Understanding nicotine addiction is key to developing programmes that successfully aid individuals who want to stop nicotine consumption. According to the Office of National Statistics, in 2018, 14.7% of the UK's adult population presented nicotine addiction, around 7.2 million people. Is the individual's environment responsible for the development of addiction? Or is it influenced mainly by biological factors?
- We will first define what we mean by nicotine addiction.
- Then, we will explore the signs and symptoms of nicotine addiction.
- We will briefly cover nicotine addiction treatment plans and then explore the different explanations for nicotine addiction.
- Then, we will delve deep into how nicotine affects the brain and nervous system, exploring research into the topic.
- We will cover how nicotine affects the blood-brain barrier before finally providing an evaluation of the various explanations for nicotine addiction.
Fig. 1 - Nicotine addiction affects around 7.2 million in the UK.
Nicotine Addiction
To understand how nicotine affects the brain, we must first understand the role of addiction in substance use and abuse.
Addiction is a mental disorder characterised by the presence of tolerance and subsequent withdrawal symptoms upon not consuming a substance. Addiction can be both physical and psychological.
Nicotine addiction refers to the dependency on nicotine, the toxic active agent in tobacco, which works as a stimulant drug.
Signs and Symptoms of Nicotine Addiction
Nicotine addiction generally has the same effects on people across the board. Signs and symptoms of nicotine addiction include:
- Urges to smoke.
- Unable to stop smoking.
- Withdrawal symptoms when quitting smoking (anxiety, restlessness, cravings, sadness and depression, irritability, frustration, and difficulty concentrating).
- Continued smoking when physical health declines.
- Inability to continue social activities to a full extent, as smoking takes precedence.
Nicotine Addiction Treatment
Treating nicotine addiction typically involves various psychological and biological therapies. Treatment for nicotine addiction includes:
- Nicotine replacement therapy (NRT), i.e., patches, chewing gum, oral strips.
- Bupropion (Zyban).
- E-Cigarette usage (reduced nicotine), although addiction issues are becoming increasingly problematic if e-cigarettes merely replace cigarettes rather than treat nicotine addiction.
- Cognitive behavioural therapy (CBT)
- Motivational interviewing (MI).
Multiple theories of why nicotine addiction develops have been proposed, including learning theory and the biological approach.
Learning Explanations for Nicotine Addiction
Learning theory has been proposed to explain nicotine addiction. It states that people who start smoking do so because they see people around them - such as family or friends - engaging in such behaviours (observation and modelling) and understand the consequences.
Based on operant conditioning, this can be positively or negatively reinforced or vicariously reinforced (witnessing the positive consequences of behaviours in others).
Given the social nature of humans, individuals are more likely to imitate role models and the behaviours role models engage in.
Once an individual has started smoking (initiation phase), the individual is likely to continue smoking for a certain period (maintenance phase). During the maintenance phase, the individual develops an addiction. Finally, the last step, according to the learning theory, is the relapse phase, in which an individual may try to stop smoking but would not be able to do so.
Positive reinforcement can be seen as fitting in with peers because of smoking (an immediate reward, alongside the pleasurable effects of smoking), and negative reinforcement can be seen in experiencing withdrawal symptoms when attempting to stop (they will begin smoking again to avoid symptoms).
In addition to the above, learning theory states that addiction occurs when an association is made between the consumption of a substance and being in certain environments, which prompts the need to smoke when placed in similar environments. This is known as cue reactivity (classical conditioning), and is associated with relapse rates.
Carter and Tiffany (1999) conducted a meta-analysis of cue-reactivity in addiction research. 41 cue-reactivity studies compared alcoholics, cigarette smokers, cocaine addicts or heroin addicts' responses to drug-related versus neutral stimuli.
They calculated effect sizes through self-reports of cravings and physiological responses to the stimuli.
They found a large effect size of +0.92 for cravings across all addict groups mentioned above. They suggested the study can be used during treatment planning for those with drug abuse issues to identify potential triggers that could induce cravings, impacting relapse rates.
Support can be seen in the study conducted by Akers and Lee (1996). They conducted a longitudinal test of social learning theory in adolescent smoking, examining 454 students in Grades 7–12 from Iowa, over five years using self-report questionnaires.
They examined social learning variables and how this related to smoking behaviours. They found positive correlations between social learning variables (such as differential association, differential reinforcement, definitions (attitudes), and modelling) and smoking.
