1. Addiction A BioPsychoSocial approach Dr Bob Patton
Addictions Department
2. In this 45 minute introductory lecture you will learn about
the biopsychosocial approach to addiction At the end of this
session you should: Have an understanding of the neurological
systems that underpin addiction. Appreciate that the ways addiction
is explained has a direct influence upon treatment. Be aware that
there is no unified theory of addition, but that an integrated
approach can help explain onset and maintenance of addictive
behaviour.
3. There are many different drugs that can be abused legal and
illegal. This table is from an article published in 2004; there
would be a few more additions to the table for 2013 Its a drug! The
most obvious omissions are the ones that can be loosely described
as legal highs. Never the less drug misuse remains a persistent
issue worldwide
4. A continuum of harm Drug Use Any psychoactive recreational
substance use Experimental Use Drug Misuse, Abuse Any unsanctioned
recreational substance use Harmful Use Use of a psychoactive
substance which leads to harm whether to health, psychological
well-being, or socially need not be dependent use Dependent Use
Persistent uncontrolled drug use repeatedly leading to (multiple)
harmful consequences
5. All theories of addiction attempt to explain the processes
that underpin the onset and maintenance of drug taking behaviors.
When considering the various theories remember that each should be
able to: Explain the onset of addiction Account for the maintenance
of addictive behaviors Suggest mechanisms for treatment There is NO
single unified theory of addiction (although attempts are being
made to integrate existing ones refer to ALICE-RAP, 2011 for more
details) Theories of Addiction
6. Any 3 of the following: Tolerance Withdrawal syndrome Larger
amounts, or longer use, of drug than intended Persistent desire, or
unsuccessful attempts, to control / quit Excessive time spent
obtaining & using drug, or recovering from its effects
Important social, occupational or other activities reduced
Continued use despite physical or psychological harms What is
addiction? DSM-IV definition
7. Addiction can be seen as a disease of the brain. This
approach suggest that the neural pathways of executive function
become distorted and motivational processes become amplified as a
consequence of the interaction between behaviours and their effects
in the brain. That behavior is the ingestion of certain drugs.
Robert West, 2013 What is addiction? Expert opinion
8. There are many chemical messengers in the brain, and of
these Dopamine is the one most associated with addiction. All drugs
of abuse increase dopamine in the brain systems associated with
addiction. Dopamine is the key to reward, acting as a precursor to
the actual stimulus provided by the substance itself. Dopamine
9. The brain repeats pleasurable experiences and avoids pain,
but automatic brain mechanisms do not think behaviour through to
its conclusion, and do not learn from delayed negative outcomes.
The brain is like a reckless infant, wanting what it wants right
now. Behaviour that produces right not pleasure is repeated,
regardless of the long-term consequences. DuPont The Selfish Brian,
1997
10. A neat description the brains specific areas of function
with relation to addiction (note the work was based on impulse
control disorders, but has a clear analogue to addictions per se.):
The amygdala is important in the assignment of emotional
significance and learned associations between motivationally
relevant and otherwise neutral stimuli; the orbitofrontal cortex
(OFC) encodes outcome expectancies and, via its strong anatomical
connections with the basolateral amygdala (BLA), may facilitate
associative learning in the amygdala; and the anterior cingulate
cortex (ACC) is implicated in discriminative learning and cognitive
control Brewer & Potenza, 2008
11. Additional structures that are important in this process
include the hippocampus, which provides contextual memory relevant
to motivational stimuli, and the hypothalamic and septal nuclei,
which provide information relevant to primitive motivational
behaviours such as sexual drives and nutrient ingestion. As
motivated behaviours become increasingly subordinated to the
addictive behaviours as addiction progresses, changes in the
structure and function of these brain regions contribute to the
excessive engagement in behaviours Brewer & Potenza, 2008
(2)
