E-cigarette and Cognition


E-cigaretteand Cognition

E-cigaretteand Cognition

Tobaccohas been one of the most abused drugs not only in the contemporarybut also in the traditional human society. Research and statistics in2012 showed that about 16 percent of adults in the United Kingdom or10 million people currently smoke cigarettes. Out of these people,about 68% were daily smokers, while the remaining 22% smoke in somedays (Levin &amp Rezvani, 2000). Of course, there are variations inthe rates of smoking across the genders and individuals in differentsocial statuses. Indeed, research showed that the rates of smokingwere considerably higher among poor people, where 33% of individualsin manual and routine occupations smoked while only 14% of people inprofessional and managerial positions did the same. Further, theprevalence of smoking among men is highest at 32% in the 25-34 agegroup, while the same is at 29% in the 20-24 year age group. Nevertheless, it has well been acknowledged that the use of tobaccois the single largest cause of preventable diseases and death in theUnited Kingdom. Indeed, tobacco kills over 124,000 Americans everyyear, 22,000 of which result from exposure to second-hand smoke(Centers for Disease Control and Prevention, 2014). Scholars havetried to comprehend smoking habit in the wider social-culturalcontext and stated that the wider cultural context would beinfluential in determining or shaping smoking, either as an isolatedactivity at home or as a social activity in the case of individualswhose chances of smoking in private are restricted by the disapprovalof their loved ones. In such contexts, social smokers would beconsiderably constrained, which would reduce their smokingtendencies.

Thesedevastating effects of tobacco smoking resulted in a need to reinventthe smoking so as to make it safer and reduce the devastatingeffects. This is what gave rise to e-cigarettes, which are in factvaporizers that incorporate a mechanism that heats up a liquid ratherthan the traditional burning of tobacco (Balfour, 2009). They arebattery-operated devices that are designed to provide nicotine withflavorings, alongside other chemicals in vapor rather than smoke.This liquid would then become vapor, which would then be inhaled(Hukkanen et al, 2005). Questions have been asked regarding the truthin the notion that e-cigarettes are advantageous to the smokers orrather that they do not have similarly devastating effects. This isespecially with regard to their effects on cognitive (memory)functioning of an individual (Gudehithlu et al, 2012).

E-cigarettesare made in such a way that they would stimulate tobacco smokingthrough the production of an appealingly-flavored aerosol that hasthe look and feel of tobacco smoke, while delivering nicotine withlower amounts of toxic chemicals than those produced through theburning of tobacco leaves (Dubuc, 2013). Since the nicotine isdelivered without the burning of tobacco, e-cigarettes are seen assafer and less toxic.

However,as much as they do not generate tobacco smoke, e-cigarettes stillincorporate nicotine, as well as other potentially harmful chemicals.The effects of nicotine on the functioning of the brain have alwaysbeen in question (Benowitz et al, 2009). Nevertheless, studies haveshown that nicotine would improve the memory and cognitive capacityof an individual. The brain incorporates neurons that assist in thetransfer and integration of information. As much as signals arecarried out via neurons, the actual relaying of the messages fromneurons to other cells is carried out by neurotransmitters (Soderpalmet al, 2000). Nicotine is known to imitate neurotransmitteracetylcholine, binds itself to the receptors. However, the body doesnot regulate nicotine unlike the case of acetylcholine. Researchersnote that nicotine would stimulate cholinergic neurons in numerousvaried regions across the brain at the same time, unlike neuronswhich release minute amounts of acetylcholine in controlled amounts(Kapoor &amp Jones, 2005). On the same note, nicotine is known tostimulate or activate the release of glutamate, a neurotransmitterthat plays a fundamental role in memory and learning, while alsoimproving the connections or links between the varied sets of neurons(Tariot et al, 2000). The enhanced connections are thought to be thephysical foundation of what is known as memory, in which case the useof glutamate may generate a memory loop of desirable feelings.

Onthe same note, nicotine is known to enhance other chemicals andneurotransmitters levels that regulate the functioning of the brain(Graham, 2007). As a result of the unregulated disruption andstimulation, the body would increase the release of acetylcholineresulting in increased activity in the brain’s cholinergic pathways(Centers for Disease Control and Prevention, 2010). This is whatwould stimulate the brain and body to action, making the individualfeel re-energized (Graham, 2007).