They concluded that social learning theory could explain why adolescents begin smoking.
Learning theory explains nicotine addiction. However, it is not exempt from criticism.
- The learning theory may predict smoking behaviours but does not offer a model based on which all human smoking behaviour is explained. It does not account for the negative consequences of smoking, such as health issues.
- Learning theory tends to ignore individual differences and free will.
Effects of Nicotine on the Brain and Nervous system
Several hypotheses and models have been suggested that explain the effect of nicotine on the brain. Theories and models typically explain nicotine addiction in terms of the dopaminergic system, which is associated with the reward system.
Nicotine Receptors: Desensitisation
The desensitisation hypothesis explains nicotine addiction at the synaptic level. When it comes to nicotine, the neurotransmitter (NT) that comes into play is acetylcholine (ACh). ACh binds to ACh receptors. However, one type of ACh receptor is nicotinic acetylcholine receptors (nAChRs).
Nicotine seems to have a specific effect on these receptors. It stimulates the nAChRs, and shortly after that, the receptors are less sensitive due to ion channel inactivation (Ochoa et al., 1989). The phenomenon by which a response is diminished or absent is called desensitisation.
- Nicotine addicts (typical daily smokers) continue to smoke throughout the day, which results in a near-constant state of saturation of the nAChRs (Brody et al., 2006). When sleeping or attempting to stop smoking, smokers experience cravings and withdrawal symptoms because nAChRs return to a sensitised state. To reduce cravings and withdrawal symptoms, smokers will take in nicotine once more, which will desensitise the receptors again.
Nicotine also stimulates dopamine release, especially in the nucleus accumbens and ventral tegmental area, all of the dopaminergic reward pathways.
- Dopamine provides feelings of reward and relaxation.
Once smoking stops, dopamine goes through the reuptake process and the reward-like feeling stops, so smokers may want to increase their nicotine intake to regain these feelings.
Fig. 2: The reward structures in the brain.
In general, nicotinic receptors can be found throughout the brain. Areas of the brain include the hippocampus, the thalamus, the basal ganglia, and the cerebellum, to name a few.
Evidence from Studies using Brain-Imaging techniques
Evidence of this model comes from studies using imaging techniques which compare blood flow in certain brain areas. In 2005, Zubieta and colleagues conducted a PET study investigating brain activation patterns when participants consumed tobacco.
- The study presented a double-blind design, meaning neither participants nor researchers knew which participants consumed nicotine or a placebo. Brain scans were taken after the day's first and second cigarette.
- The VTA and NAcc (and other brain areas) were activated in the scans.
Brain Regions Affected by Nicotine
Olds and Milners (1954), two scientists working in Canada, conducted a study using rats.
- Researchers implanted electrodes in the NAcc of rats.
- The electrode would stimulate the NAcc once a lever would be pressed.
- Interestingly, once rats learned the association between pressing the lever and receiving the stimulation, they would keep pressing the lever to receive the stimulation (up to 2000 times in one hour).
The NAcc activation would trigger the activation of the VTA, which both are part of the reward system, which aligns with the desensitisation hypothesis. The consumption of nicotine triggers the reward system.
Nicotine and the Blood-Brain Barrier
The blood-brain barrier (BBB) is the brain's protective system, which keeps neurotoxins away from the brain. It was in the 1800s when Ehrlich noticed that staining when rats were injected with a blue stain, the stain would spread across all cells except those in the central nervous system.
- In this way, the brain and spinal cord would remain the same colour. When the stain was injected between the brain and the skull, the whole brain would change colour, while the rest of the body would remain the same colour.
Ehrlich discovered that the BBB was a barrier formed of cells strategically placed very close to one another. This allowed some materials, such as water and glucose, to cross the barrier and enter the brain, while at the same time, the barrier prevented other materials, such as neurotoxins, from entering the brain.
Interestingly, nicotine is a substance which can cross the BBB. This, in turn, has the effect of nicotine reaching the brain in around 15 seconds 2. The fact that nicotine can enter the brain in such a short amount of time contributes to nicotine addiction.
Impulsivity, Serotonin and Smoking
Research has pointed attention to the role serotonin has in smoking initiation and relapse. It is well established that serotonin plays a role in the inhibition of impulses 4.
Low levels of serotonin have been associated with higher impulsive behaviours. At the same time, nicotine consumption has been shown to increase serotonin levels in the brain, while nicotine withdrawal decreases serotonin levels.
