Addiction

Question 1

costs of substance use

Answer 1

• AUD/SUDs are one of the largest contributors to the global burden of mortality and premature death.
• Infer a high economic cost.
• They are preventable (non-communicable disease).
  Disability Adjusted Life Years (DALYs): The sum of years of potential life lost due to premature mortality and the years of productive life lost due to disability

Question 2

Alcohol

Answer 2

• Approx. 18.4% of the population (39.6% of the drinking population) report heavy drinking (bingeing)
• DALYS: 85 m
  Cirrhosis, traffic accidents, cancers
• In 2022 there were 10,048 alcohol specific deaths in the UK- the highest number on record.
• 4.2% higher than in 2021 and 32.8% higher than in 2019 (the last year before COVID-19).
• Drug and alcohol-related deaths as of 2022 25.9 per 100 000 people in England and 30.2 per 100 000 in Wales.
  Increasing since 2019.

Question 3

Illicit substances

Answer 3

• Cannabis 3.8%
• Amphetamine 0.77%
• Opioids 0.37%
• Cocaine 0.35%
• Injecting drugs 0.25%
• DALYS: 27.8 m
• Cirrhosis, HIV, liver cancer
  Harms and prevalence etc. are much more difficult to keep track of when drug use is unsanctioned

Question 4

chemical brains

Answer 4

• The human brain uses numerous chemical messengers to:
  
  • sense changes in external/internal milieu
  • process and transmit information
  • manage neural function
    constantly adapt to changing context and bodily needs.

Question 5

Phytochemistry

Answer 5

• Plants synthesise a wide spectrum of chemicals, including specialised compounds designed to encourage beneficial interactions with other species, or to discourage ‘predators’ and parasites.
• Human have exploited these phytochemicals for years.
• Some plant chemicals share structural properties with mammal neurotransmitters
• Phytochemicals act on receptors to produce psychopharmacological effects.
• We know that lots of different plants produce chemicals in order to interact with other species and animals
  Humans have exploited these- similar structural properties to human neurotransmitters to start a psychoactive effect e.g. magic mushrooms

Question 6

implication for human substance use

Answer 6

• Drug use in modern humans may be an inheritance of our evolutionary past.
• There may have been adaptive benefits to consuming substances.
• They incur a survival advantage.
• Almost every culture has consumed substances as part for health or ritualistic reasons.
• ‘Fourth-drive’ (Siegel, 2005).
  Fourth drive- implicit drive to experience intoxication like there is to eat, have sex etc

Question 7

drug administration and absorption

Answer 7

• Drugs are usually administered in one of four ways (each has different psychoactive effects
  
  • 1. Oral ingestion
  • 2. Injection
  • 3. Inhalation
    4. Absorption through mucous membranes

Question 8

drug administration: oral

Answer 8

• Once swallowed drugs dissolve in stomach and carried to intestine, where they are absorbed into the bloodstream.
• Some drugs pass through stomach wall and so act sooner (e.g. alcohol which is lipid and water soluble).
• Some substances are metabolised by liver reducing the concentration.
• Relatively safer than other methods.
• But effects can be unpredictable (e.g. delayed action).
• Rate can depend on other factors (e.g. food in stomach).
  Normally associated with a lower risk potential

Question 9

drug administration: injection

Answer 9

• The effects of injected drugs are fast and predictable
• Drugs can be injected in
  
  • the fat under the skin (subcutaneous)
  • a muscle (intramuscular)
  • a vein (intravenous)
• Drug users prefer the intravenous way because the blood takes the drug directly to the brain
• This is a mixed blessing
  Little to no opportunity to counteract the effects of overdose, impurity or allergic reaction.

Question 10

drug administration: inhalation

Answer 10

• Some drugs can be absorbed through capillaries in the lungs.
• Difficult to regulate the dose that is inhaled.
  Causes lung damage.

Question 11

drug administration: absorption through the mucus membranes

Answer 11

• Some drugs can be absorbed through the mucous membranes in the nose, mouth and rectum.
  Can cause damage to membranes.

