Keywords
bipolar disorder; suicidality; reductionism and non-reductionism;
multi-dimensional frameworks
Introduction
Contemporary psychiatry is facing an identity crisis. Is it a scientific
discipline? Is it a social-political movement? Or is it strictly a
healthcare practice that relies largely on practitioners’ insights and
experience? Philosophy of psychiatry is a relatively new field that
draws from centuries-long debates in philosophy of mind and philosophy
of science. It has the potential to reinvent psychiatry’s identity.
However, it needs to emancipate from its predecessors and the scholastic
debates that dominate them. In particular, debates over reductionism may
stall the development of the field if not dealt with in radically novel
ways. Our goal in this paper is to show that taking a side in the
“reductionist wars” is not feasible for psychiatry. We usesuicidality in bipolar disorder (BD) , also known as
manic-depressive disorder, as an example to make the case that
traditional debates over reductionism are nothing more than scholastics
and that resolving the controversy requires abandoning the assumption of
the fundamentality of “levels” in the ontology of neuroscience,
psychology, and psychiatry.
Suicidality covers “all the suicidal behavior/acts and suicidal
thinking/thoughts referring to an intention to end life” (Nanayakkara
et al., 2012, p. 234). It is the outcome of “a complicated sequence of
cognitive and behavioural events, beginning with ideation through to
planning and an intention to act” (Malhi et al., 2013, p. 559).
Suicidality thus highlights the contributions of cognitive,
psychosocial, behavioural, and biological dimensions alike. These
characteristics are further underscored in suicidality in persons with
BD. Suicidality in BD illustrates the interplay between
cognitive-affective, neurophysiological, environmental, and social
causal factors: it demonstrates the need to account for these components
to comprehensively account for a complex phenomenon. This pluralistic
framework is reflected in the heterogeneous interventions for managing
suicidality, which can be pharmaceutical, technological, psychosocial,
cognitive, or a combination of all. It is also reflected in individual
responsiveness to such interventions: for instance, suicidality in some
persons may be alleviated by medication, while for others a cognitive
approach, such as talking or group therapy, is more effective.
The case of suicidality in BD is especially suitable for our purpose
because it is a multi-dimensional phenomenon whose study has been
productive through the methods of several disciplines. For instance,
suicidality in BD is partly due to genetic factors (Kim et al., 2007),
and can be aggravated by symptomatic periods. This suggests that its
causality has a significant physiological component. However, some
features of suicidality in BD underscore the causal roles of cognitions.
Notably, suicidality can persist beyond depressive periods, and is
sometimes experienced during manic periods (Dilsaver et al., 1994;
Miklowitz & Gitlin, 2014). It is believed that this is due to the
persistence of suicidal ideation, a cognitive phenomenon, thereby
highlighting the need to appeal to cognitive concepts in accounting for
suicidality. This is reflected in actual scientific practice: models of
suicidality in BD typically adopt a pluralistic approach that does not
reduce cognitive or mental factors to neurobiological ones or vice
versa.Rather, it treats them as different dimensions of a complex
phenomenon that interact and influence each other. Moreover, recent
studies have shown the promise of physical interventions on
neuromodulation such as electroconvulsive therapy (ECT) in the treatment
of suicidality in BD (Kucuker et al., 2021; Liang et al., 2018; Tondo et
al., 2021). Additionally, social and environmental interventions have
been successful in suicide prevention more generally (Platt &
Niederkrotenthaler, 2020). This demonstrates how multi-disciplinary,
multi-dimensional explanations are most likely to productively account
for how cognitive, affective, psychosocial, and environmental factors
contribute to suicidality alongside genetic and physiological
determinants.
What follows is a brief historical overview of the relationship between
the body and the mind, expositions of suicidality in BD followed by how
it is modelled, a discussion on how suicidality in BD demonstrates the
usefulness of multi-dimensional approaches, and finally, endorsement of
levelless, multi-dimensional explanatory frameworks.
The Psychoneural Relation in Psychiatry
Three competing conceptualizations of mental illness dominated 20th
century psychiatry: the medical model, antipsychiatry , and thebiopsychosocial model . According to the medical model, mental
illness is an organic disease just like any other disease studied and
treated in medicine. Even though environmental and social factors may be
relevant to the etiology of the disease and its diagnosing, a disease is
identified as a biological dysfunction that results from the interaction
of genetic and environmental factors. Consequently, neurobiology is the
relevant scientific discipline to advance psychiatry (Guze, 1978). The
mirror image of the reductive medical model is antipsichiatry which
denies any organic cause to mental illness. Psychiatry should instead be
considered a practice of helping a struggling individual overcome
personal, moral or other problems in living (Szasz, 1960). This
conceptualization has been particularly influential in the disabilities
rights movement. The biopsychosocial model is an alternative to both of
these views as it promotes an integrated multidimensional
conceptualization of mental illness, and all disease for that matter.
