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Neuropsychoanalysis: An Interdisciplinary Journal for

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Response to Commentaries
E. J. Khantzian
Published online: 09 Jan 2014.

To cite this article: E. J. Khantzian (2003) Response to Commentaries, Neuropsychoanalysis: An Interdisciplinary Journal
for Psychoanalysis and the Neurosciences, 5:1, 53-56, DOI: 10.1080/15294145.2003.10773409
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Neuro-Psychoanalysis, 2003, 5 (1)

53

Response to Commentaries

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E. J. Khantzian

It is indeed an honor to have been invited to present

an evolving contemporary psychodynamic perspective of addictive vulnerability for this issue of
Neuro-Psychoanalysis. With the exception of Dr.
Yorkes response, it has also been validating and
instructive to have the benefit of the responses of
Drs. Koob, Johnson, Panksepp, and, to a somewhat
lesser degree, Dr. Morrison. As I indicate in my
concluding remarks, I believe there is more complementarity than competition between the paradigms
of neuroscience and psychoanalysis, and we need
not and should not compete.
For the most part, I welcome this opportunity to
respond in kind to the commentaries on my paper by
Drs. Koob, Johnson, Panksepp, Morrison, and
Yorke. I say, for the most part, in that in some
respects it feels daunting to adequately do justice to
the thoughtful and scholarly input of my colleagues.
In another respect some of the responses by Dr.
Yorke, and to a lesser extent, Dr. Morrison, could
degenerate into quibbling over whose pet psychological slant is better or more relevant for understanding the addictions.
Given that the principal aim of Neuro-Psychoanalysis is to stimulate discourse between neuroscience and psychoanalysis, I will give priority to
the responses of Drs. Koob and Panksepp. For starters, I was gratified with Dr. Koobs clarity and
precision in capturing the essence of my perspective. This is important to me for two reasons: First,
too many of the published criticisms of the selfmedication hypothesis (SMH) have not got it right,
thus spuriously arguing against its merits. Second,
in Dr. Koob getting it right, it has made it possible
for me, him, and the reader to consider its relevance
to neuroscientific findings and to consider further
the other half of the storynamely, what are the
neurobiological consequences for addiction-prone
individuals who self-medicate their self-regulation
problems? One immediate and reassuring revelation
to me of Dr. Koobs response is that both perspec-

tives place self-regulation problems, and particularly dysregulation of affects (or emotions), as a
central focus of concern in addictive behaviors. I
cannot agree more, as patients repeatedly convey
that suffering is at the heart of addictive disorders
(Khantzian, 1999). Dr. Koob instructs, similarly,
that there is a neurobiological basis for the negative affective state(s) [which are] important for the
development of addiction and the vulnerability to
relapse. Dr. Koob lucidly elaborates on the neurotransmitter and neuroanatomic substrates by which
emotions are experienced and expressed. He does so
in such a way as to make these mechanisms and
pathways more user friendly for those of us who
do not so customarily visit this important terrain.
Not insignificantly, he cites the work of Dr.
Panksepp and his associates on the neural substrates
of emotions that are of significance for emotional
fitness. Again, I am impressed with the concordance with contemporary psychoanalytic findings,
which in slightly different terms have repeatedly
stressed an intensity, underdevelopment, or absence
of emotions associated with addictive illness. I
found Dr. Koobs comments on allostatic states
especially intriguing. The idea of how allostatic
load causes cumulative damage to the brain and
body can be likened to cumulative psychological
trauma, which, some addiction experts have
stressed, is operative in addictive disorders. Dr.
Koob makes a strong case for brain changes as a
consequence of repeated use of addictive drugs and
how they result in chronic elevation of reward
thresholds. He proposes that this disruption of normal homeostatic processes by chronic drug use replaced by allostatic ones provide a neurobiological
basis to explain progressive dysregulation in animal
models as well as humans. I agree with Dr. Koob
that this paradigm (or conceptualization), so
clearly explained by him, provides a very important
addition in explaining the dark side of addiction,
and as to why and how addictive behaviors can

