Reframing problem and pathological gambling: the new evidence

1
Re-framing problem and pathological gambling the
new evidence

• Don Ross
• U of Cape Town / U of Alabama B'ham
• don.ross_at_uct.ac.za

2
Aims of the talk

• Ill describe recent scientific evidence for two
  main claims
• (1) some people are neurochemically addicted to
  gambling
• But
• (2) they arent the locus of the main social
  problemarising from excessive gambling

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Clinical usage

• This is derived from a medical model of
  alcoholism going back to the middle of the last
  century
• Pathological gamblers are the gambling
  equivalent of alcoholics they are either in
  remission or gambling obsession dominates their
  lives.
• Problem gamblers are the gambling equivalent of
  problem drinkers they alternate between
  episodes of socially acceptable gambling behavior
  and episodes in which they struggle and fail to
  control damage caused by their gambling.

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Inconsistency of principle

• Pathological gamblers are conceptualized by
  reference to an hypothesized internal property.
• Problem gamblers are conceptualized by reference
  to externally indexed harm.

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Two cheers for inconsistency

• This turns out to be on the right track as long
  as we correct for a historical practice of
  assigning (far) too many problem gamblers to the
  pathological group.

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DSM operationalization of Pathological gambling

• PG is a variety of impulse control disorder in
  which a person manifests a chronic inability to
  refrain from gambling to an extent that causes
  serious disruption to core life aspects such as
  career, health and family. A person is diagnosed
  as a probable pathological gambler if they agree
  with five or more of the following statements

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• 1. You have often gambled longer than you had
  planned.
• 2. You have often gambled until your last dollar
  was gone.
• 3. Thoughts of gambling have caused you to lose
  sleep.
• 4. You have used your income or savings to gamble
  while letting bills go unpaid.
• 5. You have made repeated, unsuccessful attempts
  to stop gambling.
• 6. You have broken the law or considered breaking
  the law to finance your gambling.
• 7. You have borrowed money to finance your
  gambling.
• 8. You have felt depressed or suicidal because of
  your gambling losses.
• 9. You have been remorseful after gambling.
• 10. You have gambled to get money to meet your
  financial obligations.

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Problem gambling

• Not defined in DSM.
• But US Committee on the Social and Economic
  Impact of Pathological Gambling defines as
  gambling behavior that results in any harmful
  effects to the gambler, his or her family,
  significant others, friends, co-workers etc.
• Rendered literally meaningless by use of any
  and lack of quantitative restriction.
• Then Disordered gambling defined as union of
  Pathological and Problem gambling.

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Is Problem gambling low-severity Pathological
gambling (PG)?

• There is no underlying model of PG by which one
  can define a common scale for quantifying the two
  phenomena together and the inconsistency makes
  this a fools errand anyway..
• Not all statements in the DSM operationalization
  are equally weighted clinically (5), (6), and
  (10) are more strongly diagnostic and (8) is
  highly statistically predictive.

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Problems with clinical screens as research
instruments

• Screens are designed to avoid false negative
  identifications thus they are biased (heavily)
  toward false positives.
• Research is forced to frequently rely on clinical
  samples. But there are ethical objections, based
  on interference with treatment, in using
  different instruments to re-classify clinical
  populations. Instead, we refine the screen
  classifications using structured clinical
  interviews based on DSM operationalizations. But
  these are impractical for use in most studies
  unless samples are small.

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PG screens

• 90 of studies to date used the South Oaks
  Gambling Screen (SOGS). We now believe that this
  resulted in overestimating prevalence by about
  100.
• More sophisticated screens have been used in
  superior prevalence studies over the past 2
  years. This suggests typical prevalence rates
  (UK, US, NZ, pilot data from SA) as follows
  4-5 experience transient gambling problems
  0.5-0.7 are true PGs. Just a few years ago,
  some scientists were estimating the US prevalence
  of PG at 7! The media continues to use this
  figure.

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Severity measures

• Only one screen, the Canadian Problem Gambling
  Index (CPGI), tries to measure severity. Given
  the inconsistency, were going to need different
  such measures for pathological and problem
  gambling.

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Comorbidities

• One clear predictor of PG severity that has
  broken through the data and analysis problems is
  other Axis-I comorbidity. This raises further
  questions about the underlying model. Is PG an
  expression of other comorbidities, or are
  multiple Axis-I problems consequences of a common
  causal factor (or factors)?

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The sample problem

• It is hard to resolve these issues by running
  surveys. The basic problem is the very low
  prevalence of PG, which interferes with efforts
  to estimates shapes of distributions and to
  obtain balanced samples. This blocks use of
  econometric regression techniques. So
  correlations pile up while causal models remain
  elusive.

