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 behavior.

2. Addiction
A BioPsychoSocial approach
Dr Bob Patton
Addictions Department

3. 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.

4. 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…
It’s 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

5. 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

6. 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

7. 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

8. 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

9. 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

11. 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

13. 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

14. 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)

15. 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)

16. 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

18. 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

19. 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

20. 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)

21. 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.

22. 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

23. 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)

24. 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.

25. 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

26. 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.

27. 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

28. 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.

29. 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.

30. 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.

31. Classical Conditioning (Pavlov)

32. 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

34. Learning and the brain
In non–dependent 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

35. 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. Cognitive–behavioural therapy (CBT) is a product of social learning
theory.

36. 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.

38. 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.

39. 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 patient’s 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 individual’s life that are affected by drinking. This information, Donovan
hypothesized, would improve diagnosis and treatment.

40. 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.

41. 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.

42. 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 São Paulo Sept. 2001 http://dx.doi.org/10.1590/S0004-282X2001000500001
7. Paquette V, Lévesque 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): 502–505.
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

43. THANK YOU!