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Commentary on Understanding Addictive

Vulnerability
a

Jaak Panksepp Ph.D.

a

Bowling Green State University, Bowling Green, Ohio, U.S.A.

Published online: 09 Jan 2014.

To cite this article: Jaak Panksepp Ph.D. (2003) Commentary on Understanding Addictive Vulnerability,
Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 5:1, 21-29, DOI:
10.1080/15294145.2003.10773404
To link to this article: http://dx.doi.org/10.1080/15294145.2003.10773404

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Neuro-Psychoanalysis, 2003, 5 (1)

21

Commentary on Understanding Addictive Vulnerability

Jaak Panksepp

TOWARD A COMPREHENSIVE PSYCHOBIOLOGICAL

THEORY OF ADDICTIONS

Professor Khantzian shares an emotion-regulation

centered depth-psychological perspective on addictive processes. Rather than critique his even-handed
coverage, I would merely supplement his views with
some current neuroscientific perspectives in the
area. There is still a vast chasm between these
approaches, and the needed bridges can only sustain
commerce if there is substantive building from both
sides with concrete empirical predictions that can be
evaluated in laboratory and clinic. To some extent
that has already happened, with the recognition
by both sides that certain evolved psycho-neuro
Jaak Panksepp, Ph.D.: Bowling Green State University, Bowling
Green, Ohio, U.S.A.

mechanisms of the brain, such as the mesolimbic

and mesocortical dopamine SEEKING pathways
(ML/MC DAp), are essential in all kinds of appetitive urges, including ones related to most drugs of
abuse (Berridge & Robinson, 1998; Ikemoto &
Panksepp, 1999; Kelley, 1999; Koob & Le Moal,
2001; Wise, 1998). However, I will highlight certain
problems that still impede progress across the modest bridges that we already have, in the hope that
those fragile constructions can be replaced by sturdier ones.
The key issue for depth-psychology is how to
utilize the emerging neuroscientific knowledge to
hew new insights. I think this largely boils down to
evaluating and utilizing the new neurochemical/
psychopharmacological manipulations that modern
neuroscience has provided in ways that permit ever
more rigorous evaluation and characterization of

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22

psychobiological vectors that contribute to addiction. Since this topic remains fairly poorly developed experimentally and I have outlined some
relevant approaches previously (i.e., the development of neurochemically based psychoethological
research endeavors, Panksepp, 1999a, 1999b), I will
here largely focus on what basic brain researchers
may need to do to contribute to positive interdisciplinary building efforts. As Khantzian indicates,
explanations are too often presented as competing
with or in isolation from alternative theories, and
this is certainly a common attitude in neuroscience,
where many are acutely aware of the rewards that
attend substantive solutions to this area of great
societal concern.
Since psychoanalytic approaches are less experimental, they are less likely to yield profound new
insights, unless connections to neuroscientific perspectives are cultivated. In the absence of ample
funding, the competitive spirit is also not so fierce,
providing fertile ground for the emergence of more
complementarity than competition among those
who pursue the Holy Grail of deep psychobiological insights to understanding the core sources of
addictions. In general, my view will be complementary with Khantzians in developing the claim that if
we do not better understand emotional/affective
processes, we cannot have a coherent theory of
addiction (see Koob & Le Moal, 2001; Panksepp,
Knutson, & Burgdorf, 2002). In short, I do not
believe addictions exist unless the addictive agents
generate experienced affective states in both humans and other animals. If true, this simple assertion
should be a major call for behavioral neuroscience
to pay better heed to the global emotional issues that
must frame our molecular investigations.
At present, the emerging brainemotion area is
having great difficulty coming to terms with the
affective nature of the mammalian neuromental apparatus (for a contentious coverage of some recent
trends, see Panksepp, 2002a, 2003), and the integrative approach advocated by Khantzian will hinge
very much on how that difficult issue is finally
resolved by the larger community of interested
scholars. Since this point bears emphasis, my own
view is that addictions would never emerge, and
would not be as troublesome as they are, without our
ability to experience life and a large array of endogenous neurochemistries and man-made molecules
with experiential affective intensity (Panksepp,
Burgdorf, Gordon, & Turner, 2002; Panksepp,
Nocjar, Burgdorf, Panksepp, & Huber, 2003). This
has traditionally been an intellectually unattractive
view in basic neuroscience, which is still guided
heavily by twentieth-century behavioristic biases.
Hence emotional issues currently remain a minority
approach in behavioral neuroscience. Even among

