Week 10-Psychiobiology & Motivation Flashcards

1
Q

What’s addiction?

A

■ 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)

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2
Q

What are SUDs?

A

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)

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3
Q

The development of an AUD or SUD typically follows what pattern?

A

1.Experimental drug use
2.Casual drug use
3.Heavy drug use (abuse/misuse)
4.Compulsive drug use (dependence)
5.AUD / SUD

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4
Q

What’s the prevalence and impact of AUD/SUDs?

A

■ AUD/SUDs are one of the largest contributors to the global burden of mortality and premature death.
■ Also a high economic burden
■ Importantly, they are preventable (i.e. 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.

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5
Q

How much of the population are heavy drinkers?

A

■ Approx. 18.4% of the population (39.6% of the drinking population) report heavy drinking (bingeing)
■ DALYS: 85 m
■ Cirrhosis, traffic accidents, cancers

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6
Q

What % of the population takes illicit substances?

A

■ 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

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7
Q

What % of people use tobacco?

A

■ 15.2% of the adult population smoke daily (approx. 933.1 million people)
■ DALYS: 170.9 m
■ Cancers, chronic respiratory disease, chronic obstructive pulmonary disease

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8
Q

What are the difference between countries in regards to prevalence?

A

■ Countries with predominantly Muslim populations: lower rates of alcohol problems, higher rates of tobacco smoking.
■ Tobacco smoking is declining in Western countries but increasing in developing countries.
■ Other regional trends, e.g., methamphetamine in
some states of the USA

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9
Q

What are the trends seen over in the UK?

A

■ rates of smoking are declining (taxation and the smoking ban have helped)
■ the number of people who drink alcohol has declined, but among drinkers the number of people who drink too much has increased (pricing and availability probably played a role again)
■ New drugs become fashionable (e.g. mephedrone), others fall out of favour (e.g. ecstasy)

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10
Q

Addiction as a (free) choice?

A

-Historical account: Moral failure, lack of willpower or a weakness of self.
-Drug use as a cost-benefit analysis (West, 2006)
Benefits:
Pleasurable high
Increased alertness
Social aspects
Costs:
Death
Hangover
Illness

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11
Q

What are the consequences of a free choice
model?

A

-Addicts are stigmatised
-Funding and research is unnecessary - a punitive response to the problem is required
-Doesn’t really account for the preference shift in addiction

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12
Q

What are the key claims in the opposing view: addiction is a disease?

A

-All drugs of abuse affect (directly or indirectly) a pathway deep within the brain.
-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.
-‘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’
-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.

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13
Q

What are the reward systems in the brain?

A

■ 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.

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14
Q

What’s Incentive Sensitization Theory?

A

■ Repeated drug administration = sensitization
■ Brain mesolimbic dopamine system becomes ‘hyper-responsive’ to the drug. – Not hyperactive, hyper(RE)active.
■ Sensitization = drug effects increase over repeated use (opposite of tolerance)
■ However, not everything is sensitized just:
1) Psychomotor effects (e.g., blinking, vigour)
2) Incentive motivational effects (incentive salience)
■ Robinson & Berridge argue that the most important psychological change is ‘sensitization’ (i.e. hypersensitivity) to the incentive motivational effects of drugs

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15
Q

What’s Incentive salience? Robinson and Berridge (1993, 2003)

A

– 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’

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16
Q

What’s the Incentive Sensitization Theory - The Paradox?

A

-As incentive sensitization develops, drugs are wanted more but liked less.
-Although to begin with most drugs produce positive effects (e.g., euphoria) which can maintain drug use, over time these effects seems to decrease (as addiction develops - tolerance).
-The incentive sensitization theory: repeated drug use sensitizes the neural systems that mediate the motivational process of incentive salience (wanting), but NOT the neural systems that mediate the pleasurable effects of drugs (liking).
-Therefore, drugs will be wanted more but liked less over time.
(See Hobbs & Glautier (2005) for a series of human studies separating wanting/liking in the reference section)

17
Q

What’s the paradox?

A

■ 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.
-The incentive salience model, therefore, has considerable intuitive appeal.

18
Q

What’s Robinson and Berridge’s theory based on?

A

-It’s based on incentive sensitization (core principle)
-However, the theory acknowledges that drugs do have other effects (e.g., cognitive impairments)…
-This is why you need to read some of their later papers/reviews (especially 2008, 2016)

19
Q

What’s IST & Learning?

A

-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

20
Q

Why are associative learning processes important?

A

-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
CSs (Vezini & Leyton (2009) Neuropharmacology, pp160–168)

21
Q

What’s IST & Cognitive dysfunction?

A

-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

22
Q

What’s drug addiction according to Koob & Volkow, 2010?

A

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

23
Q

What’s impulsivity and compulsivity and why are they important? (Koob & Volkow, 2010)

A

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.

24
Q

What’s Inhibitory Control / Response
inhibition? Jones, A. (2017).

A
  • Executive function is a global term, so measurements must focus on specific components
  • One of the most well-researched is inhibitory control / AKA response inhibition / AKA disinhibition
  • Idea is that self-control becomes diminished, while drug salience, learned responses toward the drug, and motivation to obtain the drug all increase
  • IC allows people to inhibit (stop/withhold) dominant behavioural responses
  • It can help us stop, change or delay an inappropriate response and is related/overlapped with our self- control
    Measured via:
     Stop-Signal Task
     Anti-Saccade Task
     Stroop
25
Q

How can cognitive dysfunction be treated?

A

■ The brain is ‘plastic’ and so volumetric deficits could theoretically be reversed or at least improved – however, there’s no clear evidence this actually happens
■ You would think that treating the cognitive deficits would be easier than treating brain deficits, but here too the evidence is not promising:

26
Q

What are the consequences of a disease model?

A

■ 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)