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6 Comorbid Psychiatric Illnesses 159
activity, genetics, inadequate diet, gut dysfunction, circadian rhythm dys-
function, and comorbidity (e.g. with anxiety and/or fatigue). Supporting
theories, for the most par t, articulate that singular processes underpin the
development of depression. That is, few if any of the theories properly
address the ‘elephant in the room’—the common presence of psychologi-
cal andsomatic comorbidities. Nonetheless,recent biological theories(e.g.
cytokine theory of depression) have sought to integrate psychological and
biological factors together into the same model. So what should we make
of all the disparate theories and their supporting empirical research? Is
there a way forward?
Obviously, there is a need to incorporate existing depression theories
into more complex real-world models of depression causation. Witten-
born and colleagues [87] recently sought to do just this by mapping out
the multiple feedback loops that likely exist between different psychoso-
cial risk factors and biological processes; but the model is disconcerting in
its complexity, and it is unclear where the strongest linkages exist among
the various pathways. However, there is hope for a ‘grand unified theory’
of depression causation that links together the likely psychological and
biological antecedents, maps out their likely interactions, and predicts the
major causal pathways in depression causation. That is to say, a depres-
sion model is needed that can meaningfully link together, in a functional
way, the various risk factors, interactions between them, and depression
outcomes and also takes comorbidity into account.
As detailed in Chapters 2 and 9, only two models have meaningfully
sought to do this. The utility of the two models, in integrating together
the various singular depression theories, willtherefore be briefly examined.
First, the network model of comorbid symptom development [88, 89, 179]
broadly posits that there may be many different causal pathways to comor-
bidity, including the development of specific disorders (e.g. depression)
in different individuals and in the same individual over time; or alterna-
tively, multiple different causation events could contribute to comorbid
illness in some individuals. Nevertheless, the model asserts that the shared
symptoms of the comorbid disorders are most likely to be causally linked to
the development of comorbidity. Similarly, our clinical theory of concurrent
symptom development asserts that there may be multiple potential path-
ways to comorbidity, and the shared symptoms of the disorders will most
160 E. Thorsteinsson and R. Brown
likely contribute to comorbidity. Both models also assert that particular
symptom groups(e.g. impaired sleep,physical inactivity) are most likely to
contribute to comorbidity via homeostatic pathways (e.g. hypothalamic–
pituitary–adrenal axis, sympathetic nervous system) that are regulated by
human circadian clocks.
As discussed in Sect. 6.2, an elevated nocturnal BT and the disruption
of the circadian rhythm of core BT are linked to an increased risk of affec-
tive disorders,including bipolar disorder[123, 180, 181],whereas positive
affect is linked to a normal circadian rhythm of core BT [182]. Addition-
ally, many of the hallmark features of depressed mood can potentially be
parsimoniously explained by circadian rhythm dysfunction, especially a
phase advancein thecircadian rhythm ofcore BTand the sleep-wakecycle.
Thus, thereis broad supportfor the assertions of the two models.However,
can the two models reconcile the various singular theories of depression
causation? Our model clearly accommodates many of the singular theo-
ries inasmuch as it asserts that acomplex bio-psycho-behavioural mechanism
underpins the development of comorbidity, including depression causa-
tion. Italso asserts that impaired sleep plays a pivotal and bidirectional role
in contributing to the causation, worsening, and/or perpetuation of some
comorbid conditions, via an increase in nocturnal BT. In this respect, the
model may have some utility in providing a framework for structuring the
various depression risk factors and theories in a systematic way; that is,
linking psychological risk factors together with physical symptoms, sleep-
disrupting behaviour, and homeostatic pathways (e.g. SNS, HPA axis),
circadian rhythm of core BT, and the sleep-wake cycle. More broadly, the
clinical model could potentially accommodate theories that are related to
stress,psychological vulnerability, infection, braininflammation, circadian
rhythm dysfunction, and gut–brain dysfunction, via changes in BT and
circadian rhythm function, as evidenced in this chapter and in Chapter 7,
aside from taking into account physical and psychological comorbidities.
To a similar extent, the network model of comorbid symptom develop-
ment can accommodate the likelihood of multiple causal pathways.
Finally, thetwo theories haveimplications forthe treatmentof depressed
mood. First, depression may be co-treated by treating a person’s comorbid
sleep problem (as detailed in Chapter 9). Second, removing impediments
to normal circadian rhythm functioning may improve depression (and
6 Comorbid Psychiatric Illnesses 161
other related) outcomes. Third, therapies that are known to normalise
circadian rhythm functioning might have utility in treating depression.
For example, bright light therapy is effective in treating seasonal affec-
tive disorder [183] using light that is brighter than normal lighting, and
which can alter melatonin secretion, BT, and circadian rhythm function-
ing [184]. Bright light that is administered in the early morning can
suppress melatonin and advance the circadian rhythm such that the nadir
of BT occurs earlier in day; whereas if it is used in the evening, it will
delay the circadian rhythm such that the nadir of BT occurs later in the
day [185]. Nonetheless, both of the comorbidity theories can also accom-
modate other models of depression causation, which might have specific
implications for therapy.
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