Question 12

drug penetration

Answer 12

• Following administration, the drug will enter the bloodstream.
• To exert an effect drugs must cross the blood-brain barrier.
• Psychoactive drugs are typically lipid soluble they can dissolve in the fatty membrane of the brain and pass through the barrier.
• Many psychoactive substances have small molecules these can pass through more easily.
  How quick it passes through the blood brain barrier depends on how soluble it is and hoe small the molecule is

Question 13

mechanisms of drug action

Answer 13

• After passing the blood brain barrier drugs can then influence the nervous system.
• Some drugs (e.g. alcohol) act on lots of different membranes throughout the CNS.
  Others are more specific and bind to synaptic receptors influencing, synthesis, transport release of deactivation

Question 14

tolerance

Answer 14

State of decreased sensitivity to a drug that develops because of use (Pinel et al., 2017)

Question 15

withdrawal

Answer 15

• Sudden elimination can trigger adverse reactions (withdrawal syndrome).
  Severity dependent on duration and degree of drug use, speed in which drug eliminated from the body. (Pinel et al., 2017)

Question 16

what is addiction?

Answer 16

• The term is widely used (and you probably already have an idea of what it means), but it has not been used as an ‘official’ diagnosis for decades.
• The official diagnostic labels are currently:
  
  • ‘(substance) use disorder’ (e.g. ‘alcohol use disorder’) (DSM V)
    ‘harmful use’ and ‘dependence syndrome’ (ICD-10)

Question 17

what are SUDs?

Answer 17

• Often described as a chronically relapsing disorder characterized by:
• Compulsion to seek and take substance
• Loss of control limiting intake
  Emergence of a negative emotion state when access to substance is prevented (e.g. withdrawal)

Question 18

animal models

Answer 18

• One way to gain insight into the neurobiology of drug abuse in humans is to create animal models of substance use.
• There are a number of different ways this can be done.
• For example, we may see what factors affect the extent to which animals self-administer drugs.
• Can be used to assess abuse potential of new drugs and classify them.
• Animals will administer most drugs that are abused by humans (especially stimulants).
  Some drugs notoriously difficult to get animals to self-administer (e.g. THC).

Question 19

drugs self admin model

Answer 19

• Rat has infusion pump and cannula linked directly to the brain
• Drugs are administered straight into the brain of rats
• When the animal presses the lever they receive some of the drug
• Animal studies often begin with a period of continuous reinforcement in which each response leads to the outcome (drug use).
  
  • Continuous reinforcement- when it presses the lever it gets the drug (builds a habit of pressing the lever)
• There is often a short timeout period to allow the substance to exert its effects.
• Can be used to investigate initial drug use, acquisition of drug behaviours, rates and patterns of drug use.
  Continuous reinforcement often used initially then the schedule can be changed.

Question 20

schedules of reinforcement

Answer 20

• Interval schedules require a minimum amount of time that must pass between successive reinforced responses (e.g. 5 minutes).
  Fixed Interval schedule: fixed time-period between reinforcers. Getting a raise at the end of every year. Produce accelerated rate of response as the time of reinforcement approaches. (Scalloped response pattern).
• Variable Interval schedule: variable time period between reinforcers: produce a steady rate of response.
  Waiting for a lift (an unpredictable amount of time). May press elevator button over and over again even though this does nothing. (Steady response pattern).
• Ratio schedule require a certain number of operant responses (e.g., 10 responses) to produce the next reinforcer
• Fixed Ratio schedule: The required number of responses is fixed from one reinforcer to the next: they support a high rate of response until a reinforcer is received, after which a discernible pause in responding may be seen, especially with large ratios.
• Sales people who are paid on a “commission” basis may work feverously to reach their sales quota, after which they take a break from sales for a few days. (Break and run behaviour with a post-reinforcement pause).
  Variable Ratio schedule: The required number of responses may vary from one reinforcer to the next. The power of this schedule of reinforcement is illustrated by the gambler who persistently inserts coins and pulls the handle of a “one-armed bandit” produces a high and steady rate of responding.