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54

become so compelling and consuming. What it does

not explain so well is the human capacity for readaptation and resiliency. That is, even the most
debilitated addicted patients recover and, in my
experience, often achieve greater degrees of maturity and emotional stability compared to their preaddiction states. It remains to be seen whether this is
a result of treatment (or recovery) working more on
the brain or on the mind, or some interaction between the two. Finally, I agree with Dr. Koob that
our respective commentaries help to bridge the gap
between neurobiological and psychoanalytic approaches, and perhaps, as Dr. Koob suggests, we do
not need to wait on the Renaissance person as I
had suggested in my paper. Nevertheless, I am not
quite as optimistic and convinced as Dr. Koob that
we simply need to read and comment on each others work to bridge the gap. There still is the fundamental problem that there are too many on each side
of the margins of the two worlds who are oblivious
or indifferent to the others domain.
To Dr. Panksepps response, I want to say, Hurrah! for challenging clinicians and neuroscientists
alike to more actively and vigorously pursue the
centrality of how substances of abuse influence
affect states. I agree with him entirely that we would
not have the problem of addiction were it not the
fact that as humans we experience life with affective intensity and that a wide array of man-made
and naturally occurring substances powerfully impact on our affects (or emotions). He instructs us
that interest in emotional issues has traditionally not
been popular (he says it is unattractive) in basic
neuroscience because it has been heavily influenced
by twentieth-century behaviorist biases.
Although some psychoanalysts might disagree
with me, Dr. Panksepp might find it interesting and
surprising that as psychoanalysts we have not done
so well either with affect experience during the first
seventy-five years of the twentieth century. It is only
over the last three decades that empathic fine tuning,
interest in affect development, and the vicissitudes
of real trauma on emotional life have gained some
ascendance in psychoanalysis. I was fortunate to
have mentors (Semrad, Havens, Mack) and a training analyst (Levin) who all were preeminently tuned
in to the primacy of affective life. Most psychoanalysts during the twentieth century were more focused on drives, psychic structures, a topographic
model, and intrapsychic mechanisms; therapeutically, the emphasis was on interpretative approaches as the gold standard, and less on an
appreciation of what all this meant in terms of
ramifications on affective experiences. As my appreciation of the neural substrate of affects and
interpersonal relations grows, I agree with Drs.
Panksepp and Koob that the focus on the biological

E. J. Khantzian

substrate for emotions resides less in higher neocortical functions but more predominantly at subcortical levels. Flores (2003) has recently elaborated on
this from a psychodynamic perspective. He views
addiction as an attachment disorder, and that the
attachment problem in addicts resides in the emotional brain and not at higher cognitive/cortical
levels. I also appreciate Dr. Panksepps appeal to
neuroscientists to more rigorously study neuroaffect in animal research and to focus more
on brainmindbehavior (vs. brainbehavior) to
bridge more effectively to in-depth psychological
issues in humans.
I understand the parsimony and heuristic value of
terms such as reward/reinforcement and pleasurable feelings employed by neuroscientists, including Dr. Panksepp. From my perspective, however,
such terms border on the pejorative and hark back to
early psychoanalytic theories of libidinal and pleasure drives, which conjure up images of addicted
individuals simply as pleasure seekers. Fairbairn,
the great British psychoanalyst, emphasized that
libido was object (i.e., relations) seeking and not
pleasure seeking, and the main drive of the developing child (and, from my perspective, adults as well)
is not toward pleasure but toward contact (cited in
Khantzian, 1993). This latter perspective is more in
keeping with Dr. Panksepps admonitions about the
hedonia concept and the need to parse positive
affect in a variety of distinct forms to really understand the natural order of emotional feelings [my
italics]. Both Dr. Panksepp and Dr. Koob refer to
the opponent-process theory of addictions, developed by Solomon and associates, in which positive
affect states cycle with negative ones. Dr. Panksepp
underscores the neuroadaptations and changes that
result. I have described a similar cycling in psychodynamic terms:
Burgeoning interest has arisen in a range of behaviors or activity characterized as addictive in nature, including compulsive or habitual behaviors
such as gambling, bulimia/anorexia, compulsive
running, violence, risk taking, and even sexuality.
These behavioral excesses share with the addictions
an inordinate mental preoccupation with the
behavior or activity, an excessive desire or need to
pursue it, a seeming inability to control it, and a
persistent, repeated reversion to it despite deleterious consequences. Like the addictions, they also
seem to be associated with short-term comfort,
pleasure, and gratification, but invariably also with
short- and long-term deleterious and destructive
consequences, often entailing much suffering.
[Khantzian, 1993, p. 26l]

