5.4 Adolescence and brain maturation

Last updated April 2012 

The human brain does not reach full maturation until early adulthood, with significant changes to brain structure occurring during adolescence. This prolonged and complex developmental period results in a 'long window of vulnerability' (p 333 1) during adolescence.1 Initiation of substance use during this time is known to increase the risk of developing an addiction later in life; in addition, adolescence is typified by a tendency to engage in risk-taking behaviours, accompanied by a relatively high level of access to and experimentation with psychoactive substances.1 Adolescents are particularly susceptible to the effects of tobacco exposure,2 with evidence suggesting that adolescence marks a period of heightened biological sensitivity to the stimulatory and reinforcing properties of nicotine.3 Young smokers may rapidly become addicted to smoking, even at low levels of consumption,4,2 and at significantly lower nicotine levels than adults.5 For example, preliminary research among young people aged 13–17 years found that light smokers (1–5 cigarettes daily, mean duration of daily smoking 1.9 years) exhibited neural activation in response to smoking cues in brain regions important during the developing stages of addiction, areas similar to those observed in adult and teenage heavy smokers.5

Young people's tobacco use and nicotine addiction have both been classified as paediatric medical disorders, rather than for example attributing youth tobacco consumption to social habits or rebellious behaviour.6 This implies the need for a medical approach that acknowledges potential differences between diagnosis and treatment strategies for young people compared with adults, and adapts such strategies accordingly.6 However, there is a need for better understanding of how the effects of nicotine, including how nicotine dependence becomes established, interact with physiology and behaviour during child and adolescent development such that the young adult perceives substantial benefit and need from continued nicotine administration.6 Clinical assessment of individual risk of addiction, such as nicotine dependence, requires improved understanding and acknowledgement of the complex relationships between biological and environmental factors affecting neural development and subsequent behaviour.1

The adolescent neurophysiological response to nicotine is likely to be mediated by comparative brain immaturity.7,8,9 There is evidence that adolescent exposure to nicotine may trigger long-term changes in brain function relating to reward pathways, learning, memory and mood10 as well as a permanent susceptibility to nicotine addiction.11 Long-term changes in brain function associated with adolescent exposure to nicotine may also predispose the individual to later use of other addictive substances, and to mental illness.12 There is some evidence linking adolescent smoking with impaired affective decision-making (decision-making that requires appraisal of the emotional and motivational significance of stimuli i.e. their potential for rewards or punishments).13 Numerous studies have demonstrated that impaired decision-making is associated with the loss of control contributing to substance abuse.13

O'Dell14 proposes a neural framework to explain why adolescents are particularly likely to initiate tobacco use and are more vulnerable to long-term nicotine dependence. The model accounts for differences in experiences of the effects of nicotine between adolescents and adults (i.e. adolescents experience enhanced short-term positive and reduced aversive effects of nicotine, and fewer negative effects during nicotine withdrawal) through developmental differences within the mesolimbic pathway based on the established role of dopamine in addiction.14

Early experiences of the physiological response to inhaling nicotine might also be an important predictor of continued smoking behaviour. For example, individuals who experience strong aversion may follow a different trajectory in ongoing smoking behaviour from those for whom the first rush of nicotine provides a 'buzz' or a 'high'.15 It is also likely that the social context in which early experimentation occurs will influence an individual's perception of the experience.15 Adolescence coincides with a marked shift in emphasis of psychosocial influences, including increased awareness of peer structures and changes in schooling. These factors are discussed in Sections 5.8 and 5.9 respectively. For further discussion on nicotine, addiction and the adolescent brain, see Chapter 6, Section 7.

5.4.1 Onset of puberty

The onset of the physiological changes associated with puberty may be associated with increased experimentation with tobacco and other drugs, independent of age or education level of the individual.16 Recent research from the US has shown that adolescents who mature early are twice as likely to try cigarettes as those with an average age of physical maturity.17 A variety of reasons have been postulated for an association between earlier pubertal maturation and behaviours such as tobacco use, including that early-maturing girls may associate with older adolescents and copy their behaviour.18 Girls who are more physically mature and developed for their age might not have developed psychological maturity, thus lacking the cognitive skills to resist social pressures from peers;19 in addition, such behaviours may be perceived as more adult-like or acceptable in adolescents who appear more 'grown-up', such that early maturers may receive fewer deterring comments than other adolescents.20 Early-maturing girls also appear to be at greater risk for internalising and externalising behaviour problems, suggesting that tobacco use may be one of a group of unhealthy activities adopted as a means of mood regulation in stressful situations.20 Similarly, greater disruption of parent–child relationships has been associated with early development; for example, early-maturing girls appear to experience more parental conflict than other adolescents, which may subsequently reduce those factors that are typically protective against tobacco use and other psychosocial risks.20