Jaak Panksepp

the few who are prominently interested in the neural

underpinnings of emotions, no fewer than two (e.g.,
LeDoux, 1996; Rolls, 1999) out of three scholars
(e.g., Panksepp, 1998a), as a rough estimate, believe
that affective experiences arise from higher neocortical functions, especially frontal cortical ones,
which are only really well developed in humans,
who have spectacular working memories and linguistic abilities. For some perplexing reason, the
massive evidence for the subcortical locus-of-control for most affective processes is not well accepted
by most (Panksepp, 2003). Partly, I suspect, this
denial is based on psychic reasons similar to those
that delayed the acceptance of the fact that the world
was not the center of the universe, just 400 years
ago.
The major behavioral neuroscience
approaches
Before proceeding to extol the importance of a basic
brain process such as affective consciousness (see
Panksepp, 1998a, 2000a, 2000b) in resolving key
issues in recreational and addictive drug use, it
might be useful to summarize six general approaches to addiction that are presently prominent
in the field of behavioral neuroscience. The first
five are widely touted, and the last one (i.e., our
own), is generally less well considered since it
accepts the issue of a diversity of experienced emotions as a (perhaps the) key neuroscientific issue
that can allow us to generate a comprehensive psychobiological theory of addictions. Not that the
others neglect emotional issues, but they generally
do not recognize experienced neuro-affect as either
a workable or a key issue in animal research. As a
consequence, most behavioral neuroscience approaches may not yet be able to deal forthrightly
with certain neuro-experiential aspects of brain
functions that may be essential conceptualizations
to bridge to human addiction issues. By not explicitly including affective dimensions in their discussions, most neuroscientists tend to remain at the
level of brainbehavior relations, rather than brain
mindbehavior ones that might relate more directly
to depth-psychological issues that can only be well
evaluated in humans.
So here are the half dozen major approaches
(which overlap with each other extensively, in various synergistic and cross-current ways), along with
a few remarks about how they might be related to
issues of affective consciousness. There is one
key piece of agreement among all the theories,
which has arisen from the massive weight of evidence from the past quarter-century of brain reward research: the ML/MC DAp, along with the

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Understanding Addictive Vulnerability Commentaries

key dopamine target zones of the nucleus accumbens and ventral pallidum, lie at the core of addictive and appetitive urges, and this provides an
umbrella concept for pretty much all subvariants of
psychobiological theories that we consider here,
including the important issue of how plastic neuropsychobiological processes (such as sensitization)
are critical for the transition to addiction. These
thumbnail sketches are simply aimed to provide a
context for discussing neuroscience issues, and I
will not attempt to weigh the pros and cons of each
approach in the limited space available here. For a
more detailed summary and critique, see the recent
review by Robinson and Berridge (2003); an overall
neuropsychiatric view of addictions is available in
Graham and Schultz (1998).
1. The most generic theory in behavioral-neuroscience is that which comes down to us directly
from human studies and the generally accepted role
of rewardreinforcement processes in the guidance of behavior. In everyday parlance, this straightforward view is that people are likely to consume
drug agents that cause pleasurable feelings. In the
past twenty years, Roy Wise (1982, with subtle
transitions to 1998) has been the most prominent
proponent of this perspective in neuroscience, although it has faltered on the ambiguity of the hedonia concept and on the probable need to parse
positive affect in a variety of distinct forms to really
understand the natural order of emotional feelings.
2. A more sophisticated variant of this theory is
the opponent-process theory of addiction, originally enunciated by Richard Solomon (1977) and
colleagues, which posits that one key component of
addictionsthe initial positively experienced state
of drugsis followed by accruing negative affective consequences (opponent processes), which set
the stage for a vicious addictive cycle. These unpleasant feelings, and the capacity of drugs to alleviate them, sustain addictive behavior. This, of course,
is a formalization of the classic view that abstention
from addictive agents can generate negative withdrawal symptoms that are critical for sustaining
addictions. Neural versions of this theory (Koob &
Le Moal, 1997) also focus on the fact that the
positive hedonic effects of drugs sensitize the underlying neural substrates, which can magnify not only
the positive hedonic effects of certain drugs, but also
the affectively aversive after-effect. Of course, the
neuro-adaptations that can emerge during these
stages of addiction can also be conceptualized in
learning terms.
3. Among the learning-theory approaches, investigators focus on addiction reflecting natural, albeit
intense, learning processes that are known to be
controlled to some extent by the ML/MC DAp. The
specific types of learning that may be affected are

