Biological explanations of addiction

Thought I'd make a start on the addiction topic! AO2 in this can come from two styles of question - the first being evaluation (of theories or studies), the second being application. Questions can give a specific scenario and ask you to apply your knowledge to the situation - make sure you specifically reference the situation they describe in order to gain AO2 credit for application. They can also ask about either smoking or gambling in specific detail - so make sure to learn points relating to both addictions rather than just one or the other. You can also be asked about addiction, maintenance and relapse as separate elements of addiction - so make sure you can specifically apply theory to each of the three stages!

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points/IDAs
Purple: My notes/hints/tips

Dopamine Reward System (DRS)

According to this hypothesis, when the brain experiences pleasure dopamine is released from the mesolimbic pathway in the midbrain. The original purpose of this was to promote behaviours that aided survival and reproduction, such as eating, drinking, and sex. However, the use of certain drugs such as alcohol or nicotine, or events such as winning money when gambling, can also trigger mesolimbic dopamine release, as well as a glutamate release from the limbic system, stimulating areas of the prefrontal cortex responsible for memory - creating a memory of pleasurable feelings.

Continued drug use has been shown by Volkow et al (1999) to reduce the sensitivity and activity of the D2 dopamine receptors in the brain's reward system. This can explain the maintenance and progression of an addictive behaviour - it is suggested that this leads people to taking more or "harder" drugs in order to compensate for their decreased sensitivity.

Pontieri et al (1996) found supporting evidence for the role of the DRS in addiction. They found that nicotine produces its pharmacological effects through the activation of nicotinic acetylcholine receptors (nAChRs). The activation of these receptors then increases dopamine levels, causing pleasurable feelings.

The Parkinson’s Disease Society estimates that 14% of patients who take drugs such as Pergolide, which increase dopamine activity, will develop compulsive behaviours such as gambling. (Breen 2008)  Similarly, Grosset (2009) found that dopamine agonists used to treat Parkinson’s disease turned 10% of patients in to compulsive gamblers. This suggests that dopamine levels can play a role in the initiation of addictive behaviour  - this is far higher than in the general population, implying that rather than just being released by addictive behaviours, dopamine plays a role in triggering these behaviours in the first place. Supporting this, Kim & Grant (2001) found that administering Naltrexone, a dopamine antagonist, was successful in reducing compulsions to gamble. These results also help explain initiation of addictive behaviour - drug induced deviations from normal drug levels can stimulate or kill urges to initiate an addictive behaviour.

Cocaine inhibits the action of a protein called DAT (which controls the removal of excess dopamine from the junctions between nerve cells in the brain). This leads to nerve cells being overloaded with dopamine, which contributes to the "high" associated with taking cocaine - supporting the hypothesis that behaviours that cause a dopamine surge will be registered as "pleasurable" and become addictive.

However, Volkow et al (1997) found that while drugs increased dopamine activity the limbic systems of addicted participants, they also raised dopamine levels in non-addicted controls to an even greater degree without them becoming addicted, suggesting that raised dopamine levels cannot entirely explain addiction, and it is overly reductionist to suggest this - there must be other factors that cause somebody to develop a dependence after just taking the drug.

Prefrontal Cortex

The prefrontal cortex (PFC) deals with rational decision-making and social behaviour. It also plays a role in regulating the emotionally-driven and impulsive limbic system. Raised dopamine levels suppress the PFC, leading to it being unable to regulate the more primitive amygdala, leading to risk-taking and impulsive behaviour such as drug-taking.

Research has found a grey matter reduction in the frontal lobes in addicts to heroin, cocaine and alcohol, damaging "synaptic plasticity"  which then leads to a loss of PFC function. This explains maintenance of addiction - drug addiction damages our own ability to regulate our addictive behaviours, making us less likely to be able to quit.

However, it is difficult to establish cause and effect here - an alternate explanation is that a reduction in PFC activity pre-dates addiction, and is actually responsible for the loss of control and impulsive behaviours such as gambling and drug-taking, rather than drug-taking causing PFC damage.

Frontal lobe volume loss has been found in cocaine addicts (Franklin et al 2002), alcoholics (Jernigan et al (1991) and heroin addicts (Liu 1998), suggesting that drugs which increase dopamine levels cause damage to the PFC's frontal lobes.

Endogenous Opioid System

The opioid system controls pain, reward and addictive behaviours. Opioid receptors in the brain are activated by a family of endogenous peptides such as enkephalins and endorphins, released by neurons that are stimulated by addictive behaviours such as gambling and smoking - the activation of this system causes a pleasure response similar to that of the mesolimbic pathway's dopamine reward circuit.

Herz (1997) found that endogenous opioids play a key role in the addictive properties of alcohol, as results showed that opioid antagonists (reducing EOS activity) reduce both pleasure from and urge to drink alcohol.

