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It has been found that between 70 to ninety percent of adults gamble at some point in their life. (Ladoucer, 1991). These figures are from Canada but can be genralised to most developed civilisations. According to the DSM criteria pathological gambling is am impulse control disorder, which is displayed by a persistent and uncontrolled gambling, failure to stop gambling, feeling withdrawal symptoms and uneasiness when not aloud to take part in a gambling activity and finally increased gambling. (ref). The increased availability of gambling opportunities often makes this a hard condition to recover from, as well as increasing the amount of people suffering from pathological gambling(ref). Pathological gambling causes the obvious financial problems (ref), but like any other “addiction” it causes social problems as well (ref). Along with this pathological gambling has been linked in some cases to higher rates of suicide attempts (ref).
Pathological gambling is classified as a behavioural addiction, rather than a chemical addiction. Although seemingly different these both manifest in the same way, that is “the enduring engagement in uncontrolled self-destructive behaviour, despite its negative consequences” (ref).
There are many different theories of behavioural addiction, in particular pathological gambling and how it should be treated, which will be critically reviewed and considered.
It would seem that in the seemingly distant past psychodynamic approaches such as those put forward by Freud and Bergler were prevalent. Since then many approaches and theories to the causes of pathological gambling have been found, these models include; the medical model, some behavioural models, psychological models, cognitive behavioural approaches and of coarse biological, physiological and models of personality. Some of these models are reviewed and considered in greater depth.
To start with psychodynamic approaches will be looked at. As is commonly known amongst academic community, these approaches are relatively old, mostly carried out in the early 1900’s. Due to the age of these theories and the pace at which theories are changed these psychodynamic approaches may seem quite irrelevant. It is important to gain an understanding of this area as some theories take a basis from psychodynamic approaches. According to the psychodynamic approach, gambling is a way of expressing feelings connected with the pre-genital psychosexual stages (Greenson). In true psychodynamic style pathological gamblers often feel that they have been denied the attention and love they deserved from their parents and as a result need erotic satisfaction, which in tern seems to create a need for excitement and pleasure, as well as a “promise of gain.” According to psychodynamic theories gambling caters for these needs (Simmel 1920). So in a nut shell gambling is a substitute for feelings of subconscious sexual conflicts. Arguably the founder of psychodynamics, Freud (1928), reported that gamblers do not play to win money, quite the opposite. In fact Freud states that gamblers gamble to loose in order to provide a self-inflicted punishment for the guilt carried with an over compulsion to masturbate, which can be related to an Oedipal conflict. This idea put forward by Freud seems quite masochistic, in the way that that the gambler is actually taking part to loose and there for punish themselves. Bergler (1967) agreed with Freud in the respect that a gambler unconsciously desires to lose. Bergler had a different opinion on why compulsive gamblers get addicted. This is that in their unconscious they dislike authority figures, who during childhood, made them consider the “reality pleasure” instead of the “pleasure principle.” These could be parental figures or teachers. This unconscious feeling causes them to try and almost rebel against the people who support the “reality principle” as well as he principle it’s self, this in turn causes a need to punish themselves as a bi-product of having too much built up unconscious aggression.
So far only the very surface of the psychodynamic approach towards pathological gambling has been looked at. In summary according to the psychodynamic approach there seems to be three ideas to explain pathological gambling “an unconscious substitute for pre-genital libidinal and aggressive outlets associated with Oedipal conflicts,” a desire “for punishment in reaction to the guilt,” and a means for recurrent “re-enactments, but not resolutions, of the conflict” (Allcock, 1986, p. 262). So these being the main ideas a treatment plan can be called upon.
Treatments of pathological gamblers offered by the psychodynamic approach are concerned with the narcissistic personality and the related characteristics. Psychoanalysis has been used in an attempt to try and help pathological gamblers, but in most cases have failed. Bergler’s (1957) study is one of the more classic studies and showed a 75% rate of success. This though was only based on 30% of the overall group looking for treatment, meaning that it was in fact a lot lower than 75%. Another issue is the lack of follow up treatment given, with no information given about possible relapses. This is not the only study where this is the case. In a review Greenberg (1980) stated “Effectiveness rates of gamblers treated psychoanalytically have ranked from poor to guarded optimism.” This simply means that results are not very good or are shadowed by other factors, such as selection bias and lack of follow ups. It would seem that a lot of the studies and journals available to view for the psychodynamic approach deal with small sample sizes and do not have important experimental factors, such as control groups. This causes problems with generalisability and also shows why the psychodynamic approach was disregarded as a treatment for behavioural conditions, this coupled with their lack of consideration for social factors.
The next theory that will be looked at is the disease or medical model. This is often seen as a very black and white model (Blume, 1987), meaning that it’s ether on or off, someone either has a condition or they don’t, there is no in-between. Every condition is viewed as a disease. So in terms of pathological gambling, the gambler is pathological or quite simply is not. The disease model, as the name suggests, views pathological gambling as a disease and so the cause is physiological, and pathological gamblers are often predisposed. According to Blume, being a disease, addictive conditions, such as gambling, manifests through stages of development, has signs characteristic to the condition and has symptoms, much like a disease. This is all out of the person’s conscious control, not so different to the psychodynamic ideas.
