Connection between Brain’s Reward Pathway and the Development of Drug Addiction: Discursive Essay

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Introduction

Drug addiction is increasingly becoming a universal issue, both expense wise, but also the impact it has socially. With an estimated cost to the healthcare of $1 trillion, it is clear why there is a high demand for further knowledge and treatments (NIoDA, 2017). Not only does the cost of addiction put a strain on a country’s economy, but it also has a disruptive effect on an addict’s personal life, the impact of drugs is not just to the individual, but also the person’s family, work-life etc. As of 2017, almost 21 million Americans have at least one addiction, yet only a small 10% of Americans receive treatment for their addiction. Drug overdose death has more than tripled since 1990, with more than 700,000 Americans dying from drug use. Finding out applications to help understand drug abuse and treatments on how to help dependents overcome their addicts is fundamentally vital (Addiction Centre, 2019).

It is common knowledge that drug abuse has an extensive impact on the mesolimbic pathway (often referred to as the reward pathway). Drug use releases dopamine neurons within the ventral tegmental area (VTA), which creates a pleasurable euphoria for the addict (Di Chiara & Bassareo, 2007). Research has shown that the reward pathways have a direct link with drug addiction, this opens a gateway of opportunity for future researchers to study the causes and mechanisms that are within addiction.

Whilst the reward brain pathway offers valuable knowledge and does explain a huge part of drug addiction, there are alternative explanations that can be put forward. It is undisputed that an environmental situation a person finds themselves in could have a major impact on the pathway they take. A person who may have an upbringing of deprivation and see no way out of their surroundings may turn to delinquent behaviours, such as drug abuse, this can be further influenced through the people who share these environments with them. Genetics is also another explanation behind why people may be at a higher risk of drug abuse, studies have shown that a person’s likelihood of developing an addiction could be hereditary.

The present essay will be explaining not only what drug addiction is but how it links with the brain’s reward pathway, the dopamine hypothesis will be explored by focusing on studies that have supported this process. The essay also aims to show alternative explanations in which contrast to the dopamine hypothesis and offer an alternative viewpoint, this will be ranging from animal vs human models to social learning theory.

What is drug addiction?

The National Institute of Drug Abuse (NIDA) was established 45 years ago, this has produced decades worth of research which has contributed to the viewpoint and understanding that drug addiction is a neuropsychiatric disorder (disease of the brain), and treatments to help individuals deal with their addiction. Hyman and Malenka (2011) described drug abuse as being “characterised by the compulsive seeking and taking of drugs despite serious negative consequences”, concluding that addiction is a behavioural disorder. In the UK alone, statistics showed that 3256 people died due to overdose in 2016, it is vital to understand and develop our knowledge of drug abuse to prevent such cases (EMCDDA, 2019).

When an individual takes certain substances such as cocaine or heroin, a euphoric sensation is felt, leading to the individual’s brain pathway to see this as a ‘reward’. When the high decreases (the reward declines) an addict will then take the drug again to replicate the pleasurable sensation, constantly chasing the same reward feeling again. This is otherwise known as ‘reinforcement’, as the brain is subjected to the repeated reward, which as a result begins the dependency.

How is ‘reward’ linked to the brain?

It is valuable information understanding how drug addiction works, but there needs to be understanding on how the reward system works directly with the brain. Neurobiologists research has revealed that activity within the brain’s reward system is boosted when euphoria chemicals are induced from the usage of substance abuse. (Volkow, Fowler & Wang, 2003)

Research indicates that chronic drug use changes behaviour within key parts of the structure and function of the brain’s neurons, in particular, the reward system pathway that extends from dopamine-producing nerve cells, (otherwise known as neurons) of the ventral tegmental area to the dopamine sensitive cells located within the nucleus accumbens. This can have lasting effects from days, weeks, months or even years. Each use decreases the euphoric feeling that an addict feels, however, due to the reinforcement that the brain will be rewarded, the reward system will create a craving and dependency that often leads to a lifetime of drug abuse or multiple relapses. (Nestler & Malenka, 2004)

The Dopamine Hypothesis

Dopamine (DA) is a neurotransmitter within the brain, which acts as a control for numerous functions such as motor activity, cognition and emotion. The dopaminergic system (consisting of dopamine receptors, transporters and enzymes) has been subjected to masses amounts of research due to its potential contribution to treatment to conditions such as drug addiction and schizophrenia (Le Foll, Gallo, Le Strat, Lu & Gorwood, 2009; Gorwood et al., 2012).

