Social learning theory was built upon by Akers (1973) to explain ‘deviant and conforming behaviour’ under which smoking would lie. This theory is drawn upon by Akers et al. (1979), where four key mechanisms are described. 

The mechanisms are:

-       Differential association = direct and indirect interaction with others 

-       Differential reinforcement = instrumental learning through rewards and punishers. ‘Social’ and ‘non-social’

-       Imitation = observational learning 

-       Cognitive definitions = attitudes 

Using the mechanisms described, increased chances of an adolescent smoking should occur if the person associates themself with others who smoke, and expects more positive than negative reactions from others, The others who smoke, in this scenario, act as the aforementioned models on which the adolescent can model their own behaviour. So with deviant others, (those who smoke) the adolescent can expect positive reinforcement from smoking in the form of positive attitudes, leading to their own imitation. 

 

Akers and Lee (1996) tested the previously constructed mechanisms over 5 years in a longitudinal study which supported the social learning theory as an explanation for smoking behaviour. A 3-year longitudinal study (Krohn et al., 1985) also confirmed this. This would indicate that the social learning theory can be used as an explanation as to the learnt behaviour of smoking.

 

Akers and Lee also identified primary and secondary social learning factors that influence smoking behaviour: primary are parents and peers, secondary are the media. Furthermore, they described a strong correlation between other drug use and smoking.

Akers, R. L., Krohn, M. D., Lanza-Kaduce, L., & Radosevich, M. (1979). Social Learning and Deviant Behavior: A Specific Test of a General Theory. American Sociological Review, 44(4), 636. https://doi.org/10.2307/2094592

Akers, R. L., & Lee, G. (1996). A Longitudinal Test of Social Learning Theory: Adolescent Smoking. Journal of Drug Issues, 26(2), 317–343. https://doi.org/10.1177/002204269602600203

Bandura, A. (1977). Social learning theory. Englewood Cliffs, N.J. Prentice-Hall.

Krohn, M. D., Skinner, W. F., Massey, J. L., & Akers, R. L. (1985). Social Learning Theory and Adolescent Cigarette Smoking: A Longitudinal Study. Social Problems, 32(5), 455–473. https://doi.org/10.2307/800775

·       Social environment very important in adolescent attitudes towards smoking – family and peers

·       Social environment much more important than personal characteristics in taking up smoking.

·       Being in presence of smoking important

·       Study suggests observation of smoking more important than adopting friends’ behaviour (slt over social influence

Vitória, P. D., Salgueiro, M. F., Silva, S. A., & de Vries, H. (2011). Social influence, intention to smoke, and adolescent smoking behaviour longitudinal relations. British journal of health psychology, 16(4), 779-798.

·       Social influence has an effect on intention to smoke (smaller than behaviour)

o   Parents subjective norms, peers descriptive norms

·       Social influence has an effect on smoking behaviour

o   Parents subjective and descriptive norms, peers descriptive norms

o   Also self-efficacy mediator as well as intention

·       Social influence has both direct and indirect effects on smoking

·       Descriptive behaviour, subjective intention

·       Subjective norms: how you believe others want you to act

·       Descriptive norms: how you see others act

 

Fauzan, & Firman, Firman & Daharnis, Daharnis. (2018). Relationship between self-control 

and peer conformity with smoking behavior. 

 

·       Peer conformity high in adolescents in regard to smoking due even if they didn’t want to smoke (don’t want to go against the group)

·       Peer conformity and self-control both influence whether students will smoke.

Harakeh, Z., & Vollebergh, W. A. (2012). The impact of active and passive peer influence on young adult smoking: An experimental study. Drug and alcohol dependence, 121(3), 220-223.

·       Masked study asking young adults about music taste preference but actually testing passive and active influences in peer pressure to smoke

·       Peer smoking increased likelihood to smoke but not peer pressure. Passive influence rather than active influence (more likely to smoke if confederate was smoking opposed to being offered a cigarette)

o   Less explicitly encouraged to behave a way

o   Potentially nsi (asch) of seeing other smoke, or imitation.

o   Cue-reactivity paradigm: exposure to smoking cues increase craving

Carter, B. L., Robinson, J. D., Lam, C. Y., Wetter, D. W., Tsan, J. Y., Day, S. X., & Cinciripini, P. M. (2006). A psychometric evaluation of cigarette stimuli used in a cue reactivity study. Nicotine & Tobacco Research, 8(3), 361-369.

·       Supports cue reactivity paradigm for cravings to smoke

o   Showing images of smoking to smokers.

Moran, S., Wechsler, H., & Rigotti, N. A. (2004). Social smoking among US college students. Pediatrics, 114(4), 1028-1034.