12. The nucleus accumbens (NAcc) also plays an important role.
The NAcc shell is proposed as important in modulating incentive
salience, while the core is involved with the expression of learned
behaviours in response to stimuli that predict motivationally
relevant events experienced as pleasurable. The ventral tegmental
area (VTA), which projects the amygdala, NAcc and prefrontal cortex
(PFC, which includes the OFC and ACC), facilitates learned
associations with motivationally salient events using bursts of
dopamine release. Dopaminergic neurons are inhibited, probably
through the dorsal medial thalamus (habenula), when expected
rewards do not occur. Brewer & Potenza, 2008 (3)
13. Amygdala assignment of emotional significance and learned
association Orbitofrontal Cortex (OFT) encodes outcome expectancies
Basolateral Amygdala (BLA) facilitates associative learning
Anterior Cingulate Cortex (ACC) discriminative learning and control
Hippocampus Contextual memory Hypothalamic and Septal nuclei Basic
drives Nucleus Accumbens (NAcc) responses to pleasure Ventral
Tegmental Area (VTA) facilitates learning and releases dopamine
PreFontal Cortex (PFC) OFT and ACC Dorsal Medial Thalamus inhibits
dopamine The neural circuitry of behaviour - summary
14. Drugs stimulate the midbrain dopamine system which in turn
projects to the PFC, ACC and basal ganglia. Positive experiences
result in increased dopamine release. So there is associative
learning of cues, behaviours, rewards and punishments, which
ultimately results in levels of want that far exceed expectation
This occurs because the dopamine signal is amplified, thus
increasing motivation and this in turn will over-ride cognitive
control of behaviours. Dopamine rewards logical and illogical
expectations. Expectancy & Reward Theory
15. What is the evidence? (1) This is imaging that compares
problem Gamblers (B) with Controls (A):. There is limited
activation of the ventral striatum (reward response) in the
addicted brain. The controls display much higher levels of activity
the differences are due to sensitisation
16. Tolerance - Phenomena where the effects of a drug diminish
with repeated use Develops at different rates to different drug
effects Once developed, it does NOT last indefinitely
Cross-tolerance between members of same class of drug After a
prolonged period of abstinence, a user will require a much small
dose to gain the same effect. This is particularly problematic in
the case of heroin users released from long term prison sentences
most overdose deaths occur in the week following release What is
the evidence? (2)
17. Agonists and Antagonists Agonists such as Methadone binds
to the same receptor as the heroin, but does not produce the
euphoria / high. Taken orally, it does not rapidly increase opioid-
receptor activity, but does maintain enough activity to avoid
withdrawal. Naltrexone is an opioid antagonist. It prevents heroin
from binding to the receptor, but does not activate the receptor.
Naloxone (Narcan) also works in this way, and can be used to
address overdose by replacing the heroin.
18. Fighting fire with fire Pharmaceutical solutions to
pharmaceutical problems What is the evidence? (3) Medication
Treatment for addiction to Mechanism Methadone Heroin
Opioid-receptor agonist Naltrexone Heroin Opioid-receptor
antagonist Naloxone Heroin, alcohol Opioid-receptor antagonist
Buprenorphine Heroin Mixed opioid-receptor agonist and antagonist
Nicotine gum, patches Nicotine Provide low doses of nicotine
19. Has work on the biological basis for addiction contributed
towards the development of effective interventions? The utilisation
of antagonists to reduce cravings and reverse overdose are good
examples of this. What is the evidence? (4)
20. We are more than our biology Although it is important to
understand the brain mechanisms that underpin the onset and
maintenance of additive behaviours, it is necessary to place these
systems in the context of the individual and their surroundings.
Genetics and individual differences in brain architecture do not
adequately explain why particular individuals initiate drug taking,
develop addictions and then may or may not respond to a variety of
interventions. Several psychological traits have been associated
with addiction impulsivity, depression, anxiety, reward sensitivity
and learning capacity. Such characteristics are the product of
biology, personality and circumstance.