23

diverse, with considerable variety in specific points

of view that will not be detailed here (Everitt,
Dickinson, & Robbins, 2001; Hyman & Malenka,
2001; Schultz, 2000). These learning-theory approaches fade into the more cognitive views, some
of which focus largely on perceptual processes
(Theory 4) and those that focus more on higher
executive processes, or lack thereof (Theory 5).
4. The incentive-sensitization theory of Robinson
and Berridge (2000) has posited the relatively novel
idea that arousal of the ML/MC DAp makes environmental stimuli associated with drugs that arouse
these systems more psychologically compelling
(i.e., facilitating an incentive motivational state) and
capable of drawing organisms toward a potentially
vicious cycle of behavioral activities magnetized
by those psychological states. It also emphasizes the
consequences of neural sensitization in promoting
the cycle of events governing transitions to addiction.
5. This view is based on the recognition that the
frontal cortex is not only a major brain area that
mediates a large variety of executive processes that
help an organism negotiate between its basic bodily
and emotional needs and the long-term opportunities that exist in the environment. Without frontal
lobes, one would be at the mercy of the basic animal
urges. The recognition that people prone to developing addictions exhibit frontal-lobe deficits has lead
to the specification of this brain area as a potential
key to understanding the changes in decision making (commonly with impaired judgment and impulsivity) that are common in addicts (Bechara &
Damasio, 2002; Bolla, Cadet, & London, 1998).
6. Finally, a view that focuses on the many ingrained emotional systems of the brain (Panksepp,
1982, 1998a) is emerging and, in agreement with
Khantzians overall perspective, suggests that there
may be many affective changes that underlie addictive potentials (Panksepp, Knuston, &Burgdorf,
2002; Panksepp et al., 2003). In this view, emotional
systems are evolved action-to-perception systems,
each with its own affective characteristics, providing a broad naturalistic view of brain organization
that focuses on a diversity of brain operating systems that can figure in different emotional aspects
of addictions. The central ML/MC DAp system is
one that is conceptualized to mediate SEEKING
urges that can generate appetitive expectancies and
is thereby conceived of as an emotive action system
of the brain that can mediate habits in specific ways
(Ikemoto & Panksepp, 1999; Kelley, 1999). Since
emotional systems are conceived to modulate sensory-perceptual input channels, this perspective is
largely consistent with the incentive salience view
(Theory 4 above), but it is considerably broader,
putting substantial emphasis on the intrinsic psycho-

