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243
Depression as a
MindBody Problem
Walter Glannon
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Theories of Mind
In addressing a mental disorder like depression, it is necessary to frame it by a satisfactory
theory of the relation between mind and body.
Descartes raised the problem of causal interaction between the mind and body by arguing that
they were ontologically distinct substances. His
legacy of substance dualism says that, although
mind and body causally interact through the
pineal gland in the brain, the metaphysical relation between these substances is contingent rather than necessary. It is possible for the mind to
exist and function independently of the body and
brain. Few philosophers today defend substance
dualism; most agree that the mind necessarily
depends on the body and brain to generate and
sustain it. Instead, many philosophers defend
reductive materialism. This theory says that consciousness and other forms of mentality are not
simply caused by neural processes in the brain;
mental states just are neural processes or neural
states (Dennett 1991; Churchland 1995; Churchland 1989). This form of materialism is reductionist because it says that mental states can be
explained entirely in terms of the material or
physical structures and functions of the brain.
But insofar as our mental states have a subjective phenomenology, and insofar as their content
involves features of the social and natural environment, the mind cannot be explained entirely
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ty of the mitochondria. When the system is considered as a whole, the mitochondria contribute
to the emergence of the lung. And the lung in
turn constrains the mitochondria. (Feinberg
2001, 1289)
Similarly, the higher-level properties of the
mind constrain the lower-level properties of the
brain and body. But this relation can be understood only in terms of the purpose the mind
serves for a human organism as a whole. In
evolutionary terms, the mind serves an adaptive
purpose by enhancing the survival of the organism by protecting it from external threats and
preventing various physiologic disorders. Strictly
speaking, the mind as such is not adaptive.4 Rather, mental states like beliefs and emotions are
adaptive when they enable the organism to discriminate between threatening and benign events
by processing sensory information from the environment accurately and efficiently. When they
accurately represent these events to the organism, the relevant mental states modulate physiologic systems in the body so that they are neither
understimulated nor overstimulated. By constraining or modulating bodily systems, the mind plays
a critical role in maintaining homeostasis of the
systems that constitute the organism. Consistent
with this role, the mind cannot be so inattentive
to environmental stimuli that it renders the brain
and body unable to sense and respond appropriately to real threats. At the same time, the mind
cannot be so overly attentive to external events
that beliefs misrepresent benign situations as
threats and emotions are out of proportion to
the problems at hand. In these instances, the
mind becomes maladaptive and can trigger pathologic processes in the brain and body.
The model of the mind as an emergent feature
of a nested hierarchy serving an adaptive purpose has several advantages over both supervenience and non-nested models. First, because it
specifies interdependence among different levels
and different regions of physical and mental organization, it provides a more accurate picture of
mindbrain interaction than the linear causation
in supervenience, which treats this interaction as
a one-to-one relation between particular physical events and particular mental events. Second,
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it assumes that the mind emerges from the interaction of the body and brain of the entire organism in interaction with the environment. Third,
as a teleological rather than causal model, it
offers a more helpful way of understanding how
the mind plays a role in preserving bodily homeostasis and maintaining health or generating
disease in human organisms. Fourth, by focusing
on purposive rather than causal processes, and
thus on evolutionary biology rather than physics, the nested hierarchy model sidesteps worries
about physical events causally determining mental events in accord with psychophysical laws. It
also sidesteps worries about how the mind in a
non-nested hierarchy could interact with physical properties from which it emerges but of which
it presumably becomes independent. Given that
mind and brain are two aspects of one biological
system, we can account for interaction between
them. But we can only do this provided that any
causal explanation of the interaction between
physical and mental events is subsumed under a
more general teleological explanation specifying
their role in terms of the organism as a whole in
interaction with the environment.
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organism, the body is put on the constant defensive. As a consequence, the feedback loop between cortisol and CRH is disrupted. The mind
fails to constrain the central nervous, endocrine,
and immune systems, disrupting homeostasis and
thereby working against the adaptive purpose
for which it is designed. An adaptive mechanism
turns into a maladaptive response. The psychological and physiologic stress responses persist
beyond the point where they are useful in enhancing the survival of the organism.
Overproduction of cortisol adversely affects
levels of the neurotransmitters noradrenaline and
serotonin by disrupting the presynaptic reuptake
of them. This appears to be the major physiologic cause of chronic depression. In addition, overproduction of cortisol can prompt the immune
system to release cytokines and immune molecules such as interleukin I and II, which can also
adversely affect the relevant neurotransmitters
and contribute to or exacerbate depression. Although the underlying mechanisms are still unclear, research suggests that impaired feedback
regulation of the HPA axis found in many depressed patients is positively correlated with immune activation of cytokines (Krionfel and
Remick 2000; Ader et al., 2001). Chronic psychological and physiologic stress responses can
trigger the release of cytokines from leukocytes
in the blood circulation, which can penetrate the
bloodbrain barrier and combine with cytokine
receptors in the hypothalamus and pituitary. By
altering normal hormone secretion in these two
structures, cytokines can disrupt modulation of
noradrenaline and serotonin, leading to depression. The links among nervous, endocrine, and
immune systems may help to explain why depression is often correlated with suppressed immune function and increased susceptibility to
infectious diseases in patients who have the disorder. Too much cortisol suppresses the immune
system and increases susceptibility to infection.