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Progress nevertheless

• Two approaches are coming to the rescue where the
  true addicts are concerned
• Neuroscience based on imaging studies
• Molecular genetics

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Neuroscience of addiction

• Thanks to fMRI work, a neuroeconomic model of
  addiction is coming together. The mesolimbic
  dopamine reward system gains control of the
  organisms molar behavior by chemically
  attenuating feedback serotonin (and other)
  circuits from frontal and prefrontal cortex that
  normally bid for attention to, and for scheduling
  consumption of, longer-range sources of reward.
  The reward system achieves this mutiny by
  exploiting the discovery that, through
  relentlessly searching for cues to the arrival of
  an addictive target, and then organizing
  consumption of that target, it can reliably
  produce floods of dopamine in striatum that
  constitute the reward it is itself evolved to
  maximize and which simultaneously overwhelms the
  functioning of normally rival circuits.

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The brains of PGs

• People who report greatest behavioral disturbance
  with respect to gambling closely resemble drug
  addicts in having hyperactive striatal dopamine
  responses in the presence of cues for gambling
  (drugs), including their own fantasizing about
  gambling (drugs), and hypoactive opponent
  neurotransmitter responses.

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A conceptual proposal

• In the book Midbrain Mutiny (2008), Ross et al
  (2008) marshal evidence for the suggestion that
  it would be best for both research and treatment
  to identify PG with neurochemical addiction to
  gambling. The present DSM operationalization
  fails to cut nature at a joint, as philosophers
  like to say.

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An heritable component?

• Based on examination of 3359 twin pairs, Eisen et
  al (1998) conclude that inherited factors explain
  between 35 and 54 of reports of five DSM
  symptoms that could be estimated statistically,
  56 of the report of three or more symptoms, and
  62 of diagnoses. Potenza et al (2005) find a
  matched genetic contribution with near-perfect
  overlap to pathological gambling and major
  depression, while Slutske et al (2000) report
  common genetic vulnerability to pathological
  gambling and alcohol dependence in male subjects.

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Genetics

• Seven association studies by Ibáñez et al (2003)
  separating evidence between conceptions of
  pathological gambling as an obsessive-compulsive
  disorder the category in which DSM places
  pathological gambling but not drug addiction
  and the family of dopaminergic pathologies that
  clearly include the classic addictions.
• (Implicated genetic structures Promoter
  polymorphism sequence for expression of MOA-A
  protein DRD4 7-repeat allele Taq-A1 allele of
  the D2 dopamine receptor gene. All of these are
  associated with dopamine, or with the
  dopamine-serotonin interaction.)

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Conclusion I what the PGs need is to be fixed

• We should reconceptualize the phenomenon
  operationalized as PG in DSM-IV as a specific
  manifestation of disruption in frontal-cortical
  governance of the mesolimbic dopamine system. PG
  so conceptualized facilitates construction of
  testable models, predicts the observed dramatic
  fall-off in natural remission at the extreme end
  of CPGI scores, and shows evidence of gathering
  patients into a class that responds similarly to
  drug therapies.

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Conclusion II for problem gamblers, focus on the
transience

• The crucial fact about most problem gamblers is
  that they recurrently stop and start. I thus
  doubt that their typical main problem is
  misunderstanding of the house advantage if it
  were, why would they regularly make (successful)
  efforts to quit?

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Other forms of transient self-undermining are a
clue

• Why do some people go through recurrent episodes
  in which they drink too much?
• Here are the leading reasons, in order (1) they
  suffer relationship break-ups (2) they suffer
  major employment / career setbacks (3) they come
  to feel oppressed by the rules other
  peoples, and/or their own.

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How do most transient problem drinkers get out of
the problem zone?

• Answer on their own or with their partner, they
  decide to drink less and then they follow through
  on their decision.

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What do we most need to know about this
population?

• (1) How long are typical remission periods is
  there a standard pattern? Are there any data that
  would tend to predict such patterns?
• (2) How many of these people want outside help?
  What are the policy implications if this turns
  out to be a low number?

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The NRGP / NCSG team

• David Spurrett, University of KwaZulu-Natal
• Harold Kincaid, University of Alabama at
  Birmingham
• Graham Barr, University of Cape Town
• Carla Sharp, Baylor College of Medicine (Houston)
• Martine Visser, University of Cape Town
• Rudy Vuchinich, University of Alabama at
  Birmingham
• Robert Ladouceur, Laval University
• George Ainslie, Veterans Medical Centre,
  Coatesville PA
• Jacques Rousseau, University of Cape Town
• Andre Hofmeyr, University of Cape Town
• Andrew Dellis, University of KwaZulu-Natal