·       Study of US college students found a large proportion are social smokers

·       Do so to gain peer acceptance, don’t perceive themselves as having addiction 

Leshargie, C. T., Alebel, A., Kibret, G. D., Birhanu, M. Y., Mulugeta, H., Malloy, P., ... & Arora, A. (2019). The impact of peer pressure on cigarette smoking among high school and university students in Ethiopia: A systemic review and meta-analysis. PLoS One, 14(10), e0222572.

·       Meta analysis of 19 studies of students in Ethiopia showed peer pressure had a significant influence on smoking.

Nicotine entering your body through cigarettes activates nicotinic acetylcholine receptors (nAChRs; Dani & Heinemann, 1996). When activated, these receptors release dopamine (a chemical for feeling pleasure). Therefore, dopamine, specifically midbrain dopamine, neurons are a major role in nicotine addiction and the behaviours following it (Faure et al., 2014). Over time, the brain develops more nicotine receptors. Active nicotine-addicted smokers have billions more receptors than non-smokers (Olincy et al., 1997); however, not all smokers have high levels of these receptors, meaning they can quit smoking without difficulty (Benowitz, 1992; 2008). 

When trying to quit, the receptors do not receive nicotine, so your brain stimulates no pleasure. Unfortunately, most addicts fall into nicotine withdrawal due to their receptors failing to receive nicotine (McLaughlin et al., 2015). Symptoms of withdrawal include anxiety, jumpiness, irritability, upset, strong cravings / urges to smoke, difficulty concentrating, depression difficulty sleeping and increased hunger (Centers for Disease Control and Prevention, 2023). Ultimately, the quickest way to stop the symptoms is by smoking a cigarette (releases dopamine, which resumes the pleasure response). 

Even after the person is no longer a smoker for a few months or even years, brain receptors are conditioned to expect nicotine in certain situations after smoking has been stopped (Benowitz, 2008); in these circumstances, the dead nicotine receptors in the brain anticipate a rush of dopamine, and these can briefly resume strong withdrawal symptoms. However, with time the brain will return to the normal number of nACh (nicotine) receptors (Marks et al., 1985), meaning that the symptoms will eventually disappear (Toll et al., 2007).

Benowitz, N. L. (2008). Neurobiology of nicotine addiction: implications for smoking cessation treatment. The American journal of medicine, 121(4), S3-S10. https://doi.org/10.1016/j.amjmed.2008.01.015

Benowitz, N. L. (2009). Pharmacology of nicotine: addiction, smoking-induced disease, and therapeutics. Annual review of pharmacology and toxicology, 49, 57-71. https://doi.org/10.1146/annurev.pharmtox.48.113006.094742 

Centers for Disease Control and Prevention. (2023, February). Tips for Former Smokers. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention. https://www.cdc.gov/tobacco/campaign/tips/quit-smoking/7-common-withdrawal-symptoms/index.html

Dani, J. A., & Heinemann, S. (1996). Molecular and cellular aspects of nicotine abuse. Neuron, 16(5), 905-908. https://doi.org/10.1016/S0896-6273(00)80112-9 

Faure, P., Tolu, S., Valverde, S., & Naudé, J. (2014). Role of nicotinic acetylcholine receptors in regulating dopamine neuron activity. Neuroscience, 282, 86-100. https://doi.org/10.1016/j.neuroscience.2014.05.040 

Marks, M. J., Stitzel, J. A., & Collins, A. C. (1985). Time course study of the effects of chronic nicotine infusion on drug response and brain receptors. Journal of Pharmacology and Experimental Therapeutics, 235(3), 619-628. 

McLaughlin, I., Dani, J. A., & De Biasi, M. (2015). Nicotine withdrawal. The Neuropharmacology of Nicotine Dependence, 99-123. https://doi.org/10.1007/978-3-319-13482-6_4 

Olincy, A., Young, D. A., & Freedman, R. (1997). Increased levels of the nicotine metabolite cotinine in schizophrenic smokers compared to other smokers. Biological psychiatry, 42(1), 1-5. https://doi.org/10.1016/S0006-3223(96)00302-2 

Toll, B. A., O'Malley, S. S., McKee, S. A., Salovey, P., & Krishnan-Sarin, S. (2007). Confirmatory factor analysis of the Minnesota nicotine withdrawal scale. Psychology of addictive behaviors, 21(2), 216. https://doi.org/10.1037/0893-164X.21.2.216

An Individuals genetic makeup can play a part in making an individual more vulnerable to a nicotine addiction.