Too little cortisol overstimulates the immune system and increases susceptibility to autoimmune
diseases like rheumatoid arthritis. This illustrates
how an imbalance in or between bodily systems
involved in the stress response can disrupt homeostasis and lead to disease.
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An Adaptive Response?
There are fewer stressors on humans from the
natural environment now than there were centuries ago, largely because we are better able to
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Treatment Modalities:
Biomedicine and Psychotherapy
Antidepressant therapy should be tailored to
fit the relative causal roles that the four systems I
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late neurotransmitter levels in each patient. Owing to this lack of precision, they do not always
effectively stabilize mood in all patients, and
they may cause debilitating side effects. Each
persons brain has a great degree of plasticity and
develops uniquely in response to the social and
natural environment as the person develops over
the course of his or her life. Our brains are
systems that are in dynamic interaction with the
environment and as such facilitate our relatedness to it (Edelman 1992; Gillett 1999). Also,
antidepressants can positively modulate neurotransmitters and the qualitative aspects of beliefs and emotions and thereby influence how we
perceive their representational content. But antidepressants cannot completely determine this content. The nature of the states of affairs toward
which our mental states are directed is independent of our minds and brains. Because this content can elicit a psychological stress response in
our beliefs and emotions, there are causes of
depression that are not located in the brain and
body.
Given the role that beliefs and emotions play
in the sequence of events leading to depression,
biomedicine is insufficient because therapeutic
intervention must also take place at the mental
level where the sequence is initiated. Behavior
therapy, for example, can help to block stimuli
that prompt a conditioned response involving an
unconscious memory that can generate conscious
fear or anxiety out of proportion to the problem
at hand (McCullough 2000). In constructive
avoidance, patients are taught to develop appropriate responses to stimuli by working through
harmless to gradually more difficult stimuli until
the stimuli become manageable. Ideally, the conditioned signals that prompt attacks will be eliminated. This is difficult to achieve in practice,
though, because it is extremely difficult to rewire the amygdala, where unconscious emotional memory is entrenched. Emotional memory is distinct from conscious memory of emotion,
which is controlled by the hippocampus. Because
the amygdala is hard-wired as a defense mechanism that responds automatically to stimuli as
potential threats to the organism, psychotherapy
that utilizes more recently evolved (soft-wired)
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Conclusion
Mind and body (and brain) are not independent substances. The mind is generated and sustained by the body and brain and could not exist
without them. Nor is the mind reducible to them.
For the qualitative and intentional aspects of
mental states cannot be explained entirely in
terms of physical processes in the body and brain.
Mind and body are interdependent higher- and
lower-level features of a nested hierarchy in a
biological system that is a human organism. Mind
and body interact as part of an adaptive purpose,
which is to maintain homeostasis of bodily systems and thereby enhance the survival of the
organism by protecting it from disease.
With the help of the cerebral cortex that sustains it, the minds role is to process sensory
information in a more refined way than the comparatively primitive processing of the thalamus
and amygdala in the brain. By distinguishing
between threatening and benign events and relaying this information to the relevant bodily
systems, the mind constrains these systems and
prevents the body from undergoing a chronic
stress response that can lead to physical and
mental disorders. Chronic depression is a psychoneuroimmunologic disorder that results when
the mind fails in its constraining role. Negative
beliefs or emotions relay information to the nervous, endocrine, and immune systems in such a
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way as to trigger a stress response with pathologic consequences for these systems and the organism as a whole. Against the evolutionary hypothesis that depression is a defense mechanism
preventing us from pursuing unattainable goals,
I have argued that it is an adaptive disorder.
Mental states that are designed to serve as an
adaptive mechanism become part of a maladaptive response to the social environment.
We do not know, and perhaps never will know,
precisely how the mind arises from the brain. Yet
by explaining mindbody interaction in terms of
a medical rather than metaphysical model,
progress can be made toward achieving a better
understanding the psychological and physiologic
mechanisms of depression and other mental and
physical disorders. Psychiatrists treating patients
with this disorder must try to enable them to
reestablish a normal connection between mind
and environment. Ultimately, the aim of all psychiatric interventions is to restore the balance
between the mind and the body so that they
interact in accord with the adaptive purpose for
which they are naturally designed in preserving
the health and life of human organisms.
