisciplinary set-
ting—could be considered to be the optimal management of comor-
bid illness patients. In some countries, patients with comorbid over-
weight/obesity and diabetes mellitus type-II already have their conditions
co-managed in the hospital or general practice (GP) setting. For example,
in Australia and other countries, GP management plans (e.g. Australian
Medicare #s 721, 723) are provided to chronic illness patients with com-
plex illnesspresentations; and the GP typically coordinates the care team to
co-manage the patient’s illnesses. Further, early intervention group-based
approaches could be used to manage the weight of diabetes patients in this
context, and such an approach is suggested to be cost effective [68]. How-
ever, mental health services have remained largely separated from physical
health services, making it difficult to provide optimal care to patients
with a physical and mental health problem/s. Thus, a more collaborative
approach is required to co-manage the patients with the comorbidities, in
particular, patients with comorbid physical and mental health problems.
9 Typing It All Together 259
More broadly, there is a need to evaluate the cost effectiveness of alter-
nate organisational models of care (e.g. multidisciplinary care clinics) to
encourage a more collaborative approach in detecting and managing dis-
ease comorbidity [3]. However, as indicated above, multidisciplinary care
approaches are currently, for the most part, not utilised in the treatment
of comorbid conditions. Nevertheless, it is clear that patients with a sig-
nificant comorbid illness burden require an integrated therapy approach,
which separately (and together) addresses patient’s medical and psycho-
logical conditions. As mentioned in Chapter 1, multidisciplinary ther-
apy approaches are likely to have considerable utility in managing these
comorbid illnesses as the care provided in them tends to be coordinated;
evidence-based; utilises co-therapy and/or sequential therapy protocols;
and, clinicians typically communicate with each other about the precise
sequencing of the prescribed care andthe management of relatedproblems
(e.g. depressed mood).
A third approach in exploring the potential of certain therapies to treat
comorbidity is to examine predictions derived from theory. We therefore
used our clinical model of concurrent symptom developmentto make pre-
dictions aboutthe potential utility of new (or existing) therapyapproaches.
First, if as asserted, impaired sleep plays a pivotal and bidirectional role in
facilitating disease comorbidity, it would appear prudent to co-manage a
patient’s impaired sleep at the same time as managing their other comor-
bidities, usingan evidence-basedtherapy approach such as CBT-I.Treating
a patient’s comorbid sleep problem at the same time as treating their other
disorder/s (e.g. obesity) might result in additional clinical improvements
in the condition/s. However, it might also be necessary to address the pres-
ence of sleep-disrupting behaviour (e.g. binge-eating), which aside from
disrupting sleep, may also contribute to the development of comorbidities
(e.g. impaired sleep, obesity).
Second, if as asserted, circadian rhythm dysfunction underpins the devel-
opment of comorbidity then therapies that can correct this dysfunction
might be clinically useful. For example, bright light therapy is known to
reduce nocturnal coreBT (e.g. in seasonal affective disorder patients) [69],
and it can normalise the circadian rhythm of core BT in anorexia nervosa
and bulimia nervosa patients [70]. Together, the results suggest that bright
light therapy may be useful in treating affective disorders as well as certain
260 R. Brown and E. Thorsteinsson
eating disorders. Additionally, a recent review by Zimmet et al. in 2019
[31] posited that circadian rhythm dysfunction (i.e. Circadian Syndrome )
is likely to contribute to metabolic syndrome and related comorbidities;
which in turn can increase the risk of cardiovascular disease and diabetes
mellitus type-II. On this basis, they suggested that ‘circadian medicine’
approaches might be useful in treating the disorders, by altering the timing
of light exposure, exercise, food consumption, sleep, and/or medication
use. As detailed below, ‘thermal exercise’ approaches can also normalise
a person’s circadian rhythm function to treat sleep problems (e.g. insom-
nia). However,additional work is required to examine whetherthe therapy
approach is useful in treating other comorbid illnesses.
One final assertion of our clinical theory is that comorbidity may be
linked to an elevated BT. It is therefore possible that therapies that can
reduce BT (or correct the circadian rhythm of core BT) might be useful in
treating comorbidities. Several therapies are thought to result in clinical
improvement via a correction in BT, especially an elevated nocturnal BT.
For example, sleep restriction therapy has been shown to reduce BT [71],
as has antidepressant use [72] and bright light therapy [69]. However,
the chronic administration of SSRIs can lead to an increase (rather than
a decrease) in core BT [73], whereas electroconvulsive therapy increases
or decreases it [74], and amphetamines consistently elevate it [75]. In
contrast, prolonged caloric restriction is known to reduce a person’s BT
[76, 77]. Further, aside from their antipyretic effects, anti-inflammatory
agents such as aspirin have been shown to reduce depressive symptoms,
either taken alone, taken for their anti-platelet effects or to reduce the
risk of myocardial infarction [78] or in combination with SSRIs, relative
to SSRIs alone [79]. Antidepressants (e.g. SSRIs) are also known to have
anti-inflammatory effects [80–83]. However, few studies have examined
the effects of any treatments on human BT, and mostly only in patients
with uncomplicated clinical trajectories, rather than complex comorbid
illnesses. Nevertheless, the existing studies suggest that normalising a per-
son’s BT and/or circadian rhythm of core BT may result in the clinical
improvement that is seen with some therapies, although the proposition
has rarely been examined in the scientific literature.
Interestingly, sleep restriction therapy, a type of psychological therapy was
shown to reduce patients’ BT during sleep, without leading to a change