According to this model, diabetes and schizophrenia are both
experienced, identified, and diagnosed as complex phenomena which
require accounting for biological, psychological, and social factors.
Moreover, the success of the treatment of each depends to a large extent
on the relationship between the physician and the patient (Engel, 1977).
With certain modification, all three of these views have their
contemporary proponents. As we indicated earlier, our affinity is with a
biopsychosocial approach. However, the main point we are making is that
the debates between the proponents of the three models, while
overlapping to various degrees with traditional philosophical debates
over psychoneural reduction, do not involve any references to levels of
any kind.
Traditional discussions of reduction in philosophy of mind are largely
motivated by the need to articulate a solution to the mind-body problem,
the problem that arises when assuming Descartes’ substance dualism which
postulates that the ideal (mind) and the material (body) substances
which make up reality are so fundamentally different that it is not
clear how the two can interact. How do our desires produce actions in
our bodies and how do our bodily needs produce ideas in our minds, for
example? One way to solve the problem is to show that the distinction is
faulty. Either the world is completely ideal or it is completely
material. While both options have their proponents, only the latter has
gained credence in the analytic philosophy tradition which claims close
allegiance with science. Thus, the debates have shifted towards the role
of science, or scientific discipline(s), in shedding light on the true
nature of the mind-body relation.
20th century psychology was the discipline identified as the science of
the mind while physiology was the science of organisms in general. Human
minds could now be studied by psychology, while their bodies by
physiology. Those who sought to solve the mind-body problem through a
scientific study, then aimed at articulating the relationship between
psychology and physiology in order to provide a unified account of
humans, including their minds and their bodies. Oppenheim and Putnam
(Oppenheim & Putnam, 1958) famously introduced their account ofintertheoretic reduction as a model of unified science. In their
view, the relationship between scientific disciplines, or branches, is
defined by the theoretical vocabulary, or universe of discourse,
corresponding to a level of the multilevel real world where every higher
level can be decomposed into the entities of the level below it.
Further, a scientific discipline has the potential to reduce the
theories of a discipline of a higher level to the vocabulary of its own
theories gradually level-by-level, starting with sociology through
psychology, biology, and chemistry all the way down to elementary
particle physics. Any whole that can be decomposed to the parts of a
lower level, in their model, belongs to that level even though its
“proper” level is the highest level to which it belongs (Oppenheim &
Putnam, 1958, pp. 9–10). Thus the mind can be reduced to a physical
entity as psychology can be reduced to neurophysiology, and ultimately
physics. Early critics of this reductive view of mind and psychology
objected that the reduction of the vocabulary of a higher level theory
presupposes a direct correspondence to the vocabulary of a lower level
theory in order for the reduction to be possible. Furthermore, this also
presupposes identities between the corresponding properties at the
psychological and neurological levels (Fodor, 1974, p. 101). Fodor
famously considers this an absurdity and argues for the relative
independence of the “special” sciences from physics. Rather than
unity, he then advocates disunity of science.
The 20th century philosophy of mind and philosophy of science have
proposed numerous versions of reductive and non-reductive accounts of
the psycho-neural relation. However, the debates have degenerated into
scholastic rhetoric and seem to be of little relevance to real-life
experiences such as mental illness. Early 21st century proposals that
criticized both the proponents and the opponents of intertheoretic
reduction have included ruthless reduction (Bickle, 2006),nonreductive mechanistic explanations (Craver, 2007), andmechanistic reduction (Bechtel, 2007). Variations of these three
models of the psycho-neural relation have dominated the reduction wars
over the past two decades in philosophy of psychology and neuroscience.
However, all three of them have assumed some kind of level-based model.
Bickle proposes a direct jump from molecular/cellular interventions to
behavioural observations without the need to go up and down the ladder
identified by Oppenheim and Putnam. Craver articulates an ontic account
of compositional levels of mechanisms which are thus irreducible.
Whereas Bechtel assumes an epistemic model of compositional levels and
allows for reductive explanations in terms of the lowest compositional
level of a given model. However, these level-based accounts of the
psycho-neural relation based have, at best, shown to be insufficient to
capture the complexity of psychiatric phenomena as it is widely
acknowledged that comprehensive approaches to treatment that include
psychosocial, pharmacological, and lifestyle interventions are superior
to any “single-level” interventions.
