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Introduction
Historically,
societal attitudes toward gambling were influenced by the effects of gambling on
public order, the erosion of prevailing moral values and social mores, and the cheating
and exploitation of the masses (Peterson, 1950; Ploscowe, 1950; Blakely, 1977). The
move to medicalize pathological gambling originated from the case studies of early
psychoanalytic writers (Von Hattinger, 1914; Bergler, 1957), and by the inclusion
of pathological gambling in DSM-III (American Psychiatric Association, 1980), as
a psychiatric disorder of impulse control. The formalization of pathological gambling
as a psychiatric disorder led to recent attempts to develop theoretical models, which
explain the aetiology of problem gambling (Ferris, Wynne & Single, 1998).
Contemporary
psychological models include gambling as:
- an addictive disorder (Jacobs, 1986; Blume, 1987)
- an unresolved intrapsychic conflict (Bergler, 1957; Rosenthal, 1992; Wildman,
1997)
- having its causation through a biological/psychophysiological dysregulation (Blaszczynski,
Winter & McConaghy, 1986; Carlton & Goldstein, 1987; Lesieur & Rosenthal,
1991; Rugle, 1993; Comings, Rosenthal, Lesieur & Rugle, 1996)
- a learned behaviour (McConaghy, Armstrong, Blaszczynski & Allcock, 1983;
Anderson & Brown, 1984)
- a result of distorted/irrational cognitions (Sharpe & Tarrier, 1993; Ladouceur
& Walker, 1996).
This diversity
of models has led to the search for qualitative similarities and differences between
social and pathological gamblers in personality traits (Blaszczynski, Buhrich &
McConaghy, 1985; McCormick, Taber, Kruedelbach & Russo, 1987; Castellani &
Rugle, 1995), co-morbidity (Kruedelbach & Rugle, 1994) and biological correlates
(Rugle, Semple, Goyer & Castellani, 1995; Comings et al., 1996).
The fundamental
assumption contained within each model is that pathological gamblers constitute a
homogenous population, and that theoretically derived treatments can be effectively
applied to all pathological gamblers. There is minimal evidence to support this implicit
assumption. On closer inspection, learning theories (Dickerson, 1979) refer to fixed
and variable schedules of reinforcement. But these learning theories fail to explain
why not all gamblers suffer impaired control. Cognitive theories (Sharpe & Tarrier,
1993; Ladouceur & Walker, 1996) emphasize irrational cognitive schemas but have
not demonstrated that these are of causal significance. Heated debate continues on
the validity of the addiction model of gambling, particularly by those adhering to
the socio-cognitive approach.
Divergent
frameworks, however, can be reconciled if gamblers are accepted as a heterogeneous
group (Blaszczynski, 1996) with multi-factorial causes. It cannot be denied that
the majority of gamblers seek monetary gain. But some continue to participate and
persist because they are inexorably motivated to find relief from boredom, to dissociate
and to escape from negative life circumstances, or to modulate negative mood states.
The task confronting clinicians is to refine the categorization of problem gamblers
into increasingly homogenous subgroups or typologies of gamblers.
In a series
of long-term controlled outcome studies (Blaszczynski, 1988; McConaghy, Blaszczynski
& Frankova, 1991), three types of responses to treatment were observed: controlled
gambling, abstinence and uncontrolled gambling. Controlled gamblers were characterized
by an absence of psychopathology, abstinent gamblers continued to exhibit moderate
levels of affective disturbances and elevated neuroticism; while uncontrolled gamblers
persisted in showing high levels of psychopathology across a number of domains. These
findings matched my clinical experience. I found that some gamblers displayed integrated
personalities; others showed evidence of depressive affect and situational stresses
which precipitated increased gambling. Others manifested traits of impulsivity and
severe disruptive behaviours in gambling and in other parts of their lives.
These findings
made me question if the response to treatment was predicated on personality or demographic
differences, which were present between groups prior to treatment. However, no such
differences emerged when statistical comparisons were applied to group variables.
An alternative possibility was therefore considered: that is, that the end results
of gambling had affected their psychological profile so that it masked group differences.