Thus, it has been hypothesised that nicotine withdrawal increases individuals' impulsivity, making them more prone to maintaining their nicotine consumption.
Opioid System and Nicotine Addiction
There is preliminary evidence of the role that the opioid system may be playing in nicotine addiction. Nicotine consumption results in the increase of levels of opioids in the brain, which have an effect on the brain's reward system.
- Krishnan-Sarin et al. (1999) conducted a study to investigate whether the opioid system was different in smokers compared to non-smokers. Twenty participants were tested in four experimental conditions in which they received different amounts of naloxone.
Naloxone is a substance used to reverse the effects of opioids. In the presence of the substance, individuals addicted to nicotine present withdrawal symptoms, cravings to smoke and tiredness.
- The comparisons between smokers and non-smokers suggested that those who consumed nicotine regularly had a different response to naloxone. This, in turn, was taken as evidence suggesting that nicotine consumption can alter the opioid system.
Evaluation of the Biological Explanation of Nicotine Addiction
The biological approach to the research on Nicotine Addiction has offered great insights into the topic. We need to consider the strengths and weaknesses of the explanations for nicotine addiction.
Among the strengths:
- A significant amount of research has supported the link between nicotine and the dopaminergic system.
- Understanding the brain neurochemistry behind the consumption of nicotine has practical implications in the programmes supporting individuals quit the consumption of nicotine.
And of course, there are limitations to this approach:
- The biological explanation of addiction is criticised for being reductionist. Explaining addiction in terms of brain neurochemistry does not account for other components, such as social learning and environmental influences, that may also be playing a role in nicotine dependency.
- Further, the approach is criticised for being deterministic. One of the biological approach's assumptions is that biological foundations determine behaviour. This, in turn, cancels out individuals' rational ability to freely choose their actions.
Nicotine Addiction - Key takeaways
- Addiction is a mental disorder characterised by the presence of tolerance and subsequent withdrawal symptoms when a given substance is not consumed. Addiction can be both physical and psychological.
- Nicotine addiction is an addiction to smoking substances containing nicotine. Many people have a nicotine addiction.
- Brain neurochemistry can explain nicotine addiction, as seen in how nicotine affects neurotransmitters such as dopamine in the brain's reward pathways and serotonin in impulse control. Quitting smoking affects dopamine levels, explaining withdrawal symptoms and the need to continue.
- Nicotine addiction can also be explained by learning theory through operant conditioning. Cue reactivity can be explained through classical conditioning and how environmental cues can trigger smoking.
- Nicotine is not stopped by the blood-brain barrier, which allows the substance to reach the brain quickly, contributing to the development of an addiction. Both the biological approach and the learning theory approach have their strengths and weaknesses.
References
- Zubieta, J. K., Heitzeg, M. M., Xu, Y., Koeppe, R. A., Ni, L., Guthrie, S., & Domino, E. F. (2005, March). Regional Cerebral Blood Flow Responses to Smoking in Tobacco Smokers After Overnight Abstinence. American Journal of Psychiatry, 162(3), 567–577. https://doi.org/10.1176/appi.ajp.162.3.567
- Cisternino, S., Chapy, H., André, P., Smirnova, M., Debray, M., & Scherrmann, J. M. (2012, December 5). Coexistence of Passive and Proton Antiporter-Mediated Processes in Nicotine Transport at the Mouse Blood–Brain Barrier. The AAPS Journal, 15(2), 299–307. https://doi.org/10.1208/s12248-012-9434-6
- Fig. 2: Oscar Arias-Carrión1, Maria Stamelou, Eric Murillo-Rodríguez, Manuel Menéndez-González and Ernst Pöppel.Substantially modified by Seppi333, CC BY 2.0 , via Wikimedia Commons
- Krakowski, M. (2003, August). Violence and Serotonin: Influence of Impulse Control, Affect Regulation, and Social Functioning. The Journal of Neuropsychiatry and Clinical Neurosciences, 15(3), 294–305. https://doi.org/10.1176/jnp.15.3.294
- Fig. 2: Reward pathways by Oscar Arias-Carrión1, Maria Stamelou, Eric Murillo-Rodríguez, Manuel Menéndez-González and Ernst Pöppel.Substantially modified by Seppi333, CC BY 2.0 https://creativecommons.org/licenses/by/2.0, via Wikimedia Commons
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