In what follows, we will review the literature on modelling of
psychiatric phenomena, and suicidality in people with BD more
specifically. This kind of modelling draws from methods in genetics,
physiology, pharmacology, and psychology. Later, we will reference
emerging literature on technological interventions for neuromodulation
employed in the treatment of several psychiatric conditions, including
suicidality in BD. This will ultimately enable us to make the case for a
levelless account of reduction in psychiatry.
Bipolar disorder and suicidality
BD is a common, heritable, and lifelong psychiatric condition. Due to
its distinctive symptom profile, BD can provide novel philosophical
standpoints on various dimensions of human experience and how they are
impacted by the interplay between cognitive, psychological,
socio-environmental, and physiological factors.
BD is a spectrum of disorders characterized by alternating elevated and
depressed periods, which in turn are accompanied by changes to neural
activity, cognition, behaviour, and personality (Angst, 2007). The
symptomatic periods of BD are divided into mania (or its milder
form of hypomania ), depression , and mixed states .
Among the typical characteristics of manic or hypomanic periods are
euphoric mood, increased energy or decreased need for sleep, rapid
thinking, associational fluency, impulsivity, and feelings of
grandiosity. In some severe cases of mania, psychosis can occur. Common
symptoms of depression include low mood, feelings of hopelessness or
worthlessness, lack of energy or motivation, restricted thinking,
rumination, and cognitive slowness. Mixed states are periods that
exhibit a combination of manic or hypomanic and depressed symptoms (for
instance being in a low mood yet having increased energy). The fifth
edition of the Diagnostic and Statistical Manual (DSM-V) categorizes BD
into different types, depending on severity, frequency, and presentation
of symptoms, which vary extensively between individuals. The trajectory
of BD also varies from person to person: some have more severe and
frequent manic or hypomanic periods, while for others depression is more
common.
BD is associated with a predisposition towards suicidality. As
previously mentioned, suicidality is an umbrella term that encompasses
suicidal ideation, i.e., thoughts or preoccupation about suicide, and
suicidal behaviour, or actions and attempts related to suicide
(Borders, 2020). The population with BD is one of the highest suicide
risk groups, in comparison to the general population and all other
psychiatric illnesses (Miller & Black, 2020). The suicide rate within
the BD population is 10-30 times higher than that of the general
population, with up to 20% of persons with BD dying by suicide, and
about 20-60% having attempted suicide at least once (Dome et al.,
2019). It is estimated that “about one-third to one-half of bipolar
patients attempt suicide at least once in their lifetime and
approximately 15-20% die due to suicide” (Miller & Black, 2020, p.
2). Individuals with BD who have comorbid personality disorders, a
history of suicidal behaviour, or family histories of suicide or suicide
attempts are more likely to themselves attempt or die by suicide (Miller
& Black, 2020). It is also well established that genetic risk factors
are involved in suicidality in BD (Kim et al., 2007). Additional factors
contributing to suicidality in persons with BD include poor quality of
life, relationships or social support, and childhood abuse or neglect
(Miller & Black, 2020).
Suicidality typically—but not exclusively—occurs during depression,
wherein feeling low, a sense of hopelessness, rumination, mental pain,
and increased susceptibility to stress are common. Suicidality usually
arises due to the interaction of these psychological and cognitive
factors with stressful social and environmental circumstances,
physiological states, and other cognitions pertaining to taking one’s
own life (Jamison, 1995; Malhi et al., 2018). (NB: “cognitions” refer
to thoughts, beliefs, and motivational states, which are sometimes
referred to in philosophical literature as mental states .)
Emphasizing the cognitive dimension, Kay Redfield Jamison (1999, p. 91)
writes that “much of the decision to die is in the construing of
events, and most minds, when healthy, do not construe any event as
devastating enough to warrant suicide.” In addition to the
aforementioned symptoms, depressed periods are also accompanied by
negative construal of social or environmental circumstances, such that
one is more likely to regard one’s situation as hopeless or inescapable,
while at the same time having a diminished ability to see other
solutions to perceived problems (Jamison, 1999). Thus, during
depression, a person may view death as the only escape from or solution
to circumstances experienced as stressful and problematic, and may
consequently contemplate suicide. Moreover, persons with BD are believed
to be prone to suicidal ideation (Miklowitz & Gitlin, 2014), thereby
increasing exposure to cognitive or psychological states that may be
translated into suicidal actions. This tendency is further compounded
when death is viewed as an end to one’s problems and pain (Jamison,
1999).
