Motivation and emotion/Book/2023/Hijack hypothesis of drug addiction
What is the hijack hypothesis and how does it help to understand drug addiction?
Overview
[edit | edit source]Scenario: Who is Sarah?
Sarah, a vibrant and ambitious young woman in her early twenties who initially experimented with drugs out of curiosity . 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
. The result is a vicious cycle where drug cravings intensify while other aspects of life lose importance (Robinson & Berridge, 1993).Focus questions:
|
Hijack hypothesis
[edit | edit source]
Explanation of hijack hypothesis
[edit | edit source]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 , 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).[1]
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
[edit | edit source]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
[edit | edit source]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
[edit | edit source]
The role of dopamine in addiction
[edit | edit source]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
[edit | edit source]Neurotransmitter imbalances play a significant role in addiction vulnerability according to this
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
[edit | edit source]
Self-control
[edit | edit source]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
[edit | edit source]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).
Quiz
[edit | edit source]
Conclusion
[edit | edit source]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).
See also
[edit | edit source]- Hijack hypothesis of drug addiction (Book chapter, 2022)
- Addiction (Wikiversity)
- Dopamine and drug addiction (Book Chapter, 2017)
- Evolutionary models of human drug use (Wikipedia)
- Hijack hypothesis of drug addiction (Book Chapter, 2022)
References
[edit | edit source]Baumeister, R. F., & Vohs, K. D. (2007). Self-regulation, ego depletion, and motivation. Social and Personality Psychology Compass, 1(1), 115-128.
Beck, J.S., & Haigh, E.A.P. (2014). Cognitive therapy: Basics and beyond (2nd ed.). Guilford Press.
Beloate, & Coolen, L. M. (2017). Influences of social reward experience on behavioral responses to drugs of abuse: Review of shared and divergent neural plasticity mechanisms for sexual reward and drugs of abuse. Neuroscience and Biobehavioral Reviews, 83, 356–372. https://doi.org/10.1016/j.neubiorev.2017.10.024
Bevilacqua, L., Goldman, D., & Lee, F. S. (2010). Genetic approaches to addiction: genes and alcohol. Addiction, 105(8), 1514–1528.
Blum, K., Sheridan, P. J., Wood, R. C., Braverman, E. R., Chen, T. J., Cull, J. G., & Comings, D. E. (1996). The d2 dopamine receptor gene as a determinant of reward deficiency syndrome. Journal of the Royal Society of Medicine, 89(7), 396-400.
Bogdan, R., & Agrawal, A. (2017). The genetics, neurogenetics and pharmacogenetics of addiction. Current behavioral neuroscience reports, 4(2), 126-136.
Borsari, B., & Carey, K. B. (2001). Peer influences on college drinking: A review of the research. Journal of Substance Abuse, 13(4), 391-424.
Brown. (2010). A linguistic interpretation of Welford’s hijack hypothesis. Corporate Social-Responsibility and Environmental Management, 17(2), 81–95. https://doi.org/10.1002/csr.233
BURDMAN. (2023). DIACHRONIC AND EXTERNALLY-SCAFFOLDED SELF-CONTROL IN ADDICTION. Manuscrito, 46(1), 77–116. https://doi.org/10.1590/0100-6045.2023.v46n1.fb
Dube, S. R., Felitti, V. J., Dong, M., Chapman, D. P., Giles, W. H., & Anda, R. F. (2003). Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: The adverse childhood experiences study. Pediatrics, 111(3), 564-572.
Everitt, B. J., & Robbins, T. W. (2016). Drug addiction: updating actions to habits to compulsions ten years on. Annual Review of Psychology, 67, 23-50.
Goldstein, R.Z., & Volkow, N.D. (2011). Dysfunction of the prefrontal cortex in addiction: Neuroimaging findings and clinical implications. Nature Reviews Neuroscience, 12(11), 652-669. https://doi.org/10.1038/nrn3119
Guerri, & Pascual, M. (2019). Impact of neuroimmune activation induced by alcohol or drug abuse on adolescent brain development. International Journal of Developmental Neuroscience, 77(1), 89–98. https://doi.org/10.1016/j.ijdevneu.2018.11.006
Hagen, Roulette, C. J., & Sullivan, R. J. (2013). Explaining human recreational use of “pesticides”: The neurotoxin regulation model of substance use vs. the hijack model and implications for age and sex differences in drug consumption. Frontiers in Psychiatry, 4, 142–. https://doi.org/10.3389/fpsyt.2013.00142
Hulse G.K., Morris N., Arnold-Reed D., Tait R.J., & Parrott A.C. (1999). Improving clinical outcomes in treating heroin dependence: randomized, controlled trial of oral or implant naltrexone. Archives of General Psychiatry, 56(10), 848-852. doi:10.1001/archpsyc.56.10.848
Hyman SE, Malenka RC, Nestler EJ. (2006) Neural mechanisms of addiction: the role of reward-related learning and memory. Annu Rev Neurosci.