Asmuch as this information may assist in the examination of the effectsof e-cigarettes, it is worth noting that the composition of chemicalsin these devices is always varying. Indeed, there are varied brandsof e-cigarettes, each of which have distinctive characteristics(Charlton, 2004). The effects of nicotine on the brain may be partlydefined, but little is known on the effects of e-cigarettes as awhole. Indeed, there are questions on whether the effects wouldchange with varying levels of nicotine in the e-cigarettes or varyingcompositions of the same (Tizabi et al, 2002). What would be theduration of these effects? Such information would be crucial tovaried stakeholders including the smokers themselves, as well aspolicymakers. Indeed, there have been concerns that e-cigarettes willbe illegalized in the near future (Dugdale, 2012). Such informationwould be crucial to informing the basis for the enactment or evenrepelling of such legislations. This study would be based on thehypothesis that while e-cigarettes may enhance the functioning andcognitive capabilities of an individual, the long-term effects wouldinvolve a reduction in the cognitive and memory capabilities.


Balfour,DJ. (2009) &quotThe Neurobiology of Tobacco Dependence: aPreclinical Perspective on the Role of the Dopamine Projections tothe Nucleus Accumbens [corrected].&quot Nicotine&amp Tobacco Research.Vol. 6, no. 6. Pages 899-912.

Benowitz,N. L., Hukkanen, J &amp Peyton, J (2009). &quotNicotineChemistry, Metabolism, Kinetics and Biomarkers.&quotHandbook of Experimental Pharmacology. Vol. 192. Pages 29-60.

Centersfor Disease Control and Prevention (2014).&nbspCurrent CigaretteSmoking Among Adults—United States, 2005–2012. Morbidityand Mortality Weekly Report.Vol. 63(02):29–34

Centersfor Disease Control and Prevention (2010).&nbspVital Signs:Nonsmokers` Exposure to Secondhand Smoke—United States, 1999–2008.Morbidityand Mortality Weekly Report.Vol. 59(35):1141–6&nbsp

Charlton,A (2004). &quotMedicinal uses of tobacco in history.&quot Journalof the Royal Society of Medicine. Vol. 97, no. 6. Pages 292-296.

Dubuc,B (2013). &quotHowdrugs affect neurotransmitters.&quotThe Brain from Top to Bottom.

Dugdale.D. C. (2012).&quotNicotine and tobacco.&quot U.S.National Library of Medicine.

Graham,M (2007). &quotResearchers Light Up for Nicotine, the Wonder Drug.&quotWired.

Gudehithlu,KP Duchemin AM Tejwani GA Neff, NH &amp M Hadjiconstantinou(2012). &quotNicotine-induced changes of brain B-endorphin.&quotNeuropeptides. Vol. 46, no. 3. Pages 125-131.

Hukkanen,J., Pleyton III, Jacob &amp Neal L. Benowitz (2005). &quotMetabolismand Disposition Kinetics of Nicotine.&quot Pharmacological reviews.Vol. 27, no. 1. Pages 79-115.

Kapoor,D, &amp Jones, T.H (2005). &quotSmoking and hormones in health andendocrine disorders.&quot EuropeanJournal of Endocrinology.Vol. 152. Pages 491-499.

Levin,E.D. &amp Rezvani, A.H (2000).&nbspDevelopmentof nicotinic drug therapy for cognitive disorders.&nbspEurJ Pharmacol.Vol.&nbsp393:&nbsp141–146

Soderpalm,B. Ericson, M. Olausson, P (2000). Nicotinic mechanisms involved inthe dopamine activating and reinforcing properties of ethanol.Behaviorand Brain Research113:85–96

Tariot,P.N., Solomon, P.R., Morris, J.C., Kershaw, P., Lilienfeld, S., &ampDing, C (2000).&nbspA5-month, randomized, placebo-controlled trial of galantamine in AD.The Galantamine USA-10 Study Group.&nbspNeurology.Vol.&nbsp54:&nbsp2269–2276

Tizabi,Y. Copeland, R.L., Jr. Louis, V.A. &amp Taylor, R.E (2002).Effects of combined systemic alcohol and central nicotineadministration into ventral tegmental area on dopamine release in thenucleus accumbens. Alcoholism:Clinical and Experimental Research26:394–399