Nevertheless, in persons with BD, suicidality is not limited to
depressed periods. Mixed states, particularly those with a significant
depressive component (sometimes referred to as mixed depression )
are likewise high-risk periods for suicidality. Periods wherein a person
with BD appears to be recovering from depression also pose a high risk
(Jamison, 1999). Suicidality during mania is sparsely documented, but
nevertheless occurs (Dilsaver et al., 1994; Malhi et al., 2018;
Miklowitz & Gitlin, 2014). It has been proposed that “persons
experiencing mania may have components of the suicidal process in mind
but are incapable of putting them into action. It is only when they
shift from the manic phase or a depressive or mixed state that they may
regain the capacity to do so” (Malhi et al., 2018, p. 341). This thus
indicates that being in a depressed state is not a necessary condition
for suicidality. Furthermore, in BD, the use of antidepressants (in
contrast to mood stabilizers) can also lead to increased suicidality
(Miklowitz & Gitlin, 2014). It is believed that the “emergence of
suicidal ideation during antidepressant treatment might be genetically
driven” (McGuffin et al., 2010, p. 276). When depressed, a person may
experience suicidal ideation, but may not have sufficient energy or
motivation to carry out suicidal actions to a lethal degree. However,
when their energy and motivation increase (e.g., due to the effects of
anti-depressants, during mixed depressions with manic/hypomanic
components such as agitation or impulsivity, or when the depressed state
is beginning to lift) they may become psychologically “strong” enough
to complete suicide.
Rapid-cycling BD, defined as “presenting four or more manic or
depressive episodes during at least 2 weeks” (Garcia-Amador et al.,
2009, p. 74), compounds suicide risk and predisposition towards
suicidality (MacKinnon et al., 2005). It has been found that
rapid-cycling BD is associated with a higher rate of suicide attempts
and a “marked increase of lifetime history of suicidal ideation”
(Garcia-Amador et al., 2009, p. 76), in comparison to its
non-rapid-cycling counterparts. A person with rapid-cycling BD is
potentially faced with briefer asymptomatic periods and more frequent
mood episodes throughout their life than their counterparts with
non-rapid-cycling BD (Garcia-Amador et al., 2009). It can be inferred
from the existing literature that rapid cycling results in exposure to
the stressors associated with symptomatic periods, which in turn can
aggravate any suicidal tendencies that may be present.
In BD, suicidality has a genetic component (Kim et al., 2007; McGuffin
et al., 2010), although what aspects of suicidality are genetically
transmitted is yet unclear. Nevertheless, “[a]ll the genetic
epidemiology evidence suggests that suicide and suicidal behaviours are
complex traits where there are probably multiple genes with each
individual gene having a small effect” (McGuffin et al., 2010, p. 276).
Among the candidate genes that stand out are those related to serotonin
(McGuffin et al., 2010). There may be an overlap between genes that
predispose towards suicidality and those that predispose towards
affective disorders, although the extent of this overlap is yet unclear.
It has been theorized that expressions of certain BD-related genes are
associated with neural, physiological, cognitive, behavioural, and
personality processes, traits, or patterns implicated in suicidality.
For instance, some genes relevant to stress regulation increase the
sensitivity of certain neural systems to stress, making them more
reactive to stress-inducing factors in a manner that increases the
predisposition to suicidality (Malhi et al., 2018; Mathews et al.,
2013). The periodic dysregulation brought about by BD’s symptomatic
periods, physiological features, and adverse life
experiences—including those directly related to the experience of
BD—can also bring about “abnormalities in the hypothalamic pituitary
adrenal (HPA) axis as well as the serotonergic, dopaminergic, and
noradrenergic systems” (Mathews et al., 2013, p. 204) implicated in
suicidality. It is also hypothesized that candidate genes may affect the
development of brain areas or neural activity in ways correlated with
suicidality (Kim et al., 2007). Another possibility is that certain
genes are related to the development of the personality traits
impulsivity and aggressiveness—which are not uncommon in persons with
BD, particularly during manic periods—and which have been identified
as suicide risk factors. There are also findings that in BD, suicidal
ideation that emerges upon treatment with antidepressants have a genetic
basis (Laje et al., 2007), although it is yet unclear how the cognitive
component, i.e., suicidal thinking, arises from these neurobiological
interactions.
A family history of suicidality is one of the more consistent risk
factors for suicide, in the BD population and in general. There is
extensive evidence that suicidality aggregates within families (Brent &
Mann, 2005; Voracek & Loibl, 2007), partly due to genetically
transmitted biological or psychiatric features, but also as a result of
other heritable factors such as behavioural patterns. Nevertheless, not
all families with a history of suicide have a history of psychiatric
illness; likewise, a history of psychiatric illness is insufficient to
account for aggregation of suicidality within families. It has been
proposed that familial transmission of suicidality can be attributed to
a combination of genetically inherited responses to stress, the presence
of psychiatric disorders, imitation of behaviour and cognitive patterns,
and exposure to similar environments and the stressors therein (Brent &
Mann, 2005).