Dopamine within the brain reward system, responds to every type of reward, from basic needs such as food and drink to sexual desires and addiction. Dopamine is vital to an addict’s cravings and desire. Evidence has shown that drugs directly link to dopamine, e.g. cocaine and heroin, both of which involve dopamine-releasing as a neurotransmitter but differ in how they access this. Cocaine, on one hand, has more direct access, as it goes straight to the dopamine levels within the nucleus accumbens. Whereas heroin first attaches to opiate receptors, stimulating dopamine neurons which react with the prefrontal cortex. Psychostimulants, e.g. cocaine and amphetamine, reduces activity within the ventral tegmental area dopamine (VTA DA) neurons, as they block DA reuptake, which then increases DA release and activates the reward mechanism. (Bunney et al., 1973)

Evidence in support of the Dopamine Hypothesis

Di Chiara and Imperato (1988), studied the effect that various drugs would have on extracellular concentration levels in the nucleus accumbens and the dorsal caudate nucleus, within rats by using brain dialysis. Rats self-administrated drugs such as nicotine and cocaine, which increased dopamine levels in both areas, but mainly in the accumbens. The drugs also induced hypermotility (excessive movement) at even the smallest of doses. In contrast, drugs with aversive properties e.g. bremazocine, which blocked receptors, reduced dopamine within the accumbens and caudate, and elicited no hypomotility. Further tests were done for non-abusive drugs, such as anti-depressants and antihistamines, which neither modified any dopamine concentration within the dopaminergic areas. These findings proved that there is clear biochemical evidence in support that drug abuse and dopamine release within the limbic area are directly linked.

This was supported by a study in 1995, by Pontieri, Tanda and Di Chiara, who also studied rats, but this time they administrated drugs (cocaine, amphetamine and morphine) via IV. They used a range of doses levels, however, even the lowest dose of amphetamine increased dopamine. These experiments showed that if the dopamine becomes blocked, the drug high is no longer pleasurable, highlighting the impactful role dopamine plays within cravings and addiction.

A study which helped support the Dopamine Hypothesis, was the usage of Knock out Mice, these mice are used as science have genetically modified or “knocked out” genes within the mice. In this case, mice had their dopamine receptors within the nucleus accumbens biochemically deleted or disrupted. Findings showed that the knock out mice consumed less alcohol than normal mice, as they did not receive the “reward” feeling from consuming alcohol. However, the mice did not display the withdrawal affects other studies had found, and thus cannot explain this aspect (Phillips, 1998).

Similar studies researching drug abuse, in particular, the administration of cocaine and ethanol to nonhuman primates (monkeys) over 6 months. Findings reported that extracellular DA levels were increased. This suggests that an increased dopaminergic transmission centralises the memory of how the drug experience made the addict feel and explains why nonhuman primates will continue to self-administrate drugs (Bradberry 2000; Bradberry et al., 2010).

Critiques

The Role of Dopamine Receptors: Molecular Genetics

Molecular genetics has been used to try and identify if addiction is biologically inherited through families and if so how. Functionality within the D2 Dopamine receptor could potentially explain why responses to drugs differ and the likelihood that someone may be more inclined to be an addict.

Human brain imaging studies have shown that responses to cocaine can be subjective which does not correlate with the dopamine process. Studies in mice, where dopamine transport molecules had been deleted, showed that mice had reduced overall cocaine administration but overall, it was not completely diminished, showing that whilst the dopamine hypothesis, does hold some key roles in drug addictions, it does not fully explain. (Sora, 2001)

Genetics of Addiction

Epidemiological studies (the study of how often diseases occur in different groups of people and why (BMJ, 2019)) proposes that addiction is operated by genetic factors such as vulnerability to taking drugs, continuing taking them and the likelihood of becoming dependent. Researchers have favoured using twin studies to investigate how genetics and environmental factors impact addiction. Twin studies supply information on environmental factors, such as the availability of drugs and the exposure dependents face. Studies have shown that genetic influences on addiction have proven to be useful and the heritability of becoming addictive is moderately high. (Li & Burmeister, 2009)

A genetic study by Tsuang et al. (1996) researched 3,372 twins and looked in a clinical setting whether drug use disorders ran through families. 10.1% of the sample had been either abused or had been dependent on at least one illicit drug. There was a significant difference between monozygotic twins (26.2%) vs. dizygotic (16.5%) twins showed a genetic influence on drug addictive disorders. Biometrical modelling of the twins showed that genetic factors had a 34% of the variance, the environment the twins shared had 28% and the non-shared environment had 38%, which indicated a significant influence over the individual’s chances of developing drug dependency.