I argued that with gambling the common manifestation of affective disturbances (anxiety,
substance use and criminality) were a complex mixture and/or interaction of both
primary and secondary processes involved in gambling. In some cases, depression was
instrumental in causing impaired control over gambling; while in others, gambling
produced depression resulting from financial and marital difficulties. During a psychometric
assessment, both groups obtained similar scores on depression. But this depression
had significantly different implications in respect to etiological significance and
relevance to treatment strategies. This led to the postulate that specific subgroups
of gamblers existed and shared features in common, yet differed significantly in
many respects.
I have proposed
a prototypical model that attempts to integrate biological, personality, developmental,
cognitive, learning theory and environmental factors into one model. This model is
based on clinical experience and attempts to integrate relevant research findings.
It suggests the existence of three major types of gamblers: the gambler who is not
pathologically disturbed, the gambler who is emotionally vulnerable, and the gambler
whose impulsivity is biologically based.
There are
three elements relevant to all gamblers irrespective of subgroup membership. The
first relates to ecological determinants. These determinants revolve around public
policy issues that promote availability and access to gambling facilities. Substantive
data clearly demonstrates that the incidence of pathological gambling is inextricably
tied to the number of available gambling outlets (Abbott & Volberg, 1996; Volberg,
1996; Productivity Commission, 1999).
The second
element resides in the role of classical and operant conditioning. Studies have demonstrated
that gambling produces a state of subjective excitement (Dickerson, Hinchy &
Fabre, 1987), dissociation (Jacobs, 1986) and increased heart rate (Anderson &
Brown, 1984; Leary & Dickerson, 1985; Brown, 1988; Griffiths, 1995). Wins, delivered
at variable ratios that are resistant to the effects of extinctions, produce states
of excitement described as equivalent to a "drug-induced high." Repeated
pairings classically condition this arousal to stimuli associated with the gambling
environment (Dickerson, 1979; Sharpe & Tarrier, 1993). Through second order conditioning,
gambling cues elicit an urge to gamble, which results in a habitual pattern of gambling.
As Rosenthal and Lesieur (1992) observe, excitement can be experienced in anticipation,
during, or in response to exposure to gambling situations or cues. This process of
conditioning can be used to explain gambling as an addiction produced by the effects
of positive and negative conditioning, tolerance and withdrawal.
An alternative
non-addiction explanation has also been offered, and is based on a neo-Pavlovian
"neuronal model" of habitual behaviour, which relies on the concept of
cortical excitation (McConaghy, 1980).
Superimposed
on the conditioning framework and irrespective of whether or not an addiction type
model is adopted, is the development of cognitive schemas. Early and repeated wins
result in irrational belief structures that promote gambling as an effective source
of income. These schemas shape illusions of control, biased evaluations, erroneous
perceptions, superstitious thinking and faulty understandings of probability (Langer,
1975; Gilovich, 1983; Ladouceur & Walker, 1996; Walker, 1992; Griffiths, 1995).
The reinforcing
properties of gambling and the irrational cognitive schemas combine to consolidate
and strengthen habitual gambling practices. At this point, the downward spiral of
gambling, perceptively described by Lesieur (1984), takes its toll. When gamblers
lose they attempt to recoup losses through further chasing, which results in accumulating
financial debts. Despite acknowledging the reality that gambling led them into financial
problems, they irrationally believe that gambling will solve their problems.
It is emphasized
that the above processes are applicable to all gamblers. At this point additional
factors can be invoked to differentiate between three broad subgroups of gamblers.
Subgroup one: "Normal" problem gamblers
The first
subgroup can be labelled, perhaps somewhat oxymoronically, as the "normal"
pathological gambling subgroup. Members of this subgroup may meet formal criteria
for pathological gambling at the height of their gambling disorder. What distinguishes
this subgroup is the absence of any specific premorbid psychopathology. Conceptually,
these gamblers can be seen as occupying the diffuse domain between regular-heavy
and excessive gambling. Excessive gambling behaviour occurs as a result of bad judgments
or poor decision-making strategies, which are independent of any intrapsychic disturbance.
Features of a preoccupation with gambling, chasing losses, substance dependence and
depression and anxiety are all seen as the end response to the presence of financial
pressures caused by continual losses. These symptoms are the consequence not the
cause of excessive gambling.
Clinically,
the severity of difficulties in the "normal" gambling subgroup is the lowest
of all pathological gamblers. They do not manifest gross signs of major premorbid
psychopathology, substance abuse or impulsivity behaviours. Placed at the low end
of the problem-gambling scale, these gamblers move between heavy and problem gambling.
