(2009).

Neuropsychoanalysis, 11:76-80
An Integrated Theory of Depression
Otto F. Kernberg
Douglas Watt and Jaak Panksepp's elegant, comprehensive, and thought-provoking essay provides
not only an up-to-date review of neurobiological systems involved in depression, and a clear and
convincing relationship between these mechanisms and those involved in the panic/separation-distress
system, but convincing evidence throughout the painstaking analysis of the interaction of the various
neurobiological systems involved that strengthens their overall thesisnamely, thatdepression is an
evolutionarily conserved mechanism in mammalian brains, selected as a shutdown mechanism to
terminate protracted separation distress (a prototype mammalian emotional state), which, if sustained,
would be dangerous for infant mammals. Following Bowlby's (1980) terminology,
the separation/distress syndrome is described as a series of psychological responses to social loss on a
continuum from protest to despair and, finally, to detachment. The broad spectrum of depressive
syndromes results from an exaggerated activation and persistence of this mechanism, particularly the
transition phase between protest and despair. A genetic predisposition to an excessive activation of this
biological constellation, particularly a genetically determined hypersensitivity combined with excessive
negative affect in response to the loss of social supportabandonment by essential sources of physical
and psychic securitywould reflect the biologically determined vulnerability todepression. This
vulnerability becomes reinforced by psychological experiences that further augment the threat of
social loss or psychological abandonment and constitute the psychodynamic disposition to depression.
In my view, the authors' thesis fits harmoniously with contemporary
psychodynamic thinking regarding depression, particularly with respect to the intrapsychic mechanisms
that determine the experience of loss of support not only from external objects, but also as a consequence
of pathological internalization of early object relations and their role in dysfunctional regulation of self-
esteem and of the confirmation of self-regard by the internalized value systems represented by
the superego and its ego-ideal component.
In exploring this thesis further, there are two reasons for caution. One is the risk posed by the attempt
to fit neurobiological systems into the procrustean bed of psychoanalytic theories; the other is the risk of a
reductionistic effort to link specific psychic functions to specific neurobiological structures, a danger that
Panksepp himself (2008) has warned against, by stressing the epigenetic, in contrast to the genetic, source
of organization of psychic functions. In other words, from a general viewpoint, neurobiological functions
permit the development of the psychic structure of primary affects and their cognitive contextualization.
But further elaboration of affective disposition, which reflects the development of symbolic thinking,
depends on this structure formation at the level of symbolic functions and not directly on the underlying
neurobiological structures and functions. What follows, I trust, will illustrate my efforts to respect these
two reasons for caution.
Mourning and Melancholia (1917e [1915]) is Freud's first and fundamental contribution to the
psychoanalytic understanding of normal and pathological mourning, the psychopathology of
major affective disorders, and the psychodynamic determinants of depression.
Freud described fundamental differences between normal and pathological mourning processes. In
normal mourning, he proposed, there are no guilt feelings regarding the lost object. The work of
mourning culminates in the introjection of the lostexternalobject; the narcissistic gratification
of being alive contributes to the successful working through of the mourning process. In melancholia, in
contrast, the ambivalent relation to the lost object arouses intense guilt feelings and leads to the turning of
the unconscious aggressive attack on the external object into an internal attack on a part of the ego
identified with the lost object. This attack on the selfprevents the narcissistic gratification of being alive
and thus intensifies and prolongs the pathological mourning process.
Melanie Klein (1940) postulated the splitting, in the mind of the infant, of idealized and persecutory
relations with its mother and the generation of guilt anddepression
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when integration of these split segments of the ego or self and of the corresponding internal objects would
bring about the infant's awareness that its own aggression was directed against the ideal mother: this is the
depressive position. Klein pointed to the normal consolidation of the good internal object and the ego
when aggression is not excessive and described how conditions promoting marked dominance of
aggressive over libidinal investments prevent such a normal integration. The result is intolerance of
ambivalence and lack of assurance of one's own goodness, creating the predisposition to
pathological mourning and melancholia.
In contrast to Freud, Klein felt that in normal mourning there was an unconscious process of
reinstating the early good internal object and that ambivalence characterized normality as well as
pathology. Normal mourning, she proposed, includes unconscious guilt feelings related to the reactivation
of the depressive position, together with the activation of reparative urges, gratitude, and longing for the
lost good object, but also by the reinstatement of the good internal one. Pathologicalmourning is
characterized by the failure to work through the depressive position due to the sadism and cruelty of
the superego, its demands for perfection, and its hatred of instincts. In melancholia, Klein stated, this
hatred has destructive consequences for both the internal and the external good objects, leading to a sense
of internalemptiness and loss. Because of the attack on and the destruction of the idealized object, a
vicious circle of guilt evolves, with an attack on the bad self, not on the internalized object. Suicide would
be an unconscious effort to destroy the bad self and rescue the good object.