The role of Serotonin

Dopamine is not the only neurotransmitter that drugs react strongly with, serotonin receptors also strongly react with drugs especially cocaine. Levels of serotonin become unsteady through the process of addiction and make going through withdrawal a struggle. Serotonin is responsible for how the brain processes emotions, judgement and conditioned cues. Serotonin functions to produce happy and positive feelings when consuming drugs, serotonin levels become overstimulated and thus released brain transmitters, which causes dependency to continue taking drugs. When illicit drugs and serotonin mix, a person’s learning, memory, sleep pattern, emotions, and feelings are all negatively impacted. (Mueller & Homberg, 2015)

Withdrawal and serotonin interaction can lead to severe aftereffects when abstaining from drugs, addicts will often feel emotions such as depression, suicidal thoughts etc, due to the ‘come down’ they will feel. This often leads to addicts relapsing to prevent these emotions and thoughts. (EGDR, 2017)

Animal vs. Human studies

Studying into the animal of addiction has been said to have had valuable progression in the understanding of human addiction and treatments for it. However, most pharmacological treatments that have been developed in response to animal models have failed to be effective in treating addiction, which has wasted plenty of resources that could have been used elsewhere. It could also be said that addiction, may be unique to humans, which would reduce the validity of animal models. The addicted brain should be one component of a broader network of symptoms, environmental and social factors that are just not prevalent in an animal’s model, especially laboratory animals. So, it could be stated that addiction within animal models does not contribute as much understanding and treatment of addiction within humans, as previously stated, and instead has been exaggerated. (Field & Kersbergen, 2019)

Theoretical Models

Theoretical perspectives a divided into four categories, basing on the role of social factors which condition and model addiction. First, social learning theory, which states there needs to be a strong bond within society to stay engaged and feel inclusive. When these bonds are weak, people tend to shy away from social norms and begin to rule-break such as turning to drug use. Second, behavioural choice theory, the key focus being the reward and reinforcements, drug users receive from their addiction, (‘reward’ not to be confused with the same ‘reward’ in the brain pathways). Third, role modelling, linking with social learning theory, if a young adult whose role model is an addict, this may have a huge influence on their behaviour. Lastly, stress and coping theory, individuals who may have poor life circumstances may turn to addiction as a result of the distress and alienation they face in their daily life. People who have poor coping skills often cannot manage these misdemeanours in their life and so turn to more high-risk engagement such as drug abuse (Miller & Carroll, 2006).

A study by Teasdale (1976), revealed that when addicts were exposed to pictures that related to forms of opiates, they had significant reactions of emotional and physical distress when viewing the pictures. This would indicate that former drug addicts may have potentially relapsed due to their environment or settings they have found themselves in, where they had once taken drugs. This suggests the idea that addicts tend to stick with their peers who also have a drug dependency due to society’s negative connotations that have been applied to drug-taking. In environments such as these, addicts will be constantly encouraging each other to take hits, which is where social learning and modelling can play a prominent role.

Implications for Treatment

Addiction treatment should be tailored to meet the needs of the addicts, as it is a personal process they go through. Pharmacological treatments alone can be quite insufficient, however combining pharmacotherapy with other treatments such as psychosocial therapy, this can help establish the individual differences the addict has and what may have influenced their choice of lifestyle.

Current treatments for dependencies on heroin, use methadone, which replicates the euphoric state heroin brings, but it is not as dangerous, however, it could be argued this is not helping overcome addiction, rather replacing a dangerous drug dependency with a lesser one.

Talking therapies can be useful however, it is not beneficial to only discuss the drug the addict is dependent on, all forms of addictions should be discussed, as it is not uncommon for an addict to replace one addiction with another, this could result in continuous relapsing, as the addict will supplement their current drug for a new one.

Conclusion

In conclusion, the brain’s reward pathway and the dopamine hypothesis do contribute and give valuable knowledge to the understanding of drug addiction, such as the euphoria feeling the drugs bring, altering the brain to think it is being rewarded, could offer solutions such as altering dopamine receptors, however, this comes with risks. Alternative explanations have shown that the dopamine hypothesis cannot stand alone as an effective explanation for drug dependency. Environmental cues also have a substantial impact on a person’s risk of developing a drug dependency, this is due to their scenario, whom there with etc.

Models on how drug addiction is looked at within the brain, need to be updated, whilst animals do have similar brain imaging, they cannot be applied when combined with the environmental cues a human faces. An addiction in a human is entirely different to addiction within an animal, as an animal does not know the consequences it faces due to its dependency.

In response to the initial proposed question on whether the brain’s reward pathway is responsible for the development of drug addiction, the answer is clear, partly. It cannot be concluded that the pathway is entirely responsible for drug addiction, but it can be agreed it plays a significant role. Drug addiction is far more complex than categorising it in one explanation. Genetics, theoretical models and psychobiology all play a hand in how we can understand and develop our knowledge and treatment of drug addiction. However, drug addiction is still quite ambiguous as new information is found continuously, meaning there is still a lot more research does not know.

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