They are more motivated to seek treatment, to comply with instructions and post treatment
are able to achieve controlled levels of gambling. Counselling and minimal intervention
programs are of benefit.
Subgroup two: Emotionally disturbed gamblers
The next
subgroup is characterized by the presence of predisposing psychological vulnerability
factors where participation in gambling is motivated by a desire to modulate affective
states and/or meet specific psychological needs. This subgroup manifests a history
of problem gambling in the family, negative developmental experiences, neurotic personality
traits and adverse life events. These problems may contribute in a cumulative fashion
to produce an emotionally vulnerable gambler.'
Evidence
in support of this contention comes from a number of sources. Jacobs (1988), Lesieur
and Rothschild (1989), Gambino, Fitzgerald, Shaffer, Renner, and Courtage (1993)
observed that a family history of pathological gambling was an important predisposing
risk factor for children. Jacobs (1986), in his General Theory of Addiction, postulated
that certain personality characteristics and life events, which interacted with physiological
states of arousal, influenced the development of gambling problems. He stated that
excessive gambling was produced by the interaction between abnormal physiological
resting states of hyper or hypo-arousal, and a history of negative childhood experiences.
Personal vulnerability was linked to negative childhood experiences of inadequacy,
inferiority, low self-esteem and rejection (McCormick, et al., 1987; McCormick, Taber
& Kruedelbach, 1989).
This subgroup
of gamblers displays higher levels of premorbid psychopathology. In particular, they
display depression, anxiety, substance dependence, and deficits in their ability
to cope with and manage external stress. Gamblers within this subgroup cannot express
their emotions directly and effectively, and they show a tendency to engage in avoidance
or passive aggressive behaviours. Emotionally vulnerable gamblers see gambling as
a means of achieving a state of emotional escape through the effect of dissociation
on mood alteration and narrowed attention (Anderson & Brown, 1984; Jacobs, 1986).
The abstinent
gamblers in Blaszczynski's (1988) and Blaszczynski, McConaghy and Frankova's, (1991)
two-to-five year treatment outcome study appear to fall within this subgroup. In
respect to psychopathology, the abstinent gamblers were placed on an intermediate
position between the more adjusted controlled and severely disturbed uncontrolled
gamblers. Because of their negative developmental history and poor coping skills,
these gamblers were regarded as too fragile to maintain sufficient control over behaviour
to permit controlled gambling.
Subgroup three: Biological correlates of gambling
The third
subgroup of pathological gamblers is defined by the presence of neurological or neurochemical
dysfunction reflecting impulsivity (Steel & Blaszczynski, 1996) and attention-deficit
features (Rugle & Melamed, 1993). Briefly, evidence supporting neurological deficits
in gamblers is found in electrophysiological, neuropsychological and biochemical
studies.
Goldstein
and his colleagues (Goldstein, Manowitz, Nora, Swartzburg & Carlton, 1985; Carlton,
Manowitz, McBride, Nora, Swartzburg & Goldstein, 1987) reported differential
patterns of EEG activity and self-reported symptoms among gamblers found in childhood
attention deficit disorder. Supporting this finding, Rugle and Melamed (1993) on
the basis of neuropsychological measures of executive functions concluded that childhood
differences in behaviours related to overactivity, destructibility and difficulty
inhibiting conflicting behaviours were of primary importance in differentiating gamblers
from controls. These authors noted that attention- deficit related symptoms reflecting
traits of impulsivity were present in childhood. These traits predated the onset
of pathological gambling behaviour and gave rise to the hypothesis that impulsivity
precedes gambling; and that impulsivity is independent of it and is a good predictor
factor for severity of involvement in at least a subgroup of gamblers.
From preliminary
evidence in the field of genetics and from neurotransmitter activity comes the tentative
hypothesis which links receptor genes and neurotransmitter dysregulation in reward
deficiency, arousal, impulsivity and pathological gambling (Roy, De Jong & Linnoila,
1989; Lopez-Ibor, 1988; Moreno, Saiz-Ruiz & Lopez-Ibor, 1991; Carrasco, Saiz-Ruiz,
Hollander, Cesar & Lopez-Ibor, 1994; Comings et al, 1996; Bergh, Eklund, Sodersten
& Nordin, 1997; DeCaria, Hollander, Grossman, Wong, Mosovich & Cherkasky,
1996).