It remains to be seen how much such processes are

driven by the psychodynamic of repetition to
which I refer in this issue of the Journal, and how

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Understanding Addictive Vulnerability Response to Commentaries

much the cycle is a consequence of the neuroadaptations/brain changes resulting from chronic drug
abuse.
I am remiss in not acknowledging at the outset
what must be obvious to all namely that all psychological and emotional processes reside in the
brain. What is more interesting is how early life
experiences get into the brain, and, conversely, how
the brain processes life experiences. In this respect,
it impresses me how Dr. Panksepps description of
how emotions evolve to action-to-perception systems resonates with the developmental notion that
troubled early-life experiences of addicted individuals are not encoded in words, but are expressed
without conscious memories in perceptual-actionaffect responses (Gedo, 1986; Lichtenberg, 1983).
These paradigms obviously have implications for
the predisposition to addictive behaviors and, as Dr.
Panksepp suggests, for prevention.
Dr. Panksepp goes to some length in elaborating
upon an exemplary study of morphine self-administration by Lamb. In this study he feels colleagues do
not sufficiently appreciate how conscious appreciation of changes in feelings was operative. Again, I
am gratified that Dr. Panksepp appreciates as well
as he does the problem so central to addiction,
namely that individuals prone to addiction and relapse consciously experience how addictive drugs
change feeling states. Put another way, the problem
with becoming addicted to a substance (or behavior)
is that the individual remembers (often quite vividly) the relief of or change in their suffering (i.e.,
the reinforcementin this case a conscious
onein neurobehavioral terms).
As a final commentary, I wish to applaud Dr.
Panksepps capacity to translate the complex neural
underpinnings of addictive processes into such clear
and humane terms, an approach that enhances
the interdisciplinary dialogue to which this Journal
aspires.
In responding briefly to Dr. Morrisons and Dr.
Yorkes commentaries, I am impressed that at the
outset both express displeasure with my conceptualization of addictive vulnerability. To this I can only
respond by saying I have worked hard over my
career to place my evolving psychodynamic perspective into the mainstream of modern psychoanalytic theory. It has gained fairly wide acceptance, as
well as some criticism. I cannot be or articulate what
I am not. I am not an empiricist, a behaviorist, or a
cognitive behavioral theorist. This is not a function
of antipathy on my part against these paradigms. It
is more a function of my temperament and preference for narrative approaches and sensitivity to the
primacy of emotions in psychological life. Dr.
Yorke criticizes my work because I hardly mention
the unconscious. This is like saying that Drs. Koob