Of all the risk factors for suicide, the most consistent and precarious
is a history of prior suicide attempts (Gonda et al., 2012). At least
half of completed suicides in the BD population were carried out by
individuals with a history of attempted suicide (Miller & Black, 2020).
In the same vein, having previously attempted suicide “increases the
risk of suicide by 37-fold in bipolar patients” (Miller & Black, 2020,
p. 4). Moreover, “the lifetime rate of prior suicide attempts was found
to be significantly higher in bipolar patients compared to unipolar
[depression] patients” (Gonda et al., 2012, p. 18). Prior suicide
attempts can raise the threshold and habituation to pain, which in
effect serve as “cognitive rehearsal” (O’Connor & Kirtley, 2018, p.
4) or preparation for subsequent suicide attempts that may have a
greater likelihood of pain and lethality (Malhi et al., 2018). From a
cognitive perspective, it is also believed that “[e]ach time a
suicidal mode becomes activated, it becomes increasingly accessible in
memory and requires less triggering stimuli to become activated the next
time” (van Heeringen, 2012, p. 118).
Modelling suicidality in BD
Although there is a substantial corpus of literature documenting the
quantitative aspects of suicidality in persons with BD, far less is
known about why people take their own lives (Jamison, 1999).
There is still much to be learned about the mechanisms and processes
over which implicated factors interact to generate suicidality. Issues
that have been addressed yet remain incompletely answered include how
suicidal ideation leads to suicidal action, why suicidality and suicide
are not uniform outcomes of being faced with the same risk and
predisposing factors, and how internal (e.g., neurobiological,
physiological, and genetic features) and external factors (e.g.,
environmental stressors, quality of life and relationships) mediate or
aggravate suicidality across individuals. Furthermore, to
comprehensively understand the causality of suicidality, thereasons for suicide must be explored. This involves examining the
cognitive dimensions of suicidality, which are extensively intertwined
with psychological, social, and environmental factors. A number of
models (Malhi et al., 2013, reviewed in 2018) exist that aim to explain
why suicidality in persons with BD (as well as in those without BD)
occurs. Significantly, these models account for suicidality in terms of
the interplay between cognitive, psychological, social, and
physiological factors, thereby highlighting the effectiveness of
multi-dimensional explanatory frameworks. Some of these models are
briefly reviewed in what follows.
The stress-diathesis model (Brent & Mann, 2005) proposes that
suicidality depends on interactions between the individual’s threshold
for stress and the presence of internal and external predisposing
factors. This threshold is influenced by the interactions between
pre-existing risk factors (such as psychiatric history, genetic
predisposition to suicidality or psychiatric illness, previous trauma,
and other factors that affect neural and physiological systems
responsible for regulating stress and emotional responses) and presently
or recently experienced stressors in the environment (such as difficult
life circumstances or poor quality of relationships). Importantly, this
model holds that “the development of suicidal behavior involves a
vulnerability or diathesis as a distal risk factor, which predisposes
individuals to such behavior when stress is encountered” (van
Heeringen, 2012, p. 114). In BD, symptomatic periods, substrates of the
disorder, and their effects on physiology and lived experience act as a
diathesis, as they can increase vulnerability to suicidality, in
particular through difficulty regulating affect, restricting thought
patterns, causing psychic pain, increasing impulsivity and/or
aggression, decreased resilience to stress, frequent or prolonged
exposure to depressive periods or that may be accompanied by
suicidality.
The cry of pain (CoP) model identifies three cognitive components
of suicidality (van Heeringen, 2012 citing Williams and Pollock 2001;
Williams, 2002). The first is sensitivity to signals of defeat ,
wherein “an involuntary hypersensitivity to stimuli signaling ‘loser’
status increases the risk that the defeat response will be triggered”
(van Heeringen, 2012, p. 118). Of the three, feelings of defeat appear
to be the most influential in generating suicidal behaviour (Malhi et
al., 2013). The second, perceived “no escape,” is the outcome
of a restricted capacity for problem-solving that leads to perception
that one cannot escape from problems or difficult circumstances.