21. What are the risk factors for addiction? Permissive family
attitudes to substance use Use of substances by parents, family
members Family conflict Early and persistent behaviour problems
Academic problems Low commitment to school Early peer rejection -
alienation Association with peers who use drugs Attitudes
favourable to drug use Early onset of alcohol/drug use
22. Nature and Nurture Are some people born to be addicts? Do
our thoughts control our behaviour or does our behaviour change the
way we think? Could a combination of both heredity and environment
make people the way they are? All of these questions are addressed
by the various modalities of addiction theory. The following slides
provide a rapid summary of how different theoretical perspectives
influence the understanding of, and treatment for, addiction.
23. Disease model With the development of physiology and
scientific research, more and more emphasis has been given to
medicine and scientific explanations of human behaviours The
concept of alcoholism as a disease was first initiated by three
physicians: Benjamin Rush (1785), Thomas Trotter (1804) and Magnus
Huss (1849-1851). Now Addiction is attributed to the
genetic/biological make-up of the individual. Genetic factors Twin
studies start to uncover the influence of learned behaviour &
genetic inheritance Identification of a predisposing genetic marker
Genetic inheritance neither predicts onset nor suggests longer term
decline
24. Moral Theory One of the earliest models of addiction. The
moral theory denotes substance misuse as a vice or a sin. The
theory implies that some individuals, through their own free will,
make a conscious choice to become substance misusers.
25. The Moral Brain.. Recent work by Eslinger and colleuges has
identified certain brain regions (the amygdala, thalamus, and upper
midbrain) that were consistently activated by emotional stimulus
(with and without moral content). But some areas, including the
orbital prefrontal cortex (OFC), located just above the eye
sockets, and the superior temporal sulcus, at the furrow between
the frontal and temporal lobes, fired specifically in response to
moral content alone.
26. Learning Theory This theory contends that substance misuse
is learned through the complex processes of behavioural acquisition
and reinforcement. Many learning theories have evolved from simple
classical and operant conditioning theories through to more
complicated social learning theories that emphasize the
interactions between personal dispositions and environmental
situations. We will briefly examine classical and operant
conditioning.
27. Classical Conditioning (Pavlov)
28. Operant Conditioning (Skinner) Positive Reinforcement
Increases probability of a behaviour occurring by presentation of
reward Behaviour (take drug): Reward (get high) Negative
Reinforcement Increases probability of a behavior by removing
discomfort Stimulus (withdrawal, depression): Response (Take drug)
Intermittent reinforcement strengthens a behaviour Animals learn to
avoid as well as escape discomfort Cues (discriminative stimuli)
are important and ties in well with classical conditioning Strength
of learning is influenced by the nature of the reinforcer, the
schedule of reinforcement and for how long the schedule is in place
Underpinning this is the release of dopamine in the meso-limbic
pathway in anticipation of the potential reward
29. Learning and the brain In nondependent drinkers, drinking
alcohol results in stimulation of the pleasure pathway: Dopamine
release. Whereas in dependent drinkers, alcohol serves to supress
the stress pathway, to mitigate the release of cortisol
30. Social Theory This theory hypothesizes that substance
misuse develops and endures as a result of disruptive social forces
such as unemployment, poverty, violence, family dysfunction, as
well as gender and age inequities. These forces are believed to act
as social stressors and substance misuse is considered to be an
adaptation to the resultant misery and unhappiness. Cognitive
factors or processes such as anticipation, planning, expectancies,
attributions, self-efficacy and decision-making were all shown to
play a part in learning. Cognitivebehavioural therapy (CBT) is a
product of social learning theory.
31. Cognitive Behaviour Therapy Change the mind and you change
the brain: Paquette et al, 2003 CBT can also change the prefrontal
cortex, the part of the brain responsible for higher-level
thinking. So it seems that CBT might be able to make real, physical
changes to both our "emotional brain" (instincts) and our "logical
brain (thoughts). Similar patterns of brain changes have been seen
with CBT and with drug treatments, suggesting that psychotherapies
and medications might work on the brain in parallel ways.