55

and Panksepp hardly mention molecules. The unconscious is so basic that I choose to go elsewhere
in focusing on addictive vulnerabilities. Of course I
am interested in the unconscious, and, for example,
with my patients I constantly try to make conscious
subconscious processes involving affects, relationships, self-esteem, and self-care that are operative in
their addictive behaviors. My psychoanalytic focus
obviously does not focus on rebellion or having
fun, as Dr. Morrison suggests it might, because
such goals or motives are not sufficient in my
experience, or that of my respected psychoanalytic
colleagues, whom I cite, to explain the consuming,
compulsive, destructive nature of addictive behaviors. I also have not stressed peer influences because
here too, we all have peers and their influence, but
adequate self-care functions protect most individuals from succumbing to destructive behaviors with
which peers can be involved. I also cannot apologize that my focus causes me to predominantly
examine the person and inner psychological life, but
in my own defense I do not ignore how addictive
vulnerability involves problems with adapting to
external reality. I would also contend that Dr.
Morrison misleads when she maintains that individuals with SUDs and psychopathology are in the
minority. This runs contrary to epidemiological and
comorbidity studies, which contradicts such a contention. Remember, our dialogue here is about addictive disorders and not off-again, on-again
recreational or social drug use. Furthermore, I
would question Dr. Morrisons emphasis on intentionality. Powerful affects and drives that are beyond their control or awareness more often drive
individuals who become addicted. As tactfully as I
can, I am forced to suggest that Dr. Morrisons and
Dr. Yorkes approach in their responses more promotes their preference to elaborate on their preferred conceptualizations rather than enjoins my
work with respectful discourse. This latter approach
better succeeds in what this Journal is about
namely, dialogue between and the bridging of the
worlds of neuroscience and psychoanalysis. I find it
both fascinating and bewildering that this is better
accomplished with my neuroscience colleagues,
Drs. Koob and Panksepp, and my psychoanalytic
colleague, Dr. Johnson.
Dr. Johnsons comments are refreshing and welcome responses coming from a psychoanalyst who
better joins the issues than the responses of Drs.
Yorke and Morrison. As I suggest in my paper, he
better straddles the domains between neuroscience
and psychoanalysis. As Drs. Panksepp and Koob
well appreciate, and Dr. Johnson underscores, the
locus of appetitive systems resides in the ventral
tegmentum, and addictive substances produce extremely stable changes in that part of the brain.

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56

As Dr. Johnson rightfully points out, other compulsive behaviors, such as gambling, shopping,
food, etc., which seem addictive in nature, are not as
well explained by brain motivational systems. Dr.
Johnsons responses suggest to me that psychological/psychodynamic factors converge with neurobiological mechanisms to make compulsions, of both
a chemical and a behavioral nature, more likely.
Could it be that the dysphoria and anhedonia that
predisposes to addictive behaviors are a function of
life experiences interacting with genetic influences?
Perhaps on this dual basis, reward mechanisms
are preset at lower levels and thus make it more
likely that certain behaviors or substances produce
more dramatic changes on emotions. As a consequence, individuals so constituted are prone to finding such experiences more compelling.
Dr. Johnson astutely considers the possibility
that one class of drugs (e.g., benzodiazepines) can
set up the brain to find the effect of another drug
such as opiates more compelling, a progression
that I considered clinically in an early articulation
of the SMH (Khantzian, 1975). Johnson cites laboratory animal models and early human traumatic
experiences to describe the early developmental
origins of affect intolerance that can predispose to
addiction. He suggests that anxiety and mood disorders affect appetitive behaviors and, on such a basis, create a connection to addictive behaviors, a
formulation that gives further support for the SMH.
Johnson also nicely joins the issues of disordered
personality function and degree of substance dependence, and the implications for treatment, sever-

E. J. Khantzian

ity dictating the level of activity and support required from the therapist. He caps off his discussion with a sophisticated reframing and discussion
of drive concepts and the repetition compulsion and
their relationship to the addictions, formulations
that resonate well with my paper and the responses
of Dr. Koob and Panksepp.
In conclusion, I thank the editors, Drs. Nersessian
and Solms, and my respondents for providing me a
special collegial experience. It has allowed me to
present a perspective that, I believe, is an important
one; at the same time it has stimulated me to integrate, consider, understand, and respond to alternative and important perspectives on addictive
vulnerability.

REFERENCES

Flores, P. (2003). Addiction as an Attachment Disorder.

Northvale, NJ: Jason Aronson.
Gedo, J. (1986). Conceptual Issues in Psychoanalysis: Essays in History and Method. Hillsdale, NJ: Analytic
Press.
Khantzian, E. J. (1975). Self selection and progression in
drug dependence. Psychiatry Digest, 10 (1): 922.
Khantzian, E. J. (1993). Affects and addictive suffering: A
clinical perspective. In: Human Feelings, ed. S. L. Ablon,
B. Brown, E. J. Khantzian, & J. E. Mack. Hillsdale, NJ:
Analytic Press.
Khantzian, E. J. (1999). Treating Addictions as a Human
Process. Northvale, NJ: Jason Aronson.
Lichtenberg, J. D. (1983). Psychoanalysis and Infant Research. Hillsdale, NJ: Analytic Press.