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24

motor energizing (i.e., mass-action states that

arouse the instinctual apparatus) aspects of the ML/
MC DAp system. In other words, changes in the
intrinsic emotional action systems of the brain are
critical in addictions, and it is assumed that affective
feelings are critically linked to the dynamics of such
intrinsic brain operating systems that help construct
distinct types of cognitive spheres of influence in
the brainmind during development (Panksepp,
2001). One main aim of this view is to parse affective space in terms of evolved neural systems shared
by all mammals, which can link up easily with
human self-report studies. It also provides a ready
gateway to linkage with the types of contextual and
personality issues that may be important in resolving who is likely to get addicted in certain situations
and who is less prone to succumb to cognitively
unregulated behavioral urges.
Of course, the degree of overlap among these
viewpoints is enormous. For practically all viewpoints, the neuro-adaptive changes that result from
chronic exposure to addicting drugs, under various
contextual and physiological conditions, become a
key issue of concern. The most salient feature of
these changes is the sensitization that has been
repeatedly shown to occur in the ML/MC DAp
(Stewart, in press; Vanderschuren & Kalivas, 2000),
which promotes heightened neuronal responsivity
of certain emotional systems, yielding a greater
eagerness for drugs as well as conventional rewards
(Fiorino & Phillips, 1999; Nocjar & Panksepp,
2002).
It is now widely considered that some of the
neuro-adaptive changes that result from drugs of
potential abuse may provide major insights into
prophylaxis. This hope remains to be realized, and I
suspect it would be hastened if neuro-psychoanalysts began to closely analyze the psychoethological
changes in people who can give testimony to the
types of depth-psychological changes that result
from the relevant neurochemical challenges to their
nervous systems.
This hope is based on the debatable assumption
that consciously experienced states of the brain
mind are as important in understanding addictions
as the increasingly touted (and ubiquitous) unconscious neuronal processes. One of the dirty little
secrets shared by most behavioral neuroscientists is
that practically no investigator is willing to invest
much credence or devotion to the view that affective
states of mind exist in the brains of the animals they
study. Most are satisfied to assert that such issues
are epistemologically unworkable, and many also
seem to believe that such positions (i.e., the view
that other animals have no experienced feelings) are
likely to be ontologically incorrect. This, of course,
puts an enormousand probably an ontologically

Jaak Panksepp

incorrect and hence arbitrarybarrier between the

types of views advocated by Khantzian and the type
of discourse indulged in by behavioral neuroscientists, who are revealing the neural details that are
essential for an in-depth scientific discussion of
addictions.
The role of conscious experiences
in addictions
The most common view in behavioral neuroscience
is that most psychological changes are mere epiphenomena and not causally efficacious factors in the
control of behavior. From the vantage that the only
thing the brain does is to process information, it
has been hard for many to imagine how psychological aspects of brain functions would have much
importance in a fully causal analysis of what people
or other organisms do. Of course, this way of looking at things does not readily acknowledge that
psychological processes reflect fairly global network functions of the brain, and that a neuron
doctrine is typically of too fine a scale to really
yield powerful explanatory schemes for global
organismic processes such as addiction. In fact (or
at least in my estimation), a network doctrine that
accepts the global and coordinated activities of
many brain systems to yield psychological processes is the most productive way, at the present
time, to view behaviorally important psychological
functions.
In any event, psychobiological viewpoints are
currently not very popular in neuroscience, and that
prevents neuroscientists from looking at brain functions in psychologically meaningful ways, including
the role of emotional experience in controlling
behavior. Indeed, the totally unconscious mechanistic view of animate actions that a radical neuron
doctrine promotes discourages discussions about
what animals may or may not experience (i.e., scientists must be agnostic and hence silent on issues that
cannot be directly measured) As a corollary, such
difficulties concerning what we can or cannot know
tends to make most behavioral neuroscientists more
eager to talk about unconscious brain processes than
about conscious ones.
Parenthetically, if there is one contribution of
Freud that has been thoroughly accepted in neuroscience, it is the importance of unconscious neural
processes in the governance of behavior. Indeed,
this bias is so strong that investigators often see
unconscious processes where the assumption is
simply not justified. In the addiction literature, the
premier experiment that is routinely misused is that
by Lamb and colleagues (1991) which is commonly
claimed to be the pice de resistance for the con-

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Understanding Addictive Vulnerability Commentaries