Edward Bibring (1953) described depression as the result of acknowledgment of the loss of
an ideal state of self in the context of a severe discrepancy between theideal self and the real self. This
pointed to the affect of depression as an ego potential predating the differentiation of the superego from
the ego. In contrast to the Kleinian view that depression necessarily involves superego mechanisms,
Bibring stressed the early emergence of the loss of an ideal state of self under conditions of severe failure
of the protective environment, thus foreshadowing, I suggest, the catastrophic reaction to prolonged
early separation described by Bowlby (1969) in the pathology of attachment. A potential for
depressive affect, triggered by the loss of an ideal state of self, may be caused by early maternal failure as
well as by a later internal, superego-determined attack on the self. The basic mechanism is a loss of
an ideal state of self related to the loss of an ideal object. In my view, the potential for the affective
reaction of depression to loss of an ideal ego or self state is compatible with Melanie Klein's
description (1946) of the depressive position when theaggression stemming from the self can be
acknowledged, when ambivalence can be tolerated, and when the implicit comparison between a past
illusory, split-off, idealized self and the realistic, integrated, present one signals the loss of that ideal self
state.
Edith Jacobson's analysis (1971) of normal, neurotic, borderline, and psychotic depression mapped
out a comprehensive psychoanalytic theory of the psychopathology of depression. In describing the
dyadic, internalized object relations reflected in the affective connection between libidinally invested self
and object representations and the corresponding aggressively invested self- and object-representations,
she originated what I consider the contemporary object-relations theorymodel in psychoanalysis. I believe
that she accomplished this independently from, although at the same time as, Ronald Fairbairn (1954) in
Scotland. Jacobson described the originally fused or undifferentiated units of self- and object-
representations in both the libidinal and the aggressive domains of experience and the defensive refusion
of libidinal self- and object-representations under conditions of psychotic regression. In
psychotic depression, this regressive refusion would affect the aggressively invested self- and object-
representations in the ego and would also involve a refusion of the earliest aggressive superego precursors
with the later idealized ones. It is the regressive fusion of persecutory and idealized object representations
in the superego, she proposed, that brings about the sadistic demand for perfection and the typical cruelty
of the superego in melancholia. The attacks of this sadistic superego are directed toward the units of fused
aggressive self- and object-representations in the ego. In the process, the frail remnant of the idealized
segment of the self that was overwhelmed in the total refusion process occurring in the ego succumbs to
the generalized activation of guilt, despair, and self-accusation. As a consequence, the nihilistic,
hypochondriacal, and self-devaluing delusions of psychotic depression evolve.
Jacobson proposed that in borderline conditions the boundaries between self- and object-
representations in both libidinal and aggressive domains of internalizedobject relations persist, facilitating
the defensive processes of dissociation, depersonalization, and projection that help these patients avoid
the sadistic superego attacks characteristic of depression. In neurotic depression, a sufficiently well-
integrated self relating to integrated representations of significant others still experiences the attacks of
the superego in the form of exaggerated, pathological guilt and self-devaluation,
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but such a self suffers neither the fusion processes that, in melancholia, transform guilt into a total
delusional devaluation of the self-identified with the object nor the primitive defenses characteristic of
borderline conditions.
In all these psychoanalytic theories of depression except Bibring's, depressive affect emerges as the
connection between the basic experience of loss of an ideal state of self as the result of the loss of an
object and the assumption that the loss of the object itself was caused by one's own aggression. The
empirical research of JohnBowlby (1969) and his followers on normal attachment and its pathology and
their description of the stages of protest, despair, and detachment as a result of catastrophically
prolonged separation of the infant from mother provided a fundamental link between the psychoanalytic
theory of depression, on the one hand, and the reaction to early separation, on the other.
Depressive affect as a basic psychophysiological reaction is triggered by early separation from
the mother, if excessive or traumatic, and similarly by an internal sense of loss of the relation between the
self and the good internal object derived from the superego's attack on the self. Early separations provoke
depressive affectsa chain reaction of rage, despair, and despondency, and their neurohormonal
correlates, in humans as well as in other primates(Suomi, 1995). This link between felt emotion and
neurochemical response begins to connect the psychoanalytic theory of internalized object relations with
biological research into the genetic and neurobiological determinants of aggressive and depressive affect.
Prolonged separation of the infant from its mother powerfully activates the affects of rage first,
despair later, and, under extreme circumstances, despondency and reduction of the capacity for object-
relatedness. Neurobiological studies in both humans and other mammals have confirmed the
corresponding activation of the hypothalamus-pituitary-adrenal (HPA) axis, the resulting
hypercortisolemia, and, more recently, the resulting long-range consequences in terms of lowered blood
cortisol, excessive stress response to later traumatic stimuli, and reduction in the hippocampal volume, the
brain structure most directly involved in explicit affective memory(Panksepp, 1998).