Question 21

Breakpoint (Roberts et al., 2007)

Answer 21

• A progressive ratio schedule can be used also
• Reward presented after a fixed number of responses, but the number of responses needed increase progressively. 1,2,4,8,16.
• Animals finally reach a ‘breakpoint’ in which they will stop responding.
• Different drugs have different break points
• Drugs with high breakpoints are prone to abuse in humans.
  These breakpoints are dose dependent.

Question 22

substitution procedure

Answer 22

• Can substitute the drug the animal is currently administering for another drug.
• Assess whether this new drug becomes sought after (rate of response).
  Allows the assessment of abuse potential in new drugs.

Question 23

conditioned place preference

Answer 23

• Conditioned place preference (CPP) paradigm is used to study the rewarding and aversive effects of drugs.
• Typically, the animal is injected with one drug (e.g. heroin) before being placed in a particular environment.
• On alternate days, the animal is injected with a vehicle (control drug) and placed in a different environment.
• Sometimes there is a third environment in which no drug is given.
• After training with these drugs/environments, the animal is placed in the chambers in a drug-free state and the animal is free to move among the different environments.
• Drugs often result in a conditioned place preference, i.e. the animal spends more time in the environment that is associated with the drug.
• Advantages: high sensitivity to low drug doses; can test positive and negative reinforcement and aversion; drug reinforcement is tested in a drug-free state; study the interaction between environmental cues and drugs.
  Disadvantages: costly, effortful, and takes time to get results; need to test different doses in different animals (and multiple animals at each dose); conduct lots conditions to control for confounding factors (e.g. familiarity, hyperactivity, initial preference bias).

Question 24

inter cranial self stimulation model (ICSS model)

Answer 24

• Researchers realised that the actual substances are not needed to show which brain areas are involved
• Electrical stimulation administered directly into specific areas of the brain.
• No substances used
• Allows the investigation of which specific brain processes may be involved in substance seeking behaviour.
• Supports notion of so-called ‘pleasure centres’ in the brain.
• Often implicated is the Nucleus Accumbens (Nacc).

Question 25

NAcc and addiction

Answer 25

• Using the methods we have discussed a number of findings implicate the NAcc (Deadwyler et al, 2004; Nestler et al, 2005, Pierce & Kumaresan, 2006).
• Laboratory animals self-administer addictive drugs straight into the nucleus accumbens.
• These injections have been shown to induce a conditioned place preference for the compartment in which they are administered
• Lesions to the nucleus accumbens or the ventral tegmental area blocks self- administration of drugs and development of conditioned place preference.
  Both self-administration of addictive drugs and experience of natural reinforcers found to be associated with elevated levels of extra-cellular dopamine in nucelus accumbens.

Question 26

reward systems in the brain

Answer 26

• Mesolimbic dopamine system: the ventral tegmental area and areas that project to and from it.
• All drugs of abuse stimulate dopamine release in the mesolimbic system (directly or indirectly; Nestler et al., 2005).
  Also stimulated by food, sex, warmth, and other “natural” rewards.
• Originally believed that DA release meant experience of pleasure, or the rewarding aspects of a stimulus - oversimplistic
• Natural rewards (food, sex, water) also stimulate the mesolimbic pathway (good for survival).
  DA is also triggered when drug-related cues are present (BEFORE drug is taken)

Question 27

the paradox

Answer 27

• Individuals who are dependent on drugs often report they ‘want’ drugs but no longer ‘like’ them.
• Think back to the DSM 5 criteria.
  
  • Craving, strong urges… despite wanting to cut down, no longer finding the drug appealing.
• Robinson and Berridge (e.g. 1993, 2008) developed the incentive salience model of addiction.
  They argued that dopamine was important in the process of WANTING the drug but not liking the drug. Dopamine function attributes incentive salience to a stimulus (e.g. drug), determining how important it is to the individual (how much they want it)

Question 28

incentive salience

Answer 28

• Robinson and Berridge (1993, 2003)
  
  • Repeated drug use leads to a sensitized (increasing) spike in DA activity in the mesolimbic pathway
  • Importantly, this is not only seen when the drug is ingested but ALSO when they are exposed to drug related cues (Pavlovian conditioning)
  • Exaggerated dopamine response manifests as incentive salience. Drug cues have strong motivational properties
    Exposure to drug-related cues increase ‘wanting’

Question 29

the difference between wanting and liking in alcohol consumption

Answer 29

• Hobbs et al (2005)
• Experiment 1: Separated individuals into heavy and light drinkers and examined liking ratings of a variety of drinks (alcoholic and non-alcoholic).
  
