Addiction Flashcards
Addiction
A chronically relapsing disorder characterised by compulsion to seek and take drugs, unable to control intake and the emergence of a negative emotional state when drugs are prevented
One of the largest global burden of mortality and premature death
Gowing 2015
10-16 billion a year by NHS
1 billion addicted to nicotine
76 million to alcohol - a third of those who drink
Nutt 2007
Doctors and psychologist rated drugs on physical and social harms
No correlation between harm and classification - a flawed system
Lewis 2015
Questions the myth of addiction that it is a choice and a moral failure, why would you ever want to be an addict?
Now addiction is seen as a brain disease
Lesher 1997
Drug use effects pathways within the brain and changed the structure
Addicted Brian is very different so we should treat addicts not marginalise them
Koob 2009
Addiction is a cycle, binge, withdrawal and finally anticipation leads to further intoxication
Dopamine theory of addiction
Nestler 2005
Drugs of abuse all stimulate dopamine release in the mesolimbic system
So early theories thought that drugs stimulate reward and that why we take drugs
O’Connor 2011
Rats self administer most drugs directly into the NAcc - the more it it self administered the more likely it will be abused
Pettit 1984
Destroying NAcc decreases cocaine intake decreases in rats suggesting it is important in motivation for reward not heroin (pain relief)
Lenore 1995
Rats prefer to be in a drug administration environment even if no drug is administered. Dose dependent
Humans also display this phenomenon (Childs 2009)
Due to classical conditioning the UC stimuli stimulates an UC response (pleasure) things associated with the drug then become a conditioned stimuli that trigger a response
Simplistic Natural rewards (sex food) stimulate mesolimbic pathway - so are we more likely to be addicted to drugs??
Insentive sensization theory
Brains mesolimbic system becomes hyper responsive to the drug
The drug effect increases over time but only psychomotor effects (blinking) and incentive motivational effects
Incentive salience means repeated drug use leads to a increased spike in dopamine activity in the mesolimbic system
The exaggerated dopamine responses manifest as incentive salience and drug cues have strong motivational properties and they increase wanting (Robinson 2003)
Wanting and liking
Hobbs 2005
Heavy and light drinkers should have a difference in liking, they rated different drinks. If wanting and liking worked together heavy liking would like drinks more however this is false. People were primed with alcohol and measured liking and wanting of drinks. No change in liking after some alcohol but an increase in wanting
Berridge 2007
Manipulated dopamine with aminoacid drinks so dopamine levels deplete when consumed. If taken after cocaine euphoria (liking) doesn’t change but wanting does - dopamine as a reward is wrong
This has a behavioural effect on humans
We have an attention all bias to drugs we want (field and cox, 2008)
A Pavlovian to instrumental transfer effect - cues are associated with the high of the drug and then we learn that we can work for the drug (hogarth 2003)
Wanting - prediction of reward?
Is this not just the prediction of the reward??
Need to separate learning and wanting
When presenting a conditioned stimulus animals can act in two ways
1- it stimulates the conditioned response (psychomotor - blinking) this is called sign tracking
2-stimulates a response which achieves the goal - goal tracking (learning)
Dopamine is associated with sign tracking not goal (flagel, 2011)
So dopamineis linked with incentive salience (wanting)
Tomie et al (2002)
Sign tracking not limited to animals and may confer a vulnerability to addiction because similar behaviour is seen in relapse (2008) and not effected by time, after 6mth stimuli can initiate the response
Paradox - want stings but don’t like them – this is addiction they want them despite wanting to stop
Sensitisation is a long term adaptation which explains chronic relapse disorder
Hedonic homeostatic dyregulation theory
Contradicts incentive model
During withdrawal there is a reduction in dopamine and this is associated with negative effect which drives reward seeking behaviour to relieve the negative effect (koob)
The body tries to maintain homeostasis
When you take a drug you have a massive A state (high) and the body produces a B process to return you to the baseline. The B state becomes dominant and gets larger and larger so that your baseline becomes lower. You then take the drug to get the A state which gets you back to your original baseline
Both models could be used to explain different stages in the addiction cycle
Prefrontal cortex
Human imaging studies identify that the prefrontal cortex is involved in higher order behaviours such as executive functioning which make us goal directed behaviours associated with this are the ability to shift mind set, updating (memory) and inhibition (Miyake 2000)
Tasks that involve these cause activation in the prefrontal cortex
Goldstein and Volkow I-RSA model
Addiction not explained by dopamine in the limbic pathway alone
Dopamine involvement is likely to be mediated by functional and structural changes in the frontal cortex
Cravings are due to the memories of pleasure (hippocampus) and are a result of conditioned response (amygdala)
We should be able to inhibit behaviour due to the prefrontal cortex, however drugs destroy the structure and function of it.
Brains of dead addicts gave up to 11% loss of structure of the prefrontal cortex
Dopamine is needed for the functioning of the PFC but there is a loss in receptors
I-RSA Evidence
Response inhibition is the ability to stop change or delay a response (Logan 1984) and this over laps with self control (Baumeister)
Stop trials measure response inhibitions and a meta analysis shows a robust effect that addicts have less response inhibition (smith, 2014)
Nigg 2006
Longitudinal study that showed deficit in response inhibition in childhood were predictive of illegal drug use
Rubio 2008
Heavy drinkers with poor inhibition are more likely to develop dependency than harvey drinker with good inhibition
Drinking does not predict response inhibition (Fernie)
Erache 2011
Cocaine dependence is associated with volumetric loss of PFC
Treatment
Baclofen
There are identified brain structures in addiction and so offers possibilities for effective medical treatment
Targeting the dopamine system because we believe that’s we’re wanting comes from which is linked to salience craving and motivation
Baclofen inhibits release of dopamine, so in rats there is a dampened effect when given nicotine, morphine or cocaine - has potential to help addiction as it acts on the mesolimbic system
Maccioni 2005
Reduction of wanting and intaking alcohol in rats once taken. Dose dependent
Addolorate
Same in humans
Treatment
Target PFC
Naltrexone
Improves activation of PFC and reduces number of pps who relapse or return to heavy drinking (Boettinger)
Modafinil
Cognitive enhancer that wasn’t developed for addiction.
Thought to help inhibition
Alcoholics are better at inhibition
However may have abuse potential as it increases dopamine in NAcc
IDAs
Only successful studies published - over investment in funding
Most widely drugs used were created in the 40s - all this funding but can’t find a better way to treat?!
Can’t explain spontaneous remission or unassisted recovery
AA use not drugs
Smoking fallen to lowest since 40s - culture plays a major role - smoking ban in 2007
American medical association has looked into reducing nicotine in cigarettes so smokers take in less nicotine - what if they just smoke more?
Benowitz 2007 - small study were smokers were given cigarettes with gradually less nicotine and results suggested none increased the amount of cigarettes smokers