Kalivas PW, O'Brien C. (2008) Drug addiction as a pathology of staged neuroplasticity. Neuropsychopharmacology, 33.
Kauer JA, Malenka RC. Synaptic plasticity and addiction. Nat Rev Neurosci. 2007; 844-858.
Kendler, K. S., Davis, C. G., & Kessler, R. C. (1997). The familial aggregation of common psychiatric and substance use disorders in the National Comorbidity Survey: A family history study. British Journal of Psychiatry, 170(6), 541-548.
Goldstein RZ, Volkow ND. Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry. 2002;159(10):1642-1652.
Koob GF, Le Moal M. Drug abuse: hedonic homeostatic dysregulation. Science. 1997;278(5335):52-58.
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction. Neuropsychopharmacology Reviews: Official Publication Of The American College Of Neuropsychopharmacology, 35(1), 217-238.
Koob, G. F., & Volkow, N. D. (2016). Neurobiology of addiction: a neurocircuitry analysis. The Lancet Psychiatry, 3(8), 760-773.
Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635-641.
Nestler, E. J. (2001). Molecular basis of long-term plasticity underlying addiction. Nature Reviews Neuroscience, 2(2), 119-128.
Nestler, E.J. (2005). Is there a common molecular pathway for addiction? Nature Neuroscience, 8(11), 1445-1449.
Oesterle, Thusius, N. J., Rummans, T. A., & Gold, M. S. (2019). Medication-Assisted Treatment for Opioid-Use Disorder. Mayo Clinic Proceedings, 94(10), 2072–2086. https://doi.org/10.1016/j.mayocp.2019.03.029
Olds, J., & Milner, B. (1954). Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. Journal of Comparative and Physiological Psychology, 47(6), 419-427.
Robinson, T. E., & Berridge, K. C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research Reviews, 18(3), 247-291.
Simons-Morton, B., Haynie, D., Crump, A. D., Eitel, P., & Saylor, K. E. (2009). Peer and parent influences on smoking and drinking among early adolescents.
Smith, A. B. (2008). Understanding Addiction: A Comprehensive Guide to Behavioral Science-Based Treatment Methods. Wiley.
Volkow ND et al., (2016) Imaging the Addicted Human Brain Scientific American.
Volkow, N.D., Fowler, J.S., Wang, G.J., Swanson, J.M., Telang, F. (2004). Dopamine in Drug Abuse and Addiction: Results from Imaging Studies and Treatment Implications. Molecular Psychiatry 9(6), 557–569.
Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic Advances from the Brain Disease Model of Addiction. New England Journal of Medicine, 374(4), 363-371. doi:10.1056/NEJMra1511480
Volkow ND, Koob G F, McLellan AT (2020). Neuroscience of Addiction: Relevance to Prevention and Treatment. Am J Psychiatry, 177(9), 803–807
Volkow ND, Koob GF.Therapeutic potential of mesolimbic dopamine D3 receptor antagonists for drug addiction: A critical review. Neuropsychopharmacology, 40(12),2145–2158
Volkow, N. D., & Morales, M. (2015). The brain on drugs: from reward to addiction. Cell, 162(4), 712-725.
Volkow, N. D., & Schelbert, H.R. (1994). Effects of chronic cocaine abuse on postsynaptic dopamine receptors measured with PET. The Journal of Nuclear Medicine: Official Publication Society Of Nuclear Medicine, 35(2), 228-238.
Volkow, N. D., Wang, G.-J., Smith, L., & Fowler, J. S. (2016). Addiction: Beyond dopamine reward circuitry. Proceedings of the National Academy of Sciences, 113(42), 11818–11820. https://doi.org/10.1073/pnas.1613309113
Volkow N.D., Wang G.J., Fowler J.S., Tomasi D., Telang F., & Baler R. (2017). Addiction: beyond dopamine reward circuitry. Proceedings of the National Academy of Sciences, 108(37), 15037-15042. https://doi.org/10.1073/pnas.1112120108
External links
[edit | edit source]- Explaining human recreational use of ‘pesticides’: the neurotoxin regulation model of substance use vs. the hijack model and implications for age and sex differences in drug consumption (Frontiers in Psychiatry)
- A linguistic interpretation of Welford's hijack hypothesis (Wiley Online Library)
- Addictive Substances “Hijack” Brain Reward Systems (National Library of Medicine)
- The Neuroscience of Drug Reward and Addiction (Physiological Reviews)
- Highway to addiction: how drugs and alcohol can hijack your brain (University of Cambridge)
- Drugs, Brains, and Behaviour: The Science of Addiction (Safe Space)
- Dopamine and Addiction: Separating Myths and Facts (Health Line)
- How Drug Addiction Hijacks the Brain (Live Science)
- ↑ The Hijacker || Episode 1, retrieved 2023-08-19