This concept of a disease suggest that the condition worsens, which will eventually require treatment in order to prevent worsening. It is thought that the physiological underpinning means that there is no out right cure and that it is irreversible. This means that according to the disease model that the most appropriate treatment is abstinence, similar to that of alcohol (ref). This seems like an odd treatment, as it would suggests that there is in fact no real way of recovering, just a treatment.
This model is not used so much now(refbig paper), but is more of a halfway house with other theories, such as the biological explanations of pathological gambling.
The biological approach to pathological gambling is, in relative terms a rather new theory. It is made up of many components to try and explain different aspects of pathological gambling. These all make the same assumption that a physiological cause is behind addiction, much like both the psychodynamic and the disease model.
The first aspect with in the biological approach to be considered is that of hemispheric dysregulation (Goldstein et al, 1985). By comparing EEG patterns of recovered pathological gamblers, Goldstein observe that pathological gambler’s EEG readings where similar to those of patients suffering with ADHD (Carlton and Goldstein, 1987). This means that they had a shorter attention span, frontal lobe lesions. This is also very similar to findings of alcoholism which have also led to more reported symptoms of ADHD symptoms with in the population of problem gamblers (Rugle and Melamed, 1993). This all seems very convincing, but the original 1985 study by Goldstein was only carried out on eight participants, such a small study provides problems with generalisability.
Other suggestions are that it is connected to faults in the neurotransmitter systems (Blanco et al, 2000). This includes the Serotoneric system, which as the name suggests holds the function of serotonin release. If this is not functioning, to a healthy level, then psychiatric syndromes, such as impaired impulse control, can become present. This has been linked with pathological gambling (Blanco et al, 1996). Later research by Berg et al (1997) failed to support these findings, stating in the following wel used quote, “risk-taking does not have a unitary neurochemical correlate. If risk-taking is a form of loss of control over impulse, it follows that impulse control is not merely a simple function of the neural serotonin systems.” (p.475).
Links have also be found in DNA, supporting the biological idea Perez de Castro (1999). According to Brunner et al (1993) these is a link between genetic deficit coding and impulsivity, possibly providing a good explanation.
The increased release of Dopamine has also been linked to pathological gambling (Berg et al 2007), this is much like a positive reinforcement. It can though also be linked to a negative inforcment, with more gambling causing a withdrawal, which creates the release of more dopamine, not unlike that of an opiate withdrawal (Berg, 1997).
The evidence for the biological approach seems quite strong. There is a few outstanding issues that need to be looked at. For example almost all of the above studies use male participants. This creates an issue as whether they can be used with women. The samples are also very small in most cases. The main problem that can be observed in all the studies in this area is whether the biological processes cause the addiction of the addiction it’s self, causes these biological processes.
So as can be seen the medical/disease model and the biological model are both very similar but can be separated in the way that the biological model believes that pathological gambling can be treated with certain drugs.
So far all models, with the exception of psychodynamic, have been based on biological internal processes. The cognitive social learning and behavioural theories are based on external and behavioural processes. The learning theories suggest that gambling is a learned behaviour that has resulted from both operant and classical conditioning. According to the behavioural view point there are a mixture of different positive reinforcement these are, the amount of money that is won (Moran, 1979), excitement gained (Brown, 1986). Obviously there are also negative reinforcement, namely the escapism that gambling can produce (Diskin, 1997). Some how though theses models don’t seem complete. They can not explain punishments, like the cost of gambling, as discouraging to the gambler, which using a classic behavioural model it would be.
Despite this, studies into using behavioural theories of addiction as treatment have been very successful.
Behavioral treatment studies have, however, provided some of the most comprehensive treatment literature on PG. Treatments based on learning principles (i.e., behavior modification) have involved aversion therapy using physical or imaginal stimuli (Barker; Barker and Goorney), controlled gambling/behavioral counseling (Dickerson & Weeks, 1979), positive reinforcement of gambling abstinence, paradoxical intention (Victor & Krug, 1967), covert sensitization (Bannister and Cotler), and imaginal desensitization (McConaghy, Armstrong, Blaszczynski, & Allcock, 1983). These have been administered singularly or in combination. However, due to methodological shortcomings in such studies, it is difficult to assess how effective these treatments are. Most of these treatment studies have small sample sizes and limited follow-up periods. They have unspecified or poorly operationalized dependent variables/criteria for successful outcome or treatment objectives (Allcock, 1986). Also, there is usually a lack of controlled comparisons of one treatment with another or with a placebo procedure, or combinations of several techniques are used concurrently so that identification of the active component is impossible (Blaszczynski & Silove, 1995).
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