32. The environment affects behaviour The effect of posters on
drinking behaviour: In this example (Dyer & Moss, 2013;
unpublished) posters designed to reduce consumption actually
resulted in increased alcohol use. Note the difference when the
study was repeated in Bar and Laboratory surroundings.
33. A BioPsychoSocial approach (BPS) With many differing
theories all purporting to explain addiction, some sort of
integrative approach was inevitable. First articulated by George
Engel in 1977, The BPS model was originally designed as an
alternative to the prevailing biomedical model, which tends to
reduce illness to a single source, then treat the illness with
little regard for other contributing factors such as a patients
psychological experiences or social behaviours. A decade later,
Donovan (1988) and Wallace (1990) articulated a BPS model for
addictive behaviours in recognition that drinking behaviour and
alcohol problems are multidimensional. Donovan recommended
comprehensive assessment that could capture the biological,
psychological and social aspects of the individuals life that are
affected by drinking. This information, Donovan hypothesized, would
improve diagnosis and treatment.
34. Pezoa-Jares et al, 2012 From a Biopsychosocial perspective,
addiction (in this case referring to compulsive use of the
internet) is the result of maladaptive behaviours which originate
from an interaction between various biological, psychological and
environmental factors.
35. Summary Addiction is a complex process of the CNS that
results from recurring drug intoxication and is moderated by
genetic, developmental, experiential, psychological and
environmental factors. There is no single over-arching theory of
addiction, however the BioPsychoSocial approach does attempt to
integrate component theories Given that addiction is a complex
process, often co-occurring with other psychological disorders,
treatment can be complex and multi-dimensional. Recent developments
in agonist, antagonist and partial antagonist medications can help
to retain patients in treatment systems where other
non-pharmacological interventions may be applied.
36. References and further reading 1. T P Enevoldson,
Recreational drugs and their neurological consequences. J Neurol
Neurosurg Psychiatry, 2004;75:iii9-iii15
doi:10.1136/jnnp.2004.045732 2. ALICE RAP. http://www.alicerap.eu/
3. Robert West. Models of addiction. EMCDDA, Lisbon, June 2013.
http://www.emcdda.europa.eu/publications/insights/models-addiction
4. Robert L. DuPont, The Selfish Brain: Learning from Addiction,
American Psychiatric Pub, 1 Jan 1997 5. Brewer, J.A., Potenza,
M.N., 2008. The neurobiology and genetics of impulse control
disorders: relationships to drug addictions. Biochemical
Pharmacology 75(1); 63-75. Doi: 10.1016/j.bcp.2007.06.043 6. Jorge
Moll, Paul J. Eslinger, Ricardo de Oliveira-Souza FRONTOPOLAR AND
ANTERIOR TEMPORAL CORTEX ACTIVATION IN A MORAL JUDGMENT TASK:
Preliminary functional MRI results in normal subjects. Arq.
Neuro-Psiquiatr. vol.59 no.3B So Paulo Sept. 2001
http://dx.doi.org/10.1590/S0004-282X2001000500001 7. Paquette V,
Lvesque J, Mensour B, Leroux JM, Beaudoin G, Bourgouin P,
Beauregard M. "Change the mind and you change the brain": effects
of cognitive-behavioral therapy on the neural correlates of spider
phobia. Neuroimage. 2003 Feb;18(2):401-9. 8. J Wallace. The New
Disease Model of Alcoholism. West J Med. 1990 May; 152(5): 502505.
9. D M Dononvan.. Assessment of addictive behaviors: Implications
of an emerging biopsychosocial model (1988) In DM Donovan & GA
Marlatt (eds.) Assessment of Addictive Behaviors. 10. Rodolfo
Eduardo Pezoa-Jares, Isabel Lizarindari Espinoza-Luna and Josue
Alberto Vasquez-Medina. Internet Addiction: A Review. J Addict Res
Ther S6:004. doi:10.4172/2155-6105.S6-004
