By: Antara Kothare and Vritee Shah
This literature review provides an overview of some of the neurocognitive impairments (attention, mood, memory, and the impact on the prefrontal cortex) that adolescents face as a result of active smoking. The key findings of this paper include diminished attentional problems that can persist into adulthood, deteriorating mood, reduced working, and verbal memory, and lesser functionality of the prefrontal cortex.
Adolescence is the transitional phase of growth between childhood and adulthood. The World Health Organization has defined an adolescent to be between ages 10-19. The human brain develops until the age of 20 by the process of synaptic pruning and myelination in the prefrontal cortex. This period is critical for an adolescent as their developing brain is not completely mature and hence is vulnerable to negative influences of the environment like
subjection to nicotine, a highly addictive chemical that is present in tobacco smoke. This exposure could impact the maturation process of the frontal cortical regions; it destroys the grey matter in the brain, making the cerebral cortex, the part of the brain responsible for learning and memory, thinner.
Many smokers try their first cigarette during adolescence. Research suggests that 9 out of 10 daily smokers first try smoking at the age of 18.
Active smoking is the direct inhalation of mainstream smoke (MS) that is drawn directly through the end of the cigarette. It has been found to be detrimental to human health and is considered the leading cause of lung cancer. An active smoker smokes at least one cigarette per day. Infamously held accountable for a myriad of chronic diseases including larynx or esophagus cancers, lung disease, and cardiovascular damage, active smoking has also been discovered to have a degenerative effect on the brain and its neurocognitive functions.
Neurocognitive functions are cognitive processes that are connected to the operation of certain areas in the human brain, cortical networks, and neural pathways. Although there is limited research, recent findings have discovered that chronic cigarette smoking has a lasting effect on neurocognitive functions like deficiencies in mood, attentional performance, executive functions like working and verbal memory, and reduced functionality of the prefrontal cortex.
Considering the hazardous effects of smoking on the brain and neurocognition, this review aims to discuss some neurocognitive defects caused by active smoking in adolescents. These adverse effects are outlined below to increase awareness of this overlooked research area.
Nicotine’s effects on the brain
Nicotine is a chiral alkaloid made by the tobacco plant that can also be produced synthetically. It has powerful pharmacologic and psychodynamic (inducing euphoria, increased alertness, and a sense of relaxation) effects. Nicotine is also highly addictive – it is widely used as a stimulant and anxiolytic. It is the chemical present in tobacco that causes addiction. Nicotine that enters the body while smoking a cigarette activates brain receptors.
Figure 1 shows nicotine mimicking acetylcholine (a natural neurotransmitter) and binding to its receptor, which becomes known as the nicotinic receptor. Once activated, dopamine, a brain chemical that gives people the feel-good effect, is released in the same way as it would be released naturally but at a much higher rate. This effect results from the body’s reaction to nicotine, which disrupts the body\’s natural balance. It is the cause of addiction. As a result of addiction, nicotine receptors in the brain keep increasing as smoking continues; because of this, addicted smokers have more receptors than nonsmokers.
Fig 1 showing nicotine mimicking neurotransmitter acetylcholine and binding to acetylcholine receptors.
Smoking eventually reduces the natural supply of dopamine. This is due to the reduction of acetylcholine levels that subside electrically stimulated dopamine release. When people quit smoking, there is no pleasure response since nicotine does not bind to the receptors. Additionally, this leads to nicotine withdrawal, so symptoms like anxiety, a depressed mood, frustration, and anger are prominent. Since dopamine can no longer be released naturally, the quickest way to relieve oneself from these symptoms would be to smoke a cigarette. This would release dopamine, activating the pleasure response.
The prefrontal cortex aids the brain to plan, organize and even pay attention to certain events. Professor Stephen Williams of the Queensland Brain Institute at UQ explains, \”If we want to give our full concentration, something happens in the brain to enable us to focus and filter out distractions.\” Dopamine, norepinephrine, as well as acetylcholine, are responsible for attention and focus. Nicotine at first increases the user’s alertness as a result of strengthened neural communications in the brain.
