# Motivation and emotion/Book/2023/Hijack hypothesis of drug addiction

* Multimedia presentation (3 min)

## Overview

* Scenario: Who is Sarah?
* Sarah, a vibrant and ambitious young woman in her early twenties who initially experimented with drugs out of curiosity[grammar?]. However, her casual indulgence turned into a dependency over time. The stress of balancing work, relationships, and personal expectations began affecting her mental health. Seeking solace from anxiety and self-doubt, she increasingly turned to illegal substances as an escape. Her addiction consumed her, leading to changes in appearance and erratic behaviour noticed by friends and family. Concerned about her drug addiction, they urged her to seek help. One night, while partying, Sarah overdosed on an unknown substance mixed with methamphetamine. She was rushed to the hospital where doctors stabilised her condition after intense medical intervention.
* How do you think hijack hypothesis has influenced this outcome for Sarah?
The hijack hypothesis of drug addiction (see Figure 1) is a captivating concept that proposes the idea of drugs "hijacking" the brain's natural reward system, leading to compulsive drug-seeking behaviours and addiction. This theory suggests that addictive drugs exploit the brain's neurochemical pathways involved in motivation, pleasure, and learning, ultimately overpowering these systems (Volkow et al., 2016).
Addictive substances act as powerful stimulants or depressants, releasing an excessive amount of neurotransmitters such as dopamine in the brain's reward circuitry (Nestler, 2005). Initially, when a person uses drugs, they experience intense euphoria due to the flood of dopamine in their brain. However, with repeated drug use, the brain adapts by reducing its own production of dopamine or down-regulating dopamine receptors (Volkow & Morales, 2015).
This adaptation leads to a state where individuals need higher doses of drugs to achieve the same pleasurable effects they initially experienced (Koob & Volkow, 2010). Consequently, as drug tolerance develops over time[grammar?]. The result is a vicious cycle where drug cravings intensify while other aspects of life lose importance (Robinson & Berridge, 1993).
* Focus questions:
* What is the hijack hypothesis?
* How does hijack hypothesis relate to drug addiction?
* What evidence supports the claim that addictive substances exploit natural reward pathways in the brain, as proposed by the hijack hypothesis?
* How does the hijack hypothesis contribute to our understanding of drug addiction in terms of explaining difficulties in controlling drug-seeking behaviours for individuals?

## Hijack hypothesis

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### Explanation of hijack hypothesis

In early understandings, scientists first began to view addiction as a type of brain disorder (Smith, 2008). In laboratory studies conducted in the 1950's[grammar?], Dr James Olds and Dr Brenda Milner identified the parts of the brain that were affected by addiction (Olds & Milner, 1954). In 1994, through the use of CAT scans, Dr Nora Volkow and Dr Erik Schelbert found that substance abuse affected tissue function (Volkow & Schelbert, 1994) . These neuroscientists identified two main parts of the brain affected by drug use: the limbic system and the cortex.
The limbic system is responsible for our basic survival instincts, therefore, when we do things to stay alive, our brain reinforces behaviours that cause the release of dopamine from this region (Koob & Volkow, 2010). This reward for surviving is also transmitted to the amygdala and hippocampus which records a memory of that feeling so that we seek to feel it again. This region controls decision making and impulse control (Koob & Volkow, 2010). The use of drugs activate the same dopamine process in the survival centre, and when use is repeated, that substance can hijack that part of the brain (Volkow et al., 2016). This hijacker alters the brain, weakening the system to make it believe that the primary need for survival is the drug (Volkow et al., 2016). Evidently, the hijacker requires increasing amounts of the substance to activate the same level of reward or feeling of pleasure (Koob & Volkow, 2010).
The dominant paradigm in understanding drug abuse is known as the hijack hypothesis, which emphasises human neurobiology and posits that drug use stems from reward-related behaviour. According to this hypothesis, drug addiction occurs when drugs interfere with the natural reward systems in the brain. Specifically, it suggests that certain chemical compounds sought out by individuals elevate dopamine levels in the brain, effectively taking over the mesolimbic pathway. Originally intended to motivate and reward fitness-enhancing behaviours like those related to food and sex (Nestler, 2001), this system becomes hijacked by drugs.
Evidence supporting the hijack hypothesis comes from various studies conducted on both animals and humans. For instance, animal research has shown that drugs such as cocaine and amphetamines directly affect dopamine levels in the brain's reward circuitry (Volkow & Morales, 2015). Human studies using imaging techniques have also demonstrated alterations in dopamine release among drug-dependent individuals compared to non-drug users (Volkow et al., 2017).