clusion that opiates do not have to produce conscious euphoria to sustain addictive behavior. By
generalization, this is seen as a piece of research
that strongly implicates unconscious reinforcement
processes in the governance of addictive behavior
in humans (e.g., Berridge & Robinson, 1998). That,
unfortunately, is a conclusion that is not justified
by the experiment that Lamb et al. actually conducted.
To set the record straight on that seminal and oftmisinterpreted study, let me describe it in some
detail and indicate why it should not be used to
argue against the role of conscious processes in
drug-seeking behavior patterns. Although this classic experiment was highly creative from various
methodological perspectives, it said nothing important about the role of consciousness in the mediation
of addictive behaviors. Lamb and colleagues studied five heroin addicts who were allowed to work
for one of five doses of morphine (vehicle placebo,
3.75, 7.5, 15, or 30 mg per dose). Their task was a
cognitively mediated fixed-ratio schedule during a
daily, one-hour access session freely provided for
five continuous days each week, under each of the
five dose conditions. Subjects were permitted to
work on a strenuous Fixed-Ratio 3000 schedule for
slowly absorbed intramuscular injections administered by the nursing staff, which typically allowed a
maximum of 46 infusions per session if the subjects worked at maximal rates. Not only was their
operant response rate monitored (they typically responded at a rapid average rate of about 45 lever
presses per second), but several affective and autonomic responses were also monitored about an hour
and a half after the end of each session.
The major finding of the study was that the
subjects would continue working vigorously for
pretty much all of the doses of morphine, but subjects only exhibited significant levels of drug-induced liking at the highest 30-mg dose (in fact, only
three of the five subjects experienced substantial
levels of drug liking, even at that dose). It should be
noted that even for the placebo injections, responding was sustained at a very high level on the first
placebo (or extinction) day (and rapidly declined
on succeeding days), suggesting that cognitive mediation sustained asymptotic behavior for at least
one full session. Thus, the role of reinforcement
in drug-seeking behavior (at least in the Thorndikian sense of short-term law of effect processes
that presumably help shape behavior) was probably
not even evaluated by this experimental design.
The widely touted mystery emerged at the three
intermediate dose conditions, with the lowest dose
being the most perplexing. Four of the five subjects
continued to work quite hard for the morphine, but
they did not exhibit any subjective drug-liking when

25

asked about such matters 90 minutes after the session. Thus behavior was clearly dissociated from
conscious experiences of euphoric reward.
Fair enough? Well, not quite. After all, this was
more of a cognitively mediated operant task rather
than a reinforced self-administration task (after
all, the subjects were explicitly told about the contingencies, but not the dose being administered;
under such conditions it seems unlikely the subjects
would ever have picked up the behavior on their
own with those outrageous reinforcement contingencies). Perhaps the subjects knew that they were
getting some drug and were aspiring to go even
faster to get more. (Data that may have helped
resolve this issue, on the daily response rates for the
two lowest doses, were not provided.) Also, the
subjects were heroin addicts, and it is known that
during a stable level of opiate addiction, the euphoric subjective effects of agents have almost completely diminished. However, when unable to obtain
the mega-doses needed to re-establish euphoric
states, an addict may still be satisfied to take the
lower doses that simply help him/her feel a bit more
normal.
If the investigators were taking the conscious
mediation of behavior into account more seriously,
they might have been tempted to study the changing
feelings associated with returns to psychological
normalcy, which is affectively positive, especially if one is experiencing a mild background
discomfort of protracted withdrawal (but which may
not leach into measures of drug liking, especially
if the individuals have had experiences with many
highs). During withdrawal symptoms, might there
not even be a reasonable psychological concept
such as craving for normalcy, at least in humans
who can have desires about desires?
The investigators could also have harvested other
relevant subjective feelings, such as the urge to
respond or the desire for drug reward. In other
words, since the range of relevant subjective feelings was not adequately assessed, especially those
psychological states related to response urgency or
desire, the Lamb et al. (1991) study was, at best,
measuring only a few of the relevant subjective
issues that may have been contributing to the mediation of behavior. Indeed, they apparently did not
even ask the most important question: Why were
the subjects continuing to respond on this cognitively mediated task? If the answer had been a
consistent dunno or there was nothing else to
do, then perhaps their data might be justifiably
used to conclude that the subjects were really behaving unconsciously.
Were the investigators biased? We doubt it, but
we would note a bias against detecting positive
affective responses in the sequence of morphine