The Columbia group identified a nicotinic receptor complex found at the place of neuron communication in the brain that nicotine acts on. When it is low in concentration, nicotine activates this receptor causing the release of more neurotransmitters by the neuron. Lorna Role, a professor in the Center for Neurobiology and Behavior at Columbia-Presbyterian Medical Center, explains that “nicotine apparently can increase the strength of communication between neurons in the brain by increasing the release of glutamate – the key central nervous system excitatory transmitter.” This stronger signal leads to increased alertness. In addition, nicotine also has a calming and soothing effect on the user since it stimulates the release of dopamine, a reward chemical that triggers positive feelings.
However, this is only temporary, as proven by animal and human studies that confirm smoking in adolescence leading to attention problems that persist into adulthood.
Nicotine is a key component of cigarettes that initially raises a person’s mood. It takes about ten seconds for the nicotine to reach the brain when a person smokes. Initially, nicotine boosts mood and concentration, reduces stress and appetite, and relaxes muscles in the body. This is due to nicotine’s effect on dopamine, a chemical in the brain that plays a significant role in reward-motivated behaviour and emotional responses. But since smoking causes the brain to shut down the natural supply of dopamine, in the long term, people have a reduced dopamine supply, leading to them becoming nicotine dependent and inclined to smoke more.
Working memory refers to the different processes used by the brain to organize and store information temporarily. This stored information can then be used to execute neurocognitive tasks. Verbal memory is the memory of information that is verbally represented. Certain tasks like learning and remembering word lists and story recall fall under this category. Nicotine produces temporary improvements in cognitive functions and sometimes even neuroprotection in humans. However, further research has found that nicotine cessation after addiction during adolescence can be detrimental to their memory due to the high neurotoxicity levels.
The prefrontal cortex is a part of the brain that has not completed maturing until the adolescent stage. It is one of the last parts of the brain to mature, making it vulnerable and susceptible to the effects of psychotropic substances like nicotine. This brain area is responsible for attention performance and executive functions like decision making.
Animal models are useful for gaining deeper insights into the adolescent brain as they can explore the causal links between nicotine exposure during adolescence and neurocognition in adulthood (in the absence of nicotine). An animal study assessing the long-term effects of nicotine in adolescent rats found that nicotine exposure in adolescence led to reduced attention spans in adulthood. Although the research was conducted in adolescent rats, the findings can still be useful since the neural structures, and signal processing in rats and humans are similar.
This data was supported by a human twin study conducted in 2014. They found that during youth and adolescence, between a twin who does not smoke and the other who does, the latter twin has diminished attentional performance. Before initiating smoking, their attention span was more or less the same, suggesting that smoking during teens would lead to attention issues that could last into adulthood. Prolonged nicotine exposure can lead to noticeably impaired concentration levels along with a reduction in the functioning of mGluR2, an inhibitory autoreceptor in the prefrontal cortex. This autoreceptor is responsible for preventing overstimulation of nerve cells. Reduction of mGluR2 signaling can cause reduced attention and disinhibition of the frontal lobe.
Although there is limited research conducted for the long-term effects that adolescent smoking has on executive functions like attentional performance, the findings of the above studies are consistent with studies like the one by Jacobsen et al  indicating short-term deficits in auditory attention among male adolescent smokers. These findings correlate with the hypothesis that smoking increases attention problems due to its effect on the brain and neurocognition.
A study conducted by Li-Tzy Wu and James C. Anthony  explored the possible link between tobacco smoking leading to depressed mood in adolescence. An epidemiologic sample of 1731 youth was taken, and researchers concluded that an increase in the onset of a depressed mood was due to tobacco smoking. The possibility of nicotine damaging brain pathways (by taking over the “reward pathway”) and, in turn, being responsible for regulating mood supports the conclusion stated above. They also claimed that antecedent depressed mood was not linked to the initiation of smoking.
On the contrary, a study conducted in 2007 on the different patterns and relationships between a ‘depressed mood’ and smoking occurrence opposes the above claim. The findings suggest that the severity of the depressed mood in nonsmokers caused them either to progress towards smoking initiation or progress to regular smoking.
Overall, there is a clear link between depressed moods and adolescents who regularly smoke. However, further research is required to conclude which causes which.
Cigarette smoke components are known to have high toxicity. Persistent smoking leads to these components inducing oxidative stress, atherosclerosis, and inflammation of the human brain. This toxicity and its effects on the brain are unfavorable to cognitive functions like memory.