 

Different DNA variants:

- Gene CHRNA5 variation can double the likelihood of developing a nicotine dependence. Variants within this gene can soften nicotine’s negative effects making the individual more likely to continue smoking. (Fowler & Kenny, 2014)

- The genotype CYP2A6 is the primary catalyst of nicotine metabolism. Individuals' metabolism plays a role in smoking addiction as individuals with slower metabolisms require fewer cigarettes and therefore find quitting smoking easier than those with fast metabolisms to nicotine who suffer more severe withdrawal symptoms. (Bloom et al., 2011)

- DNA variant located in the DNMT3B gene. Creating a risk factor for heavy smoking as well as a nicotine dependence. A study of 38,000 current and former smokers from the US, Iceland, Finland, and the Netherlands found that this variant occurs in 44% of Europeans/European Americans and 77% of African Americans. (RTI International, 2017)  

 

Nicotine stimulates mesolimbic dopamine release. Dopamine Receptor genes can significantly influence smoking behaviour via genetic variations of certain dopamine receptors.

-         DRD1, DRD2 and DRD3 all have polymorphisms associated with nicotine dependence.

- Polymorphisms are defined as the “presence of 2 or more variant forms of a specific DNA sequence that can occur among different individuals or population” (National Human Genome Research Institute, 2019).

-         DRD1, DRD2, and DRD3 alter the dopaminergic response to nicotine, which contributes to smoking behaviour. As found in a study of 476 Malaysian men aged 18-50. (Ruzilawati et al., 2020)

 

Finding out how much of a role genetics have in smoking can be tested via twin studies, comparing environmental factors to genetics.

Twin Studies examples:

- In a large-scale Dutch Twin Study of 2621 twin pairs aged 12-25. Factors influencing the initiation of smoking between adolescents and young adults varied substantially. Initiation for 12–16-year-olds was mainly influenced by the same environmental factors whilst for young adults the association was down to the same genetic risk factors. (Koopmans et al., 1997)

- A Virginia Twin Study of 2804 twins aged 12-32 tested for the strength between initiation of smoking and current quantity of smoking and found that genetic factors did not come into significant play until young adulthood (ages 22-32). Suggesting as access to cigarettes become easier the genetic predispositions towards increased smoking and addiction potentially increase after initiation. (Do et al., 2015)

 

Fowler, C. D., & Kenny, P. J. (2014). Nicotine aversion: Neurobiological mechanisms and relevance to tobacco dependence vulnerability. Neuropharmacology, 76 Pt B(0 0), 533–544. https://doi.org/10.1016/j.neuropharm.2013.09.008

 

 Bloom, J., Hinrichs, A. L., Wang, J. C., von Weymarn, L. B., Kharasch, E. D., Bierut, L. J., Goate, A., & Murphy, S. E. (2011). The contribution of common CYP2A6 alleles to variation in nicotine metabolism among European–Americans. Pharmacogenetics and Genomics, 21(7), 403–416. https://doi.org/10.1097/fpc.0b013e328346e8c0 

 

 Koopmans, J. R., van Doornen, L. J. P., & Boomsma, D. I. (1997). Association between Alcohol Use and Smoking in Adolescent and Young Adult Twins: A Bivariate Genetic Analysis. Alcoholism: Clinical and Experimental Research, 21(3), 537–546. https://doi.org/10.1111/j.1530-0277.1997.tb03800.x 

 

 Do, E. K., Prom-Wormley, E. C., Eaves, L. J., Silberg, J. L., Miles, D. R., & Maes, H. H. (2015). Genetic and Environmental Influences on Smoking Behavior across Adolescence and Young Adulthood in the Virginia Twin Study of Adolescent Behavioral Development and the Transitions to Substance Abuse Follow-Up. Twin Research and Human Genetics, 18(1), 43–51. https://doi.org/10.1017/thg.2014.78 

 

RTI International. (2017, October 10). Gene that influences nicotine dependence identified: Discovery creates the possibility for new research in addiction treatment. ScienceDaily. Retrieved March 5, 2023 from www.sciencedaily.com/releases/2017/10/171010124112.htm

 

 Ruzilawati, A. B., Islam, M. A., Muhamed, S. K. S., & Ahmad, I. (2020). Smoking Genes: A Case–Control Study of Dopamine Transporter Gene (SLC6A3) and Dopamine Receptor Genes (DRD1, DRD2 and DRD3) Polymorphisms and Smoking Behaviour in a Malay Male Cohort. Biomolecules, 10(12), 1633. https://doi.org/10.3390/biom10121633 

 

National Human Genome Research Institute. (2019). Polymorphism. Genome.gov. https://www.genome.gov/genetics-glossary/Polymorphism