Acknowledgment
I am grateful to George Graham and two
anonymous reviewers for this journal for very
helpful comments on earlier versions of this paper.
Notes
1. Damasio (1994, 1999) and LeDoux (1996, 1999)
distinguish between feelings and emotions. Feelings are
the conscious manifestations of emotions, which are
largely unconscious. I ignore this complication for the
issue at hand and simply distinguish between conscious and unconscious emotions.
2. Most philosophers in the analytic tradition defend the localized view of mind, especially Dennett
(1991) and Kim (1998), as do most cognitive scientists.
3. According to the non-nested view, once higherlevel mental properties emerge at the top of the hierarchy, they become independent of lower-level physical
properties. This is a form of property dualism. It is
defended by, among others, Sperry (1966) and Scott
(1995).
4. There has been much discussion of whether the
mind is or is not adaptive, as well as of the different
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On the Evolution of
Depression
Mike W. Martin
What Is Depression?
Explaining the psychology, sociology, physiology, and evolution of depression presupposes
knowing what depression is and hence what is
being explained. As a blunt but important distinction, let us contrast depression as a mood
and as a mood disorder.
As a mood, depression is a state of low spirits,
typically involving painful and low affect (of a
kind needing further specification). Not all negative low moods are depressions. It is notoriously
difficult to distinguish depression from grief, sadness, gloom, and a host of additional ways to feel
downespecially because today many people use
Im depressed as a blanket expression for virtually any low mood. For the purposes of this
paper, it is not necessary to attempt a full-blown
analysis of depressed moods (and emotions). I
would emphasize, however, that depressed moods
involve values. They involve negative evaluations
of ourselves, major events in our lives, life in its
entirety, or the values that have been guiding us.
Typically, to be depressed is to experience such
things as feelings of worthlessness, dejection about
failures, despair and hopelessness, and loss of
caring and commitment. Thus, we might be sad
or grieving but not depressed because we retain a
solid grip on what is valuable and worthwhile. In
any case, there should be no general presumption that depressed moods are all bad or undesirable. Instead, we should be prepared to appreciate the importance of depressed moods in
connection with questions of value, identity, and
even moral insight (Martin 2000). Depressed persons are not necessarily sick.
In contrast, depression as a mood disorder is,
by definition, pathologic. Moreover, usually it is
not a depressed mood, although it involves depressed moods. On the one hand, depression as a
disorder is defined as pathologic, a notion that is
itself understood in terms of valuesthe values
of health and, indirectly, moral values that define
what is culturally acceptable. Thus, even severe
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grief can be nonpathologic, even though it involves depressed moods, when it is within the
range of culturally-sanctioned responses (APA
2000, xxxi). On the other hand, only sometimes
is depression a single pathologic mood, as in
major depressive episodes that can strike with a
terrifying and suicidal severity (APA 2000, 375).
Usually, however, the pathology is not a single
depressed mood, but instead a longer-term state
involving recurring depressed moods and additional features, such as poor concentration, insomnia, poor appetite or overeating, and so on.
For some purposes, such as research funding and
billing insurance companies and government
health providers, these pathologies can be equated with what is currently in the DSM. Yet, there
are many additional states of suboptimal health,
in which the DSM criteria are only partly met.
What does Glannon mean by depression? He
does not define it, but he makes it perfectly clear
that he intends depression as a disorder. Or rather, it is a set of mental disorders, including the
depressive disorders of major depressive disorder, dysthymic disorder, depressive disorder
not otherwise specified, and a variety of bipolar
disorders and some anxiety disorders. Glannon
sometimes indicates his primary topic is severe
depression, which of course is not a DSM category (nor always a mark of pathology). For the
most part, however, he says his topic is chronic
depression, which might suggest dysthymia, a
chronically depressed mood for most of the day,
for more days than not, as indicated either by
subjective account or observation by others, for
at least 2 years (APA 2000, 380). I suspect,
however, that Glannon intends something broader
than dysthymia, perhaps including most pathologic states that significantly involve depression that
is severe and recurrent. Such a broader conception
would allow him to bypass the vagaries of the
DSM classifications, which fluctuate as its editions
change. Nevertheless, he seems to target disorders that involve primarily depressed moods, rather than bipolar disorders, and he explicitly sets
aside posttraumatic stress disorder. In any case,
because parts of his paper are concerned with the
physiology of depression, it might be helpful to
more fully specify the disorders being explained.
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References
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Reductionism: Neurobiology tends to regard subjectivity as a mere by-product of the brains activity as a symbol-manipulating machine or an
information processor. Consciousness becomes
an epiphenomon of the neuronal machinery that,
operating behind our back, creates the illusion of
a continuous self and of an autonomous will
(Churchland 1995; Roth 1996).
Reification: Mental or subjective states seem to
be localizable in the brain; thoughts or feelings,
it appears, may be observed in the colored illumination of cortical and subcortical structures.