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26

doses they employed. Four of the five subjects,

living together and apparently allowed to communicate with each other about their experiences, had the
following weekly sequence of doses: 15, 15, 0, 7.5,
3.75, and 30 mg (the remaining subject, tested
alone, had the same series, except he received only a
single 15-mg week at the outset). Thus, the 3.75
dose was given after three higher-dose weeks and
one presumably frustrating experience of nothing
(again, a psychological state that was not monitored). In other words, the study established the
possibility of negative psychological contrast effects that may have been shared with other participants being run concurrently on the same schedules.
Perhaps the subjects consciously decided that there
had to be something in the injected juice and
decided to simply pound away at the lever, since
there was nothing else to do for an hour.
Also, it is noteworthy that the two subjects who
found the 30-mg dose quite likeable were tested
at the same time, while the two subjects who found
it much less satisfactory were tested together in a
different cohort. The subject tested alone rated the
drug at about half the level of the above sets of
individuals, who obviously may have been talking
with (and hence biasing) each other. Surely, these
issues are of substantial importance for understanding how they were actually interpreting the uncanny
operant situations in which these postdependent
addicts found themselves.
In any event, this is not an optimal way to evaluate the relevant subjective effects that may have
been mediating behavior. First, the individuals have
had lots of experience with much higher doses of
opiates compared to those used in the study. Also,
presumably these subjects may have been fairly
emotionally unresponsive males (high levels of psychopathic tendencies exist in addict populations),
who had little desire to talk about their feelings.
Finally, the investigators did not attempt to measure
feelings of returning toward normality and feelings of ease that exist on the sensory-perceptual
side of consciousness and the felt urges and desires
for drugs and other experiences that may be present
on the output (i.e., intentional) side. Considering all
this, we are actually impressed that even at the low
3.75-mg dose, the subjects still responded to the
question Do you feel the drug? with yes responses only 38% of the time (p. 1167, emphasis
added). This, in our estimation, is an impressive and
relevant experiential response, especially when
compared to the 0% yes responses for the placebo.
In any event, this study should not be used as
evidence against consciously experienced consequences of the low doses of morphine. These doses
sustained operant output in a situation where the

Jaak Panksepp

only behavioral alternative was sitting in one place

and being bored for an hour. To address affective
experiential issues comprehensively, a different experimental perspective needs to be taken. For instance, one might place individuals in a peaceful
setting by themselves (perhaps alone in a waveless flotation tank, to minimize distractions and
other attentional biases that may disrupt the experience of internal feelings), and various doses of drug
are infused as individuals give on-line reports of
their experiential states.
Likewise, in operant situations such as the above
study by Lamb and colleagues (1991), the response
action side of consciousness needs to be evaluated
as well (i.e., by measures of urges and intentionality). Such studies have rarely been done, and they
would give us a better psychoethological perspective on what is happening to mental processes as
brain neurochemical environments are systematically modified. In other words, the time is ripe for
the establishment of a psychoethological tradition
that attempts to capture the ongoing dynamics of
the human mind in various emotionally challenging situations (for an extended discussion, see
Panksepp, 1999a, 1999b). Without such studies,
claims of unconscious information processing may
be little more than studies of context-dependent
distractibility or cue-induced expectancycontingency testing.
I do not summarize this study to criticize Lamb
and colleagues, but only those who take an uncritical attitude when they use such data to claim that
some type of unconscious reinforcement process
was mediating behavior in this situation (e.g.,
Berridge & Robinson, 1998; LeDoux, 2001). The
type of work described by Lamb et al. is simply not
sufficient to argue for the absence of conscious
motivational and emotional contributions to the observed low-dose drug-seeking behaviors. Thus, in
our estimation, the matter remains as open as it
always has, except for the recognition that the
amount of perceived drug rewardeuphoriapleasure (Theory 1 summarized above) is certainly not
the only psychological factor that plays a role in the
maintenance of drug taking. If we were to take the
full spectrum of emotional and motivational factors
that may contribute to drug consumption, as does
Khantzian, we might be less tempted to believe that
euphoria is the only thing addicts are seeking. Addictive urges surely reflect multidimensional affective processes.
I have detailed this classic experiment to highlight that before affective consciousness is
marginalized further in addiction research, better
studies of human mental processing/states to drug
challenges need to be conducted. Indeed, it is the
failure of behavioral psychology to invest more