  • No interaction between drinking status and type of drink on liking.
• Experiment 2: Manipulated ‘wanting’ by a small priming dose of alcohol.
  Again, no changes in liking for the alcoholic drink. But an increase in wanting.
  Mean consumption (left hand side) of fruit juice and beer after placebo (P) and alcohol (A) (+SEM) from experiment 2. The right hand side show the number of times alcohol chosen after placebo and alcohol (+SEM) from experiment 2

Question 30

incentive sensitisation theory- withdrawal and relapse

Answer 30

• The sensitization process lasts a long time (longer than tolerance or physical withdrawal).
• Even after the negative effects of withdrawal have diminished, the brain’s neural system underlying ‘wanting’ is sensitized.
• This long-term sensitization results in enhanced, long-term risk of relapse.
• For example, if the circumstances are right, relapse may be likely even after years of abstinence.
  Sensitization is a long-term adaptation. Remember addiction is a ‘chronic relapsing disorder’; IS can help to explain this.

Question 31

IST and learning

Answer 31

• We focus on drugs because of an interaction between incentive salience and associative learning mechanisms which usually directs our motivation to appropriate targets (e.g., food, sex).
• Although learning processes identify the stimulus of interest, it is sensitization of brain circuits that mediate Classical conditioned incentive motivational processes (i.e., incentive sensitization) that result in pathological drug-related motivation
• Associative learning processes are important because they can determine where, when, and how sensitised behaviour is expressed.
• This helps explain why pathological drug behaviour can be restricted to certain environments (i.e., those that have been previously associated with drug taking)
• So there is contextual control over the expression of sensitization, and this stems from associative learning.
• Null research findings may be due to absence of conditioned stimuli
  Vezini & Leyton (2009) Neuropharmacology, pp160–168)

Question 32

IST and cognitive dysfunction

Answer 32

• Cognitive Dysfunction
• Drug addicts show significant cognitive impairment; executive function, decision making, inhibitory control etc are all affected (via adaptations to prefrontal cortex).
• Incentive Sensitization Theory: impairment of executive function has an important role in addiction, esp. the bad choices about drugs. Combine this with the pathological incentive motivation for drugs (via incentive sensitization) and the result is addictive behaviour.

Question 33

IST summary

Answer 33

• Naturally, the brain directs animals to stimuli that hold incentive salience, that is, can help survival (e.g., food, water, sex). Drugs hijack this system, so that the brain system attends to substance cues rather than natural reward cues.
• The activation of neural structures which support wanting (incentive salience) persists, increasing the risk of relapse.
• Wanting and liking are served by different neural systems. Drug wanting increases while drug liking can decrease.
  Other cognitive mechanisms, such as associative learning and cognitive dysfunction, interact with sensitization to produce addiction.

Question 34

drug addiction

Answer 34

• Drug addiction: chronically relapsing disorder characterized by
• compulsion to seek and take the drug
• loss of control in limiting intake
• a negative emotional state reflecting a motivational withdrawal syndrome when access to the drug is prevented
  Koob & Volkow, 2010

Question 35

addiction pathway

Answer 35

• 3 stages:
  
  • Binge/intoxication
  • Withdrawal/negative effect
  • Preoccupation/anticpation
• The development from recreational to dependent use is due to brain adaptations:
• As with most brain models, lots of research from animal models. For example, animal models can be used to represent the withdrawal/negative affect stage of Koob et al’s (2009) addiction cycle.
  