Finally, perceived “no rescue” refers to the inability or
difficulty in imagining that the future can have in store positive
events and experiences. A “biologically mediated mental
helplessness script” (Malhi et al., 2013, p. 560) can arise when these
states are experienced. Depending on the individual’s internal and
external circumstances, this script may be acted on in the form of
suicidal behaviour. Importantly, these cognitions tend to accompany
depressed periods, and thus may be recurrent or frequent in persons with
BD.
According to the bipolar suicidality model (BSM) (Malhi et al.,
2013), the appraisal system , which assigns valence to information
about one’s circumstances or internal states, is likewise implicated in
generating suicidality. When the appraisal system evaluates one’s
situation negatively, it is possible for feelings of defeat, entrapment,
and hopelessness to arise, which can thus give rise to a suicide script
wherein suicide appears as a viable option for relief or escape.
Importantly, in BD, the appraisal system is affected by the cognitive
and emotional dysregulation engendered by symptomatic periods (Kelly et
al., 2012; Malhi et al., 2013), so that appraisal of circumstances may
be disproportionately negative or positive during depression and mania
or hypomania, respectively.
The interpersonal theory of suicide (IPTS) (Joiner, 2005) argues
that a sense of thwarted belongingness and perceived
burdensomeness , combined with an acquired capability for suicide are responsible for suicidality (Malhi et al., 2018). Thwarted
belongingness is defined as “feelings of isolation that emerge from
actual or perceived rejection by peers/friends and/or family, and
exclusion from social interactions and gatherings,” while perceived
burdensomeness refers to the “perception that one is implicitly or
explicitly a burden on others” (Malhi et al., 2018, p. 342). While the
degree to which a person experiences these thoughts can change over
time, especially during symptomatic periods, it is nevertheless possible
for them to become deeply entrenched or relatively permanent in the
construal of one’s situation, at times to the point that one begins to
view suicide as the only viable option. According to the model, this is
how suicidal ideation can arise. However, transformation of
ideation into action requires having the actual capacity for suicidal
behaviour. This capacity may manifest as a tolerance for the level of
pain involved in suicidal actions, or a diminished fear of death. These
aspects of the capacity for suicide are dynamic and variable over time,
and are susceptible to influence by the symptoms of BD (Malhi et al.,
2018). It is when all these factors are present and sufficiently salient
that suicidal actions are likely to be carried out.
The integrated motivational and volitional (IMV) model (O’Connor
& Kirtley, 2018) is a biopsychosocial model that “delineates the final
common pathway to suicidal ideation and behaviour” (p. 2). According to
the IMV, suicidal ideation is engendered by defeat and entrapment, while
the translation of suicidal ideation to suicidal behaviour is driven byvolitional moderators. The model has three phases:pre-motivational , which elucidates the biopsychosocial context of
individual predispositions toward suicidality, such as by “identifying
vulnerability factors and triggering negative events” (O’Connor &
Kirtley, 2018, p. 3); motivational, which refers to the emergence
of suicidal ideation and formulation of suicidal intentions; andvolitional, wherein suicidal actions are implemented. Among the
constructs central to the model are defeat/humiliation andentrapment. Individuals who possess vulnerability factors are more likely to develop suicidal ideation when faced with adverse
experiences (pre-motivational phase). Vulnerability factors can be
biological, psychosocial, environmental, or cognitive; BD and its
symptoms act as a constellation of vulnerability factors that fall
within these different domains. Vulnerability factors increase
susceptibility to feelings of defeat or humiliation, which in turn can
lead to a sense of entrapment. Depending on which motivational
moderators , i.e., aggravating or protective factors, are present,
suicidal ideation can naturally progress from entrapment (motivational
phase). Importantly, these motivational moderators are largely cognitive
or psycho-social, and include “reasons for living, attainable positive
future thinking, adaptive goal pursuit, belongingness or
connectedness”, or “feeling a burden, having little or no social
support, and depleted resilience” (O’Connor & Kirtley, 2018, p. 4).
Finally, volitional moderators bring about the last, volitional
phase of the model, by mediating the translation of suicidal cognitions
into suicidal behaviour. Volitional moderators can be understood as
factors that reinforce or facilitate the implementation of suicidal
actions. Similar to the IPTS, volitional moderators encompass the
“components of the acquired capability for suicide (fearlessness about
death and increased physical pain tolerance),” as well as other
internal and external factors like prior suicide attempts, availability
of instruments for suicide, “exposure to the suicidal behaviour of
others…, [and] exposure to inappropriate representations of
suicide” (O’Connor & Kirtley, 2018, p. 4).