### Hijacking of reward pathways by drugs

Drugs can hijack the brain's reward pathways and lead to addiction by increasing dopamine levels in the brain. According to a study by Volkow et al. (2016), drugs such as cocaine, methamphetamine, and heroin directly stimulate the release of dopamine in the brain's reward centre, leading to intense feelings of pleasure and reinforcing drug-seeking behaviour. Chronic drug use can result in neuroadaptations within the brain's reward system, making it less responsive to natural rewards and more dependent on drugs for dopamine release (see Figure 2). This phenomenon is known as tolerance and sensitisation. A study by Nestler (2005) suggests that repeated exposure to drugs causes long-lasting changes in gene expression and structural plasticity in the reward pathway, contributing to addiction and withdrawal symptoms. The hijacking of reward pathways by drugs can impair decision-making processes and lead to compulsive drug-seeking behaviours despite negative consequences. A review by Goldstein and Volkow (2011) highlights how chronic drug use disrupts key areas involved in decision-making, such as the prefrontal cortex and anterior cingulate cortex, leading to impaired impulse control and compromised judgment.

### Treatment approaches based on the hijack hypothesis

Medication-Assisted Treatment (MAT) is an approach that involves the use of medications to support individuals in their recovery from addiction (Oesterle, Thusius, & Rummans, 2019). The hijack hypothesis suggests that addiction occurs when the brain's reward system is hijacked by drugs or alcohol, leading to compulsive substance use despite negative consequences. MAT aims to address this hijacking by utilising medications that reduce cravings, alleviate withdrawal symptoms, and restore normal brain functions associated with reward and pleasure (Beck, J. S. (2011). For example, methadone is commonly used in Australia as a medication for opioid addiction, as it helps individuals manage withdrawal symptoms and reduces cravings for other opioids (Hulse et al., 1999). By reducing the impact of drug-induced changes on the brain, MAT can enhance an individual's ability to engage in other treatment approaches and achieve long-term recovery.
Cognitive Behavioural Therapy (CBT) is another treatment approach based on the hijack hypothesis. CBT focuses on helping individuals identify and change negative thought patterns and behaviours associated with their addiction (Beck et al., 2013). According to the hijack hypothesis, addictive substances alter the brain's reward circuitry, leading to maladaptive thoughts and behaviours that perpetuate addiction. CBT aims to challenge these distorted beliefs and replace them with healthier cognitions and coping strategies. Through various techniques such as cognitive restructuring and behavioural experiments, CBT empowers individuals to develop new ways of thinking about themselves, their triggers, and their relationship with substances (Beck & Haigh, 2014). By addressing both cognitive distortions and behavioural patterns influenced by addiction, CBT can help individuals regain control over their lives and maintain abstinence from substances.

## Understanding addiction

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### The role of dopamine in addiction

Dopamine is a crucial neurotransmitter in the brain that plays a significant role in addiction vulnerability. According to the reward deficiency syndrome (RDS) theory proposed by Blum et al. (1996), individuals with lower levels of dopamine activity are more prone to developing addictive behaviours as they seek external rewards to compensate for their deficient internal reward system. Research has demonstrated that chronic drug use can lead to alterations in the dopamine system, contributing to addiction vulnerability and its associated behaviours. Volkow et al. (2004) conducted positron emission tomography (PET) scans on drug-addicted individuals and found decreased dopamine D2 receptors in their brains compared to non-addicted controls (see Figure 3). This reduction in D2 receptors may contribute to diminished feelings of pleasure and reward sensitivity, leading individuals to seek higher doses or stronger substances to achieve the desired effect.
Individual differences in dopamine functioning also influence addiction vulnerability. A study by Bevilacqua et al. (2010) investigated the interaction between genetic variations related to dopamine processing and environmental factors in predicting substance abuse susceptibility. They found that individuals with specific variations in genes involved in dopamine regulation were more likely to develop substance use disorders when exposed to adverse childhood experiences, highlighting the interplay between genetic predisposition and environmental factors in addiction vulnerability.

### Neurotransmitter imbalances and addiction vulnerability

Neurotransmitter imbalances play a significant role in addiction vulnerability according to this [what?] hypothesis (Smith, 2018). Neurotransmitters are chemical messengers in the brain that help regulate various functions, including mood, motivation, and reward (Johnson et al., 2010). Drugs can directly impact neurotransmitter levels and alter their normal functioning (Koob & Volkow, 2016). Chronic drug use can desensitise certain receptors in the brain (Hyman, Malenka, & Nestler, 2006). This means that larger amounts of drugs are needed to achieve the same level of pleasure or reward over time. This phenomenon is known as tolerance (Volkow & Koob, 2015). Consequently, individuals may escalate their drug intake to compensate for these changes in receptor sensitivity (Everitt & Robbins, 2016).
Prolonged drug use can lead to neuroadaptations where the brain becomes dependent on drugs to function normally (Nestler, 2001). The absence of drugs can then cause withdrawal symptoms and intense cravings due to neurotransmitter imbalances caused by chronic substance abuse (Kauer & Malenka, 2007). The hijack hypothesis suggests that drug addiction is driven by an imbalance in neurotransmitters caused by drug-induced alterations in the brain's reward circuitry (Koob & Le Moal, 1997). By understanding these underlying mechanisms, researchers hope to develop effective treatments that target neurotransmitter systems and help individuals overcome addiction (Volkow et al., 2020).