Understanding Addictive Vulnerability Commentaries

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effort on ethological approaches that is delaying our

understanding of the true nature of addictions.
Without a full consideration of the many evolved
brain-action systems that generate adaptive behavioral tendencies (e.g., the intrinsic emotional tendencies of the brain), many of the confusions in
drug-addiction literature may be difficult to resolve
and various important avenues of research will remain unexplored. For instance, certain addictions
may be based on consummatory types of pleasure,
others on appetitive types, and yet others on the
alleviation of pain, fear, anger, and other forms of
suffering and irritability.
The role of individual temperamental factors
and emotional contexts in the generation
and governance of addictive behaviors
A key issue that theories of addiction must now
consider is that all animals, to some extent or another, have the basic affect-generating neural systems that lead to addictions, while only a small
percentage of people who sample potentially addictive agents become addicted. A classic example of
this is the fact that the high level of opiate use
among American soldiers during the Vietnam War
was not translated into continued addictive behaviors following repatriation. Clearly, a great
number of affective contextual variables (from environmental stressors to peer pressures) are very important for the continuation of addictive behaviors,
but so are the variety of personality and other constitutional factors emphasized by Khantzian.
Perhaps the most poignant example from current
American society is the high tendency for individuals with attention-deficit hyperactivity disorder
(ADHD) types of personalities to exhibit high levels
of impulsive behaviors, including addictive ones.
This may be partly due to lower-than-normal frontal-lobe inhibitory-executive functions among individuals with ADHD, and the way such issues
intersect with the advocacy of the American medical
community to provide children with such disorders ready access to weak forms of cocaine such
as methylphenidate, which may sensitize the
brain, is an issue that deserves a great deal more
discussion, research, and perhaps different forms of
social engineering that respect early childhood activities that promote more natural forms of frontallobe maturation (Panksepp, 1998b, 2002b). For
instance, the claim that administration of psychostimulants to ADHD kids may actually protect
against future drug abuse (Biederman, Wilens,
Mick, Spencer, & Faraone, 1999) is debatable from
various perspectives (Panksepp, Burgdorf, Gordon,
& Turner, 2002).

27

Conclusion
If one is willing to provisionally accept these admittedly radical points of view (at least for many neuroscientists and pure animal behaviorists), then we
might also conclude that biology-alone approaches,
even when linked to rigorous behavioral analyses,
will not suffice to completely understand changes in
brain functions that can lead to addiction. Psychological perspectives are essential for an adequate
confrontation with the problem, and to do that cogently requires us to link certain brain-system functions to psychological issues. Since the details of the
relevant brain circuitries can only be worked out in
animal models, we must also try to fathom the types
of psychological experiences that these circuits may
generate. A blending of basic behavioral neuroscience in other animals and relevant neuropsychological studies in humans is essential for progress.
Addiction, I would submit, operates largely
through the modulation of the organic-affective
state-control rather than the sensory-perceptual
channel-control functions of the brain. In short,
neither we nor other animals are unconscious zombies, but inheritors of an emotionally guided neuromental apparatus that has psychologically relevant
organizational aspects. Such approaches may facilitate translation of substantial parts of the animal
neuroscience data to new predictions in the human
realm (such as specifying neurochemical modulators of human feelings). This liberalization could
broaden the types of experiments and interpretive
structures that we might be more likely to conduct
and consider in animal brain research laboratories
(e.g., Panksepp & Burgdorf, 1999, 2000). Again, the
big payoff might be more rapid translations between
the basic neuroscience data and advances in neuropsychiatric practice.
It is unreasonable to think that affective states do
not govern human behaviors, and we think it equally
unreasonable to believe that they do not in related
mammals. In my estimation, the most reasonable,
data-based position is that emotional states simply
could not exist without a variety of instinctual
subcortically concentrated, emotional operating
systems that natural selection constructed into the
neural matrix a long time ago (Panksepp, 1998a). In
other words, our cognition-mediating neocortex
simply could not have any emotional feelings without the ancestral neural heritage we share with many
other animals. This does not imply that the various
neuroscientific nuts and bolts needed to construct
emotional operating systems are conscious in and of
themselves, only that experiential properties do
emerge when certain global state-control systems of
the brain come to interact in a hierarchical fashion
with each other as well as with the many sensorimo-

28

tor channel-control functions that exhibit such enormous variability across species.

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