Karras and Kane (1980) found that tobacco smoking and cravings are reduced in humans when they are given naloxone, a narcotic opioid antagonist. The resulting suppression of the EOS resulted in less urge to carry out an addictive behaviour and fewer withdrawal symptoms (cravings), suggesting that the EOS has a role in both the formation and relapse of addictive behaviour.

Pierzchala et al. (1987) showed that repeated short-term administration of small doses of nicotine to male rats produced significant increases in enkephalin, supporting the central idea of the EOS playing a role in the pleasurable feelings from addictive drugs and behaviours.

Anthropomorphism is an issue with Pierzchala's study, as research carried out on rats cannot necessarily have its results accurately applied to humans. The physiological differences between rats and humans could mean that the biological mechanisms that influence addiction such as the EOS function differently too.

Research into the endogenous opioid system can only explain maintenance and relapse of addictive behaviour (see Karras + Kane - EOS suppression reduced cravings.) It cannot explain initiation of an addictive behaviour, as one must take a drug first in order to know that it has pleasurable effects stemming from opioid release - we don't know that something will be pleasurable until we try it.

Genes

There are certain genes or combinations of genes that have been implicated in increasing or decreasing the likelihood that an individual will engage in addictive behaviours. There is also evidence suggesting that the concordance for many addictions rises as people become more genetically similar.

Breen (2006) identified a variant of a gene responsible for inhibiting the production of DAT, which controls dopamine levels. It was found that those who had 2 copies of the variant gene were 50% more likely to become addicted to cocaine, suggesting that genetics can play a role in addiction.

Studies have identified the presence of the gene SLC6A3-9 as reducing the risk of starting smoking, pushing back the age of beginning, and making quitting more likely to succeed - also causing a lower dopamine release from nicotine. This gene reduces the risk of "thrill-seeking" behaviour such as smoking, gambling and drug-taking.

Lerman (1999) compared the DNA of non-smokers and chronic smokers, and found that non-smokers were more likely to have the SLC6A3-9 gene present, and smokers with the gene were less likely to have started below age 16, suggesting that the gene's absence powerfully influences the risk of nicotine addiction. 

Hamer (1999) studied smokers, former smokers, and non-smokers. Participants with the SLC6A3-9 gene scored 1 point lower in the "novelty seeking" index and were rated as less impulsive, deriving less of a "thrill" from nicotine.

These studies that identify SLC6A3-9 absence as a genetic risk factor can certainly help explain initiation of addiction. The absence of this gene makes people more likely to indulge in thrill-seeking and impulsive behaviours such as trying smoking or drugs for the first time, starting up a habit that can quickly develop into addiction.

Shields (1962) investigated 42 pairs of monozygotic twins raised apart, to control for environmental factors in their upbringing, and found a 79% concordance rate for smoking addictions. Due to being able to control for environmental factors such as peer groups that could have played a role in addiction initiation, this is strong supporting evidence for the role of genes providing an inherent susceptibility to nicotine addiction.

Neuroadaptation

Neuroadaptation is the process whereby the body compensates for the presence of a chemical in the body so that it can continue to function normally. As a person uses a drug more regularly, the body will become used to the presence of the substance and adapt its normal responses accordingly, meaning somebody develops tolerance to a drug, and needs more of the substance to give a desired effect. Tolerance leads to dependence and addiction - significant changes occur in the brain to support the constant presence of drugs in the body, and a person will feel withdrawal symptoms when the drug is removed from their system. Withdrawal symptoms occur because the body has adapted to the drug's presence, and now requires it in order to maintain normal functioning.

With nicotine, withdrawal symptoms that can lead to relapse include anger, anxiety, depression, insomnia, weight gain and an inability to concentrate.

While neuroadaptation can explain the maintenance and relapse of addiction, with the body adjusting to a constant level of the drug in its system and suffering withdrawal when it is removed, it cannot explain addiction. 

Only really bring up neuroadaptation if the question asks about maintenance or withdrawal, as there really isn't anything in this theory that explains initiation. There isn't much AO2 here - so use it sparingly. It's very useful for application questions, though.

Overall

Biological explanations of addiction can be considered overly reductionist, ignoring environmental factors such as the role of the peer group, and cognitive processes such as self-medication in the process of addiction. Social factors such as the peer group are very important in the initiation of addiction - most addicts are first exposed to the drug through a member of their peer groups, and many people take a drug only in a specific social scenario.

Biological explanations of addiction are also overly deterministic, suggesting that people are completely controlled by their neurological systems such as the DRS and the EOS, as well as inherited genetic predispositions. Not everyone with a thrill-seeking personality due to genetics goes on to develop an addiction, and nor does everyone with raised dopamine levels - free will must play a powerful part in addiction formation.

Generally, genes best explain initiation, EOS and DRS best explain maintenance, and neurodaptation/withdrawal best explain relapse.