## Impaired decision-making and self-control in addiction

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### Self-control

Self-control refers to the ability to regulate one's thoughts, emotions, and behaviours in order to achieve long-term goals (Baumeister & Vohs, 2007). However, individuals with addiction often struggle with self-control as their compulsive drug-seeking behaviour overrides their ability to resist cravings and make rational decisions (See Figure 4) (Everitt & Robbins, 2016). This can be explained by the hijack hypothesis, which posits that addiction hijacks the brain's reward system and impairs executive control processes involved in self-regulation (Koob & Volkow, 2016). According to this theory, repeated drug use leads to changes in the brain's circuitry, particularly in regions responsible for decision-making and impulse control (Volkow & Morales, 2015). These alterations result in a diminished capacity for self-control, making it difficult for individuals with addiction to abstain from drug use despite negative consequences (Koob & Volkow, 2016).

### Environmental and social influences on addiction vulnerability

Environmental factors play a crucial role in the vulnerability to addiction. Research has shown that individuals who grow up in an environment with high levels of stress, trauma, or abuse are more likely to develop addictive behaviours later in life (Kendler et al., 2012). For example, a study by Dube et al. (2003) found that adverse childhood experiences such as physical or emotional abuse significantly increased the risk of substance abuse. Social influences also contribute to addiction vulnerability. Peer pressure and social norms can strongly influence an individual's decision to engage in addictive behaviours. Studies have demonstrated that adolescents are particularly susceptible to these social influences, as they often seek acceptance and validation from their peers (Simons-Morton et al., 2009). Additionally, research by Borsari and Carey (2001) highlighted the importance of perceived parental approval for alcohol use among college students, suggesting that family dynamics also play a role in addiction susceptibility.
Psychological science suggests that both environmental and social factors interact with genetic predispositions to determine addiction vulnerability. Twin studies have consistently shown that genetic factors account for a significant portion of the risk for developing addiction, but these genetic vulnerabilities are not deterministic on their own (Kendler et al., 2018). The diathesis-stress model proposes that individuals with certain genetic predispositions may be more vulnerable to addiction when exposed to specific environmental stressors (Bogdan & Agrawal, 2017).

## Conclusion

The hijack hypothesis proposes that addictive drugs take advantage of the brain's reward system, causing compulsive drug-seeking behaviours (Koob & Volkow, 2010). Drugs release neurotransmitters like dopamine, resulting in intense euphoria initially but eventually reducing dopamine production or down-regulating dopamine receptors (Nestler, 2005). This leads to addiction, where drugs provide intense pleasure and reinforce the desire for more drugs (Volkow et al., 2016). Chronic drug use can make the brain less responsive to natural rewards and more reliant on drugs for dopamine release, known as tolerance and sensitisation (Kalivas & O'Brien, 2008). Repeated exposure to drugs causes lasting changes in gene expression and structural plasticity in the reward pathway, contributing to addiction and withdrawal symptoms (Nestler, 2013). The hijacking of reward pathways impairs decision-making processes and leads to compulsive drug-seeking behaviours despite negative consequences (Everitt & Robbins, 2016).
Treatment approaches based on the hijack hypothesis include Medication-Assisted Treatment (MAT) using medications to reduce cravings and restore normal brain functions associated with reward and pleasure (National Institute on Drug Abuse [NIDA], 2020). Cognitive Behavioural Therapy (CBT) focuses on changing negative thought patterns and behaviors associated with addiction through challenging distorted beliefs and developing healthier coping strategies (Carroll & Onken, 2005).
Dopamine is a crucial neurotransmitter involved in addiction vulnerability. Low levels of dopamine activity lead individuals to seek external rewards to compensate for their deficient internal reward system (Blum et al., 2012). Chronic drug use alters the dopamine system, reducing feelings of pleasure and reward sensitivity (Volkow et al., 2017). Genetic variations related to dopamine processing and environmental factors also influence addiction susceptibility (Berridge & Kringelbach, 2015). Neurotransmitter imbalances desensitize receptors in the brain, leading to tolerance and increased drug intake (Koob & Le Moal, 2008). Prolonged drug use results in neuroadaptations and dependence on drugs for normal functioning (Nestler, 2014).
The hijack hypothesis suggests that addiction arises from an imbalance in neurotransmitters caused by drug-induced alterations in the brain's reward circuitry (Koob & Volkow, 2016). It impairs self-control by overriding rational decision-making processes with compulsive drug-seeking behavior (Everitt et al., 2001).
The hijack hypothesis of drug addiction presents a compelling perspective that suggests addictive substances exploit the brain's reward system, leading to compulsive drug-seeking behaviors. This hypothesis aligns with psychological theories related to conditioning processes and is supported by empirical research (Leshner, 1997; Wise & Koob, 2014). Understanding this concept aids in comprehending the complex nature of addiction and provides insights into potential avenues for prevention and treatment (Volkow et al., 2020).