  • Conditioned place aversion (animals avoid environments paired with withdrawal)
  • Increased motivation for self-administration in dependent animals (animals are motivated to take drugs to remove withdrawal state)
    Anxiety-like responses (e.g. freezing, burying)

Question 36

Koob & Volkow (2010)

Answer 36

• Impulsivity and compulsivity are important
• Impulsivity tends to be more important in earlier stages
• Both impulsivity and compulsivity are important in later stages
• Impulsivity: behavioural disposition for fast, unplanned actions triggered by ext/int stimuli with no regard to potential negative consequences. Impulsivity is a core deficit in SUD.
• Measured: 1) choice of small immediate over large delayed reward
• 2) Inability to inhibit behaviour by changing or stopping a behaviour once initiated (i.e. response inhibition).
  Compulsivity: persevere in responding despite adverse consequences, and incorrect responding in choice situations. Persistent reinstatement of habit-like acts. DSM-V: persistent use despite knowledge of negative physical/psychological problems; lots of time spent in activities trying to obtain the substance.
  Repeated drug use leads to repeated spikes in dopamine activity… which eventually leads to long-term suppression of dopamine function. Key point of this theory is that dopamine is involved in mood regulation, not just salience attribution

Question 37

hedonic homeostatic dysregulation

Answer 37

• Koob & Le Moal, 1977
• Both sensitization and opponent-processes contribute to ‘hedonic homeostatic dysregulation’: dysregulation of brain reward (DA) that gets progressively out of control.
• Sensitization occurs in the early stages of addiction and causes increased liking for drugs (results in bingeing). Represents a break from homeostasis.
  Counteradaptation (e.g., opponent-processes) occur in the latter stages to produce withdrawal and negative affect.
• The brain tries to respond to the continued presence and effects of drugs and so alters set-points (so drugged brain is ‘normal’)
• Sensitization and counteradaptation processes cause further attempts to maintain mood at this new set point (allostasis) > but with increasing drug use, it becomes more difficult to maintain this set point…
• At some point, allostasis breaks down and the individual cannot maintain a set point > ‘spiralling distress’, or mood disturbance
• Hedonic homeostatic dysregulation drives dependent drug use.
• Hedonic homeostatic dysregulation drives dependent drug use.
• Hedonic homeostatic dysregulation is a negative emotional state which is apparent when drug use is prevented (which creates craving, etc.)
• Hedonic homeostatic dysregulation is a result of a combination of decreased reward system function and increased brain stress response system function
  Hedonic homeostatic dysregulation lasts a long time (into protracted withdrawal), therefore there is a residual negative state which is an ongoing relapse risk

Question 38

Koob and Allostasis

Answer 38

• The brain works to maintain homeostasis. Counter adaptation is one mechanism of maintaining homeostatic regulation.
• Over prolonged drug use, the brain tries to adapt and counter adaptations / opponent processes alter set-points
• Deviation from normal brain-reward threshold regulation is described as an allostatic state.
• Allostasis: stability through change.
  Allostasis is more complex than homeostasis and it results in changes to reward mechanisms in an attempt to achieve stability.

Question 39

brain adaptations

Answer 39

1. Mesolimbic dopamine system (incentive salience and reward)
2. Ventral striatum (increase in DA activates the VS)
3. Ventral striatum/dorsal striatum/thalamus circuits(activity shifts from ventral to dorsal striatum (fMRI). Corresponds with drug use going from acute/goal-directed to chronic/habitual)
4. Prefrontal cortex /hippocampus circuits (impaired executive function, poor decision making, e.g. choose reward now [drug] rather than longer term reward)
5. Extended amygdala (stress system activated, leads to a negative states which drives use of natural reinforcers)
   Koob & Volkow, 2010