Genetic
studies have recently reported that pathological gamblers, similar to substance abusers,
are much more likely to have the D2A1 allele for the dopamine D2 receptor gene than
controls leading Comings et al., (1996) to suggest that the D2A1 allele may be a
major risk factor in pathological gambling. When gamblers were evaluated on severity,
63.8 per cent of them in the upper range carried the D2A1 allele compared to 40.9
per cent in the lower range. Of note: 76.2 per cent of pathological gamblers who
were co-morbid alcohol abusers carried the gene compared to 49.1 per cent of males
without co-morbid alcohol abuse or dependency.
It is argued
that gamblers manifest differential responses to reward and punishment because of
their biologically based impulsivity. These gamblers manifest a marked propensity
for seeking out rewarding activities. They are unable to delay gratification, and
have a diminished response to punishment. When the consequences of their actions
are painful, they fail to modify their behaviour.
Clinically,
impulsive gamblers display a broad spectrum of behavioural problems which are independent
of gambling. These problems include substance abuse, suicidality, irritability, low
tolerance for boredom, sensation seeking and criminal behaviours. Poor interpersonal
relationships, excessive alcohol and poly-drug experimentation, non-gambling related
criminality, and a family history of antisocial behaviour and alcoholism are characteristic
of this group. Gambling commences at an early age, rapidly escalates in intensity
and severity, occurs in binge episodes and is associated with early gambling-related
criminality. These gamblers are less motivated to seek treatment in the first instance,
have poor compliance rates, and respond poorly to any form of intervention.
Discussion
The starting
premise of the proposed pathway typology model is that problem gamblers form a heterogeneous
population; the end result of a complex interaction of genetic, biological, psychological
and environmental factors. From this population, subgroups of gamblers sharing commonalties
can be extracted. The strength of this approach is that it integrates disparate findings
reported in the literature. It takes into account the notion that there are groups
of non-disturbed gamblers. These gamblers lose transient control over their behaviour
because of irrational cognitions, which lead to a series of poor judgments and they
become temporarily over-involved in gambling. Fluctuations between heavy and excessive
gambling are observed; their disordered gambling may remit spontaneously or with
minimal interventions. At the same time, the pathway typology recognizes subgroups
of gamblers who participate for emotional reasons: to dissociate as a means of escaping
painful life stresses, to reduce boredom, or to deal with unresolved intrapsychic
conflicts or childhood traumas. The model also acknowledges that there are some gamblers
who exhibit biological correlates of disturbed behaviours. These traits qualify them
as sufferers of a medical and/or psychiatric condition characterized by impulsivity
and features of attention deficit disorder.
All three
subgroups are affected by environmental variables, conditioning and cognitive processes.
From a clinical perspective, each pathway contains different implications for managing
ement strategies and treatment interventions. "Normal" pathological gamblers
require minimal interventions, counselling and support strategies and may resume
controlled gambling post intervention. Self-help groups such as Gamblers Anonymous
are effective, as are self-control self-help educational materials.
The needs
of emotionally vulnerable gamblers who seek solace through dissociation produced
by gambling (Anderson & Brown, 1984) to deal with emotional distress, life circumstances
or trauma and loss (Taber, McCormick & Ramirez, 1987) require more extensive
psychotherapeutic interventions. Relevant here are stress management and problem-solving
skills, as are therapeutic endeavours directed toward resolving intrapsychic conflicts
and procedures designed to enhance self-esteem and self-image.
For those
gamblers with biological correlates, clinicians must attend to problems related to
attention and organizational deficits, emotional liability, stress intolerance, and
poor problem solving and coping skills. These gamblers may require intensive cognitive
behavioural interventions aimed at impulse control, which is administered over longer
terms. Medication aimed at reducing impulsivity through its calming effects may be
considered (for example, Prozac); although more random-controlled outcome trials
are needed before the benefits of the medication can be established with confidence.
The proposed
pathway model is a conceptual framework that attempts to integrate research data
and clinical observation to assist clinicians in the identification of distinct subgroups
of gamblers requiring different treatment strategies. It is hoped that the model
will provide a practical clinical guide that will improve the effectiveness of treatment
by refining diagnostic processes and matching gamblers to intervention techniques.
The model is open to empirical testing.
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