Finally, the three-step model (3ST) (Klonsky & May, 2015) is
explicitly described as an “ideation-to-action framework” by its
proponents. These steps are 1) the development of suicidal
ideation , 2) strong versus moderate ideation, and 3)progression from ideation to attempts. The model has four
concepts: “pain, hopelessness, connectedness, and suicide capacity”
(Klonsky & May, 2015, p. 116). It is proposed that suicidal ideation is
the outcome of the conjunction of pain—especially prolonged
pain—and feelings of hopelessness. Both pain and hopelessness
must be experienced, as neither on its own is sufficient to give rise to
suicidal ideation. However, a sense of connectedness can act as a
protective factor that can moderate or alleviate suicidal ideation.
While connectedness is typically interpersonal or social, it can also
“refer to one’s attachment to a job, project, role, interest, or any
sense of perceived purpose or meaning that keeps one interested in
living” (Klonsky & May, 2015, p. 117). Finally, the translation of
suicidal ideation into suicidal action depends on the capacity for
suicide, the lack of which hinders the process from moving to the third
step. Expanding Joiner’s (Joiner, 2005) conceptualization, the
proponents distinguish between dispositional, acquired, andpractical contributors to the capacity for suicide. Dispositional
factors refer to “relevant variables that are driven largely by
genetics, such as pain sensitivity or blood phobia” (Klonsky & May,
2015, p. 119), and other physiological predispositions such as those
associated with suicidality in BD (see §3). Acquired factors refer to
“habituation to experiences associated with pain, injury, fear, and
death,” while practical factors consist of “concrete factors that make
a suicide attempt easier” (Klonsky & May, 2015, p. 119).
Taken together, these models demonstrate the effectiveness of
multi-dimensional frameworks in elucidating the complex causality of
suicidality. While the models are not limited to suicidality in BD, they
have provisions for constellations of predisposing factors such as the
biological, cognitive, and psychosocial features associated with BD.
Although suicidality is not unique to BD, their intricate relationship
forms a distinctive starting point for investigating the structure of
suicidality.
Suicidality and the need for multi-dimensional approaches
What suicidality in BD demonstrates is that rather than developing
traditional reductionist frameworks, it would be productive to develop a
heterogeneous framework that can bring together multiple disciplines. On
one hand, it could provide insight into experiential aspects since this
is the kind of phenomenon that cannot be alienated from experience. On
the other hand, it could direct neuroscience inquiry and provide
“validation of a neurobiological proposal” (Varela, 1996, pp.
344–345). A benefit of heterogeneous frameworks that incorporate mental
states as constructs is able to accommodate unpredictability (Chang,
2012), such as individual presentations of BD and experience of
suicidality. While there are patterns in the risk and predisposing
factors, there is extensive variation in suicidality across individuals.
Aspects of individual life experience such as culture, mores, norms,
social circumstances, personal values, or character traits act as
differential factors with significant and not entirely predictable
influence on suicidality. These factors affect how suicidal cognitions
(e.g., “I want to end my suffering by killing myself”) interact with
other cognitions (e.g., “If I kill myself nobody will look after my
dog”), as well as how the courses of action they give rise to (e.g.,
“I won’t kill myself because I’m worried about what will happen to my
dog if I do”). A heterogenous framework can thus present a
comprehensive picture of suicidality that accounts for physiological
processes and their effects on lived experience and phenomenology, a
particularly crucial aspect of understanding why suicidality occurs.
Suicidality is an exemplar of a phenomenon calling for a heterogenous
approach, since it is characterized by multiple dimensions—from the
biological through to the psychological and cognitive to the
sociocultural. It can likewise be addressed through multidisciplinary
methodologies, depending on its individual presentation. While
suicidality is largely regarded as a phenomenon that must be prevented
or alleviated, the type of intervention through which it can be
addressed successfully varies across individuals: some may be more
responsive to a pharmaceutical approach that intervenes biologically,
while for others a psychological approach that addresses its cognitive
aspects is more effective. On the other hand, treatment based on one
dimension may not always be effective if suicidality is the outcome of
factors from another. For instance, medication may not sufficiently
address suicidality arising from how one construes one’s circumstances,
whereas talking therapy may not successfully alleviate suicidality when
it is caused largely by biological factors. An important component of
treatment strategies is thus to identify which dimension—mental,
physical, or environmental—is more salient to suicidality in a
particular case, and address it accordingly.