Question 40

brain model and treatment

Answer 40

• Pharmacological strategies that target specific clinical components of addiction are developing. These may target alcohol/substance-induced euphoria (e.g. naltrexone), hedonic dysregulation, cue- or stress-induced craving (e.g. acamprosate??) etc.
• For instance, naltrexone may work by reducing opiate and alcohol-induced reward, modafinil may reduce cocaine-induced euphoria (e.g. Anton (2008) Naltrexone for the Management of Alcohol Dependence)
• Research suggests vaccines may be possible which blocks the drug entering the brain (e.g. Kosten (2005) Future of anti-addiction vaccines)
• Disulfiram disrupts the metabolism of alcohol to induce sickness, so people avoid drinking (serious side effects, including death can occur if a person persists in drinking heavily/regularly on disulfiram) (e.g. Skinner (2014) Disulfiram Efficacy in the Treatment of Alcohol Dependence: A Meta-Analysis)
• Naltrexone = opiate receptor antagonists; alcohol releases opioids, and naltrexone blocks the receptors which opioids want to attach to. This reduces the please produced by alcohol (by blocking endogenous opioid transmission).
• Acamprosate is less well understood
  There have been fatalities from disulfiram

Question 41

animal models of addiction

Answer 41

• Field & Kersbergen (2020) argue:
• Animal models have failed to deliver effective pharmacotherapies for addiction
  
  • While they acknowledge some treatments, they argue others lack transferability. Other pharmacotherapies began with human research and were confirmed in animal research.
• Animal models have generated a misleading picture of the nature of addictive behaviour in humans
  
  • Animal models (and brain disease models) suggest drug use is compulsive and habit like. But drug users will perform complex tasks to use a substance and can reduce drug use if paid to do so.
• Field & Kersbergen (2020) argue:
• Addiction may be uniquely human
  
  • We don’t know that animals intend not to use drugs and then use drugs anyway. We do not understand animals subjective state. Language may play a key role (i.e. talking therapies for addiction).
• Network models suggest there is limited value to animal models
  Recent research in a variety of spheres understands the complex interplay between many different factors. E.g. economic effect on opioid use in America. Animal models can’t begin to explain such complex interactions.

Question 42

excessive focus on stimulants

Answer 42

• Vast majority of rat studies conducted with stimulants (i.e. cocaine).
• Thought that all addictive drugs act similarly
  But there may be differences for (i.e. some lesions affect cocaine administration but not heroin administration; Badiani et al, 2011).

Question 43

the opposing view: addiction is is a brain disease

Answer 43

• Key claims:
• All drugs of abuse affect (directly or indirectly) a pathway deep within the brain. (True)
• Both acute and prolonged drug use causes pervasive changes in brain structure and function that persist long after the individual stops taking the drug. The ‘addicted’ brain is different than the non addicted brain in terms of structure and function. (True, but with caveats)
• ‘A metaphorical switch in the brain seems to be thrown as a result of prolonged use’ Leshner (1997)…. That addiction is tied to changes in brain structure and function is what makes it, fundamentally, a disease’. (Murky at best – everything changes the brain!)
  Implications: We shouldn’t marginalize those with an A/SUD, but rather we should be trying to treat them. Similarly, incarcerating individuals won’t work.

Question 44

consequences of a disease model

Answer 44

• Led to over investment: 41% of addiction funding is for basic neuroscience; additional 17% developing ‘biological cures’.
  
  • But are we any closer to really understanding and treating addiction?
• A good theory of alcohol/substance use should be able to inform development of treatments.
• The disease model has supported development of new pharmacotherapies BUT few new drugs have been developed based on neurobiology.
  
  • The most widely used drugs in addiction?
  • Methadone Replacement Therapy
  • Nicotine Replacement Therapy
  • What about spontaneous remission / unassisted recovery?
  • Recovery is a social process – we change our identity, we become empowered.
    It’s argued to have helped reduce stigmatization of ‘addicts’(but see Buchman et al (2010) The Paradox of Addiction. Neuroethics DOI 10.1007/s12152-010-9079-z)

Question 45

summary

Answer 45

• Animal models may be useful to understand the abuse potential of substances and have provided insights into the potential neurochemical basis of addiction.
• Although brain changes (adaptations) do occur following substance use a disease model of addiction may be too simplistic
• Brain adaptations due to chronic use impair recovery making abstinence difficult
• Perhaps a better explanation that there is a continuum of brain adaptations
  If addiction was a brain disease would anyone ever get ‘better’? Some people ‘recover’ spontaneously.

