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Introduction to the BioPsychoSocial approach to Addiction

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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.

Published in: Health & Medicine
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Introduction to the BioPsychoSocial approach to Addiction

  1. 1. Addiction A BioPsychoSocial approach Dr Bob Patton Addictions Department
  2. 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. 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… 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
  4. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 27. Classical Conditioning (Pavlov)
  28. 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. 29. 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
  30. 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. Cognitive–behavioural therapy (CBT) is a product of social learning theory.
  31. 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. 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. 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 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.
  34. 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. 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. 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 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
  37. 37. THANK YOU!

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