The mechanisms by which the HPA stress response activates the basic affective responses of
rage, panic, and depression probably are still insufficiently elucidated, although the brain structures
mediating rage and pain have been circumscribed more clearly. As Panksepp (1998) points out, the
complexity of affect activation demands the simultaneous analysis of the brain structures involvedthe
generally activating genic amines (particularly, in the case of depression, the serotonergic and
noradrenergic systems), but also particular neuropeptides related to specific affect systems that are as yet
only partially knownin the context of the analysis of behavioral manifestations and subjective
experience. Basic autonomous vegetative functions of affects involve the hypothalamus, the amygdala,
and the periaqueductal gray; early emotional experience involves the amygdala, the hippocampus, and the
ventral striatum; but mature emotionality, with the development of complex later emotions, involves the
prefrontal cortex along with cognitive control of emotions mediated particularly by the orbital, frontal,
and cingulated cortex.
At this time, psychoanalysis and neurobiology are still too far apart in their focus and methodology to
permit any satisfactory integration. I believe, however, that it is reasonable to assume that the
psychopathology of depression is determined by a complementary set of etiological factors. These
include, on the biological side, an abnormal, genetically determined, and neurochemically controlled
activation of the affect of depression under conditions of early separation and object loss, most probably
mediated by abnormal biogenic amine systems. Early, severely traumatic circumstances, particularly
failed or insecure attachment, further contribute, triggering not only an exaggerated stress response but a
disposition to later excessive activation of negative, particularly depressive, affect, mediated by the
corresponding hypercortisolemia and, presumably, by the loss of the modulating influence of the
hippocampusaffective memoryon deeper affect-activating centers.
On the psychological side, depressive affect is activated by loss of the ideal state of self
when anxiety is aroused by need, and seeking gratification fails to produce the expected maternal
response, and, later, when active rejection by an ideal object is no longer perceived as an external attack
but resonates with the internal build-up of archaic superego structures. Here, what is relevant is the build-
up of complex affective memory structures that are symbolically manipulated and integrated
unconsciously, leading to the concepts of self and the world of internalized object representations. The
extraordinary richness of the human neocortical brain structures constitutes the basis for this evolution of
psychological structures. In short, on the psychological side, the development of pathological ego
and superego structures in response to the aggressive affects activated by a hostile, depriving,
abusive environment, with the consequent threat to the normal dominance of libidinally invested
internalized object relations in ego and superego over those invested with
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aggression, determines the potential for pathological depression.
The work of Melanie Klein and Edith Jacobson has enriched the analysis of normal and pathological
depressive reactions by delineating the role of the primitive defensive operations
of splitting, idealization, projection and introjection, projective identification, denial, omnipotence, and
devaluation. Both authors described a vicious cycle of early aggressive response to frustration, the infant's
tendency to project its own aggression onto the frustrating object, and the re-internalization of that
aggressively perceived object into the basic layer of the early superego in the form of persecutory
internalized object representations. A constitutional disposition to excessive depressive affect may
contribute significantly to the intensity of depressive response to superego-mediated attacks on the self.
Perhaps the major theoretical formulation initiated in Mourning and Melancholia, transcending the
subject of depression, is the concept of identification. This concept is relevant for the understanding of
the relation between affect activation and the internalization of object relations, the consistent
contextualization of affects inrelation to self- and object-representation. Here, I believe, the work
of Fairbairn (1954) and of Jacobson (1964), who arrived independently at remarkably similar
conclusions regarding this essential mechanism, provides major contributions to Freud's original
observations in Mourning and Melancholia. Briefly summarizing how I conceptualize the
contemporary view of identification, I would stress as a central concept the definition of identification as
the internalization of a representation of the object interacting with a representation of the self under the
impact of an intense affect. The more intense the affect, the more significant the object relation; the more
significant the object relation, the more intense the affect state. This theory of identification overlaps with
the theory of the centrality of depressive affect in normal and pathological mourning: the more intense the
predisposition to react with depressive affect to separation or loss, the more powerful
the identification with an abandoning object and with an abandoned self. The more profound the
experience of rejection or loss of a good external or internal object, the greater the potential
for depression.