A study conducted by Jacobsen et al found that abstinence from smoking has adverse effects on working memory in smokers, especially adolescents. The findings indicated that termination of tobacco intake by adolescent smokers leads to an increase in tobacco craving, depressed mood (discussed above), and symptoms of nicotine withdrawal. Impairments were identified in the accuracy of the working memory performance in these adolescents. These findings were irrespective of the recency of smoking. Nonetheless, reduction in performance was found to be worse with earlier age of onset of smoking – male smokers with an earlier onset of smoking performed significantly worse than female smokers with a later onset of smoking.
During cessation, the interference of working and verbal memory in adolescent smokers was observed: the fMRI scans showed a failure to exhibit functional connectivity between the components of the working memory neurocircuit. This worsened as the working memory load increased, which led to more alterations in the coordination between these components, causing the failure of the functional connectivity.
All-inclusive, regular smoking causes brain damage that reduces working and verbal memory, worsening once adolescents stop smoking due to nicotine withdrawal. The findings are consistent with previous studies concluding that these neurotoxic effects due to exposure to nicotine are more serious when nicotine exposure takes place at earlier periods of growth and development, i.e., adolescence.
Research surrounding the prefrontal cortex in the brain has been a key area for collecting evidence on deteriorating neurocognition in adolescents due to smoking. Nicotine, in the prefrontal cortex, regulates and adjusts the processing of information. This is done by the activation and desensitization of nicotine receptors. It takes place on a large variety of cell types, hence affecting cognition.
UCLA researchers conducted a study to find the changes in the prefrontal cortex of adolescent smokers and nonsmokers. The results displayed a negative correlation between teen addiction to nicotine and the functionality of the prefrontal cortex. The greater the teen’s addiction to nicotine, the worse the functionality of the prefrontal cortex. The prefrontal cortex was less active in adolescent smokers suggesting that smoking affects brain function.
Increased nicotine consumption causes increased levels of nicotine dependency. This is because of the neurotoxic effects exerted by nicotine in the prefrontal cortex, which interfere with cognitive processes required for adolescent development like executive functioning and inhibitory control.
The adolescent phase is critical in the development of cognitive processes in the brain. Chronic smoking at this age has been found to not only damage the maturation of certain brain parts but also impair certain neurocognitive functions, which may persist into adulthood.
This paper discussed the impacts of active smoking on mood, attentional performance, executive functions like working and verbal memory, and functionality of the prefrontal cortex in adolescents. Valid and reliable studies back these discussions. But in a few studies, like that of Jacobsen et al’s, this reliability was questioned due to the small sample size used to form conclusions. Additionally, another drawback was the generalisability of the findings of many studies like the animal and twin studies. In most studies, only age, gender, and education were taken into consideration. The involvement of other factors like genetics and lifestyle could have led to more precise conclusions. However, due to limited research in this field, these studies are considered important in uncovering significant data.
Smoking has been found first to elevate but gradually worsen moods, sometimes leading to depression. However, this can differ from person to person depending on a range of factors like genetic predisposition, diet, and lifestyle. Reduced attention spans and weakened working and verbal memory were recorded in smokers. Lastly, the functionality of the prefrontal cortex is significantly reduced in smokers than that of nonsmoker adolescents.
The hazardous effects mentioned may be reduced, and some even reversed, if smoking among adolescents is stopped instantly. However, the motivation to stop may be missing due to psychosocial risk factors, including peer pressure, intrafamilial linkage, and perception of smoking. Seeking support from family, friends, and professionals could help terminate the addiction.
Further research that is more streamlined on factors associated with smoking such as genetics, diet, and lifestyle, and diagnosed mental health disorders could aid in determining the extent of neurocognitive damage in adolescents.
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About the Authors
She is a first-year IBDP student at Aditya Birla World Academy, Mumbai, India. Biology has always intrigued her, and she hopes to pursue it later on. She is a national-level swimmer and has always been committed to the sport. She is a determined and hard-working student.
She is a first year IBDP student at JBCN International, Mumbai, India. She is an avid Biology enthusiast, she wishes to pursue Biological sciences later on. She enjoys swimming, and it is something she does regularly to distress. She is a Trinity Grade 5 Piano player who wishes to perform live in front of a large audience in the near future. She is extremely committed to everything she learns!
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