This results in the belief that brain images could
also show the cause of a mental illness, or even
the illness itself, which then manifests, for instance, in a reduced metabolic activity in certain
areas of the cortex.
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Glannon regards depression as a psychoneuroimmunologic disease involving psychological as well as physiologic stress responses. In a
similar approach, I have described depression as
a psychophysiologic desynchronization (Fuchs
2001): a perceived backlog or gap between ones
expectations and achievements is translated by
the brain into a neurobiochemical pattern associated with depressed mood. It also entails an
uncoupling of rhythmic physiologic (e.g., endocrine) processes otherwise synchronized to each
other and to the environment. In the course of
this desynchronization, the production of stress
hormones and, subsequently, immunologic processes may become autonomous and inadequate,
resulting in negative feedback loops and, in turn,
increasing depressed mood. Thus the subjective
reactions to the disorder become intertwined with
the disorder itself. Psychosocial and physiological desynchronization influence each other.
As we can see, subjective experience is more
than a mere by-product of an underlying real or
brain depression. Depressed mood, distorted
thinking, or perceived insufficiency, are not just
accidental or epiphenomenal symptoms whose
only importance is to give cause to consult a
psychiatrist (who actually is rather a brain doctor). Depression, on the contrary, is triggered by
the subjective perception of meaningful, mainly
interpersonal situations, and it is also to a high
degree maintained or worsened by negative feeling, thinking, and interacting with others.
Finally, given the inadequacy of monocausal
accounts that invoke specific brain abnormalities, it would be inappropriate for the psychiatrist to treat the brain exclusively. Instead, a
therapeutic pluralism is required. One could argue here that because the brain translates input
in both directions, a biochemical or bottom-up
treatment suffices to attain the desired purpose.
However, in view of the limited effectiveness of
pharmacologic treatment, it would be imprudent
to neglect the top-down options on the psychotherapeutic level. But what is more important,
we do not have any biochemical means to change
the maladaptive dispositions of perception and
behavior that have led to depression and may
lead to relapse in the future. Such dispositions
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are only accessible to change by new and repeated subjective experiencesemotional, verbal, and
interpersonal processes of learning that stabilize
new attractors of perception and behavior in the
brain. Only conscious experience is able to correct the corresponding dysfunctional patterns of
neuronal activity. Because the brain is a historical organ, there will probablyand hopefully
never be a way to create new views of the self
and the world by brain manipulation.
Conclusion
I have briefly outlined a systemic view of mind
and brain as embedded in the relation of organism and environment. There is no such thing as a
brain for itself, as long as it is not separated from
the living organism by autopsy. Its role may be
seen in the mutual translation of single elements
of a given situation into higher-order units that
are experienced as meaningful wholes and vice
versa. Only subjectivity contains the gestalt-like
wholes that for the organism represent an integrated model of reality. And it is only subjective
experience that is capable of gradually changing
the dysfunctional patterns of perception and behavior that may lead to mental disorders.
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pharmacologic interventions can do the necessary work at the nonconscious neural level that
cannot be done at the conscious level of beliefs
and feelings. The fact that the emotions involved
in depression function outside of our conscious
control is what makes combined psychotherapy
and pharmacotherapy necessary and sufficient
interventions. Still, in more severe forms of depression, the dysfunctions in the underlying brain
mechanisms may be so deep-seated that they are
completely refractory to any intervention at the
psychological level. Trying to reframe the dysfunctional beliefs and emotions that led to major
or severe depression may be of limited therapeutic value. Beyond a certain point, the dysfunction
in the neural and endocrine mechanisms involved
in depression may be too advanced to be corrected by working through the mind alone. In these
cases, the critical pathway is not between the
prefrontal cortex and the amygdala, but instead
between the adrenal cortex and the amygdala.
And the main culprits are not neurotransmitters,
but stress hormones such as cortisol.
To be sure, it is not the brain but the mentally
ill patient who suffers from a mental disorder
like depression. Because the patient is a psychological subject, we need to attend to his or her
subjective experience in understanding depression. This includes the contents of the experience
as a subject in the natural and social environment. Yet, even if we can alter the environment,
some people will still perceive events as stressors.
In these and other cases, we need to explore the
role that neural and endocrine mechanisms play
in sustaining pathologic states of body and mind.
Pharmacologic interventions may be the only
way to reverse dysfunctional neural and endocrine mechanisms underlying these states.
A good example of the therapeutic value of
drug intervention for severe depression is a recent study showing the effectiveness of the antiglucocorticoid mifepristone in treating psychotic
depression (Belanoff et al. 2002; Gold et al. 2002).
Researchers have found that mifepristone can
mitigate the pathophysiologic effects of amygdala activation in severe depression by blocking the
action of cortisol from the adrenal cortex on
glucocorticoid receptors in the amygdala. This
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