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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…
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Jetzt kostenlos anmeldenUnderstanding 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?
Fig. 1 - Nicotine addiction affects around 7.2 million in the UK.
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.
Nicotine addiction generally has the same effects on people across the board. Signs and symptoms of nicotine addiction include:
Treating nicotine addiction typically involves various psychological and biological therapies. Treatment for nicotine addiction includes:
Multiple theories of why nicotine addiction develops have been proposed, including learning theory and the biological approach.
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.
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.
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 also stimulates dopamine release, especially in the nucleus accumbens and ventral tegmental area, all of the dopaminergic reward pathways.
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 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.
Olds and Milners (1954), two scientists working in Canada, conducted a study using rats.
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.
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.
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.
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.
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.
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 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:
And of course, there are limitations to this approach:
Nicotine is addictive for a variety of reasons, including its effects on the reward systems in the brain (dopamine), impulsivity control issues (serotonin), and learning theory explanations suggesting role models affect addiction behaviours.
A variety of treatments for nicotine addiction are available, including biological treatments such as patches and inhalers, as well as cognitive behavioural therapy.
The brain responds to nicotine as it would to drugs, such as heroin and cocaine. So in a way, it is as addictive as them.
Yes, the physical effects of nicotine (pleasure) and withdrawal can contribute to addiction by making a person want to smoke.
Nicotine receptors stimulate the release of dopamine in the brain, inducing feelings of pleasure and relaxation. Eventually, repeated use results in addiction, as the body no longer produces enough to feel the normal effects of dopamine alone, without nicotine.
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