Question 46

human research- objective measures

Answer 46

• First measures of substance use began by trying to translate animal models to humans.
  
  • Ludwig, Wikler and Stark (1974), had participants ride on an exercise bike. The longer the rode the more alcohol they’d receive.
  • Subsequent research has attempted to assess substance use (particularly alcohol-seeking) through more direct methods.
    A variety of similar measures. E.g. progressive ratio task and alcohol purchase task, which measures how much people would be willing to pay for alcohol (Kiselicia, 2016).
  • But
  • Self-reported alcohol consumption explains surprisingly small amount of variance.
  • Occurs in isolation (usually)
  • Unfamiliar setting (usually)
  • Short time period
    Not representative of actual drinking.

Question 47

craving subjective measures

Answer 47

• We can also measure subjective alcohol-seeking behaviour (i.e. craving).
  
  • Craving: an intense desire for something
  • A complex and multifaceted concept.
  • Often measured using questionnaires
    E.g. The Desire for Alcohol Questionnaire or Alcohol Urge Questionnaire.

Question 48

students

Answer 48

• Students are overrepresented in all psychology research including alcohol consumption.
  
  • A particular issue with alcohol research as your alcohol use is not normal.
    Two thirds of university students are hazardous drinkers; weekly binge drinking estimated range from 70-85% (Davoren et al, 2016).

Question 49

alcohol administration- background

Answer 49

• Researchers may wish to assess the effect of alcohol on a variety of cognitive and behavioural mechanisms.
  
  • My own research has focused on the effect of acute (small) doses of alcohol on subsequent alcohol-seeking behaviour (de Wit et al, 1996).
  • Also known as the ‘alcohol priming effect’.
    This may underlie binge drinking (e.g. Field et al, 2010).

Question 50

alcohol administration

Answer 50

• Needs to be systematic
  
  • Have sufficient control
  • Account for individual differences when possible (i.e. weight).
  • Therefore, alcohol is often delivered based on weight.
  • I.e. 0.50g/kg.
  • The dose of alcohol that is administered should be theoretically driven.
    I.e. some effects of alcohol are dose dependent.

Question 51

alcohol priming effect- dose and time

Answer 51

• Dose
  * The alcohol priming effect is dose dependent.
  * I.e. de Wit and Chutuape (1993) found a 0.5g/kg dose but not a 0.25g/kg dose to increase desire for alcohol.
  
  • Time
    
    • The time that alcohol-seeking is assessed is also important.
      i.e. Rose and Duka (2006) found craving following a 0.6g/kg dose, 30 minutes after administration. But this began to decrease at after 30 minutes.

Question 52

inhibitory control and alcohol priming

Answer 52

• Alcohol impairs inhibitory control, there may be a dose response relationship.
  
  • One suggestion is that alcohol impairs inhibitory control, and this impairment leads to further alcohol consumption (see Field et al, 2010).
  • Weafer & Fillmore (2008) found the extent that alcohol impairs performance on inhibition to be related to alcohol consumption (measured via a bogus taste test) in a subsequent session.
  • BUT
  • There are some inconsistent findings which have not found alcohol to impair inhibitory control (e.g. Christiansen et al, 2013) or only under certain conditions (e.g. Knibb et al, 2018).
  • When assessed in the same session inhibition does not mediate the alcohol priming effect. (Christiansen et al, 2018; Knibb et al, 2018).
    Lack of adequate control groups in lots of alcohol administration research.

Question 53

summary of RF lecture

Answer 53

• Animal models may not be a valid measure of testing substance use in humans
• A number of paradigms have been designed to assess alcohol-seeking in humans
• These measures have their own issues
• Alcohol administration studies use controlled doses to assess the effect of alcohol on a number of mechanisms
• The effect of alcohol on such mechanisms depends on the dose and time
• One such mechanism is the alcohol priming effect which may underlie binge drinking
• A number of theories have attempted to explain the alcohol priming effect
• One example is that alcohol effects inhibition but there is conflicting evidence.
• Alcohol administration procedures should employ proper control conditions