In addition, findings from a longitudinal Canadian study (following over 8000 children for 10 years, from age 4–11 to 14–21) suggest that various aspects of low family socio-economic status (including father's employment status and education level) may act as a psychosocial stress for early pubertal maturation, which may lead to engagement in drinking and smoking at a younger age, at least for girls.21

Other research has suggested that drug use during puberty may also be mediated by the desire for sensation seeking, and that level of sensation seeking may be more closely related to an individual's pubertal stage than to chronological age. Degree of sensation seeking is linked with levels of sex steroids.22 The increase in sensation seeking and risk taking associated with puberty may come into play before those parts of the brain that weigh consequences and exert judgement reach maturity.12 However, social factors such as peer group smoking behaviours and attitudes, and parental17 and school connectedness, also mediate the effects of puberty.16,23

Recent news and research

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References

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2. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/2010/index.htm

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10. Slotkin T. Nicotine and the adolescent brain: insights from an animal model. Neurology and Teratology 2002;24:369-84. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12009492

11. Slotkin T, Ryde I, MacKillop E, Bodwell B and Seidler F. Adolescent nicotine administration changes the responses to nicotine given subsequently in adulthood: adenylyl cyclase cell signaling in brain regions during nicotine administration and withdrawal, and lasting effects. Brain Research Bulletin 2008;76:522-30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18534261

12. The National Centre on Addiction and Substance Abuse at Columbia University. Tobacco: the smoking gun. New York: CASA, prepared for The Citizens' Commission to Protect the Truth, 2007. Available from: http://www.casacolumbia.org/absolutenm/articlefiles/380-Tobacco-%20The%20Smoking%20Gun%20final.pdf

13. Xiao L, Bechara A, Cen S, Grenard JL, Stacy AW, Gallaher P, et al. Affective decision-making deficits, linked to a dysfunctional ventromedial prefrontal cortex, revealed in 10th-grade Chinese adolescent smokers. Nicotine & Tobacco Research 2008;10(6):1085–97. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18584472

14. O'Dell L. A psychobiological framework of the substrates that mediate nicotine use during adolescence. Neuropharmacology 2009; 56(suppl.1):263-78. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18723034

15. Turner L, Mermelstein R and Flay B. Individual and contextual influences on adolescent smoking. Annals of the New York Academy of Sciences 2004;1021:175–97. Available from: http://www3.interscience.wiley.com/journal/118766022/abstract

16. Patton G, McMorris B, Toumbourou J, Hemphill S, Donath S and Catalano R. Puberty and the onset of substance use and abuse. Pediatrics 2004;114:300-6. Available from: http://pediatrics.aappublications.org/cgi/reprint/114/3/e300.pdf

17. Westling E, Andrews J, Hampson S and Peterson M. Pubertal timing and substance use: the effects of gender, parental monitoring and deviant peers. Journal of Adolescent Health 2008;42:555-63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18486864

18. Jaszyna-Gasior M, Schroeder JR, Thorner ED, Heishman SJ, Collins CC, Lo S, et al. Age at menarche and weight concerns in relation to smoking trajectory and dependence among adolescent girls enrolled in a smoking cessation trial. Addictive Behaviors 2008;34(1):92–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18940275

19. Ge X, Conger RD and Elder Jr GH. Coming of age too early: pubertal influences on girls' vulnerability to psychological distress. Child Development 1996;67(6):3386-400. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9071784

20. Graber JA and Gunn JB. Developmental transitions: linking human development with tobacco prevention research. Nicotine & Tobacco Research 1999;1(suppl.1):S73-7. Available from: http://ntr.oxfordjournals.org/content/1/Suppl_1/S73.abstract

21. Arim R, Tramonte L, Shapka J, Susan Dahinten V and Douglas Willms J. The family antecedents and the subsequent outcomes of early puberty. Journal of Youth and Adolescence 2011;40(11):1423-35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21298330

22. Martin C, Kelly T, Rayens M, Brogli B, Brenzel A and Smith W. Sensation seeking, puberty, and nicotine, alcohol and marijuana use in adolescence. Journal of the American Academy of Child & Adolescent Psychiatry 2002;41:1495-502. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12447037

23. Marklein E, Negriff S and Dorn L. Pubertal timing, friend smoking, and substance use in adolescent girls. Prevention Science 2009;10(2):141–50. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19067163

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