One step towards developing a stable heterogeneous approach towards
addressing suicidality is to establish points of contact regarding the
“biological realization of [cognitive] structures” (Murphy, 2008,
p. 128). An example of this task would be identifying neural correlates
of typical types of suicidal cognitions—such as feelings or beliefs of
“hopelessness…, perceived burdensomeness…, thwarted
belongingness…, defeat…, and unbearability” (Bryan et al.,
2022, p. 270)—or determining the physiological and neurological
characteristics accompanying them. Another step is to use explanations
from one dimension to formalize or describe cognitive concepts, while
not dismissing the relevance of their content (Smith et al., 2022). The
importance of cognitive content is underscored by BD, wherein the
physiological effects of symptomatic periods can generate suicidal
cognitions, which however may not always be responsive to physical
interventions such as medication. It would be helpful to recognize which
physiological processes contribute to realizing the different types of
suicidal cognitions (Bryan et al., 2022, 2022; Rudd & Bryan, 2021).
This could then help trace their interactions with physical factors
associated with other factors implicated in suicidality, such as the
types of brain activity and physiological processes associated with BD’s
symptoms, thereby helping to understand how certain sets of
physiological conditions contribute to certain types of cognitions.
Concluding remarks: Making the case for levelless reduction
So far, we have shown that in psychiatry, both psychological and
neurobiological conceptualisations of mental illness are widely utilised
with seemingly no tension. In this section, we discuss recently explored
treatments of suicidality in BD that demonstrate further the inadequacy
of level-based models of reduction of the psychoneural relation.
Psychosurgery and electro-magnetic neuromodulation interventions for the
treatment of psychiatric conditions have seen a resurgence with recent
developments in biomedical technology (Staudt et al., 2019).
Cutting-edge techniques include vagus nerve stimulation (VNS),
transcranial magnetic stimulation (TMS), deep brain stimulation (DBS),
electro convulsive therapy (ECT), magnetic seizure therapy (MST), among
others (Trapp & Williams, 2021). There is growing literature on the
effectiveness of neuromodulation techniques for the treatment of
depression (Conroy & Holtzheimer, 2021), bipolar disorder (Mutz, 2023)
and suicidality (Kucuker et al., 2021). ECT has shown positive results
specifically in the treatment of suicidality in BD (Kucuker et al.,
2021; Liang et al., 2018; Tondo et al., 2021). These interventions are
typically recommended as add-ons to the better established psychosocial
and pharmacological interventions, though they are often last resort
interventions for treatment-resistant conditions.
DBS, and human-machine interfaces more generally, clearly challenge the
ontological assumptions underlying the traditional level-based views of
the psychoneural relation and the corresponding scientific disciplines
that study each component at a specific level. In human-machine
interfaces, a mechanical part is directly connected with a biological
organism as its proper part. However, a mechanical arm is functionally
and compositionally at the same “level” as a biological arm. In the
case of DBS, the mechanical parts—electrodes, pulse generator, and
connecting wire—are not meant to provide a functional analogue of any
organic part of an organism. Rather, they help the brain restore some
specific function by being novel mechanical parts augmenting the
organism’s nervous system. Thus, the “levels” of scientific
disciplines cannot align with the levels of organisation in the thus
blended organism. This goes to show that debating over the proper
account of levels so as to reduce them or make sure that they are
independent from one another threatens to turn into mere scholastic
bickering and philosophy would fail to make a meaningful contribution to
psychiatry.
Another set of interventions for suicide prevention also poses a
challenge for the level-based view of the psychoneural relation in
psychiatry. Environmental programs for suicide prevention may include
restricting access to commonly used means for suicide such as firearms
or pharmaceuticals, raising public awareness, and providing guidance on
news reporting. Restricting access to bridges, tall buildings and
railway tracks have proven to be among the most successful interventions
for suicide prevention (Platt & Niederkrotenthaler, 2020). Here, the
intervention is out of the scope of the composition of the organism, but
it restricts behaviour. So, the intervention is indirectly on the whole
organism. However, it is based on physics rather than biology or
psychology.
All this goes to show that the integration of all factors would be
better conceptualised through a levelless model of the psychoneural
reduction. We are not alone in this motion for abandoning the notion of
levels in the conceptualisation of the psychoneural relation. Recently,
Bickle et al. (2022) have proposed a case study that exemplifies the
inadequacy of the level-based reduction debates to capture the reality
of contemporary scientific practice in the field of cellular and
molecular cognition. We suggest focusing on multi-dimensional rather than multi-level accounts of psychiatric phenomena. In our
view, reduction may occur in psychiatry, but it is a reduction of
boundaries between the disciplines employed in the study of psychiatric
phenomena in which multiple disciplines blend for the purpose of
providing multi-dimensional explanations. Consolidation, or reduction in
number, occurs. However, it does not entail one discipline subsuming
another. Thus, our approach could be considered asinterdisciplinary reduction as opposed to the outdated view ofintertheoretic reduction .