Returning once more to the determinants of normal and pathological depression, we can now
conceive of a genetic disposition to pathological activation of aggressive affects that will be integrated
into the aggressive drive in the form of a structured sense of self or object as victim or persecutor, self and
object bound byaffects of fear, rage, and despair. The result is proneness to the excessive activation of
rage, anxiety, and despair under conditions of frustration and object loss. It is important to keep in mind
that the stress response mediated by the activation of the HPA axis includes intensive rage and panic as
well as the disposition to depression. In fact, the combination of an intense rage response and panic may
be the origin of the later structured internalized relation between a rageful self and a frustrating, sadistic
object. The projection of rage onto the object intensifies the fear and wish to destroy the persecutory
object, thus transforming rage into hatred, a complex affect that will later constitute the core affect of the
aggressive drive. Here, I refer to my theory, spelled out in earlier work (Kernberg, 1992), that the
libidinal and aggressive drives are hierarchically superordinate integrations of the libidinal and
aggressive affects, respectively, and that affects constitute the primary motivational systems first and,
later, the signals of the drives in terms of the affective quality of reactivated internalized object relations. I
believe that this theory does justice to the convincing clinical implication of Freud's dual-drive theory and
to the emerging knowledge of the fundamental motivational functions of affects in neurobiology.
Temperament as a genetically determined, constitutionally given disposition to a certain intensity,
rhythm, and threshold of affect activation links the innate disposition to aggression with the traumatic
impact of early separation, trauma, and frustration on the internalization of object relations. By far the
most important determinant of the internalized object relations expressed in the tripartite psychic structure
is the earliest mother-infant interaction. Severe frustration and trauma in this early interaction, with
consequent excessive activation of aggressive and depressive affect, would then give rise to the structural
consolidation of a psychic apparatuswith a hypertrophic superego and the predisposition to react
with depression to relatively minor triggering factors from the environment. An extremely severe inborn
disposition to depressive affect would exacerbate the development of such pathological structures. At
the other extreme, even without any genetic disposition, the structural consequences of
severe frustration and trauma, with a consequent activation of excessive aggression, would contribute to
the build-up of a severely pathological, though well-integrated, superego structure predisposing
to depression in later life.
A depressive-masochistic personality structure predisposes to characterological depression and to
a loss of normal self-esteem, determined by the superego, under conditions of multiple sources
of unconscious
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guilt. This is the counterpart to the activation of anxiety as nonspecific manifestation of danger derived
from unconscious intrapsychic conflict (Kernberg, 1992). Anxiety, in fact, also may function as a
warning of the impending danger of unconscious guilt and object loss leading to depression.
Once depressive affect is structured into an internalized object-relations frame that reflects the
relationship between a guilty, internally abandoned self and an idealized, abandoning or critical object, it
would seem reasonable to hypothesize that any critique, disqualification, or abandonment in everyday life
would immediately activate depressive affect as part of such an object relation. And vice versa: when,
given such a structured internalized object relation, depressive affect is triggered or accentuated by a
constitutional disposition to pathological affect activation, the entire constellation of
intensive guilt feelings, self-devaluations, and the experience of abandonment will be activated as well.
The major emphasis in this discussion has been on the attempt to integrate the psychoanalytic
approach to depression with evolving knowledge regarding the neurobiology of depression. For
neurobiology, contemporary psychoanalytic theory offers an instrumental approach to
higher symbolic functions that cannot be reduced to neocortical circuitry. For psychoanalysis,
neurobiological progress offers the challenge of reexamining older theories of drives, the impact of
neurobiological structures on stress and trauma, and the mutual relations
of unconscious interpsychic conflict and the genetic and temperamental disposition to depressive affect as
causes ofdepression.
This completes my outline of the organization of the psychodynamic features that contribute to
the development both of normal mourning and grief reactions on the one hand and of
clinical depressionfrom characterologically determined chronic dysthymic reaction to major
affective illnesson the other. From a clinical psychiatric viewpoint, it is possible to differentiate the
milder, chronic dysthymic reactions from major depression because of the lesser degree of
depressive symptoms in the former and the stronger presence in those cases of particular environmental
triggers and specific characterological predispositions, in contrast to the greater degree of clinical
severity, the prominence of neurovegative symptoms, and the alteration of biological rhythms evident in
major depressive disorder. Genetic factors predominate in majordepression, while intrapsychic and
environmental factors predominate in chronic dsythymic disorders. In general, psychopharmacological
(and electroconvulsive) treatments are the treatment of choice in the major depressions, while
characterologically determined depression responds optimally to psychotherapeutic treatments, often
combined with medication.
Finally, from a general viewpoint of the interaction of biological and intrapsychic predisposing
features, it is of great interest that the psychological impact of a graveloss of social support may trigger
the entire constellation of the neurobiology of depression, while, equally, a strong genetic disposition
to depression reflected in the activation of the corresponding neurobiological systems may trigger the
entire complexity of psychodynamically structured, psychological symptomatology ofdepression,
including severe and unrealistic self-attack and self-devaluation. The study of the intimate mechanisms of
these interactions between symbolic thinking and genetic disposition, and between genetic and epigenetic
structures, is a major task ahead, and Watt & Panksepp have advanced fundamentally in this direction.
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Article Citation [Who Cited This?]
Kernberg, O.F. (2009). An Integrated Theory of Depression. Neuro-Psychoanalysis, 11:76-80