Authors

  1. Snow, Diane PhD, RN, PMHNP-BC, FAANP, FIAAN

Article Content

Most e-cigarettes contain nicotine in various "doses," and the public health message is very clear: If you start using aerosol nicotine (vaping), you are at risk of developing an addiction to nicotine, a powerfully reinforcing drug. The neurobiological basis for nicotine addiction results from its reinforcing properties in the brain, mechanisms that produce cravings, and high levels of anxiety relieved only by using more nicotine. As with other addicting drugs, dopamine is released with every puff activating the mesolimbic dopamine reward system neurons. The brain learns, through repeated use, to seek nicotine to get the same "reward." Along with the dopamine reward mechanism, acetylcholine neuroreceptors get "hijacked" by nicotine, and the brain becomes controlled by them (Stahl, 2013).

  
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After only four puffs of a cigarette or e-cigarette, the nicotinic receptors are 95% full, yet most people smoke an entire cigarette or many more inhalations of an e-cigarette (Stahl, 2013). Flavors that are added to e-cigarettes make their use even more attractive and may increase the dopamine surge. Sweet flavors act in the brain's dopamine signaling mechanism to increase the amount of nicotine used (Wickham et al., 2018) when tested in rats. The Centers for Disease Control and Prevention (CDC) and Food and Drug Administration (FDA) found increasing use of flavored e-cigarettes in high school students in 2014-2018 and in middle school students in 2015-2018 when analyzing data from the 2014-2018 National Youth Tobacco Surveys (Cullen et al., 2019). FDA regulations and individual states' regulations must act to limit the flavor additives to e-cigarettes.

 

Nicotine by classification is a stimulant. It can boost energy and cause mild euphoria, and yet it can calm anxiety, curb hunger, and reduce pain. It is unique in its ability to react to the state of the individual. Nicotine withdrawal symptoms, as discovered in rat research, occur as a result of corticotropin-releasing factor activation (CRF-CRF1) in the central nucleus of the amygdala, creating a powerful stressor (anxiety) that is relieved by increasing amounts of self-administration of nicotine, making nicotine addiction very difficult to treat and abstinence difficult to sustain (George et al., 2007). The good news is that nonnicotine medications may help block the activation of the CRF-CRF1 system.

 

There are several reasons why nicotine is so reinforcing. Nicotine stimulates the release of dopamine in the nucleus accumbens, prefrontal cortex, amygdala, hippocampus, and other brain regions, "teaching" the brain to use nicotine (Volkow, 2018). The amount of dopamine released from one puff of a cigarette is less than those from other drugs, but the frequency of smoking and the activities carried out while smoking enhance the reward. "Smokers' brains have learned to smoke, and just like unlearning to ride a bike, it is incredibly hard to unlearn that simple, mildly rewarding behavior of lighting up a cigarette"(Volkow, 2018, p. 2).

 

The adolescent brain is under construction until around the age of 25 years and maybe even longer in some men. Dendrites are being pruned, and new synapses are being formed, preparing the brain for adulthood. Executive control, namely, good judgment, good decision making, organizing, and sequencing, is largely the work of the prefrontal cortex. If the adolescent brain is exposed to nicotine or other drugs of abuse, it is more likely to have poor cognitive control and be dominated by the limbic system's impulsive, emotional decision making. The younger the teen who starts using nicotine (in any form), the greater the chances of developing not only addiction but also long-term attentional and impulsive issues. Some states require e-cigarettes to be sold only in adult tobacco stores; however, the internet provides easy access to e-cigarettes in the United States.

 

There is controversy about whether nicotine is a gateway drug. Certainly, there are many individuals who smoke cigarettes or e-cigarettes who do not go on to use other drugs. However, the changes in the brain from nicotine prime the brain to use other substances such as cocaine. Nicotine's reward mechanism stimulates gene expression of FOSB, which teaches the brain to repeat the use of other drugs that are tried (Kandel & Kandel, 2014; Volkow, 2018). Nicotine also increases the enjoyment of other activities such as music and visual stimuli (Perkins et al., 2015). It is clear that the difficulties in quitting cigarettes and e-cigarettes are very challenging. Smoking only one cigarette or one e-cigarette can start the cycle of addiction that the brain knows so well.

 

Health care providers should be screening patients of all ages for nicotine use at each visit. Anyone using e-cigarettes should be assessed for the amount of nicotine they are using. This can be determined by the milligrams in each cartridge and the number of cartridges used daily. This should be documented at each visit. Initially, many patients will not know the exact amount used, but explaining the importance of documentation may motivate the patient to calculate and report their usage. Motivational interviewing should be used to assess the desire/plan to change their use patterns. Providing facts on the milligrams in e-cigarettes compared with a pack of cigarettes may help raise awareness of the severity of the problem. For example, the average pack of cigarettes is 20-21 mg of nicotine. The number of milligrams of nicotine in e-cigarettes can then be compared with the number of cigarettes. However, JUUL e-cigarettes have much higher nicotine concentrations. Patients may be shocked at their usage patterns. They can be encouraged to agree to a trial of abstinence if they are motivated to change. A decisional balance exercise can help the patient assess the pros and cons of continuing and the pros and cons of cutting down or stopping e-cigarettes. Follow-up appointments will address progress toward abstinence. Cues that trigger cravings, such as places, people, smells, music, dates, and times, should be identified and avoided early in recovery from nicotine addiction. Withdrawal symptoms should be discussed along with developing a plan that includes strategies to choose when times are especially difficult. Educating the patient on the length of withdrawal and what physical symptoms to expect may help, with days 3-5 being the hardest. Ideally, heavy e-cigarette users will choose a slow taper with a planned stop date; others will choose a stop date with no taper. The goal is total abstinence, which will require support and recognition of successful completion as well as frequent monitoring for relapse prevention.

 

REFERENCES

 

Cullen K. A., Liu S. T., Bernat J. K., Slavit W. I., Tynan M. A., King B. A., & Neff L. J. (2019). Flavored tobacco product use among middle and high school students-United States, 2014-2018. Morbidity and Mortality Weekly Report, 68(39), 839-844. https://dx.doi.org/10.15585/mmwr.mm6839a2[Context Link]

 

George O., Ghozland S., Asar M. R., Cottone P., Zorrilla E. P., Parsons L. H., O'Dell L. E., Richardson H. N., & Koob G. F. (2007). CRF-CRF1 system activation mediates withdrawal-induced increases in nicotine self-administration in nicotine-dependent rats. Proceedings of the National Academies of Science, 104(43), 17198-17203. [Context Link]

 

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Perkins K. A., Karelitz J. L., & Michael V. C. (2015). Reinforcing enhancing effects of acute nicotine via electronic cigarettes. Drug and Alcohol Dependence, 153(1), 104-. https://doi.org/10.1016/j.drugalcdep.2015.05.041[Context Link]

 

Stahl S. M. (2013). Stahl's essential psychopharmacology (4th ed). New York: Cambridge University Press. [Context Link]

 

Volkow N. (2018). Recent research sheds light on why nicotine is so addictive. https://blogs.scientificamerican.com/observations/recent-research-sheds-new-ligh[Context Link]

 

Wickham R. J., Nunes E. J., & Addy N. A. (2018). Evaluating oral flavorant effects on nicotine self-administration behavior and phasic dopamine signaling. Neuropharmacology, 128, 33-42. doi.org/10.1016/j.neuropharm.2017.09.029 [Context Link]